Objective:To investigate the effect of DEAD-box helicase (DDX) 21 on myocardial ischemia-reperfusion (I/R) injury and its potential mechanisms.Methods:In vivo, adult male Bama pigs and C57BL/6J mice were used to establish a myocardial I/R injury model by ligating the left anterior descending coronary artery, with sham-operated groups set as controls. The expression of DDX21 in myocardium after I/R injury was assessed by quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescence staining. Following the establishment of the myocardial I/R injury model in mice, AAV9 vectors with cardiac-specific expression were injected in situ into the peri-infarct region (The I/R+DDX21 group, I/R+negative control (NC) group, I/R+sh-NC group and I/R+sh-DDX21 group were injected with AAV9:cTnT-DDX21, AAV9:cTnT-NC, AAV9:cTnT-sh-NC and AAV9:cTnT-sh-DDX21, respectively). Additionally, the I/R+A-485 group received intraperitoneal injections of the cAMP response element-binding protein (CREB) binding protein inhibitor A-485, while the I/R+PBS group was injected with an equivalent volume of phosphate-buffered saline (PBS) as the control. Echocardiography was performed on postoperative days 1 and 28 to evaluate cardiac function (left ventricular ejection fraction and fractional shortening). At 28 days post-surgery, mice were euthanized and heart tissues were harvested for histological sectioning. Myocardial fibrosis was evaluated using Masson′s trichrome staining. In vitro, primary cardiomyocytes were isolated from neonatal day 1 C57BL/6J mice using enzymatic digestion method. Cardiomyocytes were transfected with plasmids or small interfering RNA (siRNA). The cardiomyocytes transfected with DDX21-siRNA were assigned to the siDDX21 group, those transfected with the DDX21 plasmid were assigned to the DDX21 group, and those transfected with the corresponding empty plasmid or siRNA were assigned to the NC group. Additionally, cardiomyocytes were treated with A-485 (A-485 group) or PBS (PBS group). An oxygen-glucose deprivation/reoxygenation (OGD/R) model was used to simulate cellular injury. Transcriptome sequencing was performed to identify downstream mechanisms of DDX21. Differential gene expression analysis was conducted using software such as DESeq2, and alternative splicing events in the mRNA transcriptome were analyzed using rMATS software. Mitochondrial superoxide, mitochondrial membrane potential, ATP content, and mitochondrial respiratory chain complex enzyme activity in cardiomyocytes were detected using immunofluorescence staining and commercial assay kits. The oxidative phosphorylation level of the cells was assessed by the Seahorse extracellular flux analyzer. Acetylated DDX21 levels were measured using co-immunoprecipitation and Western blot assays.Results:The expression levels of DDX21 in myocardium from the Bama pigs and mice in the I/R injury model were significantly higher than those in the sham group (all P<0.001). Echocardiographic results showed that at 28 days post-surgery, compared to the I/R+NC group, the I/R+DDX21 group exhibited higher left ventricular ejection fraction and fractional shortening, while the I/R+sh-DDX21 group showed lower values; Masson staining results demonstrated that, compared to the I/R+NC group, the myocardial fibrosis area in the I/R+DDX21 group was significantly reduced, whereas it was significantly increased in the I/R+sh-DDX21 group (all P<0.001). Transcriptomic sequencing results suggested that DDX21 may influence myocardial injury by regulating mitochondrial metabolic activity. In vitro, compared to the OGD/R+NC group, the OGD/R+DDX21 group exhibited lower mitochondrial superoxide levels, higher polymer/monomer ratio, maximal oxygen consumption, reserve capacity, and ATP content. In contrast, the OGD/R+siDDX21 group showed the opposite results, with reduced activity of mitochondrial respiratory chain complex V (all P<0.05). Mechanistically, rMATS software and other analyses indicated that knockdown of DDX21 affected the alternative 3′ splicing sites of ATP5J precursor mRNA, inhibiting the splicing of certain exonic sequences. Overexpression of DDX21 upregulated both mRNA and protein levels of ATP5J. Co-immunoprecipitation experiments showed that, compared to the PBS group, acetylated DDX21 levels were reduced in the A-485 group. Further in vivo experiments showed that, compared to the I/R+PBS group, the I/R+A-485 group exhibited higher left ventricular ejection fraction and fractional shortening, and a lower proportion of left ventricular fibrosis (all P<0.001). Conclusions:DDX21 improves cardiomyocyte energy metabolism and alleviates I/R injury by regulating the alternative splicing of ATP5J. A-485 holds potential as a novel small molecule candidate for the treatment of myocardial injury.

