排序方式: 共有75条查询结果,搜索用时 265 毫秒
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TM?Matthews RK?Duncan M?Zidanic TH?Michael PA?FuchsEmail author 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2005,191(6):491-503
In the inner ear of birds, as in mammals, reptiles and amphibians, acetylcholine released from efferent neurons inhibits hair cells via activation of an apamin-sensitive, calcium-dependent potassium current. The particular potassium channel involved in avian hair cell inhibition is unknown. In this study, we cloned a small-conductance, calcium-sensitive potassium channel (gSK2) from a chicken cochlear library. Using RT-PCR, we demonstrated the presence of gSK2 mRNA in cochlear hair cells. Electrophysiological studies on transfected HEK293 cells showed that gSK2 channels have a conductance of approximately 16 pS and a half-maximal calcium activation concentration of 0.74±0.17 M. The expressed channels were blocked by apamin (IC50=73.3±5.0 pM) and d-tubocurarine (IC50=7.6±1.0 M), but were insensitive to charybdotoxin. These characteristics are consistent with those reported for acetylcholine-induced potassium currents of isolated chicken hair cells, suggesting that gSK2 is involved in efferent inhibition of chicken inner ear. These findings imply that the molecular mechanisms of inhibition are conserved in hair cells of all vertebrates. 相似文献
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Abandoning ineffective medical practices and mitigating the risks of untested practices are important for improving patient health and containing healthcare costs. Historically, this process has relied on the evidence base, societal values, cultural tensions, and political sway, but not necessarily in that order. We propose a conceptual framework to guide and prioritize this process, shifting emphasis toward the principles of evidence-based medicine, acknowledging that evidence may still be misinterpreted or distorted by recalcitrant proponents of entrenched practices and other biases. 相似文献
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Elisabeth APM Romme David A McAllister John T Murchison Edwin JR Van Beek George S Petrides Cameron OS Price Erica PA Rutten Frank WJM Smeenk Emiel FM Wouters William MacNee 《Respiratory research》2013,14(1):129
Background
Cardiovascular disease, osteoporosis and emphysema are associated with COPD. Associations between these factors and whether they predict all-cause mortality in COPD patients are not well understood. Therefore, we examined associations between markers of cardiovascular disease (coronary artery calcification [CAC], thoracic aortic calcification [TAC] and arterial stiffness), bone density (bone attenuation of the thoracic vertebrae), emphysema (PI-950 and 15th percentile) and all-cause mortality in a COPD cohort.Methods
We assessed CAC, TAC, bone attenuation of the thoracic vertebrae, PI-950 and 15th percentile on low-dose chest computed tomography in COPD subjects. We measured arterial stiffness as carotid-radial pulse wave velocity (PWV), and identified deaths from the national register.Results
We studied 119 COPD subjects; aged 67.8 ±7.3, 66% were males and mean FEV1% predicted was 46.0 ±17.5. Subjects were classified into three pre-specificed groups: CAC = 0 (n = 14), 0 < CAC ≤ 400 (n = 41) and CAC > 400 (n = 64). Subjects with higher CAC were more likely to be older (p < 0.001) and male (p = 0.03), and more likely to have higher systolic blood pressure (p = 0.001) and a history of hypertension (p = 0.002) or ischemic heart disease (p = 0.003). Higher CAC was associated with higher PWV (OR 1.62, p = 0.04) and lower bone attenuation (OR 0.32, p = 0.02), but not with 15th percentile, after adjustment for age, sex and pack-years of smoking. In a Cox proportional hazards model, CAC, TAC and 15th percentile predicted all-cause mortality (HR 2.01, 2.09 and 0.66, respectively).Conclusions
Increased CAC was associated with increased arterial stiffness and lower bone density in a COPD cohort. In addition, CAC, TAC and extent of emphysema predicted all-cause mortality.Trial registration
Lothian NHS Board, Lothian Research Ethics Committee, LREC/2003/8/28. 相似文献26.
