tbuckley/cabot-search huggingface dataset:
On the Relevance of History
Authors: Ruben D. Rumbaut
Journal: JAMA (1982)

To  Editor.—  As physicians, we are trained to think of  patient in historical terms. A clinical history is an indispensable part of any examination. In psychiatry, Freud, taking  concept from  poet Wordsworth, postulated that the child is father to  man. Yet we do not apply  same reasoning to medicine as a whole. If a person's presence can not be fully understood unless we see it in context and longitudinally, as  result of a lifelong process of development, how can we disregard  same logic when it applies to our profession? Santayana's dictum is inescapable: Those who ignore history are condemned to repeat it.  The history of medicine makes us aware of all facets of our endeavor. It shows us how wise Hippocrates was when he admonished us to first, do not harm and how innumerable iatrogenic symptoms and diseases have emerged throughout
Case 34-1987
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, Shirley H. Wray, Edward P. Richardson
Journal: New England Journal of Medicine (1987)

Presentation of CaseA 30-year-old woman was admitted to the hospital because of increasing ataxia.She was born at 39 weeks of gestation after an uncomplicated pregnancy of a mother 44 years old who used no tobacco, alcohol, or medications; the cord was around the child's neck at birth, and the birth weight was 2.2 kg. A reduced muscle mass was observed in infancy, and a diagnosis of cerebral palsy was made. Limited eye movements and bilateral ptosis were noted in childhood. Her motor development was slow; she could never run or jump as well as her peers. Through the . . .
Risk of cardiovascular events among women with high normal blood pressure or blood pressure progression: prospective cohort study
Authors: David Conen, Paul M Ridker, Julie E Buring, Robert J Glynn
Journal: BMJ (2007)

<b>Objective</b> To compare cardiovascular risk among women with high normal blood pressure (130-9/85-9 mm Hg) against those with normal blood pressure (120-9/75-84 mm Hg) and those with baseline hypertension. <b>Design</b> Prospective cohort study. <b>Setting</b> Women9s health study, United States. <b>Participants</b> 39 322 initially healthy women classified into four categories according to self reported baseline blood pressure and followed for a median of 10.2 years. <b>Main outcome measures</b> Time to cardiovascular death, myocardial infarction, or stroke (major cardiovascular event—primary end point); progression to hypertension. <b>Results</b> 982 (2.5%) women developed a major cardiovascular event, and 8686 (30.1%) women without baseline hypertension progressed to hypertension. The age adjusted event rate for the primary end point was 1.6/1000 person years among women with normal blood pressure, 2.9/1000 person years among those with high normal blood pressure, and 4.3/1000 person years among those with baseline hypertension. Compared with women with high normal blood pressure (reference group), those with normal blood pressure had a lower risk of a major cardiovascular event (adjusted hazard ratio 0.61, 95% confidence interval 0.48 to 0.76) and of incident hypertension (0.42, 0.40 to 0.44). The hazard ratio for a major cardiovascular event in women with baseline hypertension was 1.30 (1.08 to 1.57). Women who progressed to hypertension (reference group) during the first 48 months of the study had a higher cardiovascular risk than those who remained normotensive (adjusted hazard ratio 0.64, 0.50 to 0.81). Women with high normal blood pressure at baseline who progressed to hypertension (reference group) had similar outcome rates to women with baseline hypertension (adjusted hazard ratio 1.17, 0.88 to 1.55). <b>Conclusion</b> The cardiovascular risk of women with high normal blood pressure is higher than that of women with normal blood pressure. The cardiovascular risk of women who progress to hypertension is increased shortly after a diagnosis of hypertension has been made. <b>Trial registration</b> Clinical trials NCT00000479.
Leiomyosarcoma of the Anterior Mediastinum
Authors: J. C. R. Lincoln
Journal: Thorax (1965)

