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BACKGROUND: Although many studies have suggested that biomass smoke is a risk factor for COPD, the relationship between the two has not been firmly established. In particular, the extent of the association between exposure of biom...
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BACKGROUND: Although many studies have suggested that biomass smoke is a risk factor for COPD, the relationship between the two has not been firmly established. In particular, the extent of the association between exposure of biomass smoke and COPD in different populations, as well as the relationship between biomass smoke and cigarette smoke, is not clear. To ascertain the relationship between biomass smoke and COPD, we performed a metaanalysis. METHODS: We searched MEDLINE, EMBASE, and the Latin American and Caribbean Literature in Health Sciences Database and analyzed 15 epidemiologic (11 cross-sectional and four case-control) studies that met our criteria. Data were extracted and analyzed independently by two investigators using a standardized protocol. RESULTS: Overall, people exposed to biomass smoke have an odds ratio (OR) of 2.44 (95% CI, 1.9-3.33) for developing COPD, relative to those not exposed to biomass smoke. Biomass smoke exposure was clearly identified as a risk factor for developing COPD in both women (OR, 2.73; 95% CI, 2.28-3.28) and men (OR, 4.30; 95% CI, 1.85-10.01), and in both the Asian population (OR, 2.31; 95% CI, 1.41-3.78) and the non-Asian population (OR, 2.56; 95% CI, 1.71-3.83). This risk factor has also been revealed in patients with chronic bronchitis (OR, 2.56; 95% CI, 1.77-3.70) and COPD (OR, 2.65; 95% CI, 1.75-4.03), and in cigarette smokers (OR, 4.39; 95% CI, 1.40-4.66) and non-cigarette smokers (OR, 2.55; 95% CI, 2.06-3.15). CONCLUSIONS: Exposure to biomass smoke is a risk factor for COPD.
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We investigated the potential of human hair follicle cells for multilineage differentiation and as a source of functional smooth muscle cells (SMCs). We report that human hair follicle stem cells (HFCs) isolated from individual fo...
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We investigated the potential of human hair follicle cells for multilineage differentiation and as a source of functional smooth muscle cells (SMCs). We report that human hair follicle stem cells (HFCs) isolated from individual follicles expressed surface markers that are characteristic of mesenchymal stem cells such as CD44, CD49b, CD73, CD90, and CD105 but lacked hematopoietic markers CD45 and CD34. In addition, HFCs differentiated toward adipocytes, chondrocytes, osteoblasts, or SMCs in the appropriate induction medium. Treatment with basic fibroblast growth factor increased proliferation and prevented myogenic differentiation, suggesting that basic fibroblast growth factor can be used to expand the population of undifferentiated HFCs to the large numbers needed for therapeutic applications. SMCs were isolated from HFCs using tissue-specific promoters and flow cytometry sorting. Cylindrical vascular constructs engineered with HF-SMCs showed remarkable contractility in response to receptor and nonreceptor agonists such KCl, endothelin-1, and the thromboxane mimetic, U46619, as well as superior mechanical properties compared to their counterparts with human vascular SMCs. Our results suggest that HF is a rich source of mesenchymal stem cells with great potential for myogenic differentiation providing functional SMCs for tissue regeneration and cell therapies.
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The essential role of the transcription factor Foxp3 in the development and function of Treg has been well documented. The role of Foxp3 in non-Treg, however, is not fully understood. Emerging evidence indicates that Foxp3 express...
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The essential role of the transcription factor Foxp3 in the development and function of Treg has been well documented. The role of Foxp3 in non-Treg, however, is not fully understood. Emerging evidence indicates that Foxp3 expression is not confined to CD4+CD25+ Treg. The present study shows that in Foxp3 transgenic (Foxp3-Tg) mice, in which the transgene is driven by the lck distal promoter, CD4+CD25- T cells that express the Foxp3 transgene do not upregulate the expression of CD25-, GITR, or CTLA-4, and do not have suppressive function; however, the Foxp3-Tg+CD4+CD25- T cells exhibit significantly reduced proliferative response to TCR engagement. Foxp3-Tg mice are resistant to collagen-induced arthritis via reduced cellular proliferation of activated T cells. These findings indicate that Foxp3 upregulation in activated non-Treg may be a mechanism to suppress immune responses by reduced clonal expansion of activated T cells.
