tbuckley/cabot-search huggingface dataset:
Distinct Mitotic Segregation Errors Mediate Chromosomal Instability in Aggressive Urothelial Cancers
Authors: Yuesheng Jin, Ylva Stewénius, David Lindgren, Attila Frigyesi, Olga Calcagnile, Tord Jonson, Anna Edqvist, Nina Larsson, Lena Maria Lundberg, Gunilla Chebil, Fredrik Liedberg, Sigurdur Gudjonsson, Wiking Månsson, Mattias Höglund, David Gisselsson
Journal: Clinical Cancer Research (2007)

Abstract Purpose: Chromosomal instability (CIN) is believed to have an important role in the pathogenesis of urothelial cancer (UC). The aim of this study was to evaluate whether disturbances of mitotic segregation contribute to CIN in UC, if these processes have any effect on the course of disease, and how deregulation of these mechanisms affects tumor cell growth. Experimental Design: We developed molecular cytogenetic methods to classify mitotic segregation abnormalities in a panel of UC cell lines. Mitotic instabilities were then scored in biopsies from 52 UC patients and compared with the outcome of tumor disease. Finally, UC cells were exposed in vitro to a telomerase inhibitor to assess how this affects mitotic stability and cell proliferation. Results: Three distinct chromosome segregation abnormalities were identified: (a) telomere dysfunction, which triggers structural rearrangements and loss of chromosomes through anaphase bridging; (b) sister chromatid nondisjunction, which generates discrete chromosomal copy number variations; and (c) supernumerary centrosomes, which cause dramatic shifts in chromosome copy number through multipolar cell division. Chromosome segregation errors were already present in preinvasive tumors and a high rate mitotic instability was an independent predictor of poor survival. However, induction of even higher levels of the same segregation abnormalities in UC cells by telomerase inhibition in vitro led to reduced tumor cell proliferation and clonogenic survival. Conclusion: Several distinct chromosome segregation errors contribute to CIN in UC, and the rate of such mitotic errors has a significant effect on the clinical course. Efficient tumor cell proliferation may depend on the tight endogenous control of these processes.
Physostigmine Reversal of Diazepam-lnduced Hypnosis
Authors: G. R. AVANT
Journal: Annals of Internal Medicine (1979)

Under randomized double-blind conditions, 1.00 to 1.67 mg of intravenous physostigmine (Antilirium) reversed sleep induced by administration of 0.102 to 0.238 mg/kg body weight of intravenous diazepam in eight healthy human volunteers. Awakening occurred 330 to 740 s after initiation of the physostigmine infusion at a rate of 0.5 mg/min every 4 min. Diazepam plasma levels were not significantly different at the start of either the physostigmine or placebo infusion. Physostigmine did not effect plasma binding of diazepam. Six subjects experienced nausea, and one subject developed an arrhythmia. Physostigmine reverses diazepam-induced hypnosis but causes side-effects requiring cautious administration.
p53 Mutation, Expression, and DNA Ploidy in Evolving Gliomas: Evidence for Two Pathways of Progression
Authors: D. J. van Meyel, D. A. Ramsay, A. G. Casson, M. Keeney, A. F. Chambers, J. G. Cairncross
Journal: JNCI Journal of the National Cancer Institute (1994)

