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排序方式: 共有8908条查询结果,搜索用时 15 毫秒
61.
Rosie Ashbolt Jenny Barralet Robert Bell Dennis Bittisnich Andrew Black Barry Combs Christine Carson Scott Crerar Craig Dalton Joy Gregory Michelle Harlock Gillian Hall Geoff Hogg Martyn Kirk Karin Lalor Tony Merritt Sally Munnoch Jennie Musto Lillian Mwanri Leonie Neville Chris Oxenford Rhonda Owen Jane Raupach Cameron Sault Russell Stafford Barbara Telfer Hassan Vally Kefle Yohannes 《Communicable diseases intelligence》2005,29(1):85-88
62.
Ines Lessa Maria Jenny Araújo Lucélia Magalh?es Naomar de Almeida Filho Estela Aquino Maria Cecília R Costa 《Pan American journal of public health》2004,16(2):131-137
OBJECTIVE: To estimate the frequency of modifiable cardiovascular risk factors, with and without inclusion of arterial hypertension, occurring simultaneously in a racially-mixed population. METHOD: A cross-sectional study was carried out with 1,298 adults aged > or = 20 years in the city of Salvador, Brazil, in 2000. Eight modifiable cardiovascular risk factors were assessed, in any combination: total cholesterol > or = 240 mg/dL; high density-lipoprotein cholesterol (HDL-c) < 40 mg/dL; triglycerides > or = 200 mg/dL; glycemia > or = 126 mg/dL + well-controlled diabetes; body mass index > or = 25 kg/m2, waist > or = 102 cm for males and > or = 88 cm for females, smoking and alcoholism. The results were stratified according to the number of simultaneous risk factors (zero to five or more and two or more risk factors). The data were analyzed in terms of estimated proportions and 95% confidence intervals (95%CI), with and without the inclusion of arterial hypertension (VI Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure [JNC-VI], United States of America), ratio of proportions and chi-square for proportions as a measure of association. RESULTS: Among men (41.4% of participants), 7.5% (95%CI: 2.5 to 9.7) did not present risk factors; 68.8% (95%CI: 65.0 to 72.8) presented two or more risk factors, not including hypertension. After inclusion of hypertension, 73.4% (95%CI: 69.7 to 77.1) presented two or more risk factors. Among women, 11.6% did not present risk factors. The presence of two or more risk factors, not including hypertension, was observed in 67.7% (95%CI: 64.8 to 71.4). After inclusion of hypertension, 71.7% (95%CI: 68.5 to 74.9) of the women presented two or more risk factors. Significant differences were observed for the presence of two or more risk factors in men with not more than 4 years of schooling vs. 5 to less than 11 years of schooling (P < 0.05); in women with not more than 4 years of schooling vs. 5 to less than 11 years of schooling; in women with not more than 4 years of schooling vs. 11 or more years of schooling (P < 0.01); and in black vs. white women (P < 0.01). CONCLUSIONS: The high proportion of clustering cardiovascular risk factors in Salvador, with or without hypertension, especially in the population with little schooling and in black individuals, suggests the need for broad social strategies to reduce social inequality, promote health, and facilitate the treatment of cardiovascular risk factors. 相似文献
63.
