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321.
Adela Paez Jimenez Mostafa K. Mohamed Noha Sharaf Eldin Hasnaa Abou Seif Said El Aidi Yehia Sultan Nasr Elsaid Claire Rekacewicz Mostafa El-Hoseiny May El-Daly Mohamed Abdel-Hamid Arnaud Fontanet 《PloS one》2009,4(9)
Objective
To identify current risk factors for hepatitis C virus (HCV) transmission in Greater Cairo.Design and Setting
A 1∶1 matched case-control study was conducted comparing incident acute symptomatic hepatitis C patients in two “fever” hospitals of Greater Cairo with two control groups: household members of the cases and acute hepatitis A patients diagnosed at the same hospitals. Controls were matched on the same age and sex to cases and were all anti-HCV antibody negative. Iatrogenic, community and household exposures to HCV in the one to six months before symptoms onset for cases, and date of interview for controls, were exhaustively assessed.Results
From 2002 to 2007, 94 definite acute symptomatic HCV cases and 188 controls were enrolled in the study. In multivariate analysis, intravenous injections (OR = 5.0; 95% CI = 1.2–20.2), medical stitches (OR = 4.2; 95% CI = 1.6–11.3), injection drug use (IDU) (OR = 7.9; 95% CI = 1.4–43.5), recent marriage (OR = 3.3; 95% CI = 1.1–9.9) and illiteracy (OR = 3.9; 95% CI = 1.8–8.5) were independently associated with an increased HCV risk.Conclusion
In urban Cairo, invasive health care procedures remain a source of HCV transmission and IDU is an emerging risk factor. Strict application of standard precautions during health care is a priority. Implementation of comprehensive infection prevention programs for IDU should be considered. 相似文献322.
Matthew B. West Zaneer M. Segu Christa L. Feasley Pilsoo Kang Iveta Klouckova Chenglong Li Milos V. Novotny Christopher M. West Yehia Mechref Marie H. Hanigan 《The Journal of biological chemistry》2010,285(38):29511-29524
The cell surface glycoprotein γ-glutamyl transpeptidase (GGT) was isolated from healthy human kidney and liver to characterize its glycosylation in normal human tissue in vivo. GGT is expressed by a single cell type in the kidney. The spectrum of N-glycans released from kidney GGT constituted a subset of the N-glycans identified from renal membrane glycoproteins. Recent advances in mass spectrometry enabled us to identify the microheterogeneity and relative abundance of glycans on specific glycopeptides and revealed a broader spectrum of glycans than was observed among glycans enzymatically released from isolated GGT. A total of 36 glycan compositions, with 40 unique structures, were identified by site-specific glycan analysis. Up to 15 different glycans were observed at a single site, with site-specific variation in glycan composition. N-Glycans released from liver membrane glycoproteins included many glycans also identified in the kidney. However, analysis of hepatic GGT glycopeptides revealed 11 glycan compositions, with 12 unique structures, none of which were observed on kidney GGT. No variation in glycosylation was observed among multiple kidney and liver donors. Two glycosylation sites on renal GGT were modified exclusively by neutral glycans. In silico modeling of GGT predicts that these two glycans are located in clefts on the surface of the protein facing the cell membrane, and their synthesis may be subject to steric constraints. This is the first analysis at the level of individual glycopeptides of a human glycoprotein produced by two different tissues in vivo and provides novel insights into tissue-specific and site-specific glycosylation in normal human tissues. 相似文献
323.
