Targeting Mitochondrial Dysfunction With LncRNAs in a Wistar Rat Model of Chronic Obstructive Pulmonary Disease.

BACKGROUND/AIM: Chronic obstructive pulmonary disease (COPD) has become a prominent healthcare issue in recent years. Cigarette smoking (CS) and fine particulate matter (PM2.5) are important causative factors for COPD. This study assessed the aberrant lncRNA profiles in the tissue of rats with COPD caused by CS or PM2.5 Materials and Methods: A COPD rat model was developed using CS (CSM) or PM2.5 (PMM), and lung tissue RNA was extracted. The Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) were used to investigate the correlations between the distinct lncRNAs and mRNA pathways. A coding-non-coding gene co-expression network (CNC) was constructed by establishing connections between differentially expressed long non-coding RNAs (lncRNAs) and messenger RNAs (mRNAs) associated with mitochondrial dysfunction and the inflammatory response. RESULTS: A quantitative real-time reverse transcription PCR (qRT-PCR) experiment was performed to verify the expression of the particular lncRNAs. Microarray analysis of lung tissue from the COPD model revealed that 123 and 444 lncRNAs were substantially raised and reduced in PMM vs. the control group (Ctrl), respectively, as were 621 and 1,178 mRNAs. Meanwhile, 81 and 340 lncRNAs were consistently raised and lowered in CSM vs. Ctrl, respectively, as were 408 and 931 mRNAs. GO enrichment and KEGG pathway analysis indicated that the COPD model was connected to inflammatory responses, mitochondrial dysfunction, and others. CONCLUSION: XR_340674, ENSRNOT00000089642, XR_597045, and XR_340651 were decreased, and XR_592469 was elevated. These lncRNAs were shown to be related to mitochondrial dysfunction in the lung tissue of animals exposed to CS or PM2.5.

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation.

Background: Transforming growth factor beta-induced protein (TGFBI, encoded by TGFBI gene), is an extracellular matrix protein, widely expressed in variety of tissues. It binds to collagens type I, II, and IV and plays important roles in the interactions of cell with cell, collagen, and matrix. It has been reported to be associated with myocardial fibrosis, and the latter is an important pathophysiologyical basis of atrial fibrillation (AF). However, the mechanism of TGFBI in AF remains unclear. We aimed to detect the potential mechanism of TGFBI in AF via bioinformatics analysis. Methods: The microarray dataset of GSE115574 was examined to detect the genes coexpressed with TGFBI from 14 left atrial tissue samples of AF patients. TGFBI coexpression genes were then screened using the R package. Using online analytical tools, we determined the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, Gene Ontology (GO) annotation, and protein-protein interaction (PPI) network of TGFBI and its coexpression genes. The modules and hub genes of the PPI-network were then identified. Another dataset, GSE79768 was examined to verify the hub genes. DrugBank was used to detect the potential target drugs. Results: In GSE115574 dataset, a total of 1818 coexpression genes (769 positive and 1049 negative) were identified, enriched in 120 biological processes (BP), 38 cellular components (CC), 36 molecular functions (MF), and 39 KEGG pathways. A PPI-network with average 12.2-degree nodes was constructed. The genes clustered in the top module constructed from this network mainly play a role in PI3K-Akt signaling pathway, viral myocarditis, inflammatory bowel disease, and platelet activation. CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 were identified and finally verified as the hub genes, mainly enriched in pathways like leukocyte transendothelial migration, PI3K-Akt signaling pathway, viral myocarditis, rheumatoid arthritis, and platelet activation. Pegcetacoplan, ocriplasmin, and carvedilol were the potential target drugs. Conclusions: We used microdataset to identify the potential functions and mechanisms of the TGFBI and its coexpression genes in AF patients. Our findings suggest that CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 may be the hub genes.

Evaluation of a Cryptococcus capsular polysaccharide detection FungiXpert LFA (lateral flow assay) for the rapid diagnosis of Cryptococcosis.