Two lines of evidence indirectly implicate the tumor suppressor p53 (also known as TP53) gene in glioma development. First, germline mutations of the p53 gene are associated with increased susceptibility to glioma. Second, chromosome 17p deletions and p53 gene mutations are found frequently in sporadic gliomas of all malignancy stages. These observations suggest that mutations of the p53 gene may be early events in glioma development.Our purpose was to analyze 15 low-grade astrocytic gliomas that progressed to higher-grade gliomas, examining the status of the p53 gene in both the initial and recurrent tumors. Also, we explored the relationships between p53 status, DNA ploidy, tumor grade, and patient survival.Fifteen low-grade gliomas that recurred as tumors of higher grade 17-102 months after initial treatment (biopsy, resection, radiotherapy, or chemotherapy) were identified from hospital records of patients (eight male and seven female) aged 31-68 years. Pathologic diagnosis was re-evaluated. Polymerase chain reaction (PCR)-single-strand conformation polymorphism and DNA sequencing were performed on tissue samples from the initial and recurrent tumors of each patient, using oligonucleotide PCR primers directed to exons 5-9 of the p53 gene. p53 expression was determined by immunohistochemistry and DNA ploidy evaluated by DNA flow cytometry.Eight (53%) of fifteen tumors had p53 mutations in exons 5-9. Nine (64%) of fourteen were immunopositive initially, and eight of these were also immunopositive at recurrence. p53 gene status was significantly associated with p53 expression in the initial tumor (P = .02), and p53 expression at initial diagnosis was significantly related to tumor pathology at recurrence (P = .03). Patients with p53 mutant tumors survived nearly twice as long as those without mutations (median survival, 61 versus 33 months; P = .031). There was no significant difference in recurrence-free survival between patients with p53 mutant and nonmutant tumors (48 versus 33 months; P = .37), but there was a significant difference in postrecurrence survival (17 versus 2 months; P = .019).Low-grade tumors that recurred as anaplastic gliomas were characterized by p53 gene mutation, immunopositivity, and DNA non-diploidy. Low-grade tumors that recurred as glioblastomas generally had intact p53 genes and were immunonegative. These findings suggest that histologically indistinguishable, low-grade astrocytic gliomas that are destined to progress to higher grades, do so along two distinct clinicopathologic pathways (either stepwise to anaplastic glioma, then glioblastoma, or directly to glioblastoma) marked by the presence or absence of p53 mutation.
Toxic Shock Syndrome Following Submucous Resection and Rhinoplasty
Authors: Stephanie W. Thomas
Journal: JAMA (1982)

IN 1978, the illness known as toxic shock syndrome (TSS) was first described by Todd and co-workers.<sup>1</sup>During 1979 and 1980 the number of patients recognized as having this disease increased dramatically, and recent publications have described in detail the epidemiology and nature of the illness.<sup>2,3</sup>Although there is a striking association between vaginal colonization with<i>Staphylococcus aureus</i>, menstrual bleeding, and the use of vaginal tampons, the pathogenesis of TSS is not completely understood. The presence of an occlusive tampon together with breaks or abrasions of the vaginal mucosa may allow multiplication of<i>S aureus</i>and perhaps enhance the absorption of a toxin elaborated by this organism.<sup>3</sup> The combination of menstruation and tampon use is thought to contribute to production of the disease in the great majority of instances. Recently, Reingold and associates<sup>4</sup>described a number of patients with TSS that was not associated with menses
Malpractice Risk in Ambulatory Settings
Authors: Gianna Zuccotti
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Progress in Neurology and Psychiatry, an Annual Review
Authors: C. C. BURLINGAME
Journal: American Journal of Psychiatry (1947)

false fabrication, oi tnat tallacy called by Whitehead "the fallacy of misplaced concreteness."Another fallacy is in- volved, "the belief that it is not too difficult to know the truth."Another precept which has always guided the best physi- cians, "So far as possible do no harm.""You can do harm by the process that is quaintly called telling the truth.You can do harm by lying.""The doctor is never privileged to lie to the patient, but he is privileged to tell the patient part of the truth."Even though this series of essays and opinions does not give a final answer to the question, it does give much help in telling how much or how little of the truth should be told.The most valuable parts of the book are those written by nurses, religious leaders and psychiatrists.They seem to point the way toward a more cooperative effort on the part of all concerned.
Less than 10% of obese adults accept that they have a serious weight problem, survey finds
Authors: J. Wise
Journal: BMJ (2014)

Most obese people in Britain do not recognise themselves as obese or even very overweight, new research has shown. The researchers said that public health initiatives were likely to be hampered by people’s lack of recognition of their weight status.1

The study, published in BMJ Open , examined participants’ perception of their weight by using data from two population based surveys, each of around 2000 people, carried out in 2007 and 2012. From those groups 160 men and 182 women in 2007 and 166 men and 149 women in …
Chronic Amlodipine Treatment During the Development of Heart Failure
Authors: Francis G. Spinale, Rupak Mukherjee, R. Stephen Krombach, Mark J. Clair, Jennifer W. Hendrick, Ward V. Houck, Latha Hebbar, Scott B. Kribbs, James L. Zellner, Michael G. Dodd
Journal: Circulation (1998)

