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Ke F.,Fujian Medical University | Wu W.,Xiamen Maternity and Child Health Care Hospital
Acta Crystallographica Section E: Structure Reports Online | Year: 2013

In the title compound, [Cu3I3(C5H8NS)3] n , a polymeric structure is formed along [100] through bridging iodide and pyridine-2-thione ligands. The metal atoms are engaged in [Cu3S3] and [Cu2S2] rings sharing Cu - S edges, with the [Cu2S2] rings located about inversion centers. CuI atoms bridged by iodide ions exhibit the shortest Cu⋯Cu separation in the polymer [2.8590 (14) Å]. The three independent CuI atoms all display distorted tetrahedral coordination geometries. Source

Huang W.-F.,Xiamen Medical Research Institute | Zhang H.,Xiamen Medical Research Institute | Ouyang S.,Xiamen Medical Research Institute | Lu C.-J.,Xiamen Maternity and Child Health Care Hospital
World Chinese Journal of Digestology | Year: 2011

AIM: To evaluate the effect of 5-hydroxytryptamine (5-HT) and electrical stimulation on gastric electric activity (GEA) in rabbits with gastric dysrhythmia (GD). METHODS: GD was induced in rabbits by peripheral injection of glucagon. Peripheral injection of 5-HT, gastric pacemaking, and electrical stimulation of the paraventricular nucleus (PVN) and raphe magnus (RM, P7) were performed in GD rabbits. Four pairs of bipolar Ag-AgCl electrodes implanted on the serosa along the gastric greater curve were used for recording GEA. The stimulation of PVN and RM was carried out using brain stereotaxis apparatus (SN-2). The analyzed parameters included frequency (F), phase difference (PD), ratio of negative PD (RNPD) and corresponding rate of waves (CRW). RESULTS: The F of GEA in the gastric corpus 2 increased (from 4.29 ± 0.60 to 4.56 ± 0.59, P = 0.05) and that in the gastric antrum decreased (from 4.54 ± 0.51 to 4.27 ± 0.44, P = 0.013) in GD rabbits. Injection of 500 μg 5-HT accelerated the F of GEA in the gastric corpus 1 (from 4.06 ± 0.45 to 4.25 ± 0.37, P = 0.031), corpus 3 (from 4.32 ± 0.51 to 4.58 ± 0.36, P = 0.041) and gastric antrum (from 4.54 ± 0.47 to 4.73 ± 0.44, P = 0.017) and improved the CRW in the gastric corpus 3 (from 0.78 ± 0.13 to 0.83 ± 0.10, P = 0.030) in GD rabbits. The F of GEA in the gastric corpus 3 was (from 4.27 ± 0.53 to 4.52 ± 0.47, P = 0.022) increased by gastric pacing. Electrical stimulation of PVN decreased the F of GEA in the gastric corpus 3 (from 4.47 ± 0.44 to 4.14 ± 0.46, P = 0.046) and gastric antrum (from 4.05 ± 0.54 to 3.69 ± 0.55, n = 12, P = 0.039), increased the RNPD in the gastric antrum (from 0.32 ± 0.19 to 0.40 ± 0.19, P = 0.046), and greatly inhibited GEA in GD rabbits. Electrical stimulation of P7 slowed the F of GEA in the gastric antrum (from 4.31 ± 0.44 to 3.86 ± 0.47, P = 0.012) in GD rabbits. CONCLUSION: A rabbit model of GD has been successfully developed by injection of glucagon. Peripheral injection of 500 μg 5-HT and gastric pacemaking prominently improved the waves of GEA. Electrical stimulation of the PVN and RM decreased the F of GEA in GD rabbits, which demonstrate that there exists a "descending inhibition system" in the centre nervous system. Source

Peng S.,Chinese Institute of Urban Environment | Zhang J.,Chinese Institute of Urban Environment | Liu L.,Chinese Institute of Urban Environment | Zhang X.,Xiamen Maternity and Child Health Care Hospital | And 4 more authors.
Journal of Proteome Research | Year: 2015

Recently, the number of women suffering from gestational diabetes mellitus (GDM) has risen dramatically. GDM attracts increasing attention due to its potential harm to the heath of both the fetus and the mother. We designed this case-control study to investigate the metabolome response of newborn meconium and urine to maternal GDM. GDM mothers (n = 142) and healthy controls (n = 197) were recruited during June-July 2012 in Xiamen, China. The newborns metabolic profiles were acquired using liquid chromatography coupled to mass spectrometry. The data showed that meconium and urine metabolome patterns clearly discriminated GDM cases from controls. Fourteen meconium metabolic biomarkers and three urinary metabolic biomarkers were tentatively identified for GDM. Altered levels of various endogenous biomarkers revealed that GDM may induce disruptions in lipid metabolism, amino acid metabolism, and purine metabolism. An unbalanced lipid pattern is suspected to be a GDM-specific feature. Furthermore, the relationships between the potential biomarkers and GDM risk were evaluated by binary logistic regression and receiver operating characteristic analysis. A combined model of nine meconium biomarkers showed a great potential in diagnosing GDM-induced disorders. © 2015 American Chemical Society. Source