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Elthon G. Ferreira Diego V. Wilke Paula C. Jimenez Julieta R. de Oliveira Otília Deusdênia L. Pessoa Edilberto R. Silveira Francisco A. Viana Cláudia Pessoa Manoel Odorico de Moraes Eduardo Hajdu Letícia Veras Costa‐Lotufo 《化学与生物多样性》2011,8(8):1433-1445
Five guanidine alkaloids, mirabilin B ( 1 ), 8bβ‐hydroxyptilocaulin ( 2 ), ptilocaulin ( 3 ), and a mixture of the 8β‐ and 8α‐epimers, 4 and 5 , of 8‐hydroxymirabilin (1,8a;8b,3a‐didehydro‐8‐hydroxyptilocaulin), were isolated from Monanchora arbuscula colonies collected off the northeastern Brazilian coast. All structures were elucidated by spectroscopic analysis, including 1D (1H‐, 13C‐ (BB), and 13C‐DEPT) and 2D (COSY, HSQC, and HMBC) NMR experiments, and comparison with the literature data. The cytotoxicity of the isolated compounds were evaluated against four tumor cell lines, showing that mirabilin B ( 1 ) and the two epimers were inactive, while 8bβ‐hydroxyptilocaulin ( 2 ) and ptilocaulin ( 3 ) presented IC50 values in the range of 7.9 to 61.5 μM , and 5.8 to 40.0 μM , respectively. Further studies on the mechanism of action of ptilocaulin, using HL‐60 leukemia cells, demonstrated that this guanidine compound induced apoptosis of the treated cells. 相似文献
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Systems Biology involves the study of the interactions of biological systems and ultimately their functions. Down''s syndrome (DS)
is one of the most common genetic disorders which are caused by complete, or occasionally partial, triplication of chromosome 21,
characterized by cognitive and language dysfunction coupled with sensory and neuromotor deficits. Neural Tube Disorders
(NTDs) are a group of congenital malformations of the central nervous system and neighboring structures related to defective
neural tube closure during the first trimester of pregnancy usually occurring between days 18-29 of gestation. Several studies in the
past have provided considerable evidence that abnormal folate and methyl metabolism are associated with onset of DS & NTDs.
There is a possible common etiological pathway for both NTDs and Down''s syndrome. But, various research studies over the years
have indicated very little evidence for familial link between the two disorders. Our research aimed at the gene expression profiling
of microarray datasets pertaining to the two disorders to identify genes whose expression levels are significantly altered in these
conditions. The genes which were 1.5 fold unregulated and having a p-value <0.05 were filtered out and gene interaction network
were constructed for both NTDs and DS. The top ranked dense clique for both the disorders were recognized and over
representation analysis was carried out for each of the constituent genes. The comprehensive manual analysis of these genes yields
a hypothetical understanding of the lack of familial link between DS and NTDs. There were no genes involved with folic acid
present in the dense cliques. Only – CBL, EGFR genes were commonly present, which makes the allelic variants of these genes –
good candidates for future studies regarding the familial link between DS and NTDs.
Abbreviations
NTD - Neural Tube Disorders, DS - Down''s Syndrome, MTHFR - Methylenetetrahydrofolate reductase, MTRR– 5 - methyltetrahydrofolate-homocysteine methyltransferase reductase. 相似文献29.
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Barbosa KC Oba-Shinjo SM Uno M Carvalho PO Rosemberg S Aguiar PH Carlotti CG Malheiros SM Toledo S Lotufo P Marie SK 《The International journal of biological markers》2008,23(3):140-146
Epidermal growth factor receptor (EGFR) gene overexpression has been implicated in the development of many types of tumors, including glioblastomas, the most frequent diffusely infiltrating astrocytomas. However, little is known about the influence of the polymorphisms of EGFR on EGFR production and/or activity, possibly modulating the susceptibility to astrocytomas. This study aimed to examine the association of two EGFR promoter polymorphisms (c.-191C>A and c.-216G>T) and the c.2073A>T polymorphism located in exon 16 with susceptibility to astrocytomas, EGFR gene expression and survival in a case-control study of 193 astrocytoma patients and 200 cancer-free controls. We found that the variant TT genotype of the EGFR c.2073A>T polymorphism was associated with a significantly decreased risk of astrocytoma when compared with the AA genotype [sex- and age-adjusted odds ratio 0.51, 95% confidence interval 0.26-0.98]. No association of the two promoter EGFR polymorphisms (or combinations of these polymorphisms) and risk of astrocytomas, EGFR expression or survival was found. Our findings suggest that modulation of the EGFR c.2073A>T polymorphism could play a role in future therapeutic approaches to astrocytoma. 相似文献