tbuckley/cabot-search huggingface dataset:
Children of the Painter
Authors: M. Therese Southgate
Journal: JAMA (2006)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
S60 Cigarette smoke induced oxidation of -1 antitrypsin amplifies the pulmonary inflammatory response
Authors: S. Alam, Z. Li, R. Mahadeva
Journal: Thorax (2010)

Alpha-1 antitrypsin (AT) is the major elastase inhibitor within the lung. Oxidation of critical methionine residues in AT (Ox-AT) has diminished ability to inhibit neutrophil elastase, which is thought to contribute to the pathogenesis of COPD. Ox-AT may also be pro-inflammatory. We investigated whether cigarette smoke would promote production of Ox-AT and an exaggerated inflammatory response. Adult female transgenic mice for human M-AT and wild type CBA mice (n=9 per group) were exposed to cigarette smoke (CS) from 1R3F research grade cigarettes for 5 days and killed 1 day later. Control mice were exposed to air. Ox-AT and inflammatory chemokines were assessed in BALF and lung homogenates (LH) by ELISA and Western blot. Ox-AT was not detected in control M-AT mice nor CS-CBA mice, but was significantly increased in BALF, 72.3 ng/ml (SEM±11.7), p=0.017 and LH, 1351.3 (±111.6) p=&lt;0.001 of CS-M-AT mice. This was confirmed on western blot of SDS-PAGE using a monoclonal antibody to Ox-AT. There was a significant increase in BAL polymorphonuclear cells (1.53(10<sup>4</sup>) (±0.02) vs 0.16 (10<sup>4</sup>) (±0.04) p=0.022) and macrophages (16.36 (10<sup>4</sup>) (±0.69) vs 10.19(10<sup>4</sup>) (±1.94) p=0.008) in CS-M-AT mice compared with CS-CBA mice. There was significantly greater MCP-1 and KC in CS-M-AT vs CS-CBA; BALF, MCP-1 521.35 pg/ml (±46.7) vs 264.63 (±17.65), respectively; p=0.006, and KC 440.5 pg/ml (±53) vs 171.4 (±17), p=0.024. In LH, CS-M-AT MCP-1, 779.6 (±55) vs CS-CBA 368.8 (±30) (pg/ml) p=0.003, and CS-M-AT KC 466.1 (±67) vs 250.9 (±14), p=0.003. Similarly there was significantly increased NF-кB (p=0.015) and AP-1 (p=0.015) activity in CS-M-AT lungs compared with CS-CBA lungs. These findings demonstrate that oxidation of methionines in AT by oxidants released from cigarette smoke not only reduces the anti-elastase lung protection but converts AT into a pro-inflammatory stimulus. Ox-AT generated in the airway interacts directly with epithelial cells to release MCP-1 and IL-8, so enhancing lung inflammation. This mechanism could potentially contribute to the abnormal inflammatory response seen in COPD.
ACUTE INTESTINAL OBSTRUCTION
Authors: FRANK SMITHIES
Journal: JAMA (1930)

Whatever may be the cause, or (from the duodenum to the rectum) whenever acute, persistent stricture of the lumen of the alimentary tract develops, there is created the gravest form of abdominal emergency.  Initial manifestations, as mild as a common, transient gas colic, may progress so swiftly that but few hours suffice to accumulate pathologic changes of a degree and extent indicative of early death. Again, abrupt, stormy, painful beginning-symptoms, suggesting rapid and extensive enteric damage, often enough are followed by such quiescence of distress as to present a problem equally puzzling from the points of view of diagnosis and of management. In either type of onset, physical examination of the abdomen may yield few anomalies; the classic or textbook signs of intestinal obstruction are lacking or confused. Indeed, as our material shows, what most commonly are considered as signs of entero or colonic obstruction represent largely the manifestation of
Activation mapping in patients with coronary artery disease with multiple ventricular tachycardia configurations: Occurrence and therapeutic implications of widely separate apparent sites of origin
Authors: Lawrence E. Waspe, Richard Brodman, Soo G. Kim, Jeffrey A. Matos, Debra R. Johnston, Gale M. Scavin, John D. Fisher
Journal: Journal of the American College of Cardiology (1985)
Dietary Patterns and Risk for Type 2 Diabetes Mellitus in U.S. Men
Authors: Rob M. van Dam, Eric B. Rimm, Walter C. Willett, Meir J. Stampfer, Frank B. Hu
Journal: Annals of Internal Medicine (2002)

