OBJECTIVE:To prepare urapidil osmotic pump tablet(OPT) characterized by 24 h constant drug release in vitro.METHODS:OPT of urapidil was prepared using NaCl and low or high moleculan weight PEO(Mr 4?106、2?105) as core,CA and PEG-400 as the coating material.Similarity factor was used to evaluate formulation of osmotic pump tablets.The drug release mechanism was investigated as well.RESULTS:The optimal core formulation consisted of urapidil 60 mg,NaCl 190 mg,PEO(Mr 4?106) 90 mg,PEO(Mr 2?105) 90 mg.The drug was released from OPT at controlled rate 24 h.CONCLUSION:The preparation of osmotic pump tablets was simple and characterized by zero-order release.

This paper introduces the principium of data exchange between different information systems by COM technology, and the one between HIS and RIS is taken as an example.

ObjectiveTo investigate the effect of cerebroprotein hydrolysate on diabetic peripheral neuropathy.Methods105 diabetic patients were randomly divided into the treatment group (34 cases, treated with intravenous injection of cerebroprotein hydrolysate), standard control group (38 cases, treated with intramuscular injection of Metrycobal combined with intravenous injection of Actovegin) and blank control group (33 cases, treated with oral vitamin B1, B6, B12). Curative effects of three groups were evaluated.ResultsIt was shown that intravenous injection of cerebropotein hydrolysate could improve patients' symptoms, raised speed of nerve conduction and its curative effect was as same as intramuscular injection of Metrycobal combined with intravenous injection of Actovegin.ConclusionIntravenous injection of cerebropotein hydrolysate has a curation effect on diabetic peripheral neuropathy.

Objective To investigate the effects of transient receptor potential vanilloid 1 activation by capsaicin on the oxidative stress in lipopolysaccharide-induced lung injury in mice in order to elucidate the potential mechanisms.Methods A total of 108 specific pathogen free (SPF) ICR male mice were randomly divided into six groups:normal control group (n =18),capsaicin control group (CAP control group,n =18),capsazepine control group (CAPZ control group,n =18),acute lung injury group (n =18),capsaicin treatment group (CAP treatment group,n =18) and capsazepine treatment group (CAPZ treatment group,n =18).After modeling,superoxide dismutase (SOD),catalase (CAT) and malondiachehyche (MDA) levels in lung were measured with the method of chromatometry,and the expression of heme oxygenase 1 (HO-1) in lung tissue was assessed with enzyme linked immunosorbent assay (ELISA),while the level of NF-E2-related factor-2 (Nrf2) was determined by western blotting and the expression of Nrf2 mRNA was measured by RTPCR.Pathological changes of lung tissue were observed under light microscope.Results The activities of SOD and CAT in lung tissue at 3,8,16 h were dramatically lower in acute lung injury group than those in normal control group (P ＜ 0.05),while the level of MDA was higher.Compared with acute lung injury group,the lung levels of SOD and CAT at 8 h and 16 h were higher in CAP treatment group (P ＜0.05),while the lung level of MDA was lower (P ＜ 0.05).The levels of SOD and CAT in CAPZ treatment group were decreased at 8 h and 16 h,while the levels of MDA in this group were increased at 3,8,16 h (P ＜0.05).The pulmonary levels of HO-1,Nrf2 and expression of Nrf2 mRNA were significantly higher in acute lung injury group than those in normal control group (P ＜ 0.05).Compared with acute lung injury group,the levels of HO-1,NRF2 and expression of NRF2 mRNA were increased markedly in CAP treatment group (P ＜ 0.05)and were obviously decreased in CAPZ treatment group (P ＜0.05).At 8 h,16 h after modeling,the degree of lung damage was ameliorated in CAP treatment group compared with acute lung injury group under light microscope,while the lung damage was aggravated in CAPZ treatment group.Conclusions The activation of TRPV1 could apparently up-regulate the levels of CAT,SOD,Nrf2,HO-1,and reduce the MDA level in lung tissue of mice with acute lung injury,ultimately protecting the endotoxemia mice from oxidative stress.

OBJECTIVE:To optimize the purification technology of total alkaloid from the flos of Aconitum kusnezoffii. METH-ODS:The content of total alkaloid from the flos of A. kusnezoffii was determined by acid-base titration. The purification technology of total alkaloid from the flos of A. kusnezoffii was optimized by ion resin with resin type,mass concentration of loading liquid and exchange speed as factors,maximum adsorption quantity,desorption rate and mass fraction of total alkaloid as index,and verifica-tion test was conducted. RESULTS:The optimal purification technology was as follows as type 732 cation exchange resin,mass concentration of loading liquid 0.32 g/L,exchange speed of 7 column volume(BV)/h. In validation test,the content of total alka-loid was 86.88%(RSD=0.52%,n=3),and desorption rate was 92.81%(RSD=0.40%,n=3)averagely. The extraction trans-port rate of total alkaloid from 3 batches of the flos of A. kusnezoffii was 81.76% and purification transport rate was 89.47% in av-erage. CONCLUSIONS:The established method is stable and feasible,and shows high transport rate.

