Objective To study the detection rate of early esophageal carcinoma using magnifying endoscopy,and to evaluate the relationship between the imaging patterns of microvasculature change and his- tological diagnosis.Methods Two hundred and fourteen patients with esophageal mucosa roughness,ero- sion,plaque,abnormal color and indentation in conventional endoscopy and 16 healthy volunteers were en- rolled.The magnifying endoscopy images were graded as four patterns by intraepithelial papillary capillary loop(IPCL)changes after iodine dyeing.The biopsies underwent pathologic evaluation.The comparison be- tween the imaging patterns of endoscopy and histological diagnosiswas was evaluated.Results 80.4%(90/ 112)esophagitis was type 2,and 85.7%(12/14)early esophageal carcinoma was type 3 and type 4.The difference was significant between early esophageal carcinoma and normal mueosa(?~2=27.32,P

The present study was undertaken to define whether intracarotid injection of capsaicin induces Fos expression associated with the activation of NOS-containing neurons in brainstem nuclei by combining the immunocytochemical method for Fos with NADPH-d histochemical technique for NOS. The results obtained are as follows: (1) Intracarotid injection of capsaicin caused a significant increase of Fos-like immunoreactive neurons in area postrema (AP), nucleus tractus solitarius (NTS), paragigantocellularis lateralis (PGL) and locus coeruleus (LC), without influence upon the neurons of raphe nuclei (RN) and periaqueductal gray (PAG). (2) NO-containing neurons in PGL and NTS and the double-labeled neurons in PGL were also increased significantly following intracarotid injection of capsaicin. Small numbers of NO-containing neurons were found in LC, but there was no change in the number of NO-containing neurons in RN and PAG. No NADPH-d histochemical activity could be found in AP. (3) The above responses to capsaicin were significantly inhibited by pretreatment with either a capsaicin receptor antagonist ruthenium red or a NMDA receptor antagonist MK-801. The above results indicate that intracarotid injection of capsaicin may activate the neurons in brainstem nuclei involved in cardiovascular regulation, and that NO only plays an indirect role in the modulation of the responses of brainstem nuclei to capsaicin. These effects of capsaicin are mediated by capsaicin receptors with involvement of glutamate.

AIM:To explore the expression and possible function of histamine H3 receptor (H3R) in striated myogenesis and the differentiated C2C12 cells.METHODS: H3R and myogenesis late marker myosin heavy chain (MHC) were detected at mRNA and protein levels during C2C12 myogenesis.H3R antagonist ciproxifan was added and the expression of the myogenesis early marker desmin, intermediate markers myogenin and MHC was detected.Differentia-ted myoblasts were loaded with Fluo-4 calcium indicator dye and the effect of R-( a)-methylhistamine ( RMeHA) on the cy-toplasmic calcium concentration was determined under the 200 mA electrical stimulation.RESULTS: The expression of H3R and MHC was increased during myogenesis.Ciproxifan incubation had no influence on the 3 striated myogenesis mar-kers (P>0.05).In C2C12 myoblasts, RMeHA (10 nmol/L~100 μmol/L) effectively diminished cytoplasmic calcium peak when the cells were electrically paced (P<0.05).The best inhibitory effect of RMeHA was observed at dose of 100 nM for 10 min and 20 min, which was higher than that for 5 min (P<0.05).CONCLUSION: H3R might have little effect on the myogenic differentiation, but diminishes cytoplasmic calcium peak of the differentiated myoblasts under electri-cal stimulation.

