Serotyping of hepatitis C virus in hemodialysis patients: comparison with a standardized genotyping assay

The aims of this study were to investigate the prevalence of hepatitis C virus (HCV) genotypes and serotypes in anti-HCV-positive hemodialysis patients and determine the concordance between genotyping and serotyping methods. Sixty-two hemodialysis patients were included in this study. HCV RNA was determined using polymerase chain reaction assay and genotypes using a line probe assay. HCV serotyping was performed with competitive enzyme-linked immunosorbent assay. Genotype 4 (52 patients) was the most predominant genotype, followed by type 1 (10 patients). The most prevalent HCV serotype was type 4 (41 patients), followed by serotype 1 (6 patients). We detected multiple serotypes in 4 patients and untypeable strains in 11. The overall sensitivity of serotyping assay was 82% for the study patients. According to the genotyping results, the sensitivity of serotyping was 60% and 86.5% for HCV types 1 and 4, respectively. There was a 100% concordance between results of serotyping and genotyping in the identification of HCV type 1 and 91% concordance in HCV type 4. Serological typing method may be of great value in microbiology laboratories that require a simple assay for identification of HCV genotypes, although the sensitivity of this assay may be limited by the immunocompetence of infected hemodialysis patients.     

Comparison between Glidescope,Airtraq and Macintosh laryngoscopy for emergency endotracheal intubation in intensive care unit: Randomized controlled trial

Background

Emergency endotracheal intubation in intensive care is a major challenge that can be associated with life-threatening complications. The aim of this study was to evaluate the success of the first attempt of endotracheal intubation and incidence of complications using Macintosh laryngoscopy, Airtraq or Glidescope during emergency intubation in intensive care.

Acute brucellosis in Saudi families: relationship between brucella serology and clinical symptoms.

OBJECTIVE: To determine if screening family members of patients with acute brucellosis will enhance the detection rate of brucellosis and also to determine the relationship between symptoms and brucella serology. MATERIALS AND METHODS: Family members from patients with acute brucellosis were interviewed and serologically screened. All seropositive family members were clinically and serologically followed for six months. RESULTS: Twenty-five acute brucellosis patients and their 178 family members were enrolled from January 2001 to February 2002. Of the 178 family members, 40 (23%) manifested various symptoms, 138 (77%) were asymptomatic, with an overall seroprevalence rate of 34 (19%). The rate of seropositivity among the symptomatic family members was 23 (58%) and for the asymptomatic was 11 (8%) (P<0.001). The majority of the symptomatic family members (13 (57%)) had a high Brucella titer in comparison to one (9%) of the asymptomatic group (P<0.001). Acute brucellosis was diagnosed and treated in 18 (78%) of the symptomatic seropositive family members and in four (36%), of the asymptomatic seropositive family members with an acute brucellosis prevalence rate of 22 (12%). All family members with acute infection recovered without sequelae; one patient relapsed (5%). CONCLUSION: Symptomatic family members are more likely to be seropositive with a high titer in comparison to the asymptomatic members.     

Does the surgical approach for treating mandibular condylar fractures affect the rate of seventh cranial nerve injuries? A systematic review and meta-analysis based on a new classification for surgical approaches

Purpose

The purpose of this study was to determine the rate of facial nerve injury (FNI) when performing (ORIF) of mandibular condylar fractures by different surgical approaches.

