tbuckley/cabot-search huggingface dataset:
Nurse-training Scheme for Ex-Tuberculosis Patients
Authors: W. M. Robson
Journal: BMJ (1952)

<h3>Background</h3> Reducing intestinal phosphorus absorption is a cornerstone in CKD-MBD management. Yet, knowledge gaps include how CKD pathophysiology affects intestinal phosphorus absorption. <i>In vivo</i> rodent studies suggest that intestinal phosphorus absorption remains inappropriately normal in early-moderate CKD, despite declining 1,25-dihydroxyvitamin D (1,25D). We measured intestinal phosphorus absorption in patients with moderate CKD versus healthy adults using a direct radiotracer method. <h3>Methods</h3> Patients with CKD and healthy adults matched for age, sex, and race were enrolled in this 8-day controlled diet study: the first 6 days outpatient and the final 2 days inpatient. Oral and intravenous doses of <sup>33</sup>P and serial blood and urine sampling determined intestinal phosphorus absorption during the final 2 days. Secondary outcomes included fasting biochemistries and 24-hour urine phosphorus (uP). <h3>Results</h3> In total, <i>n</i>=8 patients with CKD (eGFR=29–55 ml/min per 1.73 m<sup>2</sup>) and <i>n</i>=8 matched healthy controls completed the study. On a controlled diet, no difference in fractional intestinal phosphorus absorption was detected between patients with CKD and healthy adults (0.69 versus 0.62, respectively; <i>P</i>=0.52), and this was similar for 24-hour uP (884 versus 935 mg/d, respectively; <i>P</i>=0.70). Fractional intestinal phosphorus absorption was not significantly related to 24-hour uP. Patients with CKD had higher serum intact PTH and intact FGF23 and lower 1,25D. The relationship between 1,25D and fractional intestinal phosphorus absorption was not statistically significant. <h3>Conclusions</h3> Intestinal phosphorus absorption with typical dietary intake did not differ in patients with moderate CKD compared with controls, despite lower serum 1,25D levels. In this setting, a relationship between 24-hour uP and fractional or absolute intestinal absorption was not evident. Further investigation is needed to determine what factors influence intestinal phosphorus absorption in CKD and the apparent lack of compensation by the intestine to limit phosphorus absorption in the face of declining kidney function and reduced 1,25D. Whether this is evident across a range of dietary phosphorus intakes, as well as CKD severity, also needs to be determined. <h3>Clinical Trial registry name and registration number:</h3> Phosphorus Absorption in Healthy Adults and in Patients with Moderate Chronic Kidney Disease, NCT03108222
New allergy society, formed to advocate in vitro laboratory test, wins reimbursement victory
Authors: P. Cotton
Journal: JAMA (1990)

A SOCIETY formed to promote in vitro allergy testing has won approval for the controversial technology from Blue Cross and Blue Shield. "The Blues' decision at the top level indicates that this test is reasonable, the cost-benefit ratio is reasonable, the way it is being done is not abusive, and it contributes to patient care," says American In Vitro Allergy and Immunology Society president-elect Russell Williams, Jr, MD. However, the national Blues' statement is only "informational." Independent local plans that are considering a change in their own reimbursement policy are bound to hear reservations from other allergists. The technology "just is not at the point yet where we're ready to shift," says Donald Aaronson, MD, immediate past president of the American College of Allergy and Immunology. And in declaring in vitro tests "eligible for coverage," the Blues' revised Uniform Medical Policy statement equates them to other widely used but controversial
Evidence of Autoimmune-Related Effects of Trichloroethylene Exposure from Studies in Mice and Humans
Authors: Glinda S. Cooper, Susan L. Makris, Paul J. Nietert, Jennifer Jinot
Journal: Environmental Health Perspectives (2009)

