Geophagia is not associated with Trichuris or hookworm transmission in Zanzibar, Tanzania

Geophagia may be harmful as a method for the transmission of geohelminths. In this study, we pose two questions in a representative sample of 970 pregnant women from Pemba Island, Zanzibar, Tanzania. Can consumed earth be a vector for geohelminth infection? And do geophagists have differential parasitic infection? The parasitological content of 59 non-food substance samples was analysed. Cross-sectional data regarding pica behaviour were collected through interviews conducted by local researchers. Ascaris, Trichuris and hookworm status was ascertained through Kato-Katz smears. The prevalence of geophagia at baseline was 5.6% and the overall prevalence of Ascaris, Trichuris and hookworm infection was 5.6%, 33.2% and 32.9%, respectively. No consumed soil samples contained infectious parasitic stages, and only one of the consumed pica substances (charcoal) contained parasites of potential risk to human health. In bivariate analyses, neither the prevalence nor the intensity of infection with Ascaris, Trichuris or hookworm differed significantly by geophagia status. Furthermore, in multivariate models, geophagia was not a significant predictor of helminth infection status. We conclude that geophagia is not a source of Trichuris or hookworm infection among pregnant women in Pemba (insufficient power to evaluate the effect of Ascaris), which is in contrast to existing findings of helminth infection and geophagia.     

Bacterial RNA induces myocyte cellular dysfunction through the activation of PKR

Severe sepsis and the ensuing septic shock are serious life threatening conditions. These diseases are triggered by the host's over exuberant systemic response to the infecting pathogen. Several surveillance mechanisms have evolved to discriminate self from foreign RNA and accordingly trigger effective cellular responses to target the pathogenic threats. The RNA-dependent protein kinase (PKR) is a key component of the cytoplasmic RNA sensors involved in the recognition of viral double-stranded RNA (dsRNA). Here, we identify bacterial RNA as a distinct pathogenic pattern recognized by PKR. Our results indicate that natural RNA derived from bacteria directly binds to and activates PKR. We further show that bacterial RNA induces human cardiac myocyte apoptosis and identify the requirement for PKR in mediating this response. In addition to bacterial immunity, the results presented here may also have implications in cardiac pathophysiology.     

Administration of gallium nitrate by continuous infusion: lack of chronic nephrotoxicity confirmed by studies of enzymuria and beta 2-microglobulinuria

Enzymuria and beta 2-microglobulinuria are sensitive markers of injury to renal tubular cells. We evaluated these markers in 41 patients with advanced malignant lymphoma who received gallium nitrate administered as a continuous infusion during a recent phase I-II study. In contrast to our findings with cisplatin, we observed no significant increase in enzyme excretion or beta 2-microglobulinuria in these patients even after long-term treatment. Our results indicate that gallium nitrate administered by infusion does not produce cumulative renal tubular toxicity.     

Quantitative image analysis of F-actin in endothelial cells

OBJECTIVE: Filamentous actin (F-actin) plays a central role in maintaining endothelial barrier function. Thrombin and histamine, two inflammatory mediators that increase endothelial permeability, can alter F-actin production and distribution. In this study, we use a newly developed image analysis technique to show that these two inflammatory mediators differentially alter F-actin structure. METHODS: Human umbilical vein endothelial cells were grown to confluence and treated with either histamine (1 microM), thrombin (1 microM) or the agonist's vehicle. The endothelium was stained with BODIPY-phallodin, and digitized images were taken of the treated cells. The digitized images of individual human umbilical vein endothelial cells (HUVEC) were imported into a F-actin image analysis program (FAAP) and converted to layers, each one pixel thick. The program then determined the mean gray level (which corresponded to the amount of F-actin) in each layer starting from the outside of the cell (layer 1) and progressing in one pixel layer increments towards the center of the cell (layer 32). RESULTS: Both inflammatory mediators increased endothelial F-actin production, however, the distribution of the actin was different. Thrombin increased the presence of stress fibers, while also decreasing peripheral banding actin. In contrast, histamine had no effect on peripheral actin compared to control, but did increase the presence of F-actin stress fibers. CONCLUSIONS: These results establish that thrombin and histamine alter endothelial F-actin production in different locations within the cell, which can be quantified using an image analysis program.