We conducted a randomized, open-label, parallel-controlled, multicenter trial on the use of Shuanghuanglian (SHL), a traditional Chinese patent medicine, in treating cases of COVID-19. A total of 176 patients received SHL by three doses (56 in low dose, 61 in middle dose, and 59 in high dose) in addition to standard care. The control group was composed of 59 patients who received standard therapy alone. Treatment with SHL was not associated with a difference from standard care in the time to disease recovery. Patients with 14-day SHL treatment had significantly higher rate in negative conversion of SARS-CoV-2 in nucleic acid swab tests than the patients from the control group (93.4% vs. 73.9%, P = 0.006). Analysis of chest computed tomography images showed that treatment with high-dose SHL significantly promoted absorption of inflammatory focus of pneumonia, which was evaluated by density reduction of inflammatory focus from baseline, at day 7 (mean difference (95% CI), -46.39 (-86.83 to -5.94) HU; P = 0.025) and day 14 (mean difference (95% CI), -74.21 (-133.35 to -15.08) HU; P = 0.014). No serious adverse events occurred in the SHL groups. This study illustrated that SHL in combination with standard care was safe and partially effective for the treatment of COVID-19.
COVID-19 ; Humans ; Medicine, Chinese Traditional ; Research ; SARS-CoV-2 ; Treatment Outcome

Clopidogrel is one of the anti-platelet drugs, which is widely used in the world.It plays an important role in the treatment of patients with acute coronary syndrome and those undergoing percutaneous coronary intervention.Clopidogrel is effective in inhibiting the activity of platelets, decreasing the incidence of thrombosis in the stent, and then reducing the risk of adverse cardiovascular events in affected individuals. However, some patients still have coronary thrombosis after taking clopidogrel.This phenomenon is known as clopidogrel resistance or clopidogrel non-response or low response. Identification of clopidogrel resistance is of great significance in preventing the occurrence of adverse cardiovascular events.This paper provides guidance for the clinical treatment of clopidogrel resistance by discussing the definition, mechanisms and laboratory evaluation of clopidogrel resistance.

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 trace human umbilical cord mesenchymal stem cells (MSCs)labelled by USPIO-PLL which were transplanted into mouse subcutaneous xenotransplanted lung cancer by using 3.0T MR,to investigate the relationship between MSCs and VEGF expression and tumor angiogenesis by using SABC immunohistochemical method and to comprehensively analyze the effect of MSCs transplantation on lung cancer.Methods Cultured MSCs and poly lysine (PLL)was as a transfection agent which was magnetically labeled by USPIO and implanted into mice with subcutaneous xenotransplanted lung cancer through the tail vein.MRI was performed at pre-transplantation, 1 d and 10 d after transplantation and the tissues were performed by immunohistochemistry respectively.Results (1)MSCs could reach the tumor area at the first day after the transplantation and be monitored by MRI.MSCs increased at the 10th day.MRI signal intensity was reducedand the difference was statistically significant (P <0.05).The inhibitory rate of the 1st day and 10th day was positive;(2)At the 10th day after the transplantation,the rate of the VEGF positive expression in MSCs group was 86.67％,the value of MVD was 44 .22 ± 12 .36 ,and the rate of the VEGF positive expression in NS group was 26 .67 ％ ,the value of MVD was 20 .29 ±8.47 (P <0.05).Conclusion Tracing stem cell transplantation in vivo can be proceeded effectively by using 3.0T MR.Stem cell has bidirectional effect on lung cancer which inhibites the tumor growth by directional chemotaxis and differentiation,and also enhances expression of VEGF and angiogenesis at a certain extent.

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 .

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.

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.

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 Iκ B-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 Iκ B-α in both adipose and liver.It was concluded that telmisartan administration in vivo may improve insulin resistance through attenuated inflammatory response 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.

Tubulointerstitial fibrosis(TIF)is a common pathological feature of end-stage kidney disease.Previous studies showed that upregulation of TGFβ1 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 TGFβ1 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 TGFβ1 which was up-regulated in operation groups.Western blot showed that irbesartan treatment down-regulated the expression of TGFβ1,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-β1,p-smad2,AT1 and p-p38 MAPK.