Objective To explore the early predictive factors of intestinal necrosis in patients with acute superior mesenteric arterial occlusive disease and its significance for the decision of exploratory laparotomy.Methods This retrospective study enrolled 29 patients diagnosed with acute superior mesenteric artery embolism or thrombosis in Peking University People's Hospital between July 1995 and June 2015.Results 12 patients developed intestinal necrosis.Patients with intestinal necrosis had a poorer prognosis than those who did not develop intestinal necrosis (x2 =14.867,P =0.000).In univariate analysis,the early predictive factors for intestinal necrosis were D-Dimer ≥ 600 μg/L (x2 =11.455,P =0.002),INR≥1.2 (x2 =3.948,P =0.047),pH values ＜7.4 (x2 =8.191,P =0.004),BE ＜ -1.0 mmol/L (x2 =8.191,P =0.004),blood lactate ≥ 2.2 mmol/L(x2 =7.535,P =0.006),BUN ≥ 6 mmol/L (x2 =10.076,P =0.002),CK ≥ 80 U/L (x2 =8.191,P =0.004),LDH ≥ 210 U/L (x2 =13.079,P=0.000),AST ≥25 U/L (x2 =10.076,P =0.002),SIRS (x2 =10.076,P =0.002).Multivariate logistic regression analysis found no independent predictive factors of intestinal necrosis in patients with acute superior mesenteric arterial occlusive diseases.Conclusion Intestinal necrosis in acute mesenteric arterial occlusive diseases indicates a poor prognosis.Coagulation abnormalities,liver or kidney dysfunction,metabolic acidosis and SIRS necessitates an immediate exploration.

To observe the protective effect and mechanism of Sailuotong capsule in focal cerebral ischemia/reperfusion. The 90 min middle cerebral artery occlusion (MCAO) reperfusion model was established. The expressions of dynamin-related protein 1 ( Drp1) and optic atrophy 1 (Opa1) were tested by Western blot. The transmission electron microscope was used to observe the changes in the mitochondrial ultra-structure. The pathological morphological changes were observed through the HE staining. The immunohistochemical method was used to test Drp1 and Opa1 expressions. Sailuotong capsule (33, 16.5 mg x kg(-1), ig) can inhibit the abnormal mitochondrial fission and fusion in the cortical area on the ischemia side and the mitochondrial fission gene expression and promote the mitochondrial fusion gene Opa1 expression, so as to alleviate the energy metabolism disorder caused by ischemia/reperfusion. Sailuotong capsule can inhibit the abnormal mitochondrial dynamics in peri-ischemic regions and maintain the normal morphology of mitochondria, which may be the mechanism of Sailuotong capsule in promoting the self-recovery function in the ischemic brain region.
Animals ; Brain ; drug effects ; metabolism ; Brain Ischemia ; drug therapy ; genetics ; metabolism ; surgery ; Drugs, Chinese Herbal ; administration & dosage ; Dynamins ; genetics ; metabolism ; GTP Phosphohydrolases ; genetics ; metabolism ; Humans ; Male ; Mitochondria ; drug effects ; metabolism ; Rats

Objective:To analyze the effects of essential medicine system on revenue structures at primary med-ical institutions. Methods:Data on revenue status and structures from 58 township health centers in Shanxi Province was collected to analyze changes and trends. Results:Along with growing government investments in primary medical institutions, the essential medicine system has fundamentally realized full coverage. The percentage of essential medi-cine revenue to pharmaceutical revenue rose from 20 . 45% in 2009 to 97 . 03% in 2013 , though the percentage of pharmaceutical revenue to total revenue dropped by 18 . 43%. The percentage of fiscal subsidy revenue in total reve-nue rose from 25 . 77% in 2009 to 54 . 16% in 2013 , though the percentage of business revenue to total revenue dropped in general. Conclusions:The essential medicine system requires the government’s financial support. Essen-tial medicine lists and primary financial aid policies should be further improved;doctor reimbursement and incentive mechanisms should be improved as well and unreasonable doctor service pricing and reimbursement mechanisms should be reformed.

OBJECTIVETo validate the hypothesis that the phenotypic transformation occurs in the smooth muscle cells in the corpus cavernosum of hypertensive rat and explore its impact on the erectile function of rats.

METHODSEighteen 16-week-old male spontaneously hypertensive rats (SHR) and 10 syngeneic normotensive rats (WKY) were used in this experiment. After measurement of systolic blood pressure of the caudal artery and examination of the erectile function with subcutaneous injection of apomorphine (APO), the rats were divided into 3 groups, namely hypertensive with erectile dysfunction (HBP-ED) group (n=6), hypertensive (HBP) group (n=12) and control group (n=10). Immunohistochemical staining and color image analysis system were used to observe expression of calponin 1 and osteopontin (OPN) in rat corpus cavernosum. Real-time quantitative RT-PCR was used to determine the expression of calponin 1 and OPN mRNAs in different groups.

RESULTSThe expressions of calponin 1 protein and mRNA were the highest in the control group and the lowest in HBP-ED group, while the expressions of OPN protein and mRNA were the highest in HBP-ED group and the lowest in the control group.

