Aim: The aim of this study was to determine the treatments and their outcomes in horses with colic in Nairobi County, Kenya.
Materials and Methods: This is a retrospective study to determine the occurrence, treatments, pain management, and outcomes of colic in horses in Nairobi County. Association between pain management protocols and the outcomes of colic with regard to recovery or death was also determined. Data collected from four equine practitioners were organized manually and given numerical codes as appropriate to facilitate entry into the computer. The coded data were entered into Microsoft Excel 2010 and exported to StatPlus pro 5.9. 8 statistical package for analysis. Simple association tests were done between various factors and occurrence of colic.
Results: The incidence of colic for the 11 years was 3.1%, which constituted 68.0% spasmodic colic, 27.8% impaction colic, and 4.2% displacement …

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Major losses in sheep and goats have been incurred from Peste des petit ruminants (PPR), a relatively new disease in East Africa. It first appeared in Eastern Uganda but has since spread to most of Kenya and Northern Tanzania. Small ruminants are the source of income for most pastoralists in East Africa. In this study the epidemiology of PPR including risk factors, prevalence, and socio-economic effects will be analyzed using participatory tools in Turkana, Kenya and Longido in Tanzania.

North Eastern Province, camel is the dominant livestock; it provides subsistence to many people especially during the frequent droughts when other animals either die or are unthrifty. This is beca use camel is highly suited for hot environments. In this region, camels number approximately 3 million and are the main producers of milk for the residents, who are mainly of Somali origin, and are pastoralists. Currentl y, the milk is also sold in Nairobi and other far places; and there is a fast growing demand for it. This has necessitated examination of the milk quality, in response to food safety awareness, especially noting that some of the bacteria causing subclinical mastitis can cause disease in humans. This study was carried out to establish the hygienic quality of camel milk from this area, zeroing down to 2 districts, Garissa and Wajir. T hree hundred and eighty four bulk camel milk samples were collected in volumes of 200 to 300 ml. They wer e transport ed to the laboratory in cold/ice boxes and bacterial isolation and characterization done not later than 24 h after arrival at the laboratory. Before culturing, the milk samples were screened using Ca lifornia Mastitis Test (CMT); samples testing positive (a n indication of subclinical mastitis) were then subjected to bacteriological investigation, using standard methods. Results of this study have shown that subclin ical mastitis is prevalent in dromedary camels of Garissa and Wajir districts of North Eastern province of Kenya, and that Gram positive cocci ( Staphylococcus and Streptococcus) are the dominant mastitis pathogens isolated. Other isolated bacteria included Klebsiella/Enterobacter, E scherichia coli and Bacillus. The positive correlation of CMT with the presen ce of mastitis pathogens in camel milk showed that CMT is a useful screening test in the detection of subclinical mastitis in camels; it is thus a useful tool for farm ers, aiding them in picking the affected animals, segregating and treating them. The resu lts also contribute towards coming up with respective control measures so as to keep camel milk fresh for longer periods and als o make it safe for human consumption.

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Interleukin-18 (IL-18) plays an important role in innate and acquired immunity, in particular against intracellular pathogens. However, little is known about the microbial factors that trigger IL-18 secretion by dendritic cells (DCs). To determine the influence of bacterial virulence factors on the activation and release of IL-18, we infected human monocyte-derived DCs with virulence mutants of the facultative intracellular pathogen Salmonella typhimurium. Our results show that infection by S. typhimurium causes caspase-1-dependent activation of IL-18 and triggers the release of IL-18 in human DCs. The secretion of IL-18 by the DCs was closely correlated with the ability of the S. typhimurium strains to induce apoptosis. We demonstrate that activation and release of IL-18 are blocked by mutations in the Salmonella sipB gene, which encodes a virulence factor that activates caspase-1 to induce apoptosis. These findings indicate that the activation and release of IL-18 induced by bacterial virulence factors may represent one component of innate immunity against the intracellular bacteria.

Salmonella typhimurium (ST) can cause infection in man, and attenuated strains are under consideration as live vaccine vectors. However, little is known about the interaction of ST with human dendritic cells (DC). Here, we compared the consequences of exposure of human, monocyte-derived DC with different attenuated strains of ST. Infection was observed with all four strains tested (wild type, PhoP-, PhoPc, and AroA), but the PhoPc strain was by far the most efficient. Intracellular persistence of wild type and PhoP- was longer than that of PhoPc and AroA, both of which were largely eliminated within 24 h. Most DC survived infection by the attenuated strains, although apoptosis was observed in a fraction of the exposed cells. All strains induced DC maturation, independent from the extent of infection. Although all strains stimulated secretion of TNF-alpha and IL-12 strongly, PhoPc induced significantly less IL-10 than the other three strains and as much as 10 times less IL-10 than heat-killed PhoPc, suggesting that this mutant suppressed the secretion of IL-10 by the DC. These data indicate that infectivity, bacterial elimination, and cytokine secretion in human DC are controlled by the genetic background of ST.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Street food play a significant role in feeding urban population with cheap accessible and nutritious foods. Most street foods vendors are not trained on food hygiene and safety........