AIM:To observe the changes of macular thickness in patients after cataract operation.
METHODS: A total of 126 patients ( 133 eyes ) were divided into two groups that were included in this study. The group (68 eyes of 64 case) with phacoemulsification combined intraocular lens implantation and ( 65 eyes of 62 cases ) with manual small incision cataract surgery ( MSICS) . There was no complication before and during the surgery. Optical coherence tomography ( OCT) was examined 1, 3mo before and after surgery. The visual acuity and macular thickness were compared after surgery. The SPSS 17. 0 software was used for statistical analysis. The paired t-test was used before and after surgery. Independent-samples t test was used in two groups before and after surgery,α=0. 05.
RESULTS: The cataract phacoemulsification group:preoperative and 1mo after surgery, the mean macular thickness was 241. 3±10. 9μm and 279. 7±16. 5μm, with significant difference ( P < 0. 01 ). The mean macular thickness was 245. 6±12. 6μm 3mo after surgery without statistical difference compared with preoperative ( P>0-05). The mean macular thickness was 279. 7±16. 5μm 1mo after surgery and 245. 6±12. 6μm 3mo after surgery with statistical difference(P<0. 05). Three eyes displayed cystoid macular edema at 1mo after surgery and 2 eyes of them was resolved 3mo after surgery. The group of MSICS: preoperative and 1mo after surgery, the mean macular thickness was 240-5±11. 9μm and 280. 7±16. 8μm, with significant difference (P<0. 01). The mean macular thickness was 246. 6±13. 2μm 3mo after surgery without statistical difference compared with preoperative ( P >0-05). One month after surgery and 3mo after surgery, the mean macular thickness were 280. 7±16. 8μm and 246-6±13. 2μm, with statistical difference (P<0. 05). Two eyes displayed cystoid macular edema at 1mo after surgery and 2 eyes were resolved 3mo after surgery. Between the two groups pre-operation or after operation for 1, 3mo respectively P values were without statistical difference (P>0. 05).
CONCLUSION: The macular thickness and macular edema can be found 1mo after cataract phacoemulsification and MSICS. Three months post-operatively, macular edema disappears and does not show statistical difference compared with preoperative. The increase of macular thickness has no obvious relationship with the choice of surgery.

Objective To investigate the onset of left ventricular remodeling (LVRM) after acute myocardium infarction (AMI) and its changes within 6 hours in dogs on echocardiography. Methods AMI was induced in 14 dogs by ligating the left anterior descending arteries. Eight myocardium infarcted models were successful and were sacrified for pathological study. The indices of LVRM: wall infarction thickness (WIT), the wall motion score index (WMSI), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV) and left ventricular ejection fraction (LVEF) were evaluated before and 1 h, 2 h, 3 h, 4 h, 5 h and 6 h after operation. Results Compared with the pre-operation, WIT and LVEF were decreased (P<0.01), LVESV and WMSI were increased (P<0.01), and LVEDV was increased (P<0.05 or P<0.01) at every time point after operation. WIT had no significant difference at 1 h, 2 h, 3 h, 4 h, 5h and 6h after operation (P＞0.05). LVEDV, LVESV were higher (P<0.05) and LVEF was lower (P<0.05 or P<0.01) at 4 h, 5 h, and 6 h than at 1 h, and 2 h after operation. WMSI was higher at 3 h, 4 h, 5 h, and 6 h than at 1h (P<0.05). Conclusions In our experiment, LVRM occurred at 1 h after AMI in dogs. Thus echocardiography may evaluate early LVRM.

Objective To investigate the effects of penehyclidine hydrochloride on activities of nuclear factor kappa B (NF-kB) and activator protein-1 (AP-1) during actue lung injury induced by blunt chest trauma-hemorrhagic shock and resuscitation (HSR) in rats.Methods Thirty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly assigned into 3 equal groups (n =10 each) using a random number table:sham operation group (group S),blunt chest trauma-HSR group (group THSR) and penehyclidine hydrochloride group (group PHCD).The model of actue lung injury induced by blunt chest trauma-HSR was induced by dropping a 300 g weight onto a precordium in anesthetized rats.Blood was withdrawn via the femoral artery 5 min later until MAP was decreased to 35-45 mmHg within 15 min and maintained at this level for 60 min,followed by resuscitation.In PHCD group,PHCD 2 mg/kg was injected intravenously at 60 min after hemorrhagic shock.At 6 h after the model was established,blood samples were obtained for measurement of concentrations of tumor necrosis factor-alpha (TNF-α) in serum.The lungs were then removed for determination of lung water content,myeloperoxidase (MPO) activaty (by colorimetric assay),NF-κB and AP-1 activaties (using electrophoretic mobility shift assay) in lung tissues,and for microscopic examination of pathologic changes (under light microscope).The left lung was lavaged,and lung permeability index (LPI) was calculated.Results Compared with S group,lung water content,LPI,serum TNF-α level and activites of MPO,NF-κB and AP-1 were significantly increased in THSR and PHCD groups.Compared with THSR group,lung water content,LPI,serum TNF-α concentrations and activites of MPO,NF-κB and AP-1 were significantly decreased in PHCD group.The pathological damage to lung tissues was significantly reduced in PHCD group as compared with THSR group.Conclusion PHCD can inhibit activities of NF-κB and AP-1 in lung tissues,thus mitigating acute lung injury induced by blunt chest trauma-HSR in rats.

