Decidualisation of ovarian endometriomas in pregnancy: a management dilemma. A case report and review of the literature     

Louise Helen Taylor  Thumuluru Kavitha Madhuri  Woodruff Walker  Karen Morton  Anil Tailor  Simon Butler-Manuel 《Archives of gynecology and obstetrics》2015,291(5):961-968

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Karyomapping—a comprehensive means of simultaneous monogenic and cytogenetic PGD: comparison with standard approaches in real time for Marfan syndrome     

Alan R. Thornhill  Alan H. Handyside  Christian Ottolini  Senthil A Natesan  Jon Taylor  Karen Sage  Gary Harton  Kerry Cliffe  Nabeel Affara  Michalis Konstantinidis  Dagan Wells  Darren K. Griffin 《Journal of assisted reproduction and genetics》2015,32(3):347-356

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Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models     

Jenny U. Johansson  Nathaniel S. Woodling  Qian Wang  Maharshi Panchal  Xibin Liang  Angel Trueba-Saiz  Holden D. Brown  Siddhita D. Mhatre  Taylor Loui  Katrin I. Andreasson 《The Journal of clinical investigation》2015,125(1):350-364

Microglia, the innate immune cells of the CNS, perform critical inflammatory and noninflammatory functions that maintain normal neural function. For example, microglia clear misfolded proteins, elaborate trophic factors, and regulate and terminate toxic inflammation. In Alzheimer’s disease (AD), however, beneficial microglial functions become impaired, accelerating synaptic and neuronal loss. Better understanding of the molecular mechanisms that contribute to microglial dysfunction is an important objective for identifying potential strategies to delay progression to AD. The inflammatory cyclooxygenase/prostaglandin E2 (COX/PGE₂) pathway has been implicated in preclinical AD development, both in human epidemiology studies and in transgenic rodent models of AD. Here, we evaluated murine models that recapitulate microglial responses to Aβ peptides and determined that microglia-specific deletion of the gene encoding the PGE₂ receptor EP2 restores microglial chemotaxis and Aβ clearance, suppresses toxic inflammation, increases cytoprotective insulin-like growth factor 1 (IGF1) signaling, and prevents synaptic injury and memory deficits. Our findings indicate that EP2 signaling suppresses beneficial microglia functions that falter during AD development and suggest that inhibition of the COX/PGE₂/EP2 immune pathway has potential as a strategy to restore healthy microglial function and prevent progression to AD.  相似文献   

Acute respiratory distress syndrome in patients with and without diffuse alveolar damage: an autopsy study     

José A. Lorente  Pablo Cardinal-Fernández  Diego Muñoz  Fernando Frutos-Vivar  Arnaud W. Thille  Carlos Jaramillo  Aida Ballén-Barragán  José M. Rodríguez  Oscar Peñuelas  Guillermo Ortiz  José Blanco  Bruno Valle Pinheiro  Nicolás Nin  María del Carmen Marin  Andrés Esteban  Taylor B. Thompson 《Intensive care medicine》2015,41(11):1921-1930

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The ten diseases that look like ARDS     

Claude Guérin  Taylor Thompson  Roy Brower 《Intensive care medicine》2015,41(6):1099-1102

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Polymorphisms in glutathione-S-transferase genes (GST-M1, GST-T1 and GST-P1) and susceptibility to prostate cancer among male smokers of the ATBC cancer prevention study.   总被引：2，自引：0，他引：2  

La Creis R Kidd  K Woodson  P R Taylor  D Albanes  J Virtamo  J A Tangrea 《European journal of cancer prevention》2003,12(4):317-320

