Cardiovascular diseases are now the leading cause of serious harms to human health,have drawn widespread attention both domestically and internationally. But the current research on mechanism of cardiovascular diseases is not keeping up with the current status of their treatment. The microbiota in the gut,the largest microecological system in the human body and its interaction with the human host have been implicated in a variety of diseases. The relationship between gut microbiota and cardiovascular diseases has been increasingly understood in recent years. The changes of gut microbiota and its metabolites are the major contributing factor for the occurrence and development of cardiovascular diseases,therefore,correction of gut microbiota dysbiosis may provide a novel therapeutic alternative for cardiovascular diseases. This article reviews the role of gut microbiota and its metabolites in cardiovascular diseases,aiming to provide reference for future related studies.

Objective:To investigate the possible mechanism of high mobility group box-1 (HMGB1) in amplifing inflammatory responses in Leptospira interrogans hemolysin Sph2-treated J774A.1 macrophages. Methods:Recombinant Sph2 was incubated with J774A.1 macrophages. The damage of cell membrane was detected by lactate dehydrogenase(LDH) determination; the changes of cell structure were observed by cryo-electron microscope; ELISA was used to determine the expression of HMGB1. After the commercial recombinant HMGB1 was incubated with mouse J774A.1 macrophages, the phosphorylation of NF-κB, p38-MAPK and JNK signaling pathway wsa detected by Western blot, and the expression of IL-1β, IL-6, and KC (IL-8) was detected by ELISA.Results:Recombinant hemolysin rSph2 induced significant changes in the structures of J774A.1 cells, including nucleus disappearance, cell membrane structure damage, cell lysis and membrane swelling. The yields of LDH and HMGB1 also increased significantly. Phosphorylated-NF-κB, -p38-MAPK and -JNK were increased by HMGB1. The expression of IL-1β, IL-6 and KC in J774A.1 cells was up-regulated by HMGB1 and inhibited via inhibitors of NF-κB, p38-MAPK and JNK signal pathways.Conclusions:Hemolysin rSph2 damaged the membrane of J774A.1 cells, and induced the secretion of HMGB1. Secreted-HMGB1 might induce the expression of IL-1β, IL-6 and KC in J774A.1 cells via NF-κB, p38-MAPK and JNK signal pathways, thus amplifying the inflammatory responses caused by Sph2.

The incidence of metabolic rheumatism gout has been increasing with a trend of more younger patients and atypical symptoms. Typical gout is easy to be diagnosed, but it is difficult for atypical cases. Finding uric acid crystal in articular fluid by polarizing light microscope is a gold standard of diagnosis, but it is an invasive diagnostic method and difficult to be widely used. The patients need further imaging examination for assistance of diagnosis and guide of follow-up treatment. This article reviews the research progress of different imaging methods used for diagnosis of gouty arthritis.

Glycosides are the active ingredients (AIs) of many Chinese herbs and have become hot spots along with the findings of their new functions,such as anti-inflammatory,antivirus,enhanced immunity and anti-cancer.It has been found that glycosides exert their effects by converting to aglycons or other AIs in vivo.Therefore,the transformation of glycosides to the corresponding AIs in vitro becomes very important to enhance their bioavailabilities.The microbial transformation has an unparalleled advantage in the transformation of Chinese herbs in vitro for its reaction specificity,less by-products,mild reaction conditions and environmental protection.This paper summarized and prospected researches of glycosides' microbial transformation.