OBJECTIVE To study the antidepressant effects of ammoxetine(AMX)and the underlying mechanisms. METHODS Two behavioral despair models,the tail suspension test (TST) and the forced swimming test(FST),were used to evaluate the antidepressant-like effects of AMX 2.5-20 mg · kg-1 following oral administration. Monoamine neurotransmitter p-chloro-phenylalanine(p-CPA)andα-methyl-p-tyrosine(AMPT) depletion models in mice were used to investigate the effects of AMX on levels of 5-serotomin(5-HT)and norepinephrine(NE)in the brain. RESULLTS The results of behavioral study showed that compared with normal control group,AMX(10 and 20 mg · kg-1)reduced the immobility time of mice by 51.4% and 80.7% in the TST(P<0.05,P<0.01) or by 48.0% and 66.2% in the FST (P<0.05),respectively. Locomotion activity test indicated that AMX did not increase or decrease the movement distance of mice,demonstrating that AMX had no excitatory or inhibitory actions on the central nervous system. Moreover,AMX(5,10 and 20 mg·kg-1)exerted antidepressant effects in the p-CPA induced 5-HT depletion model and AMPT induced NE depletion model,as evidenced by the significantly reduced immobility time,ie,63.9%,93.4%,90.5% and 61.9%,77.2%,100% reduction in the TST (P<0.01),respectively,and AMX at the dose of 20 mg·kg-1 significantly increased the concentrations of 5-HT and NE by 144.7% and 57.2% in the mouse brain(P<0.05) ,respectively. CONCLUSION AMX has strong antidepressant-like effects in behavioral despair models and monoamine neurotransmitter depletion models in mice,which is involved in the increased levels of 5-HT and NE in the brain.

Objective To assess the safety and efficacy of a novel biodegradable polymer and rapamycin-coating stent, the EXCEL stent, in the treatment of coronary artery disease (CAD), as compared with the CypherTM stent. Methods In this prospective, non-randomized study, 60 consecutive patients with symptomatic CAD received either an EXCEL stent (n=32), or a CypherTM stent(n=28),according to their respective treatment intention. Follow-up angiography was performed at a mean of 180±40 days. The primary endpoint of the study was the occurrence of a major adverse cardiac event (MACE), including death, myocardial infarction, or target-vessel revascularization during the 6 months after stenting. The secondary end points included the in-stent late luminal loss (LLL), percentage of in-stent stenosis of the luminal diameter, and the rate of restenosis (luminal narrowing of 50 percent or more) at 6 months. Results There were no significant differences between the two groups in baseline characteristics, including the distribution of target vessel and lesion types. During the follow up period of 6 months, there were no occurrences of MACE in either group. Twenty-seven patients(84%) in the EXCEL group and 10 (36 %) in the CypherTM group underwent quantitative coronary angiography at 6 months. For these patients, no restenosis occurred, and there were no differences in the in-stent stenosis of the luminal diameter (5.98±5.52% vs 5.21 ±6.3%,P＞0.05) and the LLL (-0.02±0.09 mm vs -0.01±0.07 mm, P＞0.05). Conclusions Compared with the CypherTM stent, the EXCEL Stent with biodegradable polymer and rapamycin-coating showed similar efficacy in the prevention of neointimal proliferation, restenosis, and associated clinical events in CAD patients.