CONCLUSIONThe smooth muscle cells may transform from the contractile phenotype into synthetic phenotype in the corpus cavernosum of the hypertensive rats, resulting ultimately in erectile dysfunction.

Animals ; Calcium-Binding Proteins ; genetics ; metabolism ; Erectile Dysfunction ; etiology ; pathology ; Hypertension ; complications ; pathology ; Male ; Microfilament Proteins ; genetics ; metabolism ; Myocytes, Smooth Muscle ; pathology ; Osteopontin ; genetics ; metabolism ; Penis ; pathology ; Phenotype ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Inbred SHR

A large amount of nicotinamide adenine dinucleotide phosphate (NADPH) is required for fatty acid synthesis and maintenance of the redox state in cancer cells. Malic enzyme 1(ME1)-dependent NADPH production is one of the three pathways that contribute to the formation of the cytosolic NADPH pool. ME1 is generally considered to be overexpressed in cancer cells to meet the high demand for increased de novo fatty acid synthesis. In the present study, we found that glucose induced higher ME1 activity and that repressing ME1 had a profound impact on glucose metabolism of nasopharyngeal carcinoma(NPC) cells. High incorporation of glucose and an enhancement of the pentose phosphate pathway were observed in ME1-repressed cells. However, there were no obvious changes in the other two pathways for glucose metabolism: glycolysis and oxidative phosphorylation. Interestingly, NADPH was decreased under low-glucose condition in ME1-repressed cells relative to wild-type cells, whereas no significant difference was observed under high-glucose condition. ME1-repressed cells had significantly decreased tolerance to low-glucose condition. Moreover, NADPH produced by ME1 was not only important for fatty acid synthesis but also essential for maintenance of the intracellular redox state and the protection of cells from oxidative stress. Furthermore, diminished migration and invasion were observed in ME1-repressed cells due to a reduced level of Snail protein. Collectively, these results suggest an essential role for ME1 in the production of cytosolic NADPH and maintenance of migratory and invasive abilities of NPC cells.
Carcinoma ; Cell Line, Tumor ; Cell Movement ; Cell Survival ; Glucose ; metabolism ; Glycolysis ; Humans ; Malate Dehydrogenase ; metabolism ; NADP ; metabolism ; Nasopharyngeal Neoplasms ; metabolism ; pathology ; Neoplasm Invasiveness ; Oxidation-Reduction ; Oxidative Phosphorylation ; Pentose Phosphate Pathway ; Proto-Oncogene Proteins c-akt ; metabolism

Objective To investigate the phenotypes and genotypes of a hereditary protein C(PC) deficiency pedigree.Methods Imrnunoassay(ELISA)was used for PC antigen and PS antigen; Immunoturbidimetry assay was used for measuring AT antigen;Chromogenic substrate assay was used for measuring the activity of PC,PS and AT in Sysmex 1500 automatic Blood Coagulation Analyzer.Polymerase chain reaction(PCR)for amplification of the fragment of each exon and side sequences of PC gene in 10 members of the 3 generations;Direct DNA sequencing was used to examine the mutation site.Results Among 10 members of the 3 generation pedigree,8 of them had a PC:Ag level of 1.06-1.92 mg/L(normal references 3.00-6.00 rag/L),the activity of PC was between 41% and 67%(normal references 70%- 140%),which was significantly lower than the normal references while the levels of PS:Ag,PS:A,AT:Ag and AT:A were all within normal range.DNA sequencing analysis showed that there was a G to T mutation in exon IX of the PC gene at 12 918 position in 8 members.This mutation resulted in the substitution of terminator TGA for TGG which encoding tryptophan at 372 amino acid.There was a polymorphism in 2 405C/ T,2 418A/G,2 583A/T in the promotor area.Conclusions This pedigree is a type I hereditary protein C deficiency.There is a G12 918T mutation in exon IX of PC gene.This mutation is reported for the first time and there is a polymorphism in 2 405C/T,2 418A/G,2 583A/T in the promotor area.

The complete coding sequences of Eya gene family was amplified by standard PCR fromhuman tissues or cells cDNA library.The product of PCR was cloned into the eukaryotic expression vector pcDNA3-FLAG,generating pcDNA3-FLAG-Eya1～4.Thenhuman embryo kidney 293T cells were transfected with the recombinant plasmids and the expression of Eya genes were identified by Western blot.Transcriptional assay using a reporter containing myogenin enhance factor indicated that expression of Eya cooperation with Six in 293T cells affected the Myogenin gene expression.The expression vectors of Eya genes were constructed and confirmed by restriction enzyme digestion and DNA sequence analysis.Transcriptional assay using a reporter containing myogenin enhance factor indicated that expression of Eya in coordination with Six in 293T cells stimulated the Myogenin gene expression.Eya proteins are transcriptional activator of Six and can improve the activity of myogenin promoter.

OBJECTIVETo investigate the effects of pioglitazone on transforming growth factor beta1 (TGFbeta1) expression in ischemia/reperfusion injury myocardium of rats.

