Objective To evaluate the effect of isoflurane anesthesia on noise-induced hearing loss in guinea pigs.Methods Forty-eight healthy adult male guinea pigs,aged 3 months,weighing 400-500 g,were randomly divided into 4 groups (n =12 each) using a random number table:control group (C group),isoflurane group (I group),noise-induced hearing loss group (N group),and isoflurane + noise-induced hearing loss group (I + N group).Isoflurane was inhaled for 140 min at a concentration of 1％ in I and I + N groups.N and I + N groups were exposed to the noise of 4 kHz center frequency and 118-122 dB sound pressure level for 120 min starting from 20 min after administration.Mean arterial pressure (MAP) was recorded at 10,40,70,100 and 120 min of exposure to noise and cochlear blood flow (CoBF) was recorded before administration and at 10,40,70,100 and 120 min of exposure to noise.Auditory brainstem response (ABR) threshold was recorded before administration and at 1 h,72 h,and 10 days after the end of exposure to noise.Arterial blood samples were obtained and the plasma noradrenaline (NE) concentration was detected by HPLC before exposure to noise and immediately after the end of exposure to noise.Results Compared with group C,MAP and the change rate of CoBF were significantly decreased,and the plasma NE concentration was increased immediately after the end of exposure to noise in I group,and MAP was increased,the change rate of CoBF was decreased,and the plasma NE concentration immediately after the end of exposure,and ABR threshold after the end of exposure were increased in N and I + N groups.Compared with N group,MAP was significantly decreased,the change rate of CoBF was increased,the plasma NE concentration immediately after the end of exposure,and ABR threshold at 1 and 72 h after the end of exposure were increased,and no significant was found in ABR threshold at 10 days after the end of exposure in I + N group.Conclusion Isoflurane anesthesia exerts temporary but not permanent protective effects against noise-induced hearing loss in guinea pigs and partial inhibition of activation of sympathetic nerve and increased CoBF may be involved in the mechanism.

Objective To optimize the preparation process for Fangji Huangqi Granules. Methods With the extraction rates of tetrandrine, fanchinoline, astragaloside Ⅳand solid as the parameters, the extract conditions of Fangji Huangqi Granules were optimized by orthogonal design . Then the anti-inflammation effect of the extracts was observed on the mice and rats. Results The optimal preparation process was as follows:the mixture of medical materials was firstly refluxed twice with total 10 times of 70 %alcohol,1.5 hours for each time, and then extracted twice with total 12 times of boiling water ,1.5 hours for each time. The anti-inflammation effect of the extracts was obvious on the mice and rats. Conclusion The optimal preparation process is reasonable and with high extraction rate of active components.

Background and purpose: The diagnosis of thyroid papillary carcinoma sometimes is difficult, metastasis of lymph node is the major reason of local relapse and influence prognosis.This study explores the immunohistochemical expression and their diagnostic value of CK19,HBME-1,galectin3,p27 and cyclinD1 in thyroid papillary carcinoma and the relations between p27,cyclinD1 and lymph node metastasis of papillary carcinoma.Methods: Immunohistochemical staining was used on 50 specimens of benign lesions (40 speciments of nodular goiters and 10 cases of follicular adenomas) and 50 specimens of papillary carcinomas (40 specimens of classic variants and 10 specimens of follicular variants) operated in our hospital from January of 2005 to December of 2008. Results: CK19,HBME-1 and galectin3 were expressed in cytoplasm or on the membrane, but p27 and cyclinD1 were expressed on the nucleus. The expressions of CK19,HBME-1 and galectin3 in thyroid papillary carcinoma were middle to strong positive, the positive ratios were 100%,96% and 100%, respectively;their expressions in benign lesions were negative or low positive, the positive ratios were 10%,10% and 6%, respectively;there were statistical differences between them (P<0.01). The expression of p27 in thyroid papillary carcinoma was low positive or negative, the positive ratio was 14%, but the expression of p27 in benign lesions was middle to strong positive, the ratio was 84%, there was also significant difference between them(P<0.01). The expression of CyclinD1 were similar in benign and malignant lesions of thyroid, the positive ratios were 68% and 78%, respectively, there was no statistical difference between them(P>0.05). There were significant differences(P<0.01) between the benign lesions and the papillary carcinomas in terms of the combination of CK19,HBME-1 and galectin3 expression and there were no significant differences(P>0.05) in the group of the former with underexpression of p27 between the two groups. The differences were not statistically significant (P>0.05) between the underexpression of p27 with the expression of cyclinD1 (the positive ratios in metastasis group and no metastasis group are 72.7% and 71.4%) in the lymph node metastasis. Conclusion: The combined immunohistochemical stainings of CK19,HBME-1 and galectin3 are useful on the diagnosis and differential diagnosis of thyroid papillary carcinoma, there is no predicted value of the underexpression of p27 with the expression of cyclinD1 for lymph node matastasis of thyroid papillary carcinoma.

