Objective To explore the psychological intervention effect of ulinastatin combined with Xuebijing in the treatment of severe sepsis. Methods 76 patients with severe sepsis in our hospital from January 2016 to March 2017 were selected,and according to the different nursing intervention divided into observation group and control group,38 cases in each groups. control group with Ulinastatin and Xuebijing treatment, observation group with Ulinastatin and Xuebijing plus psychological intervention; before and after treatment in two groups of patients with clinical symptoms, psychological status (SAS and SDS score) to improve the situation, and the related data for comparative analysis. Results Ulinastatin and Xuebijing+psychological intervention (observation group) the clinical effect of treatment of severe sepsis patients than Ulinastatin and Xuebijing (control group) the clinical treatment effect of inflammatory factors in patients with improvement than the control group, SAS and SDS was better than that of control group, the difference was statistically significant (P<0.05). Conclusion severe sepsis patients choose the Ulinastatin+Xuebijing+psychological intervention of ulinastatin Xuebijing significantly, can effectively reduce the level of inflammatory factors in the patients, and fully improve the psychological status of patients, is worthy of clinical application.

Objective: To investigate the antiatherosclerotic effect of Wujibaifeng Pills and its mechanism. Methods: Rat dyslipidema was induced by ovariectomy (OVX), the levels of serum lipids, superoxide dismutase (SOD) activities and malondialdehyde (MDA) were detected after 12 weeks with the treatment of wujibafeng pills. Results: Wujibaifeng Pills lowered serum oxidized-low density lipoprotein cholesterol (OX-LDL,P

AIM: To optimize and establish the extraction techn ology of water-soluble polysaccharides from Ulva pertusa. TLC was employed to determine the mainly neutral sugars in the Ulvan. METHODS: The orthogonal test was employed to test the effects of th e four factors including volume of water, temperature of extraction, time of ext raction and pH of water on the yield and total carbohydrate contents of water-s oluble polysaccharides from Ulva pertusa and optimize the extraction technol ogy. Five groups of parallel tests were carried out by the optimum parameters es tablished and the sugar constituents of products were analyzed by TLC. RESULTS: Temperature of extraction and time of extraction have sign ificant effects on the extraction yield of water-soluble polysaccharides from Ulva pertu sa, but, for total carbohydrate content, only temperature of extraction was a significant factor. The mainly neutral sugars were composed of rhamnose, xylose and glucose. CONCLUSION: The optimum extraction technology was A 1B 3C 3D 3 when the yield and total carbohydrate content were considered as preferential pa rameters.

AIM:to investigate the effects of extract of ginkgo biloba (EGB) on human tubular epithelial-mesenchymal transition induced by transforming growth factor-?1.METHODS: HK2 cells were induced to epithelial-mesenchymal transition by transforming growth factor-?1 (TGF-?1, 10 ?g/L). EGB was added into the medium of HK2 cells 2 h before TGF-?1 was added. The expressions of E-cadherin, ?-smooth muscle actin (?-SMA), NADPH oxidase p67phox and superoxide dismutase (SOD) were determined by Western blotting. Malondialdehyde (MDA) in the mediums of HK2 cells was detected. RESULTS: EGB significantly attenuated the downregulation of E-cadherin, the upregulation of ?-SMA and p67phox, the downregulation of SOD and the upregulation of MDA in HK2 cells induced by TGF-?1.CONCLUSION: EGB significantly attenuates human tubular epithelial-mesenchymal transition induced by TGF-?1, and its underlying mechanism is that EGB attenuates the upregulation of p67phox and the downregulation of SOD induced by TGF-?1.

