The role of OmpC and OmpF in acidic resistance in Escherichia coli

The roles of OmpC and OmpF in acidic resistance (AR) were examined. When ompC and ompF were deleted, AR was decreased. The decreased level of AR seen in the mutant that was deficient in ompC and ompF was elevated by the addition of glutamate, but not by the addition of arginine or lysine. The expression levels of adiA and cadB were diminished by the deletion of ompC and ompF, and the conversion of arginine to agmatine and lysine to cadaverine by intact cells were reduced in the mutant. The expression of gadA/gadB was not affected by the deletion of ompC and ompF. These results suggest that the transport of arginine, lysine, and their decarboxylated products through OmpC and/or OmpF is essential for the survival of Escherichia coli cells under extremely acidic conditions.     

Chronic treatment with tempol does not significantly ameliorate renal tissue hypoxia or disease progression in a rodent model of polycystic kidney disease

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In vivo requirement of TGF-β/GDNF cooperativity in mouse development: focus on the neurotrophic hypothesis

Neurotrophic factors are well-recognized extracellular signaling molecules that regulate neuron development including neurite growth, survival and maturation of neuronal phenotypes in the central and peripheral nervous system. Previous studies have suggested that TGF-β plays a key role in the regulation of neuron survival and death and potentiates the neurotrophic activity of several neurotrophic factors, most strikingly of GDNF. To test the physiological relevance of this finding, TGF-β2/GDNF double mutant (d-ko) mice were generated. Double mutant mice die at birth like single mutants due to kidney agenesis (GDNF−/−) and congential cyanosis (TGF-β2−/−), respectively. To test for the in vivo relevance of TGF-β2/GDNF cooperativity to regulate neuron survival, mesencephalic dopaminergic neurons, lumbar motoneurons, as well as neurons of the lumbar dorsal root ganglion and the superior cervical ganglion were investigated. No loss of mesencephalic dopaminergic neurons was observed in double mutant mice at E18.5. A partial reduction in neuron numbers was observed in lumbar motoneurons, sensory and sympathetic neurons in GDNF single mutants, which was further reduced in TGF-β2/GDNF double mutant mice at E18.5. However, TGF-β2 single mutant mice showed no loss of neurons. These data point towards a cooperative role of TGF-β2 and GDNF with regard to promotion of survival within the peripheral motor and sensory systems investigated.     

Impact of SEN virus on immunoblot INNO-LIA HCV reactivity pattern and disease outcome in Egyptian hepatocellular carcinoma patients

Recently, a novel virus designated SEN virus (SENV), which is thought to be related to posttransfusion hepatitis, was discovered. The aim of the present study was to investigate the prevalence and clinical significance of 2 SENV variants (SENV-D and SENV-H) in patients with hepatocellular carcinoma (HCC) and healthy adults. Also, to investigate the possible effect of SEN virus on the humoral immune response against different proteins of HCV through analyzing reactivity patterns of the confirmatory INNO-LIA HCV Ab III update in relation to SEN viremia. We investigated SEN virus infection in 41 patients with HCC (25 males and 16 females) and twenty healthy blood donors (12 males and 8 females). All samples were taken from the National Cancer Institute, Cairo University. We used semi nested polymerase chain reaction (PCR) amplification to detect SENV-D and SENV-H strains in serum. All patients were tested against HCV antibody by ELISA and HCV viremia by RT-PCR. Furthermore, nineteen patients positive for HCV antibody by EIA (10 positive for SEN DNA and 9 non viremic for SEN) were confirmed in the immunoblot assay. SENV DNA was detected in 68 % (28 of 41) of patients with HCC and in 64 % (21 of 33) HCV-related HCC, in comparison to 5% (1 of 20) healthy blood donor populations. The blood biochemical parameters, and performance status did not differ significantly between the SENV DNA-positive and- negative patients. However, the overall survival rate was 50 % after two years follow up in SENV DNA-positive and 14 % in SENV DNA-negative HCC patients. Reactivity to NS5 and E2 were less (22 % and 44 % of cases) in SENV negative cases, than in SENV positive cases (70 % and 80 % of cases, respectively). In conclusion, SENV DNA seems to be highly prevalent among Egyptian HCC patients. Cross reactivity between SENV proteins and HCV NS5, E2 or the increased immune response in SENV positive cases and consequently the increased reactivity to HCV NS5 and E2 proteins could not be ruled out. Although there was no apparent effect of SENV on biochemical tests, survival rates of SENV DNA-positive HCC patients were higher thannegative cases, which might be due to other factors affecting survival in our Egyptian HCC patients.     

Three-dimensional isotropic wavelets for post-acquisitional extraction of latent images of atherosclerotic plaque components from micro-computed tomography of human coronary arteries

