Angioplasty, Balloon ; methods ; Aortic Valve Stenosis ; therapy ; Cardiac Pacing, Artificial ; methods ; Child, Preschool ; Heart Ventricles ; Humans ; Infant ; Male

Angioplasty, Balloon ; methods ; Aortic Coarctation ; diagnostic imaging ; pathology ; therapy ; Aortography ; Cardiac Catheterization ; methods ; Child ; Humans ; Male ; Platinum ; Prosthesis Design ; Stents ; Tomography, X-Ray Computed ; Treatment Outcome

Cannula ; Catheters ; Drainage ; Duodenal Diseases ; Humans ; Intestinal Fistula/surgery*

OBJECTIVESyncope is a common problem in children and adolescents. Such an event may have multiple possible causes, ranging from benign conditions to life-threatening diseases. Syncope is a major challenge for the practicing physicians. It is very important to know the etiologic and clinical characteristics of syncope in children. This study aimed to improve diagnostic efficacy of syncope in children by analyzing the etiology and clinical characteristics of syncope.

METHODSThe investigators retrospectively analyzed the causes of syncope and diagnostic workup of 154 consecutive children seen in Department of Pediatrics, Peking University First Hospital because of a syncopal event.

RESULTSAutonomic-mediated reflex syncope (AMS) was the most common cause of syncope (65.6%), whereas cardiac disorders were found in 10 cases (6.5%) comprising the second cause of syncope in children. Other causes included psychologic problems and neurological and metabolic disorders. Although many causes were studied, 25 cases (16.2%) were found to have uncertain etiologies yet. The children with AMS were commonly seen in pubertal girls, and they had clear inducement of syncope and prodromes. The children with cardiac syncope often had history of cardiac diseases, and they were often younger than those with AMS. Lack of prodromes of syncope, exercise-related syncope, syncope spells seen in any body position, frequent syncope spells and sudden death in family were clues of cardiac syncope. Neurological disorders should be considered if there are any of the followings: syncope with seizure activity, syncope spells seen in any position, and a postictal phase of disorientation or neurologic abnormal signs. A metabolic cause was entertained when the child had a history of metabolic diseases, prolonged anger, or violent vomiting and diarrhea. Children with psychiatric disorders were adolescent girls with prolonged syncope spells, and had more frequent syncopal episodes. Most children with syncope were evaluated by many of diagnostic tests, but most of those tests were not goal-directed approach. Since persons with cardiac syncope were at increased risk for death from any cause, electrocardiography was recommended in almost all children with syncope. Neurologic testing including electroencephalography, computed tomography, etc. were rarely helpful unless neurologic signs and symptoms are present. Holter electrocardiography and echocardiography were most useful in children with suspected cardiac syncope. There was little benefit of screening cardiac enzyme in children with syncope. Routine blood tests (blood electrolytes and blood glucose, etc) rarely yield diagnostically useful information unless the children had the history of metabolic diseases. Head-up tilt testing was most useful in children with recurrent syncope in whom heart disease was not suspected. The children with frequent syncope, long lasting syncopal episode and clear psychiatric inducement of syncope should be evaluated by psychiatric testing.

CONCLUSIONSyncope in children may result from a wide variety of causes, and clinicians often use a wide range of investigation to try to achieve a diagnosis. But most of investigations have low diagnostic yield. Thorough history taking, physical examination and electrocardiography are the core of the syncope workup.

Adolescent ; Child ; Child, Preschool ; Electrocardiography ; Female ; Humans ; Male ; Retrospective Studies ; Syncope ; diagnosis ; etiology

Acute Disease ; Biomarkers, Tumor ; analysis ; Child ; Cyclin-Dependent Kinase Inhibitor p16 ; analysis ; Histocytochemistry ; Humans ; Leukemia ; metabolism ; pathology ; Proliferating Cell Nuclear Antigen ; analysis ; Proto-Oncogene Proteins c-bcl-2 ; analysis

OBJECTIVETo study the effects of genistein on the proliferation, apoptosis induction and expression of related gene proteins of human colon cancer cells in vitro and in vivo, and its mechanisms of action.