Objective To investigate the interference and associated mechanism of hnman tissue kallikrein (HK) gene on renal interstitial fibrosis in rats with 5/6 nephrectomy. Methods Human kallikrein cDNA was packed in a recombinant adeno-associated virus(rAAV)-based plasmid vector. The rAAV-HK was produced by transfection in 293 cells. Twenty-four male Wistsr rats were divided into sham operation and operation groups. The rats with 5/6 nephrectomy were randomly divided into simple operation, control and experiment groups. The rats in experiment group received single dose rAAV-HK via the tail vein with 1×1011 pfu. Before nephrectomy and every month after surgery until the rats were sacrificed, the caudal arterial pressure was measured using tail cuff blood pressure determinator. Three months after HK gene delivery, the rats were sacrificed. The expression of HK in rats was assessed by RT-PCR, Western blot and enzyme-linked immunosorbent assay (ELISA). The pathological changes of renal interstitium were evaluated by Masson stainning, and the distribution of bradykinin B2 receptor (BKB2R) and angiotensin Ⅱ typel receptor (ATIR) was examined by immunohistochemistry. The expressions of BKB2R, AT1R, p-MAPK protein in renal tissue were detected by Western blot. Results Three months after HK gene delivery, the systolic blood pressure of experiment group was significantly decreased compared with the control group [(163±13) nun Hg vs (217±16) mm Hg, P<0.01](1 mm Hg=0.133 kPa). Compared with sham rats, the rats in simple operation group and control group had much more renal interstitial collagen deposition and more serious fibrosis performance, but renal interstitial collagen deposition and fibrosis were significantly ameliorated in the rats of experiment group. In addition, the tubulointerstitial injury index of HK transgenic rats was significantly lower than that of the rats in control group (1.33±0.73 vs 3.01±0.62, P<0.01). Up-regnlating expression of bradykinn B2 receptor protein and down-regulating expression of AT1 receptor and p-MAPK protein were found in renal tissues of experimental group after three months (P<0.05). Conclusion HK gene delivery significantly alleviates renal interstitial fibrosis in rats with 5/6 nephrectomy through regulating the expression of bradykinin B2 receptor, AT1 receptor and p-MAPK in renal tissue.

Objective To describe the general characteristics of patients with acute chest pain in order to analyze factors associated with patients’utilization of emergency medical services (EMS).Methods A total of 747 eligible patients with acute chest pain admitted to emergency department of Qilu Hospital were consecutively enrolled from October 2014 to April 2015.Clinical data including demographic features, mode of arrival,past medical history,risk factors,symptoms and signs were collected prospectively by using standardized case report form.Univariate and multivariate analyses were carried out to investigate the association between the decision to use EMS and related factors including demographic features,past medical history,risk factors,symptoms and signs.Results Of the total 747 eligible patients,414 (55.4%)were male ,and the mean age was (57.2 ± 15.8)year;333 (44.6%)were female,and the mean age was (61.7 ±14.9)year.Of them,171 (22.9%)patients used EMS,and 143 chest pain patients with more than 75 years old were more inclined to use EMS (P <0.01),whereas 152 patients in 65 -75 years age group accounted for the lowest proportion of using EMS.Men were more inclined to use EMS than women (P <0.05),and 483 patients with typical chest pain used more EMS than patients with atypical chest pain (P <0.05);Of them,356 patients with a history of hypertension and 54 patients with a history of cerebral infarction were more inclined to use EMS (P <0.05 and P <0.01,respectively).Multivariate logistic regression analysis showed that male,older than 75 years,history of cerebral infarction were independent factors associated with EMS use (P <0.05).Conclusions This study indicated that only less than one-third of emergency department visits with acute chest pain decide to use EMS when symptoms occurred. Factors including male,older than 75 years,and a history of cerebral infarction were associated with more use of EMS.In order to promote patient asking for EMS timely,more work should be done.

BACKGROUND:Cytochrome P450 ( CYP) epoxygenases metabolize arachidonic acids ( AA) to form epoxyeicosatrienoic acids
(EETs), which exert beneficial roles in the treatment of cardiovascular diseases , but little is known about its role on adventitial remo-deling.METHODS:We used C57BL/6J mice in vivo and primary rat adventitial fibroblasts ( AFs) in vitro treated with angiotensin II (Ang II) to investigate the effects of CYP2J2 gene delivery and exogenous EETs administration on adventitial remodeling .RESULTS:CYP/sEH system was found to exist in human adventitia , and involved in adventitial remodeling process .Exogenous EETs administra-tion significantly inhibited Ang II-induced AFs activation , characterized by differentiation , proliferation, migration, and collagen syn-thesis.These protective effects were partially reversed by PPARγantagonist GW9662 pretreatment or SOCS3 siRNA transfection.EETs suppressed Ang II-induced IκBαphosphorylation , subsequent NF-κB nuclear translocation via PPARγdependent signaling pathway in AFs.Additionally, EETs reduced Ang II-induced JAK2, STAT3 phosphorylation and subsequent phosphor-STAT3 nuclear transloca-tion, which were mediated by SOCS3 induction but independent of PPARγactivation.Furthermore, rAAV-CYP2J2 gene delivery re-duced vessel wall thickening , AFs differentiation , proliferation and collagen deposition in aortic adventitia induced by Ang II infusion , which were mediated by NF-κB and SOCS3/JAK/STAT signaling pathways in blood pressure-dependent and -independent manners , re-spectively.CONCLUSION:We concluded that CYP2J2 overexpression attenuated Ang II-induced adventitial remodeling via PPARγ-dependent NF-κB and PPARγ-independent SOCS 3/JAK/STAT inflammatory signaling pathways .

