Bronchial asthma and risk of 4 specific cardiovascular diseases and cardiovascular mortality: a meta-analysis of cohort studies.

OBJECTIVE: It has been shown that asthma is significantly associated with the risk of cardiovascular disease (CVD). Under this background, this study aimed to systematically classify and summarize the epidemiological evidence of asthma and the risk of 4 specific cardiovascular diseases (CVDs) and cardiovascular mortality (CVM). MATERIALS AND METHODS: PubMed and Embase databases were searched from inception to December 1st, 2021 in order to identify relevant studies. The random-model was used to assess the pooled results. All pooled results were expressed as risk ratios (RRs) and corresponding 95% confidence intervals (CIs). RESULTS: Finally, a total of 18 studies were included in the present meta-analysis. Compared with non-asthmatic group, patients with asthma had significantly increased risks of subsequent cardiovascular heart disease (CHD, RR 1.33; 1.19-1.50, I2=80.3%; p<0.001), and CVM (RR 1.35; 1.15-1.59, I2=0%; p<0.001). Similarly, the risks of heart failure (HF, RR 2.10; 1.98-2.22, I2=17.4%; p<0.001) and myocardial infraction (MI, RR 1.39; 1.16-1.66, I2=59.3%; p<0.001) were higher in the asthmatic population. However, the higher risk of atrial fibrillation (RR 1.70; 1.45-2.00, I2=0%; p<0.001) was observed only in the active asthmatic population. CONCLUSIONS: In general, asthma is associated with subsequent increased risks of CHD, MI, AF, HF, and CVM. In addition, among patients with asthma, females have a higher risk of CHD than males, while active asthmatic patients have a higher risk of CVM than non-active asthmatic patients.

Correlation between serum microRNA-136 levels and RAAS biochemical markers in patients with essential hypertension.

OBJECTIVE: The aim of this study was to investigate the correlation between microRNA-136 levels and biochemical markers of renin-angiotensin-aldosterone system (RAAS) in patients with essential hypertension (EH). PATIENTS AND METHODS: The subjects were divided into EH group (n=110) and healthy control group (n=110). MicroRNA-136 expression, angiotensin-converting enzyme (ACE) activity, and expression of renin (RA) and angiotensin II (Ang II), and aldosterone (ALD) in peripheral blood serum were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), equine glycylglycine glycine method, magnetic particle chemistry, and radioimmunoassay, respectively. In addition, the correlation between microRNA-136 and RAAS biochemical markers was estimated by Pearson linear regression. Meanwhile, ROC curve analysis was carried out to evaluate the potential of microRNA-136 for the diagnosis of EH. Follow-up data were recorded for assessing the influence of microRNA-136 on the prognosis in patients with EH. RESULTS: It was found that microRNA-136 expression was remarkably elevated in peripheral blood serum of patients with EH, and the expression levels of biochemical markers of RASS, such as ACE, RA, Ang II, and ALD were also found higher than those in healthy controls. Meanwhile, a significant positive correlation was confirmed between microRNA-136 level and ACE activity, RA, Ang II, as well as ALD levels in patients with EH. In addition, the area under the ROC curve (AUC) was calculated as 0.8662, with a sensitivity of 82.73% and a specificity of 80.91%. After two-months medication intervention, patients with EH expressing a high level of microRNA-136 had better therapeutic efficacy than those with a low level. CONCLUSIONS: In peripheral blood serum, microRNA-136 expression was dramatically negatively correlated with biochemical markers of RASS. High level of microRNA-136 predicts a good prognosis in patients with EH following medication. Therefore, microRNA-136 can be used as a potential biomarker for the diagnosis of EH.

Measurement of cytokines and chemokines and association with clinical severity of dermatomyositis and clinically amyopathic dermatomyositis.

