tbuckley/cabot-search huggingface dataset:
Maternal Cigarette Smoking and the Ghost of Yerushalmy—Will It Ever Rest?
Authors: Philip R. J. Burch
Journal: JAMA (1986)

<h3>To the Editor.—</h3> The results of two randomized controlled intervention trials of antismoking advice during pregnancy have now been reported.<sup>1,2</sup>In the first, carried out by Donovan<sup>1</sup>in 1972 and 1973 in London, the mean birth weight for singleton live births in the control group was 12 g higher than in the intervention group; the difference was not statistically significant.<sup>1</sup>In the second trial, carried out in the United States and reported in 1984, the mean birth-weight difference (92 g) was in the opposite direction; it was statistically significant (<i>P</i>&lt;.05) and corroborated the hypothesis that cigarette smoking during later stages of pregnancy causes a reduction in fetal growth.<sup>2</sup> There is no clear explanation<sup>2</sup>for the divergent results between the two trials but Berman and colleagues<sup>3</sup>suggest that if answers to three questions could be given "in the causal direction, we may then truly be
Autoimmune Endocrine Disease
Authors: Robert Volpé
Journal: JAMA (1984)

This volume consists of a series of chapters by different authors on various aspects of autoimmune endocrine diseases, edited by a well-known figure in the field of thyroid autoimmunity. The contributors vary considerably in their treatment of the subject matter, comprehensiveness, and handling of other viewpoints. They are, however, all experts in their fields, with interesting and sometimes controversial perspectives, and the book makes interesting reading and is a worthwhile contribution.  Chapter 1, by Duncan Adams, a pioneer and seminal contributor to our understanding of thyroid autoimmune disease, deals with an overview of autoimmune mechanisms. This rather lengthy and rambling chapter is not tightly constructed but goes through the history of the epochal discoveries in relation to the immune system in an entertaining fashion. Adams, however, appears to reject summarily any evidence favoring an antigen-specific defect in suppressor T-lymphocyte function as a cause of organ-specific autoimmune diseases by stating that
Audit of compliance with antenatal protocols.
Authors: A. F. Yoong, J. Lim, C. N. Hudson, T. Chard
Journal: BMJ (1992)

OBJECTIVE--To assess the implementation of action protocols dictated by antenatal risk factors noted at the initial (booking) antenatal visit. DESIGN--Retrospective study of 2000 women delivered between 1 March 1990 and 29 March 1991. SETTING--Maternity department of a district general hospital supporting a multiethnic population in inner London. MAIN OUTCOME MEASURES--Comparison of clinical actions performed against those dictated by the department9s protocols. Analysis according to clinical importance, gestation at booking, maternal age, parity, birth order, ethnic origin, and certainty of gestational age. RESULTS--Interobserver agreement between the two auditors was good (kappa statistic for risk factors detected, 0.78; for actions generated, 0.80). Of the 15,658 actions dictated by department protocols, 3673 (23.5%) were actually performed by the clinicians. The 63 combinations of risk factors and actions believed by consultants to be of particular clinical importance had an action rate of 28.3% compared with 18.6% for those considered less important (p &lt; 0.001). Mothers who first visited the hospital antenatal clinic at or before 24 weeks9 gestation had 25.2% of relevant protocols fulfilled (p &lt; 0.001). Compliance was significantly improved in women aged 36 or over (32.4%), black women (24.9%), and cases of uncertain gestation (24.5%). Parity and birth order were not associated with an altered action rate. Ethnic origin deemed as "other" (than white, black, Asian, or oriental) or "unknown" was associated with poor compliance (19.3%). CONCLUSIONS--Compliance to a set of agreed protocols was poor even though a computer system was available and a protocol manual had been distributed. Protocols were more likely to be implemented in women who booked early and in some groups of women deemed at high risk including older mothers, black women, and those denoted as having uncertain gestational age.
ASSESSMENT OF LEFT VENTRICULAR FUNCTION USING SPECKLE TRACKING ECHOCARDIOGRAPHY DURING VASOPRESSOR-INDUCED INCREASES IN AFTERLOAD IN A RABBIT MODEL
Authors: David J. Sahn, Anneka Hooft, Jonathan Ho, Wei Zhou, Jennifer Corniea, Elizabeth Sanchez, Aman Mahajan, Muhammad Ashraf
Journal: Journal of the American College of Cardiology (2010)
Placental Insufficiency Associated with Loss of Cited1 Causes Renal Medullary Dysplasia
Authors: Duncan B. Sparrow, Scott C. Boyle, Rebecca S. Sams, Bogdan Mazuruk, Li Zhang, Gilbert W. Moeckel, Sally L. Dunwoodie, Mark P. de Caestecker
Journal: Journal of the American Society of Nephrology (2009)

