Objective:To explore the expression and clinical meaning of plasma soluble receptor of advanced glycation end product (sRAGE) in patients with gestational hypertension heart disease.Methods:Our research included in 2 groups:Observation group,n=57 patients with gestational hypertension heart disease who were diagnosed and treated in our hospital from 2013-06 to 2016-07;Control group,n=57 healthy pregnant women at the same period of time.Based on cardiac function,the patients in Observation group was divided into 4 subgroups as NYHA Ⅰ,Ⅱ,Ⅲ and ⅣV;according to 28-day surviving,the patients were divided into another set of 2 subgroups as Survival subgroup,n=49 and Death subgroup,n=8.Plasma levels of sRAGE and BNP were examined within 24h of admission.The changes of sRAGE were compared among different groups and the impact of sRAGE on gestational hypertension heart disease prognosis was analyzed.Results:Compared with Control group,Observation group had increased plasma sRAGE (939.2±184.3) pg/mL vs (467.3±116.2) pg/mL,P＜0.05;sRAGE level was positively related to NYHA grading (r=0.76,P＜0.001),sRAGE had an elevating trend upon NYHA grade increasing accordingly,P＜0.05.Compared with Survival subgroup,Death subgroup had increased plasma sRAGE (1647.6±249.7) pg/mL vs (776.9±146.2) pg/mL,P＜0.05.The areas of sRAGE and BNP under ROC curve were 0.91 and 0.88 respectively,P＜0.05.Conclusion:Plasma sRAGE was increased in patients with gestational hypertension heart disease;it was related to severity of heart failure (HF) and could be used for predicting the early prognosis in HF patients.

Objective To explore the effect of miRNA-195 (miR-195) on Smad7 expression and rat hepatic stellate cells line (HSC-T6) activation incuced by transforming growth factor-β1 (TGF-β1).Methods HSC-T6 were cultured in vitro,with 5 ng · mL-1 TGF-β1 as an injury factor simulating the rats liver fibrosis models.The cells divided into six groups:control group,model group (TGF-β1 group),miR-195 mimic experimental group,miR-195.mimic NC experimental group,miR-195 inhibitor experimental group and miR-195 inhibitor NC experimental group.After the HSC-T6 treated with 5 ng · mL-1 TGF-β1for 24,48,72 h,the mRNA expression of miR-195,Smad7,and α-SMA was detected by Real-time PCR.The protein expression of Smad7 was detected by Western blot.Results Under the induced by TGF-β1,the expression of miR-195 increased gradually (P ＜ 0.01),the expression of Smad7 showed a decreasing trend (P ＜ 0.05),and the expression of oα-SMA was gradually upregulated (P ＜ 0.01) with time.Compared with the model group,miR-195 mimic could promote activation of HSC-T6 induced by TGF-β1,and increase miR-195,α-SMA mRNA expression (all P ＜0.01),as well as reduce Smad7 mRNA and protein expression (all P ＜0.01);while miR-195 inhibitor could inhibit activation of HSC-T6 induced by TGF-β1,decrease miR-195,α-SMA mRNA expression (all P ＜ 0.01),as well as upregulate Smad7 mRNA and protein expression (all P ＜ 0.01).Conclusion miR-195 is involved in pro-activation of HSC-T6 by inhibiting Smad7 expression.

Multilateral mechanisms are important platforms and vehicles for cooperation in traditional medicine.Relying on multilateral platforms,China is able to enhance the international influence of the domestic traditional Chinese medicine and form synergies with other member countries to enhance regional or cross-regional radiation effects in order to promote sustainable development of traditional medicine around the world.This paper focuses on China's participation in major multilateral health cooperation mechanisms,including global initiatives(WHO-led global cooperation framework,the Belt and Road Initiative),regional multilateral mechanisms(ASEAN countries,China-Japan-Korea Health Cooperation Mechanism,Shanghai Cooperation Organization(SCO),The Greater Mekong Subregion(GMS)),and cross-regional multilateral mechanisms(BRICS,Forum On China-Africa Cooperation(FOCAC),G20),and sorts out the cooperation policies and actions in traditional medicine under different mechanisms,to analyze the characteristics and challenges of the existing mechanisms in traditional medicine cooperation,and to provide evidence for China's promotion on multilateral cooperation in traditional medicine.