Background: The role of diet in the development of type 2 diabetes mellitus remains unsettled. Objective: To examine the association between major dietary patterns and risk for type 2 diabetes mellitus. Design: Prospective cohort study. Setting: United States. Participants: 42 504 male health professionals, 40 to 75 years of age, without diagnosed diabetes, cardiovascular disease, or cancer at baseline. Measurements: Using factor analysis based on data from food-frequency questionnaires, we identified and validated two major dietary patterns that we labeled "prudent" (characterized by higher consumption of vegetables, fruit, fish, poultry and whole grains) and "western" (characterized by higher consumption of red meat, processed meat, French fries, high-fat dairy products, refined grains, and sweets and desserts). Relative risks and 95% CIs were adjusted for potential confounders, including body mass index (BMI), physical activity, and cigarette smoking. Results: During 12 years of follow-up (466 508 person-years), we documented 1321 cases of type 2 diabetes. The prudent dietary pattern score was associated with a modestly lower risk for type 2 diabetes (relative risk for extreme quintiles, 0.84 [CI, 0.70 to 1.00]). In contrast, the western dietary pattern score was associated with an increased risk for type 2 diabetes (relative risk, 1.59 [CI, 1.32 to 1.93]; P < 0.001 for trend). A high score for the western dietary pattern combined with low physical activity (relative risk comparing extreme quintiles of dietary pattern score and physical activity, 1.96 [CI, 1.35 to 2.84]) or obesity (relative risk for BMI ≥ 30 kg/m2 vs. <25 kg/m2, 11.2 [CI, 8.07 to 15.6]) was associated with a particularly high risk for type 2 diabetes. Conclusion: Our findings suggest that a western dietary pattern is associated with a substantially increased risk for type 2 diabetes in men.
Berek and Novak’s Gynecology
Authors: Ronald T. Burkman
Journal: JAMA (2007)

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
A case of peptic ulcer.
Authors: L I Zander, J Bennett
Journal: BMJ (1977)

The patient's story is really very straightforward, but it raises several problems of deciding management. He is 52 and has a clerical job in local government with a fair amount of respon sibility that he enjoys, and he does not feel he is working under undue stress. He is married with two children, one still at home, and again no obvious problems arise in this part of his life. He has had intermittent dyspepsia for some 20 years and a barium meal examination 10 years ago showed duodenal scar ring. He normally controls exacerbations with milk or by taking baking soda; he drinks little alcohol but smokes about 10 cigarettes daily. He has never lost work because of his symptoms. He consulted yesterday evening because of a two-week long current episode of dyspepsia of greater than usual severity that has not responded to his usual self-medication. He has not vomited but is losing sleep and having considerable epigastric pain as the day wears on. He looks unhappy and has moderate abdominal tenderness localised to the usual peptic ulcer area. He seems thin but says he has not lost weight recently. I feel reasonably happy that the diagnosis is duodenal ulcer and no doubt antacid treatment would help his pain. I also feel further investigation could reasonably be delayed. Our local gastroenterologist however, has asked for this type of patient to be referred to him because of his co-operation in a trial of one of the new bismuth-containing preparations. This would mean three gastroscopies but equally could help both the patient's illness and the proper evaluation of a possibly important new drug. I find my position between the patient and progress difficult and need advice both in general and particular terms.
Controversies in Lactic Acidosis
Authors: Barry A. Mizock
Journal: JAMA (1987)

