OBJECTIVETo explore the repair of Xiangsha Liujunzi Decoction (XSLJZD) on interstitial cells of Cajal (ICC) and gap junction (GJ) in the gastric muscular layer of rats of Pi-qi deficiency syn- drome (PQDS).

METHODSPQDS was established using purgative method with bitter and cold drugs in 30 healthy Wistar rats. After successful modeling they were randomly divided into the treatment group and the model group, 15 in each group. Another 15 healthy Wistar rats were recruited as the healthy control group. Rats in the treatment group were gastric administered with XSLJZD at 2 mL/100 g body weight, once daily for 14 successive days. Equal volume of normal saline was gastrically administered to those in the healthy control group and the model group. The gastric muscle tissues were taken out before modeling, before intervention, and after intervention, respectively. Ultrastructural changes of ICC and GJ were observed using transmission electron microscope (TEM). The number and distribution of Connexin43 (Cx43) were detected using immunohistochemistry.

RESULTSResults of TEM indicated that compared with the healthy control group, both ICC and GJ in the model group showed obvious injury. ICC and GJ were apparently repaired after intervention in the treatment group. Compared with the same group before modeling, the integrated optical density (IOD) of the Cx43 expression significantly decreased in the model group before and after intervention (P <0.05). Compared with before intervention, the IOD of the Cx43 expression significantly increased in the treatment group (P <0.05). Compared with the healthy control group, the IOD of the Cx43 expression significantly decreased in the model group before and after intervention (P <0.05). Compared with the model group, the IOD of the Cx43 expression significantly increased in the treatment group (P <0.05).

CONCLUSIONSUltrastructures of ICC and GJ in the gastric muscular layer of rats of PQDS were obviously damaged. XSLJZD could repair the structural damage of ICC and GJ in the gastric muscle tissues of rats of PQDS.

Animals ; Connexin 43 ; Drugs, Chinese Herbal ; pharmacology ; Gap Junctions ; Interstitial Cells of Cajal ; drug effects ; Leydig Cells ; Male ; Muscle, Smooth ; Qi ; Rats, Wistar ; Syndrome

ZHU Lian is a deceased famous acupuncture and Moxibustion specialist, the first director and the founder of institute of Acupuncture-Moxibustion of China Academy of Chinese Medical Sciences. This article discusses the thought and idea of education and teaching of acupuncture-moxibustion from the following three aspects: diversified education and training mode, teaching idea of new acupuncture-moxibustion with a lot of characteristics, and the founding of professional acupuncture-moxibustion college. All above have both distinct characteristics of the times and positively enlightening significance of reality.
Acupuncture ; education ; history ; Acupuncture Therapy ; history ; China ; Education, Medical ; history ; History, 20th Century ; Humans ; Teaching ; history

Objective To explore the early diagnosis and risk factors for judging prognosis of acute respiratory distress syndrome (ARDS),and to provide references for clinical intervention.Methods Using the method for prospective cohort study,clinical data were collected from 64 ARDS and 66 high-risk ARDS patients in Department of Respiratory Diseases of Xinqiao Hospital from January 2013 to March 2016.They included patients' demographic data,Acute Physiology and Chronic Health Evaluation system Ⅱ (APACHE Ⅱ) score,oxygenation index,blood routine test,coagulation function and inflammatory markers (procalcitonin,C-reaction protein,tumor necrosis factor and interleukin-6) within 24h and the state of survival or death of the 24th day.Risk factors for predicting progression of the high-risk ARDS patients into ARDS patients and influencing the prognosis of the ARDS patients were analyzed by using logistic regression.Results Univariate logistic regression analysis found that the independent risk factors for progression of ARDS were APACHE Ⅱ score (OR=6.764,P=0.001),hypoproteinemia (OR=10.54,P=0.002),white blood cell count (OR=3.912,P=0.012),fibrinogen (OR=9.953,P=0.064),and D-dimer (OR=4.239,P=0.029).The mortality rate was 43.75％ (36/64) in ARDS group,and the oxygenation index (OR=6.573,P=0.014),platelet count (OR=9.376,P=0.003),hypoproteinemia (OR=10.738,P=0.056) were the independent risk factors of death in ARDS patients.Multivariate logistic regression showed that combination of multiple indicators for predicting ARDS improved the specificity,but reduce the sensitivity.APACHE Ⅱ and hypoproteinemia (sensitivity 62.50％,specificity 92.42％) and APACHE Ⅱ and D dimmer (sensitivity 62.07％,specificity 93.33％) had better specificity and sensitivity.The specificity and sensitivity of combining hypoproteinemia and platelet count to predict the risk of death in these patients were 77.78％ and 60.71％.Conclusions In high-risk ARDS patients,combining hypoproteinemia or APACHE Ⅱ score with D-dimer to judge the development of ARDS has good specificity but poor sensitivity.For ARDS patients,low oxygenation index,thrombocytopenia and hypoproteinemia indicate a poor prognosis.

