Because of the medical industry valla,the medical market is in a state of oligopoly.Hospitals and patients are in a state of asymmetric information in the medical market,which could lead to moral hazard,adverse selection,and low social and medical efficiency.Based on the gaming model,we analyze the gaming process and equilibrium between hospitals and patients under the circumstances of asymmetric information.The analyzing result suggests that asymmetric information in the medical market is harmful for patient's benefit and the development of medical market as well.Therefore,it's necessary to strengthen the entire social medicare,set up an opening system of medical information and strengthen the national health education so as to relieve the asymmetric information between hospitals and patients,and improve the efficiency of medical market.

Objective To stuay the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1,and the expression of CD40L of the CD4+T cells in patients withacute coronary syndrome(ACS),and to explore the relationship between CD40L and inflammatory factors and the effects of CD40/CD40L on ACS.Method Thirty-two coronary heart disease patients without history of other discernible systemic disease and medicine of steroids or immunosuppressants taken were divided into acute myocardial infarction group(AMI,n=11),unstable angina pectoris group(USP,n=14)and stable angina pectoris group(SAP,n=7).The control group was composed of eight healthy volunteers(CON group).Theexpression of CD40L Was determined by flow cytometry(FCM).Serum sCD40L.ICAM-1 and VCAM-1 were determined by using ELISA.The serum hsCRP was assayed by using immunoturbidimetry.Data were analyzed with SPSS 11.0 software for windows.Results The expression percentage(%)of CD40L of the CD4+T cells,and the serum levels of sCD40L,hsCRP,ICAM-1 and VCAM-1were sifnificantly higher in patients of AMI group than those in patients of other groups(P＜0.05 or P＜0.01).Similarly,those biomarkers in patients of UAP group were usually higher than those in patients of CON or SAP groups(P＜0.05).There Was a positive correlation between the expression of CD40L and the serum level of VCAM-1 in paients of AMI group(P＜0.05),and likewise,a positive correlation also existed between the serum level of sCD40L and other factors,hsCRP,ICAM-1 as well as VCAM-1,in patients of AMI group(P＜0.05).Conclusions The enhanced expression of CD40L of the CD4+T cells and high serum level of sCD40L are present in patients with acute coronary syndrome.The hsCRP,ICAM-1 and VCAM-1 play roles in the pathogenesis of ACS,and they have correlation with enhanced expression of CD40L and high serum level of sCD40L.Therefore,CD40L and sCD40L may be used as indicators of risk in coronary heart disease.

Objective To determine the levels of soluble thrombomodulin(sTM) in patients with acute pulmonary embolism (PE), and evaluate sTM clinical significance.Methods The sTM levels were determined with enzyme linked immunosorbent assay in PE patients, and compared with healthy control group. Eighteen PE patients were divided into massive PE group and non - massive PE group, non - respiratory failure group and respiratory failure group, and compared the sTM level in the groups. Results Level of sTM in PE patients was higher than that of control group (P

Objective MicroRNAs (miRNAs) are endogenous short stranded RNAs with a length of about 22 NT, which are highly conserved and have no coding function.Mature miRNAs play a role by specifically binding to the 3′untranslated region of the target gene, degrading the mRNA of the gene or hindering its translation at the post transcriptional level, so as to negatively regulate the expression of the target gene and play a biological role.In recent years, the research of miRNAs in cardiovascular diseases is increasingly in-depth.A large number of evidences show that miRNAs play a role in the pathogenesis of many cardiovascular diseases, and will become a potential marker and new treatment target for the diagnosis and prognosis evaluation of cardiovascular diseases.