Cryptococcus is an opportunistic pathogenic fungus and is the major cause of fungal meningitis. The cryptococcal antigen (CrAg) lateral flow assay (LFA) is an immunochromatographic test system that has simplified diagnosis as a point-of-care test. In this study, we evaluated the diagnostic performance of Cryptococcal capsular polysaccharide detection FungiXpert (Genobio Pharmaceutical, Tianjin, China) using serum and cerebrospinal fluid (CSF) samples for the diagnosis of cryptococcosis and investigated the cross-reaction of the assays to pathogenic fungi and bacterium by comparing it to the U.S. Food and Drug Administration (US FDA)-approved IMMY CrAg LFA. Eighty CSF and 119 serum/plasma samples from 158 patients were retrospectively collected to test for qualitative or semi-quantitative detection of CrAg. Cross-reaction of the assays was tested using 28 fungi and 1 bacterium. Compared to IMMY CrAg LFA, the FungiXpert LFA demonstrated 99.1% sensitivity and 98.9% specificity in the qualitative test. In the 96 semi-quantitative CrAg assay results, 39 (40.6%) test titers of FungiXpert LFA were 1-2 dilutions higher than those of IMMY CrAg LFA. The Intraclass Correlation Coefficient of the Semi-quantitative results of CrAg titer tests via the two assays was 0.976. Similar to IMMY CrAg LFA, FungiXpert LFA showed cross-reactivity with Trichosporon asahii. Compared with the IMMY CrAg LFA, the FungiXpert LFA showed an equal, yet, excellent performance. However, it is important to note that these two assays have potential cross-reactivity to T. asahii when diagnosing patients. FungiXpert LFA is a rapid screening method for the effective and practical diagnosis and treatment of cryptococcosis. LAY SUMMARY: The FungiXpert LFA was developed to diagnose fungal meningitis caused by Cryptococcus yeasts, by using serum or cerebrospinal fluid. It was compared to an existing lateral flow assay (LFA). The FungiXpert LFA performed well in qualitative and semi-quantitative tests.

[Galactomannan Tests of Bronchoalveolar Lavage Fluid for Diagnosing Invasive Pulmonary Aspergillosis].

OBJECTIVE: To determine the value of galactomannan (GM) in bronchoalveolar lavage fluid (BALF) for diagnosing invasive pulmonary aspergillosis. METHODS: According to the European Organization for Research and Treatment of Cancer / Invasive Fungal Infection Group (EORTC / IFICG) and the American Mycosis Research Group (MSG),and the American College of Infectious Diseases (IDSA) guidelines,295 patients with pulmonary aspergillosis (IPA) and high risk of invasive infections were divided into four groups: IPA group (42 cases),clinically diagnosed group (68 cases),suspected group (61 cases),and non-IPA group (124 cases). Their serum and BALF concentrations of GM were detected by enzyme-linked immunosorbent assay (ELISA).The clinically diagnosed and confirmed invasive pulmonary fungal infections (IPFI) were treated as golden standards (+). A GM value ≥ proposed threshold was deemed diagnostic test positive. Receiver operating characteristic (ROC) curves were drawn to determine the diagnostic efficiency of BALF GM assay for IPFI. The optimal cut-off point of BALF GM was determined using Youden index. RESULTS: BALF GM had an area under the curve (AUC) of 0.932 in diagnosing IPFI,with 87.5% sensitivity, 96.7% specificity, 87.5% positive predictive value,and 96.7% negative predictive value when the BALF GM value was set at 1.5 ng/mL as the optimal cut-off point. Higher BALF and serum GM values were found in the confirmed IPA group,followed by the clinical diagnosed group compared with the non-IPA group ( P<0.05). The threshold value was set at 0.5 ng/mL for serum GM and 1.5 ng/mL for bronchoalveolar lavage GM. Higher positive rates were found in the confirmed IPA group and the clinical diagnosed group compared with the non-IPA group ( P<0.05). Serum GM appeared to have higher false positives and false negative rates. CONCLUSION: BALF GM is a rapid and accurate indicator with high sensitivity and specificity for the early diagnosis of IPA.

[Antibiotic Resistance and Risk Factors for Mortality of Blood Stream Infections (BSIs) with Escherichia coli in Patients with Hematological Malignancies].

