Objective: To investigate the awareness of and participation in Healthy City construction among residents in Hangzhou City, so as to provide insights into promotion of participation in Healthy City construction. Methods: Residents at ages of 15 to 75 years were sampled using the multi-stage stratified random sampling method, from 30 townships in Jianggan, Xiaoshan and Tonglu counties of Hangzhou City from November 2019 to July 2020, and a questionnaire survey of 10 representative projects pertaining to Healthy City construction in Hangzhou City was performed to investigate the awareness of and participation in Healthy City construction. Results: A total of 5 559 questionnaires were allocated, and 5 211 valid questionnaires were recovered, with an effective recovery rate of 93.74%. The respondents had a mean age of ( 43.82±17.25 ) years, and included 2 280 males ( 43.75% ) and 2 931 females ( 56.25% ). The overall standardized awareness and participation rates of Healthy City construction were 81.73% and 48.58% among the respondents. The projects with the three highest awareness included healthy environment improvements ( 92.67% ), travelling by public transportation ( 92.22% ) and tobacco control action ( 91.04% ), while the projects with the three lowest awareness included chronic disease management ( 75.57% ), maternal and child healthcare ( 72.73% ) and “Healthy Cell” Program ( 45.56% ). The projects with the three highest participation rates included travelling by public transportation ( 74.59% ), healthy environment improvements ( 65.17% ), tobacco control action ( 61.52% ), while the projects with the three lowest participation rate included chronic disease management ( 35.92% ), “Healthy Cell” Program ( 34.96% ) and maternal and child healthcare ( 33.20% ). Conclusions The overall proportion of participation in Healthy City construction is low among residents in Hangzhou City, and notably, the awareness rate of and the proportion of participation in chronic disease management, maternal and child healthcare and “Healthy cell” Program are both low.

Objective To observe the effect of RNAi targeting Livin gene on biology characteristics such as apoptosis and proliferation in human prostate cancer cells.Methods siRNA expression vector targeting Livin gene was constructed and transfected into human prostate cancer cell line PC3.The expressions of Livin mRNA and protein were detected by real-time PCR and Western-blot,cell apoptosis and cell cycle were assayed by flow cytometry,proliferation and colony formation were detected by MTT and colony formation assay,and the tumor growth in vivo was observed in nude mice.Results After transfection,downregulation of Livin mRNA and protein expression in PC3 cells was observed (P＜0.01).Compared with the control group,the proliferation of cancer cells was inhibited significantly (P＜0.01) and the apoptotic ratio was (26.5±3.3) ％ (P＜0.01).The Caspase3 activity increased obviously (P＜0.05),and the experimental group showed a decreased colony formation rate (P＜0.01).The tumor volume of xenografts in nude mouse in experimental and control group was (1.79± 0.07) and (4.40 ± 0.06) cm3 respectively (P ＜ 0.01).Conclusions The siRNA recombinant expression vector targeting Livin gene was constructed and can knockdown the expression of Livin mRNA and protein.It can inhibit PC3 cell proliferation,induce apoptosis and inhibit tumor growth in vivo.

