The immunopathogenesis of chronic hepatitis B (CHB) has not been clarified yet. Toll-like receptors (TLR) are a receptor family that initiates immunity with exogenous-endogenous ligands and plays a role in the pathogenesis of infections. In this study, we aimed to investigate the frequency of TLR 3 1377C/T (rs3775290) polymorphism and its role in patients with CHB. We included 50 healthy individuals as control group and 73 active and 43 inactive hepatitis B patients. All DNA samples were isolated from blood samples. For the detection of TLR 3 1377C/T single-nucleotide polymorphism, restriction fragment length polymorphism was used. A statistically significant difference was determined in Hepatitis B virus (HBV) DNA levels of CHB patients with the CC, CT, and TT genotypes (p = 0.013). The highest levels of HBV DNA were detected in individuals with TT genotypes. Additionally, the frequency of CC genotype was higher in the active CHB patients compared with that of the inactive CHB patients (p = 0.044). No statistically significant difference in TLR 3 1377C/T polymorphism was detected between healthy controls and the hepatitis B patients (p = 0.342). In conclusion, HBV DNA level was higher in the individuals with TT genotype, and CC genotype was more frequent in the active CHB patients. These results suggest a possible association between CHB and TLR 3 gene (1377C/T) polymorphism.
Introduction:The human population is aging at an astonishing rate. The aim of this study is to capture a situation snapshot revealing the proportion of individuals aged 65 years and over among inpatients in healthcare institutions in Turkey and the prevalence and type of infections in this patient group in order to draw a road map. Materials and Methods: Hospitalized patients over 65 years at any of the 62 hospitals in 29 cities across Turkey on February 9, 2017 were included in the study. Web-based SurveyMonkey was used for data recording and evaluation system. Results: Of 17,351 patients 5871 (33.8%) were !65 years old. The mean age was 75.1 AE7.2 years; 3075 (52.4%) patients were male. Infection was reason for admission for 1556 (26.5%) patients. Pneumonia was the most common infection. The median length of hospital stay was 5 days (IQR: 2-11 days). The Antibiotic therapy was initiated for 2917 (49.7%) patients at the time of admission, and 23% of the antibiotics prescribed were inappropriate. Healthcare-associated infections developed in 1059 (18%) patients. Urinary catheters were placed in 2388 (40.7%) patients with 7.5% invalid indication. Conclusion:This study used real data to reveal the proportion of elderly patients in hospital admissions. The interventions done, infections developed during hospitalization, length of hospital stay, and excessive drug load emphasize the significant impact on health costs and illustrate the importance of preventive medicine in this group of patients.
Objective: Roberts syndrome is a very rare genetic disease, and it has an autosomal recessive inheritance pattern. It develops as a result of the mutation in ESCO2 gene located in the 8th chromosome. In our study, we aimed to present a case which was found to have Roberts syndrome coexisting with multiple anomalies, particularly skeletal system anomaly, in the 17 weeks of gestation. Case(s): In the fetal ultrasonographic evaluation performed on the pregnant women who referred to our hospital for routine gestational examination in the 17 weeks of gestation, anomalies in the bilateral upper and lower extremities, contracted legs, bilateral cleft palate and lip, intrauterine growth restriction and cardiac anomaly were found in the fetus. Roberts syndrome was considered first with these ultrasonographic findings. The diagnosis of Roberts syndrome was confirmed by cytogenetic and molecular analyses. Early segregation of centromeres and early breaking up of heterochromatic regions near centromeres were found at metaphase stage. By cytogenetic and molecular analyses, homozygous mutation in ESCO2 gene of the fetus and heterozygous mutation in the parents were found. The termination of pregnancy was decided after the genetic consultation with the parents. Physical examination findings and prenatal ultrasound findings after termination were found similar. Conclusion: Many severe skeletal dysplasia cases can be diagnosed ultrasonographically before 20 weeks of gestation. Early diagnosis ensures to take necessary actions for medical support during postnatal period and in terms of labor if pregnancy continues as well as genetic consultation opportunity. If the genetic disease that causes skeletal dysplasia can be identified and parents are found to have this gene, healthy pregnancies can be achieved by obtaining normal embryos via pre-implantation genetic diagnosis in order to prevent the relapse of the disease.
Background: Previous studies in an experimental model of rabies showed neuronal process degeneration in association with severe clinical disease. Cultured adult rat dorsal root ganglion (DRG) neurons infected with CVS-11 strain of rabies virus (RABV) showed axonal swellings and immunostaining for 4-hydroxy-2-nonenal (4-HNE) indicating evidence of lipid peroxidation associated with oxidative stress and reduced axonal growth versus mock-infection. We have demonstrated that RABV induces alterations in a variety of mitochondrial parameters, including an increase in reactive oxygen species production after addition of substrates or inhibitors and increased activity of Complex I of the respiratory chain vs. mock infection. We have hypothesized that a RABV protein targets the mitochondria and triggers its dysfunction. Methods & Materials: We used immunocytochemistry, Western immunoblotting, immunoprecipation and proteomics methods to study RABV-and mock-infection of mouse neuroblastoma (MNA) cells. Results: Immunocytochemistry of CVS-infected cells after 72 h post-infection showed strong colocalization of mitochondria with the RABV phosphoprotein (P). Extracts of MNA cells from the mitochondrial subcellular fractionation were analyzed with a proteomics approach. We identified peptides belonging to the RABV P, glycoprotein (G), and nucleocapsid protein (N) with 67% of protein coverage at 95% confidence for P vs. N (8%) and G (6%). Our data show that the majority of viral peptides (79%) belong to P vs. N (13%) or G (8%), indicating that the extract was highly enriched with P. P was detected by immunoblotting in RABV-infected purified mitochondrial extracts and in Complex I immunoprecipitates from the extracts, but not in mock-infected extracts. A plasmid expressing P in cells produced an increase in Complex I activity, whereas expression of other RABV proteins did not. We have analyzed a variety of recombinant plasmids encoding various segments of the P gene. Expression of a peptide from amino acid 139 to 172 produced an increase in Complex I activity similar to expression of the entire P protein, whereas most peptides that did not contain this region did not produce increased activity of Complex I. Conclusion: The RABV phosphoprotein is present in mitochondria and may interact with Complex I causing mitochondrial dysfunction, oxidative stress, neuronal process degeneration, and severe clinical disease in experimental rabies.
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