RATIONALE AND OBJECTIVES: The capability of wavelet transforms to separate signals into frequency bands is the basis for its use in image compression and storage, data management and transmission, and, recently, extraction of latent images of tissue components from noisy medical images. Analysis of temporal variations of radiofrequency backscatter of intravascular ultrasound with one-dimensional wavelets can detect lipid-laden plaque in coronary arteries with a sensitivity and specificity of >80%. In this study we evaluate the capability of a novel, 3-dimensional isotropic wavelet analysis to perform high resolution, non-directionally biased, statistically reliable, non-invasive discrimination between components of human coronary atherosclerotic plaques in micro-CT. MATERIALS AND METHODS: Coronary artery segments (5-15 mm) were excised at necropsy from 18 individuals with advanced coronary atherosclerosis. Specimens were imaged using a GE Locus SP ex vivo micro-CT scanner and processed for histological correlation (833 sections). The isotropic wavelet constructs were applied to the entire volume of CT data of each arterial segment to distinguish tissue textures of varying scales and intensities. Voxels were classified and plaque characterization achieved by comparing the relative magnitudes of these wavelet constituents to that of several reference plaque tissue components. RESULTS: Processing of micro-CT images via these isotropic wavelet algorithms permitted 3-D, color-coded, high resolution, digital discrimination between lumen, calcific deposits, lipid-rich deposits, and fibromuscular tissue providing detail not possible with conventional thresholding based on Hounsfield intensity units. Using the isotropic wavelets (with histology as the gold standard), lipid-rich pools approaching the size of the filter for the isotropic wavelet algorithm (0.25 mm [250 microns] in length) were identified with 81% sensitivity and 86% specificity. Calcific deposits, fibromuscular tissue, and lumen equal to or larger than the wavelet filter size were detected without error (100% sensitivity and specificity). CONCLUSION: Isotropic wavelet analysis permits high resolution, multi-dimensional identification of coronary atherosclerotic plaque components in micro-CT with sensitivity and specificity similar to that achieved with data obtained invasively (from IVUS in vivo) using one-dimensional wavelets. Further studies are necessary to test the applicability of this technology to clinical, multi-detector scanners.     

Tunisian hereditary spastic paraplegias: clinical variability supported by genetic heterogeneity

Hereditary spastic paraplegias (HSP) constitute a clinically and genetically heterogeneous group of neurodegenerative disorders characterized by slowly progressive spasticity of the lower extremities. We performed the first clinical, epidemiological and genetic study of HSP in Southern Tunisia. We investigated 88 patients belonging to 38 unrelated Tunisian HSP families. We could establish the minimal prevalence of HSP in the district of Sfax at 5.75/100,000. Thirty‐one percent of the families had a pure HSP, whereas 69% had a complicated form. The mode of inheritance was almost exclusively compatible with an autosomal recessive trait (97%, 37/38). Taking into account previously published results and new data generated in this work, genetic studies revealed significant or putative linkage to known HSP loci in 13 families (34.2%) to either SPG11 (7/38, 18.4%), SPG15 (4/38, 10.5%) or to SPG4 and SPG5 in one family each. The linkage results could be validated through the identification of two recurrent truncating mutations (R2034X and M245VfsX246) in the SPG11 gene, three different mutations (Q493X, F683LfsX685 and the novel S2004T/r.?) in the SPG15 gene, the recurrent R499C mutation in the SPG4 gene as well as the new R112X mutation in the SPG5 gene. SPG11 and SPG15 are the major responsible HSP genes in Tunisia.     

Phytochemical and biological studies of Adiantum capillus-veneris L.

Chromatographic fractionation of the alcoholic extract of the dried fronds of Adiantum capillus-veneris L. (Adiantaceae) yielded seven compounds: four triterpenoidal compounds belonging to adiantane and filicane groups were isolated from the hexane fraction and identified as isoadiantone (1); isoadiantol-B (2); 3-methoxy-4-hydroxyfilicane (3) and 3,4-dihydroxyfilicane (4) and three flavonoids were isolated from the ethyl acetate fraction and identified as: quercetin (5), quercetin-3-O-glucoside (6) and quercetin-3-O-rutinoside (rutin) (7). The identification of the isolated compounds has been established through their physical, chemical and spectroscopic methods including IR, ¹H NMR, ¹³C NMR, HSQC, HMBC, NOESY and MS. Biological studies of the total alcoholic extract, hexane fraction and some of the isolated compounds showed an anti-inflammatory activity while the hypoglycemic study of the total alcoholic extract showed a significant activity.     

PI3 kinase integrates Akt and MAP kinase signaling pathways in the regulation of prostate cancer

PI3 kinase (PI3K), Akt and MAP kinase (MAPK) pathways are central to many classical signaling cascades and are often de-regulated in many cancers. Due to this, inhibitors for a number of key signaling molecules in these pathways such as PI3K, Akt, mTOR, Raf and ERK are currently in clinical trials. In the current study, we investigated the effects of specific inhibition of these signaling molecules, alone or in combinations, on prostate cancer cells. Our study showed that integration of Akt-mTOR and MAPK signaling by PI3K was essential for the EGF-stimulated TRAMP cell migration, proliferation, survival and invasion as well as PC3 and LNCaP C4-2 (C4-2) colony/foci formation. Adenovirus-mediated expression of constitutively active Akt (Ad-myrAkt) in PC3 cells resulted in significant increase in number of foci. Even though PI3K inhibition significantly reduced foci formed by C4-2 cells, none of the Akt, ERK or mTOR inhibitors showed any significant inhibition. This indicated that functional redundancies and/or feed back loops between Akt-mTOR and MAPK signaling exist in prostate cancer. Further studies on cotargeting these signaling molecules revealed that combined inhibition of Akt (or mTOR) and ERK, but not Akt and mTOR, resulted in significant reduction in number of foci formed by the C4-2 cells. Overall, our study demonstrated that the effects of PI3K-mediated prostate cancer growth necessitates a synergism between the Akt and MAPK pathways and suggests cotargeting Akt (or mTOR) and MAPK as an effective method for prostate cancer therapeutic interventions.