Objective Acute respiratory dysfunction (ARD) can occur after aortic surgery with the use of cardiopulmonary bypass and deep hypothermic circulation arrest, but relatively little is known about acute respiratory dysfunction in the patients with type A aortic dissection. This study aims to analyze the independent risk factors of acute respiratory dysfunction after A type aortic dissection surgery and to assess possible prevention and treatment option in the future. Methods Clinical data of the 252 patients including 193 male patients and 59 female patients who underwent type A aortic dissection surgery from February 2009 to October 2010 were collected. The mean age was 47 years. Postoperative acute respiratory dysfunction was defined as oxygenation impairment (PaO2/FiO2 ＜ 150) that occurred within 72 h of surgery except pleural effusion, cardiogenic pulmonary edema, pneumonia, pulmonary embolism and haemato-/ pneumothorax. There were 187 acute A type aortic dissection patients and 65 chronic type A aortic dissection patients. Clinical characteristics including age, gender, weight, height, history of hypertension, history of smoking, preoperative complications such as preoperative shock and acute renal failure, pericardial effusion, previous cardiac surgery, time from event to surgery, malperfusion syndrome, cardiopulmonary time, cross-clamp time,deep hypothermia circulation arrest time, surgical procedure, duration of intensive care unit stay and postoperative complications including tracheotomy, dialysis dependent renal failure and hospital mortality were gathered. Arterial blood analysis, chest X ray, ventilator parameters, number of blood transfusion and flood balance were assayed after operation. All the factors were evaluated by means of univariate and multivariate logistic regression analysis to identify relative risk factors of ARD. Results Acute respiratory dysfunction occurred in 32 (12.7% ) patients. The in-hospital mortality was significant difference between acute respiratory dysfunction group and non- acute respiratory dysfunction group (P ＜ 0.05). The value of BMI, incidence of acute aortic dissection, preoperative SBP level, cardio-pulmonary bypass time, aortic clamp time and total arch replacement in acute respiratory dysfunction group were significantly higher than the values in non- acute respiratory dysfunction group. Multivariate Logistic regression analysis showed blood transfusion more than 10 units and cardio-pulmonary bypass time more than 160 minutes were independent risk factors of early stage acute respiratory dysfunction after type A aortic dissection surgery.Conclusion Acute respiratory dysfunction after type A aortic dissection was a severe early stage postoperative complication and was associated with in-hospital mortality. The patients in acute aortic dissection were prone to have acute respiratory dysfunction. The independent risk factors of acute respiratory dysfunction included blood transfusion more than 10 units and cardio-pulmonary bypass time more than 160 minutes.

Objective To explore whether combined olmesartan angiotensin Ⅱ receptor type 1 blocker(ARB) and angiotensin-converting enzyme inhibitor(ACEI) temocapril have synergistic effect on reversal of left ventricular hypertrophy (LVH) in stroke-prone spontaneously hypertensive rats (SHRsp). Methods Fourty-four SHRsps and 11 Wistar-Kyoto rats(WKY) were divided randomly into 5 groups:WKY-control group, SHRsp-control group, SHRsp-olmesartan 10 mg/(kg?d)group, SHRsp-temocapril 10 mg/(kg?d)group, and SHRsp-Olmesartan 3 mg/(kg?d)+temocapril 3 mg/(kg?d) group for 6 weeks. Hearts weight were measured and histologically studied. The mRNA expression of angiotensin Ⅱ receptor type 1(AT1R) and integrin ?1 in myocardium was detected by RT-PCR. Results Olmesartan, temocapril and the their combination significantly reduced systolic blood pressure in a similar magnitude. Combination therapy was shown not greater effect in reversal of LVH than by olmesartan alone, although the effect by both of them was greater than temocapril monotherapy. The mRNA levels of AT1R and integrin ?1 in SHRsp were significantly decreased by treatment with olmesartan, temocapril, or combination therapy. Olmesartan and combination therapy result in greater decreases in expression of AT1R and integrin ?1 mRNA in myocardium than that by temocapril. Conclusion Compared with olmesartan alone, the combination of ARS and ACEI didn't show synergistic effect on reversal of left ventricular hypertrophy as were down-regulation of AT1R and suppression of integrin ?1 mRNA in myocardium.