BACKGROUND: Dermatomyositis (DM) is an autoimmune disease affecting primarily the skin, muscle and lung. Dysregulations of cytokines and chemokines are commonly found in inflammatory disorders. OBJECTIVES: To investigate the association between serum cytokines and chemokines and clinical severity, especially cutaneous lesions and interstitial lung disease (ILD) in patients with DM and clinically amyopathic DM (CADM). METHODS: Clinical features, laboratory findings and serum of 40 patients with DM or CADM were collected and analysed. Serum cytokines and chemokines were measured by enzyme-linked immunosorbent assay or cytometric bead array. A multiple unpaired t-test was performed to compare cytokines and chemokines in patients with DM and healthy controls. Correlations of serum cytokines and chemokines with disease severity were evaluated by Spearman's rank correlation test. RESULTS: Serum interferon (IFN)-ß [rs  = 0·37, 95% confidence interval (CI) 0·078-0·62; P = 0·019] and CXCL10 (rs  = 0·32, 95% CI to -0·004 to 0·57; P = 0·045) were significantly correlated with the Cutaneous Dermatomyositis Disease Area and Severity Index activity score in the subset of patients with DM or CADM. Serum levels of interleukin (IL)-6, IL-10, IL-18 and IFN-ß were significantly higher in the patients with acute/subacute interstitial pneumonia (A/SIP) than in the subset without A/SIP (P < 0·05). IL-6 (rs  = 0·54, 95% CI 0·27-0·72; P < 0·001) and IL-18 (rs  = 0·46, 95% CI 0·21-0·65; P = 0·003) were significantly correlated with the serum level of anti-melanoma differentiation-associated protein 5 antibody. CONCLUSIONS: Serum levels of IFN-ß and CXCL10 may be useful biomarkers for assessing cutaneous disease activity in patients with DM and CADM. In addition, serum IL-6, IL-10, IL-18 and IFN-ß were highly correlated with the occurrence of A/SIP. These cytokines may play a role in the pathogenesis of DM and CADM.

[Prevalence of hyperuricemia in the elderly in 7 areas of China].

Objective: To investigate the prevalence of hyperuricemia (HUA) in the elderly in China. Methods: A randomized stratified cluster sampling survey was conducted. And 5 376 residents aged ≥60 year in 7 Beijing, Xi'an and Harbin in northern China and Chengdu, Chongqing, Changsha and Shanghai in southern China were surveyed. A unified questionnaire was used to collect their basic information, and blood samples were taken from them to detect the level of plasma uric acid (UA). The differences in hyperuricemia prevalence among different groups were compared with χ(2) test. Results: The mean concentration of plasma UA was 302.8 µmol/L in the elderly surveyed, 329.5 µmol/L in males and 282.7 µmol/L in females, 272.4 µmol/L in rural residents and 315.5 µmol/L in urban residents. Our study showed the prevalence of hyperuricemia was 13.1% in the elderly surveyed. The prevalence of hyperuricemia in women (14.1%) was higher than that in men (12.0%) (P<0.05); and the prevalence of hyperuricemia was higher in urban residents (15.8%) than in rural residents (6.9%) (P<0.01); in southern area (16.0%) than in northern area (11.6%) (P<0.01). Both the plasma UA level and the prevalence of hyperuricemia increased with age in those aged ≥60 years. The average prevalence of hyperuricemia were 9.5%, 11.9%, 14.5%, 16.4% and 21.9% and the plasma UA levels were 287.7, 295.9, 308.1, 311.6 and 323.3 µmol/L respectively in age group ≥60, 65, 70, 75 and 80 years (P<0.01). Conclusion: The result showed that mean concentration of plasma UA was 302.8 µmol/L and the overall prevalence of hyperuricemia was 13.1% in the elderly surveyed in China. The prevalence of hyperuricemia in females was higher than in males, in urban residents than in rural residents and in southern area than in northern area. Both the UA level and prevalence of hyperuricemia increased with age.

Association of HLA-DQ alleles with the presence of an anti-ß2-glycoprotein I antibody in patients with recurrent miscarriage.