Our objective was to examine experimental and epidemiologic studies pertaining to immune-related, and specifically autoimmune-related, effects of trichloroethylene (TCE).We performed a literature search of PubMed and reviewed bibliographies in identified articles. We then systematically reviewed immune-related data, focusing on clinical and immunologic features and mechanistic studies.Studies conducted in MRL+/+ lupus mice report an accelerated autoimmune response in relation to exposure to TCE or some metabolites. Effects have been reported after 4 weeks of exposure to TCE at doses as low as 0.1 mg/kg/day in drinking water and have included increased antinuclear antibodies and interferon-gamma (IFN-gamma) and decreased secretion of interleukin-4 (IL-4), consistent with an inflammatory response. Autoimmune hepatitis, inflammatory skin lesions, and alopecia have been found after exposures of 32-48 weeks. Recent mechanistic experiments in mice examined oxidative stress and, specifically, effects on lipid-peroxidation-derived aldehydes in TCE-induced autoimmune disease. Two studies in humans reported an increase in IL-2 or IFN-gamma and a decrease in IL-4 in relation to occupational or environmental TCE exposure. Occupational exposure to TCE has also been associated with a severe, generalized hypersensitivity skin disorder accompanied by systemic effects, including hepatitis. In three case-control studies of scleroderma with a measure of occupational TCE exposure, the combined odds ratio was 2.5 [95% confidence interval (CI), 1.1-5.4] in men and 1.2 (95% CI, 0.58-2.6) in women.The consistency among the studies and the concordance between the studies in mice and humans support an etiologic role of TCE in autoimmune disease. Multisite collaborations and studies of preclinical immune markers are needed to further develop this field of research.
Amplification of MDS1/EVI1 and EVI1, Located in the 3q26.2 Amplicon, Is Associated with Favorable Patient Prognosis in Ovarian Cancer
Authors: Meera Nanjundan, Yasuhisa Nakayama, Kwai Wa Cheng, John Lahad, Jinsong Liu, Karen Lu, Wen-Lin Kuo, Karen Smith-McCune, David Fishman, Joe W. Gray, Gordon B. Mills
Journal: Cancer Research (2007)

Abstract Increased copy number involving chromosome 3q26 is a frequent and early event in cancers of the ovary, lung, head and neck, cervix, and BRCA1 positive and basal breast cancers. The p110α catalytic subunit of phosphoinositide-3-kinase (PI3KCA) and protein kinase Cι (PKCι) have previously been shown as functionally deregulated by 3q copy number increase. High-resolution array comparative genomic hybridization of 235 high-grade serous epithelial ovarian cancers using contiguous bacterial artificial chromosomes across 3q26 delineated an ∼2 Mb–wide region at 3q26.2 encompassing PDCD10 to MYNN (chr3:168722613-170908630). Ecotropic viral integration site-1 (EVI1) and myelodysplastic syndrome 1 (MDS1) are located at the center of this region, and their DNA copy number increases are associated with at least 5-fold increased RNA transcript levels in 83% and 98% of advanced ovarian cancers, respectively. Moreover, MDS1/EVI1 and EVI1 protein levels are increased in ovarian cancers and cancer cell lines. EVI1 and MDS1/EVI1 gene products increased cell proliferation, migration, and decreased transforming growth factor-β–mediated plasminogen activator inhibitor-1 promoter activity in ovarian epithelial cells. Intriguingly, the increases in EVI1 DNA copy number and MDS1/EVI1 transcripts are associated with improved patient outcomes, whereas EVI1 transcript levels are associated with a poor patient survival. Thus, the favorable patient prognosis associated with increased DNA copy number seems to be as a result of high-level expression of the fusion transcript MDS1/EVI1. Collectively, these studies suggest that MDS1/EVI1 and EVI1, previously implicated in acute myelogenous leukemia, contribute to the pathophysiology of epithelial ovarian cancer. [Cancer Res 2007;67(7):3074–84]
A Contribution to the Treatment of the Professional Dyscinesiae
Authors: L. Bianchi
Journal: BMJ (1878)

country.For instance, how few provincial towns possess a (Ransome's) stethometer, or even a sphygmograph, etc.c.An organisation of this kind would also secure the introduction without delay of the newest modes of treatment, e.g., the method of curing spinal curvature, which has been so ably demonstrated to this meeting by Dr. Sayre of New York, etc.
Understanding Human Behavior in Health and Illness
Authors: Chris Meuli
Journal: JAMA (1982)