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Using statistical parametric mapping (SPM), we evaluate the feasibility and accuracy of (18) F -2-deoxy-2-fluoro-D-glucose (FDG) positron emission tomography (PET) for clinical diagnosis with characteristic hypo-metabolic regions,...
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Using statistical parametric mapping (SPM), we evaluate the feasibility and accuracy of (18) F -2-deoxy-2-fluoro-D-glucose (FDG) positron emission tomography (PET) for clinical diagnosis with characteristic hypo-metabolic regions, and examine the consistency of cerebral hypo-metabolism in Alzheimer's disease (AD) cross multicenters at both the group and the individual levels. Four groups of scan data including 39 AD patients and 52 healthy control subjects derived from three centers were analyzed and comparisons between patient subgroups or individual patient and relevant control population were performed using Two Sample T-test. In the group analysis, the hypo-metabolic regions of AD patients obtained from different PET centers were similar and consistent. The common hypo-metabolic cerebral areas were located bilaterally in the posterior cingulate and medial parietal cortex, temporo-parietal cortex, prefrontal cortex, and the middle and inferior temporal gyrus (uncorrected, p<0.001). In the analysis of each individual subject, the location of declined posterior cingulate and medial parietal cortex, temporo-parietal cortex and temporal lobe were found highly consistent with relevant characteristic regions obtained in the group analysis and were selected for diagnostic purposes. Complete typical hypo-metabolic pattern was observed in 67% and 54% of AD patients in two sets of 3D scans, respectively. Only 27% and 33.3% patients showed full typical pattern in two sets of 2D scans. The results indicated that FDG PET measures and SPM can 4 provide a valuable reference for clinical diagnosis of AD patients. The potential influence of acquisition mode on the clinical diagnosis of AD was suggested for further evaluation.
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PURPOSE: This study investigated the expression and release of tissue plasminogen activator (t-PA) in lipopolysaccharide (LPS)-induced retinal microglia activation. We evaluated change in microglia activation following down-regula...
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PURPOSE: This study investigated the expression and release of tissue plasminogen activator (t-PA) in lipopolysaccharide (LPS)-induced retinal microglia activation. We evaluated change in microglia activation following down-regulation of t-PA expression by siRNA interference. METHODS: The primary cultured microglia cells were isolated from retinas of S-D rats and activated with different concentration of LPS (0, 3, 10, 30, 100, and 300 ng/ml). Double immunofluorescence (OX42 and tPA) and Western blot were used to detect t-PA expression. Next, tPA expression was down-regulated by siRNA interference, the microglia transfected with tPA siRNA lentivirus or blank control lentivirus were activated with 30 ng/ml of LPS, the culture supernatant was collected 1, 3, 6, 12, and 24 hours after LPS treatment for IL-1beta and TNF-alpha ELISA assays, and the cells were collected 24 hours later for immunocytochemistry of microglia markers (OX42 and Iba-1) and quantitative real-time PCR to determine the inhibitory efficiency of t-PA siRNA. Transfection efficiency was evaluated with flow cytometry by EGFP expression. RESULTS: The microglia expressed t-PA when treated with LPS in a dose-dependent pattern. The expression was down-regulated by siRNA interference markedly; the inhibitory efficiency was 80% as determined by quantitative real-time PCR. Transfection efficiency during siRNA interference was 88%. The expression of Iba-1 and the release of IL-1beta and TNF-alpha were inhibited significantly when the t-PA expression was knocked down. CONCLUSIONS: Activated microglia express t-PA. Down-regulation of t-PA expression can inhibit the activation of microglial cell.
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PURPOSE: The present study was undertaken to examine the amplification and expression status of Cks1 in breast cancer and its significance. METHODS: The amplification and expression status of Cks1 gene was examined by FISH, real-t...