OBJECTIVE: To analyze the risk factors for mortality of blood stream infections (BSIs) caused by Escherichia coli in the patients with hematological malignancies. METHODS: There were 110 Escherichia coli BSIs patients with hematological malignancies included in recent five years. Among them,77 cases had BSIs caused by extended-spectrum-beta-lactamase (ESBL)-producing Escherichia coli (ESBL-EC group),while 33 cases had BSIs with non-ESBL-producing Escherichia coli (non-ESBL-EC group). The antibiotic resistance and clinical features were compared between the two groups,and the risk factors for death within 30 d were analyzed. RESULTS: Less than 10% of the isolates were resistant to carbapenems and amikacin. Between ESBL-EC group and non-ESBL-EC group,the clinical symptoms,prior use of antibiotics or antifungal agents,risk factors for infection,30 d mortality rates were not significantly different (P>0.05). A logistic regression analysis confirmed that non remission of hematologic malignancies (odds ratio=9.575,95% confidence interval 1.546-59.312,P=0.015) and inappropriate initial antibiotic therapy (odds ratio=8.806,95% confidence interval 1.527-50.772, P=0.015) were independent risk factors for 30 d mortality. CONCLUSION: The use of effective antimicrobial treatment as early as possible could reduce the risk of death for hematological malignancies patients suffering Escherichia coli BSIs.

Different characteristics of cryptococcal meningitis between HIV-infected and HIV-uninfected patients in the Southwest of China.

Cryptococcus is the major pathogen that causes fungal meningitis. In the People's Republic of China, especially in the Southwest area, cryptococcal meningitis (CM) in HIV-uninfected patients is more common than in HIV-infected patients. We compared clinical features and laboratory data pertaining to CM in patients with different immunological statuses. Demographic data, clinical manifestations, and laboratory data from inpatients in West China Hospital Sichuan University were collected from June 2009 to June 2014. Patients were grouped according to HIV status. Continuous variables were evaluated by Student t-test or Wilcoxon rank sum tests. Categorical variables were analyzed by χ2 test. Among 85 patients with CM were identified, 53 (62.4%) were HIV-uninfected patients. CM occurred more frequently in males in the HIV-infected group. Compared with HIV-infected patients, HIV-uninfected patients had more leukocytes in their blood and more leukocytes and protein in cerebrospinal fluid. More HIV-uninfected patients had increased cerebrospinal fluid (CSF)/serum albumin ratios, while intrathecal immunoglobulin G (IgG) synthesis was significantly increased. The rate of in-hospital mortality of HIV-infected CM patients was higher. Clinical signs are similar between HIV-uninfected and HIV-infected CM patients. Fewer leukocytes and protein was detected in the CSF and lower local synthesis of IgG in the central nervous system in HIV-infected patients, which reflects their diminished immune response. These characteristics should be noted in order to avoid misdiagnosis. Meningeal enhancement and intrathecal IgG synthesis in the HIV-uninfected group was significantly higher, that may be performance of aggressive inflammatory response and might contribute to a better outcome.

Current applications of graphene oxide in nanomedicine.

Graphene has attracted the attention of the entire scientific community due to its unique mechanical and electrochemical, electronic, biomaterial, and chemical properties. The water-soluble derivative of graphene, graphene oxide, is highly prized and continues to be intensely investigated by scientists around the world. This review seeks to provide an overview of the currents applications of graphene oxide in nanomedicine, focusing on delivery systems, tissue engineering, cancer therapies, imaging, and cytotoxicity, together with a short discussion on the difficulties and the trends for future research regarding this amazing material.

[Antagonism of tert-butylhydroquinone on neurotoxicity and oxidative stress induced by paraquat in PC12].

