Diabetic diarrhea is one of the chronic complications of diabetes, which is particularly closely related to the spleen and kidney. Using these two organs as the theoretical foundation, the root of diabetic diarrhea can be grasped. Pathogenic dampness is responsible throughout the whole process of diabetic diarrhea. Using syndrome differentiation, deficiency is as the basic pattern and excess is the syndrome for diabetic diarrhea; diagnosis and treatment combine symptoms and syndromes, which not only particularly pay attention to protecting the spleen and kidney, but also clearing pathogenic dampness. At the same time, flexible medication is applied according to dynamic symptoms, which can achieve good efficacy.

OBJECTIVETo conduct a systematic review and meta-analysis of randomized controlled trials (RCTs) that have assessed the effect and safety of ursodeoxycholic acid (UDCA), S-adenosylmethionine (SAMe) and UDCA-SAMe combination therapies for intrahepatic cholestasis of pregnancy (ICP).

METHODSUsing searching protocols and assessment methods recommended by the Cochrane Collaboration to reduce bias in systematic reviews, the databases of Medline, EMBASE, Cochrane Central Register of Controlled Trials (CCRT), China National Knowledge Infrastructure (CNKI), Chinese BioMedical Literature (CBM) and Wanfang China Online Journals were searched to identify relevant RCTs published from database inception to December 2011.

RESULTSTen RCTs (of 727 pregnant women) were included in the study and represented a low risk for bias. Compared to the patients who received UDCA monotherapy, those who received UDCA-SAMe combination therapy had significantly lower rates of Cesarean section (odds ratio (OR) =0.45, 95% confidence interval (CI):0.24-0.86), preterm birth (OR=0.36, 95% CI:0.20-0.63), and fetal asphyxia (OR=0.27, 95% CI:0.13-0.56) (all P less than 0.05); however, the UDCA-SAMe therapy did not provide better rates of amniotic fluid pollution (OR=0.38, 95% CI:0.14-1.01) or better new bom weight (mean difference (MD) =397.36, 95% CI:-96.17-890.89). Compared to the patients who received SAMe monotherapy, those who received UDCA-SAMe combination therapy had significantly lower rates of preterm birth (OR=0.39, 95% CI:0.21-0.73), fetal asphyxia (OR=0.23, 95% CI:0.07-0.75), and amniotic fluid pollution (OR=0.41, 95% CI:0.20-0.85) (all, P less than 0.05); however, the UDCA-SAMe therapy did not provide better rates of Cesarean section (OR =0.62, 95% CI:0.27-1.44) or better new bom weight (MD =445.95, 95% CI:-143.51-1035.42). Comparison of the two monotherapies (UCDA vs.SAMe) showed no statistical differences in rates of Cesarean section (OR=0.91, 95% CI:0.47-1.78), preterm birth (OR =0.79, 95% CI:0.49-1.38), fetal asphyxia (OR=0.90, 95% CI:0.38-2.12), and amniotic fluid pollution (OR=1.14, 95% CI:0.61-2.13), as well as of new born weight (MD =-62.86, 95% CI:-157.81-32.09). Six studies reported no side effects.None of the included studies reported use of allocation concealment or blinding.

CONCLUSIONUDCA-SAMe combination therapy is better than either UDCA or SAMe monotherapy for improving the outcome of ICP without adverse effects. Large-scale trials with adequate sample sizes and higher quality study design are needed to further confirm the efficiency and safety of UDCA and SAMe for treating ICP.

Cholestasis, Intrahepatic ; drug therapy ; Drug Therapy, Combination ; Female ; Humans ; Pregnancy ; Pregnancy Complications ; drug therapy ; Pregnancy Outcome ; Randomized Controlled Trials as Topic ; S-Adenosylmethionine ; administration & dosage ; adverse effects ; therapeutic use ; Ursodeoxycholic Acid ; administration & dosage ; adverse effects ; therapeutic use

Atherosclerosis(AS)is a chronic inflammatory disease of large and medium-sized arteries that leads to ischemic heart disease,stroke,and peripheral vascular disease.Despite the current treatments,mortality and disability still remain high.Sonodynamic therapy(SDT),a non-invasive and localized methodology,has been developed as a promising new treatment for inhibiting atherosclerotic progression and sta-bilizing plaques.Promising progress has been made through cell and animal assays,as well as clinical trials.For example,the effect of SDT on apoptosis and autophagy of cells in AS,especially macrophages,and the concept of non-lethal SDT has also been proposed.In this review,we summarize the ultrasonic parameters and known sonosensitizers utilized in SDT for AS;we elaborate on SDTs therapeutic effects and mechanisms in terms of macrophages,T lymphocytes,neovascularization,smooth muscle cells,lipid,extracellular matrix and efferocytosis within plaques;additionally,we discuss the safety of SDT.A comprehensive summary of the confirmed effects of SDT on AS is conducted to establish a framework for future researchers.

Objective To explore the possible mechanisms by which fibroblast growth factor(FGF)23 promoted atrial fibrosis in circulation of chronic kidney disease(CKD)by binding to atrial tissue fibroblast growth factor receptor(FGFR)4.Methods Twenty-two healthy male Sprague-Dawley(SD)rats were selected.Rats were randomly selected to undergo 5/6 nephrectomy and fed for 15 weeks to establish a CKD model(n=14).The remaining 8 rats were used as the sham group.The sham group(n=8)underwent the same surgery without removing renal tissue.Body weight,blood pressure,renal function,cardiac ultrasound,epicardial electrocardiography and pathological indices were monitored in both groups.Enzyme-linked immunosorbent assay(ELISA)method was used to determine the circulating levels of FGF23 in the two groups of rats.Transcriptomic analysis of left atrial tissue was performed to search for differentially expressed genes.Rat atrial fibroblasts were divided into the control group,the FGFR inhibitor group,the transforming growth factor-β(TGF-β)group and the TGF-β+FGFR inhibitor group.The expression levels of α-smooth muscle actin(α-SMA),collagenⅠ(Col Ⅰ)and phosphorylated protein kinase B(p-AKT)protein were detected by Western blot assay.Results Systolic blood pressure,blood urea nitrogen and creatinine were elevated in the CKD group of rats.Cardiac electrophysiological study showed that CKD could promote the occurrence of atrial fibrillation(AF)and atrioventricular block.Cardiac ultrasound suggested that the internal diameter of the left atrium was significantly increased in rats of the CKD group.Pathological findings showed that the left atrium in the CKD group underwent significant fibrosis,and epicardial electrical markers showed that left atrial electrical conduction velocity was significantly slower and conduction heterogeneity was significantly increased in the CKD group.These changes were accompanied by higher circulating FGF23.Western blot results showed that FGFR4 expression was upregulated in the CKD group.After blocking the FGF23/FGFR4 signaling pathway in atrial fibroblasts,the fibrosis-related proteins α-SMA,Col Ⅰ and p-AKT/AKT were decreased.Conclusion CKD promotes the occurrence of AF by inducing both structural and electrical remodeling.Increased circulating FGF23 promotes atrial fibrosis by activating the downstream AKT pathway binding to FGFR4 in atrial tissue.

A chemical investigation on