Objective:To get the basic situation of the list of low-price medicines and their sales in Tianjin to pro-vide future policy reference. Methods:The low-price medicine list was analyzed through different principles of classifica-tion including the National Essential medicine List ( NEML) , National Reimbursement medicine List ( NRML) and exclu-sive production. The study analyzed the sales status of the low-price medicines in the Tianjin from 2008 to 2011 using the Tianjin Urban Employee Basic Medical Insurance (UEBMI) database. Results:19 classes of chemical medicines and eight classes of traditional Chinese Medicine are included in the low-price medicine list. All of the medicines in the low-price list come from the NRML, and the replication ratio between the NEML and the low-price medicine list is 54. 1%. There are 41 exclusive productions and 149 exclusive formulation productions. From 2008 to 2011, the average ratio of the chemi-cal low-price medicines and traditional Chinese Medicine sales to total medicines sales are 4. 7% and 11. 0%, respective-ly. Both national essential medicines and exclusive formulation production sales ratios are increasing, however the sales ra-tio of exclusive production decreased from 2008 to 2011. Conclusion:The government should pay greater attention to the supply and production of the list’s exclusive production. The sales ratio of low-price medicines to total medicines sales is much lower in the retail pharmacies and tertiary medical institutions than other medical institutions. Suggestions:The gov-ernment should practice the shortage report system of common low-price medicine as soon as possible, with efforts made to implement the global budgeting policy and encourage sales enthusiasm for low-price medicines in retail pharmacies.

Objective To estimate direct economic burden of patients with moderate to severe psoriasis in China,and to assess its influencing factors.Methods A questionnaire survey was carried out in 150 patients with moderate to severe psoriasis from 29 third-grade class-A hospitals in 7 cities.Data on demographic characteristics,clinical features and direct economic burden were collected.Descriptive statistics were performed to analyze the direct economic burden of moderate to severe psoriasis,and multiple regression analysis was carried out to determine predictors of cost of illness.Results The patients were aged (43.87 ± 13.42) years,with an average clinical course of 3 years(range,2-6 years).Of them,82 had moderate psoriasis,and 68 had severe psoriasis.The average direct cost was (6 452 ± 6 391)RMB per patient-year,with significant difference between the patients with moderate psoriasis and those with severe psoriasis ((4 163 ± 4 605) vs.(9 212 ± 7 146) RMB,z =5.70,P ＜ 0.001).Regression analysis indicated that disease severity,clinical type,hospitalization,complications,and inhabited cities were factors influencing the direct economic burden of patients with moderate to severe psoriasis.Conclusions The direct eonomic burden of severe psoriasis seems to be twice that of moderate psoriasis in China.Physicians should strengthen the control of complications and disease severity,and pay more attention to other types of psoriasis than psoriasis vulgaris,during the treatment of psoriasis.

Objective To obtain the lung adenocarcinoma initiating cells from the A 549 cell line based on paclitaxel treatment combination with serum-free cultivation and to validate spared cells can represent tumor initiating cells (TICs) .Methods After dis-sociated by trypsogen ,about 106 /mL cells were suspended in serum-free medium supplemented with 0 .4% bovine serum albumin (BSA) ,insulin ,basic fibroblast growth factor (bFGF) ,human recombinant epidermal growth factor (EGF) and obtained spheroid cells .At the second passage ,paclitaxel was added at a concentration of 100 nmol/L for 48 h and then replaced with completely fresh medium once or twice per week until new spheroids emerged .Results The subpopulation of cells that survived serum-free cultiva-tion and paclitaxel treatment could highly express the cluster of differentiation 133/cluster of differentiation (CD133/CD326) mo-lecular markers and have features of stemness including differentiation ,high expression of cancer stem cells (CSCs)-associated genes and stronger capability of tumorigenesis .Conclusion The survived subpopulation that highly express the CD 133/CD326 molecu-lar markers presenting the characteristics of stemness in vitro and in vivo ,and could be used in future researches of biological functions .

Objective To investigate CT and MRI features of giant cell tumor of the skull.Methods CT and MRI features of 5 patients with giant cell tumor of the skull with histopathologically confirmed were analyzed retrospectively.Plain CT scanning was performed in all 5 patients.Plain MRI,contrast-enhanced MRI and HRCT scanning with facial nerve and auditory ossicle chain computer reconstruction were performed in 3 patients with giant cell tumor of temporal bone.Results Tumor occured unilateral in all cases,4 cases on the right side,1 case on the left side.CT scan showed a wide range of expanding destruction without sclerotic border,residual bone septum and bone cladding, On MRI, tumor signal variable;tumor appeared hypo-isointense on T1WI and heterogeneous hyperintense with hypointense rim on T2WI.CE-MRI: solid part of tumor show heterogeneous enhancement.Conclusion CT features of giant cell tumors of the skull was wide range of expanding destruction, residual bone septum and bone cladding.On T2WI, low signal in the rim of tumor was the disease characteristic imaging finding;Auditory ossicle chain and facial nerve CPR reconstruction made prepare for preoperative evaluation of otosteon and facial nerve,to provide more accurate image information for clinical treatment strategies.