Regulatory T cells (Treg) engage IL-2 by high affinity CD25, and anti-tumor effector T cells (Teff) use intermediate affinity CD122. We studied IL-2 complexes (IL-2c) that selectively activate CD122<sup>+</sup> Teff over CD25<sup>+</sup> Tregs. We found IL-2c but not aPD-L1 potently inhibits ID8agg, an aggressive mouse ovarian cancer (OC) model. IL-2c decreased ascites Treg functional markers (CD25, GranzymeB) while upregulating them on Teffs. IL-2c inhibited Treg suppressive function in ascites but not TDLN. Ascites Tregs after IL-2c showed a fragile phenotype (increased PD-1, T-bet, and IFNg with maintained FoxP3) known to contribute to better immunotherapy response. These data suggest IL-2c inhibits Treg in the ascites through inducing fragile Tregs. Neither CD8+ T cells nor gd T cells is required for IL-2c induced Treg fragility. Studies testing other populations are ongoing. CD8<sup>+</sup>TCF-1<sup>+</sup>T cell stem cells (TCSC) improve immune checkpoint blockade in many cancer types. In ID8agg tumors, IL-2c induces CD8<sup>+</sup>TCF-1<sup>+</sup> TCSC with tumor inhibitory capacity when transferred into Rag KO mice. tSNE analysis revealed IL-2c-induced TCSC are CXCR5<sup>+</sup>PD-1<sup>−</sup> express CCR2 CXCR3 and produce TNFa, while aPD-L1 induced TCSC are CXCR5<sup>+</sup> and PD-1<sup>+</sup>, consistent with previous reports. These data suggest IL-2c induces beneficial CD8<sup>+</sup>TCSC distinct from aPD-L1. Although aPD-L1 is not efficacious alone in ID8agg, it significantly promoted IL-2c efficacy. Mice treated with IL-2c+αPD-L1 are resistant to tumor re-challenge even 6 weeks after final dose, suggesting durable immune memory. In sum, IL-2c is a novel OC immunotherapy that targets distinct immune pathways simultaneously, including inhibiting Tregs, boosting TCSCs, and inducing immune memory when combined with aPD-L1.
Pulmonary infiltration and bone marrow depression complicating treatment with amiodarone.
Authors: A J Wright, R G Brackenridge
Journal: BMJ (1982)

lead to water losses, such as diabetes.The patient's low level of consciousness was thought at first to be due to buprenorphine, while the other signs were attributed to septicaemia.Hypernatraemia is managed by giving 5°,', dextrose to bring the plasma sodium concentration down to the normal range, taking care not to produce water intoxication.Cerebral oedema may follow over- rapid dilution of plasma at a time when the brain cells have a high sodium content.These patients usually have a pronounced diuresis with a large sodium output due to the hyperosmolality of plasma, and diuretics are not needed.3Because of massive diuresis they also lose potassium, which will need replacement.
Gastric Lavage in the Diagnosis of Tuberculosis in Children. A Survey of 75 Cases
Authors: T. W. Davies, C. J. Doherty
Journal: BMJ (1942)

of repeated dressings, adds greatly to the patient's com- fort, and the time spent in hospital is reduced to a minimum.SummaryThe treatment of compound fractures and wounds is a matter of extreme urgency.Resuscitation should be started directly the patient reaches hospital in all cases, and operation should be carried out as soon as the general condition permits.With regard to the operation, the skin should be prepared with soap and water, and the use of antiseptics in the wound should be avoided.The principles of incision and excision of the wound should be carefully followed.No wound that is of more than six hours' duration should be sutured; also, no sutures should be inserted that exert any tension on the skin margins.Local sulphanilamide may be used to advantage following adequate surgery, but to use it in an effort to replace adequate surgery is to court disaster.The general prophylactic employment of oral sulphanilamide is unnecessary.The value of anti-gas-gangrene serum as a prophylactic is doubtful; in treatment it is beyond doubt.Finally, 31 cases of compound fractures and wounds are recorded with special reference to post-operative temperature and length of stay in hospital.
Why are babies getting heavier? Comparison of Scottish births from 1980 to 1992
Authors: S R Bonellie, G M Raab
Journal: BMJ (1997)

centrations.In most reports the pleocytosis has not been examined further by differential count.A mild (3%) cerebrospinal fluid eosinophilia has been documented with immunoglobulin and in aseptic meningitis after other drug treatment. 1 5In our case cerebrospinal fluid was specifically analysed and stained to provide an accurate differential count.The presence of eosinophilia enabled aseptic meningitis to be diagnosed and antibiotic treatment to be stopped, also avoiding extensive contact tracing.
The urea decomposition product cyanate promotes endothelial dysfunction
Authors: Dalia El-Gamal, Shailaja P. Rao, Michael Holzer, Seth Hallström, Johannes Haybaeck, Martin Gauster, Christian Wadsack, Andrijana Kozina, Saša Frank, Rudolf Schicho, Rufina Schuligoi, Akos Heinemann, Gunther Marsche
Journal: Kidney International (2014)
Underrepresented Minorities in Medicine
Authors: S S Bergen
Journal: JAMA (2000)