Since a cyclooxygenase 2 (COX-2) inhibitor can reduce infarct size and improve contractility in ischemic myocardium, the aim of the present study was to explore whether COX-2 inhibitor nimesulide could protect myocardial function against oxidative stress injury in rat hearts, and to investigate the underlying mechanisms. The isolated rat hearts perfused by Langendorff method were exposed to 140 mumol/L of H2O2, and the cardiac contractility was measured. Then, the responses of coronary arteries, precontracted with U-46619, to the endothelium-dependent vasodilator serotonin (5-HT) and the endothelium-independent vasodilator sodium nitroprusside (SNP) were evaluated. The results were as follows: (1) In hearts exposed to H2O2 for 20 min, the left ventricular developed pressure [LVDP, (54.8 +/- 4.0)%] and maximal rate of rise/fall of ventricular pressure [+/-dp/dt(max), (50.8 +/- 3.1)% and (46.2 +/- 2.9) %] were reduced compared with that in the control group (100%). After pretreatment with nimesulide (5 mumol/L) for 10 min before H2O2 perfusion, LVDP and +/-dp/dt(max) were enhanced to (79.9 +/- 2.8)%, (80.3 +/- 2.6)% and (81.4 +/- 2.6)%, respectively (P<0.01), and this was partially abolished by the nitric oxide synthase (NOS) inhibitor L-NAME [(60.2 +/- 2.1)%, (63.9 +/- 2.4)% and (63.1 +/- 2.9)%, respectively, P<0.01]. (2) The vasodilatation induced by 5-HT and SNP in H2O2-treated group was significantly less than that in the control group. Pretreatment with nimesulide for 10 min antagonized the decrease of endothelium-dependent vasodilatation in H2O2-treated group [(-22.2 +/- 4.2) % vs (-6.0 +/- 2.5) %, P<0.01], but had no effect on the decline of endothelium-independent vasodilatation [(-2.0 +/- 1.8)% vs (-7.0 +/- 3.5) %, P>0.05]. (3) Pretreatment with nimesulide for 10 min increased the NO production in H2O2-treated hearts [(2.63 +/- 0.40) vs (1.36 +/- 0.23) nmol/g protein, P<0.05], and this was inhibited by L-NAME. (4) Pretreatment with the selective COX-1 inhibitor piroxicam had no effect on LVDP and +/-dp/dt(max) in isolated hearts exposed to H2O2, but the left ventricular end diastolic pressure (LVEDP) was much higher than that in the group treated with H2O2 alone. Piroxicam did not influence the coronary resistance in H2O2-treated rat hearts. These data suggest that the COX-2 inhibitor nimesulide improves myocardial function in rat hearts suffering from oxidative stress, and this may be through an improvement in endothelium-dependent arterial relaxation and an enhancement of NO production in rat heart.
Animals ; Coronary Vessels ; Cyclooxygenase 2 Inhibitors ; Endothelium, Vascular ; Endothelium-Dependent Relaxing Factors ; Heart ; drug effects ; Hydrogen Peroxide ; Myocardial Reperfusion Injury ; Myocardium ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Serotonin ; Sulfonamides ; pharmacology ; Vasodilation ; Vasodilator Agents