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

The pecten oculi is a structure peculiar to the avian eye. Three morphological types of pecten oculi are recognized: conical type, vaned type and pleated type. The pleated type has been well studied. However, there exists only scanty data on the morphology of the latter two types of pectens. The structure of the vaned type of pecten of the ostrich, Struthio camelus was investigated with light and electron microscope. The pecten of this species consists of a vertical primary lamella that arises from the optic disc and supports 16-19 laterally located secondary lamellae, which run from the base and confluence at the apex. Some of the secondary lamellae give rise to 2 or 3 tertiary lamellae. The lamellae provide a wide surface, which supports 2-3 Layers of blood capillaries. Pigmentation is highest at the distal ends of the secondary and tertiary Lamella where blood capillaries are concentrated and very scanty on the primary and the proximal ends of the secondary lamella where the presence of capillaries is much reduced. In contrast to the capillaries of the pleated pecten, the endothelium of the capillaries in the pecten of the ostrich exhibits very few microvilli. These observations suggest that the morphology of the pecten of the ostrich, a flightless ratite bird is unique to the pleated pecten and is designed to meet the balance between optimal vision and large surface area for blood supply and yet ensuring it is kept firmly erect within the vitreous

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

A novel triple co-culture model of the human airway barrier was designed to simulate the cellular part of the air-blood barrier of the respiratory tract represented by macrophages, epithelial cells, and dendritic cells. When epithelial cells (A549 cells) were grown on filter inserts with pores of 3.0 mum in diameter in a two-chamber system, they formed monolayers with polarization into apical and basolateral domains. The epithelial cell cultures were then supplemented with human blood monocyte-derived macrophages and dendritic cells on the apical and basal aspect, respectively. The single-cell cultures as well as the triple co-cultures were characterized in terms of a number of typical features, for example, morphology of cell types, integrity of epithelial layer, and expression of specific cell surface markers (CD14 for macrophages and CD86 for dendritic cells). The interplay of epithelial cells with macrophages and dendritic cells during the uptake of polystyrene particles (1 mum in diameter) was investigated with confocal laser scanning and conventional transmission electron microscopy. Particles were found in all three cell types, although dendritic cells were not directly exposed to the particles. More investigations are needed to understand the translocation pathway.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells (DCs) can release microvesicles, but the latter's numbers, size, and fate are unclear. Fluorescently labeled DCs were visualized by laser-scanning microscopy. Using a Surpass algorithm, we were able to identify and quantify per cell several hundred microvesicles released from the surface of stimulated DCs. We show that most of these microvesicles are not of endocytic origin but result from budding of the plasma membrane, hence their name, exovesicle. Using a double vital staining, we show that exovesicles isolated from activated DCs can fuse with the membrane of resting DCs, thereby allowing them to present alloantigens to lymphocytes. We concluded that, within a few hours from their release, exovesicles may amplify local or distant adaptive immunological response.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Interleukin-18 (IL-18) plays an important role in innate and acquired immunity, in particular against intracellular pathogens. However, little is known about the microbial factors that trigger IL-18 secretion by dendritic cells (DCs). To determine the influence of bacterial virulence factors on the activation and release of IL-18, we infected human monocyte-derived DCs with virulence mutants of the facultative intracellular pathogen Salmonella typhimurium. Our results show that infection by S. typhimurium causes caspase-1-dependent activation of IL-18 and triggers the release of IL-18 in human DCs. The secretion of IL-18 by the DCs was closely correlated with the ability of the S. typhimurium strains to induce apoptosis. We demonstrate that activation and release of IL-18 are blocked by mutations in the Salmonella sipB gene, which encodes a virulence factor that activates caspase-1 to induce apoptosis. These findings indicate that the activation and release of IL-18 induced by bacterial virulence factors may represent one component of innate immunity against the intracellular bacteria.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