Objective:To investigate the biological role and molecular mechanism of checkpoint kinase 1 (CHK1) in delaying cardiac aging in mice.Methods:In vitro, a senescence model of H9C2 cells (a cardiomyocyte line) was induced using H 2O 2. A control group (without H 2O 2 treatment) and three H 2O 2-treated groups (at concentrations of 10, 30, and 50 μmol/L) were set up. The CCK-8 assay was used to evaluate the proliferative activity of cells in each group; Western blot analysis was employed to detect the expression level of CHK1; and quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to determine the messenger RNA (mRNA) expression levels of P16 and interleukin-1β (IL-1β). In vivo, C57BL/6 wild-type mice aged 2 months ( n=15) and 24 months ( n=40), as well as myocardial-specific CHK1-overexpressing (CHK1-TG) mice aged 2 months ( n=15) and 24 months ( n=40), were selected. The mice were divided into four groups based on age and genotype: 2-month-old wild-type (WT-2M), 24-month-old wild-type (WT-24M), 2-month-old CHK1-TG (CHK1-TG-2M), and 24-month-old CHK1-TG (CHK1-TG-24M). Echocardiography was used to evaluate cardiac function of mice in the WT-24M and CHK1-TG-24M groups. Western blot analysis was conducted to measure the protein expression levels of CHK1, total Ras-related protein 1 (Rap1), NADPH oxidase 4 (Nox4), and Rap1-guanosine triphosphate (Rap1-GTP, the active form of Rap1) in the cardiac tissue of mice in each group. qRT-PCR was used to detect the messenger RNA (mRNA) expression levels of CHK1, collagen type Ⅰ (Coll1), matrix metalloproteinase-2 (Mmp2), alpha-smooth muscle actin (α-SMA), P53, P21, P16, thioredoxin 1 (Trx1), thioredoxin reductase (TrxR), glutathione recluctase (GR), Rap1, and Nox4. Immunofluorescence staining was employed to determine the protein expression levels of P53, P21, and P16, as well as the proportion of histone H2AX phosphorylation-positive cells. Dihydroethidium (DHE) staining was used to detect the relative intensity of DHE. Wheat germ agglutinin staining, HE staining, Masson staining and Sirius red staining were applied to measure the cross-sectional area of cardiomyocytes, cardiac morphology, and myocardial fibrosis area. Mice in the WT-24M and CHK1-TG-24M groups were intraperitoneally injected with the Rap1 activity inhibitor GGTI298 (25 μmol/kg). After injection, the oxidative stress damage in the cardiac tissue of the mice was detected, along with the mRNA expression levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P16, P21, and P53). Results:A concentration of 30 μmol/L was determined as the optimal concentration for establishing an H 2O 2-induced senescence model of myocardial cells in vitro. The expression level of CHK1 in H9C2 cells of the 30 μmol/L H 2O 2 group was lower than that in the control group ( P<0.05). Echocardiographic examination showed that the left ventricular ejection fraction ((61.08±1.13)% vs. (52.55±2.02)%) and fractional shortening ((31.80±1.27)% vs. (25.18±1.59)%) of mice in the CHK1-TG-24M group were higher than those in the WT-24M group (both P<0.05). qRT-PCR and Western blot analysis revealed that, compared with the WT-24M group, mice in CHK1-TG-24M group had higher expression levels of CHK1 and its mRNA, lower expression levels of Nox4 and its mRNA, and higher expression level of Rap1-guanosine triphosphate (Rap1-GTP) (all P<0.05). However, there were no statistically significant differences in the total expression level of Rap1 and its mRNA between the two groups (both P>0.05). In addition, the mRNA expression levels of Coll1, Mmp2, and α-SMA in myocardial tissue of mice in the CHK1-TG-24M group were lower than those in the WT-24M group (all