Objective To study the screening value of color doppler flow imaging (CDFI) for gastroesophageal reflux(GER).Methods Through the window of left lobe liver, the abdominal esophageal length,the phenomenon of GER and the frequency of GER were detected by CDFI in 55 children with GER and 55 control group.Results Abdominal esophagus was identified by CDFI in every children. The abdominal esophageal length was shorter in refluxers than that in control group. A significant correlation was found between its length and the age of control group.To diagnose GER with CDFI ,its accuracy was 98.18%,and its specificity was 76.36%.Conclusions Visualization and measurements of the abdominal esophagus are readily achieved with CDFI in children.Abdominal esophageal length is shorter in refluxers than that in control group. CDFI is a rapid method of screening GER.

Objective To study whether gastric liquid emptying is delayed in children with gastroesophageal reflux and its clinical significance. Methods At different times after meal, the gastric antral diameters were measured by real - time ultrasonography in 55 children with gastroesophageal reflux and 55 controls. Results At 20 min,60 min after meal , there was a significant difference in gastric emptying rate between case groups and control groups, respectively(P

Objective To explore the role of stromal interaction molecule 1(STIMI)on prohteration and intra- cellular Ca~(2+)change in vascular smooth muscle ceils(VSMC).Methods Rat VSMC were isolated from SD rats and primary cultured.Ad-si/rSTIM1 and Ad-hSTIM1 were transfected into VSMC.The protein of STIM1 was measured by Western blot,the proliferation of VSMC was analyzed by ~3H-thymidine(~3H-TdR)incorporation and cell count,the intracellular Ca~(2+)change was assessed By Aquaeosmos system.Ruselts Fourty-eight hours after transfection,as compared with Ad-hSTIMI group,the Ad-si/rSTIMI VSMC had lower expression of STIM1 protein (P

With the deployment of electronic medical records systems, more and more routine clinical data are recorded electronically, which become a potential data source for new drug clinical trials. In this paper, we summarized the opportunities, challenges, obstacles and the latest development in this field.
Clinical Trials as Topic ; Data Collection ; methods ; Drug Evaluation ; Electronic Health Records

The biological artificial liver(BAL) can offer reliable artificial liver support for the patients with hepatic failure.All BAL devices contain hepatocytes as their biological component,whose specific biological characteristics contribute to the function of the BAL.During the past two decades,various cells including human hepatocytes,heterogeneous hepatocytes and liver cell lines have been used and different culture methods have been studied to optimize the activity of the biological component.However,both functionality and safety of these cells should be improved before successful use in BAL. This paper summarizes the latest progress on it.

Objective To investigate whether the monthly distribution of birth was associated with congenital heart disease(CHD).Methods The monthly distribution of birth of 5 070 patients with CHD who accepted examination or treatment from Jan.2003 to Dec.2006 was investigated and compared with that of 6 627 healthy newborn children born in 2001-2006.The statistic analysis was accomplished with SPSS 12.0 software for ?2 test.Results Four hundred and forty-four of the 5 070 patients with CHD were born in January(8.8%),432 cases in February(8.5%),384 cases in March(7.6%),339 cases in April(6.7%),390 cases in May(7.7%),393 cases in June(7.8%),414 cases in July(8.2%),489 cases in August(9.6%),498 cases in September(9.8%),492 cases in October(9.7%),396 cases in November(7.8%),and 399 cases in December(7.8%).The structural ratio of the number of CHD patients were the highest for those who were born in August,September,October,and the lowest among those who were born of February and March,April.The number of CHD patients who were born in the autumnal months of August,September and October was 1 479(29.1%),much higher than those who were born in February,March and April(1 155 cases,22.8%)(P

AIMTo investigate the impact of human urotensin II (hUII) on pulmonary arterial smooth muscle cell (PASMCs) cycle in vitro.