Lactic acidosis is common in critically ill patients and is usually caused by tissue perfusion that is inadequate to meet metabolic demand. However, it has also been noted in conditions in which tissue perfusion is apparently adequate. Hyperlactatemia can occur in the absence of acidosis, usually in the setting of hypermetabolic disease. Numerous areas of controversy exist regarding the pathogenesis of lactic acidosis, as well as certain of its diagnostic, therapeutic, and prognostic features. Knowledge of these areas of controversy should facilitate the clinician's approach to diagnosis and management.
Towards optimal cut-off trough levels of adalimumab and etanercept for a good therapeutic response in rheumatoid arthritis. Results of the INMUNOREMAR study
Authors: Raimon Sanmarti, Jose Inciarte-Mundo, Paula Estrada-Alarcon, Maria Garcia-Manrique, Javier Narvaez, Jesus Rodriguez-Moreno, Antoni Gomez-Centeno, Mariona Pascal, Jordi Yagüe
Journal: Annals of the Rheumatic Diseases (2015)

We read with great interest the paper by Chen et al 1 analysing the relationship between therapeutic response to adalimumab and etanercept and serum drug trough levels in 70 patients with rheumatoid arthritis (RA). The authors confirmed a positive association between drug levels and European League Against Rheumatism (EULAR) response. Good responders showed significantly higher drug levels than moderate or poor responders, in line with other studies.2 ,3 The authors calculated (receiver operating characteristic curves) highly sensitive and specific cut-off trough levels of response (1.274 and 1.046 μg/mL for therapeutic response to adalimumab and 1.242 and 0.800 μg/mL for etanercept at 6 and 12 months, respectively). The study also highlights the importance of establishing an optimal cut-off for the …
F.D.P. in glomerulonephritis.
Authors: F E Preston, R G Malia, E K Blackburn, M Platts
Journal: BMJ (1971)

The note also states that "during 1970, 101 cases of malaria were reported by [Public Health] laboratories in the United King- dom."This figure is a serious underestimate of the total number of cases of malaria noti- fied in Britain.Information provided by the Department of Health and Social Security indicates that the quarterly returns of the Registrar General for 1970 quote 137 confirmed notifications of malaria in England and Wales.In addition to that the Scottish Home and Health Department received in 1970 not less than 24 notifications of malaria of which 19 were confirmed.This brings the known number of malaria cases in England, Wales, and Scotland to at least 156.Carswell and Stevenson2 reported recently that over the period 1965-9 the number of cases of malaria seen in Scotland averaged 20 per annum.Malaria is not notified in Northern Ireland but the cases confirmed by the Public Health Laboratories in 1970 were in- cluded in the figures reported in your note.
Efficient inhibition of multidrug-resistant human tumors with a recombinant bispecific anti-P-glycoprotein × anti-CD3 diabody
Authors: Y Gao, D Xiong, M Yang, H Liu, H Peng, X Shao, Y Xu, C Xu, D Fan, L Qin, C Yang, Z Zhu
Journal: Leukemia (2004)
Will Sulfonylurea Treatment of Impaired Glucose Tolerance Delay Development and Complications of NIDDM?
Authors: Arne Melander, Per-Olof Bitzén, Gunnar Sartor, Bengt Scherstén, Elisabeth Wåhlin-Boll
Journal: Diabetes Care (1990)