P<0.05). Immunofluorescence staining results showed that the expression levels of P53, P21, and P16 proteins, as well as the proportion of phosphorylated histone H2AX-positive cells in myocardial tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). qRT-PCR further confirmed that the mRNA expression levels of the above-mentioned proteins in cardiac tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). DHE staining results indicated that the relative intensity of DHE in cardiac tissue of mice in the CHK1-TG-24M group was lower than that in the WT-24M group ( P<0.05). Meanwhile, the left ventricular internal diameter, cross-sectional area of cardiomyocytes, and myocardial fibrosis area of mice in the CHK1-TG-24M group were all smaller than those in the WT-24M group (all P<0.05). Furthermore, the degree of DNA damage in cardiac tissue as well as the mRNA levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P53, P21, P16) in mice of the WT-24M+GGTI298 group were higher than those in the WT-24M group and the CHK1-TG-24M+GGTI298 group (all P<0.05). Conclusion:CHK1 alleviates oxidative stress-induced damage in mouse cardiomyocytes by activating the Rap1/Nox4 signaling pathway, thereby delaying cardiac aging in mice.

Objective:To investigate the effect of DEAD-box helicase (DDX) 21 on myocardial ischemia-reperfusion (I/R) injury and its potential mechanisms.Methods:In vivo, adult male Bama pigs and C57BL/6J mice were used to establish a myocardial I/R injury model by ligating the left anterior descending coronary artery, with sham-operated groups set as controls. The expression of DDX21 in myocardium after I/R injury was assessed by quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescence staining. Following the establishment of the myocardial I/R injury model in mice, AAV9 vectors with cardiac-specific expression were injected in situ into the peri-infarct region (The I/R+DDX21 group, I/R+negative control (NC) group, I/R+sh-NC group and I/R+sh-DDX21 group were injected with AAV9:cTnT-DDX21, AAV9:cTnT-NC, AAV9:cTnT-sh-NC and AAV9:cTnT-sh-DDX21, respectively). Additionally, the I/R+A-485 group received intraperitoneal injections of the cAMP response element-binding protein (CREB) binding protein inhibitor A-485, while the I/R+PBS group was injected with an equivalent volume of phosphate-buffered saline (PBS) as the control. Echocardiography was performed on postoperative days 1 and 28 to evaluate cardiac function (left ventricular ejection fraction and fractional shortening). At 28 days post-surgery, mice were euthanized and heart tissues were harvested for histological sectioning. Myocardial fibrosis was evaluated using Masson′s trichrome staining. In vitro, primary cardiomyocytes were isolated from neonatal day 1 C57BL/6J mice using enzymatic digestion method. Cardiomyocytes were transfected with plasmids or small interfering RNA (siRNA). The cardiomyocytes transfected with DDX21-siRNA were assigned to the siDDX21 group, those transfected with the DDX21 plasmid were assigned to the DDX21 group, and those transfected with the corresponding empty plasmid or siRNA were assigned to the NC group. Additionally, cardiomyocytes were treated with A-485 (A-485 group) or PBS (PBS group). An oxygen-glucose deprivation/reoxygenation (OGD/R) model was used to simulate cellular injury. Transcriptome sequencing was performed to identify downstream mechanisms of DDX21. Differential gene expression analysis was conducted using software such as DESeq2, and alternative splicing events in the mRNA transcriptome were analyzed using rMATS software. Mitochondrial superoxide, mitochondrial membrane potential, ATP content, and