Objective In order to provide support for the rational use of drugs,we summarize the clinical characteristics of patients with drug-induced liver injury (DILI) and statistics of the allergic drugs.Methods According to the common drug-induced liver injury diagnostic criteria of our country,the clinical data of 144 hospitalized cases in the third Xiangya hospital with DILI were analyzed retrospectively,then,potential pathogenic drugs were summarized.Results A total of 144 patients with DILI were enrolled in this study:male account for 53.47％ (77/144 cases),female account for 46.53％ (67/144 cases).The average age was (44.32 ± 16.02) years old,and 50.70％ (73/144 cases) of the patients were over 40 years old.Liver injury was caused by several kinds of drugs,23.61％ (34/144 cases) were traditional Chinese medicine,20.83％ (30/144 cases)were immunosuppressive agents,15.97％ (23/144 cases) were anti-tuberculosis drugs,7.64％ (11/144 cases) were antineoplastic drugs.18.75％ (27/144 cases) patients were cured,22.92％ (33/144 cases) patients got better while others account for 58.33％ (84/144 cases),and the average hospitalization days of patients with DILI were 16 days.Age,gender and duration of the disease had no significant effect on prognosis (P ＞ 0.05),while there were significant differences between liver function indexes and prognosis (P ＜0.05).Conclusion In this study,the incidence of DILI was higher in elderly people.A variety of drugs were able to cause DILI,including traditional Chinese medicine,immunosuppressive agents and anti-tuberculosis drugs.

This study adopted the policy text analysis method,review the historical background of the enactment,aimed to comparatively analyze the international pharmaceutical trade policies of the BRICS countries.The main objectives of the BRICS countries'international pharmaceutical trade policies included ensuring stable and accessible drug supply,expanding exports of domestic products and creating a favorable political environment.For these purposes,Brazil,Russia,and South Africa all ensure drug supply through substantial imports.However,they have also taken measures such as compulsory patent licensing and promoting localization of production by foreign companies to reduce import dependence.India,on the other hand,protects its domestic industry by resisting drug imports to ensure drug supply while simultaneously promoting the export of pharmaceutical products.China continually optimizes approval and data monitoring procedures to align with international standards,creating a favorable trade environment and expanding exports.China should further refine its international pharmaceutical trade policies while ensuring the autonomy of domestic drug research and supply,fostering stronger collaboration within BRICS nations and promoting global access to public healthcare products.

OBJECTIVETo study the relationship between blood pressure control status and patients' knowledge on hypertension prevention and control among hypertensive patients.

METHODSA total of 726 hypertensives were selected from four community health service centers (2 urban and 2 rural) in Beijing. All subjects were investigated by questionnaires and their blood pressures were measured at the same time.

RESULTSThe rate for blood pressure under control (< 140/90 mm Hg, 1 mm Hg = 0.133 kPa) in the rural and urban patients were 46.4% and 23.9% respectively. The control rate increased with the increase of patients' knowledge on prevention and control of hypertension in both urban and rural patients. The cumulative effect of knowledge on hypertension control status could contribute 30.0% to the difference in hypertension control rate between rural and urban patients.

CONCLUSIONPatients' knowledge on hypertension control was significantly related to the rate on hypertension control. Health education should be helpful to improve the rate on hypertension control.

