BACKGROUND: The effect of external application of capsaicin in the treatment of superficial pain has been recognized, but its effect against trigeminal neuralgia by direct action on the nerve ending or nerves in the hypodermis or deep tissues awaits intensive investigation.OBJECTIVE: To observes the effect of subcutaneous injection of capsaicin on calcitonin gene-related peptide (CGRP) and nitric oxide synthase(NOS)-positive nerve fibers in rat facial skin.SETTING: Teaching and Research Division of Anatomy, Xianning Medical College, and Department of Neurobiology, Tongji Medical College of Huazhong University of Science and Technology.MATERIALS: This experiment was conducted in the Laboratory of Neurobiology, Tongji Medical College, between October and December 2003.Twenty healthy Wistar rats of either sex with body mass of 120-170 g were used.METHODS: The rats received subcutaneous injection of capsaicin for treatment of the suborbital branch of the trigeminal nerve on the right side,with the left side serving as the control side. According to the doses of capsaicin applied, the rats were divided into 4 groups, namely 20, 30, 50and 100 μL capsaicin groups with 5 rats in each group. Twenty-four hours after the injections, samples were obtained and cut into slices for microscopic observation and the expressions of CGRP and NOS were examined immunohistochemically.MAIN OUTCOME MEASURES: [1] Changes of CGRP and NOS-positive nerve fibers on the experimental side and image analysis of the mean absorbance of CGRP and NOS; [2] changes of characteristic behaviors and body signs of the rats.RESULTS: Totally 20 rats entered the result analysis. [1] Behavioral change: A few minutes after subcutaneous injection of capsaicin, the rats exhibited a series of characteristic behavioral and symptomatic changes,which gradually diminished or even vanished with the increase of the doses. [2] Microscopic changes: On the experimental side, no obvious difference was noted in the expression of CGRP and NOS-positive nerve fibers between the groups. [3] Imaging analysis of the mean absorbance of CGRP and NOS: For CGRP, the mean absorbance was 0.984±0.056 on the control side and 0.947±0.025, 0.852±0.042, 0.756±0.028 and 0.730±0.016 in 20,30, 50 μL and 100 μL capsaicin groups, respectively. As for NOS, the mean absorbance was 0.151±0.009 on the control side, and was 0.148±0.007,0.132±0.012, 0.111±0.067 and 0.107±0.006 in 20, 30, 50 μL and 100 μL capsaicin groups. Analysis of variance revealed significant differences between the groups (P ＜ 0.01).CONCLUSION: CGRP and NOS participate in the processing of nociceptive information and modulate pain and analgesia. Capsaicin executes analgesic effect by exhausting massive neurotransmitters.

Objective: To investigate the endothelial function of chronic ischemia heart failure (CIHF) patients complicated with depression. Methods: The depression statuses were evaluated by Self-rating Depression Scale (SDS) in 56 patients with documented stable chronic ischemia heart failure. The patients were assigned to depression group (n = 20) or non-depression group(n = 36) based on their standard SDS scores. The flow-mediated dilation(FMD) of the brachial artery was assessed by ultrasound in the two groups, and the plasma ET-1 and NO levels were determined so as to evaluate the endothelial function. Results: The incidence of depression was 35.7% in the 56 patients. Patients in the depression group showed significantly lower FMD compared with the non-depression group([5.97±0.78]% vs [6.66±0.83]% , P<0.05). Plasma NO level ([48.90±9.82] μmol/L vs [55.13±10.32] μmol/L, P<0.05) was lower and ET-1 level ([83.35±13.39] ng/L vs [74.67±10.95] ng/L, P<0.05) was higher in the depression group than in the non-depression group. Conclusion: CIHF patients with depression have a more severe damage of endothelial function than those without depression.

Obiective: To compare the tissue biocompatibility of domestically manufactured NiTi alloy before and after thermal surface oxidation under 3 different temperatures. Methods: Domestically manufactured NiTi alloy was oxidized in air (group A) and subjected to 30 min heat treatment at 400°C (group B),500°C, (group C),and 600°C (group D) to form different protective oxide surface layers in presence of argon (607.95 kPa). Wire samples from A, B, C and D groups were subcutaneously implanted in guinea pigs. Guinea pigs received 317L stainless steel transplantation(group E) and sham-operation group (F) were taken as control. The order of inflammatory cell infiltration and tissue hyperplasia around implanted materials were observed 1, 2, 4, and 8 weeks after implantation. Results: The peak time of inflammatory cell infiltration and fibrous hyperplasia were at the first and fourth week after implantation. The inflammatory cell infiltration and fibrous hyperplasia were both slight and all met the GB/T 16886. 6-1997 in vivo implantation standard. The order of inflammatory cell infiltration and thickness of capsule walls from low to high was F