METHODSPASMCs dissected from Wistar rats were cultured in vitro, and incubated with series of concentrations of hUII (10(-7) mol/L, 10(-8) mol/L, 10(-9) mol/L) for 12 hours under normoxia or hypoxia condition, in order to analyze cell cycle progression and sub-G1 of PASMCs by using flow cytometric analysis stain of propidium iodide, which represented the proliferative and apoptotic changes in PASMCs.

RESULTSThe study showed a dose-dependent effect of hUII on PASMCs proliferation, which reflected the increase both in percentage of S phase of cell cycle and proliferative index (PI). The response of PASMCs to hUII was different under normoxic and hypoxic conditions. Compared with the control group, the treatment of 10(-7) mol/L, 10(-8) mol/L and 10(-9) mol/L hUII produced an increase of 175%, 136% and 118% under normoxia, respectively, and 135%, 118% and 103% under hypoxia, respectively. The concentration 10(-7) mol/L hUII played a significant role in PASMCs proliferation both under hypoxia and normoxia (P < 0.01). The results of cell cycle did not show sub-G1 of PASMCs at various concentrations of hUII.

CONCLUSIONhUII may stimulate DNA synthesis in S phase cell cycle of PASMCs and the proliferation of PASMCs under normoxia and hypoxia conditions, which promote cell growth in a dose-dependent manner.

Animals ; Cell Cycle ; drug effects ; Cells, Cultured ; Humans ; Male ; Muscle, Smooth, Vascular ; cytology ; Myocytes, Smooth Muscle ; cytology ; drug effects ; Pulmonary Artery ; cytology ; Rats ; Rats, Wistar ; Urotensins ; pharmacology

OBJECTIVETo explore the effects and molecular mechanisms of rhein on reducing starvation-induced autophagic protein expression in renal tubular epithelial ( NRK-52E) cells.

METHODHank's balanced salt solution (HBSS) was used to induce NRK-52E cells to be in the state of starvation. After the intervention of HBSS for 0, 0.5,1, 2 and 6 hours, firstly, the protein expression of microtubule-associated protein 1 light chain 3(LC3 I/II), which is a key protein in autophagy, was detected. Secondly, the protein expressions of mammalian target of rapamycin (mTOR) and phosphorylated-mTOR Ser2448 (p-mTOR S2448) were examined. And then, after the co-treatment of rhein (5 mg x L(-1)) and HBSS (1 mL) without or with mTOR inhibitor, rapamycin (100 nmol x L(-1)), the protein expressions of LC3 I/II, mTOR and p-mTOR S2448 were tested, respectively.

RESULTHBSS could induce the up-regulation of LC3 II and the down-regulation of p-mTOR S2448 at protein expression level in NRK-52E cells. The co-treatment of rhein and HBSS could reversely regulate the protein expressions of LC3 II and p-mTOR S2448 in NRK-52E cells significantly. The co-treatment of rapamycin, rhein and HBSS could recover the level of LC3 II protein expression in HBSS-intervened NRK-52E cells.

CONCLUSIONHBSS induces autophagy in renal tubular epithelial cells by inhibiting mTOR signaling pathway activation. Rhein reduces the autophagic protein expression in renal tubular epithelial cells through regulating mTOR signaling pathway activation, which is the possible effects and molecular mechanisms.

Animals ; Anthraquinones ; pharmacology ; Autophagy ; drug effects ; Cells, Cultured ; Epithelial Cells ; drug effects ; metabolism ; Isotonic Solutions ; pharmacology ; Kidney Tubules ; drug effects ; metabolism ; Microtubule-Associated Proteins ; genetics ; Rats ; Signal Transduction ; drug effects ; TOR Serine-Threonine Kinases ; antagonists & inhibitors ; genetics ; physiology