mitochondrial respiratory chain complex enzyme activity in cardiomyocytes were detected using immunofluorescence staining and commercial assay kits. The oxidative phosphorylation level of the cells was assessed by the Seahorse extracellular flux analyzer. Acetylated DDX21 levels were measured using co-immunoprecipitation and Western blot assays.Results:The expression levels of DDX21 in myocardium from the Bama pigs and mice in the I/R injury model were significantly higher than those in the sham group (all P<0.001). Echocardiographic results showed that at 28 days post-surgery, compared to the I/R+NC group, the I/R+DDX21 group exhibited higher left ventricular ejection fraction and fractional shortening, while the I/R+sh-DDX21 group showed lower values; Masson staining results demonstrated that, compared to the I/R+NC group, the myocardial fibrosis area in the I/R+DDX21 group was significantly reduced, whereas it was significantly increased in the I/R+sh-DDX21 group (all P<0.001). Transcriptomic sequencing results suggested that DDX21 may influence myocardial injury by regulating mitochondrial metabolic activity. In vitro, compared to the OGD/R+NC group, the OGD/R+DDX21 group exhibited lower mitochondrial superoxide levels, higher polymer/monomer ratio, maximal oxygen consumption, reserve capacity, and ATP content. In contrast, the OGD/R+siDDX21 group showed the opposite results, with reduced activity of mitochondrial respiratory chain complex V (all P<0.05). Mechanistically, rMATS software and other analyses indicated that knockdown of DDX21 affected the alternative 3′ splicing sites of ATP5J precursor mRNA, inhibiting the splicing of certain exonic sequences. Overexpression of DDX21 upregulated both mRNA and protein levels of ATP5J. Co-immunoprecipitation experiments showed that, compared to the PBS group, acetylated DDX21 levels were reduced in the A-485 group. Further in vivo experiments showed that, compared to the I/R+PBS group, the I/R+A-485 group exhibited higher left ventricular ejection fraction and fractional shortening, and a lower proportion of left ventricular fibrosis (all P<0.001). Conclusions:DDX21 improves cardiomyocyte energy metabolism and alleviates I/R injury by regulating the alternative splicing of ATP5J. A-485 holds potential as a novel small molecule candidate for the treatment of myocardial injury.

Objective:To investigate the biological role and molecular mechanism of checkpoint kinase 1 (CHK1) in delaying cardiac aging in mice.Methods:In vitro, a senescence model of H9C2 cells (a cardiomyocyte line) was induced using H 2O 2. A control group (without H 2O 2 treatment) and three H 2O 2-treated groups (at concentrations of 10, 30, and 50 μmol/L) were set up. The CCK-8 assay was used to evaluate the proliferative activity of cells in each group; Western blot analysis was employed to detect the expression level of CHK1; and quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to determine the messenger RNA (mRNA) expression levels of P16 and interleukin-1β (IL-1β). In vivo, C57BL/6 wild-type mice aged 2 months ( n=15) and 24 months ( n=40), as well as myocardial-specific CHK1-overexpressing (CHK1-TG) mice aged 2 months ( n=15) and 24 months ( n=40), were selected. The mice were divided into four groups based on age and genotype: 2-month-old wild-type (WT-2M), 24-month-old wild-type (WT-24M), 2-month-old CHK1-TG (CHK1-TG-2M), and 24-month-old CHK1-TG (CHK1-TG-24M). Echocardiography was used to evaluate cardiac function of mice in the WT-24M and CHK1-TG-24M groups. Western blot analysis was conducted to measure the protein expression levels of CHK1, total Ras-related protein 1 (Rap1), NADPH oxidase 