Background —This study examined the effects of chronic amlodipine treatment on left ventricular (LV) pump function, systemic hemodynamics, neurohormonal status, and regional blood flow distribution in an animal model of congestive heart failure (CHF) both at rest and with treadmill exercise. In an additional series of in vitro studies, LV myocyte contractile function was examined. Methods and Results —Sixteen pigs were studied under normal control conditions and after the development of chronic pacing–induced CHF (240 bpm, 3 weeks, n=8) or chronic pacing and amlodipine (1.5 mg · kg −1 · d −1 , n=8). Under ambient resting conditions, LV stroke volume (mL) was reduced with CHF compared with the normal control state (16±2 versus 31±2, P &lt;0.05) and increased with concomitant amlodipine treatment (29±2, P &lt;0.05). At rest, systemic and pulmonary vascular resistance (dyne · s −1 · cm −5 ) increased with CHF compared with the normal control state (3102±251 versus 2156±66 and 1066±140 versus 253±24, respectively, both P &lt;0.05) and were reduced with amlodipine treatment (2108±199 and 480±74, respectively, P &lt;0.05). With CHF, LV stroke volume remained reduced and was associated with a 40% reduction in myocardial blood flow during treadmill exercise, whereas chronic amlodipine treatment normalized LV stroke volume and improved myocardial blood flow. Resting and exercise-induced plasma norepinephrine levels were increased by &gt;5-fold in the CHF group and were reduced by 50% from CHF values with chronic amlodipine treatment. Resting plasma endothelin (fmol/mL) increased with CHF compared with the normal state (10.4±0.9 versus 3.1±0.3, P &lt;0.05) and was reduced with amlodipine treatment (6.6±1.1, P &lt;0.5). With CHF, LV myocyte velocity of shortening (μm/s) was reduced compared with normal controls (39±1 versus 64±1, P &lt;0.05) and was increased with chronic amlodipine treatment (52±1, P &lt;0.05). Conclusions —Chronic amlodipine treatment in this model of developing CHF produced favorable hemodynamic, neurohormonal, and contractile effects in the setting of developing CHF.
Unrecognized Anemia in Patients With Diabetes
Authors: Merlin C. Thomas, Richard J. MacIsaac, Con Tsalamandris, David Power, George Jerums
Journal: Diabetes Care (2003)

OBJECTIVE—Anemia is common in diabetes, potentially contributing to the pathogenesis of diabetes complications. This study aims to establish the prevalence and independent predictors of anemia in a cross-sectional survey of 820 patients with diabetes in long-term follow-up in a single clinic. RESEARCH DESIGN AND METHODS—A full blood count was obtained in addition to routine blood and urine test results for all patients over a 2-year period to encompass all patterns of review. Predictors of the most recent Hb concentration and anemia were identified using multiple and logistic regression analysis. RESULTS—A total of 190 patients (23%) had unrecognized anemia (Hb &amp;lt;12 g/dl for women and &amp;lt;13 g/dl for men). This prevalence is two to three times higher than for patients with comparable renal impairment and iron stores in the general population. Independent predictors for Hb were transferrin saturation, glomerular filtration rate (GFR), sex, albumin excretion rate, and HbA1c level (all P &amp;lt; 0.0001). Microalbuminuric patients were &amp;gt;2 times (odds ratio [OR] 2.3) and macroalbuminuric patients &amp;gt;10 times (OR 10.1) as likely to have anemia than normoalbuminuric patients with preserved renal function (GFR &amp;gt;80 ml/min). CONCLUSIONS—Anemia is a common accompaniment to diabetes, particularly in those with albuminuria or reduced renal function. Additional factors present in diabetes may contribute to the development of increased risk for anemia in patients with diabetes.
New life form to be created
Authors: D. Josefson
Journal: BMJ (2002)