Objective To investigate mobilization of the bone-marrow-derived stem cell (BMSC) into peripheral blood by granulocyte-colony stimulating factor (G-CSF) to accelerate the renal regeneration.Methods Six-week-old transgenic C57BL/6J mice labeled with green fluorescent protein (GFP) as bone marrow donors and C57BL/6 mice without fluorescence label as recipients ( n =20 ) of bone marrow transplantation were used.All recipients received lethal dose of 8.5 Gy total body γ-ray irradiation with 137 Cs before bone marrow transplantation,and the transplantation of bone marrow mononuclear cells 2 × 105 by retrobulbar injection was done two hours later after irradiation. Bone marrow reconstruction after transplantation was proved by flow cytometry five weeks after transplantation.Six weeks after the bone marrow reconstruction completed,left renal pedicles of all mice were cross-clasped for 30 minutes followed by reperfusion to establish the animal model of ischemia-reperfusion injury.Mice were divided into two groups:( 1 ) Saline control group ( n =10),saline 0.2 ml/day was injected subcutaneously into chimeric mice from 3 days before to 4 days after operation ; (2) G-CSF mobilization group (n =10),chimeric mice were injected subcutanously with recombinant human G-CSF,200μg/kg/day,once a day from three days before surgery for a week.On the 1st day after mobilization,the percentage of stem cell in non-erythroid cells of peripheral blood was detected by using flow cytometry.One week after ischemia,the homing of BMSC to kidney was identified by flow cytometory.Renal tissue sections were stained with Hemotoxylin and Eosin staining method for pathological study,and the degree of renal tubular injury was analyzed by semiquantitative method of Vyacheslav.Four weeks after ischemia,the differences in degree of renal regeneration between the two groups by analysis the numbers of vascular endothelial cells in the kidney.Results After G-CSF mobilization,the percentage of stem cells with Sca-1 +,c-Kit +,CD29 and CD34 + antigen in peripheral blood in G-CSF mobilization group were higher than those in control group.One week after ischemia,mice of mobilization group showed higher percentage of Sca-1 +,c-Kit + and CD34 + bone marrow derived stem cells in tbe kidney compared to control group (P ＜0.05).One week after ischemia,the tubular epithelial damage score of mobilization group was lower significantly than that of the control group (P ＜ 0.05 ) studied by Hemotoxylin and Eosin staining. Four weeks after ischemia,mice of G-CSF mobilization group showed more CD31 positive cells in the kidney compared to control group (P ＜ 0.05 ).Conclusions G-CSF can effectively mediate the mobilization of bone marrow derived stem cells to peripheral blood and homing to kidney.G-CSF mobilization can accelerate renal regeneration and alleviate the degree of renal histopathological changes after ischemia.

Objective To investigate the effects of hypoxia-inducible factor-1α (HIF-1α)expression on pathogenesis of retinopathy of prematurity (ROP) and to find new target for gene therapy.Methods After liposome-mediated small interference RNA (siRNA) transfection into rat retinal endothelial cells,the cells were cultured in medium with CoCl2-induced hypoxic condition.Expression of HIF-1α mRNA was determined by fluorenscence quantitative reverse transcription-polymerase chain reaction(RT-PCR),HIF-1α protein expression was detected by Western Blot after cocultured for 8 hours.Cell proliferation was measured with 3-(4,5)-dimethylthiazol (-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay after cocultured for 24 hours.Difference between groups was compared with independent samples t test.Results Rat retinal vascular endothelial cells were successfully transfected with siRNA.Fluorescence quantitative RT-PCR results showed that at 48 hours of transfection,the expression of HIF-1α mRNA in the interference group of siRNA1,siRNA2 and siRNA4 were 0.1620 ± 0.0147,0.2034 ± 0.0251 and 0.3049 ± 0.0165,which were 16.20％,20.34 ％ and 30.49％ of blank control group (1.0000±0.0344),and were lower than that of negative control group (0.8334±0.0242) (t=16.786,8.953 and 4.087,P＜0.05 respectively).Western Blot results showed that HIF-1α protein expression was significantly inhibited by siRNA1(0.4956 ± 0.0421 ) and siRNA2 (0.6544 ± 1.0032) comparing with blank control group (3.5105 ±0.4084) and negative control group (3.4019 ± 1.0677) (t =6.861,2.893,4.567 and 5.072,P＜0.05 respectively).As for cellular proliferation activity,(49.5±2.9) ％ and (67.4±1.2) ％ of cells growth inhibition were observed after transfection with siRNA1 and siRNA2,which were higher than those of negative control group [(15.7±1.5) ％ ] (t=2.786 and 6.904,P＜0.05).Conclusions The synthetic HIF-1α siRNA could effectively inhibit the expression of HIF-1α gene and reduce cell proliferation in rat retinal endothelial cells under hypoxic condition.RNA interference technology targeting HIF-1α might become a new strategy for gene therapy of ROP.