Aged ; Blood Pressure ; physiology ; Blood Pressure Monitoring, Ambulatory ; China ; Female ; Health Knowledge, Attitudes, Practice ; Humans ; Hypertension ; physiopathology ; prevention & control ; therapy ; Logistic Models ; Male ; Middle Aged ; Outpatients ; education ; Patient Education as Topic ; organization & administration ; Rural Population ; Social Class ; Surveys and Questionnaires ; Treatment Outcome ; Urban Population

Background and purpose:Colorectal cancer(CRC)is one of the major malignant tumors threatening human health worldwide,with long-term high incidence and mortality rate.Potassium channel modulatory factor 1(KCMF1)is a member of the E3 ubiquitin ligase family.It binds to target proteins through the RING domain and participates in the regulation of a variety of biological processes in vivo.However,the function of KCMF1 in CRC remains unclear.This study aimed to investigate the expression level of E3 ubiquitin ligase KCMF1 in colorectal tumor,and to explore the effects of KCMF1 on the proliferation of CRC cells and its underlying molecular mechanism.Methods:The The Cancer Genome Atlas(TCGA)and Genotype-Tissue Expression(GTEx)databases were used to analyze the expression level of KCMF1 in CRC tissues and adjacent tissues and the association between the KCMF1 expression and the prognosis of CRC patients.Furthermore,immunohistochemical staining was performed to detect the protein level of KCMF1 in 90 paired human CRC tissues and adjacent non-tumor tissues.Lentiviral shRNA delivery system was employed to specifically target the KCMF1 gene(shKCMF1)in HCT116 and HCT15 CRC cell lines.The effects of KCMF1 knockdown on cell proliferation,apoptosis and cell cycle distribution were assessed by methyl thiazoyl terazolium(MTT)assay,colony formation assay,Western blot and flow cytometry.Changes in the transcriptional profile in HCT116 cells upon KCMF1 knockdown were identified by RNA sequencing(RNA-Seq),and the affected signaling pathways were evaluated by bioinformatics analysis.Real-time fluorescence quantitative polymerase chain reaction(RTFQ-PCR),Western blot,luciferase reporter assay and cell immunofluorescence assay were utilized to validate the alteration of the affected signaling pathway.Results:The TCGA and GTEx databases and IHC results showed that the mRNA and protein expression levels of KCMF1 in CRC tissues were significantly upregulated compared with adjacent tissues(P＜0.01).KCMF1 expression level was negatively correlated with the survival time of patients with CRC(P＜0.01),and was positively associated with CRC clinical stage(P＜0.05).Compared with control cells,KCMF1 knockdown significantly inhibited the proliferation of HCT116 and HCT15 cells(P＜0.001),induced cell apoptosis(P＜0.001),and led to cell cycle arrest in G1 phase(P＜0.01).RNA-Seq analysis showed that KCMF1 was involved in the regulation of several signaling pathways,including nuclear factor-κB(NF-κB)signaling pathway.KCMF1 knockdown reduced the transcription levels of the target genes of NF-κB signaling pathway,including BCL-XL,XIAP and CIAP(P＜0.05),and suppressed the expression of phosphorylated p65 and nuclear translocation of p65(P＜0.01).Meanwhile,the activity of NF-κB reporter was reduced in tumor cells upon KCMF1 knockdown(P＜0.01).Conclusion:The expression of KCMF1 is significantly upregulated in human CRC tissues and positively associated with advanced clinical stage and poor prognosis.KCMF1 may promote the proliferation of CRC cells by activating the NF-κB signaling pathway.KCMF1 may be a potential new therapeutic target for CRC.

OBJECTIVETo evaluate the effect of Notoginseng Radix on hepatic expression of transforming growth factor beta1 (TGF-beta1) and connective tissue growth factor (CTGF) in rats with alcoholic liver disease (ALD), in order to discuss its protective effect on alcoholic cirrhosis.

METHODFifty SD male rats were divided into the normal control group, the model group, the high-dose and low-dose Notoginseng Radix groups (3.0, 12.0 g x kg(-1)) and the magnesium isoglycyrrhizinate group (24 mg x kg(-1)), with 10 rats in each group. Apart from the control group, other groups were administered with ethanol-cornoil-pyrazole for 14 weeks to establish the alcoholic liver disease model. During the establishment of the model, the high-dose and low-dose Notoginseng Radix groups were administered with 12 g x kg(-1) x d(-1) Notoginseng Radix for 14 weeks, once everyday. Efforts were made to detect liver function, pathology with Masson staining, and the expressions of TGF-beta1, Smad3, Smad7 and CTGF mRNA.