Aim To study the mechanism of DXM and NAC inhibiting the expression of IL-8 and ICAM-1 in A549 cells. Methods The expression of IL-8 and ICAM-1 was detected by ELISA and flow cytometry re-spectively; the expression of GR,HDAC,AP-1,NF-κB was detected by Western blot, while the activity of HDAC was detected by spectrophotometry. ResultsThe increasing expression of IL-8 and ICAM-1 induced by TNF-α could be inhibited by DXM and NAC in A549 cells. DXM could inhibit the transcribed activa-tion of AP-1,NF-κB, and the expression of HDAC and its activity induced by TNF-α and LPS; NAC only in-hibited the transcribed activation of NF-κB, while it had no affection on the transcribed activation of AP-1 and the expression of HDAC and its activity. Conclu-sions DXM and NAC both have the anti-inflammatory effect. DXM plays the role of anti-inflammation through increasing the expression and activation of HDAC, in-hibiting the transcribed activation of AP-1 and NF-κB, while NAC has no effect on the expression and activa-tion of HDAC, which shows that NAC does not exert anti-inflammatory effect through acetylation signal.

Objective To investigate the clinical epidemiological features of femoral neck frac-tures. Methods The clinical data of patients with femoral neck fractures admitted to Third Affiliated Hospital of Hebei Medical University from 2003 to 2007 were retrospectively analyzed. All patients were divided into children group (age < 16 years) , adult group (age ranged from 16 to 60 years) and older group (>60 years). The types of the femoral neck fractures included 31-B1, 31-B2 and 31-B3 according to AO classification. The gender, age, fracture type and injury causes were analyzed. Results A total of 2 064 patients (971 males and 1 093 females) with femoral neck fractures were involved in the study.There were 356, 381, 397, 454 and 476 patients respectively in 2003, 2004, 2005, 2006 and 2007.There were 74 patients (3.59%) in the children group, 979 (47.43%) in the adult group and 1 011 (48.98%) in the older group. There were 960 patients (46. 51%) with type 31-B1 fractures, 860 (41. 67%) with type 31-B2 fractures and 244 (11. 82%) with 31-B3 fractures. Conclusions Form 2003 to 2007, the incidence of femoral neck fracture shows a trend of increase, with the highest incidence in the old persons. The male patients with femoral neck fractures are more than female patients in adult group, while the female patients with femoral neck fractures are less than male patients in older group.The dominant fractures type according to AO classification are type 31-B2 fractures in children and adult groups, but type 31-B1 fractures in older group.