Objective To observe the effect of liver disease special-purpose enteral nutrition preparation on protein metabolism and liver function in children with liver injury.Methods Sixty cases of severe ill with liver injury in hospital,with mean age of (7.8?6.3) years old.All patients were randomly divided into experimental group (n=30) and control group(n=30).The experimental group was treated by adding the liver disease special-purpose enteral nutrition preparation homogenized diet and control group was treated by adding entire protein entire nutrition type enteral nutrition preparation.All patients in both 2 groups were nasally fed with intestinal nutrition,which contained 418-628 kJ/(kg?d).One day before nutritional support and 14 days after nutritional support,the liver function,total serum protein,albumin,hemoglobin were recorded.SPSS 11.5 software was used to analyze the data.Results The baseline indicators were similar before nutritional supports.Fourteen days after nutritional support,alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were all significantly lower in experimental group than in control group(Pa

Objective To investigate the effect of human cytomegalovirus (HCMV) on proliferation of colony forming unit T-lymphocyte (CFU -TL)and its interference methods. Methods Normal CFU - TL culture was used as blank control. Normal CFU- TL culture system plus inactivated HCMV fluid as inactivated HCMV control. The dilution of 1:10,1:100,1:1000 were added into CFU -TL colonies culture system directly as infected group. Astragalus (AMI) and ganciclovir(GCV) were added into culture system with HCMV dilution of 1:10 as experimental group. By methylcellulose semi-solid culture, different concentrations of HCMV - AD1699 affect CFU-TL and interfered by astragalus AMI, GCV. CFU - TL were surveyed. The effect of HCMV on CFU-TL proliferation was measured by MTT; HCMV-AD169 DNA in CFU-TL was found by PCR. Results 1. Compared with control group, the numbers of CFU -TL in the HCMV infection groups decreased significantly(P

Objective To investigate the effects of morroniside on activation of caspase-3 in rats with focal cerebral ischemia/reperfusion. MethodsThe model was induced with occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. Vitamin E used for the positive control. The activity of caspase-3 was detected with spectrophotometry. ResultsCompared with sham group, the caspase-3 activity increased obviously in model rat. Compared with model group, Morroniside (30 mg/kg,90 mg/kg,270 mg/kg) decreased the activation of caspase-3 remarkably, which was dose-dependent (P<0.05). ConclusionMorroniside may reduce apoptosis by decreasing the activation of caspase-3 in rats.

ObjectiveTo investigate the effects of morroniside on IL-1β in rat cortex with focal cerebral ischemia/reperfusion.MethodsThe animal model was induced by occlusion of middle cerebral artery with suture embolus, ischemia for 30 min, and reperfusion for 72 h in rats. The content of IL-1β was detected with enzyme linked immunosorbent assay(ELISA).ResultsCompared with sham group, the content of IL-1β increased obviously in model rat. Compared with model group, morroniside(30 mg/kg, 90 mg/kg, 270 mg/kg) and colchicine (0.06 mg/kg) decreased the content of IL-1β significantly (P<0.001).ConclusionMorroniside may protect the cortex from inflammatory factor IL-1β.

Cerebral ischemia-reperfusion results in damage on neuron, leading to genes and proteins related to apoptosis activation. At the same time, generous cytokines released after cerebral ischemia-reperfusion can induce the apoptosis of the neuron. Many current studies have showed that the major damage mechanisms on apoptosis of the neuron are mitochondrion impairment, calcium overload, increased levels of oxygen radicals and so on. The advance research on the mechanism contributes to explore new neuroprotective drugs, and further identify the target and therapeutic effect of drug treatment.

Atrophy ; Disability Evaluation ; Humans ; Kidney