AIM: To explore the role of purinergic signaling mediated by ATP in the Alzheimer ’ s disease (AD)-related colon motility disorder and its related molecular mechanisms .METHODS:(1)Clinical trials:AD patients in our hospital were collected and studied .Radioimmunoassay was used for the determination of plasma motilin (MTL), cholecystokinin (CCK), vasoactive intestinal peptide (VIP) and nitric oxide (NO), and high-performance liquid chroma-tography ( HPLC) was applied to test the level of adenosine triphosphate ( ATP) .The patients were assessed by neuropsy-chology and scored accordingly .( 2 ) In animal experiments , AD mice received Morris water maze test , and the spatial learning and memory function were evaluated .The plasma levels of MTL , CCK, VIP and NO were examined by radioimmu-noassay , and the level of ATP was measured by HPLC .Choline acetyltransferase ( ChAT ) , VIP, nitric oxide synthase ( NOS) and ATP synthase were detected by immunohistochemistry .Western blot and immunohistochemistry were used to detect the expression of P2Y receptor.(3) In vitro, organ bath was applied to observe the effect of α,β-methylene ATP (α,β-MeATP), an agonist of P2Y receptor, on both spontaneous and electrically evoked contraction of colonic smooth muscle strip, and the technique of intracellular microelectrode was applied to observe the effect of α,β-MeATP on the membrane potential of colonic smooth muscle cells .RESULTS:Compared with control group , the levels of MTL and CCK were decreased (P<0.01), and the levels of NO and ATP were increased (P<0.05 or P<0.01), while the VIP level was not changed.Mini-Mental State Examination (MMSE) score was decreased (P<0.05), Alzheimer’s Disease Assess-ment Scale-Cognitive Subscale (ADAS-Cog) score, Neuropsychiatric Inventory (NPI) score and Alzheimer’s Disease Co-operative Study-Activities of Daily Living Scale ( ADCS-ADL ) were all increased as compared with control group ( P <0.01).The 4~6 d escape latency of APP/PS1 AD mice was significantly prolonged (P<0.05), and the space explora-tion ability distinctly reduced (P<0.05).In AD mice, the levels of MTL and CCK were decreased (P<0.01), and the levels of NO and ATP were increased (P<0.05 or P<0.01), while the VIP level was not changed .The protein expres-sion of colonic ATP synthase was significantly increased (P<0.05), but the expression of ChAT, VIP and NOS was not changed.The expression of P2Y receptor was increased (P<0.01).The results of in vitro experiment displayed that α,β-MeATP, from 20 μmol/L to 100 μmol/L, inhibited the spontaneous contraction of colonic smooth muscle strip in the nor-mal mice and AD mice ( P<0.05 or P<0.01 ) , and this inhibition was reversed by Na +channel inhibitor tetrodotoxin (TTX) (P<0.05 or P<0.01).In addition, the effect of α,β-MeATP at 100μmol/L on the AD mice was more obvious than that on the normal mice (P<0.05), and this inhibition was also antagonized by TTX (P<0.05 or P<0.01), pro-minent in AD group as compared with control group (P<0.05).In 10 Hz electrically evoked contraction of colonic smooth muscle strip,α,β-MeATP inhibited both the normal and AD mice (P<0.05 or P<0.01), while the inhibition was more obvious in the AD mice at the concentration of 40μmol/L or 100μmol/L (P<0.05 or P<0.01).CONCLUSION:AD patients and AD mice are accompanied by decreased MTL and CCK levels , and enhanced NO level , thus inducing colonic motor dysfunction along with AD .Meanwhile, ATP in plasma, purinergic neurons , and P2Y receptor expression are in-creased in the AD mice .Purinergic signaling mediated by ATP inhibits colonic smooth muscle strip contraction and further paralyzes the colonic movement function in AD .

[ ABSTRACT] AIM: To explore the role of chemokine receptor CXCR 4 in the pathogenesis of protein C system (PCS) in ulcerative colitis (UC).METHODS:In vivo, the mice were divided into control group and UC group .The mac-roscopic score, microscopic score and ulcer index were assessed .The mRNA levels and activity of myeloperoxidase ( MPO) , cyclooxygenase-2 ( COX-2 ) , stromal cell-derived factor-1α( SDF-1α) and monocyte chemotactic protein 1 (MCP-1) both in colonic tissue and plasma were determined .The expression and location of CXCR4,β-arrestin, p-JNK, endothelial cell protein C receptor (EPCR) and thrombomodulin (TM) were detected.The activity of protein C (PC) and protein S ( PS) was measured in each group .In vitro, mouse colonic microvascular endothelial cells were isolated , cultured and identified.Both CXCR4-overexpressing and CXCR4-silencing colonic mucosa microvascular endothelial cells were con-structed.The effects of SDF-1αon the protein levels of EPCR , TM,β-arrestin and p-JNK, and on the activity of PC , PS and activated protein C ( APC) were observed .RESULTS:Compared with control group , UC mice showed increased gross score, histopathological score and ulcer index (P<0.05).The mRNA levels and activity of MPO, COX-2, SDF-1αand MCP-1 in colon and plasma were increased (P<0.01).The protein levels of CXCR4,β-arrestin and p-JNK were up-regu-lated, EPCR expression was down-regulated in colon, and the activity of PC and PS in plasma was decreased (P<0.05 or P<0.01).CXCR4 overexpression further aggravated SDF-1α-induced PCS inhibition in colonic mucosa microvascular en-dothelial cells, and further up-regulated the protein levels of β-arrestin and p-JNK (P<0.05).CONCLUSION:PCS is inhibited in UC.CXCR4 is involved in the regulation of PCS inhibition by mediating chemokines and acting on colonic mu -cosa microvascular endothelial cells through β-arrestin-JNK pathway .

Objective To observe and explore the clinical value of developmentally supportive care ( DSC) to improve the growth and development for preemy. Methods A total of 86 preterm children in this hospital since March 2013 to September 2014 were selected, and were randomized divided into two groups, 43 cases in the intervention group and 43 cases in the control group. The patients of intervention group received DSC nursing model, while the patients of control group received routine nursing. Calcium (Ca), phosphorus (P) and alkaline phosphatase (ALP) levels, bone mineral density (BMD) as well as body weight had been measured and compared at birth, 1 month, 3 months and 6 months after born in the two groups. Results After 1 month intervention, the body wight of intervention group was (1 838. 2 ± 297. 3) g higher than (1 463. 4 ± 189.4) g comparative control group (t =5. 209,P <0. 01). After 3 months intervention in the intervention group, the blood Ca (4. 92 ± 1. 26) mmol/L, blood P (2. 53 ± 0. 28) mmol/L were above those of control group, but ALP (298. 3 ± 27. 4) U/L was under that of control group (t=6. 165, 10. 500, 6. 915;P<0. 05). The BMD of intervention group was (0. 34 ± 0. 06)g/m2 and (0. 24 ± 0. 02)g/m2 in the control group 6 months after born with statistical significance between two groups (t=5. 762,P<0. 01). Conclusions DSC model can effectively improve preemy the nutrition, improve and accelerate weight gain, thereby can help the growth and development of preterm children.