In structure-function relationship studies, stereological methods are applied to quantify structural qualities under investigation. In certain organs, like the brain, it is important to count the number of neurons associated with a particular function or region. The count gives an estimate of the electronic units available for a specific task or are endowed with a quantum of electrical energy. Similar studies can be extended in organs like the kidney, glands and muscles. Therefore, stereological methods enhance our knowledge of optimization of structure to funtion in biological design. This paper expounds on the methods used in estimation of number of particles in three-dimensional space. It articulates a historical perspective of the development of particle counting techniques to date in stereology showing how the problem was solved and a sound, practical and unbiased method developed. Two approaches are applied in counting particle number. The model based and the design based approach. The model-based approach assumes that the components under investigation are regular geometrical structures whose parameters can be quantified using regular geometrical methods. This counting method is biased, inefficient and difficult to apply in biological tissues. The design based approach applies a three dimensional sampling probe, the disector and makes no assumptions about shape or size of the components under investigation as in model approach.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Live attenuated Salmonella are attractive vaccine candidates for mucosal application because they induce both mucosal immune responses and systematic immune responses. After breaking the epithelium barrier, Salmonella typhimurium is found within dendritic cells (DC) in the Peyer's patches. Although there are abundant data on the interaction of S. typhimurium with murine epithelial cells, macrophages and DC, little is known about its interaction with human DC. Live attenuated S. typhimurium have recently been shown to efficiently infect human DC in vitro and induce production of cytokines. In this study, we have analysed the morphological consequences of infection of human DC by the attenuated S. typhimurium mutant strains designated PhoPc, AroA and SipB and the wild-type strains of the American Type Culture Collection (Manassas, VA, USA), ATCC 14028 and ATCC C53, by electron microscopy at 30 min, 3 h and 24 h after exposure. Our results show that genetic background of the strains profoundly influence DC morphology following infection. The changes included (i) membrane ruffling; (ii) formation of tight or spacious phagosomes; (iii) apoptosis; and (iv) spherical, pedunculated membrane-bound microvesicles that project from the plasma membrane. Despite the fact that membrane ruffling was much more pronounced with the two virulent strains, all mutants were taken up by the DC. The microvesicles were induced by all the attenuated strains, including SipB, which did not induce apoptosis in the host cell. These results suggest that Salmonella is internalized by human DC, inducing morphological changes in the DC that could explain immunogenicity of the attenuated strains.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Interleukin-18 (IL-18) plays an important role in innate and acquired immunity, in particular against intracellular pathogens. However, little is known about the microbial factors that trigger IL-18 secretion by dendritic cells (DCs). To determine the influence of bacterial virulence factors on the activation and release of IL-18, we infected human monocyte-derived DCs with virulence mutants of the facultative intracellular pathogen Salmonella typhimurium. Our results show that infection by S. typhimurium causes caspase-1-dependent activation of IL-18 and triggers the release of IL-18 in human DCs. The secretion of IL-18 by the DCs was closely correlated with the ability of the S. typhimurium strains to induce apoptosis. We demonstrate that activation and release of IL-18 are blocked by mutations in the Salmonella sipB gene, which encodes a virulence factor that activates caspase-1 to induce apoptosis. These findings indicate that the activation and release of IL-18 induced by bacterial virulence factors may represent one component of innate immunity against the intracellular bacteria.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

In structure-function relationship studies, stereological methods are applied to quantify structural qualities under investigation. In certain organs, like the brain, it is important to count the number of neurons associated with a particular function or region. The count gives an estimate of the electronic units available for a specific task or are endowed with a quantum of electrical energy. Similar studies can be extended in organs like the kidney, glands and muscles. Therefore, stereological methods enhance our knowledge of optimization of structure to funtion in biological design. This paper expounds on the methods used in estimation of number of particles in three-dimensional space. It articulates a historical perspective of the development of particle counting techniques to date in stereology showing how the problem was solved and a sound, practical and unbiased method developed. Two approaches are applied in counting particle number. The model based and the design based approach. The model-based approach assumes that the components under investigation are regular geometrical structures whose parameters can be quantified using regular geometrical methods. This counting method is biased, inefficient and difficult to apply in biological tissues. The design based approach applies a three dimensional sampling probe, the disector and makes no assumptions about shape or size of the components under investigation as in model approach.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Formal veterinary education began in the Western world in the 1763 in Lyon, 1767 in Vienna and 1791 in London. These institutions were established in an effort to reduce the severe economic impact of animal diseases, particularly, rinderpest. However over time the profession has evolved in line with emerging issues such as animal welfare, food safety, the environment and advancement in information computer technology. Furthermore, consumers and clients are increasingly well informed, and the professionals no longer have a monopoly of knowledge in their area. Moreover, the hitherto assumption that an initial degree would confers one unlimited, life-long license to practice without any need for continuing education is being questioned. Furthermore, there is continued pressure on university resources, as well as problems in attracting competent clinical staff to teach in areas of specialization and, the universities are being expected to achieve more and more with fewer resources. The structure of the profession is also gradually changing with a move towards more specialist practices, but with mixed practice still an important employer of veterinary surgeons in rural areas. In addition, there is growing awareness that the amount of veterinary knowledge is expanding all the time and it is not possible anymore, for undergraduates to achieve high levels of expertise in all areas of the veterinary profession during the 4 to 6 years available for training. These issues have continued to model the evolution of the veterinary education. The evolution has mainly focused on 6 main areas namely, review on admission criteria and curriculum review, adoption of new teaching methods, collaboration with private clinicians, introduction of apprenticeship and mandatory continuing veterinary education. This paper will elaborate on the evolving trends in veterinary education as defined by each of

