tbuckley/cabot-search huggingface dataset:
More Than One-Third of US Individuals Use the Internet to Self-diagnose
Authors: Bridget M. Kuehn
Journal: JAMA (2013)

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
Longer sources of intracoronary brachytherapy for in-stent restenosis reduces restenosis in the real world
Authors: Annapoorna S. Kini, Ajay Agarwal, Shazia Mukaddam, Mary E. Duffy, Michael C. Kim, Mazullah Kamran, Warren Sherman, Samin K. Sharma
Journal: Journal of the American College of Cardiology (2003)
First-in-Human Study of CH5132799, an Oral Class I PI3K Inhibitor, Studying Toxicity, Pharmacokinetics, and Pharmacodynamics, in Patients with Metastatic Cancer
Authors: Sarah Blagden, Aurelius Olmin, Debra Josephs, Chara Stavraka, Andrea Zivi, David J. Pinato, Alan Anthoney, Shaun Decordova, Karen Swales, Ruth Riisnaes, Lorna Pope, Kohei Noguchi, Rie Shiokawa, Michiyasu Inatani, Jenny Prince, Keith Jones, Chris Twelves, James Spicer, Udai Banerji
Journal: Clinical Cancer Research (2014)

Abstract Purpose: This phase I dose-escalation study investigated the maximum-tolerated dose (MTD), dose-limiting toxicities (DLT), safety, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary clinical activity of CH5132799. Experimental Design: Patients with metastatic solid tumors were eligible for the study. CH5132799 was administered orally once daily or twice daily in 28-day cycles. Results: Thirty-eight patients with solid tumors received CH5132799 at 2 to 96 mg once daily or 48 to 72 mg twice daily. The MTD was 48 mg on the twice-daily schedule but was not reached on the once daily schedule. DLTs were grade 3 elevated liver function tests (LFT), grade 3 fatigue, grade 3 encephalopathy, grade 3 diarrhea, and grade 3 diarrhea with grade 3 stomatitis; all DLTs were reversible. Most drug-related adverse events were grade 1/2. Diarrhea (34%) and nausea (32%) were the most common events. Mean Cmax and AUC0-24 in steady state at MTD were 175 ng/mL and 1,550 ng·h/mL, respectively, consistent with efficacious exposure based on preclinical modeling. Reduction in SUVmax with [18F] fluorodeoxyglucose positron emission tomography (FDG-PET) was observed in 5 of 7 patients at MTD. A patient with PIK3CA-mutated clear cell carcinoma of the ovary achieved a partial response by GCIG CA125 criteria and further, a heavily pretreated patient with triple-negative breast cancer had marked improvement in her cutaneous skin lesions lasting six cycles. Conclusion: CH5132799 is well tolerated at the MTD dose of 48 mg twice daily. At this dose, the drug had a favorable PK and PD profile and preliminary evidence of clinical activity. Clin Cancer Res; 20(23); 5908–17. ©2014 AACR.
Sulfamethoxazole-Phenazopyridine and Thrombocytopenia
Authors: JONATHAN T. WILDE
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 January 1986Sulfamethoxazole-Phenazopyridine and ThrombocytopeniaJONATHAN T. WILDE, M.A., M.B., M.R.C.P., ARCHIBALD G. PRENTICE, M.B., M.R.C.P., M.R.C.Path.JONATHAN T. WILDE, M.A., M.B., M.R.C.P.Search for more papers by this author, ARCHIBALD G. PRENTICE, M.B., M.R.C.P., M.R.C.Path.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-1-128_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We report the case of a 17-year-old woman from the United States who, over a 3-day period after arrival in the United Kingdom, noticed worsening of bruising on her neck, trunk, and limbs. She also developed spontaneous gum bleeding and prolonged menstrual blood loss.She had been taking Azo Gantanol (sulfamethoxazole-phenazopyridine; Hoffmann LaRoche, Inc., Nutley, New Jersey), two tablets twice daily, over the previous 2 weeks for treatment of a urinary tract infection. She was otherwise well and was taking no other medication. On examination she had widespread skin petechiae and ecchymoses and gum bleeding. There was...References1. SMELLIEROWAN DR. A microplate enzymoimmunoassay for measuring platelet-associated IgG (PAIgG). J Clin Lab Haematol. 1982;4:41-3. CrossrefMedlineGoogle Scholar2. YOUNGVINCENT GP. Drug-induced agranulocytosis. In: GORDON-SMITH EC, ed. Haematological Effects of Drug Therapy. London: W. B. Saunders Company, Ltd.; 1980;483-504. CrossrefGoogle Scholar3. MEISCHERGRAF PJ. Drug-induced thrombocytopenia. In: GORDON-SMITH EC, ed. Haematological Effects of Drug Therapy. London: W. B. Saunders Company, Ltd.; 1980;505-19. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Plymouth General Hospital Plymouth England PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1986Volume 104, Issue 1Page: 128-129KeywordsBloodHemorrhage Issue Published: 1 January 1986 PDF DownloadLoading ...
Nosocomial pneumonia prophylaxis
Authors: M. Ferrer, A. Torres, J. González, J. Puig de la Bellacasa, J. M. Gatell, M. Roca, M. T. Jiménez de Anta, R. Rodríguez-Roisin, J. Vallés, N. Bonsoms, L. I. Blanch, F. Baigorri, D. Fontanals, P. Saura, A. Artigas, G. J. Dobb, S. M. Boyle, M. Bonten, C. Gaillard, F. Van Tiel, S. Van Der Geest, E. Stobberingh, A. N. Laggner, M. Tryba, A. Georgopoulos, K. Lenz, G. Grimm, W. Graninger, B. Schneeweiß, W. Drum, M. Palomar, F. Alvarez, R. Jorda, F. Barcerilla, J. Nava, C. Triginer, J. Luna, S. Arkengol, E. Quintana, J. Gelabert
Journal: Intensive Care Medicine (1992)
Uncovering Treatment Burden as a Key Concept for Stroke Care: A Systematic Review of Qualitative Research
Authors: Katie Gallacher, Deborah Morrison, Bhautesh Jani, Sara Macdonald, Carl R. May, Victor M. Montori, Patricia J. Erwin, G. David Batty, David T. Eton, Peter Langhorne, Frances S. Mair
Journal: PLoS Medicine (2013)

