tbuckley/cabot-search huggingface dataset:
Abstract 578: Plk1 decreases DNA double-strand break (DSB) formation during replication-stalling genotoxic stress.
Authors: Daniel Gebreselassie, Gina Chun-Kost, Elisabetta Leo, Yves Pommier, Erika Saito, Steven Patierno, Susan M. Ceryak
Journal: Cancer Research (2013)

Abstract Polo-like kinase 1 (Plk1) is a key regulator of mitosis and its over-expression/ deregulation is linked to cellular transformation. Recent studies highlight its role in resumption of cell cycle progression after DNA damage. Plk1 has also been shown to enhance DNA replication under stress of stalled replication forks. We reported Plk1 activation-induced G2/M checkpoint bypass in normal human lung cells (HLFs), in the presence of acute genotoxic stress. The present aim was to determine the effect of Plk1 on DNA double strand breaks (DSBs) during genotoxic stress. In the present study, we measured DNA DSB induction in HLFs by Cr(VI), etoposide, and H2O2 after Plk1 activation using the comet assay and γH2AX immunofluorescence staining. We used equitoxic concentrations of the different genotoxins and found that DNA DSBs increased &amp;gt; 2 fold after exposure to 3 μM Cr(VI), 12.5 μM etoposide, and 150 μM H2O2, respectively, and persisted for at least 4h. Transfection of a Plk1 constitutively active (c/a) mutant (T210D) abrogated both Cr(VI)- and etoposide-induced DNA DSBs as early as 30 min for the duration of treatment, in comparison to the vector-transfected cells. In sharp contrast, Plk1 had no effect on H2O2-induced DNA DSBs. Consistent with DNA DSB formation, Cr(VI) exposure was associated with G1 arrest, at least at 4h, as determined by BrdU incorporation. Moreover, Plk1 enhanced S phase progression during Cr(VI) treatment, which was accompanied by increased replication fork velocity and longer inter-origin distances as determined by using a single-molecule approach based on molecular combing. Expression of a Plk1 “kinase-dead” mutant (K82R) also abrogated DNA DSBs during Cr(VI) treatment, suggesting that this effect may be independent of Plk1 kinase activity. In summary, our data underline the ability of Plk1 to override DNA DSB-induced checkpoints, and to decrease DSBs after replication-stalling genotoxin exposure. We postulate these effects to be due to the replication-enhancing ability of Plk1, which may occur at the expense of genomic stability. This work was supported in part by NIH grants CA107972 and ES017334 (S.C.); ES05304 (S.R.P.); and a PhRMA Foundation predoctoral fellowship (G.C.K.). Citation Format: Daniel Gebreselassie, Gina Chun-Kost, Elisabetta Leo, Yves Pommier, Erika Saito, Steven Patierno, Susan M. Ceryak. Plk1 decreases DNA double-strand break (DSB) formation during replication-stalling genotoxic stress. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 578. doi:10.1158/1538-7445.AM2013-578
Cubital Tunnel Syndrome
Authors: Michael W. Devereaux
Journal: JAMA (1979)

<h3>To the Editor.—</h3> Clark stressed the reliability of his seven tests in preference to electrodiagnostic studies (electromyography and nerve conduction studies) for the diagnosis of the ulnar nerve cubital tunnel syndrome. The seven tests described are all part of a routine neurological examination. In actuality, positive findings on all of these tests reflect an advanced state of deficit. We have seen few patients with symptoms consistent with an ulnar neuropathy with such marked neurological deficit on examination. We are impressed that electrodiagnostic studies can often show accurately, first, the presence (or perhaps more important, the absence) of neuropathy, and second, the exact location of the injury along the nerve, often in the absence of findings on most of the seven tests. If surgery is being considered to relieve a clinically suspected nerve entrapment, electrodiagnostic studies should be performed routinely.
Failure To Thrive in Older Adults
Authors: Catherine A. Sarkisian
Journal: Annals of Internal Medicine (1997)

