tbuckley/cabot-search huggingface dataset:
Oral Thyroxine in the Treatment of Myxoedema
Authors: F. D. Hart, N. F. Maclagan
Journal: BMJ (1950)

Bthey must be worn during dusting operations and the dilu- ting of wettable powders.Thorough washing before eating or smoking is necessary, and a bath should be taken at the end of the day's work.These instructions, together with an account of the symptoms of poisoning, appear on the labels of containers as shown on the preceding page.The attention of all workers exposed to risk siould be directed repeatedly to the toxic properties of these com- pounds and the protective measures emphasized and enforced.No cases of poisoning from parathion or related com- pounds have been reported in Great Britain.Doctors should be prepared to recognize this new occupational hazard, since treatment with adequate doses of atropine is a matter of urgency if symptoms of poisoning occur.
Ribonucleic Acid Synthesis in Experimental Cardiac Hypertrophy in Rats
Authors: BARRY I. POSNER, BARRY L. FANBURG
Journal: Circulation Research (1968)

The sequence of events which lead to increased RNA synthesis in the heart following aortic constriction was studied with the use of inhibitors of protein and RNA synthesis. Puromycin given during the first 4 hours after operation inhibited the increase in RNA labeling with [ 32 P] H 3 PO 4 that occurred after 4 hours of aortic constriction without inhibiting RNA labeling in sham-operated rats. Puromycin had no effect on the 32 P labeling of the alpha-phosphate of AMP which suggests that the effect on labeling of RNA is not mediated by the lowering of precursor specific activity. The dose of puromycin used inhibited the labeling of heart muscle protein with 3 H leucine. Parafluorophenylalanine had no selective inhibitory effect on the increase of RNA labeling in the hypertrophying heart. The most likely interpretation of these data is that, following aortic constriction, synthesis of protein is required for subsequent stimulation of RNA synthesis, and this protein may be dependent upon the synthesis of new RNA templates. Any early increased synthesis would be of a minority species of protein since there was no increase in amino acid labeling of total heart protein until 4 to 6 hours after aortic constriction. The stimulation of RNA labeling by aortic constriction was unaffected by digitalis treatment. The pressure-time index did not correlate with the increased labeling of RNA.
Association Between Hospitalization for Pneumonia and Subsequent Risk of Cardiovascular Disease
Authors: Vicente F. Corrales-Medina, Karina N. Alvarez, Lisa A. Weissfeld, Derek C. Angus, Julio A. Chirinos, Chung-Chou H. Chang, Anne Newman, Laura Loehr, Aaron R. Folsom, Mitchell S. Elkind, Mary F. Lyles, Richard A. Kronmal, Sachin Yende
Journal: JAMA (2015)

<h3>Importance</h3> The risk of cardiovascular disease (CVD) after infection is poorly understood. <h3>Objective</h3> To determine whether hospitalization for pneumonia is associated with an increased short-term and long-term risk of CVD. <h3>Design, Settings, and Participants</h3> We examined 2 community-based cohorts: the Cardiovascular Health Study (CHS, n = 5888; enrollment age, ≥65 years; enrollment period, 1989–1994) and the Atherosclerosis Risk in Communities study (ARIC, n = 15 792; enrollment age, 45-64 years; enrollment period, 1987–1989). Participants were followed up through December 31, 2010. We matched each participant hospitalized with pneumonia to 2 controls. Pneumonia cases and controls were followed for occurrence of CVD over 10 years after matching. We estimated hazard ratios (HRs) for CVD at different time intervals, adjusting for demographics, CVD risk factors, subclinical CVD, comorbidities, and functional status. <h3>Exposures</h3> Hospitalization for pneumonia. <h3>Main Outcomes and Measures</h3> Incident CVD (myocardial infarction, stroke, and fatal coronary heart disease). <h3>Results</h3> Of 591 pneumonia cases in CHS, 206 had CVD events over 10 years after pneumonia hospitalization. CVD risk after pneumonia was highest in the first year. CVD occurred in 54 cases and 6 controls in the first 30 days (HR, 4.07; 95% CI, 2.86-5.27); 11 cases and 9 controls between 31 and 90 days (HR, 2.94; 95% CI, 2.18-3.70); and 22 cases and 55 controls between 91 days and 1 year (HR, 2.10; 95% CI, 1.59-2.60). Additional CVD risk remained elevated into the tenth year, when 4 cases and 12 controls developed CVD (HR, 1.86; 95% CI, 1.18-2.55). In ARIC, of 680 pneumonia cases, 112 had CVD over 10 years after hospitalization. CVD occurred in 4 cases and 3 controls in the first 30 days (HR, 2.38; 95% CI, 1.12-3.63); 4 cases and 0 controls between 31 and 90 days (HR, 2.40; 95% CI, 1.23-3.47); 11 cases and 8 controls between 91 days and 1 year (HR, 2.19; 95% CI, 1.20-3.19); and 8 cases and 7 controls during the second year (HR, 1.88; 95% CI, 1.10-2.66). After the second year, the HRs were no longer statistically significant. <h3>Conclusions and Relevance</h3> Hospitalization for pneumonia was associated with increased short-term and long-term risk of CVD, suggesting that pneumonia may be a risk factor for CVD.
Practicing Prevention With Probiotics
Authors: Vinod E. Nambudiri, Michael E. Bigby
Journal: JAMA Dermatology (2013)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast 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 Dermatology journal
Hepatic endothelial dysfunction and abnormal angiogenesis: New targets in the treatment of portal hypertension
Authors: Jaume Bosch, Juan G. Abraldes, Mercedes Fernández, Juan Carlos García-Pagán
Journal: Journal of Hepatology (2010)

