Objective : To examine the effect of moderate aerobic exercise on the 10-year risk of atherosclerotic cardiovascular disease (ASCVD) in patients with hypercholesterolemia, so as to provide insights into ASCVD prevention. Methods : The patients with hypercholesterolemia admitted to the Affiliated Hospital of Hebei University from September 2019 to September 2020 were recruited and randomly assigned into the intervention group and the control group using a random number table. Participants in both groups received routine lipid-lowering therapy and health education, and participants in the intervention group were given additional interventions of moderate aerobic exercise. Serum lipid levels were measured before and after 12 weeks of interventions. The 10-year risk of developing ASCVD was evaluated in both groups following interventions. Results : There were 50 participants with hypercholesterolemia in each of the intervention and control groups. The mean age was ( 38.80±1.42 ) years in the intervention group and ( 37.14±1.23 ) years in the control group, and males were accounted for 46.00% and 40.00%, respectively. The increase in high-density lipoprotein cholesterol ( HDL-C ), the reduction in total cholesterol ( TC ), triglyceride ( TG ), low-density lipoprotein cholesterol ( LDL-C ) and the 10-year risk of ASCVD were all significantly greater in the intervention group than those in the control group before and after the interventions ( P<0.05 ). Conclusion Moderate aerobic exercise may reduce the 10-year risk of ASCVD through regulating blood lipid levels.

Objective To investigate the differences of hand and foot morphology and genetic phenotypic characteristics in adults of Hui and Han nationality in Southwestern Henan.Methods The indicators of height,weight,hand and foot were measured by the morphological measurements,the hand and foot genetic phenotype classification was observed and performed the statistical analysis.Results The hand width,foot length and foot width of the Hui adult men and women in Southwestern Henan were(8.27±0.55,23.10±1.20,9.34±0.83)cm and(7.41±0.44,20.50±1.23,8.79±0.69) cm,respectively,while which of the Han adult men and women were(8.56±0.09,24.57±1.33,9.47±0.70)cm and(7.74±0.36,22.46±1.21,8.91±0.85) cm,respectively.The total number of both hands fingerprint ridge line in Hui adult men and women were(135.06 ± 19.87) and (125.50 ±20.44)respectively,and which in Han adult men and women were (144.46 ±14.08) and (129.20 ± 20.34)respectively,the difference was statistically significant(P＜0.05).The tPD,atd angle and a-b crest line number among the Hui and Han nationalities were 16.07± 6.46,(44.61±8.66)°,34.04±5.47 and 16.53±6.27,(43.19±9.52)°,36.73±4.22 respectively.And the handedness,fingernail form,thumb type,footedness,right type ratio of foot and toe length of the Hui and Han nationalities were 90.01％,38.52％,85.59％,70.47％,56.92％ and 89.33％,45.26％,70.91％,96.98％,74.89％,respectively,the difference between the Hui and Han nationalities was statistically significant(P＜0.05).Conclusion The national differences and gender differences exist in the multiple indicators of hand and foot morphology,finger and palm prints,and genetic phenotype among the Hui and Han adults in Southwestern Henan.

In order to investigate the expression of serum sHLA-G in hemophagocytic syndrome (HPS) patients and to evaluate its clinical significance, the clinical data of HPS patients in Capital Medical University Beijing Friendship Hospital during the period from September 2008 to July 2010 were collected. They were divided into infection-associated HPS, tumor-associated HPS and rheumatological disease-associated HPS according to cause of diseases. The serum concentration of sHLA-G in HPS patients and 25 healthy controls was measured by enzyme-linked immunosorbent assay (ELISA), the correlations between sHLA-G level and laboratory indicators were analyzed. The results showed that the level of serum sHLA-G in HPS patients was significantly higher than that in healthy controls (p = 0.003), but the difference was not statistically significant between HPS groups of different causes (p = 0.233). The positive correlation of sHLA-G level in HPS patients with platelet count was found, but there was no positive correlation of their sHLA-G levels with WBC, Hb, Plt, ALT, AST, LDH, Alb, TBil, DBil, IBil, Cr, BUN, TG, fibrinogen and ferritin levels detected on same day. It is concluded that the the increase of serum sHLA-G levels in HPS patients may be caused by different factors such as infection, tumor, T cell activation and over-stimulation of several cytokines. sHLA-G can inhibit NK cell activity, resulting in formation of abnormal immune storm, and may be play a role in the pathogenesis of HPS.
Adolescent ; Adult ; Case-Control Studies ; Child ; Child, Preschool ; Female ; HLA-G Antigens ; blood ; Humans ; Killer Cells, Natural ; metabolism ; Lymphohistiocytosis, Hemophagocytic ; blood ; Male ; Middle Aged ; Young Adult

OBJECTIVETo investigate the molecular genetic abnormalities of N-myc and C-myc, and their clinical pathological implications in pediatric neuroblastic tumors (NTs).