Tubulointerstitial fibrosis (TIF) is a common pathological feature of end-stage kidney disease. Previous studies showed that upregulation of TGFbeta1 notably contributed to the chronic renal injury and irbesartan halted the development of TIF in rats with 5/6 renal mass reduction. This study was to investigate the effects of irbesartan on chronic TIF and the mechanism involved TGFbeta1 in the rodent model of chronic renal failure involving 5/6 nephrectomy. The results showed that irbesartan significantly attenuated the rise in blood pressure and tubulointerstitial injury observed in this model. Masson staining of the renal tissue revealed that there appeared severe renal tubule atrophy and fibrosis in operation group, but the lesion was attenuated mostly in irbesartan-treated group. Immunohistochemistry showed that irbesartan treatment apparently decreased the protein expression of TGFbeta1 which was up-regulated in operation groups. Western blot showed that irbesartan treatment down-regulated the expression of TGFbeta1, phosphorylated smad2 (p-smad2), AT1R and phosphorylated p38 (p-p38) MAPK, but significantly up-regulated the protein expression of smad6 as compared with operation group. These findings suggest that irbesartan attenuates hypertension and reduces the development of TIF in rats with 5/6 renal mass reduction via changes in the expression of these proteins at least including smad6, TGF-beta1, p-smad2, AT1 and p-p38 MAPK.

3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are a kind of lipid-lowering agents and have been used for the prevention and treatment of cardiovascular diseases. Recent studies suggested that statins, besides lowering cholesterol, may protect vessels by enhancing the activity of endothelial nitric oxide synthase (eNOS). In the present study, we investigated if simvastatin increases eNOS activity through its phosphorylation in 293 cells (293-eNOS) with stable expression of eNOS. The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min . mg proteins) (P<0.01). Western blotting revealed that simvastatin increased phosphorylation of eNOS at 1177 (ser) and also 495 (thr) but did not affect the overall expression of eNOS or inducible NOS. Further study found that simvastatin raised phosphorylation levels of Akt and AMPK, and such effect could be antagonized by Akt inhibitor or AMPK inhibitor. These results suggest that simvastatin could stimulate the activity of eNOS via its phosphorylation by Akt and AMPK, which provides a new mechanism, other than lipid-lowering effect, for the cardiovascular protection of statins.
Cell Line ; Epithelial Cells/cytology ; Epithelial Cells/*enzymology ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology ; Kidney/*cytology ; Nitric Oxide Synthase Type III/*metabolism ; Phosphorylation ; Simvastatin/*pharmacology

This study investigated the effects of telmisartan on insulin resistance in high-fat diet-treated rats and the possible mechanism. A total of 40 male Sprague-Dawley rats enrolled in the study were divided into 4 groups at random: ND group (n=10) and HD group (n=10), in which the rats were given a normal chow diet or a high-fat diet for 20 weeks following a one-week adaptation; ND+telmisartan (n=10) group and HD+telmisartan group (n=10), in which the rats were initially administered in the same way as the ND or HD group, and then they were orally gavaged with telmisartan (5 mg/kg daily) additionally for 5 weeks. Related inflammatory factors were measured by ELISA. Monocyte chemotactic protein 1 (MCP-1), phosphorylated JNK and IκB-α expressions in both adipose and liver were detected by Western blotting. CRP and angiotensin II receptor 1 (AT1) mRNA expressions in both adipose and liver were determined by RT-PCR. The results showed that telmisartan administration in vivo reversed insulin resistance as evidenced by a decrease in plasma fasting glucose levels, plasma fasting insulin levels and homeostasis model of assessment-insulin resistance (HOMA-IR). Furthermore, telmisartan administration significantly reduced serum CRP, TNF-α and IL-1β levels, and elevated serum IL-10 levels. It was also found to hamper the high-fat diet-induced increase in CRP mRNA, AT1 mRNA and MCP-1, and decrease in IκB-α in both adipose and liver. It was concluded that telmisartan administration in vivo may improve insulin resistance through attenuated inflammatory response pathways.