Glutathione-S-transferase (GST) genes encode a family of detoxification enzymes that offer protection against endogenous and exogenous sources of reactive oxygen species (ROS). Germline variations in GST genes may alter the catalytic efficiency of GST isoenzymes leading to a potential increase in susceptibility to the genotoxic effects of ROS and electrophilic substances. A nested case-control study design was used to examine the association between the polymorphic GST genes and prostate cancer risk among Finnish male smokers of the ATBC Cancer Prevention Study. A case-case analysis was used to determine the association between these genetic polymorphisms and prostate cancer progression. Germline DNA was obtained from 206 prostate cancer cases and 194 controls frequency matched on age, intervention group and study clinic. Cases and controls were genotyped for three GST genes using MALDI-TOF mass spectrometry or multiplex polymerase chain reaction (PCR). Relative to the wild-type genotype, we observed a 36% reduction in prostate cancer risk associated with the GST-M1-null genotype (odds ratio (OR) 0.64, 95% confidence interval (CI) 0.43, 0.95). Unlike GST-M1, GST-T1-null (OR 0.74, 95% CI 0.42, 1.33) and GST-P1*B (OR 1.10, 95% CI 0.72, 1.69) were not strongly associated with prostate cancer risk. We did not observe any significant associations between the selected polymorphic GST genes and tumour grade or stage. In conclusion, we did not observe a direct association between polymorphic GST-T1 or GST-P1 and prostate cancer risk. Our observation of a relatively strong inverse association between the GST-M1-null genotype and prostate cancer risk needs to be confirmed in larger association studies.  相似文献   

Risk of hypertension in children with multicystic dysplastic kidney.     

C M Taylor 《Archives of disease in childhood》2006,91(3):277-8; author reply 277-8

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The successful treatment of primary cardiac lymphoma with a dose-dense schedule of rituximab plus CHOP.     

M A Dawson  J Mariani  A Taylor  G Koulouris  S Avery 《Annals of oncology》2006,17(1):176-177

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IFN-alpha1,8 inhibits tumor-induced angiogenesis in murine angiosarcomas.     

Kevin L Taylor  Rhonda K Oates  Ron Grane  Douglas W Leaman  Ernest C Borden  Daniel J Lindner 《Journal of interferon & cytokine research》2006,26(5):353-361

Interferon-alpha (IFN-alpha) has proved effective in the treatment of hemangiomas, hemangioblastomas, and Kaposi's sarcoma. To investigate the ability of IFNs to inhibit angiosarcoma, we used two transformed murine endothelial cell lines that form angiosarcomas in vivo. SVR and MS1-VEGF cell lines express oncogenic H-ras or vascular endothelial growth factor (VEGF), respectively. IFN-alpha1,8, which is active against murine and human cells, inhibited SVR and MS1-VEGF proliferation in vitro by 40% at 10(3) U/mL (p = 0.028). In vivo, IFN-alpha1,8 inhibited SVR tumor volume by 71% (p = 0.047) and MS1-VEGF volume by 79% (p = 0.003). Tumor-induced angiogenesis was decreased in SVR tumors by 52% (p = 0.005) and in MS1-VEGF tumors by 58% (p = 0.001). Sera from IFN-alpha1,8-treated mice bearing either SVR or MS1-VEGF tumors demonstrated a 5-fold increase in IP-10/CXCL10 (p = 0.001), an IFN-induced antiangiogenic protein. Both recombinant IP-10 and IFN-alpha1,8 inhibited human umbilical vein endothelial cell (HUVEC) vessel formation in the fibrin gel assay, a three-dimensional culture model of angiogenesis, by 56% at 25 ng/mL and 50% at 1.2 ng/mL, respectively (p < 0.001). An IP-10 blocking antibody restored vessel formation to 80% of untreated controls (p = 0.001). Given the magnitude of the in vivo response, these data suggested that the antitumor effects of IFN-alpha1,8 were likely mediated through angiogenesis inhibition rather than solely by direct inhibition of tumor cell proliferation.  相似文献   

Phase II trial of piroxantrone in patients with recurrent and metastatic squamous cell carcinoma of the head and neck     

Sarah A. Taylor  Jacqueline Benedetti  David Schuller  Stephen P. Richman  Goronwy O. Broun  Alexander Hantel 《Investigational new drugs》1993,11(2-3):227-229

Summary Twenty-two patients with recurrent or metastatic squamous cell carcinoma of the head and neck were treated with piroxantrone 150 mg/m² intravenously every 21 days. There were no objective responses. The 95% upper confidence bound for response is 15%. Primary toxicity was hematologic.  相似文献