The present study is to elucidate the mechanisms underlying Gleevec-induced apoptosis of chronic myeloid leukemia (CML) K562 cells in vitro. The apoptotic cell death and cell cycle distribution after Gleevec treatment and the effect of PDCD4 siRNA on Gleevec-induced apoptosis of K562 cells were analyzed by flow cytometry. The effect of Gleevec on p-Crkl, caspase-3, PARP and PDCD4 protein levels, and the knockdown efficacy of PDCD4 siRNA were detected by Western blotting. The results showed that Gleevec dramatically suppressed the phosphorylation level of Crkl in a dose-dependent manner and induced significant apoptosis and G0/G1 cell cycle arrest of K562 cells in time- and dose-dependent manners. In addition, Gleevec activated caspase-3 and its downstream substrates PARP, and the caspase pan inhibitor Z-VAD-FMK (50 micromol x L(-1)) markedly reduced Gleevec-induced apoptosis from 47.97% +/- 10.56% to 31.05% +/- 9.206% (P < 0.05). Moreover, Gleevec significantly increased the protein expression of programmed cell death 4 (PDCD4). PDCD4 knockdown by siRNA reduced Gleevec-induced apoptosis from 46.97% +/- 14.32% to 42.8% +/- 11.43%. In summary, Gleevec induced apoptosis in K562 cells via caspase-3 activation.
Amino Acid Chloromethyl Ketones ; Apoptosis ; drug effects ; Benzamides ; pharmacology ; Caspase 3 ; metabolism ; Cell Cycle ; drug effects ; Humans ; Imatinib Mesylate ; K562 Cells ; Phosphorylation ; Piperazines ; pharmacology ; Pyrimidines ; pharmacology

OBJECTIVETo study the effect of herbal compound 861 (HB861) on expression and activity of nitric oxide synthase (NOS) in hepatic stellate cells (HSC), and to explore the feasibility of its application in preventing and treating the early portal hypertension.

METHODSHSC of HSC-T6 cell line (1 x 10(5)/ml) were cultured in dish with 95% O2 plus 5% CO2 under 37 degrees C for 24 hrs, then divided into 5 groups, 6 dishes in each group. Group A was the blank control group. To Group B-E, HB861 2 mg/ml, HB861 4 mg/ml, HB861 8 mg/ml, HB861 4 mg/ml + NW-Nitro-L-Arginine Methyl Ester (L-NAME)4 mg/ml were added separately, and continuously cultured for 24 hrs. NOS activity was measured using colorimetry, NO level was determined by nitrate reductase technique. The cells were fixed by 4% paraformaldehyde for 2 hrs for test HSC-T6 iNOS expression by immunocyto-chemical method.

RESULTSHB861 in 2 mg/ml, 4 mg/ml and 8 mg/ml could increase HSC-T6 NOS activity from 1.7 +/- 0.1 to 2.5 +/- 0.3, 3.5 +/- 0.4 and 3.7 +/- 0.9 respectively (P < 0.01), the NO levels in supernatant were increased in parallel from 56.1 +/- 4.8 to 90.7 +/- 4.6, 99.7 +/- 4.1 and 109.0 +/- 2.7 respectively (P < 0.01). L-NAME could not inhibit the effect of HB861 in increasing the synthesis and secretion of NO by activated HSC-T6. Immuno-cyto-chemical study showed that there was iNOS expression in cytoplasm, and which could be increased by HB861.

CONCLUSIONThe activated HSC-T6 showed positive iNOS expression, suggesting it could produce NO. HB861 could markedly increase HSC-T6 iNOS expression and NOS activity, enhance the NO synthesis and secretion, it also could inhibit the contractility of activated HSC by way of increase HSC to secrete NO, so as to lower the resistance in hepatic sinusoid, therefore would play important role in preventing and treating of early portal hypertension.

Animals ; Cells, Cultured ; Drug Combinations ; Drugs, Chinese Herbal ; pharmacology ; Hepatocytes ; enzymology ; Hypertension, Portal ; prevention & control ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; biosynthesis ; metabolism ; Rats ; Rats, Sprague-Dawley