Immunogenetic studies have suggested that autoantibody production is commonly associated with particular human leukocyte antigens (HLA) class II genotypes in certain autoimmune diseases. The objective of this study was to investigate whether the production of anti-ß2-glycoprotein I antibody (aß2GPI) was associated with particular HLA-DQ alleles in patients with recurrent miscarriage (RM). The HLA-DQ genotypes in 126 patients with RM were determined using the polymerase chain reaction-sequence-specific primer method. Both the IgG and IgM isotypes of aß2GPI were measured via enzyme-linked immunosorbent assay. Positive results for either IgG or IgM on two occasions within an interval of 12 weeks were defined as antiphospholipid antibody-positive. The frequencies of the HLA-DQA1*01:02 [odds ratio (OR) 3.4, 95% confidence interval (CI) 1.6-7.0, Pc = 0.018] and HLA-DQB1*02:01 alleles (OR 4.6, 95% CI 2.1-10.2, Pc = 9.18 × 10(-4)) were significantly increased in aß2GPI-positive RM patients compared with aß2GPI-negative RM patients. These results suggest that the HLA-DQA1*0102 and HLA-DQB1*0201 alleles may be involved in the production of aß2GPI in RM patients.

The miR-200 family and the miR-183~96~182 cluster target Foxf2 to inhibit invasion and metastasis in lung cancers.

Metastatic lung cancer is one of the most lethal forms of cancer and molecular pathways driving metastasis are still not clearly elucidated. Metastatic cancer cells undergo an epithelial-mesenchymal transition (EMT) where they lose their epithelial properties and acquire a migratory and invasive phenotype. Here we identify that the expression of microRNAs from the miR-200 family and the miR-183~96~182 cluster are significantly co-repressed in non-small cell lung cancer cell lines and primary tumors from multiple TCGA dataset with high EMT scores. Ectopic expression of the miR-183~96~182 cluster inhibited cancer cell migration and invasion, whereas its expression was tightly modulated by miR-200. We identified Foxf2 as a common, novel and direct target of both these microRNA families. Foxf2 expression tightly correlates with the transcription factor Zeb1 and is elevated in mesenchymal-like metastatic lung cancer cells. Foxf2 expression induced robust EMT, migration, invasion and metastasis in lung cancer cells, whereas Foxf2 inhibition significantly repressed these phenotypes. We also demonstrated that Foxf2 transcriptionally represses E-cadherin and miR-200, independent of Zeb1, to form a double-negative feedback loop. We, therefore, identified a novel mechanism whereby the miR-200 family and the miR-183~96~182 cluster inhibit lung cancer invasion and metastasis by targeting Foxf2.

Association between the HER2 Ile655Val polymorphism and response to trastuzumab in women with operable primary breast cancer.

BACKGROUND: Human epidermal growth factor receptor 2 (HER2) Ile655Val polymorphism may affect the efficacy of trastuzumab treatment of breast cancer. PATIENTS AND METHODS: HER2 Ile655Val polymorphism was determined in 4167 patients with primary breast cancer using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. We investigated the associations between the HER2 Ile655Val polymorphism and clinical outcomes in women with HER2-negative breast cancer and with HER2-positive breast cancer who received trastuzumab or who did not. RESULTS: At a median follow-up of 44 months, HER2 Ile655Val polymorphism was not significantly associated with survival either in the entire study population of 4167 patients or in 2976 HER2-negative breast cancer patients. Among 816 HER2-positive patients who received adjuvant chemotherapy and/or endocrine therapy without trastuzumab treatment, patients with the Val/Ile or the Val/Val genotype had a significantly worse disease-free survival (DFS) and distant DFS (DDFS) than those with the Ile/Ile genotype (DFS, adjusted hazard ratio [HR] 1.5; 95% confidence interval [CI] 1.0-2.3; P = 0.037; DDFS, adjusted HR 1.9; 95% CI 1.2-2.9 P = 0.005). In contrast, among 212 HER2-positive patients who received chemotherapy in combination with trastuzumab treatment, patients with the Val/Ile or the Val/Val genotype had a significantly better DFS and DDFS than those with the Ile/Ile genotype (5-year DFS, 100% versus 83%; P = 0.008; 5-year DDFS, 100% versus 89%; P = 0.031). CONCLUSIONS: HER2 Ile655Val polymorphism affects the function of HER2 gene only restricted in HER2-positive breast cancers. HER2-positive breast cancer patients with the Val variant have an aggressive phenotype, but are sensitive to trastuzumab treatment.

