Surveillance of viral aetiology in children with influenza-like illness during 2015 to 2018 / 中华传染病杂志

Objective:To monitor the epidemiological characteristics of viral etiology in children with influenza-like illness and to guide the prevention and management of acute respiratory tract infections in childhood.Methods:Nasopharyngeal swabs were collected from the outpatient children seeking medical care in Children′s Hospital of Fudan University, Shanghai for influenza-like illness between January 2015 and December 2018. Multiplex real-time polymerase chain reaction was performed to detect respiratory syncytial virus (RSV), influenza virus (Flu), adenovirus (ADV), parainfluenza virus (PIV, type Ⅰ to type Ⅳ) and enterovirus (EV), and the epidemiological data were analyzed. Chi-square test was used for statistical analysis.Results:A total of 2 271 patients with influenza-like illness were enrolled, age range from two months to 182 months old, 1 280 cases(56.4%) were positive for the target respiratory viruses tested on respiratory samples. The detection rates of FluA, FluB, PIV, EV, ADV, RSV were 15.1%(343/2 271), 12.5%(284/2 271), 8.4%(191/2 271), 7.8%(177/2 271), 5.1%(116/2 271) and 6.7%(152/2 271), respectively.The detection rates of influenza virus were statistically different among the age groups ( χ2=39.33, P<0.05), which showed an increasing trend with the increasing ages. The detection rate of RSV was 9.7%(35/361) in infant group from zero to 12 months old, which was higher than other age groups. Usually, FluA had two epidemic peaks during the winter and summer seasons, the epidemics of FluB and RSV peaked during the winter season, and EV and PIV were more prevalent in the summer season. Conclusions:Influenza virus remains the most common viral pathogen responsible for childhood influenza-like illness in Shanghai.Influenza virus has high incidence in winter.Widely influenza vaccination is highly recommended for the effective prevention the influenza outbreaks.Continuous monitoring the epidemic trend of viral respiratory infections is imperative for the prevention and control of diseases.

Effects of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction / 中华老年医学杂志

Objective@#To explore the effect and mechanism of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction.@*Methods@#The acute myocardial infarction (AMI) rat model was established by ligating anterior descending branch of coronary artery for one week.A total of 60 adult male rats in SPF grade with AMI were randomized into the Sacubitril/Valsartan group and the model group, who were gavaged with Sacubitril/Valsartan (68 mg/kg, once daily, n=30) versus with normal saline once daily(n=30) for 4 weeks.Twenty-four hours after the last treatment, the left ventricular cardiac function was examined by echocardiography, and pathological changes of the left ventricle were observed under light microscope.The degree of myocardial fibrosis was quantitatively analyzed by picric acid-sirius scarlet staining.Myocardial cells and fibroblasts from rat pups of the same species were prepared in vitro and were divided into the control group, AngⅡ group, LBQ657 group, valsartan group and LCZ696 group.3[H]-leucine incorporation and 3[H]-proline incorporation were used to detect the myocardial hypertrophy and fibrosis.@*Results@#There was no significant difference in left ventricular function between the the model group and the Sacubitril/Valsartan group before medication (P>0.05). Four weeks after administration of the medications, end-diastolic diameter of left ventricle and end-systolic volume of left ventricle were lower [(9.73±0.26) mm vs.(10.52±0.21) mm, P<0.05; (0.19±0.03) ml vs.( 0.31±0.02) ml, P<0.01], and the left ventricular ejection fraction was higher [(60.17±2.18)% vs.(47.16±5.14)%, P<0.01] in the Sacubitril/Valsartan group than in the model group.The degree of myocardial cell injury in the infarct area was lower, and the area of myocardial fibrosis in the non-infarct zone and peripheral infarcted zone were less in the Sacubitril/Valsartan group than in the model group [(4.0±0.1)% vs. (6.1±0.8)%, P<0.001; (15.7±0.8)% vs. (23.8±1.2)%, P<0.001].3[H]-proline incorporation in cardiac fibroblasts was lower in the Valsartan group than in the Ang Ⅱ group [(152.77±8.46) CPM vs.(221.87±13.41) CPM, P<0.01].3[H]-leucine incorporation in myocardial cells was lower in the Valsartan group than in the Ang Ⅱ group [(113.47±2.33) CPM vs.(127.65±2.38) CPM, P<0.01].3[H]-leucine incorporation in myocardial cells was lower in LBQ657 group than in the Ang Ⅱ group [(119.78±2.98) CPM vs.(127.65±2.38) CPM, P<0.05], and the combined application of valsartan and LBQ657 can further reduce myocardial hypertrophy and fibrosis (P<0.05).@*Conclusions@#Sacubitril/Valsartan can effectively alleviate myocardial remodeling and cardiac dysfunction after myocardial infarction, and the mechanism may be related to reducing AngⅡ-induced myocardial hypertrophy and myocardial fibrosis.