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
Acidosis during early reperfusion prevents myocardial stunning in perfused ferret hearts.
Authors: M Kitakaze, M L Weisfeldt, E Marban
Journal: Journal of Clinical Investigation (1988)

Cellular calcium overload figures prominently in the pathogenesis of the contractile dysfunction observed after brief periods of ischemia (myocardial stunning). Because acidosis is known to antagonize Ca influx and the intracellular binding of Ca, we reasoned that acidosis during reperfusion might prevent Ca overload and ameliorate functional recovery. We measured developed pressure (DP) and 31P-nuclear magnetic resonance spectra in 26 isovolumic Langendorff-perfused ferret hearts. After 15 min of global ischemia, hearts were reperfused either with normal solution (2 mM [Ca]o, Hepes-buffered, pH 7.4 bubbled with 100% O2; n = 6) or with acidic solutions (pH 6.6 during 0-3 min, pH 7.0 during 4-6 min) before returning to the normal perfusate (n = 7). Ventricular function after 30 min of reperfusion was much greater in the acidic group (105 +/- 5 mmHg at 2 mM [Ca]o) than in the unmodified reperfusion group (79 +/- 7 mmHg, P less than 0.001); similar differences in DP were found over a broad range of [Ca]o (0.5-5 mM, P less than 0.001) and during maximal Ca2+ activation (P less than 0.001). Intramyocardial pH (pHi) was lower in the acidic group than in the unmodified group during early reperfusion, but not at steady state. Phosphate compounds were comparable in both groups. To clarify whether the protective effect of acidosis is due to intracellular or extracellular pH, we produced selective intracellular acidosis during early reperfusion by exposure to 10 mM NH4Cl for 6 min just before ischemia (n = 6). For the first 12 min of reperfusion with NH4Cl-free solution (pH = 7.4), pHi was decreased relative to the unmodified group. Recovery of DP was practically complete, and maximal Ca2+-activated pressure was comparable to that in a nonischemic control group (n = 5). These results indicate that transient intracellular acidosis can prevent myocardial stunning, presumably owing to a reduction of Ca influx into cells and/or competition of H+ for intracellular Ca2+ binding sites during early reperfusion.
Adverse reaction monitoring using cohort identification.
Authors: J P Griffin
Journal: BMJ (1987)

The incidence of holoprosencephaly with normal chromosomes has been estimated at between 1 in 16 000 and 1 in 53 394 live births. It has been found that during a 3-year period in the Bristol and Weston Health District there were six cases of holoprosencephaly, two of which were familial, and these cases are described. This represents an incidence of 1 in 5200 and during the preceding 3-year period the incidence in the same area was 1 in 14 520 births.
The B Cell Mutator AID Promotes B Lymphoid Blast Crisis and Drug Resistance in Chronic Myeloid Leukemia
Authors: Lars Klemm, Cihangir Duy, Ilaria Iacobucci, Stefan Kuchen, Gregor von Levetzow, Niklas Feldhahn, Nadine Henke, Zhiyu Li, Thomas K. Hoffmann, Yong-mi Kim, Wolf-Karsten Hofmann, Hassan Jumaa, John Groffen, Nora Heisterkamp, Giovanni Martinelli, Michael R. Lieber, Rafael Casellas, Markus Müschen
Journal: Cancer Cell (2009)
Discharge Education Improves Clinical Outcomes in Patients With Chronic Heart Failure
Authors: Todd M. Koelling, Monica L. Johnson, Robert J. Cody, Keith D. Aaronson
Journal: Circulation (2005)