Objective To investigate the effects of insulin on vascular diameter of the peri -infarct region and infarct volume after cerebral infarction in mice. Methods Forty male C57/BL6j mice w ere randomly divided into a control group ( n = 5), a cerebral infarction group ( n = 15), a cerebral insulin resistance group (n = 5), and a cerebral insulin resistance infarction group ( n = 15). A model of cerebral infarction w as induced by the photochemical method. A model of cerebral insulin resistance w as induced by intracerebroventricular injection of streptozocin. Tw o -photon confocal microscope w as used to in vivo evaluate the changes of vascular diameter in the peri-infarct region at 20 min after insulin injection into the cerebelomedulary cistern. After modeling of cerebral infarction, artificial cerebrospinal fluid or insulin (10 ng/ml) w as immediately injected into the cerebelomedulary cistern, and the effect of insulin on cerebral infarct volume w as evaluated at 24 h after infarction. Results Insulin did not have significant effect on various types of cerebral vascular diameters in the normal control group, but it significantly contracted cerebral arteries ( -23.16% ±6.86% and -23.32% ±6.40%, respectively; al P <0.001) and penetrating arteries ( -15.20% ±5.51% and -16.40% ±4.27%, respectively; al P < 0.001) in the cerebral insulin resistance group and the cerebral insulin resistance infarction group, but it did not have any effect on the diameters of the cerebral veins. There w ere no significant differences in the vasoactive effects of insulin betw een the cerebral infarction group and the normal control group, as w el as betw een the cerebral insulin resistance group and the cerebral insulin resistance infarction group. Insulin significantly reduced the volume of cerebral infarction in the cerebral infarction group (9.0 ±1.0 mm3 vs.6.0 ±1.2 mm3; t = 4.294,P =0.002), and it did not have significant effect on the volume of cerebral infarction in the cerebral insulin resistance infarction group ( 12.6 ±2.3 mm3 vs.11.6 ±1.7 mm3; t = 0.782, P = 0.456). Conclusions Insulin can reduce ischemic brain injury in normal mice and can not affect the cerebrovascular diameter of the peri-infarct region. The neuroprotective effect of insulin is not significant in cerebral insulin resistance in mice, and it may be associated w ith the vasoconstrictor effects of insulin in the peri -infarct region.

Objective To solve the problem of hospital Bureau class cost accounting system to manage the Branch class cost. Methods The system was optimized by extracting the raw data of localization, collecting income and expenditure account of flexible specialization, and setting subclass accounting ratio ways of rationalization. Results The optimization subsystem has been a fundamental change in cost accounting management and creates more effective. Conclusion According to the special requirement of sanatorium financial process, information system and cost accounting ways, the new system can be optimized in design and implementation method and achieve better effects during the implementation and operation.

Objective To examine cerebrovascular reactivity to CO2 inhalation in mice. Methods In vivo Two-Pho?ton imaging technique was used to record the reaction of cerebral cortical vessels including penetrating artery, surface vein and capillary in 5 male C57 mice after CO2 inhalation under a thinned-skull cranial window. Nitric oxide syntheses inhibitor L-NAME and Prostaglandin syntheses inhibitor Indomethacin were used to block different vasodilator pathways, respectively. Results Different mouse cortical vessels displayed different degrees of dilation to 1-minute 5%CO2 inhala?tion. The penetrating artery exhibited the most obvious dilation (45.01%±4.45%). L-NAME intervention significantly di?minished cerebravascular CO2 reactivity(P<0.05). Indomethacin significantly attenuated the dilation of artery but not capillary comparing with L-NAME intervention(P<0.05). Conclusions Different vessels react differently to CO2 inhala?tion in which postaglandins and NO signal pathways are involved.

The aim of this study is to construct specific shRNA expressing plasmids, and to observe their effects on H9c2 cardiomyocytes injury induced by hypoxia/reoxygenation (H/R). RIPK1 and RIPK3 are the key kinases mediating the process of necroptosis. Using recombinant DNA technology, we inserted the synthetic shRNA into pSUPER vector to construct RIPK1-shRNA or RIPK3-shRNA plasmid respectively. We transfected H9c2 cardiomyocytes with the two shRNA plasmids respectively, before we treated them with H/R stimulation. Then, we measured the relevant genes and proteins by real-time PCR and Western blot. Meanwhile,we detected the markers of necroptosis and cardiomyocytes injury. The results showed that inhibition of ripk1 or ripk3 gene expression by its specific shRNA might protect the cardiomyocytes injury induced by H/R stimulation.
Animals ; Apoptosis ; Cell Hypoxia ; Cell Line ; Gene Expression ; Myocytes, Cardiac ; pathology ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; RNA, Small Interfering ; Rats ; Real-Time Polymerase Chain Reaction ; Receptor-Interacting Protein Serine-Threonine Kinases ; genetics ; metabolism ; Transfection

Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.

The aim of this study was to observe whether necroptosis is involved in the process of cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and protein expression of receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for cardiac hypertrophy was established. The experimental data showed that the gene and protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the sham group. HE staining showed cardiomyocytes injury and hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with losartan used, the selective antagonist of angiotensin II type I receptor could improve the cardiac function of TAC rats. Moreover, losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of cardiac hypertrophy with pressure overload, and losartan could alleviate the cardiac hypertrophy and inhibit necroptosis.
Animals ; Apoptosis ; Cardiomegaly ; pathology ; Disease Models, Animal ; Echocardiography ; Heart ; physiopathology ; Losartan ; pharmacology ; Myocytes, Cardiac ; Pressure ; Protein-Serine-Threonine Kinases ; metabolism ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptor-Interacting Protein Serine-Threonine Kinases ; metabolism