Objective To evaluate the relationship between DJ?1 and diabetes mellitus ( DM )?caused influence on cardioprotection induced by ischemic postconditioning in rats. Methods Adult male Sprague?Dawley rats, aged 3 months, weighing 220-250 g, were used in the study. DM was induced by intraperitoneal injection of 1% streptozotocin 60 mg∕kg and confirmed by blood glucose≥16.7 mmol∕L. Forty?eight rats with DM were randomly divided into 3 groups ( n=16 each) using a random number table:sham operation group ( group DM?S ) , myocardial ischemia?reperfusion ( I∕R ) group ( DM?IR ) and ischemic postconditioning group (DM?IPO group). Another 48 normal rats received the equal volume of citrate buffer solution instead and served as control. Those rats were randomly divided into 3 groups ( n=16 each) using a random number table: sham operation group ( S group) , myocardial I∕R group ( IR group) and ischemic postconditioning group (IPO group). At 12 weeks after streptozotocin injection, myocardial I∕R was produced by 30 min occlusion of the left anterior descending branch of the coronary artery followed by 120 min reperfusion. Ischemic postconditioning was induced by 3 cycles of 10 s reperfusion followed by 10 s limb ischemia at the end of 30 min limb ischemia. At 120 min of reperfusion, the animals were sacrificed, and hearts were removed for determination of myocardial infarction size ( using TTC ) , and expression of DJ?1, phosphatase and tensin homologue ( PTEN) protein, and phosphorylated Akt ( p?Akt) in myocardial tissues ( by Western blot) . Results The infarction size was significantly increased in diabetic and nondiabetic rats during myocardial I∕R. The expression of DJ?1, PTEN protein and p?Akt was significantly higher during myocardial I∕R in nondiabetic rats, and the expression of PTEN protein and p?Akt was up?regulated, and no significant change was found in DJ?1 expression during myocardial I∕R in diabetic rats. Ischemic postconditioning reduced infarction size during myocardial I∕R and up?regulated the expression of DJ?1 and p?Akt, and down?regulated the expression of PTEN protein in nondiabetic rats, but not in diabetic rats. Compared with nondiabetic rats, the expression of DJ?1 and p?Akt was down?regulated, and the expression of PTEN protein was up?regulated after ischemic postconditioning in diabetic rats. Conclusion The mechanism by which DM abolishes cardioprotection induced by ischemic postconditioning is associated with down?regulation of DJ?1 expression in rats.

Partial nature of "promoting blood circulation and dieresis" of Salvia Miltiorrhizain was initially demonstrated by investigating the regulation effect of AQP2 expression in kidney of trauma blood stasis model rats with the Salvia Miltiorrhizain so as to provide guidance for its clinical deployment of administration. Random allocation was taken to averagely divide 30 SD rats into two groups: 10 rats in normal group and 20 rats in blood stasis syndrome group. Trauma blood stasis rat model was established by quantitatively beating. Then the rat model group was divided into model group and salvia group. After 7 days of treatment, the rat kidney AQP2 expression was detected, the content of urine AQP2 was compared and the damaged local muscle and kidney pathological changes were observed by immunohistochemical method and western blot method. Compared with that of the normal group, rats in model group had inflammatory cells infiltration, blood stasis and edema of the injured local muscles and up-regulated AQP2 expression, decreasing urinary output, and kidney tissues blood stasis and edema (P < 0.05). On the other hand, compared with that of the model group, those parameters of rats in salvia group were all decreasing except urine output (P < 0.05). Such result indicated that Salvia Miltiorrhiza can reduce trauma blood stasis rat content of urine AQP2 and down-regulated AQP2 expression in kidney tissue, so as to reduce the reabsorption of water by renal tubular and increase urine output. The promoting blood circulation effect of Salvia Miltiorrhizain can alleviate the degree of the damaged tissue edema and encourage urine drainage. This therapy is closely related to the effect of regulating AQP2 in kidney by salvia, so the purpose of this study by verifying "promoting blood circulation and diuresis" as the mechanism for the regulation effect of the salvia on AQP2 expression.
Animals ; Aquaporin 2 ; genetics ; metabolism ; Blood Circulation ; drug effects ; Diuresis ; drug effects ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Kidney ; blood supply ; drug effects ; metabolism ; physiopathology ; Kidney Diseases ; drug therapy ; genetics ; metabolism ; physiopathology ; Male ; Rats ; Salvia miltiorrhiza ; chemistry