Objective To investigate drug resistance and genotypes of methicillin-resistant Staphylococcus aureus (MRSA) isolated from intensive care unit (ICU). Methods MRSA strains were isolated from patients, medical staff and environment of hospital ICUs. Disk diffusion (K-B method) was used for drug resistance testing; Staphylococcal cassette chromosome mec (SCCmec) and Staphylococcal protein A (spa) typing methods were used for genotyping and identifying the homology. Results There were 78 strains of Staphylococcus aureus isolated including 62 isolates of MRSA, which were mainly from the burn ICU (22, 35.48%). Among 62 MRSA strains, 50 were hospital acquired strains, in which 43 isolates were of SCCmec Ⅲ, 4 of SCCmec Ⅰ and 3 of SCCmec Ⅱ. Twelve isolates could not be typed. Twenty-eight out of 37 hospital acquired isolates were typed by spa typing as SCCmec Ⅲ-t030, which belonged to the same clone. Conclusion MRSA in ICU is multi-drug resistant and SCCmec Ⅲ-t030 is the most prevalent genotype, which indicates that clinical MRSA strains and environmental MRSA strains may be homologous.

Background Granulocyte colony-stimulating factor(G-CSF)has been reported to have beneficial effect on cardiac dysfunction in post infarction and doxorubicin-induced cardiomyopathy.Objective To investigate the effects of G-CSF on cardiac remodeling in cardiac hypertrophy induced by angiotensin Ⅱ(Ang Ⅱ).Methods Thirty-six male wild type mice(WT)were allocated randomly to receive subcutaneously G-CSF(10 ?g/kg per day, n=9),or Ang Ⅱ(2.88 mg/kg per day,n=9),or Ang Ⅱ plus G-CSF(Ang Ⅱ 2.88 mg/kg+G-CSF 10 ?g/kg,n =9)for 4 weeks with untreated WT(n=9)as controls.Blood pressure and cardiac function were measured. Heart weight/body weight ratio,myocyte cross-sectional area and fibrosis area were determined.The mRNA ex- pression of osteopontin(OPN)in myocardium was detected by RT-PCR.The expressions of angiotensin converting enzyme(ACE),ACE2 and phosph-p70S6 kinase protein in myocardium were assessed by Western-Blot.Results Ang Ⅱ significantly elevated blood pressure(SBP,Ang Ⅱ:139.7?1.6 vs WT:108.7?2.3 mmHg,P0.05),but significantly attenuated the myocyte cross-sectional area(Ang Ⅱ+G-CSF:181.06?0.11 vs Ang Ⅱ:202.02?0.16 ?m~2,P

Hemagglutinin and neuraminidase, two important glycoproteins on the surface of influenza virus, play a considerable role in the entry and release stage of the viral life cycle, respectively. With in-depth investigation of influenza virus glycoproteins and the continuous innovation of drug discovery strategies, a new generation of glycoproteins inhibitors have been continuously discovered. From the point of view of medicinal chemistry, this review summarizes the current advances in seeking small-molecule inhibitors targeting influenza virus glycoproteins, hoping to provide valuable guidance for future development of novel antiviral drugs.

Wumei Pills is a prescription for the treatment of ascariasis of biliary tract and chronic diarrhea. It can be widely used in the treatment of many diseases with the basic pathogenesis "simultaneous occurrence of cold and heat" because of its features of cold-heat combination and tonifying-purgation combination. What should be noticed is that it is necessary to use large dose of Mume Fructus, which is also can be applied to the treatment of chronic diseases. Carefully sticking to pathogenesis in clinical treatment can obtain good efficacy.