Objective To investigate the variation of biomarker of coagulation, anti-coagulation, fibrinolysis in elderly critical patients and find out whether they are related to the disease severity. Methods Sixty-seven patients were no less than 60 years old. Eligible criteria: coincidence with the diagnostic criteria of systemic inflammatory response syndrome (SIRS) and APACHE Ⅱ score was no less than 10 scores. Blood sample was drawn from the venous for the test of biomarker (APTT, PT, TT, D-D, Fib, AT-Ⅲ , PC, PAI-1). According to the existent status,all the patients were divided into two groups:survival group (43 cases) and death group(24 cases) ,meanwhile,according to the diagnostic criteria of MODSE,all the patients were divided into MODSE group (30 cases) and non-MODSE group (37 cases). Results There were significant differences in APACHE Ⅱ score between MODSE group and non-MODSE group, survival group and death group [(25.83 ± 1.19) scores vs(18.1±20.73) scores and(18.81±0.72) scores vs(26.50 ± 1.42) scores](P <0.01). The PT and D-D in MODSE group anti death group were higher than those in non-MODSE group and survival group, the differences were significant (P <0.05),while the activity of AT-Ⅲand PC in MODSE group and death group were lower than those in non-MODSE group and survival group, the differences were significant (P <0.05). The PT,D-D and PAI-1 were positively correlated to APACHE Ⅱ score (related coefficients were 0.328, 0.308, 0.335,P <0.05). The AT-Ⅲ and PC were negatively correlated to APACHE Ⅱ score (related coefficients were -0.469, -0.559,P <0.01). Conclusions The abnormality of eoagnlation-fibfinolysis system exists in elderly critical patients. The extended PT, elevated D-D and PAI-1 ,descended PC and AT-Ⅲ are the hints of disease severity and poor prognosis.

Objective To explore the safety and rate of intraperitoneal cooling in rabbits after cardiopulmonary resuscitation(CPR). Method There were two experiments. In the experiment one: 15 healthy adult NewZealand rabbits were divided into five groups as per the various amounts, 30, 40, 60, 80, and 100 mL/kg, of priming volume of 4 ℃ cold balanced salts solution injected into peritoneal cavity of rabbits. After injection of priming cold solution, the tympanic temperature between 33 ℃～ 35 ℃. For the maintenance of this mild hypothermia, a intraperitoneal infusion device(patent number ZL200820201265) was connected to the rabbits. The rabbits were rewarmed by using the same device after 12-hour hypothermia. The biochemical parameters were assayed during the experiment. After the rabbits were sacrificed, the liver, ileocecal junction of intestine and kidneys were removed to fix them in 3 % formalin, and examined by using H.E. staining. In the experiment two, another 12 healthy adult New Zealand rabbits were induced into ventricular fibrillation by alternating electric current and then gave CPR for 2 minutes. After return of spontaneous circulation(ROSC), the priming volume of 4 ℃ cold liquid was infused into peritoneal cavity of rabbits, and then the rabbits were connected to the intraperitoneal cooling device to maintain hypothermia for 12 hours. Matched-pairs t test was used for the comparison of biomarkers before and after intraperitoneal cooling. A two-tailed value of P < 0.05 was considered statistically significant. Results In the experiment one, the tympanic temperature of rabbits with priming volume of 80 mL/kg cold solution was decreased quickly reaching the target temperature in(30±2.00) minutes. During the induction of hypothermia, the intraperitoneal temperature reached the target temperature in less than 10 minutes, and was 1 -2℃ lower than the tympanic temperature during the maintenance of hypothermia. The intraperitoneal cooling did not cause damage in the liver, ileocecal junction of intestine and kidney, and did not alter the biomarkers. In the experiment two, the tympanic temperature of rabbits after ROSC was decreased quickly after intraperitoneal infusion of 80 mL/kg 4 ℃ cold solution, and reached the target temperature in(26.00±6.99) minutes, and the intraperitoneal temperature was lowered to reach the target temperature in less than 10 minutes. This cooling method after CPR didn' t disturbance water-electrolyte and acid-base balance. Conclusions The intraperitoneal cooling can safely and quickly induce hypothermia after CPR in rabbits.

