The environmental impact on the hydrogeochemical characterization of the Kurkar aquifer system, Gaza strip, Palestine.

The Gaza strip is suffering groundwater deterioration as a result of high population density where the outflow exceeds inflow by about 20 Mm3/y. This quantity of water is believed to be replaced by deep seawater intrusion and/or upconing of deep brines in the southern areas or by anthropogenic wastewater. Large cones of depression have been formed over the last 40 years within the Gaza, Khan Younis, and Rafah governorates. The salinity increases in the northwestern and the southeastern parts of Gaza Strip. Nitrate and chloride exceed the WHO maximum permissible limits and are considered as the major pollutants of the aquifer, their high concentration values are attributed to agricultural activity and leaked wastewaters as well as the scarcity of the resource. The cluster analysis (Q-mode) classified the data into 5 clusters and 3 independent cases depending upon salinity and nitrate concentrations. The rotated factor analysis identified 3 factors. The AquaChem program clarified that the study area was supersaturated with calcite and dolomite and undersaturated with gypsum and anhydrite minerals. In general, the groundwater was unsuitable for drinking according to their TDS and NO3 contents. The groundwater can be used in permeable soils for irrigation purposes

Prevalence of hepatitis C virus in patients with tuberculosis and its impact in the incidence of anti-tuberculosis drugs induced hepatotoxicity

AbstractBackgroundThe prevalence of hepatitis C virus (HCV) infection among patients with tuberculosis (TB) has not been extensively investigated, and very limited data on rates of HCV co-infection among patients with TB exists. Hepatotoxicity is the major adverse effect of three of the first line anti-TB agents: isoniazid (INH), rifampin (RIF), and pyrazinamide (PZA). Chronic liver disease raises a risk of hepatotoxicity during anti-tuberculosis treatment, up to three to five times more than TB patients who do not have viral infection.AimTo assess the prevalence of HCV infection in patients with tuberculosis and its impact in the incidence of anti-tuberculosis drug induced hepatotoxicity (DIH).Subjects and methodsThe prevalence of HCV in patients with newly diagnosed pulmonary or extrapulmonary tuberculosis was estimated using polymerase chain reaction (PCR). Then patients were classified into 2 groups: group I (patients with HCV-TB coinfections) and group II (HCV-seronegative tuberculous patients). Baseline and monthly measuring liver transaminases was done before and following the start of 1st line anti-tuberculosis therapy.ResultsThe prevalence of HCV in patients with TB was 17.02%. Regarding DIH, in group I; 6 (40%) cases showed transient transaminase elevations and 6 (40%) cases developed DIH. In group II; 11 (20.75%) cases developed transient transaminase elevations and only 2 (3.78%) cases developed DIH, and there was a highly significant difference (<0.01) between both groups. Regarding the severity of DIH, in group I; 4 cases were mild, one case was moderate and one case was severe. While in group II, no cases was with severe DIH. The risk factors for developing DIH during anti-tuberculosis therapy were; age ⩾40, high baselines transaminases, ALP and total bilirubin, and low BMI. Most cases of DIH occurred during the 1st 4weeks of starting anti-tuberculosis therapy (66.7% and 50% in group I and group II, respectively).ConclusionsTuberculosis and hepatitis C virus co-infection is common, and elevation of liver functions during anti-tuberculosis therapy is not uncommon. HCV-positive patients with tuberculosis should be closely monitored during treatment especially if they had elevated baseline liver functions, old age and with low BMI. Monitoring should include the whole period of treatment, especially the 1st 2months

Comparison of Real-time PCR to ELISA for the detection of human cytomegalovirus infection in renal transplant patients in the Sudan

<p>Abstract</p> <p>Background</p> <p>This study was carried out to detect human cytomegalovirus (HCMV) IgG and IgM antibodies using an Enzyme-linked immunosorbent assay (ELISA) in renal transplant patients in Khartoum state, Sudan and to improve the diagnosis of HCMV through the introduction of Real-time Polymerase Chain Reaction (PCR) testing. A total of 98 plasma samples were collected randomly from renal transplant patients at Ibin Sina Hospital and Salma Centre for Transplantation and Haemodialysis during the period from August to September 2006.</p> <p>Results</p> <p>Among the 98 renal transplant patients, 65 were males and 33 females. The results revealed that HCMV IgG was present in all patients' plasma 98/98 (100%), while only 6/98 (6.1%) had IgM antibodies in their plasma. HCMV DNA viral loads were detected in 32 patients 32/98 (32.7%) using Real-time PCR.</p> <p>Conclusions</p> <p>The HCMV IgG results indicate a high prevalence of past HCMV infection in all tested groups, while the finding of IgM may reflect a recent infection or reactivation. HCMV detection by real-time PCR in the present study indicated a high prevalence among renal transplant patients in Khartoum. In conclusion, the prevalence of HCMV in Khartoum State was documented through detection of HCMV-specific antibodies. Further study using various diagnostic methods should be considered to determine the prevalence of HCMV disease at the national level.</p

Allogenic hematopoietic stem cell transplantation after reduced intensity conditioning regimen for elderly patients (60 years and older) with hematologic malignancies using unrelated donors: a retrospective study for the French society for stem cell transplantation (SFGM-TC)

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Increased FGF1-FGFRc expression in idiopathic pulmonary fibrosis

© MacKenzie et al. 2015. Recent clinical studies show that tyrosine kinase inhibitors slow the rate of lung function decline and decrease the number of acute exacerbations in patients with Idiopathic Pulmonary Fibrosis (IPF). However, in the murine bleomycin model of fibrosis, not all tyrosine kinase signaling is detrimental. Exogenous ligands Fibroblast Growth Factor (FGF) 7 and 10 improve murine lung repair and increase survival after injury via tyrosine kinase FGF receptor 2b-signaling. Therefore, the level and location of FGF/FGFR expression as well as the exogenous effect of the most highly expressed FGFR2b ligand, FGF1, was analyzed on human lung fibroblasts. Methods: FGF ligand and receptor expression was evaluated in donor and IPF whole lung homogenates using western blotting and qPCR. Immunohistochemistry for FGF1 and FGFR1/2/3/4 were performed on human lung tissue. Lastly, the effects of FGF1, a potent, multi-FGFR ligand, were studied on primary cultures of IPF and non-IPF donor fibroblasts. Western blots for pro-fibrotic markers, proliferation, FACS for apoptosis, transwell assays and MetaMorph analyses on cell cultures were performed. Results: Whole lung homogenate analyses revealed decreased FGFR b-isoform expression, and an increase in FGFR c-isoform expression. Of the FGFR2b-ligands, FGF1 was the most significantly increased in IPF patients; downstream targets of FGF-signaling, p-ERK1/2 and p-AKT were also increased. Immunohistochemistry revealed FGF1 co-localization within basal cell sheets, myofibroblast foci, and Surfactant protein-C positive alveolar epithelial type-II cells as well as co-localization with FGFR1, FGFR2, FGFR3, FGFR4 and myofibroblasts expressing the migratory marker Fascin. Both alone and in the presence of heparin, FGF1 led to increased MAPK-signaling in primary lung fibroblasts. While smooth muscle actin was unchanged, heparin+FGF1 decreased collagen production in IPF fibroblasts. In addition, FGF1+heparin increased apoptosis and cell migration. The FGFR inhibitor (PD173074) attenuated these effects. Conclusions: Strong expression of FGF1/FGFRs in pathogenic regions of IPF suggest that aberrant FGF1-FGFR signaling is increased in IPF patients and may contribute to the pathogenesis of lung fibrosis by supporting fibroblast migration and increased MAPK-signaling