Objective To investigate the effects of mesenchymal stem cells (MSCs) transplantation combining with vascular endothelial growth factor (VEGF) gene therapy on myocardium rebuilding,angiogene- sis,and heart function improvement in rats with myocardial infarction.Methods SD rat MSCs were isola- ted,cultured in vitro,labeled with BrdU and transfected by Ad.VEGF gene.Four weeks after left anterior descending artery was ligated to created rat myocardial infarction,cardiac function was examined with echocar- diography,rats were randomly divided into four groups (n=10 in each group):GroupⅠ:MSCs/Ad.VEGF implantation;GroupⅡ:MSCs implantation;GroupⅢ:Ad.VEGF injection;GroupⅣ:Control.MSCs dif- ferentiation was observed 4 weeks after transplantation.Immunohistochemistry and angiogenesis were observed. Echocardiography was performed to detect the effects on heart function.Results MSCs labeled with BrdU could be identified in host hearts in groupⅠandⅡ,most of them positively stained with cTnT antibody. Echocardiography indicated that the improvement of the LVEF value in groupⅠwas more significant than that in the other three groups (P＜0.01,respectively).Some cells were incorporated into the coronary capillaries in the infarcted region.The capillary density in groupⅠwas higher than that in the other three groups (P＜0.01,respectively).Conclusion MSCs implantation combining with VEGF gene therapy can obviously re- pair damaged myocardium and enhance the angiogenesis in ischemic heart tissue.

OBJECTIVETo observe the expression of serine protease HtrA1 in human periodontal ligament tissue and to explore the effect of HtrA1 on the proliferation of human periodontal ligament cells (hPDLC).

METHODSSix human premolars and three human third molars(patient's ages ranging from 12 to 25, with intact root, without caries and/or periodontitis) were obtained in the Department of Maxillofacial Surgery of Wuhan University Hospital of Stomatology. Reverse transcription-PCR(RT-PCR) and immunohistochemistry analysis were applied to investigate the expression of HtrA1. Primary hPDLC were obtained by tissue-culture method in vitro. The proliferation of hPDLC was determined by methyl thiazolytetrazolium(MTT). Lentivirus-mediated over-expression and reduction of HtrA1 level was performed. An empty vector was used as negative control. On days 1, 3, 5, 7 and 9, the growth of hPDLC was characterized using cell counting kit-8(CCK-8) assay.

RESULTSRT-PCR data indicated that HtrA1 mRNA was expressed in human periodontal ligament tissue. Immunohistochemistry analysis showed HtrA1 was expressed in human periodontal ligament, mainly in the cytoplasm of hPDLC and the extracellular matrix. The MTT result suggested that the growth curve was consistent with the growth characteristics of hPDLC. The stable over-expression and knockdown cell lines was successfully established by lentivirus with more than 90% transfection efficiency. CCK-8 assay showed that HtrA1 over-expression inhibited the proliferation of hPDLC(0.897±0.060, 0.890±0.083, 1.631±0.038, 1.111±0.041, 1.110±0.189), while cell proliferation increased after down-regulation of HtrA1(0.329±0.021, 0.529±0.044, 0.973±0.056, 1.626±0.102, 2.344±0.198)(P<0.05).

CONCLUSIONSHtrA1 is expressed in human periodontal ligament tissue at both mRNA and protein levels, and may play an important role in regulating the proliferation of hPDLC.

Adolescent ; Adult ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Child ; Down-Regulation ; Genetic Vectors ; High-Temperature Requirement A Serine Peptidase 1 ; Humans ; Lentivirus ; physiology ; Periodontal Ligament ; cytology ; metabolism ; RNA, Messenger ; metabolism ; Serine Endopeptidases ; genetics ; metabolism ; Transfection ; Young Adult

