tbuckley/cabot-search huggingface dataset:
Effects of lowering elevated LDL cholesterol on the cardiovascular risk of lipoprotein(a)
Authors: V. M. Maher
Journal: JAMA (1995)

<h3>Objective.</h3> —To determine if lowering elevated low-density lipoprotein cholesterol (LDL-C) levels offsets the adverse effect of raised lipoprotein(a) (Lp[a]) levels on coronary artery disease (CAD) in men. <h3>Design.</h3> —Randomized, double-blind, placebo-controlled trial of lipid lowering for CAD. <h3>Setting.</h3> —Post hoc analysis of the Familial Atherosclerosis Treatment Study. <h3>Participants.</h3> —A total of 146 men aged 62 years or younger with CAD and apolipoprotein B levels of at least 125 mg/dL. <h3>Intervention.</h3> —Patients received a Step II Diet and lovastatin (40 mg daily) plus colestipol (30 g daily), niacin (4 g daily) plus colestipol, or placebo (plus colestipol if LDL-C &gt;90th percentile) for 2.5 years. They were grouped by their LDL-C responses: "minimal" if LDL-C decreased by 10% or less from baseline (mean [SD] change, +6% [13%]) and "substantial" if LDL-C decreased more than 10% (mean [SD] change, —40% [16%]). <h3>Main Outcome Measure.</h3> —Impact of lowering elevated LDL-C on the cardiac event rate (death, myocardial infarction, and revascularization for refractory ischemia) and CAD change associated with elevated Lp(a). <h3>Results.</h3> —In multivariate analyses, the best correlate of baseline CAD severity was Lp(a) (<i>r</i>=0.30;<i>P</i>&lt;.001). For 36 patients with minimal LDL-C reduction, CAD progression correlated only with in-treatment Lp(a) levels (<i>r</i>=0.45;<i>P</i>&lt;.01), but for 84 patients with substantial LDL-C reduction, disease regressed and its change correlated with in-treatment LDL-C (<i>r</i>=0.24;<i>P</i>&lt;.05) but not with Lp(a) (<i>r</i>=—0.05). Lipoprotein(a) levels were not significantly altered in either group. For 40 patients with Lp(a) at the 90th percentile or higher, events were frequent (39%) if reduction of LDL-C was minimal, but were few (9%) if reduction was substantial (relative risk, 0.23; 95% confidence interval, 0.06 to 0.99). <h3>Conclusions.</h3> —In men with CAD and elevated LDL-C, Lp(a) levels were dominant correlates of baseline disease severity, its progression, and event rate over 2.5 years. However, with substantial LDL-C reductions, persistent elevations of Lp(a) were no longer atherogenic or clinically threatening. This provides a possible direction for treatment in such patients with elevated Lp(a) and LDL-C. (<i>JAMA</i>. 1995;274:1771-1774)
Abstract 436: The Fat1 Cadherin Intracellular Domain Interacts with Atrophin Proteins and Recruits Robust Transcription Activity
Authors: Rong Hou, Nicholas Sibinga
Journal: Circulation (2007)

Background: We recently reported that the atypical cadherin Fat1 is strongly induced after arterial injury, inhibits growth and promotes migration of vascular smooth muscle cells (VSMCs), and can undergo cleavage, with subsequent translocation of its intracellular domain (Fat1IC) to the cell nucleus. In Drosophila, dFat and Atrophin, a nuclear receptor transcriptional corepressor implicated in the control of cell polarity and migration, have been linked by both physical and genetic interaction. Together, these findings suggest an important integrative role for Fat1 in active vascular remodeling, and raise the possibility that some Fat1 effects are mediated from the nucleus via interaction with transcriptional regulators. Objectives, methods, findings: We hypothesized that the interaction of mammalian Fat1IC with nuclear proteins, such as the mammalian Atrophin homologues atro-1 and atro-2, might contribute to the phenotypic effects of Fat1 on VSMC activation. To test for such interactions, we performed co-immunoprecipitation and Western analysis, identified a physical interaction of Fat1 with atro-1 and atro-2, and mapped necessary Fat1IC sequences to a discrete domain. Immunocytochemical staining showed partial co-localization of Fat1 and atro-1 and -2 in the nucleoplasm. In mammalian two-hybrid assays, surprisingly, tethering of the Fat1IC to DNA yielded very robust transcriptional activation, not repression. This activity was augmented by COUP-TFs, orphan nuclear receptor transcription factors known to associate with atrophins and implicated in both angiogenesis and cardiac development, but not previously linked to Fat1. The biological relevance of these interactions is further supported by quantitative PCR analysis that showed induction of both atro-1 and atro-2 mRNAs after vascular injury, similar to the pattern we identified for Fat1. Conclusion: The biological significance and molecular functions of the multiple cadherin superfamily proteins expressed in VSMCs are not well understood. Our studies demonstrate the physical and functional interaction of the Fat1IC with multiple nuclear proteins involved in transcriptional regulation, and point to novel pathways by which Fat1 may affect VSMC growth and migration.
Archives of General Psychiatry, Chicago
Journal: JAMA (1967)