In this complex world of modern medical knowledge, with all of its attendant psychological dilemmas, how many of us have truly attempted to understand how "normal" people respond to the emotional stresses of growing up, growing older, being sick, and the continuum along which psychological health evolves into "illness"? In this well-written series of 73 essays, a large array of emotional and psychological issues are authoritatively addressed by many authors who have done an extraordinary job of working together in developing a synthetic and coherent textbook. The book begins by asking the physician the question, "Why learn about human behavior?" and proceeds to discuss how psychological factors affect organic diseases and vice versa. The first 15 chapters explore the physician-patient relationship and delve into common patient problems, such as the psychological aspects of pain and physical illness, the difficult patient, responses to medical advice (compliance), and the evaluation of psychosomatic
Esophageal voice prosthesis mistaken for impacted foreign body
Authors: K. Karakaya, A. Emre, O. Tascilar, H. Ucan, O. Irkörücü, E. Tas, G. Cakmak, Y. Ustundag, M. Comert
Journal: Endoscopy (2009)

A 66-year-old man presented with dysphagia and weight loss of more than 20 % in a 3-month period. His past medical history included total laryngectomy and left radical neck dissection for laryngeal cancer in 1999. Later he underwent right radical neck dissection and insertion of an esophageal Blom–Singer voice prosthesis in 2000. The patient had adjuvant chemoradiotherapy. He had lost 11 kg within the last 3-month period. Upper gastrointestinal endoscopy revealed a tumoral mass obstructing the esophageal lumen at 28 cm distal to the incisors. Meanwhile, the endoscopist also noticed a foreign-body-like object 14 cm from the incisors ([Fig. 1]) and nearby a small papillomatous lesion. The material of the object was completely unknown to us and a brief consultation with a laryngologist prevented us from taking it out with a snare. The object was a voice prosthesis.
Quality of life three years after diagnosis of localised prostate cancer: population based cohort study
Authors: D. P Smith, M. T King, S. Egger, M. P Berry, P. D Stricker, P. Cozzi, J. Ward, D. L O'Connell, B. K Armstrong
Journal: BMJ (2009)

Nicotine is thought to be the key substance responsible for tobacco-smoking habits and appears to trigger reinforcement via the ventral tegmental area (VTA). Recently, multiple anatomical substrates for drug reinforcement have been identified in the vicinity of the ventral midbrain. In addition to the posterior portion of the VTA, the central linear nucleus raphé and the supramammillary nucleus of the posterior hypothalamus mediate drug reinforcement. Using intracranial self-administration procedures, we examined whether these regions mediate the reinforcing effects of nicotine. Rats learned to lever press for self-administration of nicotine into the posterior VTA, central linear nucleus, and supramammillary nucleus, suggesting a reinforcing action of nicotine in these regions. The rats did not self-administer nicotine into surrounding regions including the anterior VTA, substantia nigra, the region just dorsal to the posterior VTA, interpeduncular nucleus, or medial mammillary nucleus. The reinforcing effects of nicotine into the three brain regions were further confirmed by a two-lever discrimination procedure, in which rats learned to selectively respond between active and inactive levers. The reinforcing effects of nicotine administration into the posterior VTA, central linear nucleus, and supramammillary nucleus were blocked by coadministration of the nicotine receptor antagonist mecamylamine. The reinforcing effects of nicotine into the posterior VTA or central linear nucleus were attenuated by coadministration of the D<sub>2</sub> receptor agonist quinpirole. These findings demonstrate that nicotine reinforcement involves multiple regions both inside and outside the VTA.
Wellcome Trust is to close its centre for history of medicine
Authors: W. Moore
Journal: BMJ (2010)

The internationally renowned Wellcome Trust Centre for the History of Medicine at University College London (UCL) is to close within two years, following allegations of mismanagement and arguments over funding.

The decision, which was announced to staff before Easter and confirmed by the Wellcome Trust and UCL this week, has shocked the academic world. In a joint statement issued on Thursday 15 April UCL and the trust announced that they had agreed “with regret” to “work towards” the closure of the centre over the next two years. The statement said that the decision followed “discussions between the senior staff of both organisations and consideration by the board of governors of the Wellcome Trust.”