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

The pecten oculi is a structure peculiar to the avian eye. Three morphological types of pecten oculi are recognized: conical type, vaned type and pleated type. The pleated type has been well studied. However, there exists only scanty data on the morphology of the latter two types of pectens. The structure of the vaned type of pecten of the ostrich, Struthio camelus was investigated with light and electron microscope. The pecten of this species consists of a vertical primary lamella that arises from the optic disc and supports 16-19 laterally located secondary lamellae, which run from the base and confluence at the apex. Some of the secondary lamellae give rise to 2 or 3 tertiary lamellae. The lamellae provide a wide surface, which supports 2-3 Layers of blood capillaries. Pigmentation is highest at the distal ends of the secondary and tertiary Lamella where blood capillaries are concentrated and very scanty on the primary and the proximal ends of the secondary lamella where the presence of capillaries is much reduced. In contrast to the capillaries of the pleated pecten, the endothelium of the capillaries in the pecten of the ostrich exhibits very few microvilli. These observations suggest that the morphology of the pecten of the ostrich, a flightless ratite bird is unique to the pleated pecten and is designed to meet the balance between optimal vision and large surface area for blood supply and yet ensuring it is kept firmly erect within the vitreous.

Dendritic cells play a central role in initiation of primary T lymphocyte responses to foreign antigens. Their potency in antigen presentation vis-a-vis reported low or lack of ability to phagocytize particulate matter has limited our understanding of the role that they play in inducing immunity to particulate antigens. One hypothesis is that dendritic cells may possess a high phagocytic capacity when immature and located in peripheral tissues, which they lose on maturation. Our goal was to characterize the phagocytic capacity in human immature dendritic cells. The phagocytic capacity of human monocyte-derived immature dendritic cells was studied by morphological and morphometric means, and compared to that of professional phagocytes, human alveolar macrophages, their progenitors, the peripheral blood monocytes, and mature dendritic cells. Phagocytic index (proportion of phagocytic cells) was decreased by 42.8% (immature dendritic cells) and 74.2% (mature dendritic cells) with respect to monocytes. Similarly, the phagocytic index was decreased by 46.5% (immature dendritic cells) and 75.9% (mature dendritic cells) with respect to macrophages. Volume density of phagocytized particles was decreased by 76.1% (immature dendritic cells) and 96.7% (mature dendritic cells) with respect to the monocytes. However, volume density was decreased by 34.3% (immature dendritic cells) and 91% (mature dendritic cells) with respect to alveolar macrophages. These results show that human monocyte-derived immature dendritic cells possess a phagocytic capacity that is lower than that of peripheral blood monocytes and alveolar macrophages but higher than that of mature dendritic cells.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

We studied the effect of using Motivational Interviewing Intervention (MII) on health facility delivery and newborn care practices among pregnant women receiving Care of the Mother and Newborn at Home (CNH) visits by Community Health Workers (CHWs). Near-Term women who had received at least one CHW home visit, were randomly assigned to one session of MII (intervention) or no MII (Control). Fifty five (55%) of intervention women, compared to 35% of control women delivered in health facilities. Intervention women also understood the need to breastfeed exclusively for 6 months better than controls (P = 0.000), and had a p-value of 0.07 for breastfeeding within one hour after birth. We concluded in the context of CHW Home visit program, adding may improve perinatal care.

We studied the effect of using Motivational Interviewing Intervention (MII) on health facility delivery and newborn care practices among pregnant women receiving Care of the Mother and Newborn at Home (CNH) visits by Community Health Workers (CHWs). Near-Term women who had received at least oneCHWhome visit, were randomly assigned to one session of MII (intervention) or no MII (Control). Fifty five (55%) of intervention women, compared to 35% of control women delivered in health facilities. Intervention women also understood the need to breastfeed exclusively for 6 months better than controls (P = 0.000), and had a p-value of 0.07 for breastfeeding within one hour after birth. We concluded in the context of CHW Home visit program, adding may improve perinatal care.

Laparostomy or the open abdomen can be a lifesaving intervention in surgical emergencies for abdominal compartment syndrome, wound dehiscence, trauma and intra-abdominal sepsis. However, the open abdomen imposes a significant burden on nursing staff caring for these critically ill patients due to the large volume of exudate and fluid loss.To achieve mechanical containment of abdominal viscera and active removal of exudate, we used NPWT to manage five patients with complex intra-abdominal sepsis laparostomy wounds. It took between 12 to 28 days to achieve full granulation for secondary closure of the wounds. The series shows that in the management of laparostomy wounds, NPWT provides an easier way to manage the large volumes of exudates and reduces the frequency of dressings changes required with traditional wound dressings.