Effects of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction / 中华老年医学杂志

Objective To explore the effect and mechanism of Sacubitril/Valsartan on myocardial remodeling and cardiac function in rats with myocardial infarction.Methods The acute myocardial infarction (AMI) rat model was established by ligating anterior descending branch of coronary artery for one week.A total of 60 adult male rats in SPF grade with AMI were randomized into the Sacubitril/Valsartan group and the model group,who were gavaged with Sacubitril/Valsartan (68 mg/kg,once daily,n=30) versus with normal saline once daily(n=30) for 4 weeks.Twenty-four hours after the last treatment,the left ventricular cardiac function was examined by echocardiography,and pathological changes of the left ventricle were observed under light microscope.The degree of myocardial fibrosis was quantitatively analyzed by picric acid-sirius scarlet staining.Myocardial cells and fibroblasts from rat pups of the same species were prepared in vitro and were divided into the control group,Ang Ⅱ group,LBQ657 group,valsartan group and LCZ696 group.3 [H]-leucine incorporation and 3[H]-proline incorporation were used to detect the myocardial hypertrophy and fibrosis.Results There was no significant difference in left ventricular function between the the model group and the Sacubitril/Valsartan group before medication (P ＞ 0.05).Four weeks after administration of the medications,end-diastolic diameter of left ventricle and end-systolic volume of left ventricle were lower [(9.73±0.26) mm vs.(10.52±0.21) mm,P＜0.05;(0.19±0.03) ml vs.(0.31±0.02) ml,P＜0.01],and the left ventricular ejection fraction was higher [(60.17±2.18)％vs.(47.16± 5.14)％,P＜0.01] in the Sacubitril/Valsartan group than in the model group.The degree of myocardial cell injury in the infarct area was lower,and the area of myocardial fibrosis in the non-infarct zone and peripheral infarcted zone were less in the Sacubitril/Valsartan group than in the modelgroup[(4.0±0.1)％ vs.(6.1±0.8)％,P＜0.001;(15.7±0.8)％ vs.(23.8±1.2)％,P＜0.001].3 [H]-proline incorporation in cardiac fibroblasts was lower in the Valsartan group than in theAng Ⅱ group [(152.77±8.46) CPM vs.(221.87±13.41) CPM,P＜0.01].3[H]-leucine incorporation in myocardial cells was lower in the Valsartan group than in the Ang Ⅱ group [(113.47 ±2.33) CPM vs.(127.65 ± 2.38) CPM,P＜0.01].3 [H]-leucine incorporation in myocardial cells was lower in LBQ657 group than in the Ang Ⅱ group [(119.78±2.98) CPM vs.(127.65±2.38)CPM,P＜0.05],and the combined application of valsartan and LBQ657 can further reduce myocardial hypertrophy and fibrosis (P ＜ 0.05).Conclusions Sacubitril/Valsartan can effectively alleviate myocardial remodeling and cardiac dysfunction after myocardial infarction,and the mechanism may be related to reducing Ang Ⅱ-induced myocardial hypertrophy and myocardial fibrosis.

