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排序方式: 共有198条查询结果,搜索用时 15 毫秒
1.
J. Philip Kuebler Terry D. Oberley Lorraine F. Meisner Younan A. Sidky Catherine A. Reznikoff Ernest C. Borden Kenneth B. Cummings George T. Bryan 《Investigational new drugs》1987,5(1):21-29
Interferon-, interferon-, and interferon- differ in their antiproliferative effects for several cell lines. Interferons were thus assessed for their activity in inhibiting proliferation of three renal cell carcinoma cell lines. The malignant epithelial phenotype of each of these cell lines was confirmed by electron microscopy, histology, karyotype and tumorigenicity. When compared on an anti-viral unit basis, naturally produced interferon- was more effective than natural interferon- for all cell lines and clones. Proliferation of each of the cell lines was inhibited by interferon-. In all cases, removal of interferons from culture media resulted in resumption of the rate of cell growth after a variable delay of 6–10 days. If the antiproliferative effects of interferons predominate in mediating tumor regression, clinical response may depend upon the type of interferon to which the tumor is exposed. 相似文献
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目的:探讨术前血清糖链抗原19-9(CA19-9)阳性和(或)甲胎蛋白(AFP)阳性的胃癌患者临床病理特征,及两者联合分析与胃癌的临床病理之间的联系。方法:回顾性分析南京医科大学第一附属医院900例术前检测血清CA19-9和AFP水平的胃癌患者临床病理资料。结果:与CA19-9阴性者相比,CA19-9阳性患者T分期更晚(T4期,94.2% vs. 65.5%),临床分期更晚(Ⅲ+Ⅳ期,89.2% vs. 61.5%),淋巴结转移率更高(80% vs. 61.3%),脉管和神经侵犯比例更高(32.5% vs. 23.3%;42.5% vs. 27.1%),差异有统计学意义(P<0.05);与AFP阴性者相比,AFP阳性患者临床分期更晚(Ⅲ+Ⅳ期,88.9% vs. 60.6%),淋巴结转移率更高(81.5% vs. 59.1%),更容易发生神经侵犯(44.4% vs. 27.0%),差异有统计学意义(P<0.05)。与CA19-9和AFP均阴性的患者相比,一种或两种肿瘤指标阳性的患者T分期更晚,临床分期更晚,淋巴结转移率更高,更容易出现脉管和神经侵犯(P<0.05)。二元Logistic回归多变量分析显示CA19-9阳性是影响胃癌侵犯深度的独立危险因素;与CA19-9(-)-AFP(-)比较,CA19-9(+)-AFP(+)是影响胃癌脉管浸润的独立危险因素,CA19-9(+)-AFP(-)是影响胃癌侵犯深度的独立危险因素(P<0.05)。结论:术前血清CA19-9和AFP水平与胃癌临床病理密切相关,术前检测其水平有助于为胃癌患者临床病理特征提供信息。 相似文献
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Duraid Younan Chee Paul Lin Robert Johnson Robert Clark Lisa Smith Jean-Francois Pittet Mali Mathru David W. Miller 《The American journal of emergency medicine》2018,36(8):1439-1443
Background
Little data is available in the literature about the role of end tidal oxygen in critically ill patients. We sought to identify the association between the level of respiratory oxygen and clinical outcomes in critically-ill ventilated trauma and burn patients.Methods
A retrospective cohort of 55 trauma and burn patients from 2010 to 2016 was collected. Exposures of interest included a) expiratory end tidal oxygen (ETO2) and b) the difference between FiO2 and ETO2 (uptake). Associations of clinical characteristics with ETO2 and oxygen uptake were examined using a Spearman correlation. The relationships between discharge status, demographics, injury type, severity, and clinical characteristics were examined using chi-square (or Fisher's exact) tests and two-sample t-tests. Multivariable analyses using linear and logistic regression were performed to determine whether expiratory end tidal oxygen or oxygen uptake was an independent predictor of clinical outcomes.Results
Mean age for the patients was 46.3 ± 18.2 years with 41 (74.6%) male and 34 (61.8%) white. In the cohort, 27 (49.1%) of patients had burns and 28 (50.9%) blunt trauma. Oxygen uptake was negatively correlated with lactic acid, minute ventilation, total ICU days, and ventilator days (p < 0.05). Patients who died demonstrated lower oxygen uptake than those alive, oxygen uptake remained significantly associated with discharge status after adjusting for potential confounders (p = 0.028).Conclusion
A narrowed difference between ETO2 and inspiratory oxygen is associated with increased mortality in a cohort of ventilated trauma and burn patients. Future research is needed to further elucidate the role of respiratory oxygen level in larger, prospective studies. 相似文献7.