Kenyan agriculture is largely rain-fed and principally dependent on rainfall. According to FEWS NET report for Kenya in August 2010 based on historical data from 70 rainfall stations and 17 air temperature stations to interpolate the long-rains precipitation and temperature trends for all of Kenya from 1960 to 2009 (Funk et al, 2010). The FEWS NET report indicate that in Kenya long-rains traditionally occur between March and June and short rains in October to December. The authors report that Kenya has experienced trend of decreasing rainfall and rising temperatures as Sudan. In Central Kenya, one of the country’s key agricultural regions, the area receiving adequate rainfall to support reliable rain-fed agriculture has declined by roughly 45 per cent since the mid 1970s (Funk et al, 2010). This study investigates change in temperature and rainfall pattern across all livelihood zones in Tharaka Nithi County. Data was collected for 39 years (1976 - 2015) period for the area of Study and in addition divisions were made to three non overlapping climate period of 30 years (1982 - 1991, 1992 – 200 and 2002 - 2012). The data were subjected to Gaussian kernel analysis, moments, regression, and non-parametric approaches based on Mann-Kendal statistics to justify any change in the average monthly and annually rain fall and temperature trend. The results indicate common change points and transitions from wet to dry (upward shift). The test indicates rainfall variation over the study area is significant (p= 0.05).The study recommended on the use of the information for Agricultural development and general socio-economic improvement.

Climate change and variability pose momentous severe threats to agricultural development and consequently to economic growth and increased poverty levels. In reference, this paper examines the determinants of household food security status and assesses the challenges of building resilience to climate variability and change posed by drought in Tharaka Nithi, Kenya. The study coverage is Tharaka North and Tharaka South sub-counties which are semiarid and cover an area of 1,569 square kilometers (km2) with a total population of 158,023 people; this is about 65% of Tharaka Nithi County (Kenya). The sub-counties have three main livelihood zones (LZs). These are marginal mixed farming at 52%, mixed farming at 38%, and rain-fed cropping at 10%.

The area is exposed to climate change, aggravated by minimal adaptive capacity. Climate variability and climate change threaten food production leading to about 20–30% of the population being in poor and borderline food consumption score. The year 2017 describes one of the cyclical drought situations with low productivity and depleted range land conditions exposing approximately 30,000 persons in need of humanitarian assistance. This study reflects on challenges of building resilience to climate variability and change posed by drought using a transdisciplinary approach. The problems of the household food security status were poor rainfall performance, high temperatures, low livestock prices, high food prices, poor crop production, poor pasture and browse quality, and inadequate water for both domestic and livestock use. The solutions to the above-listed issues lie in the increased advocacy, rainwater harvesting structures, marketing linkages, timely early warning knowledge management, and eco-based farming practices. The study also found that there was a significant relationship between the household level of education, family size, household income, and household head age with food security. Findings of this study will form a platform for policy makers.

Keywords
Climate variability Climate change Tharaka Nithi Drought and resilience

Extreme climatic events, such as droughts and floods, as well as changes in the mean climate, have a direct
effect on crops and livestock and, thus, people’s livelihoods. Food security is at risk, particularly in sub-saharan Africa where local production remains largely rain-fed. Given that climate variability is likely to increase with increasing greenhouse gas emissions, it is more important than ever to understand how this variability can be managed to reduce the negative consequences.

The impact is already significant. In Malawi, for example, as a result of the 2002 drought, approximately 5 million people needed emergency food aid, which took a long time to be delivered. A similar situation occurred in Niger in 2004–2005 when approximately 2.5 million people — or a fifth of the population — was in need of food rations (UNDP 2007). In 2009, approximately 3.8 million people in Kenya required food aid because of the prolonged drought (FEWS Net 2010). In 2006, sub-Saharan Africa accounted for 13% of the world’s population and 25% of the undernourished people in the developing world (FAO 2006).

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

Anecdotal evidence surrounding Tibetans' and Sherpas' exceptional tolerance to hypobaric hypoxia has been recorded since the beginning of high-altitude exploration. These populations have successfully lived and reproduced at high altitude for hundreds of generations with hypoxia as a constant evolutionary pressure. Consequently, they are likely to have undergone natural selection toward a genotype (and phenotype) tending to offer beneficial adaptation to sustained hypoxia. With the advent of translational human hypoxic research, in which genotype/phenotype studies of healthy individuals at high altitude may be of benefit to hypoxemic critically ill patients in a hospital setting, high-altitude natives may provide a valuable and intriguing model. The aim of this review is to provide a comprehensive summary of the scientific literature encompassing Tibetan and Sherpa physiological adaptations to a high-altitude residence. The review demonstrates the extent to which evolutionary pressure has refined the physiology of this high-altitude population. Furthermore, although many physiological differences between highlanders and lowlanders have been found, it also suggests many more potential avenues of investigation.