Facile access to regio- and stereoselective synthesis of highly functionalized spiro[indoline-3,2′-pyrrolidines] incorporating a pyrene moiety: experimental,photophysical and theoretical approach

The regio- and stereochemical polar [3 + 2] cycloaddition of azomethine ylides, which were generated in situ by the reaction of isatin and sarcosine or benzylamine, with (E)-3-aryl-1-(pyren-1-yl)prop-2-en-1-ones as dipolarophiles, was studied using experimental and theoretical methods. The chemical structures and relative configurations of all products have been fully established by 1D and 2D homonuclear and heteronuclear correlation NMR spectrometry. The effects of the electronic and steric factors of the reactions were discussed. The photophysical properties of the synthesized spiro[indoline-3,2′-pyrrolidin]-2-ones and 5′-phenyl-spiro[indoline-3,2′-pyrrolidin]-2-ones were studied. The mechanism of the reactions was investigated using global and local reactivity indices and frontier molecular orbital (FMO) analysis at the B3LYP/6-31G level of theory. The relationship between the electrophilicity index ω of the dipolarophiles and the Hammett constant σ_p has been studied. The theoretical scale of reactivity correctly explains the electrophilic activation/deactivation effects promoted by electron-withdrawing and electron-releasing substituents in the para-position of the dipolarophiles.

The regio- and stereochemical polar [3 + 2] cycloaddition of azomethine ylides with (E)-3-aryl-1-(pyren-1-yl)prop-2-en-1-ones as dipolarophiles, was studied using experimental and theoretical methods.     

Molecular updating of β-thalassemia mutations in the Upper Egyptian population

We have updated the dataset of the molecular spectrum of the β-thalassemia (β-thal) in Upper Egypt. Buccal swabs were analyzed from 94 unrelated patients with β-thal major (β-TM) using reverse dot-blot and multiplex amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). The most frequent mutation was IVS-I-110 (G>A) (57%). The IVS-I-110, IVS-I-6 (T>C) and IVS-I-1 (G>A) mutations accounted for 87% of the β-thal anomalies. The codon 39 (C>T) and frameshift codon (FSC) 6 (-A) (GAG>-GG) mutations were only detected in Al-Minya and Qina, respectively. We did not observe the IVS-II-745 (C>G) or -101 (C>T) mutations. Forty-three percent of Upper Egyptians were homozygotes. Our efforts were an important step to complete the mutation map of β-thal in Egypt restricted to Cairo and the Nile Delta regions. This study will help to develop preventative programs for Upper Egyptians. It addressed the genetic drift of the β-thal gene mutations in Africa, Asia, and Europe.     

Thrombospondin-1 null mice are resistant to hypoxia-induced pulmonary hypertension

Background and objective

Chronic hypoxia induces pulmonary hypertension in mice. Smooth muscle cell hyperplasia and medial thickening characterize the vasculature of these animals. Thrombospondin-1 null (TSP-1^-/-) mice spontaneously develop pulmonary smooth muscle cell hyperplasia and medial thickening. In addition, TSP-1 produced by the pulmonary endothelium inhibits pulmonary artery smooth muscle cell growth. Based on these observations we sought to describe the pulmonary vascular changes in TSP-1^-/- mice exposed to chronic hypoxia.

Methods

We exposed TSP-1^-/- and wild type (WT) mice to a fraction of inspired oxygen (FiO2) of 0.1 for up to six weeks. Pulmonary vascular remodeling was evaluated using tissue morphometrics. Additionally, right ventricle systolic pressures (RVSP) and right ventricular hypertrophy by right ventricle/left ventricle + septum ratios (RV/LV+S) were measured to evaluate pulmonary hypertensive changes. Finally, acute pulmonary vasoconstriction response in both TSP-1^-/- and WT mice was evaluated by acute hypoxia and U-46619 (a prostaglandin F2 analog) response.

Results

In hypoxia, TSP-1^-/- mice had significantly lower RVSP, RV/LV+S ratios and less pulmonary vascular remodeling when compared to WT mice. TSP-1^-/- mice also had significantly lower RVSP in response to acute pulmonary vasoconstriction challenges than their WT counterparts.

Conclusion

TSP-1^-/- mice had diminished pulmonary vasoconstriction response and were less responsive to hypoxia-induced pulmonary hypertension than their wild type counterparts. This observation suggests that TSP-1 could play an active role in the pathogenesis of pulmonary hypertension associated with hypoxia.