A number of studies have shown that placental insufficiency affects embryonic patterning of the kidney and leads to a decreased number of functioning nephrons in adulthood; however, there is circumstantial evidence that placental insufficiency may also affect renal medullary growth, which could account for cases of unexplained renal medullary dysplasia and for abnormalities in renal function among infants who had experienced intrauterine growth retardation. We observed that mice with late gestational placental insufficiency associated with genetic loss of Cited1 expression in the placenta had renal medullary dysplasia. This was not caused by lower urinary tract obstruction or by defects in branching of the ureteric bud during early nephrogenesis but was associated with decreased tissue oxygenation and increased apoptosis in the expanding renal medulla. Loss of placental Cited1 was required for Cited1 mutants to develop renal dysplasia, and this was not dependent on alterations in embryonic Cited1 expression. Taken together, these findings suggest that renal medullary dysplasia in Cited1 mutant mice is a direct consequence of decreased tissue oxygenation resulting from placental insufficiency.
Abstract C15: RB status alters the response of prostate cancer to ionizing radiation
Authors: Robert B. Den, Steve Ciment, Ankur Sharma, Hestia Mellert, Steve McMahon, Adam P. Dicker, Karen E. Knudsen
Journal: Cancer Research (2012)

Abstract Background: Prostate cancer is the most frequently diagnosed malignancy and the second leading cause of cancer death in U.S. men. We have previously shown that RB loss results in a castrate resistant phenotype and impacts on the sensitivity of prostate cancer to different chemotherapies. However the consequences of RB status with regard to radiation response are unknown. We hypothesized that RB loss would downregulate the G1-S cell cycle checkpoint arrest normally induced by irradiation, inhibit DNA repair, and subsequently sensitize cells to ionizing radiation. Methods: Experimental work was performed with multiple isogenic prostate cancer cell lines (hormone sensitive: LNCaP and LAP-C4 cells and hormone resistant C42, 22Rv1 cells; stable knockdown of RB using shRNA). Gamma H2AX and 53BP1 assays were used to quantitate DNA damage; PARP cleavage and Caspase 3 were used to quantitate apoptosis; FACS analysis with BrdU was used to assess the cell cycle; beta galactosidase was used to assess senescence. Cell survival was measured using the clonogenic cell survival assay. In vivo work was performed in nude mice with tumor xenografts. Results: We observed that loss of RB increased the radioresponsiveness in both transient and clonogenic cell survival assays in both hormone sensitive and castrate resistant cell lines (p&amp;lt;0.05). Cell death was not mediated through increased apoptosis or alterations in cell cycle. However, loss of RB effected DNA damage repair as well as cellular senescence. In vivo xenografts of the RB deficient tumors exhibited diminished tumor mass, lower PSA kinetics and decreased tumor growth after treatment with single fraction of ionizing radiation in comparison to RB intact tumors (p&amp;lt;0.05). Conclusions: Loss of RB results in a differential response to ionizing radiation. Isogenic cells with RB knockdown are more sensitive to DNA damage and result in reduced cell survival. The underlying mechanism appears to be related to DNA damage repair and cellular senescence. Citation Format: Robert B. Den, Steve Ciment, Ankur Sharma, Hestia Mellert, Steve McMahon, Adam P. Dicker, Karen E. Knudsen. RB status alters the response of prostate cancer to ionizing radiation [abstract]. In: Proceedings of the AACR Special Conference on Advances in Prostate Cancer Research; 2012 Feb 6-9; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2012;72(4 Suppl):Abstract nr C15.
American Medical Association Auxiliary
Authors: Betty Payne
Journal: JAMA (1984)

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
Chronic Interstitial Pancreatitis
Authors: Marion C. Anderson
Journal: JAMA (1961)

DURING the past century much investigative effort has been directed to the cause of 3 pancreatic inflammatory disease. Most of these studies have dealt with factors which initiate acute pancreatitis, and the chronic form of the disease has been relatively neglected. A number of methods have been developed which produce changes in the pancreas of experimental animals similar to those observed in human chronic interstitial pancreatitis. In most instances some form of exocrine obstruction has been employed to simulate duct obstruction, a factor considered important in the pathogenesis of pancreatic inflammation in man. Acute complete duct obstruction results in mild pancreatic edema from which most experimental animals recover quickly. There is no evidence that this simple maneuver alone will cause a progressive inflammatory reaction capable of initiating the cicatrical changes which characterize well developed chronic pancreatitis. Rather, the pancreas gradually undergoes atrophy, and within one month there is little evidence of
Vectorization of morpholino oligomers by the (R-Ahx-R)4 peptide allows efficient splicing correction in the absence of endosomolytic agents
Authors: Saïd Abes, Hong M. Moulton, Philippe Clair, Paul Prevot, Derek S. Youngblood, Rebecca P. Wu, Patrick L. Iversen, Bernard Lebleu
Journal: Journal of Controlled Release (2006)
Gene Studies Provide Window on Cancer Prognosis, Treatment Benefits, Toxic Effects
Authors: Joan Stephenson
Journal: JAMA (2002)