Portal hypertension is the main cause of complications in patients with chronic liver disease. Over the past 25 years, progress in the understanding of the pathophysiology of portal hypertension was followed by the introduction of an effective pharmacological therapy, consisting mainly of treatments aimed at correcting the increased splanchnic blood flow. It is only recently that this paradigm has been changed. Progress in our knowledge of the mechanisms of increased resistance to portal blood flow, of the formation of portal-systemic collaterals, and of mechanisms other than vasodilatation maintaining the increased splanchnic blood flow have opened entirely new perspectives for developing more effective treatment strategies. This is the aim of the current review, which focuses on: (a) the modulation of hepatic vascular resistance by correcting the increased hepatic vascular tone due to hepatic endothelial dysfunction, and (b) correcting the abnormal angiogenesis associated with portal hypertension, which contributes to liver inflammation and fibrogenesis, to the hyperkinetic splanchnic circulation, and to the formation of portal-systemic collaterals and varices. Portal hypertension is the main cause of complications in patients with chronic liver disease. Over the past 25 years, progress in the understanding of the pathophysiology of portal hypertension was followed by the introduction of an effective pharmacological therapy, consisting mainly of treatments aimed at correcting the increased splanchnic blood flow. It is only recently that this paradigm has been changed. Progress in our knowledge of the mechanisms of increased resistance to portal blood flow, of the formation of portal-systemic collaterals, and of mechanisms other than vasodilatation maintaining the increased splanchnic blood flow have opened entirely new perspectives for developing more effective treatment strategies. This is the aim of the current review, which focuses on: (a) the modulation of hepatic vascular resistance by correcting the increased hepatic vascular tone due to hepatic endothelial dysfunction, and (b) correcting the abnormal angiogenesis associated with portal hypertension, which contributes to liver inflammation and fibrogenesis, to the hyperkinetic splanchnic circulation, and to the formation of portal-systemic collaterals and varices.
Allergy from Therapeutic Products
Authors: Samuel M. Feinberg
Journal: JAMA (1961)

Drug allergy has become a common and important medical problem. At least 2 to 3 million people have had reactions to penicillin, some of which have been serious. A variety of other drugs, among which are other antibiotics as well as analgesics, sedatives, serums, and organ extracts, have frequently produced allergic symptoms. The effects have ranged from urticaria and other rashes to anaphylaxis, blood changes, periarteritis, and visceral lesions including hepatitis. The allergic state can be diagnosed by skin tests in some cases and by in vitro tests in others, but in most cases the history is most important. A large proportion of the serious reactions are preventable by a knowledge of the special proclivities of the drug, by conservatism, by using appropriate tests, and by alertness during therapy.
On "Albuminuria in the Apparently Healthy."
Authors: H. P. Hawkins
Journal: BMJ (1899)