Letters15 April 1997Failure To Thrive in Older AdultsCatherine A. Sarkisian, MD and Mark S. Lachs, MD, MPHCatherine A. Sarkisian, MDNew York Hospital-Cornell Medical Center, New York, NY 10021Search for more papers by this author and Mark S. Lachs, MD, MPHNew York Hospital-Cornell Medical Center, New York, NY 10021Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-126-8-199704150-00039 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail IN RESPONSE:We appreciate the comments of Dr. Still and concur that the morbidly obese older patient may be declining functionally just as an undernourished older patient might be; this is yet another compelling argument for abandoning failure to thrive as a diagnosis because it reinforces the stereotype of the wasting patient as the only one who qualifies for the label. Although it was not the purpose of our paper to provide a comprehensive differential diagnosis for patients who are declining, we agree with Dr. Stead that tuberculosis is a diagnosis that is often overlooked.Dr. Portnoi is mistaken in ... Author, Article, and Disclosure InformationAffiliations: New York Hospital-Cornell Medical Center, New York, NY 10021 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 April 1997Volume 126, Issue 8Page: 669KeywordsChild healthChildrenElderlyMalnutritionOverweightPatient advocacyPhysical functioning Issue Published: 15 April 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
THE WORK OF THE OPHTHALMIC SECTION FOR 1895.
Journal: JAMA (1895)

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
The Art of Anæsthesia.
Journal: JAMA (1933)

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
Visual And Eye Movement Functions Of The Posterior Parietal Cortex
Authors: R. Andersen
Journal: Annual Review of Neuroscience (1989)

Lesions of the posterior parietal area in humans produce interesting spatial-perceptual and spatial-behavioral deficits.Among the more important deficits observed are loss of spatial memories, problems representing spatial relations in models or drawings, disturbances in the spatial distribution of attention, and the inability to localize visual targets.Posterior parietal lesions in nonhuman primates also produce visual spatial deficits not unlike those found in humans.Mountcastle and his colleagues were the first to explore this area, using single cell recording techniques in behaving monkeys over 13 years ago.Subsequent work by Mountcastle, Lynch and colleagues, Hyvarinen and colleagues, Robinson, Goldberg & Stanton, and Sakata and colleagues during the period of the late 1970s and early 1980s provided an informational and conceptual foundation for exploration of this fascinating area of the brain.Four new directions of research that are presently being explored from this foundation are reviewed in this article.1.The anatomical and functional organization of the inferior parietal lobule is presently being investigated with neuroanatomical tracing and single cell recording techniques.This area is now known to be comprised of at least four separate cortical fields.2. Neural mechanisms for spatial constancy are being explored.In area 7a information about eye position is found to be integrated with visual inputs to produce representations of visual space that are head-centered 3"77 0147~006X/89/0301~)377502.
Association of Age, Sex and Deprivation with Quality Indicators for Diabetes: Population-Based Cross Sectional Survey in Primary Care
Authors: Jeremy Gray, Christopher Millett, Caoimhe O'Sullivan, Rumana Z Omar, Azeem Majeed
Journal: Journal of the Royal Society of Medicine (2006)

To determine the quality of diabetes management in primary care after the publication of the National Service Framework and examine the impact of age, gender and deprivation on the achievement of established quality indicators.Population-based cross sectional survey using electronic general practice records carried out between June-October 2003.Thirty-four practices in Wandsworth, South-West London, UK.6035 adult patients (> or =18 years) with diabetes from a total registered population of 201,572 patients.None.Success rates for the diabetes quality indicators within the General Medical Services contract for general practitioners.We identified large variations in diabetes management between general practitioner practices with poorer recording of quality care in younger patients (18-44 years). In addition, younger patients had a worse cholesterol and glycaemia profile, although hypertension was more common in older patients. Gender and deprivation did not appear to be important determinants of the quality of care received.There are large variations in diabetes management between general practitioner practices, with care seemingly worse for younger adults. Longitudinal studies are required to determine whether current UK quality improvement initiatives have been successful in attenuating existing variations in care and treatment outcomes.
Secondary prevention of vascular disease by prolonged antiplatelet treatment
Journal: BMJ (1988)