Introduction
Through binding to von Willebrand factor (VWF), platelet glycoprotein (GP) Ibα, the major ligand-binding subunit of the GPIb-IX-V complex, initiates platelet adhesion and aggregation in response to exposed VWF or elevated fluid-shear stress. There is little data regarding non-human primate platelet GPIbα. This study cloned and characterized rhesus monkey (Macaca Mullatta) platelet GPIbα.Materials and Methods
DNAMAN software was used for sequence analysis and alignment. N/O-glycosylation sites and 3-D structure modelling were predicted by online OGPET v1.0, NetOGlyc 1.0 Server and SWISS-MODEL, respectively. Platelet function was evaluated by ADP- or ristocetin-induced platelet aggregation.Results
Rhesus monkey GPIbα contains 2,268 nucleotides with an open reading frame encoding 755 amino acids. Rhesus monkey GPIbα nucleotide and protein sequences share 93.27% and 89.20% homology respectively, with human. Sequences encoding the leucine-rich repeats of rhesus monkey GPIbα share strong similarity with human, whereas PEST sequences and N/O-glycosylated residues vary. The GPIbα−binding residues for thrombin, filamin A and 14-3-3ζ are highly conserved between rhesus monkey and human. Platelet function analysis revealed monkey and human platelets respond similarly to ADP, but rhesus monkey platelets failed to respond to low doses of ristocetin where human platelets achieved 76% aggregation. However, monkey platelets aggregated in response to higher ristocetin doses.Conclusions
Monkey GPIbα shares strong homology with human GPIbα, however there are some differences in rhesus monkey platelet activation through GPIbα engagement, which need to be considered when using rhesus monkey platelet to investigate platelet GPIbα function. 相似文献8.
9.
Isen Joshua Tuvblad Catherine Younan Diana Ericson Marissa Raine Adrian Baker Laura A. 《Child psychiatry and human development》2022,53(2):199-211
Child Psychiatry & Human Development - The developmental course of antisocial behavior is often described in terms of qualitatively distinct trajectories. However, the genetic etiology of... 相似文献
10.
Xinhui Wang Diana Younan Joshua Millstein Andrew J. Petkus Erika Garcia Daniel P. Beavers Mark A. Espeland Helena C. Chui Susan M. Resnick Margaret Gatz Joel D. Kaufman Gregory A. Wellenius Eric A. Whitsel JoAnn E. Manson Stephen R. Rapp Jiu-Chiuan Chen 《Proceedings of the National Academy of Sciences of the United States of America》2022,119(2)
Late-life ambient air pollution is a risk factor for brain aging, but it remains unknown if improved air quality (AQ) lowers dementia risk. We studied a geographically diverse cohort of older women dementia free at baseline in 2008 to 2012 (n = 2,239, aged 74 to 92). Incident dementia was centrally adjudicated annually. Yearly mean concentrations of fine particulate matter (PM2.5) and nitrogen dioxide (NO2) were estimated using regionalized national universal kriging models and averaged over the 3-y period before baseline (recent exposure) and 10 y earlier (remote exposure). Reduction from remote to recent exposures was used as the indicator of improved AQ. Cox proportional hazard ratios (HRs) for dementia risk associated with AQ measures were estimated, adjusting for sociodemographic, lifestyle, and clinical characteristics. We identified 398 dementia cases during follow up (median = 6.1 y). PM2.5 and NO2 reduced significantly over the 10 y before baseline. Larger AQ improvement was associated with reduced dementia risks (HRPM2.5 0.80 per 1.78 μg/m3, 95% CI 0.71–0.91; HRNO2 0.80 per 3.91 parts per billion, 95% CI 0.71–0.90), equivalent to the lower risk observed in women 2.4 y younger at baseline. Higher PM2.5 at baseline was associated with higher dementia risk (HRPM2.5 1.16 per 2.90 μg/m3, 95% CI 0.98–1.38), but the lower dementia risk associated with improved AQ remained after further adjusting for recent exposure. The observed associations did not substantially differ by age, education, geographic region, Apolipoprotein E e4 genotypes, or cardiovascular risk factors. Long-term AQ improvement in late life was associated with lower dementia risk in older women.Consistent evidence from epidemiologic studies and toxicological experiments has shown that ambient air pollution is an important modifiable risk factor of dementia (1). Several studies have shown an increased risk of dementia associated with late-life exposures to regional fine particulate matter (PM2.5; with aerodynamic diameter < 2.5 μm) (2–15) and gaseous pollutants (e.g., NO2; NOx) (2–4, 11, 12, 15–17) in particular. Over the past 50 y, significant improvements in air quality (AQ) have been observed across the United States because of national policies and strategies aimed at regulating pollution from stationary (power plants; factories) and mobile (vehicles) sources (18). Several US studies have shown that these long-term reductions in air pollution levels are associated with improved lung function (19), decreased bronchitic symptoms (20), lower asthma incidence (21), lengthened life expectancy (22), and reduced mortality (23). However, it remains unclear whether improved AQ also benefits the aging brains.Therefore, we conducted a multiyear study to examine the association between improved AQ and incidence of dementia, which was based on Diagnostic and Statistical Manual of Mental Disorders (Fourth edition) criteria and centrally adjudicated annually (24, 25). We examined data from the Women’s Health Initiative (WHI) Memory Study (WHIMS)—Epidemiology of Cognitive Health Outcomes (WHIMS-ECHO) that included a combined 20 y of data on individual-level outdoor air pollution (1998 to 2012) estimated using regionalized national universal kriging models (26–28) and cognitive function assessed annually (2008 to 2018) in a geographically diverse sample of community-dwelling older women in the United States. We hypothesized that improved AQ over the span of 10 y, as indicated by reductions in PM2.5 and NO2 (proxy for traffic pollutants), was associated with lower dementia risk. 相似文献