4 (Nox4), and Rap1-guanosine triphosphate (Rap1-GTP, the active form of Rap1) in the cardiac tissue of mice in each group. qRT-PCR was used to detect the messenger RNA (mRNA) expression levels of CHK1, collagen type Ⅰ (Coll1), matrix metalloproteinase-2 (Mmp2), alpha-smooth muscle actin (α-SMA), P53, P21, P16, thioredoxin 1 (Trx1), thioredoxin reductase (TrxR), glutathione recluctase (GR), Rap1, and Nox4. Immunofluorescence staining was employed to determine the protein expression levels of P53, P21, and P16, as well as the proportion of histone H2AX phosphorylation-positive cells. Dihydroethidium (DHE) staining was used to detect the relative intensity of DHE. Wheat germ agglutinin staining, HE staining, Masson staining and Sirius red staining were applied to measure the cross-sectional area of cardiomyocytes, cardiac morphology, and myocardial fibrosis area. Mice in the WT-24M and CHK1-TG-24M groups were intraperitoneally injected with the Rap1 activity inhibitor GGTI298 (25 μmol/kg). After injection, the oxidative stress damage in the cardiac tissue of the mice was detected, along with the mRNA expression levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P16, P21, and P53). Results:A concentration of 30 μmol/L was determined as the optimal concentration for establishing an H 2O 2-induced senescence model of myocardial cells in vitro. The expression level of CHK1 in H9C2 cells of the 30 μmol/L H 2O 2 group was lower than that in the control group ( P<0.05). Echocardiographic examination showed that the left ventricular ejection fraction ((61.08±1.13)% vs. (52.55±2.02)%) and fractional shortening ((31.80±1.27)% vs. (25.18±1.59)%) of mice in the CHK1-TG-24M group were higher than those in the WT-24M group (both P<0.05). qRT-PCR and Western blot analysis revealed that, compared with the WT-24M group, mice in CHK1-TG-24M group had higher expression levels of CHK1 and its mRNA, lower expression levels of Nox4 and its mRNA, and higher expression level of Rap1-guanosine triphosphate (Rap1-GTP) (all P<0.05). However, there were no statistically significant differences in the total expression level of Rap1 and its mRNA between the two groups (both P>0.05). In addition, the mRNA expression levels of Coll1, Mmp2, and α-SMA in myocardial tissue of mice in the CHK1-TG-24M group were lower than those in the WT-24M group (all P<0.05). Immunofluorescence staining results showed that the expression levels of P53, P21, and P16 proteins, as well as the proportion of phosphorylated histone H2AX-positive cells in myocardial tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). qRT-PCR further confirmed that the mRNA expression levels of the above-mentioned proteins in cardiac tissue of mice in the WT-24M group were higher than those in the CHK1-TG-24M group (all P<0.05). DHE staining results indicated that the relative intensity of DHE in cardiac tissue of mice in the CHK1-TG-24M group was lower than that in the WT-24M group ( P<0.05). Meanwhile, the left ventricular internal diameter, cross-sectional area of cardiomyocytes, and myocardial fibrosis area of mice in the CHK1-TG-24M group were all smaller than those in the WT-24M group (all P<0.05). Furthermore, the degree of DNA damage in cardiac tissue as well as the mRNA levels of fibrosis-related indicators (Coll1, Mmp2, and α-SMA) and cell cycle inhibitory proteins (P53, P21, P16) in mice of the WT-24M+GGTI298 group were higher than those in the WT-24M group and the CHK1-TG-24M+GGTI298 group (all P<0.05). Conclusion:CHK1 alleviates oxidative stress-induced damage in mouse cardiomyocytes by activating the Rap1/Nox4 signaling pathway, thereby delaying cardiac aging in mice.

