[Study on the relationship between dietary quality and the risk of diabetes and prediabetes in urban women].

Objective: To explore the relationship between dietary quality and the risk of diabetes and prediabetes among urban women based on alternative healthy eating index-2010（AHEI-2010). Methods: From March to July 2016, a total of 1 061 female residents from 8 cities, Beijing, Guangzhou, Chengdu, Lanzhou, Xuchang, Jilin, Wuhu and Chenzhou in China, were selected by using the multi-stage sampling method. The basic characteristics of all participants were collected by using self-made questionnaire, and the dietary status of the subjects was collected by using 24-hour dietary recall method. AHEI-2010 scores were calculated and the diet was divided into low, medium and high dietary quality group according to the third quartile. All participants received physical examination, systolic blood pressure test, fasting blood glucose test and glycosylated hemoglobin test. Unconditional logistic regression model was used to analyze the relationship between dietary quality and the risk of diabetes and prediabetes. Results: The age of all participants was（48.0±17.5) years old. The median（P25, P75) of AHEI-2010 score was 46.52（40.04, 54.88). The prevalence of diabetes and prediabetes were 13.3%（141 cases) and 50.0%（530 cases), respectively. Unconditional logistic regression analysis showed that after adjusting for age, city, education, diet control, physical activity, energy intake and waist circumference, compared with the low diet quality group, the OR（95%CI) values of medium, high dietary quality group and diabetes risk were 0.96（0.57-1.62) and 0.63（0.36-1.09), respectively; the OR（95%CI) values of medium, high dietary quality group and prediabetes risk were 0.93（0.64-1.35) and 1.28（0.87-1.88), respectively. Conclusion: The dietary quality of urban women based on AHEI-2010 evaluation is not related to the risk of diabetes and prediabetes.

[Impact of Herpud1 in the homocysteine-induced phenotypic switching of vascular smooth muscle cells].

Objective: To investigate the impact of homocysteine inducible endoplasmic reticulum(ER) protein with ubiquitin like domain 1 protein (Herpud1) in the homocysteine (Hcy) -induced phenotypic switching of vascular smooth muscle cells (VSMCs). Methods: VSMCs were derived from thoracic aortic artery of male Sprague Dawley rats and cultured VSMCs (4-7 passage) were treated with various concentrations of Hcy (0, 100, 500 and 1 000 µmol/L) and applied to immunofluorescence to observe the morphological changes of VSMCs via SM-actin staining. Western blot was used to detect the expression of VSMCs phenotypic markers, including Osteopontin, Calponin and smooth muscle myosin heavy chain (SM-MHC) and the expression of endoplasmic reticulum stress (ERS) related proteins, including C/EBP-homologous protein (CHOP), inositol-requiring kinase 1 (IRE-1) and glucose regulating protein 78 (GRP78) in the absence and presence of non-selective inhibitor of ERS, 4-phenylbutyric acid (4-PBA, 2 mg/ml). The Herpud1 mRNA and protein levels were determined in Hcy-stimulated VSMCs treated with 4-PBA or transfected with specific siRNA targeting Herpud1. Results: Compared with the control group, SM-actin staining results showed that the shape of VSMCs treated with different concentrations of Hcy for 24 hours changed from long fusiform into round form, arrangement of myofilament became irregular and the most significant alteration was found in the 500 µmol/L Hcy group. After intervention of 24 hours, various concentration of Hcy increased protein expression of Osteopontin, and reduced Calponin and SM-MHC protein expressions in VSMCs (all P<0.05). In addition, the results showed that Hcy increased the expression of CHOP, IRE-1 and GRP78 in a dose-dependent manner, which could be reversed by 4-PBA treatment (all P<0.05). However, 4-PBA inhibited Hcy induced upregulation of Osteopontin and downregulation of Calponin and SM-MHC, suggesting that ERS was involved in Hcy-induced phenotypic switching of VSMCs. Herpud1 protein was mostly expressed in the cytoplasm and was also expressed in the nucli, both in the control, Hcy and Hcy+4-PBA groups. Moreover, Hcy increased mRNA and protein levels of Herpud1 (P<0.05), whereas treatment with 4-PBA could significantly reduce Hcy-induced upregulation of Herpud1 (P<0.05). Furthermore, knockdown of Herpud1 abrogated the effects of Hcy on VSMCs phenotype markers. Conclusion: Herpud1 plays an important role in Hcy-induced phenotypic switching of VSMCs.

A maternal hereditary deafness pedigree of the A1555G mitochondrial mutation, causing aminoglycoside ototoxicity predisposition.

OBJECTIVE: To characterise the hearing loss, and the frequency of the mitochondrial deoxyribonucleic acid 12S ribosomal ribonucleic acid A1555G mutation, in a large pedigree of aminoglycoside-induced deafness. DESIGN: Hearing loss was clinically assessed. Blood samples were collected from 27 family members (19 matrilinear and eight non-matrilinear) and leukocyte deoxyribonucleic acid was extracted. Mitochondrial deoxyribonucleic acid fragments, spanning the 1555 location, were amplified by polymerase chain reaction. Polymerase chain reaction products were analysed by restriction fragment length polymorphism and deoxyribonucleic acid sequencing. RESULTS: We detected the A1555G mutation in all 19 matrilinear relatives. Of these 19, two exhibited congenital deafness, four had no hearing deficits and the remaining 13 suffered mild to profound hearing loss. CONCLUSION: We confirmed that the A1555G mutation is a 'hot spot' associated with non-syndromic, inherited hearing loss. This mutation may play a vital role in the pathogenesis of hearing impairment, and can result in various grades of deafness.

Protease-catalyzed synthesis of the tripeptide CCK(26-28), a fragment of CCK-8.

Two enzymatically synthetic strategies of the tripeptide derivative PhAc-Asp(OMe)-Tyr-Met-OAl are reported. The second strategy gains the advantage of more economical starting materials, less reaction steps and a higher overall isolated yield of this tripeptide fragment over the first strategy. The effect of the acyl-donor ester concentration and structure, the C-alpha protecting group of the nucleophile, reaction media, enzyme and the carrier on the tripeptide derivative synthesis were studied. This tripeptide selected is a fragment of the cholecystokinin C-terminal octapeptide (CCK-8), a potential therapeutic agent in the control of gastrointestinal function and also a drug candidate for the treatment of epilepsy.