Surveillance of enteric pathogens in outpatient children with acute diarrhea / 中华传染病杂志

Objective To monitor the clinical epidemiology and etiology of acute diarrhea in children in the outpatient setting in Shanghai .Methods An active surveillance study in Children′s Hospital of Fudan University between August 2013 and July 2014 was conducted .Outpatient children with acute diarrhea were enrolled in this study and stool samples were collected .Pathogens including norovirus ,diarrheagenic Escherichia coli (DEC) , nontyphoidal Salmonella spp .(NTS),Campylobacter,Shigella,pathogenic vibrio and Yersinia enterocolitica were identified and typed .The χ2 test was used for statistical analysis .Results Of the 881 stool samples from enrolled children , the pathogens included into the target detection were identified in 246 (27 .92% ) cases . Norovirus ,DEC ,NTS ,Campylobacter and Shigella were detected in 98 (11 .12% ) cases ,74 (8 .40% ) cases , 61 (6 .92% ) cases ,34 (3 .86% ) cases and 2 (0 .23% ) cases ,respectively .Neither pathogenic vibrio nor Yersinia enterocolitica was identified .Children younger than 36 months old (3 .27% ,26/794) had a lower risk (χ2=7 .41 ,P=0 .006) of Campylobacter infection compared with older children (9 .20% ,8/87) .Vomiting (37 .76% ) and watery diarrhea (21 .34% ) were more commonly seen in children with norovirus infection;fever and mucous stool were commonly seen in diarrheal children with NTS infection (40 .98% and 21 .31% ,respectively) and Campylobacter infection (29 .41% and 26 .47% ,respectively) .Conclusion Enteric pathogens play a major role in childhood acute diarrhea in Shanghai .Continuous monitoring of enteric pathogens will be helpful for reasonable treatment and prevention of acute diarrhea in children .

Surveillance for diarrheagenic Escherichia coli in Shanghai, 2012-2013 / 中华流行病学杂志

<p><b>OBJECTIVE</b>To understand the distribution of diarrheagenic Escherichia (E.) coli in population in Shanghai and discuss the practice model of cooperation in enteric infectious disease prevention and control between public health institution and hospital.</p><p><b>METHODS</b>Sentinel hospitals were assigned, standard detection and identification of diarrheagenic E. coli were conducted, incidence curve of diarrheagenic E. coli infection was drawn and epidemiologic survey and laboratory detection were conducted for suspect diarrheagenic E. coli infection outbreaks.</p><p><b>RESULTS</b>A total of 7 204 stool specimens were collected from diarrhea patients in 4 hospitals during 2012-2013, in which 712 (9.9% ) were diarrheagenic E. coli positive, including 351 enteropathogenic E. coli (EPEC) strains, 292 enterotoxigenic E. coli (ETEC) strains, 32 enteroinvasive E. coli(EIEC) strains and 6 Shiga toxin-producing E. coli (STEC/EHEC) strains, as well as 31 mixed strains. EPEC infection mainly occurred in children aged 1-5 years; and all of these infections were caused by aEPEC. The incidence peak of ETEC infection was during August, the positive rate was >20%. The ETEC infection mainly occurred in infants aged 1-28 days in 2012 and in people aged 20-60 years in 2013 (P<0.05). ST was the major type (59.6%), followed by LT (27.8%) and ST/LT (12.6%). EIEC infection increased in children obviously in 2013 (P<0.01). No EHEC O157:H7 case was detected, but two EHEC O26:H11 (eae-hlyA-stx1a) cases in children were reported for the first time in Shanghai. The survey result indicated that the multidrug-resistant ETEC (STh-CS21-CFA/I-ClyA-EatA-ST2332-SHNL0005) strain causing outbreak in 15 newborns in Shanghai in 2012 was in the same clone as the strain detected in Zigong in Sichuan province.</p><p><b>CONCLUSION</b>Significant change has occurred in diarrheagenic E. coli distribution in Shanghai in recent years, ETEC has potential risk to cause outbreak of hospital acquired infection in neonates and food borne infection. The active surveillance on ETEC and other enteric pathogens by both public health institutions and hospitals need to be improved.</p>