Objective:To compare the tissue biocompatibility of domestically manufactured NiTi alloy before and after thermal surface oxidation under 3 different temperatures.Methods:Domestically manufactured NiTi alloy was oxidized in air (group A)and subjected to 30 min heat treatment at 400℃(group B),500℃(group C),and 600℃(group D)to form different protective oxide surface layers in presence of argon(607.95 kPa).Wire samples from A,B,C and I3 groups were subcutaneously implanted in guinea pigs.Guinea pigs received 317L stainless steel transplantation(group E)and sham-operation group(F)were taken as control.The order of inflammatory cell infiltration and tissue hyperplasia around implanted materials were observed 1,2,4,and 8 weeks after implantation.Results:The peak time of inflammatory cell infiltration and fibrous hyperplasia were at the first and fourth week after implantation.The inflammatory cell infiltration and fibrous hyperplasia were both slight and all met the GB/T 16886.6-1997 in vivo implantation standard.The order of inflammatory cell infiltration and thickness of capsule walls from low to high was F

Heart Valve Diseases ; therapy ; Heart Valve Prosthesis Implantation ; methods ; Humans

Objective To explore the roles of reactive oxygen species(ROS) and TGF-?1 in aldosterone-induced PAI-1 production.Methods Quiescent rat mesangial cells (MCs) were treated by aldosterone.The level of ROS in MCs induced by aldosterone was measured by confecal laser scanning microscopy and the TGF-?1 activity in the supematant of culture was measured by mink lung epithelial cell (Mvllu) proliferation inhibition MTT assay.Then,before the addition of aldosterone,MCs were pretreated with NAC or TGF-?1 neutralizing antibody to decrease cellular ROS or inhibit activity of TGF-?1 induced by aldosterone respectively.PAI-1 mRNA was examined by semi-quantification RT-PCR and PAI-1 protein by Western blotting.Results The intracellular ROS induced by aldosterone increased by 5-fold compared to that of control group,and the activity of TGF-?1 stimulated by aldosterone increased markedly.TGF-?1 neutralizing antibody and NAC effectively decreased aldosterone-induced PAI-1 mRNA expression by 30% and 32%,and PAI-1 protein expression by 21% and 11%,respectively.However,neither TGF-?1 neutralizing antibody nor NAC alone could regulate aldosterone-induced PAI-1 mRNA and protein expression to normal level in 24 hours.Conclusions ROS and TGF-?1 play important roles in up-regulation of aldosterone- induced PAI-1 in MCs.ROS and TGF-?1 are not the exclusive pathway of PAI-1 expression induced by aldosterone in MCs.

Objective To investigate the effect of Shexiangbaoxin pills on the heart function of patients with chronic ischemia heart failure. Methods A total of 96 patients with documented stable chronic ischemia heart failure were evenly randomized into Shexiangbaoxin pill group (Shexiangbaoxin pill plus basic treatment) and placebo group (placebo plus basic treatment) for 24 weeks. The left ventricular ejection fraction (LVEF), left ventricular end diastolic volume (LVEDV), serum brain natriuretic peptide (BNP) level, and 6 minute walk test (6 MWT) were compared before and after treatment in the two groups. Results In Shexiangbaoxin pill group, the LVEF was increased by 5.6% after 24 weeks of treatment (\[34.2±3.5\]% vs \[36.1±4.0\]%, P<0.05), the serum BNP level was significantly decreased (\[680.2±203.9\] pg/mL vs \[621.8±200.7\] pg/mL, P<0.05), and the distance of 6MWT was significantly increased (\[385.3±69.2\] m vs \[401.7±75.0\] m, P<0.05); the LVEDV had no significance before and after treatment (P>0.05). The above parameters were not significantly different in placebo group before and after treatment (P>0.05). Conclusion Shexiangbaoxin pills plus basic treatment can effectively improve the left ventricular function in patients with chronic ischemia heart failure, and further study is needed to observe whether it can reverse left ventricular remodeling.

Objective: To establish a method to determine 4 active ingredients in Jindan tablets by HPLC.
Methods: Agilent Eclipse X DB C₁₈ (4.6 mm×250 mm, 5 μm) column was adoped using acetonitrile (phase A) -0.1% phophoric acid solution (phase B) as the mobile phase with gradient program at the flow rate of 1.0 mL·min^-1, the detection wavelength was 270 nm, Column temperature was set at 30 ℃.
Results: The linear ranges of gentiopicrin, polydatin, quercetin and emodin were 7.875-78.75 μg·mL^-1（r=0.999 9）, 6.75-67.50 μg·mL^-1（r=0.999 7）, 7.726-77.26 μg·mL^-1（r=0.999 4）, 3.809-38.09 μg·mL^-1（r=0.999 8), respectively, the peak area had a good linear relationship with the mass concentration of 4 components, the average recovery were 99.31%, 99.21%, 99.04%, 99.59%, (n=6) respectively, and RSDs were 1.86%, 1.24%, 1.37%, 1.15%, respectively.
Conclusion: This method is reliable, repeatable and stable, and has strong specificity. This method can provide a reference for the quality control and standard improvement of Jindan tablets.