No reason has formally …
Drinking and Recreational Boating Fatalities
Authors: Gordon S. Smith, Penelope M. Keyl, Jeffrey A. Hadley, Christopher L. Bartley, Robert D. Foss, William G. Tolbert, James McKnight
Journal: JAMA (2001)

Alcohol is increasingly recognized as a factor in many boating fatalities, but the association between alcohol consumption and mortality among boaters has not been well quantified.To determine the association of alcohol use with passengers' and operators' estimated relative risk (RR) of dying while boating.Case-control study of recreational boating deaths among persons aged 18 years or older from 1990-1998 in Maryland and North Carolina (n = 221), compared with control interviews obtained from a multistage probability sample of boaters in each state from 1997-1999 (n = 3943).Estimated RR of fatality associated with different levels of blood alcohol concentration (BAC) among boaters.Compared with the referent of a BAC of 0, the estimated RR of death increased even with a BAC of 10 mg/dL (odds ratio [OR], 1.3; 95% confidence interval [CI], 1.2-1.4). The OR was 52.4 (95% CI, 25.9-106.1) at a BAC of 250 mg/dL. The estimated RR associated with alcohol use was similar for passengers and operators and did not vary by boat type or whether the boat was moving or stationary.Drinking increases the RR of dying while boating, which becomes apparent at low levels of BAC and increases as BAC increases. Prevention efforts targeted only at those operating a boat are ignoring many boaters at high risk. Countermeasures that reduce drinking by all boat occupants are therefore more likely to effectively reduce boating fatalities.
Risk Stratification of Patients With Barrett’s Esophagus and Low-grade Dysplasia or Indefinite for Dysplasia
Authors: Prashanthi N Thota, Hyun-Ju Lee, John R Goldblum, Xiuli Liu, Madhusudhan R Sanaka, Tushar Gohel, Mehulkumar Kanadiya, Rocio Lopez
Journal: Clinical Gastroenterology and Hepatology (2014)
Carrier Screening, Incidence of Cystic Fibrosis, and Difficult Decisions
Authors: Theodore G. Liou, Ronald C. Rubenstein
Journal: JAMA (2009)

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
Cancer Cells' Immortality May Prove Their Undoing
Authors: Andrew A. Skolnick
Journal: JAMA (1995)

WHAT MAKES cancer cells so deadly is their immortality. Normal somatic cells have a mitotic clock that keeps track of the number of times they divide. When that clock runs down, the cell ceases to replicate and becomes senescent. Most cancer cells, however, have found a way to stop their clocks.  According to research findings reported at the American Cancer Society's 37th Science Writers Seminar, in New Orleans, La, the means to stop the mitotic clock appears to be an enzyme that is expressed in early fetal development by germline cells and most cancers, but not by normal somatic cells. The enzyme, called telomerase, enables the cell to maintain the integrity of its chromosomes each time it divides. Without it, the ends of the chromosomes, called telomeres, are whittled away until too much is lost for the cell to maintain normal function. At that point, it ceases to replicate.  Telomerase
Migrant oncogene-Burkitt's lymphoma link
Authors: B. Merz
Journal: JAMA (1982)

Two teams of investigators have provided the first evidence that the translocation of a single piece of DNA from one chromosome to another involves and perhaps "turns on" an oncogene in human cells. This evidence was presented at a recent Bristol-Myers symposium, "Chromosomes and Cancer: From Molecules to Man," at the University of Chicago. The laboratories of Carlo M. Croce, PhD, associate director of the Wistar Institute in Philadelphia, and Philip Leder, MD, chair, Department of Genetics, Harvard Medical School, Boston, pursued different avenues of research to arrive at the same conclusion: The translocation between the terminal ends of chromosomes 8 and 14 in Burkitt's lymphoma cells involves an exchange of two genes (among others)— one that codes for a region of the antibody molecule and one that is an oncogene called the<i>myc</i>gene (the human homologue of the avian myelocytomatosis virus). The translocation, which occurs in 90% of
Effect of chronic administration of ciclosporin a on seric bile acids and plasma clearance of bromosulfophthalein in man
Authors: J.F. Cadranel, P. Grippon, D. Valla, F. Lunel, M. Desruenne, P. Leger, A. Cabrol, S. Erlinger, P. Opolon
Journal: Journal of Hepatology (1989)
Differing cellular infiltrates on serial biopsy of heart allograft recipients randomized to okt3 or hatg induction therapy: Implications for graft injury
Authors: Brace M. McManus, Janet E. Wilson, Gayle L. Winters, Lawrence H. Chow, E.Jeanne O'Sullivan, Roque Pifarre, Maria Rosa Costanzo-Nordin
Journal: Journal of the American College of Cardiology (1990)
Rapid decline in FEV1. A new risk factor for coronary heart disease mortality.
Authors: M S Tockman, J D Pearson, J L Fleg, E J Metter, S Y Kao, K G Rampal, L J Cruise, J L Fozard
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

