Objective To investigate the protective effects of erythropoietin (EPO) on myocardium injury after sepsis in rats in order to clarify the mechanisms.Methods The rat models of sepsis were produced by cecal ligation and perforation method (CLP).Ninty-six healthy SD rats were randomly (random number) divided into 3 groups:the sham operation group (Sham group,n =32),the sepsis group (CLP group,n =32),and the EPO treatment group (EPO group,n =32) treated with EPO 1000 IU/kg intraperitoneal injection after the CLP.The observation intervals were set at 3 h,6 h,12 h and 24 h after the surgery.The cardiac hemodynamics of the CLP group were measured.Plasma levels of inflammatory factors and myocardial enzyme indicators were determined by enzyme-linked immunosorbent assay (ELISA) ; Membrane potential levels of chondriosome of myocardial cells,cell apoptosis rates and expressions of nuclear factor-κB p65 of myocardium tissue were detected by flow cytometer; Then the pathological change of myocardium with HE staining was observed under light microscopy.Results (1) Compared with the CLP group,left ventricle systolic pressure (LVSP),left ventricle diastolic end pressure (LVEDP),the maximum rate of left ventricle rise and fall (+ dp/dtmax and-dp/dtmax) in the EPO group improved (P ＜0.05,P＜0.01); (2) Compared with the Sham operation group,plasma levels of tumor necrosis factoralpha (TNF-α),interleukin-6 (IL-6),C-reactive protein (CRP),cardiac troponin-I (cTNI),creatine kinase (CK),lactate dehydrogenase (LDH) and glutamine-oxaloacetic transaminase (GOT) in the CLP group increased at each interval (P ＜ 0.05),and those biomarkers in the EPO group were lower than those in the CLP group (P ＜ 0.05) ; On the contrary,plasma level of anti-inflammatory factor IL-10 in EPO group was higher than that in the CLP group (P ＜ 0.01) ; (3) Compared with the Sham operation group,the cell apoptosis rates in the CLP group increased significantly (P ＜ 0.01),and it decreased obviously in the EPO group (P ＜ 0.01); (4) Compared with the Sham group,membrane potential levels of chondriosome of myocardial cell in the CLP group decreased (P ＜0.01),while it increased in the EPO group in comparison with the CLP group (P ＜ 0.01) ; (5) Pathological changes of myocardium after the CLP could be lessened by the EPO treatment.Conclusions EPO may increase membrane potential levels of chondriosome and decrease the apoptosis rates of myocardial cell in rats after sepsis,and it may reduced the production of inflammatory factors to protect the myocardial cell by down-regulating NF-κB p65.Both increased membrane potential level of chonriosome and decreased inflammatory factor may implicate in myocardium protection thereby improving cardiac function after sepsis.

Objective To explore the relationship between the types of female breast density and age and breast cancer .Methods By accepting the digital mammography X -ray examination for 5 006 women cases and according to the ACR BI -RADS standard in the fourth edition ,the breast density assessment was quantified . We analysed the relationship between the breast density and age and breast cancer .Results In 5 006 cases,the average female age was between 44.22 ±8.09 years old,median age was 43 years old.The components of the breast density were fat type , small amount type , large amount type and compact type each count were 256 (5.11%),726(14.51%),3 719(74.29%),305(6.09%)respectively.By dividing into different age -group to analyze the breast density,there was significant statistical differences of the breast density among age -groups(P<0.001).Among them the breast cancer were 184 cases.Age was between 51.26 ±10.15 years old.Breast cancer in each breast density were fat type 10.16%(26/256),small amount type 9.09%(66/726),large a-mount type 2.45%(91/3719)and compact type 0.33%(1/305).There were statistical differences among age -groups and breast densities and breast (P<0.001).Conclusion Age plays a very important effects on the fe-male breast density .The lower breast density is a high risk factor to breast cancer occurrence .