Caroline C Dong Xuejun J Yin Jane Y C Ma Lyndell Millecchia Mark W Barger Jenny R Roberts Xing-Dong Zhang James M Antonini Joseph K H Ma 《Toxicological sciences》2005,88(1):150-160
Exposure to diesel exhaust particles (DEP) during the sensitization process has been shown to increase antigen-specific IgE production and aggravate allergic airway inflammation in human and animal models. In this study, we evaluated the effect of short-term DEP exposure on ovalbumin (OVA)-mediated responses using a post-sensitization model. Brown Norway rats were first exposed to filtered air or DEP (20.6 +/- 2.7 mg/m3) for 4 h/day for five consecutive days. One day after the final air or DEP exposure (day 1), rats were sensitized with aerosolized OVA (40.5 +/- 6.3 mg/m3), and then again on days 8 and 15, challenged with OVA on day 29, and sacrificed on days 9 or 30, 24 h after the second OVA exposure or the final OVA challenge, respectively. Control animals received aerosolized saline instead of OVA. DEP were shown to elicit an adjuvant effect on the production of antigen-specific IgE and IgG on day 30. At both time points, no significant airway inflammatory responses and lung injury were found for DEP exposure alone. However, the OVA-induced inflammatory cell infiltration, acellular lactate dehydrogenase activity and albumin content in bronchoalveolar lavage (BAL) fluid, and numbers of T cells and their CD4+ and CD8+ subsets in lung-draining lymph nodes were markedly reduced by DEP on day 30 compared with the air-plus-OVA exposure group. The OVA-induced nitric oxide (NO) in the BAL fluid and production of NO, interleukin (IL)-10, and IL-12 by alveolar macrophages (AM) were also significantly lowered by DEP on day 30 as well as day 9. DEP or OVA alone decreased intracellular glutathione (GSH) in AM and lymphocytes on days 9 and 30. The combined DEP and OVA exposure resulted in further depletion of GSH in both cell types. These results show that short-term DEP exposure prior to sensitization had a delayed effect on enhancement of the sensitization in terms of allergen-specific IgE and IgG production, but caused an attenuation of the allergen-induced airway inflammatory responses. 相似文献
64.
65.
Patterns of resistance and incomplete response to docetaxel by gene expression profiling in breast cancer patients. 总被引:8,自引:0,他引:8
Jenny C Chang Eric C Wooten Anna Tsimelzon Susan G Hilsenbeck M Carolina Gutierrez Yee-Lu Tham Mamta Kalidas Richard Elledge Syed Mohsin C Kent Osborne Gary C Chamness D Craig Allred Michael T Lewis Helen Wong Peter O'Connell 《Journal of clinical oncology》2005,23(6):1169-1177
PURPOSE: Chemotherapy for operable breast cancer decreases the risk of death. Docetaxel is one of the most active agents in breast cancer, but resistance or incomplete response is frequent. PATIENTS AND METHODS: Core biopsies from 24 patients were obtained before treatment with neoadjuvant docetaxel (four cycles, 100 mg/m(2) every 3 weeks), and response was assessed after chemotherapy. After 3 months of neoadjuvant chemotherapy, surgical specimens (n = 13) were obtained, and laser capture microdissection (LCM; n = 8) was performed to enrich for tumor cells. From each core, surgical, and LCM specimen, sufficient total RNA (3 to 6 microg) was extracted for cDNA array analysis using the Affymetrix HgU95-Av2 GeneChip (Affymetrix, Santa Clara, CA). RESULTS: From the initial core biopsies, differential patterns of expression of 92 genes correlated with docetaxel response (P = .001). However, the molecular patterns of the residual cancers after 3 months of docetaxel treatment were strikingly similar, independent of initial sensitivity or resistance. This relative genetic homogeneity after treatment was observed in both LCM and non-LCM surgical specimens. The residual tumor after treatment in tumors that were initially sensitive indicates selection of a residual and resistant subpopulation of cells. The gene expression pattern was populated by genes involved in cell cycle arrest at G(2)M (eg, mitotic cyclins and cdc2) and survival pathways involving the mammalian target of rapamycin. CONCLUSION: A specific and consistent gene expression pattern was found in residual tumors after docetaxel treatment. These profiles provide therapeutic targets that could lead to improved treatment. 相似文献
66.
67.
68.
Saman K. Hashmi Katie Bergstrom Alison A. Bertuch Jenny M. Despotovic Eyal Muscal Fan Xia Weimin Bi Andrea Marcogliese Rosa Diaz 《Pediatric blood & cancer》2019,66(1)
Neutropenia in pediatric patients can be due to a variety of disorders. We describe two patients who underwent extensive evaluation over many years for arthralgias and moderate neutropenia of unclear etiology. Genetic testing identified a pathogenic variant in PSTPIP1 (proline‐serine‐threonine phosphatase‐interacting protein 1) in both patients. Markedly elevated inflammatory markers and zinc levels confirmed the rare diagnosis of PSTPIP1‐associated myeloid‐related proteinemia inflammatory (PAMI) syndrome, tailoring treatment. Neutropenia is common in patients with PAMI syndrome. Unique mutations seen in PAMI syndrome may account for the specific phenotypic features of this disorder. 相似文献
69.