Primary amines react with 2,4-pentanedione at pH 6-9 to form enamines, N-alkyl-4-amino-3-penten-2-ones. The latter compounds readily regenerate the primary amine at low pH or on treatment with hydroxylamine. Guanidine and substituted guanidines react with 2,4-pentanedione to form N-substituted 2-amino-4,6-dimethylpyrimidines at a rate which is lower by at least a factor of 20 than the rate of reaction of 2,4-pentanedione with primary amines. Selective modification of lysine and arginine side chains in proteins can readily be achieved with 2,4-pentanedione. Modification of lysine is favored by reaction at pH 7 or for short reaction times at pH 9. Selective modification of arginine is achieved by reaction with 2,4-pentanedione for long times at pH 9, followed by treatment of the protein with hydroxylamine. The extent of modification of lysine and arginine side chains can readily be measured spectrophotometrically. Modification of lysozyme with 2,4-pentanedione at pH 7 results in modification of 3.8 lysine residues and less than 0.4 arginine residue in 24 hr. Modification of lysozyme with 2,4-pentanedione at pH 9 results in modification of 4 lysine residues and 4.5 arginine residues in 100 hr. Treatment of this modified protein with hydroxylamine regenerated the modified lysine residues but caused no change in the modified arginine residues. One arginine residue seems to be essential for the catalytic activity of the enzyme.

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Key messages
Effective training is a key determinant for adopting online learning in educational institutions.
Transformational leadership characteristics are important in managing change that is required in learning
institutions during the COVID-19 pandemic and beyond.
Modelling the way is a necessity in university management of online teaching and learning through COVID-19 Season

The sorption of added inorganic phosphate (P) by eight soils which varied appreciably in their ability to sorb P was evaluated using the Langmuir and Freundlich adsorption equations. When the sorption data were plotted according to the conven¬tional Langmuir and linear Freundlich equations, linear relationships were obtained. Regression analysis was used to compute the straight lines obtained. The Freundlich equations gave significantly to highly significantly correlation coefficients (r2 = 0.509 - 0.972) in all the soils tested while the Langmuir equation was non-sig¬nificant in the highest and lowest sorbing soils (r2 0.004 and 0.453 respectively) but was highly to very highly significant in the other soils (r2 = 0.816 - 0.988). The Freundlich equation was, therefore, ade¬quate in describing the sorption data in all the soils tested but with varying precision as shown by the different correlation coeffi¬cients. A comparison of the two equations indicated that Freundlich equation gives the best fit in majority of soils and would, therefore, be recommended for estimating the P-sorption characteristic of soils tested in this work.

A previous study on the feeding responses of tsetse flies, Glossina morsitans morsitans, implicated the existence of allomonal barriers, both volatile and nonvolatile, on the nonpreferred host, waterbuck, Kobus defassa. In the present study, electroantennogram-active compounds in odors from waterbuck were compared with those of two preferred hosts of tsetse flies, buffalo, Syncerus caffer, and ox, Bos indicus. Odors from the three bovids were trapped on activated charcoal and/or reverse-phase (octadecyl bonded) silica and analyzed with a gas chromatography-linked electroantennographic detector (GC-EAD) and, where possible, identified by using gas chromatography-linked mass spectrometry (GC-MS) and chromatographic comparisons with authentic samples. The GC-EAD profiles (with G. m. morsitans antennae) of the odors of the two preferred hosts were comparable, comprising medium-chain, saturated or unsaturated aldehydes and phenols, with buffalo emitting a few more EAG-active aldehydes. Waterbuck odor gave a richer profile, consisting of fewer aldehydes but more phenolic components and a series of 2-ketones (C8–C13) and δ-octalactone. This bovid also emits moderate amounts of C5–C9 straight-chain fatty acids, some of which were detected in buffalo and ox only in trace amounts. However, these did not elicit significant GC-EAD responses. Waterbuck profiles from the antennae of G. pallidipes showed broad similarity to those from G. m. morsitans, although the composition of aldehydes and ketones was somewhat different, indicating species-specific difference in the detection of host odors. Certain waterbuck-specific EAG-active components, particularly the 2-ketones and lactone, constitute a candidate allomonal blend in waterbuck odor.

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Coffee Berry Disease which affects green Arabica coffee (Coffea arabica) berries is caused by the fungus Colletotrichum kahawae and is a major problem in Arabica coffee production in African countries. Breeding for resistance to this disease is therefore to a major priority in these countries avoid intensive chemical usage for its control. Recently, microsatellite and Amplified Fragment Length Polymorphisms (AFLP) markers for a gene conferring resistance to the disease were identified and mapped onto the chromosomal region carrying the gene. To improve the repeatability of the AFLP markers, four of the marker bands were selected for cloning and sequencing to facilitate specific primers to be designed. Three of the resultant primers did not amplify products that exhibited polymorphism characteristic of the parent AFLP bands; but one primer pair amplified a product that dominantly identified the presence of the parent AFLP marker at an optimum temperature of 62°C followed by electrophoresis in agarose. The reliability of the designed primers was confirmed by analysis in 95 plants from a F2 population previously used to map the chromosomal fragment carrying the resistance. The importance of the results in enhancing the utility of the parent AFLP marker in relation to analytical costs and position on the chromosomal fragment is discussed.

