A modified rapid microprocedure for the determination of VE in serum, was described. VE reduced Fe3+ to Fe2+ and then the Fe2+ combined with bathophenanthroline to form a pink complex -which could be determined spect-rophotometrically. As little as 0.3ml (or 0.2ml) of serum or plasma sample was sufficient for determination. The reproducibility of this method was good. The CV was 4.1% (n=15). The recoveries of added VE (0.8, 0.2 and 1.6 mg/dl) were 86.3-102.5%. The mean value and SD of 99 normal adults were 1.15+ 0.31mg/dl. This spectrophotometric method was simple and could be used in common, laboratories. Some affecting frctors were discussed.

Objective to study the characteristic typing of Helicobacter pylor(Hp)phenotypes and their sub-phenotypes in the patients with duodenal bulb ulcers(DU),and its clinical significance. Methods One hundred thirty-five cases with DU and 140 casses with chronic superficial gastritis were enrolled in this study. Determinations of serum cytotoxin-associated gene protein A (CagA),vacuolating cyto-toxin A(VacA),urease (Ure)A,UreB antibodies and their sub-phenotypes by immunoblotting were carried ou. Results Positive rate of middle-phenotypes of Hp infection in DU was significantly lower than that in chronic superficial gastritis (21.5%vs 27.9%,P<0.05).VacA and CagA antibodies might express alone. There had no significant difference among the expression rate of phenotype CagA, VacA antibodies and their sub-phenotype. But expression rate of Ure antibodies in Du was higher than that in chronic superficial gasstritis (P<0.05).In infection of Hp type I, the expression rate of sub-phenotypes 30ku UreA in DU was hronic superficial gastritis (P<0.05). Conclusions The VacA is not for expressing higher than that inpression of Hp exists many sub-phenotypes ( 128 ku CagA 116 ku CagA, 95 ku VacA, 91 ku CagA 0 ku UreA),and it probably causes formation of DU by comprehensive effect. Hp type I with sub phenotype expressing 30 ku Urea may be more pathogenic in DU formation.

Objective To analyze the reliability of the Boston bowel preparation scale (BBPS) for the assessment of bowel preparation quality. Methods Demonstration video of Boston bowel preparation scale provided by Boston Medical Center were viewed by 49 clinicians,who came from several hospitals in Guangdong province and participated in an education conference.Then 3 testing colonoscopy videos were scored with BBPS and inter-observer reliability was assessed. 13 participants repeated the above test 3 months later,and intra-observer reliability was assessed.Results The correlation coefficient of inter-observer for BBPS scores was 0.987 (95％ CI:0.949 - 1.000 ),and that of intra-observer was 0.713(95 ％ CI:0.452 -0.849).Conclusion BBPS is a reliable measure of bowel preparation,while the validity of BBPS deserves further analysis.

Genetic mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to a variety of neurodegenerative diseases including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia and Parkinson’s disease. In the brain, TREM2 is highly expressed on the cell surface of microglia, where it can transduce signals to regulate microglial functions such as phagocytosis. To date, mechanisms underlying intracellular trafficking of TREM2 remain elusive. Mutations in the presenilin 1 (PS1) catalytic subunit of the γ-secretase complex have been associated with increased generation of the amyloidogenic Aβ (amyloid-β) 42 peptide through cleavage of the Aβ precursor amyloid precursor protein. Here we found that TREM2 interacts with PS1 in a manner independent of γ-secretase activity. Mutations in TREM2 alter its subcellular localization and affects its interaction with PS1. Upregulation of PS1 reduces, whereas downregulation of PS1 increases, steady-state levels of cell surface TREM2. Furthermore, PS1 overexpression results in attenuated phagocytic uptake of Aβ by microglia, which is reversed by TREM2 overexpression. Our data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function.