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
Anticholinergic Toxicity
Journal: New England Journal of Medicine (1979)

2][3][4] Plants that possess anticholinergic properties such as jimson weed, and street drugs cut with anticholinergics such as scopolamine are sources of accidental or intentional ingestion. 1,2,4Anticholinergic toxicity can cause a myriad of signs and symptoms, including agitation, seizures, hyperthermia, cardiac dysrhythmias, and death.Since poisoning from anticholinergic medications is frequently encountered in the emergency department, is it essential that emergency physicians be familiar with how to manage this toxidrome.This simulation case will allow the learner to evaluate and manage a patient presenting with anticholinergic toxicity.Educational Objectives: By the end of this simulation case, learners will be able to: 1) describe the classic clinical presentation of anticholinergic toxicity, 2) discuss common medications and substances that may lead to anticholinergic toxicity, 3) recognize the electrocardiogram (ECG) findings in anticholinergic toxicity that require specific therapy, and 4) review the management of anticholinergic toxicity.Educational Methods: This simulation is taught using a high-or moderate-fidelity manikin.Research Methods: The educational content was evaluated by the learners immediately after completion and debriefing of the scenario.This case was initially piloted with approximately twenty emergency medicine residents.The group was comprised of first, second-, and third-year residents from a three-year emergency medicine residency.The efficacy of the content was assessed by oral feedback.Results: Overall, the case was well received by learners, who felt it was useful and were engaged throughout the session.The overall feedback was positive and the case was well-received by learners.
Osteopetrosis and thalamic hypomyelinosis with synaptic degeneration in DAP12-deficient mice
Authors: Tomonori Kaifu, Jin Nakahara, Masanori Inui, Kenichi Mishima, Toshihiko Momiyama, Mitsuji Kaji, Akiko Sugahara, Hisami Koito, Azusa Ujike-Asai, Akira Nakamura, Kiyoshi Kanazawa, Kyoko Tan-Takeuchi, Katsunori Iwasaki, Wayne M. Yokoyama, Akira Kudo, Michihiro Fujiwara, Hiroaki Asou, Toshiyuki Takai
Journal: Journal of Clinical Investigation (2003)

Deletions in the DAP12 gene in humans result in Nasu-Hakola disease, characterized by a combination of bone fractures and psychotic symptoms similar to schizophrenia, rapidly progressing to presenile dementia. However, it is not known why these disorders develop upon deficiency in DAP12, an immunoreceptor signal activator protein initially identified in the immune system. Here we show that DAP12-deficient (DAP12–/–) mice develop an increased bone mass (osteopetrosis) and a reduction of myelin (hypomyelinosis) accentuated in the thalamus. In vitro osteoclast induction from DAP12–/– bone marrow cells yielded immature cells with attenuated bone resorption activity. Moreover, immature oligodendrocytes were arrested in the vicinity of the thalamus, suggesting that the primary defects in DAP12–/– mice are the developmental arrest of osteoclasts and oligodendrocytes. In addition, the mutant mice also showed synaptic degeneration, impaired prepulse inhibition, which is commonly observed in several neuropsychiatric diseases in humans including schizophrenia, and aberrant electrophysiological profiles in the thalami. These results provide a molecular basis for a unique combination of skeletal and psychotic characteristics of Nasu-Hakola disease as well as for schizophrenia and presenile dementia.
A pilot study of supraphysiologic testosterone (T) and oral etoposide (E) in men with castrate-resistant prostate cancer (CRPC).
Authors: Michael Thomas Schweizer, Emmanuel S. Antonarakis, Hao Wang, Avery N. Spitz, Haiyi Cao, Alberto Pacheco, Mario A. Eisenberger, Michael Anthony Carducci, Samuel R. Denmeade
Journal: Journal of Clinical Oncology (2014)