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PURPOSE: The present study was undertaken to examine the amplification and expression status of Cks1 in breast cancer and its significance. METHODS: The amplification and expression status of Cks1 gene was examined by FISH, real-time PCR and immunohistochemistry, respectively. RNA interference was used to detect the effects of Cks1 on migration, invasion, cell cycle progress and apoptosis of breast cancer cells. RESULTS: Cks1 gene amplification was highly correlated with protein overexpression. Overexpression of Cks1 was strongly associated with lymph node metastasis and poor prognosis (P = 0.000, 95% CI (0.00-0.02); P = 0.008, 95% CI (0.001-0.05), respectively). Knockdown of Cks1 expression by RNA interference inhibited the cell cycle progress, migration and invasion ability of breast cancer cells. Moreover, overexpression of Cks1 inhibited apoptosis of breast cancer cells through MEK-Erk pathway. CONCLUSION: Cks1 may be considered as potential novel prognostic markers and targets for the future development of specific therapeutic interventions in breast cancer.
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Activation-induced deaminase (AID) is a prerequisite for immunoglobulin (Ig) class-switch recombination and somatic hypermutation, which is critical for antibody affinity maturation. IgM and IgG autoantibodies are characteristic o...
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Activation-induced deaminase (AID) is a prerequisite for immunoglobulin (Ig) class-switch recombination and somatic hypermutation, which is critical for antibody affinity maturation. IgM and IgG autoantibodies are characteristic of the systemic autoimmune disorders such as lupus. However, the relative contributions of hypermutated high-affinity IgG antibodies and germline-encoded IgM antibodies to systemic autoimmunity are not defined fully. The role of AID in autoimmunity is unclear. The current study used AID-deficient mice to investigate the role of AID in the development and pathogenesis of murine lupus. C57BL/6 mice deficient in both Fas and AID were generated. Compared to their AID-competent littermates, AID(-/-) lymphoproliferative (lpr) mice produced significantly elevated levels of IgM autoreactive antibodies with enhanced germinal centre (GC) response, developed more advanced splenomegaly and exhibited more severe glomerulonephritis. Thus, AID may play an important role in the negative regulation of systemic autoimmune manifestations in murine lupus. The results also indicate that hypermutated high-affinity IgG antibodies are not necessary for the development of autoimmune syndrome in lpr mice on a C57BL/6 background.
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Asperosaponin VI is a saponin of the medicinal herb Dipsacus asper (Xuduan), and no pharmacological activity has been reported yet. In this study, we investigated the anti-myocardial ischemia effects of Asperosaponin VI (ASA VI) b...
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Asperosaponin VI is a saponin of the medicinal herb Dipsacus asper (Xuduan), and no pharmacological activity has been reported yet. In this study, we investigated the anti-myocardial ischemia effects of Asperosaponin VI (ASA VI) both in vivo and in vitro. An animal model of myocardial ischemia(MI) injury was induced by coronary occlusion, pretreatment with ASA VI (10 and 20mg/kg, i.v.) could protect the heart from ischemia injury by decreasing the levels of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), glutamic oxalacetic transaminase (GOT) and cardiac troponin T (cTnT) in serum, increasing the levels of catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) levels in heart, and decreasing that of malondialdehyde (MDA) level in acute MI rats. ASA VI also raised the activities of mitochondrial enzymes (succinate dehydrogenase (SDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase (MDH) and alpha-ketoglutarate dehydrogenase (alpha-KGDH)) and those of adenosine triphosphate (ATP) content, but lowered Ca(2+) level. Electrocardiograph parameters and histopathological observations demonstrated the same protective effects. In vitro experiment, neonatal rat cardiomyocytes were incubated to test the direct cytoprotective effect of ASA VI against H(2)O(2) exposure. Pretreatment with ASA VI (30 and 60 microg/ml) prior to H(2)O(2) exposure increased cell viability and inhibited H(2)O(2)-induced reactive oxygen species increase. ASA VI (15, 30 and 60 microg/ml) also increased the activities of LDH in the cultured supernatant and SOD in cardiomyocytes, but decreased the cardiomyocytes MDA level. Our results suggested that ASA VI could provide significant cardioprotective effects against acute MI in rats. The mechanisms might be attributed to scavenging lipid peroxidation products and reactive oxygen species, increasing antioxidant defense enzymes and preventing mitochondrial damage.