Peng S.,Chinese Institute of Urban Environment | Liu L.,Chinese Institute of Urban Environment | Zhang X.,Xiamen Maternity and Child Health Care Hospital | Heinrich J.,Helmholtz Center for Environmental Research | And 6 more authors.
Environmental Health: A Global Access Science Source | Year: 2015

Background: Environmental pollutant exposure may play certain roles in the pathogenesis and progression of diabetes mellitus including gestational diabetes mellitus (GDM). We hypothesize that heavy metal exposure may trigger GDM during pregnancy. The objective of this study was to investigate the possible associations between selected heavy metal exposure and GDM risk. Methods: This investigation is a retrospective case-control study nested within a cohort of 1359 pregnant women. These participants were recruited in Xiamen Maternity and Child Care Hospital, China, during June to July, 2012. All their newborns' meconium samples were collected. By reviewing the antenatal care records, 166 GDM mothers were screened out from the 1359 participants; 137 of 166 GDM mothers offered their newborns' meconium samples for the metal analysis. Those 137 mothers were set as the case group. Similarly, 294 healthy mothers without any gestational complication were initially screened out from the rest 1193 non-GDM mothers. 190 of the 294 healthy mothers offered their newborns' meconium samples for the metal analysis. Those 190 mothers were set as the control group. Arsenic (As), mercury (Hg), lead (Pb), cadmium (Cd), and chromium (Cr) levels in these case-control meconium samples were measured by inductively coupled plasma mass spectrometry. The possible association between the metal levels and maternal GDM risk of studied subjects was assessed by binary logistic regression. Results: GDM prevalence of 12.21% was observed in the investigated 1359 participants. The concentrations of As, Hg, Cr and Cd in studied cases were significantly higher (p < 0.05) than those of controls. After adjustments for maternal age, pre-pregnant body mass index, gravidity, parity, hepatitis B virus infection, and newborn sex, As, Cd and Cr were found to be positively associated with GDM prevalence in dose-dependent manners. Among them, As was detected in all samples and its levels associated the maternal GDM with the adjusted odds ratios of 3.28 [95% CI 1.24, 8.71], 3.35 [95% CI 1.28, 8.75] and 5.25 [95% CI 1.99, 13.86] for the 2nd, 3rd and 4th quartiles, respectively. Conclusions: The present work implies that exposure to some of the selected metals (noticeably As) may contribute to maternal GDM risk during pregnancy. © 2015 Peng et al.; licensee BioMed Central. Source

You J.-H.,Fujian Medical University | You J.-H.,Sun Yat Sen University | Zhuang Y.-F.,Sun Yat Sen University | Cheng J.,Quanzhou Medical College | And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

Background: An adverse intrauterine environment can predispose offspring to metabolic disorders. However, fetal programming maybe reversed by postnatal lifestyle especially physical activity levels. The goal of the present study was to determine whether predisposition induced by maternal hypoxia is aggravated or reversed by juvenile activity patterns, and to study the underlying molecular mechanisms. Methods: Sprague-Dawley rats experiencing maternal hypoxia were randomly assigned to juvenile activity patterns (sedentariness, cage activity and exercise). In male offspring, body weight, adiposity index, blood-borne factors, intramuscular oxidative/anti­oxidative status and the main proteins regulating glycolipid metabolism were evaluated by biochemical assays. Results: Maternal hypoxia offspring rats were born with reduced body weight and hyperlipemia. When full grown, lipid metabolism down-regulated and lipogenesis up-regulated. Juvenile sedentariness aggravated peripheral insu­lin resistance (Lg HOMA-IR, 1.02 ± 0.1 vs. 0.83 ± 0.0, P<0.05), increased intramuscular triglyceride levels (94.63 ± 7.6 μmol/g vs. 59.08 ± 5.5 μmol/g, P<0.05), and impaired glucose tolerance. The basal expression of fatty acid binding protein 3 and carnitine palmitoyl transferase 1 decreased, while the sterol regulatory element binding tran­scription factor 1c and fatty acid synthase increased. Following insulin stimulation, changes in membrane glucose transporter 4 and Akt expression regulating glucose metabolism occurred, and juvenile exercise normalized the observed aberrations. Conclusion: Juvenile sedentariness promoted the predisposition for metabolic syndrome in maternal hypoxia offspring, which was normalized by juvenile exercise. Changes in the intramuscular glucose up-take and lipid metabolism were responsible for the metabolic reprogramming. © 2016, E-Century Publishing Corporation. All rights reserved. Source

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