AIM:To explore the change of antithrombin Ⅲ( AT-Ⅲ) in the patients with atherosclerotic cere-bral infarction .METHODS:Chromogenic substrate assay was used to measure the activity of AT-Ⅲ in 55 patients with atherosclerotic cerebral infarction and 55 healthy controls , and the correlation analysis was applied to determine the AT-Ⅲactivity with the severity of damage in central nervous system and general biochemical parameters .The levels of TNF-αand IL-6 in the plasma were detected by ELISA .Immunocomplex in the plasma was measured by enzyme immunoassay (EIA). The number and phenotype of the monocytes in peripheral blood were analyzed by flow cytometry .ELISA was also applied to determine the secretion of TNF-αand IL-6 from the monocytes after the stimulation of immunocomplex .The expression of AT-Ⅲin human brain vascular endothelial cells after the stimulation of TNF-αand IL-6 was observed by Western blotting . RESULTS:The activity of AT-Ⅲsignificantly decreased in the patients with atherosclerotic cerebral infarction , and nega-tively correlated with the damage degree of nervous system function , systolic pressure , diastolic pressure , glucose , choles-terol, triglyceride, low-density lipoprotein cholesterol and homocysteine , while positively correlated with high-density lipo-protein.In addition, the plasma levels of TNF-αand IL-6 increased significantly , accompanied with the enhancement of immunocomplex level .The numbers of CD14 + CD16 + and CD14 + CD32 + monocytes in peripheral blood were not changed , while CD14 +CD64 +monocytes increased obviously .The secretion of TNF-αand IL-6 by monocytes were signifi-cantly enhanced after stimulated with immunocomplex , while the protein expression of AT-Ⅲ in the human brain vascular endothelial cells was down-regulated after co-incubated with TNF-αor IL-6.CONCLUSION:Decreased AT-Ⅲactivity in the patients with atherosclerotic cerebral infarction is one of the risk factors of cerebral infarction , and related with the dis-ease severity .The production of pro-inflammatory cytokines through immunocomplex from CD 14 +CD64 +monocytes may be involved in the mechanism .Improvement of AT-Ⅲactivity may protect against cerebral ischemia .

Objective To observe the tendency of the plasma concentration of plasminogen activator inhibitor type-1 (PAI-1) and thrombin activatable fibrinolysis inhibitor (TAFI) before and after thrombolytic treatment of acute ST elevation myocardial infarction (STEMI) and to explore their recanalization predictive value of PAI-1 and TAFI for acute myocardial infarction patients with thrombolytic treatment.Methods Sixty patients,who received thromobolytic treatment from January 2007 to March 2009,were prospectively recruited.The blood sample were collected within 2 hours of thromobolytic treatment ( 0,0.5 h,1 h,1.5 h and 2 h).The plasma concentration of TAFI and PAI-1 were test by ELISA.16 healthy people were recruited as control group.Results The plasma levels of PAI-1 in STEMI patients before thrombolytic treatment were higher than those of Control group ( P ＜0.01 ),however the same significant change of TAFI level was not seen.The levels of TAFI were no significant difference before and after thrombolytic therapy during whole observation periods.However,the level of PAI-1 increased at 1.5 h and 2 h after thrombolytic therapy (P ＜ 0.01 ).The plasma PAI-1 levels of no - revascularigation group at 2 h after thrombolytic therapy were significant higher than that in revascularization group ( P ＜ 0.05 ).The levels of TAFI were not significantly different between two groups (P ＞ 0.05).Conclusions The decrease of plasma PAI-1 from high level within 2 hours after thrombolysis treament may be exploring the predictive value for revascularization.The tendency of TAFI can' t forecast the result of revascularization.

Objective To investigate the map and pattern of blood oxygen level dependent(BOLD)signal changes correlated to interictal epileptiform discharges(IEDs)with EEG-fMRI in patients with partial epilepsy and then to explore the pathophysiological mechanisms of epileptic discharges and their effect on brain function in partial epilepsy.Methods Through the method of EEG-fMRI,2 patients with parial epilepsy were studied.The relationship between the regions of BOLD signal changes linked to IEDs and the electroelinical localization of epileptogenic zone in patients with partial epilepsy were investigated.Results The epileptogenic areas localized by electroclinical findings in the 2 patients all showed maximal activation and 2 sites of significant activation were found in 1 of the 2 patients;Weak activation were also manifested in the opposite side corresponding to lesions.Conclusions IED-linked BOLD response in patients with partial epilepsy is mainly in epileptogenic zones and weak activation can also be seen in the corresponding contralateral areas of epileptogenic zoiles.Activation areas ale well concordant with epileptogenie areas localized by electroclinical findings.