It was developed that a new method for measuring the ratio of pulmonary blood flow tosystemic biood flow by two-dimensional Doppler echocardiography.Qp and Qs blood flow were consid-ered to be propotional to the mitral and tricuspid Doppler flow velocity time integral multipled respectively by mitral or tricuspid valve ring diameters(MVID or TVID),I.e.MVID/TVID was equal to Qp/Qs.With the method,we calculated the Qp/Qs ratio close to 1:1(0.939+/-0.083)in 18 normal Per-sons,0-656+/-0.167 in 15 patients with Tetralogy of Fallot.Qp/Qs in TOF corrected negativly With hemoglobin.Our results demonstrated that conventional Doppler mdthod to calculate the Qp/Os ratio can be simplified.

OBJECTIVE:To study the pharmacodynamic action of Kanggan granules(KG).METHODS:After KG was administered i.g.to experiment animals,the antifebrile effect by using pyretic rats induced by fresh beer-yeast,anti-in?flammation effect by using auricle swelling in mice caused by bimethylbenzene and antitussive effect by using cough-model in mice caused by ammonia were observed and the quantity of phenolred secreted from the mouse's trachea were determined. RESULTS:KG could evidently decrease the temperature of febrile rats,lighten the auricle swelling in mice,delay the cough incubation period and reduce the cough frequency in mice,and markedly promote the secretion of phenolred from the mouse's trachea.CONCLUSION:KG has evident effects of antifebrile,anti-inflammation,antitussive and expectorant.

AIM: To study the effect of changing left ventricular afterload and isolated perfused rabbit heart on ventricular refractory period measured by subhthreshold conditioning train stimulation (St).METHODS:Ventricu- lar refractory pened strength- interval relation was measured by St method under the condition of changine left ven- tricular afterload and elimination action of nervous and body fluid.RESULTS: Reducing left ventricular afterload pro -longed ventricular refractory period measured by St method (P

The role of the hematuria examination by urinary analyzer in forensic medicine practice was evaluated in the present study.By using the chemical analysis of urinary analyzer and urinary sediment microscopy,the erythrocytes in 418 urine samples were examined simultaneously.The results showed that the negative outcome was found in 276 cases,+ in 58,++ in 35,≥++ in 84 by urinary analyzer,while negative outcome in 274 cases, +- and + in 31, ++ in 1 ,≥++ in 37 with consistent rates of 99 26%, 53 45%, 2 86% and 44 05% respectively.There was high significant difference between the positive and negative outcome and between the trauma mild (≥++) and slight trauma outcome (≤+) as determined by these two methods ( P

The 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase activity of Sclerotinia sclerotiorum is one of the multifunctional enzyme AROM activities, which catalyzes a reversible conversion of shikimate 3-phosphate (S3P) and phosphoenolpyruvate (PEP) to EPSP and inorganic phosphate, and is inhibited by the herbicide glyphosate (N-phosphonomethyl glycine). AROM protein has been purified from Sclerotinia sclerotiorum and the EPSP synthase has been analyzed. The results indicated that the optimal pH and temperature of EPSP synthase were 7.2 and 30℃ respectively. The activation energy of the heat-deactivated reaction of the enzyme was found to be 69.62 kJ/mol. Both of the substrates, S3P and PEP, were showed to inhibit the reaction rate when their concentrations exceeded 1 mmol/L and 2 mmol/L respectively. The Km of 140.98 μmol/L for PEP and 139.58 μmol/L for S3P were obtained by Dalziel equation which was a steadystate kinetic equation of the enzymatic reaction with the double substrates. The kinetic pattern of the enzyme was consistent with a sequential mechanism. Inhibition of the EPSP synthase reaction by glyphosate was competitive with respect to PEP, with the Ki 0. 32 μmol/L, and noncompetitive with regard to S3P. Activation by [ K+ ] was observed in the forward reaction. The Km (PEP) was lowered by increasing [ K+ ], while the Km (S3P) changed irregularly and the Ki (PEP) was enhanced.

Aim Telomerase is highly expression in most tumor cells, and it is an ideal target for cancer molecular targeting therapy. It has been proved that wogonin effectively inhibits telomerase activity and tumor cell growth in vitro. The study was to explore the inhibitory effect of wogonin on the growth of tumor and telomerase activity of implanted human ovarian cancer cell line SKOV3 in nude mice. Methods Nude mice with implanted human ovarian cancer cells SKOV3 were randomly divided into five groups, viz. the high dose group of Wogonin(600 mg?kg-1),low dose group of Wogonin(300 mg?kg-1),normal control group, cisplatin therapy group(3 mg?kg-1), and combined therapy group(cisplatin plus wogonin).The weight of nude mice and the volume of tumor were regularly measured. DNA、RNA and protein were extracted from the tumor tissue. The length of telomere was examined by Southern blot. The expression of telomerase hTERT gene was detected by RT-PCR. The telomerase activity was examined by TRAP-PCR-silver staining. Results The wogonin significantly inhibit the growth of tumor when compared with controlled group.The inhibitory rate of high dose group and low dose group were 56.67% (P=0.002) and 38.10%(P=0.019), respectively. The inhibition rate of cisplatin therapy group was 50.83%(P=0.004). The suppress rate of combined group reached 66.9% and higher than any single therapy(P=0.002). The length of telomere in different concentration groups of wogonin was the same as that in the control group.Wogonin inhibited the expression of telomerase gene hTERT and telomerase activity. The inhibition is related to the dose of wogonin. Conclusion Wogonin suppresses the growth and telomerase activity of tumor. The inhibitory effect is related to the dose of wogonin. Combination of wogonin and cisplatin increase the inhibitory rate in nude mice tumor.