Background Patients with chronic disease may experience complicated management plans requiring significant personal investment. This has been termed ‘treatment burden’ and has been associated with unfavourable outcomes. The aim of this systematic review is to examine the qualitative literature on treatment burden in stroke from the patient perspective. Methods and Findings The search strategy centred on: stroke, treatment burden, patient experience, and qualitative methods. We searched: Scopus, CINAHL, Embase, Medline, and PsycINFO. We tracked references, footnotes, and citations. Restrictions included: English language, date of publication January 2000 until February 2013. Two reviewers independently carried out the following: paper screening, data extraction, and data analysis. Data were analysed using framework synthesis, as informed by Normalization Process Theory. Sixty-nine papers were included. Treatment burden includes: (1) making sense of stroke management and planning care, (2) interacting with others, (3) enacting management strategies, and (4) reflecting on management. Health care is fragmented, with poor communication between patient and health care providers. Patients report inadequate information provision. Inpatient care is unsatisfactory, with a perceived lack of empathy from professionals and a shortage of stimulating activities on the ward. Discharge services are poorly coordinated, and accessing health and social care in the community is difficult. The study has potential limitations because it was restricted to studies published in English only and data from low-income countries were scarce. Conclusions Stroke management is extremely demanding for patients, and treatment burden is influenced by micro and macro organisation of health services. Knowledge deficits mean patients are ill equipped to organise their care and develop coping strategies, making adherence less likely. There is a need to transform the approach to care provision so that services are configured to prioritise patient needs rather than those of health care systems. Systematic Review Registration International Prospective Register of Systematic Reviews CRD42011001123 Please see later in the article for the Editors' Summary
Medical training did not teach me what I really needed to know
Authors: Nicola Cooper
Journal: BMJ (2004)

I have one vivid memory of medical school: being taught basic sciences by people who were neither teachers nor doctors. I vaguely remember being taught about the Frank-Starling curve in the first year. We stimulated a real myocyte at various lengths and measured its contraction. In fact, we did lots of rather bizarre experiments, but no one mentioned what relevance they might have to real life. I threw all my physiology notes away triumphantly after passing the 2nd MB (preclinical exams).



STEVIE GRAND/SPL



Later at medical school, I was taught to take a history, perform an examination, and then make a diagnosis. But no one mentioned that this would be inappropriate when faced with a critically ill patient. In fact, no one even told me that tests do not make a diagnosis. I do not recall ever being taught about oxygen (except that it's dangerous), arterial blood gases, different fluids and fluid balance in illness, how inotropes work, and all the physiology I would need to know as a …
Frank A. Seixas, MD, 72
Authors: Amy Warshawsky
Journal: JAMA (1992)

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
Biliary Excretion of Aluminum in Aluminum Osteodystrophy with Liver Disease
Authors: JAMES W. WILLIAMS
Journal: Annals of Internal Medicine (1986)