METHODSAbnormalities of N-myc were detected by interphase fluorescence in situ hybridization (FISH) technique in 246 cases of NTs, including neuroblastoma (NB,188 cases), ganglioneuroblastoma (GNB, 52 cases), ganglioneuroma (GN, 6 cases), and their association with the histological typing of the tumors and prognosis was analyzed. Abnormalities of C-myc were detected by FISH in 133 cases of NTs.

RESULTSOf the 246 cases of NTs, N-myc amplification was only found in 27 cases (11.0%, 27/246) of NB, but not in any cases of GNB or GN (P < 0.05). 89.0% (219/246) N-myc non-amplification were found in NTs, and it included N-myc gain in 175 cases (71.1%, 175/246) and normal N-myc in 44 cases (17.9%, 44/246). Univariate analysis indicated significantly (P = 0.012) poorer outcome in patients with N-myc amplification than N-myc non-amplification. However no significant difference was observed between N-myc gain cases and normal N-myc cases (P = 0.057). C-myc gain was found in 74 of 133 cases (55.6%) of NTs; no C-myc amplification or translocation was detected. Forty percent (6/15) of cases with N-myc amplification and 57.6% (68/118) of cases with N-myc non-amplification were accompanied by C-myc gain. The difference between N-myc amplification and non-amplification with C-myc gain was not significant (P > 0.05). Univariate analysis indicated that the outcome difference was not statistically significant between C-myc gain cases and normal C-myc cases (P = 0.357).

CONCLUSIONSThe incidence of N-myc amplification only found in NB is low in pediatric NTs in China. Patients with N-myc amplification predict poorer outcome. No amplification or translocation of C-myc is detected in NTs, whereas C-myc gain is relatively common in NTs. There is no obvious association between N-myc amplification and C-myc gain.

Adrenal Gland Neoplasms ; genetics ; pathology ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Ganglioneuroblastoma ; genetics ; pathology ; Ganglioneuroma ; genetics ; pathology ; Gene Amplification ; Genes, myc ; Humans ; In Situ Hybridization, Fluorescence ; Infant ; Male ; Mediastinal Neoplasms ; genetics ; pathology ; Neuroblastoma ; genetics ; pathology ; Survival Rate

OBJECTIVETo screen the differentially expressed miRNAs and their target genes in adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs) to better understand the mechanism for regulating the balance between osteoblast and adipocyte differentiation.

METHODSCultured hMSCs were induced for adipogenic differentiation, and at 0, 7, 14, and 21 days of induction, the cells were examined for miRNA and mRNA expression profiles using miRNA chip and transcriptome sequencing (RNA-seq) techniques. Correlation analysis was carried out for the miRNAs and mRNAs of potential interest. The databases including TargetScan, PicTar and miRanda were used to predict the target genes of the differentially expressed miRNA.

RESULTSThe expression of miR-140-5p was down-regulated and leukemia inhibitory factor receptor (LIFR) expression increased progressively during adipogenic differentiation of hMSCs, showing a negative correlation between them. Target gene prediction using the 3 databases identified LIFR as the target gene of miR-140-5p.

CONCLUSIONmiRNA-140-5p may play an important role by regulating its target gene LIFR during adipogenic differentiation of hMSCs.

Adipocytes ; cytology ; Adipogenesis ; Cell Differentiation ; Cells, Cultured ; Down-Regulation ; Humans ; Leukemia Inhibitory Factor Receptor alpha Subunit ; metabolism ; Mesenchymal Stromal Cells ; cytology ; MicroRNAs ; genetics ; Oligonucleotide Array Sequence Analysis ; Osteoblasts ; cytology ; RNA, Messenger ; Transcriptome

Adult ; Anti-Inflammatory Agents ; therapeutic use ; Female ; Follow-Up Studies ; Hepatitis B e Antigens ; Hepatitis B, Chronic ; drug therapy ; Humans ; Male ; Phytotherapy ; Treatment Outcome

To understand the potential causes of laboratory-acquired infections and to provide possible solutions that would protect laboratory personnel, samples from a viral laboratory were screened to determine the main sources of contamination with six subtypes of Rhinovirus. Rhinovirus contamination was found in the gloves, cuffs of protective wear, inner surface of biological safety cabinet (BSC) windows, and trash handles. Remarkably, high contamination was found on the inner walls of the centrifuge and the inner surface of centrifuge tube casing in the rotor. Spilling infectious medium on the surface of centrifuge tubes was found to contribute to contamination of centrifuge surfaces. Exposure to sodium hypochlorite containing no less than 0.2 g/L available chlorine decontaminated the surface of the centrifuge tubes from Rhinovirus after 2 min.
Equipment Contamination ; statistics & numerical data ; Humans ; Laboratories, Hospital ; manpower ; standards ; statistics & numerical data ; Occupational Exposure ; analysis ; statistics & numerical data ; Virus Diseases ; virology ; Viruses ; genetics ; growth & development ; isolation & purification

OBJECTIVETo observe the change in the number of antibodies of preneoplastic hepatocellular carcinoma (HCC) using early treatment by Compound Phyllanthus Urinaria L. (CPUL) on patients with preneoplastic hepatitis B virus (HBV)-associated HCC.