Objective:To investigate the preventive effects of intravenous N-acetylcysteine(NAC)administration on contrast-induced nephropathy(CIN)following coronary intervention in elder patients with coronary heart disease(CHD)complicated with moderate to severe renal dysfunction.Methods:In this retrospective study, 242 elderly patients with CHD and moderate to severe renal insufficiency hospitalized in the Department of Cardiology of the First Affiliated Hospital of Nanjing Medical University and undergone coronary angiography from January 2018 to February 2022 were included and divided into two groups: the treatment group(100 cases)receiving NAC plus a continuous intravenous drip of 0.9% sodium chloride solution before and after surgery and the control group(142 cases)treated with only a continuous intravenous drip of 0.9% sodium chloride solution.To ensure the comparability of important baseline data between the two groups, a 1∶1 propensity score matching analysis was used, and 70 patients in each group were finally included.Pre-and post-operative serum creatinine(Scr)and blood urea nitrogen(BUN)values were recorded, the endogenous creatinine clearance(Ccr)and estimated glomerular filtration rate(eGFR)were calculated, and the incidences of CIN and changes in renal function indicators were compared between the two groups.Results:After coronary intervention, the incidence of CIN in the treatment group was significantly lower than that in the control group(1/70 or 1.4% vs.8/70 or 11.4%, P=0.033). In the treatment group, Scr[(186.01±36.62)μmol/L vs.(195.84±36.39)μmol/L, t=4.957, P<0.001]and BUN[(13.97±2.89)mmol/L vs.(14.84±2.85)mmol/L, t=5.206, P<0.001]decreased, while Ccr[(31.84±6.54)ml/min vs.(30.08±5.65)ml/min, t=-5.076, P<0.001]and eGFR[(31.60±6.93)ml·min -1·1.73m -2vs.(29.82±5.92)ml·min -1·1.73m -2, t=-5.200, P<0.001]increased, compared with pre-operative levels.In the control group, Scr[(186.65±27.28)μmol/L vs.(182.53±22.08)μmol/L, t=-1.783, P=0.079]and BUN[(17.57±3.33)mmol/L vs.(17.13±3.35)mmol/L, t=-2.234, P=0.029]increased, but Ccr[(30.57±6.37)ml/min vs.(31.06±6.01)ml/min, t=1.435, P=0.156]and eGFR[(30.76±6.46)ml·min -1·1.73m -2vs.(31.26±6.02)ml·min -1·1.73m -2, t=1.436, P=0.156]decreased, compared with pre-operative levels, and there was no significant difference except BUN(all P>0.05). Conclusions:For elderly patients with coronary heart disease complicated with moderate to severe renal insufficiency, the use of NAC before and after coronary intervention can reduce the risk of CIN and help improve renal function.

Abstract Peer victimization is a negative peer relationship in peer communication. Research has shown that peer victimization has an important influence on physical and mental development in children and adolescents. Quantitative research methods combined with longitudinal tracking have been used to investigate children and adolescents, with a focus on special population and young Internet users. Personality characteristics, peer relationships, teacher student relationships and other factors are the main factors affecting peer victimization, which are accompanied by behavioral and emotional problems, and the construction of self concept. The negative influence has been studied in China and abroad to facilitate interventions preventing peer infringement. Research methodology should be enriched, and more in depth interventions and network peer infringement should be conducted.

Objective:To evaluate the feasibility, safety and efficacy of the magnetic resonance imaging guided focused ultrasound surgery (MRgFUS) in the treatment of localized prostate cancer (PCa).Methods:The data of 5 patients treated by MRgFUS from August 2020 to June 2021 in our institution were retrospectively analyzed. The median age was 73 (58-80) years, with the median PSA of 7.34 (5.19-8.40) ng/ml, and a median prostate volume of 27.96 (21.50-37.91) ml. The median pretreatment international prostate symptom score (IPSS) was 13(0-18). Of the 3 patients with intention of erectile function preservation, the pretreatment international index of erectile function-15 (IIEF-15) score was 12, 23 and 3, respectively. All patients had histopathology-proven PCa of grade group ≤ International Society of Urological Pathology (ISUP) 3, pre-operative PSA level <20 ng/ml, and a clinical stage ≤T 2b. A total of 6 lesions was confirmed by biopsy, with 3 of ISUP grade group 3 and 3 of ISUP grade group 1. All 5 patients underwent MRgFUS which was guided by a real-time magnetic resonance imaging (MRI). PSA, MRI and repeated biopsy were conducted to monitor recurrence. Questionnaires consisted of IPSS, IIEF-15, and the International Consultation on Incontinence-questionnaire-Short Form (ICI-Q-SF) were recorded before and after MRgFUS to evaluate the impact on functional preservation. Results:A total of 5 patients received MRgFUS. In total, 5 of the 6 lesions were treated. 1 lesion unvisible on MRI was not clinically significant and was left untreated. The median time in MRI scanner was 190 (140-355) min, and the median sonication time was 64 (35-148) min with the median sonications of 8 (5-13). The median catheter indwelling time was 1 (1-8) days. No other adverse effects were reported. The PSA level of all 5 patients decreased, with the nadir PSA of 1.196 ng/ml, 4.398 ng/ml, 4.135 ng/ml, 1.562ng/ml and 1.350ng/ml, respectively. 4 of the patients had a PSA decrease over 50%. No PCa lesion was seen on MRI at 3-month follow-up visit. As for functional preservation, the post-MRgFUS IPSS declined compared with the baseline score, and the IPSS of last follow-up was 5(0-14). Of the 3 patients with intention to preserve the erectile function, the erectile function score of IIEF-15 were 12, 30 and 9 three months after the treatment, respectively. No incontinence occurred postoperatively.Conclusions:MRgFUS is a feasible and safe way for the treatment of low- to intermediate-risk localized PCa, with satisfactory performance on functional preservation and low incidence of complications. The oncological outcomes still need to be establised with longer follow-up time and larger sample studies.