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
Medicine's Role in Mental Health Promotion
Authors: Dana L. Farnsworth
Journal: JAMA (1961)

The recent report of the Joint Commission on Mental Illness and Health reveals the inadequacy of present efforts on behalf of the mentally ill and in promoting mental health. All physicians are in an excellent position to aid in the solution of the many baffling problems involved if they would unite in attacking those conditions in their own communities which induce feelings of rejection, isolation, bitterness, hostility, and suspicion. Such unity of effort is impeded by inadequate concepts of mental illness and health, undue emphasis on particular forms of treatment, deprecatory attitudes of groups of specialists toward each other, and fear of changing the nature of medical practice. The principles of mental health are simple in theory but complex in practice. Their application constitutes one of medicine's greatest opportunities.
Orthopedic surgery puts Lucky back in the swim...
Authors: Phil Gunby
Journal: JAMA (1984)

If Lucky, a 160-kg loggerhead turtle whose flippers were bitten off by a shark, ever returns to sea, it will result from unique collaboration among medical equipment developers and physicians. Fishermen saw the shark attack, rescued Lucky, and brought her to a Florida Keys marine life center, where she continues to be cared for. Top left: After examination, physicians and veterinarians concluded that the injuries approximate amputations of human arms, one near the "elbow," the other at the shoulder. New "limbs" seemed to be needed. Bottom left: Rubber fins with metal joints were specially devised by Goodyear Tire &amp; Rubber Co, Akron, Ohio, and Howmedica Inc, Rutherford, NJ, to endure constant flexing during thousands of miles of swimming each year without inflicting undue stress on natural bone and tissue, to resist chemical attack from seawater, and to last up to 100 years—Lucky's estimated remaining lifespan. Top right: On Jan 17,
Stimulation of the BKCa channel in cultured smooth muscle cells of human trachea by magnolol
Authors: S-N Wu
Journal: Thorax (2002)

Background: Magnolol, a compound isolated from the cortex of <i>Magnolia officinalis</i>, has been found to possess anti-allergic and anti-asthmatic activity. Methods: The effect of magnolol on ionic currents was studied in cultured smooth muscle cells of human trachea with the aid of the patch clamp technique. Results: In whole cell current recordings magnolol reversibly increased the amplitude of K<sup>+</sup> outward currents. The increase in outward current caused by magnolol was sensitive to inhibition by iberiotoxin (200 nM) or paxilline (1 μM) but not by glibenclamide (10 μM). In inside out patches, magnolol added to the bath did not modify single channel conductance but effectively enhanced the activity of large conductance Ca<sup>2+</sup> activated K<sup>+</sup> (BK<sub>Ca</sub>) channels. Magnolol increased the probability of these channel openings in a concentration dependent manner with an EC<sub>50</sub> value of 1.5 μM. The magnolol stimulated increase in the probability of channels opening was independent of internal Ca<sup>2+</sup>. The application of magnolol also shifted the activation curve of BK<sub>Ca</sub> channels to less positive membrane potentials. The change in the kinetic behaviour of BK<sub>Ca</sub> channels caused by magnolol in these cells is the result of an increase in dissociation and gating constants. Conclusions: These results provide evidence that, in addition to the presence of antioxidative activity, magnolol is potent in stimulating BK<sub>Ca</sub> channel activity in tracheal smooth muscle cells. The direct stimulation of these BK<sub>Ca</sub> channels by magnolol may contribute to the underlying mechanism by which it acts as an anti-asthmatic compound.
Acute Transient Myocarditis Evaluation by Gallium Imaging
Authors: P VELUVOLU, F KAMRANI, DANIEL P HORTON, R W MILLER, JOHN G WEIR, SHARON MOEN
Journal: Clinical Nuclear Medicine (1992)

A case of acute transient myocarditis with pre-therapy and post-therapy gallium imaging that corresponded to the patient's symptomatic status is presented.
Hypocalcemia, Hypomagnesemia, and Transient Hypoparathyroidism During Therapy with Potassium Phosphate in Diabetic Ketoacidosis
Authors: William B Zipf, George E Bacon, Martha L Spencer, Robert P Kelch, Nanacy J Hopwood, Charles D Hawker
Journal: Diabetes Care (1979)