Thirty one randomised trials of antiplatelet treatment for patients with a history of transient ischaemic attack, occlusive stroke, unstable angina, or myocardial infarction were identified. Six were still in progress, and the results of the remaining 25 were reviewed. They included a total of some 29 000 patients, 3000 of whom had died. Overall, allocation to antiplatelet treatment had no apparent effect on non-vascular mortality but reduced vascular mortality by 15% (SD 4%) and non-fatal vascular events (stroke or myocardial infarction) by 30% (4%). This suggested that with good compliance these treatments might reduce vascular mortality by about one sixth, other vascular events by about a third, and total vascular events by about a quarter. There was no significant difference between the effects of the different types of antiplatelet treatment tested (300-325 mg aspirin daily, higher aspirin doses, sulphinpyrazone, or high dose aspirin with dipyridamole), nor between the effects in patients with histories of cerebral or cardiac disease. Thus antiplatelet treatment can reduce the incidence of serious vascular events by about a quarter among a wide range of patients at particular risk of occlusive vascular disease. The balance of risk and benefit, however, might be different for “primary” prevention among people at low absolute risk of occlusive disease if antiplatelet treatment produced even a small increase in the incidence of cerebral haemorrhage.
Clinicopathologic factors associated with the development of sunitinib-induced hypertension (HTN) in patients (pts) with metastatic renal cell carcinoma (mRCC).
Authors: Victoria Neiman, Maya Gottfried, Hans J. Hammers, Mario A. Eisenberger, Michael Anthony Carducci, Victoria J. Sinibaldi, Eli Rosenbaum, David Sarid, Eliahu Gez, Avivit Peer, Avivit Neumann, Svetlana Kovel, Avishay Sella, Wilmosh Mermershtain, Keren Rouvinov, Raanan Berger, Daniel Keizman
Journal: Journal of Clinical Oncology (2014)

e15551 Background: The VEGFR inhibitor sunitinib is a standard treatment for metastatic renal cell carcinoma (mRCC). HTN, an on-target class effect of VEGF signaling-pathway inhibitors, has been shown to correlate with clinical outcome. Studies have shown the association between genetic polymorphisms in several genes and the development of HTN in patients treated with targeted therapies. We aimed to study the association between readily available clinicopathologic factors and the development of sunitinib induced HTN in mRCC patients. Methods: Records from mRCC patients treated with sunitinib in 9 centers across 2 countries were retrospectively reviewed. Sunitinib induced HTN was defined as systolic blood pressure ≥ 140 mmHg and/or diastolic blood pressure ≥ 90 mmHg. Analysis of the association between clinicopathologic factors and the development of HTN was performed using logistic regression. Results: Between 2004-2013, 302 patients with mRCC were treated with sunitinib. The incidence of sunitinib induced HTN was 50% (n=152). Clinicopathologic factors included in the analysis were age (median 63), gender (67% male), HENG risk (good 22%, intermediate 59%, poor 19%), smoking status (active 21%), BMI (obese=BMI ≥30, 28%; overweight=BMI 25-29.9, 37%; normal weight= BMI <25, 35%), pre-treatment HTN (58%), past nephrectomy (83%), histology (73% clear cell), > 1 metastatic site (82%), metastatic site (lung 72%, liver 25%, bones 40%), pre-treatment neutrophil to lymphocyte ratio (>3 in 45%), treatment line (first vs advanced), sunitinib dose reduction/treatment interruption (45%). Absence of liver metastases (OR 3.5, p=0.02), pre-treatment neutrophil to lymphocyte ratio ≤ 3 (OR 5.5, p=0.001), and BMI (overweight and normal weight vs obese, OR 2.2 and 2.3 respectively, p=0.01 both) were independently associated with the development of HTN. Conclusions: In metastatic renal cell carcinoma patients treated with sunitinib, readily available clinicopathologic factors may be used to identify patients who are prone to the development of HTN.
THE ADVERTISING SWINDLER.
Journal: JAMA (1907)