OBJECTIVE: Oxidative stress contributes to joint inflammation and damage in rheumatoid arthritis. In a mobile inflamed joint, exercise induced multiple cycles of hypoxia-reperfusion injury may lead to the creation of a redox environment in which oxido-reductase systems, by NADPH mechanisms, produce highly reactive chemical species (i.e., oxygen free radicals). We investigated 2 endproducts of lipid peroxidation, malonildialdehyde (MDA) and diene conjugates (DC), and the formation of antibodies against oxidized low density lipoproteins (Ab oxLDL) in juvenile chronic arthritis (JCA), and assessed the role of oxidative phenomena in different phases and subsets of this disease. METHODS: To assess the role of oxidative stress in JCA, we measured the endproducts of lipid peroxidation, MDA and DC, by the increase of absorbance at 586 nm and 234 nm, respectively, and the levels of Ab oxLDL by ELISA in the sera of 58 patients with JCA and 21 healthy controls. Due to crossreactivity between Ab oxLDL and anticardiolipin antibodies (aCL), the sera were also tested by a standard ELISA for IgG-aCL. The patients were divided into 3 subsets: 29 with pauciarticular (pauci), 15 with polyarticular (poly), and 14 with systemic (sys) onset disease, and then were subdivided, according to different variables appropriate to each subset, reflecting active and inactive disease, into 30 active (14 pauci, 8 poly, 8 sys) and 28 inactive (15 pauci, 7 poly, 6 sys). RESULTS: Levels of Ab oxLDL were significantly increased in the whole group of patients (566.6 +/- 263.0 vs 206.6 +/- 136.3 mU/ml; p &lt; 0.001) and in each of the type of onset (pauci 660.8 +/- 272.1, p &lt; 0.001; poly 341.3 +/- 134.7, p &lt; 0.01; sys 497.8 +/- 114.8, p &lt; 0.001) compared to controls. Ab oxLDL were higher in the inactive than in the active group (743.5 +/- 231.9 and 404.4 +/- 169.9; p &lt; 0.001). MDA and DC levels were not increased significantly in patients9 sera. No patient was positive for IgG-aCL. CONCLUSION: These findings suggest that MDA and DC cannot be considered major markers of oxidative stress in JCA and that the Ab oxLDL may represent a delayed sign of oxidative stress previously induced by the inflammatory process in patients with JCA.
Hospital information booklets.
Authors: D A Spencer
Journal: BMJ (1971)

of electronic automatic counters has com- pletely altered this, for they can count many thousands of cells in a few seconds.The Coulter Model "S" counts approximately 18,000 cells in each of three replicate channels in four seconds.These three replicate counts correspond closely and the inherent error should be only a fraction of that of counts done visually.Automatic cell counters may introduce a number of errors of their own, such as co- incidence counts, incorrect setting of the threshold of discrimination, or those due to the presence of bubbles in the sample line.Nevertheless the precision now achieved with red cell counts gives the M.C.V. a status that it could not hold previously.(3) Neither the manual nor the automatic
SPATIAL CORONARY ARTERIAL DISTRIBUTION OF NON-CULPRIT LESION ATHEROSCLEROTIC EVENTS: ANALYSIS FROM THE PROSPECT TRIAL.
Authors: Adriano M. Caixeta, Alexandra J. Lansky, Ecaterina Cristea, Bernard de Bruyne, John McPherson, Akiko Maehara, Gary S. Mintz, Roxana Mehran, Eugenia Nikolsky, Barry Templin, Patrick W. Serruys, Gregg W. Stone
Journal: Journal of the American College of Cardiology (2010)
Testing of PRODIGY continues
Authors: I. Purves, G. Nestor, K. Williams
Journal: BMJ (1998)

EDITOR—Walton et al correctly state that “both CAPSULE and PRODIGY [computer support systems for prescribing] represent attempts to bring the benefits of computer support … into primary care” and highlight the lack of relevant research at the primary level.1 Their paper provides evidence that computers influence prescribing in general practice, with the potential economic benefits identified by the Audit Commission. Analysis of the cost effectiveness of prescribing interventions needs, however, to be presented within a wider assessment of overall healthcare costs, and the notions …
Beside B-type natriuretic peptide in the emergency diagnosis of systolic and nonsystolic heart failure: Results from the breathing not properly (BNP) multinational study
Authors: Alan S. Maisel, Radmila Kazanegra, Peter A. McCullough, James McCord, Richard M. Nowak, Judd E. Hollander, Alan H. Wu, Philippe Duc, Torbjorn Omland, Alan B. Storrow, Padma Krishnaswamy, William T. Abraham, Paul Clopton, Philippe Gabriel Steg, Arne Westheim, Cathrine World Knudsen, Howard C. Herrmann
Journal: Journal of the American College of Cardiology (2003)
Combined Replacement of Aortic and Mitral Valves
Authors: Robert S. Cartwright
Journal: JAMA (1962)