Expression profiling stratifies mesothelioma tumors and signifies deregulation of spindle checkpoint pathway and microtubule network with therapeutic implications.

BACKGROUND: Malignant pleural mesothelioma (MPM) is a lethal neoplasm exhibiting resistance to most treatment regimens and requires effective therapeutic options. Though an effective strategy in many cancer, targeted therapy is relatively unexplored in MPM because the therapeutically important oncogenic pathways and networks in MPM are largely unknown. MATERIALS AND METHODS: We carried out gene expression microarray profiling of 53 surgically resected MPMs tumors along with paired normal tissue. We also carried out whole transcriptomic sequence (RNA-seq) analysis on eight tumor specimens. Taqman-based quantitative Reverse-transcription polymerase chain reaction (qRT-PCR), western analysis and immunohistochemistry (IHC) analysis of mitotic arrest deficient-like 1 (MAD2L1) was carried out on tissue specimens. Cell viability assays of MPM cell lines were carried out to assess sensitivity to specific small molecule inhibitors. RESULTS: Bioinformatics analysis of the microarray data followed by pathway analysis revealed that the mitotic spindle assembly checkpoint (MSAC) pathway was most significantly altered in MPM tumors with upregulation of 18 component genes, including MAD2L1 gene. We validated the microarray data for MAD2L1 expression using quantitative qRT-PCR and western blot analysis on tissue lysates. Additionally, we analyzed expression of the MAD2L1 protein by IHC using an independent tissue microarray set of 80 MPM tissue samples. Robust clustering of gene expression data revealed three novel subgroups of tumors, with unique expression profiles, and showed differential expression of MSAC pathway genes. Network analysis of the microarray data showed the cytoskeleton/spindle microtubules network was the second-most significantly affected network. We also demonstrate that a nontaxane small molecule inhibitor, epothilone B, targeting the microtubules have great efficacy in decreasing viability of 14 MPM cell lines. CONCLUSIONS: Overall, our findings show that MPM tumors have significant deregulation of the MSAC pathway and the microtubule network, it can be classified into three novel molecular subgroups of potential therapeutic importance and epothilone B is a promising therapeutic agent for MPM.

Promoter methylation of BRCA1 in triple-negative breast cancer predicts sensitivity to adjuvant chemotherapy.

BACKGROUND: BRCA1 function is inactivated through BRCA1 promoter methylation in a substantial number of triple-negative breast cancers. We investigated the impact of BRCA1-methylation status on the efficacy of adjuvant chemotherapy in patients with triple-negative breast cancer or with non-triple-negative breast cancer. METHODS: BRCA1 promoter methylation was assessed in 1163 unselected breast cancer patients. Methylation was evaluated using a methylation-specific PCR (MSP) assay. RESULTS: In the subgroup of 167 triple-negative breast cancer patients who received adjuvant chemotherapy, patients with BRCA1-methylated tumors had a superior 10-year disease-free survival (DFS)(78% versus 55%, P = 0.009) and 10-year disease-specific survival (DSS) (85% versus 69%, P = 0.024) than those with BRCA1-unmethylated tumors, and BRCA1 methylation was an independent favorable predictor of DFS and DSS in a multivariate analysis in this subgroup [DFS: hazard ratio (HR) = 0.45; 95% confidence interval (CI) 0.24-0.84; P = 0.019; DSS: HR = 0.43; 95% CI = 0.19-0.95; P = 0.044]. In contrast, in 675 non-triple-negative breast cancer patients who received adjuvant chemotherapy, BRCA1 methylation was an unfavorable predictor of DFS and DSS in univariate analysis (DFS: HR = 1.56; 95% CI 1.16-2.12; P = 0.003; DSS: HR = 1.53; 95% CI = 1.05-2.21; P = 0.026). CONCLUSIONS: Triple-negative breast cancer patients with BRCA1-methylated tumors are sensitive to adjuvant chemotherapy and have a favorable survival compared with patients with BRCA1-unmethylated triple-negative tumors.