The chronic hyperglycemia of non-insulin-dependent diabetes mellitus (NIDDM) evolves gradually and is usually preceded by more transient hyperglycemia, classified as impaired glucose tolerance (IGT). Already in this phase, there is an increased risk of cardiovascular complications, and many IGT subjects, like NIDDM patients, often display several of the metabolic and circulatory disturbances that are associated with hyperglycemia, e.g., insulin resistance, hyperinsulinemia and/or hyperproinsulinemia, delayed insulin release, dyslipidemia, and hypertension. Therefore, and because untreated hyperglycemia is a self-perpetuating condition, early detection and early intervention may be necessary to prevent the progression and complications of NIDDM. This in turn would necessitate screening procedures, and the therapeutic goal should include both euglycemia and normalization of plasma insulin, plasma lipids, and blood pressure. A study in the German Democratic Republic indicated that the mortality in screening-detected NIDDM patients did not differ from that in patients detected in routine care. In a Swedish study on screening-detected NIDDM subjects, only those who had IGT rather than manifest NIDDM could maintain fasting blood glucose ≤6 mM for 5 yr by hypocaloric dietary regulation alone. In those with screening-detected NIDDM, the delayed acute insulin release and net postprandial hyperglycemia were improved by addition of glipizide, and most managed to attain and maintain fasting blood glucose ≤6 mM for ∼2 yr after such addition. However, after 4 yr, there was an increase in blood glucose, suggesting that preventive intervention either may not be possible or may have to start in the IGT phase. In another Swedish study, the combination of dietary advice and tolbutamide seemed to delay the progression of IGT to NIDDM, lower cholesterol and triglyceride levels and blood pressure, and reduce cardiovascular morbidity and mortality. However, no preventive effect was seen in two similar British studies. Moreover, only a few untreated IGT subjects progress to manifest NIDDM. Hence, routine screening for IGT and subsequent therapeutic intervention cannot be recommended, but more studies are needed.
Tamoxifen Induces Triacylglycerol Accumulation in the Mouse Liver by Activation of Fatty Acid Synthesis
Authors: Laura K. Cole, René L. Jacobs, Dennis E. Vance
Journal: Hepatology (2010)

Tamoxifen is an anti-estrogen drug widely used for the treatment of hormone-sensitive breast cancer. Approximately 43% of breast cancer patients treated with tamoxifen develop hepatic steatosis. The mechanism or mechanisms by which tamoxifen may induce lipid accumulation in the liver are unclear. Mice were injected with tamoxifen or vehicle (sesame oil containing 1% benzyl alcohol) for 5 consecutive days. In comparison with the vehicle, tamoxifen increased hepatic triacylglycerol levels by 72%. The levels of plasma triacylglycerol were similar between the tamoxifen-treated and control groups. We found increased radiolabeling of triacylglycerol and phospholipids from [3H]acetate (˜50%) but not [14C]oleate in hepatocytes from tamoxifen-treated mice versus control mice. Fatty acid uptake, triacylglycerol secretion, and fatty acid oxidation remained unchanged in isolated hepatocytes after tamoxifen treatment. The apparent increase in fatty acid synthesis was explained by a marked decrease in the phosphorylation of acetyl coenzyme A carboxylase, which resulted in its activation. Conclusion: Our data suggest that increased de novo fatty acid synthesis is the primary event leading to tamoxifen-induced steatosis in the mouse liver. Inhibition of fatty acid synthesis might, therefore, ameliorate steatosis/steatohepatitis in breast cancer patients treated with tamoxifen. (Hepatology 2010;52:1258-1265)
Prevention of benzene-induced myelotoxicity by nonsteroidal anti-inflammatory drugs.
Authors: G F Kalf, M J Schlosser, J F Renz, S J Pirozzi
Journal: Environmental Health Perspectives (1989)

Benzene affects hematopoietic progenitor cells leading to bone marrow depression and genotoxic effects such as micronucleus formation. Progenitor cell proliferation and differentiation are inhibited by prostaglandins produced by macrophages. Administration of benzene to DBA/2 or C57BL/6 mice caused a dose-dependent bone marrow depression and a significant increase in marrow prostaglandin E level and both were prevented by the coadministration of indomethacin and other inhibitors of the cyclooxygenase component of prostaglandin H synthase. Levels of benzene that decreased bone marrow cellularity also caused genotoxic effects measured as increased micronucleated polychromatic erythrocytes in peripheral blood, which was also prevented by the coadministration of indomethacin. These results suggest a possible role for prostaglandin synthase in benzene myelotoxicity; a mechanism by which this might occur is presented.
"Patientgate"--digital recordings change everything
Authors: G. Elwyn
Journal: BMJ (2014)

Patients’ recordings of consultations are a valuable addition to the medical evidence base

It’s 8.30 am, just before clinic opens. It is 2010. Dr Byte checks an online forum, and something catches his eye.