METHODSA total of 102 cirrhosis patients with regenerative or dysplastic nodules whose sera were tested positive for at least one of these six proteins (five up-regulated genes URG4, URG7, URG11, URG12 and URG19, and one down-regulated gene DRG2) were assigned randomly to two groups using continual random codes by SPSS software. Fifty-two patients were in the treatment group and 50 patients were in the control group. CPUL was used in the treatment group for 3 years, while the control group did not receive any treatment. The changes in HBV-DNA level, number of antibodies, and hepatocarcinogenesis occurred were observed. Patients who did not develop HCC were followed up for another 2 years.

RESULTSHBV-DNA levels decreased ⩾2log in 22.2% (10/45) of patients in the treatment group in contrast to only 5.0% (2/40) of patients in the control group (P=0.0228). The number of antibodies that were tested positive in the treatment group (1.08±1.01) was significantly lower compared with the control group (2.11±1.12) after 24 months of drug treatment (P<0.01). Both the positive rates of anti-URG11 (33/52) and anti-URG19 (31/52) were over 60% at baseline in the two groups, and were decreased to 48.1% (25/52) and 46.2% (24/52) respectively at 36 months of drug treatment, while the rates increased to 68.0% (34/50) and 66.0% (33/50) respectively (P=0.0417, P=0.0436) in the control group. The positive rate of anti-DRG2 was increased to 55.8% (29/52) at 36 months of drug treatment, while in the control group was decreased to 36.0% (18/50, P=0.0452). Among the 102 patients who developed HCC, 2 were in the treatment group and 9 were in the control group, meaning that a significant difference between the two groups (P=0.0212). In 11 patients who developed HCC, anti-URG11 and anti-URG19 were always positive, while anti-DRG2 was negative. Patients newly developing HCC were 6 (20.0%) in the control group, and only one (2.5%) in the treatment group (P=0.0441) during 2-year follow-up after the end of the treatment.

CONCLUSIONSAnti-URG11, anti-URG19 and anti-DRG2 could be used as early markers in the prediction of the therapeutic efficacy of CPUL in treating preneoplastic HCC. CPUL is useful in preventing or delaying the development of HBV-associated cirrhosis to HCC.

Antibodies, Viral ; blood ; Carcinoma, Hepatocellular ; therapy ; virology ; DNA, Viral ; analysis ; Hep G2 Cells ; Hepatitis B virus ; genetics ; immunology ; pathogenicity ; Humans ; Liver Neoplasms ; therapy ; virology ; Phyllanthus ; chemistry ; Plant Extracts ; therapeutic use ; Precancerous Conditions ; virology

OBJECTIVE: Autophagy is a highly conserved intracellular degradation pathway. Many picornaviruses induce autophagy to benefit viral replication, but an understanding of how autophagy occurs remains incomplete. In this study, we explored whether coxsackievirus B3 (CVB3) infection induced autophagy through endoplasmic reticulum (ER) stress. METHODS: In CVB3-infected HeLa cells, the specific molecules of ER stress and autophagy were detected using Western blotting, reverse transcription polymerase chain reaction (RT-PCR), and confocal microscopy. Then PKR-like ER protein kinase (PERK) inhibitor, inositol-requiring protein-1 (IRE1) inhibitor, or activating transcription factor-6 (ATF6) inhibitor worked on CVB3-infected cells, their effect on autophagy was assessed by Western blotting for detecting microtubule-associated protein light chain 3 (LC3). RESULTS: CVB3 infection induced ER stress, and ER stress sensors PERK/eIF2α, IRE1/XBP1, and ATF6 were activated. CVB3 infection increased the accumulation of green fluorescent protein (GFP)-LC3 punctuation and induced the conversion from LC3-I to phosphatidylethanolamine-conjugated LC3-1 (LC3-II). CVB3 infection still decreased the expression of mammalian target of rapamycin (mTOR) and p-mTOR. Inhibition of PERK, IRE1, or ATF6 significantly decreased the ratio of LC3-II to LC3-I in CVB3-infected HeLa cells. CONCLUSION CVB3 infection induced autophagy through ER stress in HeLa cells, and PERK, IRE1, and ATF6a pathways participated in the regulation of autophagy. Our data suggested that ER stress may inhibit mTOR signaling pathway to induce autophagy during CVB3 infection.
Activating Transcription Factor 6 ; metabolism ; Autophagy ; Coxsackievirus Infections ; metabolism ; Endoplasmic Reticulum Stress ; Endoribonucleases ; metabolism ; Enterovirus B, Human ; HeLa Cells ; Humans ; Protein-Serine-Threonine Kinases ; metabolism ; Signal Transduction ; eIF-2 Kinase ; metabolism