5052 Background: Prostate cancer (PC) cells become resistant to chronic castration via an adaptive increase in androgen receptor (AR) expression, a liability that can be exploited therapeutically. Mechanistically, supraphysiologic androgens can induce PC cell death through topoisomerase 2 (topo2) mediated double-strand DNA breaks and disruption of DNA relicensing due to persistence of AR at origins of replication during the cell cycle. Methods: We evaluated parenteral T in combination with the topo2 inhibitor E in men with CRPC and low metastatic burden (≤5 bone and <10 soft tissue metastases). To rapidly cycle from supraphysiologic (>1500 ng/dL) to near castrate T levels, men received intramuscular T cypionate 400 mg on day (D) 1 and oral E 100 mg D 1-14 of a 28 D cycle. After 3 cycles, men with declining PSA could continue T alone every 28 D. The primary endpoint was PSA response, defined as a PSA below baseline, after cycle 3. Secondary endpoints included objective response rates and safety. Results: Sixteen men enrolled of which 14 completed 3 cycles of T+E and were evaluable for response. 7/14 went on the T-only expansion stage. After 3 cycles, 6/14 men had a PSA response. 7 (50%) had a PSA response at any timepoint [4 (29%) had PSA declines ≥50%] (Table). In men with RECIST-evaluable disease, 2 had progressive and 3 had stable disease (SD), 4 had partial (PR) and 1 had a complete response (CR). Median response duration was 343 D (95% CI, 91 to 434 D). Post T, 12/12 men had a PSA decline to subsequent androgen ablative therapies. Most adverse events (AEs) were ≤grade 2 and considered effects of E. One man died from neutropenic sepsis before completing the 1st cycle. AEs possibly related to T included lower extremity edema (n=1), priapism (n=1) and asymptomatic pulmonary embolism (n=2). No one developed new pain on T. Conclusions: T with or without E demonstrated preliminary efficacy in patients with CRPC as manifested by PSA and objective responses. This regimen is generally safe. Cyclic T-based therapies warrant further study. Clinical trial information: NCT01084759.PSA/radiographic response summary. Subject Cycles (N) Maximum PSA change relative to baseline (%) RECIST response 4 15 -86 PR 6 12 -48 PR 8 3 -46 SD 9 16 -78 NA 13 14 -97 PR 15 8 -18 PR 16 5 -98 CR
Trends in HIV-Related Sexual Risk Behaviors Among High School Students--Selected US Cities, 1991-1997
Journal: JAMA (1999)

Despite recent decreases in sexual risk behaviors among high school students nationwide, human immunodeficiency virus (HIV) infection was the seventh leading cause of death among persons aged 15-24 years in the United States during 1997. To determine whether the prevalence of HIV-related sexual risk behaviors among high school students also has decreased in certain urban areas heavily affected by the epidemic, CDC analyzed data from Youth Risk Behavior Surveys (YRBS) conducted in 1991, 1993, 1995, and 1997 in eight large-city school districts: Boston, Massachusetts; Chicago, Illinois; Dallas, Texas; Fort Lauderdale, Florida; Jersey City, New Jersey; Miami, Florida; Philadelphia, Pennsylvania; and San Diego, California. This report summarizes the results of this analysis, which indicate that, from 1991 to 1997, the percentage of high school students engaging in HIV-related sexual risk behaviors decreased in some U.S. cities.
Sleep Research in Cyberspace
Journal: JAMA (1997)

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
Correction
Journal: Hepatology (2015)

described the factors associated with hepatitis B surface antigen (HBsAg) seroclearance in a cohort of Alaska Native persons with chronic hepatitis B virus (HBV) infection followed for 20 years.A secondary objective of that article was to evaluate the risk for hepatocellular carcinoma (HCC) among persons after HBsAg seroclearance.For the subanalysis on the development of HCC after HBsAg loss, the authors reported that the HCC incidence for persons with HBsAg seroclearance was 36.8 in 100,000 person-years (95% confidence interval [CI]: 13.5-80.0)and for persons without HBsAg seroclearance was 195.7 in 100,000 person-years (95% CI: 141.1-264.5).The authors concluded that HBsAg seroclearance was associated with a significant reduction in risk for developing HCC.It was recently brought to the authors' attention that the HCC incidence for persons with HBsAg seroclearance was miscalculated.The HCC incidence for persons with HBsAg seroclearance was reported in terms of personmonths, not person-years, whereas the incidence for persons without HBsAg seroclearance was reported in terms of person-years.The corrected HCC incidence for persons with HBsAg seroclearance is 441.6 in 100,000 personyears (95% CI: 162.0-958.0).Based on the corrected HCC incidence, there is no significant difference in HCC risk between persons with and without HBsAg seroclearance (P 5 0.09).The authors are grateful to the readers who brought the error in the previous HCC incidence calculation to their attention.The revised HCC incidence represents one of the few published population-based estimates of HCC risk in persons with and without HBsAg seroclearance.The results indicate that persons with HBsAg seroclearance remain at increased risk for HCC and can benefit from continued HCC surveillance.
ABSTRACTS
Authors: Joseph Ross, Helen Abstracters, Winston-Salem Belding, N Maier, Sheila Callender, England Milosnetoulek, George Cartwright, Jean Soulier, Roger Crafts, M Suarez, Puerto Rico, Charles Emerson, Wm Valentine, J Stickney, S Mills, A Hagedorn, G Higgins, K Woods, F Nichols, C Williams
Journal: Blood (1950)
Reply to Pero Bokarica's Letter to the Editor re: K. Hatzimouratidis, I. Eardley, F. Giuliano, I. Moncada, A. Salonia. Guidelines on Male Sexual Dysfunction: Erectile Dysfunction and Premature Ejaculation. European Association of Urology Website. http://uroweb.org/guideline/male-sexual-dysfunction/. Updated 2015
Authors: Konstantinos Hatzimouratidis
Journal: European Urology (2015)
CONGRATULATIONS TO THE BUREAU OF MEDICINE AND SURGERY OF THE NAVY
Journal: JAMA (1942)