Coronary heart disease (CHD) is the leading cause of mortality in the United States. The present cohort study was conducted to determine whether rate of FEV1 loss independently predicts CHD mortality in apparently healthy men. White male Baltimore Longitudinal Study of Aging (BLSA) participants without CHD underwent clinical evaluation at 2-yr intervals; 883 had satisfactory pulmonary and lipid studies and returned for a least one visit. Cases were BLSA subjects without CHD on entry who died a "coronary death" (death from acute myocardial infarction, sudden death, or congestive heart failure in the presence of coronary artery disease). Forced expiratory maneuvers followed American Thoracic Society guidelines. Serum cholesterol, blood pressure, cigarette smoking, and body mass index were obtained from the BLSA database. There were 79 CHD deaths and 804 survivors during an average follow-up of 17.4 yr. After adjustment for age, initial FEV1% predicted, smoking status, hypertension, and cholesterol, a time-dependent proportional hazards model showed that cardiac mortality, but not all causes of mortality, generally increased with increasing quintile of FEV1 decline for the entire cohort (relative risk [RR] 2.92-5.13) and separately for the subset of never-smokers. Thus, excess CHD mortality follows a large decline in FEV1, independent of the initial FEV1% predicted, cigarette smoking, and other common CHD risk factors.
HLA-DQB1-defined genetic susceptibility, beta cell autoimmunity, and metabolic characteristics in familial and nonfamilial insulin-dependent diabetes mellitus. Childhood Diabetes in Finland (DiMe) Study Group.
Authors: R Veijola, H Reijonen, P Vähäsalo, E Sabbah, P Kulmala, J Ilonen, H K Akerblom, M Knip
Journal: Journal of Clinical Investigation (1996)

Familial aggregation of insulin-dependent diabetes mellitus (IDDM) is a common phenomenon, but the reasons behind it are poorly understood. To investigate whether there is heterogeneity between familial and nonfamilial forms of IDDM we compared genetic, immunological, and clinical characteristics of diabetic children with and without an affected first-degree relative in a population-based series of Finnish children with IDDM. The frequencies of HLA-DQB1 genotypes known to be associated with high (DQB1*0302/0201) or moderate (*0302/x) IDDM risk in the Finnish population were increased, while the proportions of DQB1 genotypes associated with low or decreased risk for IDDM were reduced in the 121 familial cases as compared with the 574 nonfamilial cases (32.7 vs. 21.3%, 41.3 vs. 35.9%, 18.3 vs. 31.4%, and 7.7 vs. 11.4%, respectively; P = 0.002). The frequencies and serum concentrations of islet cell antibodies, insulin autoantibodies, and antibodies to the 65-kD isoform of glutamic acid decarboxylase were similar at diagnosis in the familial and nonfamilial cases. The 31 first-affected cases in the multiple case families were younger at diagnosis than the nonfamilial cases (6.9 vs. 8.5 yr; P < 0.05). The 90 second-affected familial cases had less severe metabolic decompensation at diagnosis than either the first-affected familial or nonfamilial cases. In conclusion, familial aggregation of IDDM in Finland is at least partly explained by a higher frequency of IDDM susceptibility genes in families with multiple affected individuals. The lack of differences in autoantibody levels between the familial and nonfamilial cases indicates homogeneity rather than heterogeneity in the pathogenetic process of beta cell destruction.