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Articles by L Shi
Total Records ( 7 ) for L Shi
  L Shi , C Mao , F Zeng , J Hou , H Zhang and Z. Xu
 

Angiotensin (Ang) II plays a critical role in cardiovascular homeostasis and neuroendocrine regulation. Little is known about whether central angiotensin-converting enzyme (ACE) is functional in the fetal brain. We investigated cardiovascular and neuroendocrinological responses to intracerebroventricular (icv) application of Ang I in the chronically prepared near-term ovine fetus in utero and examined the action sites marked by c-fos expression in the fetal hypothalamus. ACE mRNA was detected in the specific central areas. Intracerebroventricular Ang I significantly increased fetal blood pressure and c-fos expression in the supraoptic nuclei (SON) and the paraventricular nuclei (PVN) in the hypothalamus, accompanied by an increase of fetal plasma arginine vasopressin (AVP). Double labeling demonstrated that AVP neurons in the fetal SON and PVN were expressing c-fos. Captopril, an inhibitor of ACE, significantly suppressed fetal pressor responses and plasma AVP. Double labeling experiments showed colocalization of AT1 receptor (AT1R) and c-fos expression in both SON and PVN following icv Ang I. The results indicate that central endogenous ACE has been functional at least at the last third of gestation and the endogenous brain renin-angiotensin system-mediated pressor responses and AVP release via AT1Rs by acting at the sites consistent with the cardiovascular network in the hypothalamus.

  L Shi , T Remer , A. E Buyken , M. F Hartmann , P Hoffmann and S. A. Wudy
 

Whether prepubertal estrogen production impacts on the timing of puberty is not clear. We aimed to investigate prepubertal 24-h estrogen excretion levels and their association with early and late pubertal markers. Daily urinary excretion rates of estrogens of 132 healthy children, who provided 24-h urine samples 1 and 2 yr before the start of the pubertal growth spurt [age at takeoff (ATO)], were quantified by stable isotope dilution/GC-MS. E-sum3 (estrone + estradiol + estriol) was used as a marker for potentially bioactive estrogen metabolites and E-sum5 (E-sum3 + 16-epiestriol + 16-ketoestradiol) for total estrogen production. Pubertal outcomes were ATO, age at peak height velocity (APHV), duration of pubertal growth acceleration (APHV-ATO), age at Tanner stage 2 for pubic hair (PH2), genital (G2, boys) and breast (B2, girls) development, and age at menarche. Prepubertal urinary estrogen excretions (E-sum3 and E-sum5) were not associated with ATO, APHV, and age at PH2 but with duration of pubertal growth acceleration (P < 0.01) in both sexes. Girls with higher E-sum3 reached B2 0.9 yr (P = 0.04) and menarche 0.3 yr earlier (P = 0.04) than girls with lower E-sum3. E-sum3 was not associated with age at G2 in boys (P = 0.6). For most pubertal variables, the associations with E-sum3 were stronger than with E-sum5. In conclusion, prepubertal estrogens may not be critical for the onset of the pubertal growth spurt but are correlated with its duration in both boys and girls. Prepubertal estrogen levels may already predict the timing of girls' menstruation and breast development but do not appear to affect sexual maturation in boys.

  T Toyoda , T Tsukamoto , S Takasu , N Hirano , H Ban , L Shi , T Kumagai , T Tanaka and M. Tatematsu
 

Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality. Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear. Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)–associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models. The animals were allocated to H. pylori + N-methyl-N-nitrosourea administration (gerbils, 52 weeks) or H. pylori infection alone groups (gerbils and mice, 12 weeks). After H. pylori infection, they were fed basal diets containing 0 to 10 ppm of pitavastatin. The incidences of H. pylori–associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values. Expression of interleukin-1β and tumor necrosis factor- mRNAs in the pyloric mucosa was markedly up-regulated in pitavastatin-treated animals. Furthermore, in the H. pylori–infected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation. In the short-term study, H. pylori–infected gerbils and mice also showed significant up-regulation of serum triglyceride levels by pitavastatin, whereas total cholesterol was markedly reduced and low-density lipoprotein exhibited a tendency for decrease in noninfected animals. These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori–infected gerbils. Our serologic results also suggest that the H. pylori infection and consequent severe chronic gastritis interfere with the cholesterol-lowering effects of pitavastatin.