BACKGROUND:It is presumed that urinary trypsin inhibitor could have protective effects on local and systemic tissues and could inhibit osteoclast proliferation and activation under long-term chronic inflammation conditions and in ischemic and anoxic environment which was induced by prosthetic wear. OBJECTIVE:To investigate the inhibitory effect of ulinastatin on receptor activator for nuclear factor-κb ligand-induced differentiation, proliferation and osteoclastogenesis of RAW264.7 cells and its effects on matrix metal oproteinase-2, matrix metal oproteinase-9 expression level and activity. METHODS:Mouse monocyte/macrophage cellline RAW264.7 was treated with different concentrations of urinary trypsin inhibitor (0, 500, 5 000 U/mL) for 24, 48 and 72 hours. Experiments were divided into four groups:the blank group (RAW264.7 cells), receptor activator for nuclear factor-κb ligand-induced group (0 U/mL ulinastatin), 500 U/mL ulinastatin group and 5 000 U/mL ulinastatin group. RESULTS AND CONCLUSION:(1) MTT results indicated that there was no significant difference on the proliferation of RAW264.7 cells treated with urinary trypsin inhibitor at 0-5 000 U/mL (P>0.05) (2) Tartrate-resistant acid phosphatase staining results revealed that compared with receptor activator for nuclear factor-κb ligand-induced group, the number of tartrate-resistant acid phosphatase-positive cells was significantly less in the ulinastatin group (P<0.05), showing a time-dose dependent manner. (3) Immunohistochemisical results found that compared with receptor activator for nuclear factor-κb ligand-induced group, the percentage of matrix metal oproteinase-9-positive cells was apparently lower in the ulinastatin group. (4) Western blot assay results demonstrated that matrix metal oproteinase-9 expression was low in the RAW264.7 cells alone. At 48 hours after addition of receptor activator for nuclear factor-κb ligand, matrix metal oproteinase-9 protein expression was large. At 72 hours after culture in the 5 000 U/mL ulinastatin group, matrix metal oproteinase-9 protein expression was evidently reduced. (5) Gelatin zymography results showed that compared with the receptor activator for nuclear factor-κb ligand-induced group, matrix metal oproteinase-9 expression was significantly lower in the 5 000 U/mL ulinastatin group (P<0.05). Results suggested that urinary trypsin inhibitor inhibited receptor activator for nuclear factor-κb ligand-induced osteoclastogenesis and diminished matrix metal oproteinase-9 expression and activity.

Background:A recent perspective European study has shown that Chronic Liver Failure-Consortium Organ Failure score(CLIF-C OFs)is an effective diagnostic criteria for acute-on-chronic liver failure(ACLF)in alcoholic or hepatitis C virus patients with acute decompensation(AD). Aims:To assess the efficacy of CLIF-C OFs for distinguishing ACLF in non-hepatitis B virus(HBV)-related chronic liver disease patients with AD. Methods:A total of 274 consecutive non-HBV-related chronic liver disease patients with AD from Jan. 2005 to Dec. 2010 at Shanghai Ren Ji Hospital were enrolled. Patients were divided into three groups:ACLF at admission,ACLF developed within 28-day and non-ACLF according to CLIF-C OFs criteria. Clinical and biochemistry characteristics,severity of the disease and 28-day and 90-day mortality data between ACLF and non-ACLF groups were analyzed. Results:Of the patients assessed,40 had ACLF at admission,27 had ACLF developed within 28-day,207 remained not having ACLF. Patients in ACLF group had higher TB,Cr,INR,ALT,AST,ALB,WBC,score of Child-Pugh,CTP,MELD,MELD-Na than non-ACLF patients(P <0. 05),and were younger in age(P < 0. 01). Incidences of hepatic,renal,cerebral,coagulation,circulation and lung failure,28-day mortality,90-day mortality were significantly higher in ACLF group than in non-ACLF patients( P <0. 01). However,no significant differences were seen in the characteristics mentioned above between ACLF at admission group and ACLF developed at 28-day group(P > 0. 05). TB level at admission and infection occurred within 28-day were the risk factors for developing ACLF(P < 0. 05). Conclusions:ACLF constitutes a more severe subgroup in non-HBV-related chronic liver disease patients with AD,and CLIF-C OFs could help to distinguish ACLF patients out from non-HBV-related chronic liver disease patients with AD.