Two patients with chronic liver disease developed elevated serum aluminum concentrations and biopsy-proven osteodystrophy. Neither patient had chronic renal failure but both had received aluminum-containing antacids for long periods. We measured biliary and urinary aluminum excretion during antacid loading in patients with normal liver function. Our studies show that biliary excretion is an important route of elimination of orally absorbed aluminum, and we suggest that long-term antacid therapy in patients with severe liver disease be monitored with periodic serum and urinary aluminum determinations to avoid aluminum osteodystrophy.
Intestinal microbiota and blue baby syndrome
Authors: Collin L. Ellis, John C. Rutledge, Mark A. Underwood
Journal: Gut Microbes (2010)

Necrotizing enterocolitis (NEC) is the most common intestinal emergency among premature infants. Risk factors in premature infants include immature intestinal immunity and an intestinal microbiota dominated by hospital-acquired bacteria. Some probiotics have been shown to decrease the incidence of NEC in premature infants. Among term infants, NEC is rare. However, among term infants with cyanotic congenital heart disease (CCHD), the incidence of NEC is similar to that of premature infants but with even greater mortality rates. Mechanisms by which NEC occurs in term infants with CCHD are unknown. Of central interest is the potential role of changes in the intestinal microbiota and whether these can be modified with probiotic bacteria; accordingly, we review the literature, propose hypotheses, and present the rationale for future studies involving preliminary probiotic clinical trials.
Relationship between whole plasma calcitonin levels, calcitonin secretory capacity, and plasma levels of estrone in healthy women and postmenopausal osteoporotics.
Authors: J Y Reginster, R Deroisy, A Albert, D Denis, M P Lecart, J Collette, P Franchimont
Journal: Journal of Clinical Investigation (1989)

The exact role of calcitonin (CT) in the pathogenesis of postmenopausal osteoporosis remains unknown. Whole plasma calcitonin (iCT) basal levels, metabolic clearance rate (MCR), and production rate (PR) of CT were measured in 9 premenopausal and 16 postmenopausal women, including 11 osteoporotics (OP). Basal iCT levels were statistically lower in postmenopausal women than in the premenopausal group (P less than 0.01) and strongly correlated (r = 0.72; P less than 0.001) with estrone circulating levels (E1). MCR were similar in all groups. PR were similar in eugonadal women between 22 (mean +/- SD = 30.9 +/- 9.9 micrograms/d) and 37 yr (mean +/- SD = 25.5 +/- 11.1 micrograms/d) premenopausal women. In healthy postmenopausal women PR were reduced, but not significantly (mean +/- SD = 19.5 +/- 6.95 micrograms/d), whereas osteoporotic patients presented a highly significant reduction of CT PR (mean +/- SD = 9.8 +/- 4 micrograms/d) (P less than 0.01). Because there is a strong relationship between E1 and PR (r = 0.64; P less than 0.001), CT secretory capacity appears to be modulated by estrogen circulating levels. This modulation leads to a menopause-related decrease in iCT. In osteoporotics, an independent impairment of CT production drastically lowers PR and basal iCT levels. CT might be one of the determining factors in the pathogenesis of postmenopausal osteoporosis.
Aberrant Chloride Intracellular Channel 4 Expression Contributes to Endothelial Dysfunction in Pulmonary Arterial Hypertension
Authors: Beata Wojciak-Stothard, Vahitha B. Abdul-Salam, Ka Hou Lao, Hilda Tsang, David C. Irwin, Christina Lisk, Zoe Loomis, Kurt R. Stenmark, John C. Edwards, Stuart H. Yuspa, Luke S. Howard, Robert J. Edwards, Christopher J. Rhodes, J. Simon R. Gibbs, John Wharton, Lan Zhao, Martin R. Wilkins
Journal: Circulation (2014)