Objective To establish a simple,easily-producible and practical cardiopulmonary cerebral resuscitation model in rabbits.Method Cardiac ventricular fibrillation was induced in 27 New Zealand rabbits by alternating electric current.The rabbits were randomly divided into three groups according to the duration of untreated cardiac arrest(CA):CA-8 min group(n = 9),CA-5 min group(n = 9)and CA-3 min group(n = 9).All animals received cardiopulmonary resuscitation(CPR)until return of spontaneous circulation(ROSC).The sample of vein blood was collected for the measurement troponin I level at 4 hours after ROSC.The animals were sacrificed at 72 hours after ROSC,hippocampus were removed and fixed in 3%formalin,and coronal sections were analyzed by TUNEL staining and N1SSLE staining.The other two animals without ventricular fibrillation or CPR served as sham-operated group.One-way ANOVA or Mann-Whitney rank was used to determine the statistical significance among the three groups.R×C test was used for ROSC,LSD test for multiple comparisons,and t test for comparisons of means between two independent samples.A two-tailed value of P＜0.05 was considered statistically significant.Results There were no differences in rate of ROSC among groups.No animals survived until 72 hours after ROSC in CA-8 min group and CA-5 min group,while three animals in CA-3 min group survived.In group CA-8 min,CA-5 min and CA-3 min,the survival time of animals after ROSC were(1.67 ± 2.55)h,(37.78 ± 30.27)h,(12.0 ± 14.97)h,respectively.There were significant differences in the survival time of animals after ROSC and troponin I level after ROSC 4 h between CA-3 min group and the other two groups(P＜0.05).Compared with animals in CA-3 min group,sham-operated animals(n = 2)did not have neuronal degeneration or TUNEL positive cells in the hippocampus CA1 area.Conclusions CPR initiated as soon as 3 min after CA can give longer survival tome to the rabbits.The rabbits have neuronal degeneration and apoptosis in the hippocampus CA1 area at 72 hours after ROSC.It may be an ideal animal model for investigation on CPCR.

Objective To evaluate the bioequivalence of domestic and imported terazosin hydrochloride tablets after single oral dose .Methods It was a single center ,randomized ,open ,cross-over trail design ,21 subjects were fasting oral adminis-tered of 2 mg domestic and imported terazosin hydrochloride tablets in different periods ,venous blood 4 ml were collected in different time points before and 60 h after administration ,plasma concentration of terazosin was determined by LC-MS/MS . Results The main pharmacokinetic parameters of domestic and imported terazosin hydrochloride tablets were as follows :t1/2 :(13.2± 2.39)hvs(12.5±1.93)h,tmax :(1.01±0.83)hvs(1.08±0.69)h,Cmax :(40.1±10.6)ng/mlvs(37.3± 9 .57) ng/ml;AUC0- ∞ :(428 ± 82 .1) ng · h/ml vs (426 ± 85 .2) ng · h/ml .The relative bioavailability of domestic terazosin hydrochloride tablets was (101 .2 ± 14 .7)% .90% CI of domestic and imported terazosin hydrochloride tablets AUC0-t and Cmax geometric mean ratio fell between 80% -125% .Conclusion The domestic tablets are bioequivalent to the imported tablets .

Objective:To investigate the inhibitory effect and mechanism of heme oxygenase-1 (HO-1) on the inflammatory response of macrophages.Methods:Mouse macrophage strain RAW264.7 was cultured in vitro, and the cells in the logarithmic growth phase were used for the experiment. The RAW264.7 cells were divided into four groups. In blank control group, the cells were continuously incubated and received no treatment (cultured at 37 ℃, 95% air, 5% CO 2). In lipopolysaccharide (LPS) model group, 1 mg/L LPS was added to the medium to prepare LPS challenge model. In HO-1 inducer group, the cells were incubated with 30 μmol/L HO-1 inducer hemin for 1 hour, and then 1 mg/L LPS was added for incubation. In HO-1 inhibition group, the cells were incubated with 5 μmol/L HO-1 specific antagonist Zinc protoporphyrin Ⅸ (ZnPPⅨ) for 0.5 hour, and then 1 mg/L LPS was added for incubation. After 48 hours of incubation with LPS, the supernatant of each group was taken, and the protein expressions of HO-1, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), thioredoxin interacting protein (TXNIP), NOD-like receptor protein 3 (NLRP3) and mitochondrial autophagy marker microtubule-associated protein 1 light chain 3B (LC-3B) were detected by Western blotting. The expression of reactive oxygen species (ROS) was detected by immunofluorescence staining. Results:Compared with the blank control group, the cells in the LPS model group had a certain stress response, and autophagy occurred in mitochondria, but the expression of some inflammatory factors was restricted, which was related to the impairment of cell function. The protein expressions of HO-1, IL-1β, LC-3B, ROS were significantly increased, the protein expressions of TNF-α, TXNIP, and NLRP3 were decreased significantly, indicating that the cells were seriously injured after LPS challenge, and the model was successfully established. Compared with the LPS model group, HO-1 protein expression in the HO-1 inducer group was significantly increased (HO-1/GAPDH: 0.31±0.03 vs. 0.22±0.03, P < 0.05), the protein expressions of TNF-α, IL-1β, TXNIP, NLRP3, LC-3B and ROS were significantly inhibited [TNF-α protein (TNF-α/GAPDH): 0.08±0.01 vs. 0.45±0.05, IL-1β protein (IL-1β/GAPDH): 0.50±0.01 vs. 0.82±0.03, TXNIP protein (TXNIP/GAPDH): 0.21±0.02 vs. 0.28±0.02, NLRP3 protein (NLRP3/GAPDH): 0.11±0.01 vs. 0.17±0.02, LC-3B protein (LC-3B/GAPDH): 0.67±0.04 vs. 0.92±0.12, ROS (fluorescence intensity): 80.9±12.5 vs. 94.1±19.5, all P < 0.05], indicating that HO-1 could inhibit inflammatory response and oxidative stress, and reduce mitochondrial autophagy. Antagonizing HO-1 could increase inflammatory response, oxidative stress and mitochondrial autophagy, the inhibitory degree of TNF-α and IL-1β expression was significantly reduced as compared with the HO-1 inducer group [TNF-α protein (TNF-α/GAPDH): 0.26±0.02 vs. 0.08±0.01, IL-1β protein (IL-1β/GAPDH): 0.76±0.01 vs. 0.50±0.01, both P < 0.05], the protein expressions of TXNIP, NLRP3, LC-3B and ROS were significantly increased as compared with the LPS model group [TXNIP protein (TXNIP/GAPDH): 0.43±0.02 vs. 0.28±0.02, NLRP3 protein (NLRP3/GAPDH): 0.24±0.02 vs. 0.17±0.02, LC-3B protein (LC-3B/GAPDH): 1.12±0.07 vs. 0.92±0.12, ROS (fluorescence intensity): 112.0±17.0 vs. 94.1±19.5, all P < 0.05]. Conclusion:HO-1 can reduce the inflammatory response by inhibiting the activation of TXNIP/NLRP3 inflammasome and reducing the release of inflammatory mediators.