Although interventions combining patient education and postdischarge management have demonstrated benefits in patients with chronic heart failure, the benefit attributable to patient education alone is not known. We hypothesized that a patient discharge education program would improve clinical outcomes in patients with chronic heart failure.We conducted a randomized, controlled trial of 223 systolic heart failure patients and compared the effects of a 1-hour, one-on-one teaching session with a nurse educator to the standard discharge process. Subjects were contacted by telephone at 30, 90, and 180 days to collect information about clinical events, symptoms, and self-care practices. The primary end point of the study was the total number of days hospitalized or dead in the 180-day follow-up period. Subjects randomized to receive the teaching session (n=107) had fewer days hospitalized or dead in the follow-up period (0 and 10 days, median and 75th percentiles) than did controls (n=116, 4 and 19 days; P=0.009). Patients receiving the education intervention had a lower risk of rehospitalization or death (relative risk, 0.65; 95% confidence interval, 0.45 to 0.93; P=0.018). Costs of care, including the cost of the intervention, were lower in patients receiving the education intervention than in control subjects by 2823 dollars per patient (P=0.035).The addition of a 1-hour, nurse educator-delivered teaching session at the time of hospital discharge resulted in improved clinical outcomes, increased self-care measure adherence, and reduced cost of care in patients with systolic heart failure.
Cholesteryl ester transfer protein B1B1 genotype as a predictor of coronary artery disease in Taiwanese with type 2 diabetes mellitus
Authors: Ming-Chia Hsieh, Kai-Jen Tien, Shun-Jen Chang, Chao-Sheng Lo, Shih-Chieh Hsin, Jeng-Yueh Hsiao, Shih-Chieh Hsu, Hui-Ting Liang, Hung-Chun Chen, Shyi-Jang Shin, Shiu-Ru Lin
Journal: Metabolism (2007)
Biliary epithelial-mesenchymal transition in posttransplantation recurrence of primary biliary cirrhosis
Authors: Helen Robertson, John A. Kirby, William W. Yip, David E.J. Jones, Alastair D. Burt
Journal: Hepatology (2007)

Primary biliary cirrhosis (PBC) recurs in the allograft after liver transplantation. Study of early tissue changes in the time-course of disease recurrence provides a unique insight into the initial stages of the disease process, which, in nontransplant patients, occurs long before clinical presentation. We describe a patient who developed classical clinical, biochemical, immunological, and histological features of PBC within 9 months after transplantation. Use of tissue from this patient before and during the development of PBC allowed us to identify biliary epithelial cell (BEC) epithelial-mesenchymal transition (EMT) as a key pathogenetic process. BEC expression of S100A4 (an early fibroblast lineage marker established as a robust marker of EMT), vimentin, and pSmad 2/3 [a marker of transforming growth factor beta (TGF-β) pathway signaling] were identified immunohistochemically in most BECs in liver tissue from this patient at the point of diagnosis of recurrent disease. BEC expression of S100A4 and pSmad 2/3 was seen as early as 24 days after orthotopic liver transplantation (OLT), although no other features of recurrent PBC were present at this time. Conclusion: S100A4, vimentin, and pSmad 2/3 expression in early recurrent PBC after OLT suggests that BEC EMT is occurring (potentially explaining BEC loss) and that this process is driven by TGF-β. S100A4 expression by BEC appears to occur before the development of any other features of recurrent PBC, suggesting that EMT may be an initiating event. (HEPATOLOGY 2007;45:977–981.)
Probable Gastrointestinal Reaction to Soybean
Authors: Charles D. Cook
Journal: New England Journal of Medicine (1960)

FROM inability to let well alone; from too much zeal for the new and contempt for what is old; from putting knowledge before wisdom, Science before Art and cleverness before common sense; from treating patients as cases, from making the cure of the disease more grievous than the endurance of the same, Good Lord deliver us.1 In recent years the substitution of soybean preparations for milk has been urged for the relatively rare patient with milk allergy and as a result has been used for a large variety of poorly defined conditions.2 The following case is reported because it represents . . .
Inhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy
Authors: Byung-Kwan Lim, Angela K. Peter, Dingding Xiong, Anna Narezkina, Aaron Yung, Nancy D. Dalton, Kyung-Kuk Hwang, Toshitaka Yajima, Ju Chen, Kirk U. Knowlton
Journal: Journal of Clinical Investigation (2013)

Heart failure in children and adults is often the consequence of myocarditis associated with Coxsackievirus (CV) infection. Upon CV infection, enteroviral protease 2A cleaves a small number of host proteins including dystrophin, which links actin filaments to the plasma membrane of muscle fiber cells (sarcolemma). It is unknown whether protease 2A-mediated cleavage of dystrophin and subsequent disruption of the sarcolemma play a role in CV-mediated myocarditis. We generated knockin mice harboring a mutation at the protease 2A cleavage site of the dystrophin gene, which prevents dystrophin cleavage following CV infection. Compared with wild-type mice, we found that mice expressing cleavage-resistant dystrophin had a decrease in sarcolemmal disruption and cardiac virus titer following CV infection. In addition, cleavage-resistant dystrophin inhibited the cardiomyopathy induced by cardiomyocyte-restricted expression of the CV protease 2A transgene. These findings indicate that protease 2A-mediated cleavage of dystrophin is critical for viral propagation, enteroviral-mediated cytopathic effects, and the development of cardiomyopathy.
Crosstalk between KIT and FGFR3 Promotes Gastrointestinal Stromal Tumor Cell Growth and Drug Resistance
Authors: Nathalie Javidi-Sharifi, Elie Traer, Jacqueline Martinez, Anu Gupta, Takehiro Taguchi, Jennifer Dunlap, Michael C. Heinrich, Christopher L. Corless, Brian P. Rubin, Brian J. Druker, Jeffrey W. Tyner
Journal: Cancer Research (2014)