ß-Catenin/LEF1 transactivates the microRNA-371-373 cluster that modulates the Wnt/ß-catenin-signaling pathway.

The microRNA-371-373 (miR-371-373) cluster is specifically expressed in human embryonic stem cells (ESCs) and is thought to be involved in stem cell maintenance. Recently, microRNAs (miRNAs) of this cluster were shown to be frequently upregulated in several human tumors. However, the regulatory mechanism for the involvement of the miR-371-373 cluster in human ESCs or cancer cells remains unclear. In this study, we explored the relationship between this miRNA cluster and the Wnt/ß-catenin-signaling pathway, which has been shown to be involved in both stem cell maintenance and tumorigenesis. We show that miR-371-373 expression is induced by lithium chloride and is positively correlated with Wnt/ß-catenin-signaling activity in several human cancer cell lines. Mechanistically, three TCF/LEF1-binding elements (TBEs) were identified in the promoter region and shown to be required for Wnt-dependent activation of miR-371-373. Interestingly, we also found that miR-372&373, in turn, activate Wnt/ß-catenin signaling. In addition, four protein genes related to the Wnt/ß-catenin-signaling pathway were identified as direct targets of miR-372&373, including Dickkopf-1 (DKK1), a well-known inhibitor of Wnt/ß-catenin signaling. Using a lentiviral system, we showed that overexpression of miR-372 or miR-373 promotes cell growth and the invasive activity of tumor cells as knockdown of DKK1. Taken together, our study demonstrates a novel ß-catenin/LEF1-miR-372&373-DKK1 regulatory feedback loop, which may have a critical role in regulating the activity of Wnt/ß-catenin signaling in human cancer cells.

Effect of Intrafix® SafeSet infusion apparatus on phlebitis in a neurological intensive care unit: a case-control study.

OBJECTIVE: To investigate the effect of the Intrafix(®) SafeSet infusion apparatus on the incidence of phlebitis in patients being intravenously infused in a neurological intensive care unit (ICU). METHODS: Patients aged > 12 years, with no history of diabetes mellitus and no existing phlebitis, requiring a daily peripheral intravenous infusion of ≥ 8 h with the total period lasting ≥ 3 days, were enrolled. Infusions were performed using the Intrafix(®) SafeSet or normal infusion apparatus. Incidence of phlebitis (scored according to the Infusion Nursing Standards of Practice of the American Infusion Nurses Society) was analysed. RESULTS: Patients (n = 1545) were allocated to Intrafix(®) SafeSet (n = 709) or normal infusion (n = 836) groups, matched for age, gender and preliminary diagnosis. Incidence of phlebitis was significantly higher using normal infusion apparatus compared with the Intrafix(®) SafeSet (23.4% versus 17.9%, respectively). CONCLUSION: Intrafix(®) SafeSet infusion apparatus significantly reduced the incidence of phlebitis in patients in the neurological ICU, compared with normal infusion apparatus, and may be suitable for use in routine clinical practice.

Experimental research on wild-type p53 plasmid transfected into retinoblastoma cells and tissues using an ultrasound microbubble intensifier.