A female patient is complaining about a doctor. Her posting has led to strident reactions from other doctors. Patients are taking her side. It looks ugly.

It turns out that the patient had asked her family doctor whether she could use her smartphone to record the encounter. Her doctor was apparently taken aback and had paused to gather his thoughts. He asked the patient to put her smartphone away, saying that it was not the policy of the clinic to allow patients to take recordings. The patient described how the mood of the meeting shifted. Initially jovial, the doctor had become defensive. She complied and turned off her smartphone.

The patient wrote that as soon as the smartphone was turned off the doctor raised his voice and berated her for making the request, saying that the use of a recording device would betray the fundamental trust that is the basis of a good patient-doctor relationship. The patient wrote that she tried to reason, explaining that the recording would be useful to her and her family. But the doctor shouted at her, asking her to leave immediately and find …
ATROPHY IN SKELETAL MUSCLE
Authors: DONALD YOUNG SOLANDT
Journal: JAMA (1942)

Mammalian skeletal muscle is served by a number of different types of nerve fibers. Some represent the central and others the autonomic nervous system. Diagrammatic representation of the component parts of skeletal muscle innervation has been attempted in figure 1. Probably only the motor nerve fibers, axons of the lower motor neuron, make functional connection with the muscle fibers. It is generally believed that these fibers, and these alone, are responsible for the control of the activity of the muscle fiber and are chiefly responsible for the trophic state of muscle tissue. Boeke<sup>1</sup>and others have claimed that muscle fibers are also innervated by autonomic nerve fibers. Such connections may exist, but there is no satisfactory evidence that the autonomic nervous system has any direct control over the activity of skeletal muscle fibers. Sympathetic and parasympathetic nerve fibers to blood vessels in muscle give the autonomic nervous system indirect
Environmental Tobacco Smoke: The Price of Scientific Certainty
Authors: D. M. Burns
Journal: JNCI Journal of the National Cancer Institute (1992)

2:1429-1432, 1951 (4) DORN HF, CUTLER SJ: Morbidity from Cancer in the United States. Public Health Monogr No. 56. Washington DC: US Govt Print Off, 1959 (5) MACMAHON B: Breast cancer at menopausal ages: An explanation of observed incidence changes. Cancer 10:1037-1044, 1957 (6) MACMAHON B: Cohort fertility and increasing breast cancer incidence. Cancer 11:250-254, 1958 (7) MACMAHON B, TERRY WD: Application of cohort analysis lo the study of time trends in neoplastic disease. J Chronic Dis 7:24—35, 1958 (5) STEVENS RG, MOOLCAVKAR SH, LEE JAH: Temporal trends in breast cancer. Am J Epidemiol 115:759-777, 1982 (9) HOLFORD TR: The estimation of age, period and cohort effects for vital rates. Biometrics 39:311-324, 1983 (10) TARONE RE, CHU KC: Implications of birth cohort patterns in interpreting trends in breast cancer rates. J Natl Cancer Inst 84:1402-1410, 1992 (/ / ) TRICHOPOULOS D: Hypothesis: Does breast cancer originate in utero? Lancet 335:939-940, 1990 (12) TRICHOPOULOS D, LIPMAN RD: Mammary gland mass and breast cancer risk. Epidemiology. In press
Warfarin for Venous Thromboembolism — Walking the Dosing Tightrope
Authors: Andrew I. Schafer
Journal: New England Journal of Medicine (2003)

Venous thromboembolism encompasses deep venous thrombosis and pulmonary embolism, which represent different manifestations of the same disease process. Indeed, most patients in whom symptoms of either condition develop will simultaneously have overt or subclinical evidence of the other. Our understanding of the causes and natural history of venous thromboembolism has undergone considerable evolution in recent years, influencing the clinical approach to diagnosis and treatment. It is now recognized that venous thromboembolism is a chronic disease. Almost one third of patients have a recurrence within eight years after the initial event.1 Furthermore, venous thromboembolism is at least in part a systemic . . .