CTGF, a member of the CCN family of immediate early genes, is a recently discovered profibrotic growth factor, which is involved in many pathophysiologic procedures. CTGF acts as a downstream effector of TGF-? acting on interstitial cells to enhance the progression of fibrotic renal diseases. It has been shown that CTGF gene expression can be induced or blocked by some kinds of cytokine and drugs. It is an interesting candidate target for future intervention strategies of renal interstitial fibrosis. [

Objective To explore the nervous mechanism of intestinal function disorder after intestine congestion through observing the changes of acetylcholinesterase (AchE) neuron and nitric oxide synthase neuron (NOS) expression in nervous system of rat intestinal tract. Methods Sprague Dawley rats were divided into experimental groups (intestine congestion 20min and 60min group) and the control group. Then the spreading specimens of intestinal myen-teric plexus of ileums were collected and stained by AchE and nicotinamide-adenine dinucleotide phosphate-D (NADPH-d) histochemistry, to observe and compare the density of distribution and staining of AchE and NOS positive neurons. Result Compared to the control group, the number and positive expression of AchE positive neuron in intestinal myen-teric plexus of ileums in the experimental group rats decreased (P

=3) in spinal fluid. The intra and inter-day relative standard deviation of analysis were less than 3.0 % (n = 5). The recovery of lidocaine was between 98.3 % - 102.7 % . Lidocaine assay was carried out in a medical case by using the method established. Conclusion Spinal fluid is suitable for assay lidocain in forensic toxicological analysis and other medical studies by using the HPLC method which is sensitive, rapid and accurate.

Objective To investigate the relationship between the antiproliferation effects of aloe-emodin on growth of gastric cancer cells and cell cycle arrest.Methods Human gastric cancer SGC-7901 cells were treated with 2.5,5,10,20,and 40 ?mol/L aloe-emodin for 1—5 d.The cell growth was determined by MTT assay.Cell proliferation and cycle distributions were analyzed by flow cytometry.Western blotting assay was used to detect the changes of cell cycle regulators,cyclins,and cyclin-dependent kinases(CDK).Results Aloe-emodin inhibited the growth of gastric cancer cells in a dose-dependent manner.Treatment of aloe-emodin resulted in cell cycle arresting at G2/M phase.Its molecular mechanisms involved the decrease of the expression of cyclin A and CDK2,the increase of the expression of cyclin B1 and CDK1.Conclusion One of the antitumor mechanism of aloe-emodin on the growth of gastric cancer SGC-7901 cells is to arrest the cell cycle,which indicates that aloe-emodin has a potential value for the treatment of gastric cancer in clinic.

Objective To summarize the methods and results of surgical treatment of coarctation of the aorta associated with aortic dissection.Methods Analyzed the clinical data of 10 patients with aortic coarctation associated type B aortic dissection who underwent one-stage surgical repair between 2011 and 2013 in Anzhen Hospital.There were 7 males and 3 females with the age ranged from 23 to 56 years,average at 41.2 years.All patients were diagnosed by UCG and CTA.There are three key points to determine the operation method,diameter of the aortic arch and descending aorta,and the extent of dissection.Descending thoracic aortic replacement with short stented elephant trunk was performed in 3 patients,thoracic and abdominal aortic replacement in 1 patient,ascending-abdominal aorta bypass with arch or descending aortic ligature in 3 patients.Results One hospital death occurred(10％).There was no severe surgical complication.No death or reoperation occurred during follow up period.Conclusion Aortic coarctation associated type B aortic dissection is a rare and complex disease.Surgical treatment is an effective and safe method for the disease.

Objective To explore the distribution pattern of G protein-coupled receptor family C, group 6, subtype A (GPRC6A) mRNA in adult mice. Methods The distribution of GPRC6A mRNA in paraffin embedded adult mouse tissues was determined by highly sensitive nonradioactive cRNA probe in situ hybridization (ISH). We compared ISH with and without addition of tyramide signal amplification (TSA). GPRC6A wild-type and littermate GPRC6A null mice tissue sections were investigated by ISH. Results TSA greatly increased the sensitivity of ISH to detect GPRC6A mRNA in wild type mouse tissues. There was no detection of GPRC6A mRNA in GPRC6A gene specific knockout tissue in paraffin embedded tissue section. The mRNA of GPRC6A was detectable in the digestive gland or accessory digestive gland including salivary gland and pancreas, as well as in the tissues including kidney, testis, brain, muscle, and fat. Conclusion The mRNA distribution pattern of GPRC6A gene is compatible with the phenotype of GPRC6A knockout mice.