The transfection efficiency of wild-type p53 (wtp53) was investigated in retinoblastoma (RB) Y79 cells using an ultrasound microbubble technique. A human RB nude mouse xenograft tumour model was also used to investigate whether this technique could deliver wtp53 into solid tumours. Reverse transcription-polymerase chain reaction (RT-PCR) demonstrated that wtp53 was successfully transfected into Y79 cells in the plasmid with microbubbles and ultrasound group and in the plasmid with liposomes group, but not in the plasmid with ultrasound group or in the untreated control group. Flow cytometry showed that apoptosis was highest in the microbubbles and ultrasound group (25.58%) compared with the plasmid with liposomes group (19.50%), and the other two groups (< 10%). RT-PCR also showed that the wtp53 gene was successfully transfected into solid tumours in the plasmid with microbubbles and ultrasound group. This study provides preliminary evidence in support of a potential new approach to RB gene therapy.

Expression of caveolin-1 in tongue squamous cell carcinoma by quantum dots.

Quantum dots (QDs) are a new class of fluorescent probes to detect biomarker expression. The role of caveolin-1 (Cav-1) in tongue squamous cell carcinoma (TSCC) is still unknown. This study aimed to investigate the expression profile of Cav-1 in carcinogenesis and development of TSCC by QDs immunofluorescence histochemistry (QDs-IHC) and discuss the relationship between the Cav-1 expression and the clinicopathological outcomes. QDs-IHC was used to detect Cav-1 expression in tissue microarrays including normal tongue mucosa (NTM; n=10), hyperplastic tongue mucosa (HTM; n=10), tongue pre-cancer lesions (TPL; n=15) and primary tongue squamous cell carcinoma (PTSCC; n=61). Correlations between the Cav-1 expression and clinicopathologic variables were evaluated statistically. Cells positive for Cav-1 were clearly detected and bright images were obtained in a fine, granular pattern at the cell membrane and cytoplasm using QDs-IHC. The rate of Cav-1 immunoreactivity increased progressively from NTM (0%), HTM (0%), TPL (36%) to PTSCC (74%). When compared with each other, there was statistical significance among PTSCC, TPL and NTM as well as among PTSCC, TPL and HTM. Moreover, Cav-1 expression level in PTSCC was correlated positively with clinical stage and histologic grade. QDs-IHC could accurately detect protein location in tongue mucosa. An increased expression of Cav-1 in the stepwise carcinogenesis from NTM, HTM, TPL to PTSCC suggested that Cav-1 might be an oncogene in the development of tongue squamous cell carcinoma.

Use of quantum dots to detect human papillomavirus in oral squamous cell carcinoma.

OBJECTIVE: To examine the association of oral squamous cell carcinoma with human papillomavirus (HPV) using quantum dots (QD) in situ hybridization (ISH). METHODS: Expression of HPV16/18 was analyzed in a representative collection of 21 oral squamous cell carcinomas by tissue microarrays. The presence of HPV16/18 high risk was detected by applying QDISH which is compared with conventional ISH. RESULTS: Seven cases out of 21 (33.3%) were positive for QDISH while 1 out of 21 (4.8%) was positive for ISH, although all of HPV DNA were localized in the nuclei in the spinous and basal cell layer of the epithelium. The difference between these two methods was significant (P < 0.05). CONCLUSIONS: These results demonstrate that the QD might be an efficient method for determination of HPV infection and HPV-associated oral squamous cell carcinoma.

Anomalous line shape of the cross section for e{+}e{-}--> hadrons in the center-of-mass energy region between 3.650 and 3.872 GeV.

We observe an obvious anomalous line shape of the e;{+}e;{-}--> hadrons total cross sections in the energy region between 3.700 and 3.872 GeV. It is inconsistent with the explanation for only one simple psi(3770) resonance with a statistical significance of 7sigma. The anomalous line shape may be explained by two possible enhancements of the inclusive hadron production near the center-of-mass energies of 3.764 and 3.779 GeV, indicating that either there is likely a new structure in addition to the psi(3770) resonance around 3.773 GeV, or there are some physics effects reflecting the DD[over ] production dynamics.

Search for the invisible decay of J/psi in psi(2S) --> pi(+)pi(-) J/psi.