Syndecan-4 is a candidate gene for diabetic nephropathy / 中华肾脏病杂志

Objective To identify the candidate genes in the vicinity of a susceptibility locus (urinary albumin 1,UA-1) contributing to the development of albuminuria in type 2 diabetic KK/Ta mice. Methods Total RNA was extracted from the kidneys of KK/Ta (n=3) and BALB/c (n=2) mice at 20 weeks of age.The gene expression profile in kidney was investigated using the Affymetrix Murine Genome U74Av2 array.Competitive RT-PCR was used to confirm the differential expression of syndecan-4 which located in the vicinity of UA-1.Genome DNA was extracted from KK/Ta and BALB/c mice.DNA sequence analysis of the coding and promotor region of syndecan-4 gene was conducted. Results In the vicinity of the susceptibility locus (UA-1)contributing to the development of albuminuria in type 2 diabetic KK/Ta mice,10 candidate genes that showed differential expression were identified.Among them,the gene expression of syndecan-4in KK/Ta kidneys at 20 weeks of age was up-regulated by 26.1 times of age-matched BALB/c kidneys.Sequence analysis revealed two synonymous polymorphisms in the coding region (A93C and T216C) and three polymorphisms in the promoter region (-T263C,-T396C and -G669A) of the syndecan-4 gene.The TATA box was found at 321 bp upstream from the transcription start site,and the T263C polymorphism was located in the binding site of transcription factor Clox.Conclusions Syndecan-4 gene is mapped in the vicinity of the susceptibility locus contributing to the development of albuminuria in type 2 diabetes.The gene expression of syndecan-4 in KK/Ta kidneys is up-regulated than that in age-matched BALB/c kidneys at 20 weeks of age.Thus syndecan-4 may be one of the potential candidate genes responsible for diabetic nephropathy.Sequence differences in the promoter region influence the expression levels of syndecan-4 genes in KK/Ta kidneys.

Cloning and expression of a gene encoding shortened LfcinB(1-15)-Melittin(5-12) hybrid peptide in Escherichia coli BL21(DE3) / 生物工程学报

In order to get new antibacterial peptide, we designed a hybrid peptide LfcinB(1-15)-Melittin(5-12), composed of 1-15 amino acid residues of bovine Lactoferricin and 5-12 amino acid residues of Melittin. According to the bias of codon utilization of Escherichia coli, We synthesized the gene encoding the hybrid peptide. We inserted the gene between the sites of Nco I and Sal I of pET-32a and obtained the recombinant expression vector for heterologous expression of LfcinB(1-15)-Melittin(5-12) in Escherichia coli. We used Escherichia coli BL21(DE3) as expression host for the recombinant plasmid. After induced by isopropyl-beta-D-thiogalactoside (IPTG) under the optimized conditions, we realized the fusion protein was successfully expressed. The fusion protein was expressed in soluble form and the level was more than 35% of the total proteins. With (His)6 x Tag, the fusion protein was easily purified by His x Bind Purification Kit. After purification, we obtained 35 mg of fusion protein from 1 L of culture medium. At last, we accomplished that the peptide LfcinB(1-15)-Melittin(5-12) was released from the fusion protein cleaved by enterokinase. The recombinant LfcinB(1-15)-Melittin(5-12) showed antimicrobial activity assayed by agar diffusion test. This is the first report on the heterologous expression of the hybrid antibacterial peptide LfcinB(1-15)-Melittin(5-12) in Escherichia coli and also provides basis for next cost-effective expression of other antimicrobial peptides in genetic engineering.