Opinion on any subject is largely dependent on the mental perspective. Only on such an assumption can we explain those incongruities of thought and action which we see daily. A case much to the point is exhibited in an editorial that appeared in a Chicago evening paper of recent date.<sup>1</sup>In referring to the aid given an unscrupulous but plausible advertiser by the press in selling him advertising space in which to exploit his get-rich-quick schemes, the paper sums up as follows: "It is an outrage for any newspaper to trade on the trustfulness of its readers in order to share in the profits of swindlers. Reputable patrons of newspapers should demand that they cease to be the beneficiaries of financial sharks through the acceptance of advertising which has fraud written all over it in the light of ordinary business judgment. A newspaper must be honest in its advertising
Updated Recommendation From the Advisory Committee on Immunization Practices (ACIP) for Use of 7-Valent Pneumococcal Conjugate Vaccine (PCV7) in Children Aged 24-59 Months Who Are Not Completely Vaccinated
Journal: JAMA (2008)

This notice updates the recommendation for use of 7-valent pneumococcal conjugate vaccine (PCV7) among children aged 24-59 months who are either unvaccinated or who have a lapse in PCV7 administration. In February 2000, PCV7, marketed as Prevnar and manufactured by Wyeth Vaccines (Collegeville, Pennsylvania), was approved by the Food and Drug Administration for use in infants and young children. At that time, the Advisory Committee on Immunization Practices (ACIP) recommended that children aged 24-59 months who have certain underlying medical conditions or are immunocompromised receive PCV7. In addition, ACIP recommended that PCV7 be considered for all other children aged 24-59 months, with priority given to those who are American Indian/Alaska Native or of African-American descent, and to children who attend group day care centers. The recommendation also provided schedules for administering PCV7 to children aged 24-59 months who were either unvaccinated or who had a lapse in PCV7 administration; these schedules included 1) 1 dose of PCV7 for healthy children, and 2) 2 doses of PCV7 > or =2 months apart for children with certain chronic diseases or immunosuppressive conditions.
Hereditary progressive atrioventricular conduction defect. A new syndrome?
Authors: H. T. Lynch
Journal: JAMA (1973)

We studied a syndrome involving a progressive atrioventricular conduction defect in three generations of a large family. Clinical findings included a slow heart rate, episodes of lightheadedness, syncope, and absence of predisposing acquired or hereditary cardiac disorders. Electrocardiography showed a prolonged atrioventricular conduction with onset usually in the 30s, loss of R waves in the right precordial leads, and arrhythmia that occurs only as a late manifestation. Progression from first-degree to complete heart block was usually slow, but occasionally a fulminant course led to sudden death within two or three years. Specific differences from other forms of conduction defects suggest that this is a new hereditary syndrome.
From the Centers for Disease Control. Change of dosing regimen for malaria prophylaxis with mefloquine
Journal: JAMA (1991)

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
BOOK REVIEWS
Authors: PATTY DELANEY KLAFEHN
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article BOOK REVIEWS Get access Cancervive: The Challenge of Life After Cancer Susan Nessim , Judith Ellis . Boston : Houghton Mifflin , 1991 . 264 pp. $18.95. PATTY DELANEY KLAFEHN PATTY DELANEY KLAFEHN Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 1, 1 January 1992, Pages 54–55, https://doi.org/10.1093/jnci/84.1.54 Published: 01 January 1992
The birth of clinical body plethysmography: it was a good week
Authors: J. B. West
Journal: Journal of Clinical Investigation (2004)

Nearly fifty years ago, Arthur B. DuBois, Julius H. Comroe Jr., and their colleagues published two papers on the use of body plethysmography to measure lung volume and airway resistance. These two articles in the JCI are almost the most-cited doublet in the Journal’s entire archive. Remarkably, the methods described then are still in use today in clinical pulmonary function laboratories. Though body plethysmography had been used before, there were serious technical problems; it was extraordinary that DuBois managed to solve most of these in one week. Times have changed and molecular medicine now dominates the JCI, but these articles remind us that biomedical research goes beyond the molecular.
Digest of Comments on The Pharmacopoeia of the United States of America and of the National Formulary for the Calendar Year ending December 31, 1921.
Journal: JAMA (1924)

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