OBJECTIVE: To investigate the protective effects of the tert-butylhydroquinone (tBHQ) pretreatment on neurotoxicity and oxidative stress induced by paraquat (PQ) in PC12 cells. METHODS: Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with different concentrations of 100, 300 micromol/L PQ for 24 h and 48 h. PC12 cells were pretreated with or without 40 micromol/L tBHQ for 4 h, PC12 cells were exposed to PQ at the doses of 0, 100, 300 micromol/L for 24 h and 48 h, respectively. The viability of PC12 cells was measured by MTT assay, the apoptosis rates of PC12 cells were detected by flow cytometry (FCM) and the malondialdehyde (MDA) levels of PC12 cells were examine by thiobarbituric acid (TBA) method. RESULTS: When the exposure doses of PQ were 100 and 300 micromol/L for 24 h, the viability of PC12 cells pretreated with tBHQ was significantly higher than that of PC12 cells only exposed to PQ (P < 0.05 or P < 0.01). When the exposure dose of PQ was 100 micromol/L for 48 h, the viability of PC12 cells pretreated with tBHQ was significantly higher than that of PC12 cells only exposed to PQ (P < 0.01). When the exposure doses of PQ were 100 and 300 micromol/L for 24 h, the apoptosis rates and MDA levels of PC12 cells pretreated with tBHQ were significantly lower than those of PC12 cells only exposed to PQ (P < 0.05 or P < 0.01). CONCLUSIONS: tBHQ pretreatment can reduce the cytotoxicity, apoptosis and oxidative stress induced by PQ in PC12 cells.

[Induction of cell damage and change of miR-133b expression by paraquat in PC12 cells].

OBJECTIVE: To investigate the effect of paraquat on induction of cell damage and miR-133b expression in PC12 cells. METHODS: Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with 50, 100, or 300 µmol/L paraquat. Cell apoptosis was examined by the method of Annexin V-FITC/PI in flow cytometry (FCM) and the relative level of miR-133b expression was measured by real time RT-PCR, following the PC12 cells treatment with 100 or 300 µmol/L paraquat. RESULTS: Survival rate of PC12 cells treated with 100 or 300 µmol/L paraquat was lower than that of the vehicle control group (P < 0.01, P < 0.05), in the dose dependent pattern. Apoptotic rate of PC12 cells treated with 100, 300 µmol/L paraquat was higher than that of the vehicle control group (P < 0.05). The relative level of miR-133b expression of PC12 cells treated with 300 µmol/L paraquat was higher than that of the vehicle control group (P < 0.05). CONCLUSIONS: Paraquat may cause cell damage and induce apoptosis in PC12 cells, and induce miR-133b expression.

Relationship between genetic polymorphisms of ALDH2 and ADH1B and esophageal cancer risk: a meta-analysis.

AIM: To evaluate the contribution of alcohol dehydrogenase-1B (ADH1B) and aldehyde dehydrogenase-2 (ALDH2) polymorphisms to the risk of esophageal cancer. METHODS: Nineteen articles were included by searching MEDLINE, EMBASE and the Chinese Biomedical Database, 13 on ADH1B and 18 on ALDH2. We performed a meta-analysis of case-control studies including 13 studies on ADH1B (cases/controls: 2390/7100) and 18 studies on ALDH2 (2631/6030). RESULTS: The crude odds ratio [OR (95% confidence interval)] was 2.91 (2.04-4.14) for ADH1B*1/*1 (vs ADH1B*2/*2) and 1.32 (1.17-1.49) for ADH1B*1/*2. The crude OR for ALDH2*1/*2 (vs ALDH2*1/*1) was 2.52 (1.76-3.61). ADH1B*1/*1 increased the risk of esophageal cancer among never/rare [1.56 (0.93-2.61)], moderate [2.71 (1.37-5.35)], and heavy drinkers [3.22 (2.27-4.57)]. ADH1B*1/*2 was associated with a modest risk among moderate drinkers [1.43 (1.09-1.87)]. ALDH2*1/*2 increased the risk among never/rare [1.28 (0.91-1.80)], moderate [3.12 (1.95-5.01)], and heavy [7.12 (4.67-10.86)] drinkers, and among ex-drinkers [5.64 (1.57-20.25)]. ALDH2*2/*2 increased the risk among drinkers [4.42 (1.72-11.36)]. ADH1B*1/*1 plus ALDH2*1/*2 was associated with the highest risk for heavy drinkers [12.45 (2.9-53.46)]. The results of the meta-regression analysis showed that the effects of ADH1B*1/*1 and ALDH2*1/*2 increased with the level of alcohol consumption. ALDH2*1/*2 was associated with a high risk among Taiwan Chinese and Japanese drinkers, as opposed to a moderate risk among drinkers in high-incidence regions of Mainland China. ADH1B*1/*1 in heavy drinkers and ALDH2*1/*2 in moderate-to-heavy drinkers was associated with similarly high risk among both men and women. CONCLUSION: ADH1B/ALDH2 genotypes affect the risk of esophageal cancer, and the risk is modified by alcohol consumption, ethnicity, and gender.