METHODSThirty SD rats were randomly divided into five groups (n = 6): ischemia/reperfusion group, pioglitazone 5 mg/(kg x d) group, pioglitazone 10 mg/(kg x d) group, pioglitazone 20 mg/(kg x d) group and pioglitazone 20 mg/(kg x d) + peroxisome proliferator-activated receptor gamma (PPARgamma) specific antagonist GW9662 group. Left anterior descending coronary artery of rats were ligated for 30 min and reperfused for 120 min to establish the model of ischemia/reperfusion in vivo. RT-PCR was performed to detect the expression of TGFbeta1 mRNA. Western blot was performed to detect the expression of TGFbeta1 protein.

RESULTSMyocardial apoptosis was significantly suppressed by pioglitazone. Pioglitazone upregulated TGFPbeta1 expression both in mRNA and protein level. GW9662 reversed the inhibition of myocardial apoptosis and the upregulation of TGFbeta1 expression by pioglitazone.

CONCLUSIONPioglitazone can inhibit the myocardial apoptosis induced by ischemia/reperfusion. Pioglitazone may protect the myocardium from ischemia/reperfusion via upregulation of TGFbeta1. This protection may be mediated by PPARgamma.

Anilides ; pharmacology ; Animals ; Apoptosis ; Male ; Myocardial Reperfusion Injury ; metabolism ; Myocardium ; metabolism ; PPAR gamma ; antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Thiazolidinediones ; pharmacology ; Transforming Growth Factor beta1 ; metabolism

beta-CIT was labeled with 131I by the peracetic acid method. Cat model of Parkinsonism was set up with MPTP. Each of normal and PD model cats was given an injection of 74 MBq/0.5 ml 131I-beta-CIT into the femur vein. Then the blood samples were obtained at 4 h and 20 h, the radioactivity was counted with calibrator. The biodistribution data of 131I-beta-CIT in cat body was calculated (ID%/g). The cats were subjected to imaging at 0.5 h, 1 h, 2 h, 4 h, 20 h after the administration of radiopharmaceutical. The radioactivity in striatum and cerebellum was measured and striatal specific binding ratios were calculated. The Results showed that the radio chemical purity of 131I-beta-CIT was 97.62% +/- 0.31%. The 131I-beta-CIT remained stable for at least 4 h after incubation with water and serum respectively. Following intravenous administration in cats, 131I-beta-CIT showed high accumulation in striatum. The study of imaging in cats showed that striatal specific uptake of 131I-beta-CIT at 20 h after injection was 4.83 +/- 0.82 in normal cats and 2.92 +/- 0.66 in PD cats. There was a significant reduction of striatal tracer uptake in PD cats, compared to the controls. The results of biodistribution study was in agreement with the results of imaging study. These results suggest that beta-CIT is an ideal agent for dopamine transporter imaging and can be used for the diagnosis of Parkinson's disease.
Animals ; Brain ; metabolism ; Cats ; Cocaine ; analogs & derivatives ; metabolism ; Disease Models, Animal ; Dopamine Plasma Membrane Transport Proteins ; Female ; Male ; Membrane Glycoproteins ; metabolism ; Membrane Transport Proteins ; metabolism ; Mice ; Mice, Inbred Strains ; Nerve Tissue Proteins ; metabolism ; Parkinson Disease ; diagnostic imaging ; metabolism ; Tomography, Emission-Computed, Single-Photon

OBJECTIVETo determine the effect of neostigmine on antagonizing atracurium-induced neuromuscular blockage with sulfate magnesium pretreatment.

METHODSForty patients who undertook elective gynecologic laparoscopic examinations and treatments under general anesthesia were randomized into four groups (group A, B, C, and D, group A paired with group C, and group B paired with group D). Before induction of general anesthesia, patients in group A and group C received MgSO4 30 mg/kg in saline intravenously within 5 min, while patients in group B and group D received the same volume of saline. Anesthesia was induced with fentanyl and propofol; subsequently tracheal intubation was performed with 0.5 mg/kg atracurium after stabilization of the electromyography recording, and neostigmine (0.02 mg/kg) and atropine (0.01 mg/kg) were infused in group C and group D when neuromuscular recovery (T1/T(C)) reached 10%. T1/T(C) changes after neostigmine infusion as well as haemodynamic changes and other responses during induction and neostigmine and atropine infusion were recorded.

RESULTSThe neuromuscular recovery speed had no significant difference between group A and group B after the neuromuscular recovery reached 10%, but it was lower in group C than in group D (P < 0.05). Significant difference existed between group AC and group BD (P < 0.05). No haemodynamic changes and other responses were found during induction and neostigmine and atropine infusion.

CONCLUSIONNeostigmine-induced neuromuscular recovery can be attenuated in patients pretreated with magnesium sulfate.

Adolescent ; Adult ; Anesthesia, General ; Atracurium ; antagonists & inhibitors ; Cholinesterase Inhibitors ; pharmacology ; Female ; Humans ; Laparoscopy ; Magnesium Sulfate ; pharmacology ; Middle Aged ; Neostigmine ; pharmacology ; Neuromuscular Blockade ; Neuromuscular Nondepolarizing Agents ; antagonists & inhibitors