Ahmed A. Abdelhady Barbara Seuss Mostafa H. El-Dawy Nageh A. Obaidalla Kamel H. Mahfouz Samar A. Abdel Wahed 《Geobios》2018,51(4):259-268
Although foraminifers have been extensively used for biochronology, no quantitative evaluation of the quality of their application is available. In this work we apply a quantitative approach – the Unitary Association (UA) method – to evaluate the relative quality of planktic and benthic foraminifers in biostratigraphy. Based on 12,321 specimens belonging to 65 planktic and 132 benthic foraminifer species in 117 samples from the Paleocene–Eocene strata of the Kharga-Baris Oases (Western Desert, Egypt), the potential stratigraphic resolution power of benthic foraminifers is quantitatively assessed and compared to planktic foraminifers. The UA method accounts for superpositional contradictions between sets of coexisting taxa and generates unitary associations, which are conceptually similar to Oppel zones. The analysis produced fifteen unitary associations for the Paleocene–Eocene benthic Foraminifera of the studied sections, instead of three classical zones; most of these unitary associations are easily identified by the restricted occurrence of a single species. Although planktic Foraminifera have a higher seriation reality leading to a more robust biozonation, benthic Foraminifera have a higher stratigraphic resolution, at least at such regional scale. Furthermore, there was a significant positive correlation between the number of unitary associations and the number of species (R = 0.78 for planktic and 0.70 for benthic foraminifers; both with p < 0.001). These results corroborate that quantitative techniques may lead to a higher resolution in biochronology, even when applied to poor biochronological markers. Moreover, in contrast to simple spatiotemporal analyses, the Unitary Association method can accurately assess the stratigraphic potential of a given taxonomic group. 相似文献
324.
Amyotrophic Lateral Sclerosis (ALS) is a devastating adult onset neurodegenerative disease affecting both upper and lower motor neurons. TDP-43, encoded by the TARDBP gene, was identified as a component of motor neuron cytoplasmic inclusions in both familial and sporadic ALS and has become a pathological signature of the disease. TDP-43 is a nuclear protein involved in RNA metabolism, however in ALS, TDP-43 is mislocalized to the cytoplasm of affected motor neurons, suggesting that disease might be caused by TDP-43 loss of function. To investigate this hypothesis, we attempted to generate a mouse conditional knockout of the Tardbp gene using the classical Cre-loxP technology. Even though heterozygote mice for the targeted allele were successfully generated, we were unable to obtain homozygotes. Here we show that although the targeting vector was specifically designed to not overlap with Tardbp adjacent genes, the homologous recombination event affected the expression of a downstream gene, Masp2. This may explain the inability to obtain homozygote mice with targeted Tardbp. 相似文献
325.
326.
Eman AE. Badr Rasha G. Mostafa Samah M. Awad Hala Marwan Hamed M. Abd El-Bary Hossam EM. Shehab Samar Ebrahim Ghanem 《Biochemistry and Biophysics Reports》2020
BackgroundMyocardial infarction (MI) is the major cause of death and disability worldwide. Many recent studies revealed the relationship between circulating irisin levels, endothelial dysfunctions and subclinical atherosclerosis in adult patients.ObjectivesThe aim of this study was to investigate the distribution of Irisin gene single nucleotide polymorphism in patients with MI and its association with other clinical and laboratory variables in these patients.Patients and methodsThis study was carried out in 100 patients with MI, and 100 healthy subjects served as controls. All studied subjects underwent laboratory investigations, including measurement of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-c) high-density lipoprotein cholesterol (HDL-c), creatinine kinase-MB (CK-MB), troponin I (TnI) and genotyping of rs 3480 and rs726344 of Irisin genes using the TaqMan Allelic Discrimination assay technique.ResultsThere was a significant difference of Irisin genotypes in patients when compared to controls. By estimating odd ratio (OR) an association was found between G allele of rs 3480 and A allele of rs726344with increase the risk of developing myocardial infarction by 4.03 and 3.47 fold respectively. GG of rs 3480 carriers had significantly increased Troponin I and triglyceride levels, while GA carriers of rs726344 had significantly increased CKMB, Total cholesterol, LDLc, HDLc, troponin I and triglyceride levels compared with other genotypes.ConclusionG allele of rs 3480 and A allele of rs726344can considered as genetic risk factors for MI; these findings could have an impact on preventive strategy for myocardial infarction. 相似文献
327.