AIM: To analyze the effect of pigment epithelium derived factor (PEDF) on nitrogen monoxide (NO) and expression of cysteine-containing, aspartate-specific proteases-3 (caspase-3) in retinal tissues of model rats with optic nerve crush injury.METHODS: A total of 60 SD rats were randomly divided into the blank control group, model group and PEDF group, with 20 rats in each group.Except the blank control group, the optic nerve crush injury rat models were established in the other groups, and left eyeballs were taken as samples.After successfully modeling, the model group were treated with intravitreal injection of 5μL of balanced salt solution while PEDF group were treated with intravitreal injection of 5μL of PEDF (0.2μg/μL).Two weeks later, the retinal tissues were collected, and changes of shape were observed under microscope after HE staining.The changes of NO level were measured by colorimetry assay, the expression of caspase-3 mRNA and caspase-3 protein was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western-blot.RESULTS: HE staining showed that retinal tissues of the blank control group arranged neatly and clearly.Retinal ganglion cells (RGCs) arranged in a monolayer, and cells were oval, uniform in size and distribution, the cell nuclei were clear, closely arranged, with clear boundaries.The retinal tissues of the model group were sparse in shape, RGCs showed vacuolar changes, the overall number of cells was reduced, and cell nuclei of residual RGCs showed pyknosis and uneven staining.RGCs in PEDF group were with slightly edema and arranged closely, and the degree of injury was significantly milder than that in the model group.Levels of Caspase-3 mRNA and protein and NO levels in the three groups showed the model group > PEDF group > blank control group (all P < 0.05).CONCLUSION: The application of PEDF can down regulate the expression of Caspase-3 and NO in rates with optic nerve injury and reduce RGCs injury.

Cerebrospinal Fluid Otorrhea ; surgery ; Craniotomy ; Encephalocele ; Humans ; Mastoid ; surgery

Adenoids ; diagnostic imaging ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Hypertrophy ; Magnetic Resonance Imaging ; Male ; Radiographic Image Enhancement ; methods ; Tomography, Spiral Computed ; methods

OBJECTIVE Alcohol is mainly metabolized through liver and excreted by kidney in the body. Kidney damage has been considered as the secondary to liver injury and kidney dysfunction is common in hospitalized patients with severe alcoholic hepatitis. Both acute and chronic alcoholism accumulation can compromise kidney function, although alcoholic kidney disease has drawn much more attention recently,the methodology for establishing the in vivo and in vitro alcoholic renal fibrosis models are still lacking,and the underlying mechanisms are to be determined. METHODS and RESULTS Mice were feed with a liquid diet containing alcohol for 4 weeks, 8 weeks and 12 weeks respectively, results of Masson′s Trichrome staining showed that kidney fibrosis peaked in 8-week model group, which consistent with the results of albumin assay,Western blot,immunostaining and real-time PCR of collagen I and α-SMA.In vitro study also confirmed that ethanol upregulated the level of fibrotic index-es,including collagen I and α-SMA,in tubular epithelial cells(HK2 cells).Additionally,both in vivo and in vitro studies showed that Smad7 was decreased and Smad3 was highly activated. Then we further detected the underlying mechanisms by which alcohol induced the imbalance of Smad7 and Smad3. Results of Genome-wide methylation sequencing found DNA methylation of Smad7 in the alcoholic fibrosis kidney,which may be mainly mediated by DNA methyltransferase 1(DNMT1),because knock-down of DNMT1,but not DNMT2 and 3,largely restored Smad7 level in ethanol-treated HK2 cells.Con-sequently, we found that NADPH Oxidases (nox)-mediated oxidative stress is the major force upregu-lating DNMT1,since knockdown of Nox2 and 4 could both decrease DNMT1 while rebalancing Smad7/Smad3 axis, and thereby relieved ethanol-induced fibrotic response in HK2 cells. More importantly, intraperitoneal injection of apocynin,an inhibitor of NADPH oxidoreductase,attenuated renal fibrosis in alcoholic kidney fibrosis mouse model. CONCLUSION By establishing the novel in vivo and in vitro models,we found that through activating oxidative stress-induced DNA methylation of Smad7,alcohol induces renal fibrosis by breaking the balance between Smad7 and Smad3.Elimination of Nox-mediated oxidative stress may be a potential therapy for treatment of long-term alcohol abuse-induced kidney fibrosis.