[Protective effect of tert-butylhydroquinone on PC12 cells from neurotoxicity induced by manganese in vitro].

OBJECTIVE: To investigate the protective effect of the tert-butylhydroquinone (tBHQ) on PC12 cells from neurotoxicity induced by manganese. METHODS: Cytotoxicity of PC12 cells was measured by MTT assay, following the PC12 cells treatment with different concentrations of MnCl2 (300, 600, 900 µmol/L) for 24, 48 or 72 h. PC12 cells were pretreated with 40 µmol/L tBHQ for 12 h, followed by the treatment of 600 micromol/L or 300 µmol/L MnCl2 for 72 h. Cytotoxicity of PC12 cells was measured by MTT assay, and cell apoptosis was examined by the method of Annexin V-FITC/PI in flow cytometry (FCM). RESULTS: The proliferation of PC12 cells treated with 300, 600, 900 µmol/L MnCl2 was suppressed in the dose dependent pattern (P < 0.01). Proliferation of PC12 cells treated with 600 µmol/L MnCl2 was suppressed to 40% of that in control group (P < 0.01), but the proliferation rate of PC12 cell pretreated with 40 µmol/L tBHQ was 180% of that in control group (P < 0.01). Apoptotic rate of PC12 cells treated with 300 micromol/L MnCl2 was higher than the vehicle control group (P < 0.01). Apoptotic rate of 40 µmol/L tBHQ pretreatment followed by 300 µmol/L MnCl2 treatment was lower than that of MnCl2 treatment group (P < 0.01). The inhibition rate of apoptosis was 61%. CONCLUSIONS: Manganese may suppress PC12 cells proliferation and induce apoptosis. tBHQ can reduce PC12 cells proliferation suppressed by manganese and attenuate the apoptosis induced by manganese.

NF-E2 related factor 2 activation and heme oxygenase-1 induction by tert-butylhydroquinone protect against deltamethrin-mediated oxidative stress in PC12 cells.

Recent findings suggest that oxidative stress caused by pyrethroid pesticides could be closely involved in the neurotoxicity. tert-Butylhydroquinone ( tBHQ) is a known inducer of Nrf2-mediated transcription, and treatment of cells with tBHQ can confer protection against H 2O 2 and 6-hydroxydopamine (6-OHDA). In this study, we investigated the neuroprotective effect of tBHQ against deltamethrin (DM)-induced oxidative stress using rat PC12 adrenal pheochromocytoma cells. The pretreatment of PC12 cells with tBHQ significantly reduced DM-induced generation of reactive oxygen species (ROS) and increased intracellular ionized calcium ([Ca (2+)] i). We also observed that DM or tBHQ induced the expression of NF-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1), a Nrf2-regulated gene. In addition, the Nrf2 antioxidant responsive element (ARE) pathways activated by tBHQ caused a partial inhibition of the DM-induced Nrf2 and HO-1 expression. Altogether, our data clearly indicate that an activation of Nrf2/ARE pathways in PC12 cells by tBHQ treatment protects cells from DM-induced oxidative stress and regulates DM- mediated adaptive responses in PC12 cells via translocation of Nrf2.

Transcription factor Nrf2 activation by deltamethrin in PC12 cells: Involvement of ROS.