Mahfuzar Rahman Nazmul Sohel Mohammad Yunus Mahbub Elahi Chowdhury Samar Kumar Hore Khalequ Zaman Abbas Bhuiya Peter Kim Streatfield 《PloS one》2013,8(1)
Background
Arsenic in drinking water was associated with increased risk of all-cause, cancer, and cardiovascular death in adults. However, the extent to which exposure is related to all-cause and deaths from cancer and cardiovascular condition in young age is unknown. Therefore, we prospectively assessed whether long-term and recent arsenic exposures are associated with all-cause and cancer and cardiovascular mortalities in Bangladeshi childhood population.Methods and Findings
We assembled a cohort of 58406 children aged 5–18 years from the Health and Demographic Surveillance System of icddrb in Bangladesh and followed during 2003–2010. There were 185 non-accidental deaths registered in-about 0.4 million person-years of observation. We calculated hazard ratios for cause-specific death in relation to exposure at baseline (µg/L), time-weighted lifetime average (µg/L) and cumulative concentration (µg-years/L). After adjusting covariates, hazard ratios (HRs) for all-cause childhood deaths comparing lifetime average exposure 10–50.0, 50.1–150.0, 150.1–300.0 and ≥300.1µg/L were 1.37 (95% confidence interval [CI], 0.74–2.57), 1.44 (95% CI, 0.88–2.38), 1.22 (95% CI, 0.75–1.98) and 1.88 (95% CI, 1.14–3.10) respectively. Significant increased risk was also observed for baseline (P for trend = 0.023) and cumulative exposure categories (P for trend = 0.036). Girls had higher mortality risk compared to boys (HR for girls 1.79, 1.21, 1.64, 2.31; HR for boys 0.52, 0.53, 1.14, 0.99) in relation to baseline exposure. For all cancers and cardiovascular deaths combined, multivariable adjusted HRs amounted to 1.53 (95% CI 0.51–4.57); 1.29 (95% CI 0.43–3.87); 2.18 (95%CI 1.15–4.16) for 10.0–50.0, 50.1–150.0, and ≥150.1, comparing lowest exposure as reference (P for trend = 0.009). Adolescents had higher mortality risk compared to children (HRs = 1.53, 95% CI 1.03–2.28 vs. HRs = 1.30, 95% CI 0.78–2.17).Conclusions
Arsenic exposure was associated with substantial increased risk of deaths at young age from all-cause, and cancers and cardiovascular conditions. Girls and adolescents (12–18 years) had higher risk compared to boys and child. 相似文献328.
M. Kausar Neyaz R. Suresh Kumar Showket Hussain Samar Naqvi Indu Kohaar Nisha Thakur 《Biomarkers》2013,18(6):597-606
As current evidence suggests the involvement of epigenetic modification of tumour suppressor genes in human cancer, we investigated the aberrant promoter methylation of FHIT and RASSF1A genes in human papillomavirus (HPV)-mediated cervical cancer in Indian women. We analysed 60 cervical cancer tissue biopsies of different clinical stage and histological grading and 23 healthy control samples with normal cervical cytology. Methylation-specific polymerase chain reaction (MSP) was performed to analyse the methylation status of FHIT and RASSF1A genes and confirmed by sequencing. Both patients and controls were screened for HPV infection and 98% of the HPV-infected cases showed positivity for HPV type 16. Aberrant promoter methylation of the FHIT gene was found in 28.3% (17/60) of cases and of the RASSF1A gene in 35.0% (21/60) of cases; promoter methylation of both the genes was found in 13.3% (8/60) of cervical cancer cases. Methylation was significantly (p<0.01) associated with the cervical cancer cases compared with controls. None of the 23 controls was found to be methylated in either of these genes. This is the first study indicating a correlation between the promoter methylation of FHIT and RASSF1A genes and the clinical stage and histological grading of cervical carcinoma in Indian women. Future studies are underway to examine the practical implications of these findings for use as a biomarker. 相似文献
329.