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This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This integrative review on the teaching of reading in Kenyan primary schools provides a foundation for the growing movement there to improve reading education. In gathering sources for this review, we took an inclusive historical stance. Thus, we did not dismiss research reports that lacked traditional indicators of quality such as being published in peer-reviewed journals. We used multiple methods to find relevant research and associated documents, including two trips to Kenya. The review is organized by six topics: (a) language of instruction, (b) reading instruction, (c) reading materials, (d) reading culture, (e) assessment, and (f) teacher development. The review concludes with six proposals for policymakers, educational researchers, and teacher educators for the development of reading instruction based on what we learned in reviewing the literature. The first proposals are intended specifically to address the teaching of reading in Kenya, but they may be relevant to other sub-Saharan nations. The final proposal encourages others to conduct similar reviews to make possible a handbook of reading in Africa.

This paper presents results of a study aimed at quantifying soil and water management practices and identifying major constraints and implications for future adoption of appropriate technologies. The study was conducted in the Machakos and Makueni Districts of Kenya. Approximately 83% of the farmers interviewed were using manure, while only 4% use fertilizer. 60% had fanya juu terraces on their land, while only 13% were using grass strips. The study concluded that finance is a major constraint limiting farmers' adoption of practices enhancing soil fertility and that lack of conservation practices on grazing land is of great concern. The lack of knowledge of possible benefits of soil and water management practices is noted.

This paper looks at factors which influence land allocation and crop production patterns in Botswana, across traditional and commercial farmers. It found that, among smallholder traditional farmers, less land is used (on average 5.6 ha) and is subdivided into the growing of three major crops: sorghum, maize and beans, with more land allocated to sorghum, the main staple and more adaptable to the climate. The small amount of cultivated land is attributed to lack of capital, transport and labour. Although large areas of land are owned by commercial farmers a high percentage is left idle due to constraints such as poor marketing systems, poor storage facilities and shortage of labour.

This paper describes earthflow features in Nyairoko sub-location of Ol Joro Orok Division, Kenya. In 1989 more than 900 earthflows were counted in Nyandarua District, most of them in Ol Joro Orok and Ol Kalou Divisions. Individual flows affected areas between a few square metres and two hectares. More than 50% of the farms in the area were affected by earthflows. Such earthflows occurred only on grazing land and on convex slopes and were usually the result of extremely slow processes. Soils in the area are mainly moderately well drained, dark reddish brown Luvisols and well-drained, red to reddish-brown Nitisols. The first visible signs were usually shallow scars along the contour, breaking up the grass vegetation. Subsequent soil movement was very gradual. According to old residents of the area some of the earthflow features had been observed as long as 60 years ago and could not be attributed to land use change. One earthflow studied in detail revealed that soil stratification impeded drainage, leading to oversaturation of the topsoil layers and that seasonal subsurface flow generally seemed to be responsible for the soil movement. No obvious triggering could be identified.

The results of soil surveys at the ICIPE research site at Ungoye, South Nyanza, and the Ngori Ngori toposequence in Narok, Kenya, are discussed to provide insight into the applicability of soil survey information to soil and water management. It is concluded that soil survey information in soil and water management programmes can be used through understanding and appreciation of the criteria used in categorizing soils and their management implications. From the examples given it is noted that chemical aspects of the soil should be viewed not just as a means to assess its fertility, but also as a base to predict the behaviour of the soils when subjected to different types of management.

Wetlands are lands that are transitional between terrestrial and aquatic systems where the water is usually at or near the surface of the land or land that is covered with shallow water (Cowardin et al. 1979, Roggeri 1995). In the context of dry lands, wetlands are areas that are permanently, seasonally or occasionally water logged with fresh or saline water that supports characteristic animals and plants. In the dry lands of eastern Africa, wetlands cover about 3 percent of the total land area and include shallow lakes and margin s of deep lakes, swamps and marshes found on upper flood plains of major rivers, coastal river flood plains and high mountain peat bogs and tarns (Omoding 1995). These ecosystems support valuable biodiversity, including large numbers of mammals, reptiles, fishes and birds as well as diverse plant communities (Denny 1993). They also provide valuable resources and environmental benefits, such as biomass cropping for livestock pasture, water supply, agriculture, fisheries and subsistence hunting of wildlife that sustain local economies and communities (Shumway 1999).

