Application Experience of Moist Wound Healing Theory Combined with Modern New Dressings in the Treatment of Pressure Ulcers

Objective:Research on the effect of moist wound healing theory in a combination with modern new dressing treatment in patients diagnosed with pressure ulcers.Method:Selected 30 patients with pressure ulcers from our hospital,which is Shandong Tai an Municipal Hospital,from January 2019 to January 2021 were divided into experimental group(15 cases,treated with moist wound healing theory combined with modern new dressings)and control group(15 cases,applied conventional treatments).The treatment effect,time of wound edema subsidence,wound healing time,number of dressing changes,granulation tissue growth time,and diameter reduction time were compared between the two groups.Results:The total effective rate of the experimental group(93.33%,14/15)was higher than that of the control group(53.33%,8/15),P<0.05;the time to subsidence of wound edema in the experimental group was(3.11±0.22),and the time for wound healing was(12.78±0.45),the number of dressing changes(7.13±0.34)times,the growth time of granulation tissue(5.43±2.22),the diameter reduction time(6.25±3.75),compared with the control group,P<0.05.Conclusion:In the clinical treatment of patients diagnosed with pressure ulcers,the effective combination of moist healing theory and modern new dressing therapy has significant effects,whereby it speeds up the healing process of the pressure ulcers,and it is proven to be worthy to be promoted for usage.

Effectiveness and safety of Shexiang Baoxin Pill(MUSKARDIA)in patients with stable coronary artery disease and concomitant diabetes mellitus:a subgroup analysis of a randomized clinical trial

Background:Preliminary studies have indicated that Shexiang Baoxin Pill(MUSKARDIA)has a coronary artery dilation effect and increases the coronary blood flow,relieving the symptoms of angina.This study aimed to evaluate the benefit of MUSKARDIA on patients with stable coronary artery disease(CAD)and diabetes mellitus(DM).Methods:This was a subgroup analysis of a multicenter,randomized,placebo-controlled phase IV trial.CAD patients with a medical history of DM or baseline fasting blood glucose(FBG)≥7.0 mmol/L were grouped according to the treatment(standard therapy plus MUSKARDIA or placebo).The primary outcome was major adverse cardiovascular events(MACEs),which was the composite outcome of cardiovascular death,non-fatal myocardial infarction,and non-fatal stroke.The secondary outcome was the composite outcome of all-cause death,non-fatal myocardial infarction,non-fatal stroke,hospitalization for unstable angina or heart failure,and coronary angioplasty.Results:MACEs occurred in 2.6%(9/340)and 4.8%(18/376)of patients in the MUSKARDIA and placebo groups,respectively(P=0.192).Secondary composite outcome was significantly less frequent with MUSKARDIA than with placebo(15.3%[52/340]vs.22.6%[85/376],P=0.017).Risk of MACEs(hazard ratio[HR]=0.69,95%confidence interval[CI]:0.31-1.57)was comparable between two groups.In patients with uncontrolled DM(≥4 measurements of FBG≥7 mmol/L in five times of follow-up),the risk of secondary outcome was significantly lower with MUSKARDIA(5/83,6.0%)than with placebo(15/91,16.5%)(HR=0.35,95%CI:0.13-0.95).Conclusion:As an add-on to standard therapy,MUSKARDIA shows a trend of reduced MACEs in patients with stable CAD and DM.Furthermore,MUSKARDIA may reduce the frequency of all-cause death,hospitalization,and coronary angioplasty in this population,especially in those with uncontrolled DM.Trial Registration:ChiCTR.org.cn,ChiCTR-TRC-12003513.

Corrigendum to“Long non-coding RNA in liver metabolism and disease:Current status”[Liver Res.1(2017)163e167]

The authors regret<the text“to L.Wang”should be removed from the National Natural Scientific Foundation of China(Grant No.81572443).The correct acknowledgement should read as:This work was supported by the National Institutes of Health(NIH)grants(R01DK104656,R01DK080440,R01ES025909,R21AA022482,R21AA024935,R01AA026322 to L.Wang);VA Merit Award(1I01BX002634 to L.Wang);the National Natural Scientific Foundation of China(Grant No.81572443),VA Merit Award(1I01CX000361 to S.Liangpunsakul),NIH(U01AA021840,R01DK107682,R01AA025208,R21AA024935 to S.Liangpunsakul),US DOD(W81XWH-12-1-0497 to S.Liangpunsakul).>.The authors would like to apologise for any inconvenience caused.

Long non-coding RNA in liver metabolism and disease:Current status

Long non-coding RNAs(lncRNAs)are comprised of RNA transcripts exceeding 200 nucleotides in length but lacking identifiable open reading frames(with rare exceptions).Herein,we highlight emerging evidence demonstrating that lncRNAs are critical regulators of liver metabolic function and diseases.We summarize current knowledges about dysregulated lncRNAs and outline the underlying molecular mechanisms by which lncRNAs control hepatic lipid ad glucose metabolism,as well as cholestatic liver disease.Liver-specific triglyceride regulator(lncLSTR),Lnc18q22.2,steroid RNA activator(SRA),highly upregulated in liver cancer(HULC),metastasis associated in lung adenocarcinoma transcript 1(MALAT1),liver glucokinase repressor(lncLGR),maternally expressed gene 3(MEG3),and H19,lncHR1,lnc-HC,apolipoprotein A1 antisense transcript(APOA1-AS),DYNLRB2-2,and LXR-induced sequence(LeXis)are included in the discussion.