RESULTCompared with the rats in model group, rats in Notoginseng Radix groups showed significant reduction in liver ALT, AST, collagen fiber deposition, and TGF-beta1, Smad3 and CTGF mRNA expressions in liver tissues, with the increase in the expression quantity of Smad7 mRNA. There were differences between the Notoginseng Radix groups. No significant difference was observed between the high-dose Notoginseng Radix group and the magnesium isoglycyrrhizinate group.

CONCLUSIONNotoginseng Radix can affect TGF-beta1/Smads signaling pathway and reduce the expression of CTGF.

Animals ; Connective Tissue Growth Factor ; genetics ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; Gene Expression ; drug effects ; Humans ; Liver Diseases, Alcoholic ; drug therapy ; genetics ; metabolism ; Male ; Panax notoginseng ; chemistry ; Rats ; Rats, Sprague-Dawley ; Smad3 Protein ; genetics ; metabolism ; Smad7 Protein ; genetics ; metabolism ; Transforming Growth Factor beta1 ; genetics ; metabolism

OBJECTIVETo observe the effect of Schistosoma japonicum cysteine protease inhibitor (rSjCystatin) for treatment of lipopolysaccharide (LPS)-induced sepsis in mice.

METHODSAfter a week of adaptive feeding, 54 BALB/c mice were randomly divided into normal control group (group A), sepsis group (group B), and rSjCystatin intervention group (group C). The mice in group A received an intraperitoneal injection of PBS (100 µL), and those in groups B and C were injected with PBS (100 µL) containing LPS (10 mg/kg); the mice in group C were also intraperitoneally injected with 25 µg sjCystatin in 100 µL PBS 30 min after LPS injection. From each group, 10 mice were randomly selected 24 h after PBS or LPS injection for detecting serum levels of TNF-α, IL-6, and IL-10 using ELISA and the levels of ALT, AST, BUN, and Cr using automatic biochemical analyzer; the pathological changes in the liver, lung and kidney were observed with HE staining. The remaining 8 mice in each group were used for observing the changes in the general condition and the 72-h survival.

RESULTSThe 72-h survival rates of the mice was 100% in group A, 0 in group B, and 36% in group C, showing a significant difference among the 3 groups (P<0.05). Compared with those in group A, the mice in group B exhibited obvious liver, lung, and renal pathologies with increased levels of ALT, AST, BUN, Cr, IL-6, and TNF-α (P<0.05). Treatment with sjCystatin significantly lessened LPS-induced organ pathologies, lowered the levels of liver and renal functional indexes and the pro-inflammatory cytokines, and increased the serum level of IL-10 in the mice (P<0.05).

CONCLUSIONSjCystatin can produce a significant therapeutic effect on sepsis induced by LPS in mice.

High expression of Bcl-2 is associated with the development of pancreatic cancer, and downregulation of Bcl-2 is an effective approach for the treatment of pancreatic malignancy. In the present study exosomes were isolated from the cultured medium of human embryonic kidney cells (HEK293) by ultracentrifugation and exosome-coated Bcl-2 siRNA (exosiBcl-2) was synthesized using electroporation. The results showed that the particle size of exosiBcl-2 was 67.3 ± 9.7 nm and the morphology of exosomes displayed a concave ring structure as determined by transmission electron microscopy (TEM). Western blot analysis indicated that exosomal proteins including CD9, CD81, CD63 and TSG101 were highly expressed. Confocal microscopy revealed that exosiBcl-2 was widely distributed in Miapaca-2 cells, and the transfection efficiency of exosiBcl-2 in Miapaca-2 was 77.2% as determined by flow cytometry. Treatment with exosiBcl-2 at a concentration of 100 nmol·L^-1 resulted in an inhibitory effect on the growth of Miapaca-2 cells with an inhibition rate of 63%. ExosiBcl-2 treatment can downregulate Bcl-2 and upregulate Bax protein. This study provides evidence that exosiBcl-2 is able to inhibit the growth of pancreatic cancer cells and the nanoparticles have potential to be developed as a novel anticancer agent.