Maie?Alshahid Salma?M?Wakil Mohammed?Al-Najai Nzioka?P?Muiya Samar?Elhawari Daisy?Gueco Editha?Andres Samia?Hagos Nejat?Mazhar Brian?F?Meyer Nduna?DzimiriEmail author 《Human genomics》2013,7(1):15
Background
The muscle Ras (MRAS) gene resides on chromosome 3q22.3 and encodes a member of the membrane-associated Ras small GTPase proteins, which function as signal transducers in multiple processes including cell growth and differentiation. Its role in cardiovascular disease is not fully understood yet. In a preliminary study in heterozygous familial hypercholesterolaemia, we identified a locus linking the early onset of coronary artery disease (CAD) to chromosome 3q.22 and elected to sequence the MRAS gene using the MegaBACE DNA analysis system. In the present study, we investigated the association of seven single-nucleotide polymorphisms (SNPs) at this locus with CAD and its dyslipidaemia-related risk traits in 4,650 Saudi angiographed individuals using TaqMan assays by the Applied Biosystems real-time Prism 7900HT Sequence Detection System.Results
Among the studied SNPs, rs6782181 (p = 0.017) and rs9818870T (p = 0.009) were associated with CAD following adjustment for sex, age and other confounding risk factors. The rs6782181_GG also conferred risk for obesity (1,764 cases vs. 2,586 controls) [1.16(1.03–1.30); p = 0.017], hypercholesterolaemia (1,686 vs. 2,744) [1.23(1.02–1.47); p = 0.019], hypertriglyceridaemia (1,155 vs. 3,496) [1.29(1.01–1.45); p = 0.043] and low high-density lipoprotein-cholesterol (lHDL-chol) levels (1,935 vs. 2,401) [1.15(1.02–1.30); p = 0.023] after adjustment. Additionally, rs253662_(CT+TT) [1.16(1.01–1.32); p = 0.030] was associated with lHDL-chol levels. Interestingly, rs253662 (p = 0.014) and rs6782181 (p = 0.019) were protective against acquiring high low-density lipoprotein-cholesterol (hLDL-chol) levels (p = 0.014), while rs1720819 showed similar effects against CAD (p < 0.0001). More importantly, a 7-mer haplotype, ACCTGAC (χ2 = 7.66; p = 0.0056), constructed from the studied SNPs, its 6-mer derivative CCTGAC (χ2 = 6.90; p = 0.0086) and several other shorter derivatives conferred risk for obesity. hLDL-chol was weakly linked to CTAA (χ2 = 3.79; p = 0.052) and CCT (χ2 = 4.32; p = 0.038), while several other haplotypes were protective against both obesity and hLDL-chol level.Conclusion
Our results demonstrate that the genomic locus for the MRAS gene confers risk for CAD, obesity and dyslipidaemia and point to the possible involvement of other genes or regulatory elements at this locus, rather than changes in the M-Ras protein function, in these events.330.
Uversky VN Shah SP Gritsyna Y Hitchcock-DeGregori SE Kostyukova AS 《Journal of molecular recognition : JMR》2011,24(4):647-655
An intriguing regulatory mechanism is the ability of some proteins to recognize their binding partners in an isoform‐specific manner. In this study we undertook a systematic analysis of the specificity of the tropomodulin (Tmod) interaction with tropomyosin (TM) to show that affinities of different Tmod isoforms to TM are isoform‐dependent. Intrinsic disorder predictions, alignment of sequences, and circular dichroism were utilized to establish a structural basis for these isoform‐specific interactions. The affinity of model peptides derived from the N‐terminus of different TM isoforms to protein fragments that correspond to the two TM‐binding sites of different Tmod isoforms were analyzed. Several residues were determined to be responsible for the isoform‐dependent differences in affinity. We suggest that changing a set of residues rather than a single residue is needed to alter the binding affinity of one isoform to mimic the affinity of another isoform. The general intrinsic disorder predictor, PONDR® VLXT, was shown to be a useful tool for analyzing regions involved in isoform‐specific binding and for predicting the residues important for isoform differences in binding. Knowing the residues responsible for isoform‐specific affinity creates a tool suitable for studying the influence of Tmod/TM interactions on sarcomere assembly in muscle cells or actin dynamics in non‐muscle cells. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献