  L Zhang , T Deng , X Li , H Liu , H Zhou , J Ma , M Wu , M Zhou , S Shen , Z Niu , W Zhang , L Shi , B Xiang , J Lu , L Wang , D Li , H Tang and G. Li
 

microRNAs (miRNAs) are small non-coding RNAs and have been implicated in the pathology of various diseases, including cancer. Here we report that the miRNA profiles have been changed after knockdown of one of the most important oncogene c-MYC or re-expression of a candidate tumor suppressor gene SPLUNC1 in nasopharyngeal carcinoma (NPC) cells. Both c-MYC knockdown and SPLUNC1 re-expression can down-regulate microRNA-141 (miR-141). miR-141 is up-regulated in NPC specimens in comparison with normal nasopharyngeal epithelium. Inhibition of miR-141 could affect cell cycle, apoptosis, cell growth, migration and invasion in NPC cells. We found that BRD3, UBAP1 and PTEN are potential targets of miR-141, which had been confirmed following luciferase reporter assays and western blotting. BRD3 and UBAP1 are both involved in NPC carcinogenesis as confirmed through our previous studies and PTEN is a crucial tumor suppressor in many tumor types. BRD3 is involved in the regulation of the Rb/E2F pathway. Inhibition of miR-141 could affect some important molecules in the Rb/E2F, JNK2 and AKT pathways. It is well known that carcinogenesis of NPC is involved in the networks of genetic and epigenetic alteration events. We propose that miR-141- and tumor-related genes c-MYC, SPLUNC1, BRD3, UBAP1 and PTEN may constitute a gene–miRNA network to contribute to NPC development.

  L Xu , C He , C Shen , T Jiang , L Shi , K Sun , S. W Berquist and J. Feng
 

The geographical patterns of the genetic structure of Hipposideros armiger in China were assessed by analyzing sequence variation in the mitochondrial DNA control region. Analysis of molecular variance revealed a very strong genetic structure among 5 regions in H. armiger. A neighbor-joining tree, haplotype network construction by TCS and multidimensional scaling plots all showed significant geographic differentiation among 5 regions. The high genetic structure detected in H. armiger could be a consequence of poor dispersal ability, local adaptation, or marked female philopatry. The lack of genetic structure among 3 regions separated by the Gaoligong Range and the Qiongzhou Strait could be due to incomplete lineage sorting. Our estimated times of divergence for H. armiger populations suggested a relatively recent split. The S Yunnan population with the highest genetic diversity and the Hainan population with the lowest genetic diversity should be equally given priority for conservation. Although H. armiger has been shown to carry viruses implicated in human disease, we find little evidence for population mixing. We thus suggest minimizing disturbance to bats’ roosting caves for minimizing the potential risk of virus transmission.

  R. R Bidigare , F Chai , M. R Landry , R Lukas , C. C. S Hannides , S. J Christensen , D. M Karl , L Shi and Y. Chao
 

Biological responses to basin-scale climate forcing in the subtropical North Pacific Ocean are assessed based on temporal variations in plankton community structure observed at Station ALOHA and results of a coupled physical–biogeochemical model. Observational data and model simulations for the period 1990–2004 reveal distinct temporal patterns, with significant increases in net primary productivity, modeled nitrate flux into the euphotic zone and the measured downward flux of particulate nitrogen during 1999–2004. Concurrent increases in microalgae, cyanobacteria and modeled and measured zooplankton biomass were also observed during this period. We provide evidence that these responses were a consequence of climate forcing that destratified the upper ocean, making it more susceptible to mixing events and nutrient entrainment. These findings underscore the importance of nitrate flux and plankton community structure, as modulated by climate forcing, in regulating particle export over interannual and decadal time scales.

  C Wang , G Xie , B Cheng , L Du , L Shi , L Tan , Q Shu and X. Fang
 

Pediatric Risk of Mortality (PRISM), Pediatric Index of Mortality (PIM) and PIM2 could be applicable to the subset of term neonates has not been well investigated. The purpose of this study is to access and compare the performance of these scoring systems in predicting mortality probability in term Chinese neonates with critical illness. PRISM, PIM and PIM2 scores were calculated prospectively during a 1-year period on 243 neonates admitted to the neonatal intensive care unit (NICU) in the Children’s Hospital of Zhejiang University in China. Of these, 36 neonates (14.81%) died in the NICU, while the mortality rates estimated by PRISM, PIM and PIM2 were 16.19, 14.58 and 11.12%, respectively. The area under the receiver-operating characteristic (ROC) curve [95% confidence intervals (CIs)] were 0.834 (0.767–0.902), 0.851 (0.786–0.916) and 0.854 (0.790–0.918) for PRISM, PIM and PIM2, respectively. The Hosmer–Lemeshow test gave a chi-square of 1.35 (p = 0.930) for PRISM, 1.03 (p = 0.960) for PIM and 4.58 (p = 0.469) for PIM2. The standardized mortality rates (SMRs) (95% CI) using PRISM, PIM and PIM2 were 0.92 (0.79–1.08), 1.02 (0.88–1.20) and 1.33 (1.13–1.62), respectively. Although PRISM, PIM and PIM2 have displayed good discrimination and calibration in the present setting, PIM is considered as the most accurate and appropriate tool for predicting mortality in the studied NICU.

 
 
 
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