METHODSMTT colorimetric assay was used to detect the effects of genistein on the proliferation of human colon adenocarcinoma SW480 cells. Light and transmission electron microscopy were used to study the histological and ultrastructural changes. Flow cytometry was used to determine the effects of genistein on cell cycle and apoptosis. Flow cytometry and immunohistochemistry were used to determine the effects of genistein on apoptosis induction and expression of related gene proteins of colon cancer cells.

RESULTSThe MTT colorimetric assay showed that genistein inhibited the proliferation of SW480 cells in a dose-dependent and time-dependent manner, and the highest inhibition rate was 60.2% after 80 microg/ml genistein treatment for 72 h. The light microscopy revealed that many genistein-treated cancer cells were shrunken, disrupted, or showing cytoplasmic vacuolization. The electron microscopic examination showed cell shrinkage, nuclear fragmentation and pronounced chromatin condensation, sometimes formed crescent chromatin condensation attached to the nuclear membrane. The results of flow cytometry showed that: after SW480 cells were treated with 0, 20, 40, 80 microg/ml genistein for 48 h, the FI values of PCNA were 1.49 +/- 0.02, 1.28 +/- 0.04, 1.14 +/- 0.03, and 0.93 +/- 0.08; the FI values of VEGF were 1.75 +/- 0.02, 1.34 +/- 0.06, 1.32 +/- 0.04, and 1.23 +/- 0.04; the fluorescence index (FI) values of p21 were 1.26 +/- 0.05, 1.36 +/- 0.06, 1.61 +/- 0.03, and 1.73 +/- 0.03, respectively. There were statistically significant differences between the control group and each treatment group (P < 0.05 or P < 0.01). The scores of immunohistochemical staining of PCNA and VEGF proteins were decreased, while p21 increased. There were statistically significant differences between the control group and each treatment group (P < 0.05 or P < 0.01).

CONCLUSIONGenistein can inhibit the growth of colon cancer cells via apoptosis induction and cell cycle arrest at G(2)/M phase. The anti-tumor mechanisms of genistein may be related with the down-regulation of expression of VEGF and PCNA, and up-regulation of the expression of p21.

Adenocarcinoma ; metabolism ; pathology ; Animals ; Anticarcinogenic Agents ; administration & dosage ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Colonic Neoplasms ; metabolism ; pathology ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Dose-Response Relationship, Drug ; Gene Expression Regulation, Neoplastic ; Genistein ; administration & dosage ; pharmacology ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Neoplasm Transplantation ; Proliferating Cell Nuclear Antigen ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism

OBJECTIVETo investigate the cellular effects of Pien Tze Huang (PZH) in the HT-29 human colon carcinoma cell line.

METHODSThe viability of HT-29 cells was determined by MTT assay. A fluorescence-activated cell sorting (FACS) analysis with annexin-V/propidium iodide (PI) and JC-1 staining were performed to determine cell apoptosis and the loss of mitochondrial membrane potential, respectively. Activation of caspase 3 was evaluated by a colorimetric assay. The mRNA expression levels of Bcl-2 and Bax were measured by reverse transcription polymerase chain reaction (RT-PCR).

RESULTSPZH, in a dose- and time-dependent manner, reduced viability and induced apoptosis of HT-29 cells. Moreover, PZH treatment resulted in the collapse of the mitochondrial membrane potential, activation of caspase 3, and an increase in the Bax/Bcl-2 ratio.

CONCLUSIONPZH inhibits the growth of HT-29 cells by inducing cancer cell apoptosis via regulation of the Bcl-2 family and activation of caspase 3, which may, in part, explain its anticancer activity.

Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Colonic Neoplasms ; enzymology ; pathology ; Drug Screening Assays, Antitumor ; Drugs, Chinese Herbal ; pharmacology ; Enzyme Activation ; drug effects ; HT29 Cells ; Humans ; Membrane Potential, Mitochondrial ; drug effects ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo compare the specificity and sensitivity of two genotyping approaches for human papillomavirus (HPV).

METHODHPV DNA was amplified and detected in clinical specimens by polymerase chain reaction in a pair of universal primers MY09/11, and then genotyped with either sequencing method or liquid chip hybridization method (luminex method).

RESULTSequencing method obtained precise genotyping results in single-type HPV infection, while luminex method obtained accurate genotyping results in multiple-type HPV infection.

CONCLUSIONA combined method using both sequencing and luminex method is suitable for the genotyping of HPV-infected specimens.

Base Sequence ; DNA, Viral ; genetics ; Female ; Female Urogenital Diseases ; virology ; Genotype ; Humans ; Oligonucleotide Array Sequence Analysis ; Papillomaviridae ; genetics ; isolation & purification ; Papillomavirus Infections ; virology ; Polymerase Chain Reaction

Aim To investigate the effects of Bigelovii A on autophagy and its mechanism.Methods Fluorescence microscope,flow cytometry and Western blot were employed to analyze autophagy.Western blot was used to detect the protein expressions of mTOR pathway.MTT colorimetry was used to assay cell viability after treatment with 3-MA and Bigelovii A or Bigelovii A alone.Results Bigelovii A-treated MCF7 cells displayed a dramatic increase in the number of MDC-labeled vesicles and the expressions of LC3-Ⅱ,indicating cell autophagy.Ⅰt was proved that in MCF7 cells,Bigelovii A inhibited mTOR signaling by decreasing Akt and p-ERK.Consistently,Bigelovii A decreased phosphorylation levels of mTOR,p70S6K (Ser371,Thr389) and 4EBP1 proteins.Inhibiting Bigelovii Ainduced autophagy with the autophagy inhibitor 3-methyladenine significantly decreased cell viability,which suggested that Bigelovii A-induced autophagy played a pro-survival role.Conclusion Bigelovii A is likely to induce autophagy through inhibiting mTOR pathway.

Background Visual impairment influent the life quality of patient and bring about the economical burden to their families and society.Epidemiology survey of the prevalence and main causes of visual impairment is the basis of the prevention of blindness.Objective The goal of this survey was to investigate the visual impairment in the subjects aged 40 years or older living in Shunyi district and assist in the design of intervention programs.Methods A cross-sectional survey was performed in this study.Cluster sampling was used to randomly select 4549 individuals aged ≥40 years in Shunyi district,and visual impairment was evaluated based on WHO criteria and analyzed based on the 10-year interval groups.The questionnaire,best corrected visual acuity (BCVA)and comprehensive eye examination were provided for eligible residents.To evaluate the independentassociation of significant sociodemographic variables with visual impairment,a regression model was constructed including age,sex and education level.This study was approved by the Ethic Committee of Peking University Medical Department.Written informed consent was signed by each subject before any medial survey.Results A total of 4167 subjects participated in this survey with the response rate of 91.6％.The age of the subjects ranged from 40-94 years(mean:56.61±11.10 years).The numbers of visual impairment was 161 with the prevalence 3.9％.Trend x2 test showed that the number and percentage of visual impairment were elevated as the increase of age,showing a significantly difference among different age groups(x2 =159.487,P＜0.01).The prevalence rate of visual impairment in 70 and older group was 15 times more than that of 60-69-year-old group(OR =0.114,95％ CI:0.056-0.234).No significant difference was found between gender and prevalence of visual impairment(OR =0.901,95％ CI:0.627 -1.295).The prevalence rate of visual impairment in illiterate group was 5.5 fold more than that of educated group (OR =2.743,95％ CI:1.830-4.111).Conclusions Ageing and low education degree are the important factors of visual impairment.Education attainment is an independent protective factor of visual impairment.