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51.
Oxidative Status,Inflammation, and Postoperative Atrial Fibrillation With Metoprolol vs Carvedilol or Carvedilol Plus N‐Acetyl Cysteine Treatment 下载免费PDF全文
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Flow cytometry detection of minimal residual disease in multiple myeloma: Lessons learned at FDA‐NCI roundtable symposium 下载免费PDF全文
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Frank J. Molnar MSc MDCM Sophiya Benjamin MBBS MD Stacey A. Hawkins BA MA CPG PhD Student Melanie Briscoe OT Sabeen Ehsan MBBS MD MHI 《Journal of the American Geriatrics Society》2020,68(10):2207-2213
Every year, millions of patients worldwide undergo cognitive testing. Unfortunately, new barriers to the use of free open access cognitive screening tools have arisen over time, making accessibility of tools unstable. This article is in follow-up to an editorial discussing alternative cognitive screening tools for those who cannot afford the costs of the Mini-Mental State Examination and Montreal Cognitive Assessment (see www.dementiascreen.ca ). The current article outlines an emerging disruptive “free-to-fee” cycle where free open access cognitive screening tools are integrated into clinical practice and guidelines, where fees are then levied for the use of the tools, resulting in clinicians moving on to other tools. This article provides recommendations on means to break this cycle, including the development of tool kits of valid cognitive screening tools that authors have contracted not to charge for (i.e., have agreed to keep free open access). The PRACTICAL.1 Criteria ( PRACTI cing C linician A ccessibility and L ogistical Criteria Version 1 ) are introduced to help clinicians select from validated cognitive screening tools, considering barriers and facilitators, such as whether the cognitive screening tools are easy to score and free of cost. It is suggested that future systematic reviews embed the PRACTICAL.1 criteria, or refined future versions, as part of the standard of review. Methodological issues, the need for open access training to insure proper use of cognitive screening tools, and the need to anticipate growing ethnolinguistic diversity by developing tools that are less sensitive to educational, cultural, and linguistic bias are discussed in this opinion piece. J Am Geriatr Soc 68:2207–2213, 2020. 相似文献
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Purpose
Lymphomas are the third most common childhood malignant disease after leukemia and central nervous system (CNS) tumors. Early diagnosis of these complications will reduce mortality and morbidity. In this study we aimed to review the neurological complications of childhood non Hodgkin Lymphoma (NHL).Patients and methods
Forty four children with NHL between 2006 and 2012 were investigated retrospectively and 14 cases with neurological complications were identified.Results
The most common symptom was alteration of the consciousness (10 patients, 71.4 %) followed by convulsion (5 patients, 35.7 %), and hallucination (4 patients, 28.5 %); headache, eye pain, neurogenic bladder, speech disability and facial paralysis, and hemiplegia, were less common and each of them was seen in 1 (7.1 %) of the patients. The neurological complications were mostly seen in children with precursor T lymphoblastic lymphoma followed by anaplastic large cell lymphoma. The complications were secondary to medications (Eight patients) infection (two patients); CNS relapse (two patients); or CNS involvement of the primary disease (two patients). Chemotherapy-related neurologic complications were secondary to intrathecal methotrexate, l-asparaginase, vincristine, and ifosfamideConclusion
Advanced disease and PTLL subtype can be suggested as predictors of neurological complication. The survival rates of neurological complications are fairly good unless it is secondary to involvement of the primary disease. In patients with drug-induced neurological complications, the treatment can be safely re-administered after controlling the neurological complications. Therefore, clinicians managing children with NHL must be informative about neurological complications. 相似文献58.
Robert Philibert Meeshanthini Dogan Steven R. H. Beach James A. Mills Jeffrey D. Long 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2020,183(1):51-60
Many existing DNA repositories do not have robust characterizations of smoking, while for many currently ongoing studies, the advent of vaping has rendered traditional cotinine‐based methods of determining smoking status unreliable. Previously, we have shown that methylation status at cg05575921 in whole blood DNA can reliably predict cigarette consumption. However, whether methylation status in saliva can be used similarly has yet to be established. Herein, we use DNA from 418 biochemically confirmed smokers or nonsmokers to compare and contrast the utility of cg05575921 in classifying and quantifying cigarette smoking. Using whole blood DNA, a model incorporating age, gender, and methylation status had a receiver operating characteristic (ROC) area under the curve (AUC) for predicting smoking status of 0.995 with a nonlinear demethylation response to smoking. Using saliva DNA, the ROC AUC for predicting smoking was 0.971 with the plot of the relationship of DNA methylation to daily cigarette consumption being very similar to that seen for whole blood DNA. The addition of information from another methylation marker designed to correct for cellular heterogeneity improved the AUC for saliva DNA to 0.981. Finally, in 31 subjects who reported quitting smoking 10 or more years previously, cg05575921 methylation was nonsignificantly different from controls. We conclude that DNA methylation status at cg05575921 in DNA from whole blood or saliva predicts smoking status and daily cigarette consumption. We suggest these epigenetic assessments for objectively ascertaining smoking status will find utility in research, clinical, and civil applications. 相似文献
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Justin Taylor Mark T.A. Donoghue Caleb Ho Kseniya Petrova-Drus Hikmat A. Al-Ahmadie Samuel A. Funt Yanming Zhang Umut Aypar Pavitra Rao Shweta S. Chavan Michael Haddadin Roni Tamari Sergio Giralt Martin S. Tallman Raajit K. Rampal Priscilla Baez Rajya Kappagantula Satyajit Kosuri Ahmet Dogan Satish K. Tickoo Victor E. Reuter George J. Bosl Christine A. Iacobuzio-Donahue David B. Solit Barry S. Taylor Darren R. Feldman Omar Abdel-Wahab 《The Journal of clinical investigation》2020,130(12):6668
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Emine Melis Yücel Bugra Tolga Konduk Ahmet Saracaloglu Sezgin Barutu Seniz Demiryürek Fatma Kaba Belma Dogan Güngen Abdullah Tuncay Demiryürek 《The Turkish journal of gastroenterology》2021,9(9):765
Background: Wilson disease (WD) is an autosomal recessive inherited disorder of copper (Cu2+) metabolism, resulting in Cu2+ accumulation and liver and central nervous system toxicity. Oxidative stress may have a role in the pathogenesis of Wilson disease, but the roles of thiol/disulfide homeostasis and nitrosative stress have not been examined. The purpose of this study was to evaluate whether there is a modification in thiol/disulfide homeostasis and nitrosative stress in patients with Wilson disease.Methods: A total of 50 patients with Wilson disease (42 under drug treatment and 8 newly diagnosed patients with no drug treatment) and 50 healthy gender- and age-matched controls were enrolled for this study. Serum native thiol and total thiol levels were measured with a spectrophotometric method. The number of disulfide bonds and the related ratios were determined from these measurements. Serum nitric oxide (NO) and 3-nitrotyrosine (3-NT) levels were analyzed using chemiluminescence and ELISA assays, respectively.Results: The average native thiol levels of the patient group under drug treatment were found to be markedly higher than the levels of controls (P < .05). We detected no marked changes in total thiol and disulfide levels, and disulfide/total thiol, disulfide/native thiol, or native thiol/total thiol ratios between groups. We found significant elevations in NO levels in Wilson disease group before drug treatment, and the 3-NT levels in the Wilson disease groups prior to (P < .05) and under drug treatment (P < .01), when compared to controls.Conclusion: Our data are the first to show that nitrosative stress and thiol/disulfide homeostasis can contribute to the pathogenesis of Wilson disease. 相似文献