Activation of transcription factor NF-E2-related factor 2 (Nrf2) is a key initiation step in the cellular protection against a broad range of chemical oxidative stresses. To gain insights into dopaminergic cell responses to pesticides, the present study was conducted to examine the effects of deltamethrin (DM), a prototype of widely used pyrithroid pesticides, on the activation and expression of Nrf2 in PC12 rat adrenal pheochromocytoma cells as a dopaminergic cell model. We found, for the first time, that DM enhanced cellular expression of Nrf2 at the transcriptional and protein levels and activated expression of Nrf2-regulated genes in these cells. In addition, DM exposure caused nuclear accumulation of Nrf2 in association with downstream activation of Nrf2-mediated oxidative response genes, such as heme oxygenase-l (HO-1) and gamma-glutamylcysteine synthetase catalytic heavy subunit (GCSh). Furthermore, when cells were pretreated with N-acetyl cysteine (NAC), a scavenger of reactive oxygen species (ROS), DM-induced Nrf2 signaling was suppressed. These results indicate that ROS is the mediator of nuclear Nrf2 accumulation. Taken together, these data clearly show that DM increases Nrf2 expression and activity and that ROS is one of the mediators of this process.

[Effects of deltamethrin on gene expression of some antioxidase, gamma glutamylcysteine synthetase and NFE2 related factor 2 (Nrf2) in brain tissue].

OBJECTIVE: To study the effects of deltamethrin (DM) on the mRNA expression of copper-zinc dependent SOD (CuZn-SOD), glutathione reductase (GR) and gamma glutamylcysteine synthetase (gamma-GCS) light subunit (GCSl), as well as on expression of both mRNA and protein of gamma-GCS heavy subunit (GCSh) and NFE2 related factor 2 (Nrf2) in cerebral cortex and hippocampus of rats. METHODS: Eighteen Wistar male rats were randomizedly divided into three groups, six for each group. The low dosage and high dosage DM treated groups were administrated intraperitoneally with DM (the daily dosage was 3.125, 12.500 mg/kg BWT respectively) for five consecutive days while the control group was administered intraperitoneally with olive oil. The relative amount of mRNA expression of these genes was measured by the method of reverse transcription polymerase chain reaction (RT-PCR) (n = 6). The protein level was detected by the method of immunohistochemistry and image analysis system (n = 4). RESULTS: There was no change in mRNA expression level of CuZn-SOD, GR, GCSh and Nrf2 gene in both cerebral cortex and hippocampus tissue in rats administrated with DM. However, the mRNA level of GCSl gene in cerebral cortex of high dosage group as well as in both cerebral cortex and hippocampus of the low dosage group was significantly lower than that in corresponding tissue in the control group, and was decreased to 71.1%, 63.6% and 75.2% of mRNA level of corresponding tissue in the control group (P < 0.01). There was no obvious effect on protein level of both GCSh and Nrf2 in CA1, CA2, CA3 and dentate gyrus (DG) of hippocampus as well as on that in cerebral cortex in rats treated with DM. CONCLUSION: Under the experimental conditions, there is no obvious effect in the mRNA expression level of CuZn-SOD, GR gene, as well as on expression of both mRNA and protein of Nrf2 gene in both cerebral cortex and hippocampus tissue in rats administered with DM. DM depresses the mRNA expression of GCSl gene, but does not affect the mRNA expression of GCSh gene.

[Effect of cadmium on estrogen receptor from rat uterus in vitro.].