The effects of intravenous administration of potassium phosphate in the treatment of diabetic ketoacidosis were studied in nine children, ages 99/12 to 1710/12 yr. During phosphate infusion (20–40 meq/L of fluid), all children maintained normal serum concentrations of phosphorus. Transient hypocalcemia occurred in six and transient hypomagnesemia in five patients. One child developed carpopedal spasms refractory to intravenous infusion of calcium gluconate but responsive to intramuscular injection of magnesium sulfate. In three patients, serum levels of intact parathyroid hormone were low at the time of hypocalcemia, an observation that suggests transient hypoparathyroidism. This study indicates that the use of potassium phosphate as the sole source of potassium replacement might potentiate ketoacidosis-induced hypocalcemia through multiple mechanisms.
Prevention of relapse in patients with chronic non-A, non-B/C hepatitis who respond to alpha-interferon. A controlled multicenter trial of low-dose maintenance therapy
Authors: Dominique Valla, Gérard Babany, Denis Ouzan, Christian Trépo, Marc Bourlière, Paul Calès, Jean-Louis Payen, Patrice Couzigou, Catherine Buffet, Pierre Michel, Michel Veyrac, Eric Bercoff, Victor-Georges Lévy, Jean-Claude Paris, Jean-Didier Grangé, André Valla, Daniel Fischer, Claude Eugène, Jacques Denis, Jean-Jacques Voigt, Monique Fabre, Yves Le Charpentier, Pierre Opolon
Journal: Journal of Hepatology (1994)
The Coronary Arteries in Early Life in Three Different Ethnic Groups
Authors: ZEEV VLODAVER, HAROLD A. KAHN, HENRY N. NEUFELD
Journal: Circulation (1969)

The histologic changes in the coronary arteries in full-term fetuses, infants, and children of 211 consecutive necropsy specimens from Ashkenazy, Yemenite, and Bedouin groups were studied, excluding cardiac deaths. The developmental structural pattern of the coronary arteries is similar in the three ethnic groups. Differences in the intensity and quantity of the structural findings between the sexes and among various ethnic groups are found in early life. The intimal tissue in the Ashkenazy male develops in an eccentric form, has more collagen tissue components, and is more highly developed than in the Ashkenazy female. Structural findings in the internal elastic membrane and the elastic fibers of the intima are less apparent in the Bedouin group, particularly in the female, than in the Ashkenazy and Yemenite groups. Statistical analysis of the quantitative data showed the intima and musculo-elastic layers to be more developed in the Ashkenazy male than in the Yemenite and Bedouin males. However, Ashkenazy males clearly have more intima and musculo-elastic tissue than do the Ashkenazy females. This was not true for Yemenites and was found in only one of three age groups among Bedouins. The relationship between the structural findings in coronary arteries of children under 10 years and the reported prevalence of coronary heart disease in the corresponding adult population in these three different ethnic groups has been pointed out.
Cardiovascular Effects of Sustained Norepinephrine Infusions. I. Hemodynamics
Authors: Arthur J. Moss, Ingvar Vittands, Eric A. Schenk
Journal: Circulation Research (1966)

Norepinephrine (NE) in graded doses of 1, 2, and 4 µg/kg/min was infused for four hours into 14 dogs; 5 dogs served as controls. The systemic pressure and flow, blood volume, hematocrit, arterial blood pH, and oxygen saturation were measured at selected intervals throughout the infusion period. Cardiovascular performance was augmented during the first 15 minutes of the NE infusions, but this effect was not sustained. Thereafter, there was a dose-related decline in cardiac output, systemic pressure and left ventricular work, and an increase in the calculated peripheral vascular resistance. At the highest NE dose rate employed, significant left ventricular failure developed by the second hour of NE administration. The hematocrit increased during the first 15 minutes of NE infusion and remained elevated throughout the infusion period. Sustained hypovolemia was not found during the prolonged NE administration, and severe acidosis (pH &lt; 7.20) was inconstant. The processes which lead to cardiovascular dysfunction during prolonged NE infusion are discussed.
Use of Hemodynamic Algorithm After Gastrointestinal Surgery—Reply
Authors: Rupert M. Pearse, Neil MacDonald, Michael P. W. Grocott
Journal: JAMA (2014)

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
Ethical Implications of Modifying Lethal Injection Protocols
Authors: Leonidas G Koniaris, Kenneth W Goodman, Jeremy Sugarman, Uzoezi Ozomaro, Jonathan Sheldon, Teresa A Zimmers
Journal: PLoS Medicine (2008)

Teresa Zimmers and colleagues argue that it is difficult to conceive how lethal injection research activities could be carried out in a fashion consistent with ethical norms.
IS RISK FACTOR CONTROL AND EVIDENCE BASED MEDICAL THERAPY SIMILAR IN NON OBSTRUCTIVE AND OBSTRUCTIVE CORONARY ARTERY DISEASE (CAD) PATIENTS: A VETERANS AFFAIRS RETROSPECTIVE STUDY.
Authors: Tarun W. Dasari, Michael Koehler, Aneesh Pakala, Siddharth Wayangankar, Harsh Golwala, Mazen Abu-Fadel, Eliot Schechter, Udho Thadani
Journal: Journal of the American College of Cardiology (2011)