Kinase inhibitors such as imatinib have dramatically improved outcomes for patients with gastrointestinal stromal tumor (GIST), but many patients develop resistance to these treatments. Although in some patients this event corresponds with mutations in the GIST driver oncogenic kinase KIT, other patients develop resistance without KIT mutations. In this study, we address this patient subset in reporting a functional dependence of GIST on the FGF receptor FGFR3 and its crosstalk with KIT in GIST cells. Addition of the FGFR3 ligand FGF2 to GIST cells restored KIT phosphorylation during imatinib treatment, allowing sensitive cells to proliferate in the presence of the drug. FGF2 expression was increased in imatinib-resistant GIST cells, the growth of which was blocked by RNAi-mediated silencing of FGFR3. Moreover, combining KIT and FGFR3 inhibitors synergized to block the growth of imatinib-resistant cells. Signaling crosstalk between KIT and FGFR3 activated the MAPK pathway to promote resistance to imatinib. Clinically, an IHC analysis of tumor specimens from imatinib-resistant GIST patients revealed a relative increase in FGF2 levels, with a trend toward increased expression in imatinib-naïve samples consistent with possible involvement in drug resistance. Our findings provide a mechanistic rationale to evaluate existing FGFR inhibitors and multikinase inhibitors that target FGFR3 as promising strategies to improve treatment of patients with GIST with de novo or acquired resistance to imatinib.
Influence of Age on Associations Between Childhood Risk Factors and Carotid Intima-Media Thickness in Adulthood
Authors: Markus Juonala, Costan G. Magnussen, Alison Venn, Terence Dwyer, Trudy L. Burns, Patricia H. Davis, Wei Chen, Sathanur R. Srinivasan, Stephen R. Daniels, Mika Kähönen, Tomi Laitinen, Leena Taittonen, Gerald S. Berenson, Jorma S.A. Viikari, Olli T. Raitakari
Journal: Circulation (2010)

Background— Atherosclerosis has its roots in childhood. Therefore, defining the age when childhood risk exposure begins to relate to adult atherosclerosis may have implications for pediatric cardiovascular disease prevention and provide insights about the early determinants of atherosclerosis development. The aim of this study was to investigate the influence of age on the associations between childhood risk factors and carotid artery intima-media thickness, a marker of subclinical atherosclerosis. Methods and Results— We used data for 4380 members of 4 prospective cohorts—Cardiovascular Risk in Young Finns Study (Finland), Childhood Determinants of Adult Health study (Australia), Bogalusa Heart Study (United States), and Muscatine Study (United States)—that have collected cardiovascular risk factor data from childhood (age 3 to 18 years) and performed intima-media thickness measurements in adulthood (age 20 to 45 years). The number of childhood risk factors (high [highest quintile] total cholesterol, triglycerides, blood pressure, and body mass index) was predictive of elevated intima-media thickness (highest decile) on the basis of risk factors measured at age 9 years (odds ratio [95% confidence interval] 1.37 [1.16 to 1.61], P =0.0003), 12 years (1.48 [1.28 to 1.72], P &lt;0.0001), 15 years (1.56 [1.36 to 1.78], P &lt;0.0001), and 18 years (1.57 [1.31 to 1.87], P &lt;0.0001). The associations with risk factors measured at age 3 years (1.17 [0.80 to 1.71], P =0.42) and 6 years (1.20 [0.96 to 1.51], P =0.13) were weaker and nonsignificant. Conclusions— Our analyses from 4 longitudinal cohorts showed that the strength of the associations between childhood risk factors and carotid intima-media thickness is dependent on childhood age. On the basis of these data, risk factor measurements obtained at or after 9 years of age are predictive of subclinical atherosclerosis in adulthood.