Objective:To investigate the clinical and genetic characteristics of developmental and epileptic encephalopathy (DEE) caused by SLC1A2 gene mutations. Methods:The clinical manifestations, auxiliary examination results, and genetic testing results of a patient with DEE caused by SLC1A2 gene mutations who was treated at Epilepsy Center, Children's Hospital Affiliated to Shandong University on February 6, 2021 were summarized. Cases of SLC1A2 gene mutations were searched using keywords " SLC1A2" and "developmental and epileptic encephalopathy" in CNKI, Wanfang, and PubMed databases, retrieving literature published from the establishment of these databases to September 2024. Bioinformatics analysis was performed; the clinical and genetic characteristics of DEE caused by SLC1A2 gene mutations were summarized. Results:The main manifestations of the patient were rhythmic shaking of the right upper limb or focal motor seizures of bilateral upper limbs, or focal spasm of right upper limb (elevation for once). Ictal electroencephalogram showed 2-3 Hz polymorphic slow waves in the left central area, parietal area and central midline area, affecting the opposite side, or spike rhythm with decreased frequency in the right frontal area, central area and midline area, or polymorphic slow waves in the left central area and central midline area. Whole-exome sequencing indicated a heterozygous de novo mutation in the SLC1A2 gene: c.254T>G/p.Leu85Arg. A total of 7 patients with DEE caused by SLC1A2 gene mutations were retrieved from 5 related literature. All 8 patients (including the patient in our hospital) presented with epileptic seizure, developmental delay, and abnormal EEG; all of them were sporadic cases with de novo heterozygous missense mutations of SLC1A2 gene. Bioinformatics analysis showed that the 4 amino acid residues Gly82, Leu85, Pro289, and Pro333 in the 8 patients were located in the intolerance region of SLC1A2 gene encoding glutamate transporter protein 2 (EAAT2). The 5 amino acid mutations (Leu85Arg, Leu85Pro, Gly82Arg, Pro333Ser, Pro289Arg) in the 8 patients all led to significant changes in number and binding of hydrogen bonds between amino acid residues in EAAT2; except for Gly82Arg mutation, the other 4 mutations could obviously reduce the structural stability of EAAT2. Conclusion:De novo heterozygous missense mutations in SLC1A2 gene can lead to DEE, characterized by developmental delay, EEG abnormalities, and epileptic seizure; these mutations are typically located in critical regions of EAAT2, potentially resulting in reduced protein structural stability.