Objective To discuss the significance of near infrared spectroscopy (NIRS) in evaluation of intrapartum hypoxic-ischemic cerebral injury, and to provide a method to evaluate neonatal brain damage objectively and quantitatively. Methods A total of 63 neonates with fetal distress were divided into hypoxic-ischemic encephalopathy(HIE) group and non-HIE group. Thirtyfive newborns with no fetal distress were chosen as controls. Using NIRS, the brain regional oxygen saturation(rSO2) in these neonates were measured. Evaluation of brain rSO2 in the diagnosis of HIE was analyzed with receiver operating characteristic (ROC) curve. Results At the time of fetal head visible on vulval gapping and 5 min after birth, the HIE group showed decreased brain rSO2[(36. 6±5.0)% and (52. 0±4. 2)%], comparing with control group[(45. 9±4. 6)% and (59. 6±4. 4)%]and non-HIE group[(44.1±3.1) % and (57. 6±3. 5) %](P<0. 01) . The brain rSO2 was positively correlated with the pH and oxygen saturation of umbilical artery blood in all groups (P<0. 01). When the cut-off value of brain rSO2 was <39. 5% at fetal head visible on vulval gapping, the sensitivity and specificity of assessing HIE were 67% and 93%, respectively, while 70% and 86% when the cut-off value was <53. 5% at 5 min after birth. Conclusions The brain rSO2 obtained by NIRS could be used to evaluate brain oxygenation, and may be useful in predicting HIE in neonates with fetal distress.

Objective To investigate the roles of microRNA-382 (miR-382) in the pathogenesis of renal tubulointerstitial fibrosis (TIF).Methods Human kidney epithelial cells (HK2)transfected with miR-382 inhibitor (antagomiR-382) were used to examine the effect of miR-382 abundance on cell polarity,as well as to test the complementary relationship between miR-382 and its predicted target gene heat shock protein 60 (HSPD1),which was further verified by 3'-untranslated region luciferase assay and site-directed mutagenesis.The role of miR-382 played in the development of renal interstitial fibrosis and redox regulation was examined in a mouse unilateral ureteral obstruction (UUO) model.Locked nucleic acid (LAN)-modified anti-miR-382 was intravenous delivered via tail vein 30 min prior to UUO,and repeated the dosage 24 h after the surgery.For clinical verification,renal biopsy specimens from 12 IgA nephropathy (IgAN) patients were collected,6 patients with moderate to severe TIF and 6 patients without TIF.The relative abundance of miR-382 and HSPD1 protein was analyzed by using in situ hybridization and immunohistochemistry.Results HSPD1 was confirmed to be a new,direct target gene of miR-382 by in vitro 3'-untranslated region luciferase assay and sitedirected mutagenesis.The development of epithelial transition in HK2 cells was accompanied with upregulation of miR-382 [(6.54±0.96) vs (1.12±0.26),P ＜ 0.05].Blocking the expression of miR-382 could reversed the progression of epithelial transition partially.In UUO mice the abundance of miR-382 was up-regulated [(6.89 ± 2.47) vs (1.00±0.42),P ＜ 0.01] while HSPD1 and Trx were downregulated compared with the sham group.Down-regulation of miR-382 was associated with significant decrease in TIF,but increase in HSPD1 and thioredoxin protein compared with UUO group [HSPD1:(0.34±0.10) vs (0.14±0.05);Trx:(0.79±0.18) vs (0.36±0.16);all P ＜ 0.05].The expression of miR-382 was up-regulated and HSPD1 was significantly down-regulated in IgAN patients with TIF.Conclusions miR-382 play an important role in renal tubulointerstitial fibrosis in human and mice.HSPD1 is one of the target genes of miR-382.The down-regulation of HSPD1 and the decrease ability of anti-oxidative stress may be the important mechanism of miR-382 involved in renal tubulointerstitial fibrosis.

Objective To explore the early predictive factors of intestinal necrosis in patients with acute superior mesenteric arterial occlusive disease and its significance for the decision of exploratory laparotomy.Methods This retrospective study enrolled 29 patients diagnosed with acute superior mesenteric artery embolism or thrombosis in Peking University People's Hospital between July 1995 and June 2015.Results 12 patients developed intestinal necrosis.Patients with intestinal necrosis had a poorer prognosis than those who did not develop intestinal necrosis (x2 =14.867,P =0.000).In univariate analysis,the early predictive factors for intestinal necrosis were D-Dimer ≥ 600 μg/L (x2 =11.455,P =0.002),INR≥1.2 (x2 =3.948,P =0.047),pH values ＜7.4 (x2 =8.191,P =0.004),BE ＜ -1.0 mmol/L (x2 =8.191,P =0.004),blood lactate ≥ 2.2 mmol/L(x2 =7.535,P =0.006),BUN ≥ 6 mmol/L (x2 =10.076,P =0.002),CK ≥ 80 U/L (x2 =8.191,P =0.004),LDH ≥ 210 U/L (x2 =13.079,P=0.000),AST ≥25 U/L (x2 =10.076,P =0.002),SIRS (x2 =10.076,P =0.002).Multivariate logistic regression analysis found no independent predictive factors of intestinal necrosis in patients with acute superior mesenteric arterial occlusive diseases.Conclusion Intestinal necrosis in acute mesenteric arterial occlusive diseases indicates a poor prognosis.Coagulation abnormalities,liver or kidney dysfunction,metabolic acidosis and SIRS necessitates an immediate exploration.