OBJECTIVE: To investigate the inhibition effects of Tianshen Yizhi Recipe (TSYZR), a compound traditional Chinese herbal medicine, on decreased expression of nicotinic acetylcholine receptor (nAChR) and the neurotoxicity as well as lipid peroxidation induced by beta-amyloid peptide (Abeta) in human SH-SY5Y neuroblastoma cells. METHODS: The SH-SY5Y cells were treated by a certain concentration of TSYZR, and then exposed to Abeta(25-35). Methyl thiazolyl tetrazolium reduction assay was carried out to understand the influences of the drugs on cellular viability. Expressions of nAChR subunits (alpha3 and alpha7) at protein and mRNA levels were detected by Western-blotting and reverse transcription polymerase chain reaction, respectively. Lipid peroxidation was measured by thiobarbituric acid to observe the capacity of antioxidant of the drugs. RESULTS: TSYZR at a safe concentration could increase alpha7 protein in the cells, inhibit decreased expressions of alpha3 and alpha7 nAChR subunit proteins, prevent lower expression of alpha7 mRNA in SH-SY5Y cells induced by Abeta, reduce the neurotoxicity and lipid peroxidation resulting from Abeta, but had no significant effect on the lower expression of alpha3 mRNA. CONCLUSIONS: TSYZR can up-regulate the expression of alpha7 nAChR subunit protein and prevent decreased expressions of nAChRs and neurotoxicity as well as lipid peroxidation induced by Abeta. This drug may play an important therapeutic role in treatment of Alzheimer disease.

Endoscopic retrograde cholangiopancreatography (ERCP) and its derivative technologies have become the first-line treatment methods for bile duct stones. Most stones can be removed by conventional endoscopic techniques, while the treatment of large common bile duct stones requires a combination with endoscopic lithotripsy. This article summarizes the current research advances in endoscopic mechanical lithotripsy, electrohydraulic lithotripsy/laser lithotripsy, extracorporeal shockwave lithotripsy for bile duct stones in the treatment of large common bile duct stones, so as to provide recommendations and bases for the clinical treatment of large common bile duct stones.

To investigate the effects of 2-(4-methoxycarbonyl-2-tetradecyloxyphenyl)carbamoylbenzoic acid (CX09040) on protecting pancreatic β cells, the β cell dysfunction model mice were induced by injection of alloxan into the caudal vein of ICR mice, and were treated with compound CX09040. Liraglutide was used as the positive control drug. The amount and the size of islets observed in pathological sections were calculated to evaluate the β cell mass; the glucose stimulated insulin secretion (GSIS) test was applied to estimate the β cell secretary function; the oral glucose tolerance test (OGTT) was taken to observe the glucose metabolism in mice; the expressions of protein in pancreas were detected by Western blotting. The effects on the target protein tyrosine phosphatase 1B (PTP1B) were assessed by the PTP1B activities of both recombinant protein and the intracellular enzyme, and by the PTP1B expression in the pancreas of mice, separately. As the results, with the treatment of CX09040 in alloxan-induced β cell dysfunction mice, the islet amount (P<0.05) and size (P<0.05) increased significantly, the changes of serum insulin in GSIS (P<0.01) and the values of acute insulin response (AIR, P<0.01) were enhanced, compared to those in model group; the impaired glucose tolerance was also ameliorated by CX09040 with the decrease of the values of area under curve (AUC, P<0.01). The activation of the signaling pathways related to β cell proliferation was enhanced by increasing the levels of p-Akt/Akt (P<0.01), p-FoxO1/FoxOl (P<0.001) and PDX-1 (P<0.01). The effects of CX09040 on PTP1B were observed by inhibiting the recombinant hPTP1B activity with IC50 value of 2.78x 10(-7) mol.L-1, reducing the intracellular PTP1B activity of 72.8% (P<0.001), suppressing the PTP1B expression (P<0.001) and up-regulating p-IRβ/IRβ (P<0.01) in pancreas of the β cell dysfunction mice, separately. In conclusion, compound CX09040 showed significant protection effects against the dysfunction of β cell of mice by enlarging the pancreatic β cell mass and increasing the glucose-induced insulin secretion; its major mechanism may be the inhibition on target PTP1B and the succedent up-regulation of β cell proliferation.
Alloxan ; Animals ; Benzoates ; pharmacology ; Biological Assay ; Disease Models, Animal ; Glucose ; metabolism ; Glucose Tolerance Test ; Insulin ; secretion ; Insulin Resistance ; Insulin-Secreting Cells ; drug effects ; Liraglutide ; pharmacology ; Mice ; Mice, Inbred ICR ; Molecular Weight ; Pancreas ; drug effects ; enzymology ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 ; antagonists & inhibitors ; Signal Transduction