Objective To evaluate the effects of Radix Astr agali combined with prednisone and i mmunosuppressant for primary nephrotic syndrome (PNS)in adults and to compare the effects o f Radix Astragali in various prepata tions for PNS.Methods Randomized controlled trials were a pplied for systemic reviews.Electr onic and manual retrieve of Medline,Embase,Cochrane Library,CBMdisc a nd CEBM/CCD and relevant medical jou rnals in China were applied to search the RCTs of Radix Astragali,non -specific treatment,glucocorticoids and i mmunosuppresants for PNS,and the RCTs were analysed with RevMan 4.1.Results There were 14randomized controlled trials with 524cases involved.Meta-analysis showed that Radix Astragali could in crease the therapeutic effect of pre dnisone and immunosuppressant for PNS and re-duce its recurrence.Radix Astragali also had an effect in decreasing 24-hour proteinuria content and the pla sma levels of total cholesterol and albumin.There were no differences between single injection and compound decoction.Asymmetry showed in"Funnel plot"may be related to publication bias,l ow quality of methodology and small -size in sample.Conclusion Radix Astragali and its prescriptio n may become a prospect therapy for PN S and its recurrence and the com-bination of traditional Chinese med icine and western medicine can be more effective for PNS.The dedinite effect of Radix Astragali for PNS will be further con firmed by multiple -center,large -s ample randomized controlled trial.

Objective To observe the effects of CO2 pneumoperitoneum on the enteric motor function and acetylcholine esterase(AchE) neuron and nitric oxide synthase(NOS) neuron in the enteric nervous system,and explore the neuromechanism of the CO2 pneumoperitoneum on renteric motor function.Methods Thirty-six Sprague Dawley rats were randomly divided into experiment group(n=24) and control group(n=12).The experiment group was divided into two subgroups namely pneumoperitoneum 30min group and pneumoperitoneum 60min group(12 each) based on the maintenance time of pneumoperitoneum.Rats in each group were gavaged with medicinal carbon powder,and then the transmission of carbon powder in small intestine was determined.The spreading specimens of intestinal myenteric plexus of small intestine were prepared and the stained AchE and NOS neurons were observed and compared.Results The propellant velocity of carbon powder was slower in pneumoperitoneum 60min group than that in pneumoperitoneum 30min group and control group(28.55%?3.45% vs 45.90%?6.30%,48.25%?5.28%,P0.05).The number of positive expression of AchE neurons in intestinal myenteric plexus decreased in pneumoperitoneum 60min group compared with that in pneumoperitoneum 30min group and control group(48.00?3.16 vs 58.82?4.62,61.83?4.17,P0.05).The number of positive expression of NOS neurons in intestinal myenteric plexus increased in pneumoperitoneum 60min group compared with that in pneumoperitoneum 30min group and control group(42.17?4.45 vs 32.50?4.34,30.83?3.6,P0.05).Conclusions Prolonged CO2 pneumoperitoneum can affect or damage cholinergic neurons and nitroxidergic neurons in the enteric nervous system to some extent,and it may be the underlying mechanism of the intestinal motor dysfunction after operation.

Objective To investigate the effects of pyrroloquinoline quinone(PQQ) on the hippocampal neurons of aged rats induced by D-galactose(D-gal).Methods D-gal was used to induce the model of aging rat,PQQ was administered into rat lateral intracerebroventricle.After 50 days the metamorphosis of hippocampal neurons was observed by H-E and Nissl's staining.The apoptosis rate of hippocampus was tested by flow cytometry.The contents of free radical and C-FOS protern were measured.Results Compared with the control group,the size of the neurosoma was slightly changed,the optical density of Nissl's was decreased,the content of free radical and the apoptosis rate increased markedly in D-gal group.After PQQ injection with D-gal,the size of neurosoma and the optical density of Nissl's were markedly increased,the content of free radical and the apoptosis rate of hippocampus did not change.PQQ improved the expression of C-FOS protern.Conclusion PQQ can slow down the aging progress of hippocamal neurons induced by D-gal.

AIM: To explore the expression of CD14 in rat Kupffer cells (KCs). METHODS: In rat KCs induced by LPS or the mediators from KCs induced by LPS,the changes of CD14 expression were measured by RT-PCR and immunohistochemistry.The expressions of TNF? mRNA?IL-6 mRNA or the concentrations of TNF??IL-6 were estimated by in situ hybridization and radioimmunoassay,respectively. RESULTS: LPS increased the expression of CD14 in KCs in a dose-dependent fashion (LPS,1 ?g/L-10 mg/L) and in a time-dependent fashion(0.5 h-24 h,peaked at 3-6 hours). While the expression of CD14 in KCs stimulated by the active mediators from KCs which had been exposed to LPS 1 hour were obviously increased. CONCLUSIONS: There was a close relationship between LPS or the active mediators from KCs induced by LPS and the expressions of CD14. It is implied that the increase in CD14 expression may be induced by LPS and the cytokines produced by KCs,it also reveals that there is a auto-regulated loop in CD14 expression.