Objective To analyze negative lymph nodes of 34 non-small cell lung cancer(NCLC) patients with total correction by means of fluorescent quantitation PCR and immunohistcchemistry,and to form molecular bi- ology staging.Methods Clinical data and tissue samples of 193 lymph nodes were collected from 34 patients under- going resection for non-small cell lung cancer.Using fluorescent quantitation reverse transcription-polymerase chain reaction(RT-PCR) and immunohistochemistry method,lymph nodes were examined for CEA gene mRNA,P53 and CK to form molecular biology staging.All the patients were followed-up for an average of forty months.Results The CEAmRNA was identified in 21.7% (42/193) lymph nodes negative patients from 17 patients(17/34,50%); TMN staging was up-regulated in 8 patients;positive lymph nodes were increased in 9 patients.P53 and AE1/AE3 were identified 9.8%(19/193) from 11 patients,18.6 % (36/193)from 15 patients,separately;TMN staging was up-regulated in 2 patients of P53 examination and 5 patients of AE1/AE3 analysis;positive lymph nodes were in- creased in in 7 patients of P53 examination and 11 patients of AE1/AE3 analysis.There was obvious statistical sig- nificance in them,but the molecular biology staging based on the three markers was not an independent factor on re- currence and metasis of lung cancer.Conclusion CEAmRNA.P53 and AE1/AE3 analysis could find lung cancer micrometasis more sensitively to form molecular biology staging which was relative to the prognosis,but not an inde- pendent prognostic indicator.It might be good to the therapy strategy after operation.

Objective To investigate the relationship between the 5-hydroxytryptamine (5-HT)1A receptor gene C(-1019)G polymorphism and geriatric depression and Alzheimer′s disease (AD) with depressive symptoms in Han Chinese. Methods The case control study was used in the study among 106 patients with geriatric depression, 72 AD patients with depressive symptoms and 150 healthy old individuals in China. The C(-1019)G polymorphism of 5-HT1A was analyzed with the technique of polymerase chain reaction-restriction fragment length polymorphism. Results The frequencies of 5-HT1A genotype C/G (39.6%), G/G(24.5%) and allele G (44.3%) in the patients with geriatric depression were significantly higher than those in the controls (respectively 35.3%, 13.3%, 31.0%, P < 0.05). The frequencies of 5-HT1A G allele in the AD patients with depressive symptoms (41.0%) were significantly higher than those in the controls (31.0%,X2=4.2879, P<0.05). No significant difference in distribution of (5-HT)1A C (-1019) G polymorphism between the patients with geriatric depression and the AD patients with depressive symptoms was observed (P > 0.05). Conclusion The 5-HT1A gene C (-1019)G polymorphism may be associated with geriatric depression and AD with depressive symptoms and (-1019)G allele may be a risk factor for them.

Twelve patients with maple syrup urine disease were treated with restricted natural protein intake,special nutrition powder,and vitmin B1.The manifestations of these patients were greatly improved after treatment.The blood levels ofleucine and valine were significantly decreased after treatment(P＜0.01).Although the level of branched-chain α-ketoacids in urine was reduced,but not significantly.

Objective To investigate the change of the basic fibroblast growth factor(bFGF) leve in human detrusor muscle(DM)in bladder outlet obstruction(BOO)due to benign prostatic hyperplasia(BPH)and its implication.Methods Fifty-four patients with BPH were divided into two groups:the obstructive DM stability and instability groups;and 15 men with bladder tumor who underwent operation in the same period were enrolled in the control group.The bFGF mRNA level in DM was measured by reverse transcription and polymerase chain reaction(RT-PCR)and the bFGF protein level was measured by immunohistochemical staining method.Results The bFGF-mRNA expression level of bladder smooth muscle cells was significantly lower in the control group than that in the obstructive DM stability and instability groups(all P＜0.05),but there was no significant difference between the obstructive DM stability and instability groups(P＞0.05). Conclusions The expression level of bFGF mRNA in bladder DM is elevated in BOO due to BPH,but there is little or no correlation between the increased expression of bFGF mRNA and detrusor muscle instability.

Objective: To explore whether acupuncture can improve sleep disturbance, cognitive impairment and emotional disorders caused by sleep deprivation, and its association with the attenuation of oxidative stress injury in prefrontal cortex. Methods: Fifty-two male Sprague-Dawley rats were randomly divided into a control group (n=10), a model group (n=14), a manual acupuncture (MA) group (n=14), and a sham-MA group (n=14). All the groups were established as sleep deprivation models via the modified multiple platform method, except for the control group. Rats in both the MA group and the sham-MA group received corresponding intervention, respectively. After modeling and intervention, the four groups received three behavioral tests, namely sleep monitoring, by comprehensive lab animal monitoring system (CLAMS), Morris water maze (MWM) test and open-field test (OFT), followed by oxygen free radical level test and Western blot (WB) detection for the expression levels of Bax and Bcl-2. Results: The MA group derived more sleep time within 24 h than either the model group or the sham-MA group (both P<0.05). On MWM orientation navigation test day 1, there were no significant differences in escape latency among the control, MA and sham-MA groups (P>0.05), and the escape latency was significantly shorter in these three groups than that in the model group (all P<0.05). On test day 4, the escape latency was markedly shorter in the MA group than that in either the model group or the sham-MA group (both P<0.05); meanwhile, the MA group showed significantly better performance compared with these two groups in space probe test (both P<0.05). In OFT, compared with the control group, there was a significant decline in the horizontal movement score in the other three groups (all P<0.05), and the decrease was more significant in the model group and the sham-MA group than that in the MA group (both P<0.05). The superoxide dismutase (SOD) content was markedly higher and the malondialdehyde (MDA) content was markedly lower in the MA group than those in the model group and the sham-MA group (all P<0.05). Compared with the model group and the sham-MA group, the expression of Bax was significantly lower and the expression of Bcl-2 was significantly higher in the MA group (all P<0.05). Conclusion: MA therapy can lengthen the sleep time in sleep-deprived rats and improve learning and memory impairments induced by sleep deprivation, and the underlying mechanism may be associated with the enhancement of antioxidant capacity in the prefrontal cortex and the inhibition of hippocampal neuronal apoptosis.