Objective ToexplorethevalueofCTtargetreconstructionforpureground-glassnodules(pGGN)onidentifyingthe invasivenessofthelungadenocarcinoma.Methods ThepGGNs weredividedintopre-invasivegroup[atypicaladenomatoushyperplasia (AAH),andadenocarcinomainsitu(AIS)]andinvasivegroup[minimallyinvasiveadenocarcinoma(MIA),andinvasiveadenocarcinomas(IA)] accordingtothepathologicresults.ThemorphologicfeaturesofpGGNonCTincludedthelargestdiameters,CTvalue,pleuralindentation,air bronchogram,bubblelucency,vesselconvergence,vesseldilatation,lobulationandspeculation.Twodiagnosticiansevaluatedthemorphologic featuresofpGGNonCT.Binary L o g istic regressionwasusedtoassesstheassociationbetweenCTfindingsandhistopathological classification.ROCcurveanalysiswasusedindiameterandCTvalue.Results Betweenpre-invasiveandinvasivegroup,therewere significantdifferencesindiameter,CTvalue,spiculationandvesseldilatation(P<0.05).Nodifferencewasfoundinlobulated-margin,bubble lucency,airbronchogram,vascularconvergenceorpleuralindentationbetweenthetwogroups(P>0.05).Thediagnosticthresholds forpredictingpGGOinfiltrationwere8.75mminmaximumdiameterand-605HUinCTvaluerespectively.Conclusion ThepGGNwitha diametermorethan87.5mm,theCTvaluemorethan-605HU,andpresencesofspiculationandvesseldilatationsuggeststhatpGGOisinvasive.

Bladder cancer is one of the most common tumors of the urinary system. More than a quarter of the new bladder cancer cases in China are muscle invasive bladder cancer. The standard treatment of muscle invasive bladder cancer is radical cystectomy plus pelvic lymph node dissection. This operation has limitations such as large trauma, high postoperative complication rate and serious impact on the quality of life of patients. To control the condition of bladder cancer and improve the quality of life of patients, a comprehensive treatment and follow-up system after bladder sparing are being explored. In addition to the classic trimodal treatment which is consisted of "maximum transurethral resection of the tumor, chemotherapy and external radiotherapy" , the treating modes of single drug, multi-drug or combined chemotherapy/radiotherapy based on immune checkpoint inhibitors are in their heyday. Meanwhile, antibody-drug conjugates have been in the ascendant. The purpose of this article is to review the current situation of bladder sparing therapy for muscle invasive bladder cancer and look forward to the development direction of bladder sparing therapy in the current era of oncoimmunology.

OBJECTIVE: To explore the predictive value of overall longitudinal strain for the development of cardiomyopathy without hypertrophic changes. METHODS: Sixty five patients with suspected hypertrophic cardiomyopathy (HCM) but without hypertrophic changes were selected. Genetic variant, overall longitudinal strain, left ventricular ejection fraction, end diastolic volume, end systolic volume, interventricular septal thickness, left ventricular diameter and end diastolic diameter were detected. The risk factors of HCM were analyzed. RESULTS: Forty four variants of 16 genes were identified, among which MYBPC3 13659G>A was the commonest (73.20%) and MYH7 13252C>T was the second (31.25%). MYBPC3 GG genotype, overall longitudinal strain and apical longitudinal strain were correlated with HCM (P<0.05). CONCLUSION The increase of longitudinal strain is of great value in predicting the occurrence of HCM.