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 Exchange
Journal: JAMA (1988)

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
Against Diagnosis
Authors: Andrew J. Vickers, Ethan Basch, Michael W. Kattan
Journal: Annals of Internal Medicine (2008)

The act of diagnosis requires that patients be placed in a binary category of either having or not having a certain disease. Accordingly, the diseases of particular concern for industrialized countries—such as type 2 diabetes, obesity, or depression—require that a somewhat arbitrary cut-point be chosen on a continuous scale of measurement (for example, a fasting glucose level >6.9 mmol/L [>125 mg/dL] for type 2 diabetes). These cut-points do not adequately reflect disease biology, may inappropriately treat patients on either side of the cut-point as 2 homogenous risk groups, fail to incorporate other risk factors, and are invariable to patient preference. This article discusses risk prediction as an alternative to diagnosis: Patient risk factors (blood pressure, age) are combined into a single statistical model (risk for a cardiovascular event within 10 years) and the results are used in shared decision making about possible treatments. The authors compare and contrast the diagnostic and risk prediction approaches and attempt to identify the types of medical problem to which each is best suited.
Antibiotic Tolerance
Authors: JOHN A. WASHINGTON
Journal: Annals of Internal Medicine (1981)

Letters and Corrections1 November 1981Antibiotic ToleranceJOHN A. WASHINGTON II, M.D.JOHN A. WASHINGTON II, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-95-5-657_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The letter by Rajashekaraiah and Rice (1) describing their method of measuring tolerance raises a number of issues. First, penicillinase-resistant penicillins are inconsistently bactericidal to Staphylococcus aureus in trypticase soy broth (2), the medium these authors recommended for measuring tolerance. Second, the statement that S. aureus appears more tolerant to cell wall active antibiotics at concentrations of 50 μg/mL than at those near the minimal inhibitory concentration suggests that the authors have confused tolerance with the paradoxical zone phenomenon described by, among others, Eagle and Musselman (3).It is customary to define the minimal bactericidal (or lethal)...References1. RAJASHEKARAIAHRICE KT. Staphylococcal endocarditis. Ann Intern Med. 1981;95:240. Letter. MedlineGoogle Scholar2. MARCOUXWASHINGTON JJ. Pitfalls in identification of methicillin-resistant Staphylococcus aureus. Appl Microbiol. 1969;18:699-700. CrossrefMedlineGoogle Scholar3. EAGLEMUSSELMAN HA. The rate of bactericidal action of penicillin in vitro as a function of its concentration, and its paradoxically reduced activity at high concentrations against certain organisms. J Exp Med. 1948;88:99-131. CrossrefMedlineGoogle Scholar4. ANHALTSABATHBARRY JLA. Special tests: bactericidal activity, activity of antimicrobics in combination, and detection of β-lactamase production. In: LENNETTE EH, BALOWS A, HAUSLER WJ JR, TRUANT JP, eds. Manual of Clinical Microbiology. Washington, D.C.: American Society for Microbiology; 1980:478-84. Google Scholar5. MYCHAJLONKAMCDOWELLSCHOCKMAN MTG. Inhibition of peptidoglycan, ribonucleic acid, and protein synthesis in tolerant strains of Streptococcus mutans. Antimicrob Agents Chemother. 1980;17:572-82. CrossrefMedlineGoogle Scholar6. EAGLE H. Speculations as to the therapeutic significance of the penicillin blood level: I. The direct bactericidal action of penicillin. Ann Intern Med. 1948;28:260-78. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByThe System Boron-SulfurThe System Boron-Oxygen 1 November 1981Volume 95, Issue 5Page: 657-658KeywordsAntibioticsAttentionCell wallsPenicillinStaphylococcus aureus Issue Published: 1 November 1981 PDF DownloadLoading ...