Hepatitis E Virus Genotype 3 Strains in Domestic Pigs, Cameroon

Submitted by sandra infurna ([email protected]) on 2016-01-12T10:59:18Z No. of bitstreams: 1 vanessa2_depaula_etal_IOC_2013.pdf: 345946 bytes, checksum: e8608841f8a5f6994e9095f3f5b0772c (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-12T11:21:17Z (GMT) No. of bitstreams: 1 vanessa2_depaula_etal_IOC_2013.pdf: 345946 bytes, checksum: e8608841f8a5f6994e9095f3f5b0772c (MD5)Made available in DSpace on 2016-01-12T11:21:17Z (GMT). No. of bitstreams: 1 vanessa2_depaula_etal_IOC_2013.pdf: 345946 bytes, checksum: e8608841f8a5f6994e9095f3f5b0772c (MD5) Previous issue date: 2013Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil / Bernhard Nocht Institute for Tropical Medicine. Hamburg, Germany.Bernhard Nocht Institute for Tropical Medicine. Hamburg, Germany.Centre Pasteur. Yaoundé, Cameroon.Institute of Agricultural Research for Development. Ngaoundere, Cameroon.Institute of Agricultural Research for Development. Ngaoundere, Cameroon.Bernhard Nocht Institute for Tropical Medicine. Hamburg, Germany

Kidney ischemia-reperfusion injury induces caspase-dependent pulmonary apoptosis

Distant organ effects of acute kidney injury (AKI) are a leading cause of morbidity and mortality. While little is known about the underlying mechanisms, limited data suggest a role for inflammation and apoptosis. Utilizing a lung candidate gene discovery approach in a mouse model of ischemic AKI-induced lung dysfunction, we identified prominent lung activation of 66 apoptosis-related genes at 6 and/or 36 h following ischemia, of which 6 genes represent the tumor necrosis factor receptor (TNFR) superfamily, and another 23 genes are associated with the TNFR pathway. Given that pulmonary apoptosis is an important pathogenic mechanism of acute lung injury (ALI), we hypothesized that AKI leads to pulmonary proapoptotic pathways that facilitate lung injury and inflammation. Functional correlation with 1) terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling and 2) active caspase-3 (aC3) activity, immunoblotting, and immunohistochemistry (IHC) identified kidney IRI-induced pulmonary apoptosis at 24 h, and colocalization studies with CD34 identified predominantly endothelial apoptosis. Mice were treated with the caspase inhibitor Z-VAD-FMK (0.25 mg ip) or vehicle 1 h before and 8 h after sham or kidney IRI, and bronchoalveolar lavage fluid protein was measured at 36 h as a surrogate for lung leak. Caspase inhibition reduced lung microvascular changes after kidney IRI. The pulmonary apoptosis seen in wild-type control mice during AKI was absent in TNFR−/− mice. Using an initial genomic approach to discovery followed by a mechanistic approach to disease targeting, we demonstrate that pulmonary endothelial apoptosis is a direct mediator of the distant organ dysfunction during experimental AKI

Seroprevalence and Associated Risk Factors of Brucellosis among Indigenous Cattle in the Adamawa and North Regions of Cameroon

A cross-sectional seroprevalence study was conducted on cattle in the North and Adamawa Regions of Cameroon to investigate the status of bovine brucellosis and identify potential risk factors. The diagnosis was carried out using the Rose Bengal Plate test (RBPT) and indirect ELISA (i-ELISA), while questionnaires were used to evaluate risk factors for bovine brucellosis in cattle. The Bayesian approach was used to evaluate the diagnostic tests’ sensitivity and specificity. The overall individual level (n=1031) and herd level (n=82) seroprevalence were 5.4% (0.4–10.5) and 25.6% (16.2–35.0), respectively. Bayesian analysis revealed sensitivity of 58.3% (26.4–92.7) and 89.6% (80.4–99.4) and specificity of 92.1% (88.7–95.2) and 95.7% (91.1–99.7) for RBPT and i-ELISA, respectively. Management related factors such as region, locality, herd size, and knowledge of brucellosis and animal related factors such as sex and age were significantly associated with seropositivity of brucellosis. Zoonotic brucellosis is a neglected disease in Cameroon. The study highlights the need for control measures and the need to raise public awareness of the zoonotic occurrence and transmission of bovine brucellosis in the country. An integrated disease control strategy mimicking the one health approach involving medical personnel, veterinarians, related stakeholders, and affected communities cannot be overemphasized

Interactive effects of mechanical ventilation and kidney health on lung function in an in vivo mouse model

We hypothesized that the influence of acute kidney injury (AKI) on the sensitivity of the lung to an injurious process varies with the severity of the injurious process. Thus, we thought that AKI would exacerbate lung injury from low degrees of lung trauma but attenuate lung injury from higher degrees of lung trauma. C57BL/6 mice underwent AKI (30-min kidney ischemia) or sham surgery, followed at 24 h by 4 h of spontaneous breathing (SB), mechanical ventilation with low tidal volume (7 ml/kg, LTV), or mechanical ventilation with high tidal volume (30 ml/kg, HTV). Compared with LTV, median bronchoalveolar lavage (BAL) protein leak was significantly lower with SB and greater with HTV in both sham and AKI mice. Compared with LTV, median Evans blue dye-labeled albumin extravasation in lungs (L-EBD) was also significantly lower with SB and greater with HTV. L-EBD showed a significant interaction between ventilatory mode and kidney health, such that AKI attenuated the L-EBD rise seen in HTV vs. LTV sham mice. An interaction between ventilatory mode and kidney health could also be seen in BAL neutrophil number (PMN). Thus, AKI attenuated the BAL PMN rise seen in HTV vs. LTV sham mice. These data support the presence of a complex interaction between mechanical ventilation and AKI in which the sensitivity of the lung to trauma varies with the magnitude of the trauma and may involve a modification of pulmonary neutrophil activity by AKI