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Objective To observe the changes of lipoprotein‐associated phospholipase A2(Lp‐PLA2) in patients with athero‐thrombosis acute ischemic stroke and the correlation of Lp‐PLA2 with cerebra infarction volume ,neurologic impairment and early prognosis .Methods A total of 104 patients with atherothrombosis acute ischemic stroke and 100 healthy people(controls) were collected .The levels of Lp‐PLA2 were detected by immunoturbidimetry .The cerebral infarction volume was checked by Cranial MRI or CT .The neurological impairment degree was assessed by National Institute of Health Stroke Scale (NIHSS) score .The early prognosis was assessed by Barthel index .The changes of serum Lp‐PLA2 levels in patients with different infarct volumes and neurologic impairment were compared ,the influence of early prognosis were analysised .Results The levels of serum Lp‐PLA2 in the patients with atherothrombosis ischemic stroke were significantly higher than those in control group (P<0 .05) ,and signifi‐cantly correlated with the levels of serum LDLC (r=0 .859 ,P<0 .05) .The levels of serum Lp‐PLA2 were significantly correlated with the increasing of cerebral infarction volume and cerebral neurological impairments (r=0 .531 ,P<0 .05 ;r=0 .623 ,P<0 .05) . The patients with higher level of Lp‐PLA2 has poor prognosis(P<0 .05) .Conclusion The level of Lp‐PLA2 was significantly higher in patients with atherothrombosis ischemic stroke and may reflect the severity and early prognosis in patients with athero‐thrombosis acute ischemic stroke .

Objective To explore the correlation and significance of V312F locus polymorphism of PCSK9 gene in patients with coronary heart disease.Methods We selected 3560 patients with coronary heart disease who came to our hospital from January 2014 to January 2016 as the case group.They were divided into 5 subgroups:angina group,myocardial infarction group,silent myocardial ischemia group,ischemic cardiomyopathy group,and sudden death group,according to their anatomic and pathophysiological features.Data of 1 000 people for physical examination served as the control group.PCR assay combined with direct sequencing method was applied to test V312F locus polymorphism of PCSK9 gene.Logistic regression analysis was used to analyze relationship between V312F locus polymorphism of PCSK9 gene and types of coronary heart disease.The concentration of serum PCSK9 and lipids of the two groups were also measured.Results The serum levels of PCSK9,TC,TG and LDLC and ratio of positive family history in the case group were significantly higher than those in the control group,while the level of HDLC was lower than that of the controls (all P＜0.05).Indexes of sudden death subgroup in the case group showed the most significant changes,while asymptomatic myocardial ischemia subgroup showed the weakest changes.The frequency of genotype TT,GT and allele T in the case group was 3.4％,16.6％ and 11.7％,respectively,which was significantly higher than that in the control group (1.1％,10.2％ and 6.2％) (all P＜0.01).The highest frequency of genotype TT,GT and allele T was found in sudden death subgroup,and the lowest frequency of these indexes was found in asymptomatic myocardial ischemia subgroup (P＜0.05).Results of Logistic regression analysis showed that genotype TT in V312F locus of PCSK9 gene was related to the severity of coronary heart disease (OR =8.463,95％ CI from 3.505 to 17.854,P＜0.001).Conclusion The mutation of V312F (T/G)locus of PCSK9 gene might be related to the severity of coronary heart disease.

Objective To investigate the core competence of humanistic quality of the surgical nurses in primary hospitals ,therefore to detect problems and find corresponding solutions .Methods Based on the scale of core competence of registered nurses of China , we adopted the method of stratified cluster sampling , and choose one grade-three comprehensive hospital , two grade-two comprehensive hospitals and conducted the survey among 189 surgical nurses .The competence difference was compared between nurses of different professional titles and hospitals , and the correlation analysis was made .Results Among the 189 nurses surveyed , the average scores of the critical thinking and scientific research , ethics and legal practice , interpersonal relationship, and education and consultation were (21.32 ±2.54),(20.49 ±1.56),(20.75 ±1.67), (17.81 ±2.20)respectively, with the scoring rates of 53.3%,64.0%,64.8%, and 63.6%respectively.The scores of the senior nurses were higher than those of the junior and intermediate nurses with statistical significance (F=78.814,P<0.01).In terms of interpersonal relationship and ethics and legal practice the scores in grade-three hospitals were higher than those in the grade-two hospitals with statistical significance ( t=2.603,2.249,respectively;P<0.01).The four items of core competence of humanistic quality in the surgical nurses of primary hospitals were positively correlated ( P <0.01 ).Conclusions The core competence of humanity quality of the surgical nurses was comparatively low , with the phenomenon more obvious in junior and intermediate nurses .The cooperation between hospitals and colleges and universities should be promoted so as to strengthen the education on the core competence of humanistic quality in the students .Meanwhile long-term training programs should be implemented by hospitals to give stratified education on the core competence of humanistic quality .