Objective To develop an evidence-based community extended care model for patients with asthma.Methods Mixed research methods were applied to integrate best evidences:80 literatures were included in systemic review; 394 medical records were analyzed; 112 nurses admitted a test and a questionnaire to assess their competence on asthma care; clinical observation to both hospital and community centers were conducted; 6 multidisciplinary experts were consulted; and 100 patients admitted a questionnaire on patient needs and 17 of them were further interviewed.Results The nursing care model with the feature of hospital and community health service center collaborating to provide extended care for patients with asthma was established.Conclusions The development of a nursing care model for practice should be based on the current best evidence generating from the best research evidence,professional judgment on clinical practice requirement and patients' needs.

Objective:To investigate the effect and the mechanism of cordycepin on inhibiting delayed type hypersensitivity.Methods:The mouse model of delayed type hypersensitivity was established by sensitizing the skin of Kunming mice with 2,4-dinitrochlorobenzen(2,4-DNCB). There are two experimental groups respectively treated with different dosages of cordycepin:12 mg/kg and 16 mg/kg and one negative control group treated with normal saline. All the mice were intraperitoneally injected at 24 h interval(the last interval was 4 hours). We calculated the differences of the thickness and the weight between the left and right earlaps of every mouse and the edema rate, then used statistical methods to compare the edema rate and the spleen index among all the groups. After HE staining, the pathological changes of inflammatory earlap and spleen were observed and compared among these three groups.Results:Cordycepin alleviated the erythema, edema and the infiltration of peripheral mononuclear cells in the earlaps, so lowering the differences of the thickness and weight between left and right earlaps in the experimental groups. But it showed no significant effects on the spleen index and the spleen pathological changes. Compared with that in the negative control group, the anti-inflammatory effects of cordycepin in two experimental groups showed significant differences(P

AIM:To study the effects of changing right heart load on electrophysiologic parameters in anesthetized dogs. METHODS:Change of right atrial and ventricular load, right atrial and ventricular diastolic threshold (ADT, VDT), right atrial and ventricular relative refractory period (ARRP,VRRP) and right atrial and ventricular effective refractory period (AERP, VERP) were recorded. RESULTS: Increasing right heart load step by step(grade A and B) caused prolongation of ARRP, AERP, VRRP (grade B, P

Silencing ATM gene gave rise to enhanced apoptotic response to irradiation and irradiation-like chemotherapy agents, this paper explored the crucial identities of the molecular elements responsible for the enhanced apoptotic response in U937 cells mediated by silencing ATM gene. Two U937 cell mutants named U937-ASPI3K (ATM, negative) and U937-pZeosv2(+) (ATM, wild-type) were used as a cell model system to identify the critical molecule(s) responsible for the varied apoptotic response in the absence or presence of ATM gene. Apoptosis was examined by measuring concentrations of free nucleosome in U937 cells. Western blot was employed to measure nuclear protein abundance of CDC25A, CDC25B, CDC25C, total p34cdc2, p34cdc2, (Thr 161) or p34cdc2 (Thr 14, Tyr 15). RT-PCR was used to estimate CDC25 transcript levels. U937-ASPI3K exhibited an enhanced apoptotic response to lower dosage of irradiation, which could not be blocked by protein synthesis inhibitor. Protein serine-threonine phosphatase inhibitor or cyclin-dependent kinase (CDK) inhibitors, on the other hand, abolished the enhancement indicated that protein phosphorylation/dephosphorylation modification and CDK activity are required for the enhanced apoptotic response in the absence of ATM gene. Upon irradiation, p34cdc2 in U937-pZeosv2(+) was maintained in an inactive state by phosphorylation on threonine 14 (Thr 14) and tyrosine 15 (Tyr 15), which was associated with a dramatic decrease of nuclear CDC25A, CDC25B and CDC25C proteins. In contrast, p34cdc2 in U937-ASPI3K maintained in an active state by dephosphorylation on threonine 14 (Thr 14) and tyrosine 15 (Tyr 15), which was associated with constant nuclear CDC25A, CDC25B and CDC25C protein abundance before and after irradiation. The responsive decrease of nuclear CDC25 proteins occurred at the post-transcription level. Silencing ATM gene blocks the responsive decrease of nuclear CDC25 proteins, which is responsible for failure to inactivate p34cdc2 after irradiation. Active p34cdc2 and CDK2, in turn, acts as the death executors to trigger apoptosis. In summary, aberrantly activated CDK activity is the critical molecular mechanism central to enhanced apoptotic responses in the absence of ATM gene.