Objective To investigate the status of empowerment and medical support in patients with type 2 diabetes mellitus,and to explore the relationship between empowerment and medical support.Methods A multi-centered collaboration and cross-sectional survey was used in this study.With the method of simple random sampling,1512 patients with type 2 diabetes mellitus from 18 tertiary hospitals in Hunan Province were investigated from January 2016 to April 2016.General information,empowerment and medical support were investigated using general information questionnaire,Diabetes Empowerment Scale-DAWN Short Form,Patient Assessment of Chronic Illness Care DAWN Short Form.Results The mean score of empowerment ability for patients with type 2 diabetes mellitus was (53.20±16.40).The mean score of medical support for patients with type 2 diabetes mellitus was (34.56±11.64).There was positive correlation between the empowerment ability and medical support in patients with type 2 diabetes mellitus.Conclusion There is positive correlation between empowerment and medical support in patients with type 2 diabetes mellitus.But the received medical support is not enough.It is necessary to increase the supply of medical support to promote the empowerment of patients with type 2 diabetes.

Objective To investigate the feasibility and clinical results under laparoscopic resection of colorectal cancer.Methods Clinical data of 17 colorectal cancer patients with laparoscopic resection from October 2009 to September 2011 were analyzed.Results There were 16 cases of successful completion of laparoscopic surgery,conversion to open surgery in 1 case.Postoperative of incomplete intestinal obstruction and rectal vaginal fistula are each 1 case.Oncology did not occur metastasis through puncture holes in postoperative follow-up up to 2 years.Conclusion Laparoscopic resection of colorectal cancer should be widely applied,and it had more advantages such as less trauma,safety,recover quickly,consistent with the effect of laparotomy.

Objective To observe the expressions of serum insulin-like growth factor (IGF)- Ⅰ ,Ⅱ and IGF binding protein (IGFBP) 3, 5 and to explore the clinical significances in patients with clear cell carcinoma of kidney. Methods Enzyme-linked immunosorbent assay (ELISA) methods were adopted to examine serum expressions of IGF-Ⅰ , Ⅱ and IGFBP 3, 5 in 40 cases with clear cell carcinoma of kidney (renal carcinoma group) and 16 cases with hydronephrosis (control group) from May 2007 to December 2009. Results IGF- Ⅰ , Ⅱ and IGFBP 3,5 in renal carcinoma showed higher expressions before operation (985. 7 μg/L, 1154.0 μg/L,46.6 μg/L and 9.6 μg/L, respectively)than after operation (431.4 μg/L, 632.6 μg/L, 26.7 μg/L, and 6.7 μg/L, respectively, all P＜0. 05 ～0.01). There were no significant differences in those indexes between pre- and post- operation in control group (P＞ 0. 05). Conclusions There are high expressions of serum IGF-Ⅰ , Ⅱ and IGFBP 3, 5 in renal carcinoma patients, and IGF- Ⅱ has clinical significance in diagnosis.