An operative approach to the ventricular aspect of the aortic valve has permitted combined prosthetic replacement of the aortic and mitral valves. In the first clinical trial of the method, the patient recovered promptly from the surgery and was dramatically improved. This operative technique, which was developed in the experimental laboratory, consisted of a left thoracotomy, left atriotomy, and excision of the mitral and aortic valves, followed by insertion of caged-ball valve prostheses in both areas. Final evaluation of this new approach will depend on further carefully controlled clinical trials and on objective evaluation of the long-term results.
Intensive Smoking Cessation Efforts Cost-effective
Authors: Charles Marwick
Journal: JAMA (1996)

SMOKING CESSATION programs are the most cost-effective preventive intervention available to clinicians practicing in health care systems today. Overall, such programs cost about $2000 per year of life saved. In contrast, mammographic screening for breast cancer costs about $50 000 per year of life saved. In addition, the more intensive the intervention, the more cost-effective it is. All interventions are effective, but longer, more intensive ones are even more cost-effective than a 3-minute comment to the patient about the hazards of smoking. These are 2 of the findings of an unreleased study on the cost-effectiveness of antismoking programs commissioned by the Agency for Health Care Policy and Research (AHCPR). One of the key issues involved in implementing the smoking cessation guidelines recently published by the agency (<i>JAMA</i>. 1996;275:1270-1280) is cost-effectiveness, and the AHCPR has commissioned a study to look into the issue. At a meeting on smoking cessation strategies held
Abstract 3075: A novel transcriptional role of spindle assembly checkpoint protein Cdc20 regulating the expression of mitotic ubiquitin carrier protein UbcH10
Authors: Somsubhra Nath, Taraswi Banerjee, Debrup Sen, Tania Das, Susanta Roychoudhury
Journal: Cancer Research (2011)

Abstract Progression through mitosis requires precisely timed ubiquitin-dependent degradation of specific substrates. UbcH10, an ubiquitin-conjugating enzyme, plays a crucial role with anaphase promoting complex/ cyclosome (APC/C) in progression of and exit from mitotis. Similarly, spindle assembly checkpoint (SAC) protein Cdc20 plays an important role in transition from metaphase to anaphase by activating APC/C. Cdc20 itself gets ubiquitinated by UbcH10 and thus activated to bind with APC/C. Any defect in chromosome alignment activates SAC by blocking Cdc20 and thus anaphase transition is arrested. Earlier our lab reported that Cdc20 overexpression led to defective SAC resulting in aneuploidy. This prompted us to examine the regulation of UbcH10 expression in Cdc20 upregulated condition. Initially, we observed a correlation in the expression of both Cdc20 and UbcH10 in different primary tumors and cancer cell lines. Next, a dose-dependent increase in endogenous UbcH10 levels was found upon ectopic expression of Cdc20. Alternatively, CDC20 knockdown by siRNA led to downregulation of endogenous UbcH10. Activation of UBCH10 promoter-luciferase activity by Cdc20 indicated the regulation at transcriptional level. ChIP assay showed the presence of Cdc20 on UBCH10 promoter leading to chromatin remodelling by interacting with CBP/p300. APC/C-CBP/p300 complex is reported to be involved in transcription regulation. Here, we established the presence of APC/C on the UBCH10 promoter using ChIP assay. Further from ChIP and Co-IP assay we established that Cdc20 regulates APC/C and CBP/p300 association and thus modulates APC/C-CBP/p300 mediated transcriptional regulation of UBCH10. Also, we found cell cycle specific regulation of expression of UbcH10 by Cdc20. Finally, Cyclin B1 degradation assay showed physiological relevance of Cdc20 mediated UbcH10 regulation on mitotic progression. In summary, our data showed a novel role of Cdc20 as a transcription regulator and it regulates UbcH10 expression in a cell cycle specific manner. The co-regulated expression of both these proteins maintains proper mitotic progression which otherwise may results in aneuploidy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3075. doi:10.1158/1538-7445.AM2011-3075