Bettina Kuschel Georgia Chenevix-Trench Amanda B Spurdle Xiaoqing Chen John L Hopper Graham G Giles Margret McCredie Jenny Chang-Claude Catherine S Gregory Nick E Day Douglas F Easton Bruce A J Ponder Alison M Dunning Paul D P Pharoah 《Cancer epidemiology, biomarkers & prevention》2005,14(7):1828-1831
A substantial proportion of the familial risk of breast cancer may be due to genetic variants, each contributing a small effect. The protein encoded by ERCC2 is a key enzyme involved in nucleotide excision repair, in which gene defects could lead to cancer prone syndromes such as Xeroderma pigmentosum D. We have examined the association between single nucleotide polymorphisms in the ERCC2 gene and the incidence of invasive breast cancer in three case-control series, with a maximum of 3,634 patients and of 3,340 controls. None of the three single nucleotide polymorphisms were significantly associated with the incidence of breast cancer. 相似文献
70.
Inherited variation in circadian rhythm genes and risks of prostate cancer and three other cancer sites in combined cancer consortia 下载免费PDF全文
Fangyi Gu Han Zhang Paula L. Hyland Sonja Berndt Susan M. Gapstur William Wheeler the ELLIPSE consortium Christopher I. Amos Stephane Bezieau Heike Bickeb?ller Hermann Brenner Paul Brennan Jenny Chang‐Claude David V Conti Jennifer Anne Doherty Stephen B Gruber Tabitha A Harrison Richard B Hayes Michael Hoffmeister Richard S Houlston Rayjean J. Hung Mark A. Jenkins Peter Kraft Kate Lawrenson James McKay Sarah Markt Lorelei Mucci Catherine M. Phelan Conghui Qu Angela Risch Mary Anne Rossing H.‐Erich Wichmann Jianxin Shi Eva Schernhammer Kai Yu Maria Teresa Landi Neil E. Caporaso 《International journal of cancer. Journal international du cancer》2017,141(9):1794-1802
Circadian disruption has been linked to carcinogenesis in animal models, but the evidence in humans is inconclusive. Genetic variation in circadian rhythm genes provides a tool to investigate such associations. We examined associations of genetic variation in nine core circadian rhythm genes and six melatonin pathway genes with risk of colorectal, lung, ovarian and prostate cancers using data from the Genetic Associations and Mechanisms in Oncology (GAME‐ON) network. The major results for prostate cancer were replicated in the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, and for colorectal cancer in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). The total number of cancer cases and controls was 15,838/18,159 for colorectal, 14,818/14,227 for prostate, 12,537/17,285 for lung and 4,369/9,123 for ovary. For each cancer site, we conducted gene‐based and pathway‐based analyses by applying the summary‐based Adaptive Rank Truncated Product method (sARTP) on the summary association statistics for each SNP within the candidate gene regions. Aggregate genetic variation in circadian rhythm and melatonin pathways were significantly associated with the risk of prostate cancer in data combining GAME‐ON and PLCO, after Bonferroni correction (ppathway < 0.00625). The two most significant genes were NPAS2 (pgene = 0.0062) and AANAT (pgene = 0.00078); the latter being significant after Bonferroni correction. For colorectal cancer, we observed a suggestive association with the circadian rhythm pathway in GAME‐ON (ppathway = 0.021); this association was not confirmed in GECCO (ppathway = 0.76) or the combined data (ppathway = 0.17). No significant association was observed for ovarian and lung cancer. These findings support a potential role for circadian rhythm and melatonin pathways in prostate carcinogenesis. Further functional studies are needed to better understand the underlying biologic mechanisms. 相似文献