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This study was to determine if bone marrow multipotent adult progenitor cells (MAPCs) underwent cardiac specification and Oct-4 expression during their cardiomyocyte differentiation in vitro. MAPCs were isolated from rat bone marr...
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This study was to determine if bone marrow multipotent adult progenitor cells (MAPCs) underwent cardiac specification and Oct-4 expression during their cardiomyocyte differentiation in vitro. MAPCs were isolated from rat bone marrow, treated with 5-azacytidine (5-aza, 1muM) for 24h, and cultured in a serum-free medium for cardiac differentiation for up to 35 days. The cells started to express early cardiac-specific genes Nkx2.5 and GATA-4 with a significant increase in their mRNA level within 24h after 5-aza treatment. Western blotting analysis and immunofluorescence staining revealed that the cardiac-specific proteins connexin-43 and troponin I were expressed in the cells 7 days after 5-aza treatment. Flow cytometry analysis demonstrated that over 37% of the cells were positive for troponin I by 35 days of differentiation, although the cells did not display spontaneous contraction. On the other hand, the undifferentiated MAPCs expressed a significant level of the stem-cell-specific marker Oct-4 that was dramatically decreased in the cells shortly after the initiation of cardiomyocyte differentiation as evaluated using real-time (RT)-polymerase chain reaction, Western blotting, immunofluorescence staining, and flow cytometry. These data indicated that MAPCs were able to effectively differentiate into cardiomyocyte-like cells after 5-aza induction in association with downregulation of Oct-4 expression.
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Hyperleptinemia is a common feature of obese women who have a higher risk of endometrial cancer than women with normal weights, and epidemiologic studies have suggested a correlation between obesity and endometrial carcinoma. Ther...
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Hyperleptinemia is a common feature of obese women who have a higher risk of endometrial cancer than women with normal weights, and epidemiologic studies have suggested a correlation between obesity and endometrial carcinoma. Therefore, understanding of the molecular mechanism involved in leptin signaling transduction is important in endometrial cancer prevention and treatment. In this study, both isoforms of the leptin receptor (Ob-R), the long form (Ob-Rb) and short form (Ob-Ra), were detected as being expressed in six endometrial cancer cell lines with various differentiation status by western blotting, and Ob-Ra was found to be more abundant than Ob-Rb in these cells. Moreover, the expressions of both isoforms were inversely correlated with histoprognostic grading. We also showed that leptin stimulated cell proliferation and induced activations of signal transducers and activators of transcription 3 (STAT3), extracellular signal-regulated kinase (ERK1/2), AKT, and cyclooxygenase (COX)-2 in endometrial cancer cells dose-dependently by [(3)H] thymidine incorporation assay and western blotting. Leptin-stimulation resulted in increased expression of COX-2 mRNA and prostaglandin E2 (PGE2) production of endometrial cancer cells by reverse transcription-polymerase chain reaction and enzyme immunoassay, respectively, which was effectively blocked by pharmacological inhibitors of Janus tyrosine kinase 2 (JAK2), AG490; of mitogen-activated protein kinase (MAPK) kinase, U0126; of phosphatidylinositol 3-kinase (PI3K), LY294002; and of COX-2, NS398. These results suggest that leptin promotes cell proliferation of endometrial cancer cells via the aforementioned multiple signal-transduction pathways. Leptin-induced functional activation of COX-2 is JAK2/STAT3-, MAPK/ERK-, and PI3K/AKT-dependent, indicating that COX-2 may be a critical factor of endometrial carcinogenesis in obesity.
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