The effects of P supply (0, 20, 40, 80, 160 and 320 kg/ha) on growth and nodulation of cowpeas (Vigna unguiculata) cv. Vita 4 and Ife Brown grown in a podzolic soil (Haplustult) was studied in a greenhouse trial. The seeds were inoculated with Bradyrhyzobium CB 756. Plants were harvested at the beginning of flowering. The number of trifoliate leaves and DM yield in both cv. increased with increasing P application. The yield of the tops of Vita 4 was maximum at 160 kg P/ha and that of Ife Brown at 320 kg P/Ha. Extractable P related linearly to the rate of applied P, and DM yield increased with increase in extractable P. Plants grown without P had fewer and smaller nodules. An increase in P from 1 to 160 kg/ha increased the number of nodules/plant from 16 to 113 in Vita 4 and from 14 to 70 in Ife Brown. Similarly, increasing P increased nodule dry weight. The P conc. of the youngest fully expanded leaf (YFEL) and in the whole plant top increased with increasing P supply in both cv. and was generally higher in the YFEL than in the whole top. A critical P conc. of 0.3 and 0.25% was found in the YFEL and the whole top, resp., for cv. Vita 4.

Preliminary findings on the effects of land use in the Masinga Dam catchment, Kenya, on the storage capacity of the reservoir are presented. Remote sensing and GIS techniques, supplemented with ground reports, were used to determine areas most susceptible to erosion. A representative catchment was then chosen for rainy season monitoring of soil loss, river suspended sediments and discharge response to rainfall. In addition, Gerlach-type traps were used to evaluate erosion rates under different crop covers and slope gradients. A sample of 200 households was interviewed about their perceptions of erosion problems on their farms. Preliminary results suggest that the major sediment-contributing areas are the densely populated and intensively cultivated foothills of the Aberdares, rather than the semi-arid lowlands directly bordering the reservoir. Poorly drained sealed and murram roads, together with footpaths, cattle tracks and gullies, act as extensions of the drainage network during storms, channelling sediment-laden runoff from bare areas around homesteads and schools directly into the river. Subsistence crops, particularly mono-cropped maize, appear to provide poor cover for a major part of the wet season.

This paper presents results from a trial in Swara Farm, Njoro, Kenya, in which a field was sown with Sorghum almum on a volcanic ash soil. Immediately after sowing, 14 strips measuring 156 m x 9 m were marked out and alternate strips were oversown with inoculated seed of lucerne cv. Hairy Peruvian. During the first year of the trial no differences were noticed in the growth of S. almum, but during the second year it grew better when associated with lucerne. After two years the field was ploughed and sown with wheat. The strips were harvested separately with a combine harvester. Mean yields after S. almum were 2,708 kg/ha and after the S.almum/lucerne mixture were 3,244 kg/ha.

Stover placement (surface mulch, incorporated or a mixture of mulch and incorporation) was compared with stover removal in the presence and absence of 50kg N fertilizer/ha in trials over two successive seasons in continuous maize cropping systems in two regions in Kenya. Stover applied at 4 tonnes DM/ha was found to have highly variable effects on maize growth and yield according to site., method of stover placement, N application and season. Relative to controls without stover, stover incorporation reduced yield by 39% in the first season, followed by yield increases of 15% in the second season. In the first season there was little or no response to N in the presence of stover. Low N uptake and N use efficiency suggested N immobilization in the incorporation treatment. Yield responses and large N uptake in the following season suggested mineralization of N immobilized in the previous season. Surface mulching at the Kabete site increased grain yields in the first season by 39% and 6% compared to stover removal without and with fertilizer, resp. In the second season, surface mulching markedly reduced yields possibly due to a combination of reduced phytotoxicity and N immobilization. At the Katumani site, stover amendments increased yields compared to removal in both seasons with incorporation results being superior to surface mulch. At this site, in both seasons, application of N reduced the effect of stover mulching and incorporation. You must log in to CAB Direct in order to view search results. If you have forgotten your log

This paper describes a "near-farmer" applied research project working on 10 field stations scattered through the arid and semi-arid lands of Embu, Meru and Isiolo Districts of Esatern Province, Kenya. The objective of the research was to define better extension messages for resource-poor farmers to enable them to improve their land and water management techniques for improved and sustained yields. Most of the trials related to soil fertility and soil moisture, as well as trials on the use of Vetiver grass for soil conservation, control of the legume root parasite Alectra vogelii, and new introductions such as groundnuts, simsim (sesame), tubers, fodder crops and fruits.

This paper briefly presents a methodology for planning development in arid and semi-arid areas. It highlights the issues of problem identification and assessment of the natural and socio-economic environment, and describes the database contained in the Range Management Handbook. The handbook makes available baseline data for planning development in arid and semi-arid areas following a successful Farm Management Handbook that covers the high- and medium-potential areas of Kenya. In three parts, the Range Management Handbook covers: the status, principles and applications in Kenya; texts and maps relating to climate, landforms and soils, vegetation types, water sources, range unit inventory, livestock marketing and human ecology; special reports (guide to tolerant plants, pictorial key for goat stocking rates, large scale remote monitoring of vegetation, and a survey method for classification of range conditions) relevant to land planning and use in arid and semi-arid areas