Chloride intracellular channel 4 (CLIC4) is highly expressed in the endothelium of remodeled pulmonary vessels and plexiform lesions of patients with pulmonary arterial hypertension. CLIC4 regulates vasculogenesis through endothelial tube formation. Aberrant CLIC4 expression may contribute to the vascular pathology of pulmonary arterial hypertension.CLIC4 protein expression was increased in plasma and blood-derived endothelial cells from patients with idiopathic pulmonary arterial hypertension and in the pulmonary vascular endothelium of 3 rat models of pulmonary hypertension. CLIC4 gene deletion markedly attenuated the development of chronic hypoxia-induced pulmonary hypertension in mice. Adenoviral overexpression of CLIC4 in cultured human pulmonary artery endothelial cells compromised pulmonary endothelial barrier function and enhanced their survival and angiogenic capacity, whereas CLIC4 shRNA had an inhibitory effect. Similarly, inhibition of CLIC4 expression in blood-derived endothelial cells from patients with idiopathic pulmonary arterial hypertension attenuated the abnormal angiogenic behavior that characterizes these cells. The mechanism of CLIC4 effects involves p65-mediated activation of nuclear factor-κB, followed by stabilization of hypoxia-inducible factor-1α and increased downstream production of vascular endothelial growth factor and endothelin-1.Increased CLIC4 expression is an early manifestation and mediator of endothelial dysfunction in pulmonary hypertension.
1315 REPLICATED ASSOCIATION OF 170.12-21 WITH SUSCEPTIBILITY OF PRIMARY BILIARY CIRRHOSIS IN A JAPANESE COHORT
Authors: A. Tanaka, P. Invernizzi, H. Ohira, K. Kikuchi, S. Nezu, A. Shibuya, M.F. Seldin, M.E. Gershwin, H. Takikawa
Journal: Journal of Hepatology (2011)
Tissue Inhibitor of Metalloproteinase-1 Levels in Bronchoalveolar Lavage Fluid from Asthmatic Subjects
Authors: Gisèle Mautino, Corinne Henriquet, Dany Jaffuel, Jean Bousquet, Françoise Capony
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Airway remodeling is a well-recognized feature in patients with chronic asthma. The accumulation in the submucosa of fibrous proteins that are substrates of matrix metalloproteinases (MMP), and the demonstration of increased levels of MMP-9 in bronchoalveolar lavage fluid, prompted us to determine whether there was an imbalance between MMPs and tissue inhibitors of metalloproteinase (TIMP) in such patients. We investigated the presence of TIMPs and other MMPs. TIMP levels were compared with those of all MMPs and inflammatory cytokines. Adults with stable asthma, either untreated or treated with glucocorticoids (GCs), were enrolled. Healthy nonsmokers served as a control population. MMPs and TIMPs were identified through zymography or immunoblotting. TIMPs, MMPs, and cytokines were measured with enzyme immunoassays. TIMP-1 levels were significantly higher in untreated asthmatic subjects than in GC-treated subjects or controls (p < 0.0001), and were far greater than those of MMP-1, MMP-2, MMP-3, and MMP-9 combined. TIMP-2 was undetectable. TIMP-1 levels were correlated with levels of interleukin-6 (p < 0.012) and the number of alveolar macrophages recovered (p < 0.005). This observation has important implications, since an excess of TIMP-1 could lead to airway fibrosis, a hallmark of airway remodelling in patients with chronic asthma.
First day dynamic changes in antithrombin III activity after supplementation have a predictive value in critically ill patients
Authors: Satoshi Gando, Atsushi Sawamura, Mineji Hayakawa, Hirokatsu Hoshino, Nobuhiko Kubota, Akiko Oshiro
Journal: American Journal of Hematology (2006)

Abstract To evaluate the changes in the antithrombin III (antithrombin) values after initial supplementation to predict outcome in critically ill patients, we conducted a retrospective study. All consecutive patients admitted to the intensive care unit (ICU) and treated with antithrombin were enrolled in the study. Initial doses of 1,500 IU or 30 IU/kg antithrombin concentrates were administered over an hour. The clinical backgrounds of the patients were collected from computer‐based records. Serial data of antithrombin were collected from the first day of administration (Day 0) to days 1–4. The patients were subdivided into two groups based on whether they demonstrated an increased antithrombin activity of more than 60% on the first day after the initial supplementation (responders) or not (nonresponders). Four hundred thirty‐five patients were enrolled in the present study. Two hundred eighty‐eight patients could achieve an antithrombin activity of more than 60%. The outcome was significantly different between the two groups. A logistic regression analysis revealed the day 1 antithrombin level and an initial increase of less than 60% after supplementation to be independently associated with ICU mortality. We also found a significant increase in the platelet counts and fibrinogen levels, and a decrease in the disseminated intravascular coagulation (DIC) scores for the responders. In conclusion, our findings demonstrated the first‐day dynamic change in antithrombin activity, and not the basal level, to be able to predict critically ill patient death. This dynamic change was associated with an improvement in the platelet counts, fibrinogen levels, and the DIC score. Am. J. Hematol., 2006. © 2006 Wiley‐Liss, Inc.
THE ACTION OF PNEUMOCOCCUS ON BLOOD
Authors: E. E. Butterfield, F. W. Peabody
Journal: The Journal of Experimental Medicine (1913)

The reduction of the oxygen capacity which occurs after incubating pneumococcus cultures with washed rabbit corpuscles is due to the formation of methemoglobin (or some derivative of hemoglobin with identical optical constants for three regions in the spectrum). The substance which induces the change is also present in the sterile filtrate of autolyzed cultures. By analogy we feel justified in concluding that the mechanism of the reduction of the oxygen capacity in human lobar pneumonia is at least in part of the same nature. To determine the frequency and intensity of the phenomenon in lobar pneumonia, and thereby to establish its clinical significance, is the next step and a problem upon which we are now engaged.