Using psi(2S) --> pi(+)pi(-) J/psi events in a sample of 14.0 x 10(6) psi(2S) decays collected with the BES-II detector, a search for the decay of the J/psi to invisible final states is performed. No signal is found, and an upper limit at the 90% confidence level is determined to be 1.2 x 10(-2) for the ratio B(J/psi --> invisible)/B(J/psi-->mu(+)mu(-)). This is the first search for J/psi decays to invisible final states.

Measurement of psi2S radiative decays.

Using 14 x 10(6) psi(2S) events accumulated at the BESII detector, we report first measurements of branching fractions or upper limits for psi(2S) decays into gammapp, gamma2(pi+pi-), gammaKS0K+pi-+c.c., gammaK+K-pi+pi-, gammaK*0K-pi++c.c., gammaK*0K*0, gammapi+pi-pp, gamma2(K+K-), gamma3(pi+pi-), and gamma2(pi+pi-)K+K- with the invariant mass of hadrons below 2.9 GeV/c2. We also report branching fractions of psi(2S) decays into 2(pi+pi-)pi0, omegapi+pi-, omegaf2(1270), b1+/-pi-/+, and pi02(pi+pi-)K+K-.

Search for invisible decays of eta and eta' in J/psi --> phi eta and phi eta'.

Using a data sample of 58 x 10(6) J/psi decays collected with the Beijing Spectrometer II detector at the Beijing Electron Positron Collider, searches for invisible decays of eta and eta' in J/psi to phi eta and phi eta' are performed. The phi signals, which are reconstructed in K+K- final states, are used to tag the eta and eta' decays. No signals are found for the invisible decays of either eta or eta', and upper limits at the 90% confidence level are determined to be 1.65 x 10(-3) for the ratio B(eta-->invisible)/B(eta --> gamma gamma) and 6.69 x 10(-2) for B(eta' --> invisible)/B(eta' --> gammagamma). These are the first searches for eta and eta' decays into invisible final states.

[Subtype and sequence analysis of the ENV gene of HIV-1 drug users in Guangdong Pearl River delta.].

BACKGROUND: To determine the subtype of HIV-1 of drug users (DUS) in Guangdong Pearl River delta. METHODS: HIV-1 pro-viral DNA from buffy coat of 43 DUS in Guangdong was amplified by nested PCR. The C2-V3 regions of HIV-1 ENV gene was sequenced directly from the PCR product and analyzed. RESULTS: The 43 DUS were confirmed to be infected with four HIV-1 subtype or Circulating Recombinant Form (CRFs): 07-BC(n=29), AE(n=9), 08-BC(n=3) and B(n=2). Genetic distances showed that the AE group was the closest to CM240 strain isolated in Thailand which is mainly circulating in sexually transmitted infector. The 07-BC group was the closest to C54A strain isolated in Northeastern China. The 08-BC group was the closest to 97CNGX-9F strain isolated in Guangxi, China. The B strain was the closest to rl42 strain isolated in Thailand. CONCLUSION: HIV-1 CRFs 07-BC predominates in DUS in Guangdong Pearl River delta.

Observation of a near-threshold enhancement in the omega(phi) mass spectrum from the doubly OZI-suppressed decay J/psi-->gamma(omega)phi.

An enhancement near threshold is observed in the omega(phi) invariant mass spectrum from the doubly Okubo-Zweig-Iizuka-suppressed decays of J/psi-->gamma(omega)phi, based on a sample of 5.8 x 10(7) J/psi events collected with the BESII detector. A partial wave analysis shows that this enhancement favors JP=0+, and its mass and width are M=1812(+19)(-26)(stat)+/-18(syst) MeV/c2 and Gamma=105+/-20(stat)+/-28(syst) MeV/c2. The product branching fraction is determined to be B(J/psi-->gammaX)B(X-->omega(phi))=[2.61+/-0.27(stat)+/-0.65(syst)]x10(-4).