OBJECTIVE: To investigate the effect of cadmium (Cd) on estrogen receptor and to assess its endocrine disrupting action. METHODS: The estrogen receptor rich supernatant was prepared from the ovariectomized Sprague-Dawley rats. The effects of cadmium on estrogen binding were performed using a sing-dose ligand-binding assay. Extract from uterus were treated with various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for various pre-incubation time (0, 30, 60, 90 min) by means of orthogonal experimental design with orthogonal layout of L16(4(5)) (the experiment was repeated for 5 times). In addition to the radioinert competitor, each assay included a zero tube and a DES standard curve for quality control purpose. Data for cadmium and the DES standard curve were plotted as percent [3H]-E2 bound versus log (molar concentration), and the IC50 for cadmium was determined. The RBA for cadmium was calculated by dividing the IC50 of DES in terms of the IC50 of cadmium. RESULTS: Cadmium could not block the binding of estradiol to the receptor because hormone binding did not change with increasing cadmium concentration or increasing preincubation time. The results showed that the binding of [3H]-estradiol to uterine cytosols was not significant (P > 0.05). The Bmax (its unit is pmol/mg protein) of various concentrations of cadmium (0, 10(-3), 10(-5) or 10(-7) mol/L) for pre-incubating 0 min is 203.15 +/- 75.16, 203.41 +/- 22.78, 220.82 +/- 45.35, 209.10 +/- 49.66 respectively; The Bmax of them for pre-incubating 30 min is 215.67 +/- 92.97, 139.79 +/- 53.78, 205.27 +/- 23.60, 172.63 +/- 55.09 respectively. The Bmax of them for pre-incubating 60 min is 197.11 +/- 50.68, 203.24 +/- 66.33, 183.92 +/- 31.89, 183.33 +/- 32.70, respectively. The Bmax of them for pre-incubating 90 min is 229.69 +/- 76.88, 175.70 +/- 70.28, 164.26 +/- 24.46, 150.78 +/- 65.97 respectively. Mean IC50 for cadmium is 10(-4) - 10(-3) M. If the affinities of DES binding to estrogen receptors was taken to be 100%, the relative binding affinities of cadmium was 10(-6) - 10(-7). The results indicated that cadmium had only a very poor affinity with estrogen receptor. CONCLUSION: In vitro assay cadmium did not have distinct disrupting effect on binding of estradiol to estrogen receptors from rat uterine.

[A clinical study on CD178 positive T lymphocyte in hemorrhagic fever with renal syndrome].

BACKGROUND: To further probe into the role of CD178 in the pathogenesis of hemorrhagic fever with renal syndrome (HFRS). METHODS: The expression of CD178 and HLA-DR on T cell subsets in peripheral blood of patients with HFRS and their dynamic changes were detected by Flow cytometry. RESULTS: CD4+ CD178+ and CD8+ CD178+ T lymphocytes both in fever and polyuria phases were significantly higher than those in normal controls, while there was no significant difference between the both phases of HFRS (P > 0.05). CD178 expression on CD4+ HLA-DR+ and CD8+ HLA-DR+ T lymphocytes were significantly higher than those in normal controls (P < 0.05, P < 0.01, P < 0.001, P < 0.001), while there was no significant difference between CD4+ HLA-DR+ and CD8+ HLA-DR+ T lymphocytes (P > 0.05). CONCLUSION: CD178 was expressed on both CD4+ and CD8+ T cell subsets, but mainly on CD8+ T cell subsets both in early stage and in later stage in the pathogenesis of HFRS. Cytotoxic T lymphocyte (CTL) might kill target cells infected by hantavirus (HV) and eliminate HV via cell apoptosis mediated by CD178 in early stage of HFRS. In later stage of HFRS, CD178 might reduce antigen-specific T lymphocytes by activation induced cell death (AICD) and help to maintain the homeostasis of immune system.

[The effect of cadmium pollution on reproductive health in females].

OBJECTIVE: To study the relationship between cadmium pollution and its adverse effects on female reproductive health status in people living in cadmium polluted area in Zhenghe, Fujian provinces. METHODS: Data through laboratory studies on reproductive health of female residents in Cd-pollution area were studied and compared with those in control areas in Zhenghe. RESULTS: Both prevalence rates of abnormal menstrual cycle and dysmenorrhea in unmarried women in Cd-pollution area (19.1% vs. 42.6%) were significantly higher than those in control area (5.7% vs. 18.9%) and the rates of sterility in married women in Cd-pollution area (6.3%) were significantly higher than those in control area (1.1%). During the first two pregnancies, rates of queasiness, disgorgement, spontaneous abortion and stillbirth in married women in polluted area were 44.7%, 31.7%, 10.27% and 4.23%, significantly higher than those 26.5%, 17.8%, 2.85% and 1.05% in control area, with significant differences (P < 0.05). Results from cumulative odds model analysis showed that: living in Cd-pollution area was a possible risk factor related to female reproductive health (OR = 2.072), after the other risk factors being under control. CONCLUSION: The female reproductive health status of people residing in the cadmium polluted area had already been deteriorated.