Dr. Mott asks whether the toxic agent " does not lower thA -durability of the nerve elements, so that some otber factor" induces a premature decay.I have long maintained that this is an essential secret of the mysterious incidence of these .degenerativediseases.An average man inherits an equal vitality in all his structures.He goes to pieces at last like the famous " one-hoss shay," all at once, in mature, equable, -aenile decay.At the other extreme are thoee individuals who possess structural elements (it may be in some part of the nervous or the muscular system) so deficient in vital endur- ance that jhey decay as soon as, or soon.after,complete de- 'yelopment.isachieved.Such are some cases of idiopathic muscular atrophy, of con- genital atrophy of the optic nerves, in which sight fails in a whole family soon after puberty, or of " hereditary ataxy," "Friedreich's disease "-in which certain structures of the nervous system decay soon after adult age is reached.In -other cases the defect in vital endurance is only sufficient to render some structures less resistant than others, to cause, for instance, the motor nerve structures to decay before the -others under the influence of grief, or the nutrition of the cere- bral structures to give way under the strain of work or anxiety.'This disposition to decay, sometimes inherent, strongly or elightly, seems to be induced artificially by toxic and perhaps -other influences.Their effect is specific in many cases, probably in more than we can discern.They lead to failure -of nutrition, decay, degeneration.It may seem spontaneous, or be evidently excited.It may occur soon, a few years after its cause has seemed active, or the effect may be only manifest so long afterwards that the connection may be only rperceptible by these considerations.Thus tabes may be a post-syphilitic disorder in middle life, or only, yet with the same relation, when the general failure of approaching age -obscures the significance of the cause.We shall under- stand many things more clearly if we perceive that acquired influences may have the effects of congenital dispositions, that either may cause effects unaided, and may predispose to 'the results of influences that would otherwise seem to act alone.'These considerations are, I fear, somewhat beyond the question before us, but they are not, I think, beyond their indications.
149 PERSISTENT DEFICIT IN LEARNING OF RESPONSE INHIBITION FOLLOWING ONSET OF OVERT HEPATIC ENCEPHALOPATHY IN CIRRHOSIS
Authors: J. Bajaj, D.M. Heuman, C. Schubert, D.P. Gibson, J.B. Wade, A. Topaz, D. Bell, R.T. Stravitz, R.K. Sterling, A.J. Sanyal
Journal: Journal of Hepatology (2010)
Students warned not to subscribe to journal "scam"
Authors: Z. Kmietowicz
Journal: BMJ (2009)

Medical students are being warned not to respond to an email invitation to subscribe to a medical journal that lists the involvement on its editorial board of people who have never heard of the publication.

The email says the journal Scientific Medicine “comprises of several top end basic science researchers, practising clinicians, medical scientists and international journal editors from across the world (mainly US, Europe and India).”

It lists Gavin Yamey, senior editor at Public Library of Science (PloS) Medicine and formerly of the BMJ , as a member of the editorial board. The email incorrectly states that Richard Smith is still editor of …
Treatment of Rheumatoid Arthritis with Deoxycortone and Ascorbic Acid
Authors: W. S. C. Copeman, O. Savage, G. D. Kersley, J. J. R. Duthie, F. D. Hart, H. A. Burt, E. Fletcher, J. H. Kellgren, E. G. L. Bywaters, G. N. Myers, P. Ellman, S. J. Hartfall
Journal: BMJ (1950)
Prostaglandin Synthetase Inhibitors
Authors: M. Weatherall
Journal: Annals of the Rheumatic Diseases (1981)

arranged logically, and is considerably enhanced by clear and attractive line drawings by W. Brennan.The reader is not plunged into a mass of detail on individual aids but asked first, Is a hoist really necessary?While few doctors will require detailed knowledge of individual hoists, slings, and accessories, most working with patients with mobility problems would find this chapter a highly readable source of information on transferring and on toileting difficulties and their solution.This information obviously derives from Miss Tarling's experience in the Disabled Living Foundation and the Newcastle Aids Centre, and indicates the value of aids centres.Such advice is not easily obtainable elsewhere.The book deals with the use of hoists in virtually every situation, in hospital, at home, at work, and in transit.It should be available in all departments of rehabilitation, to all who are concerned with the ordering of hoists, and all who must use them, in which case its use should be reinforced by practical training.
The Utility of CPR in Elderly Persons-Reply
Authors: David B. Matchar
Journal: JAMA (1991)

<h3>In Reply.—</h3> Dr Jacobs mistakenly assumes that Longstreth et al<sup>1</sup>and we were considering the same populations when reporting outcomes of out-of-hospital cardiopulmonary resuscitation (CPR). Longstreth et al reported outcomes for all elderly, including the most robust septuagenarians. We illustrated our model using outcomes for the chronically ill elderly. It is unlikely that the Seattle system, which is one of the best in the country and, therefore, not representative of most urban areas, could achieve a 10% survival to discharge rate for chronically ill elderly. We did not dispose of advance directives. We suggested that they alone will not solve the problem of inappropriate life-sustaining care. Other strategies should supplement advance directives. Our model is based on the aggregate preferences of patients. Dr Jacobs seems to imply that all patients, regardless of prognosis, should determine what level of care is appropriate. What is touted as patient autonomy—patients having the
The Physician and the Law
Authors: R. V. Platou
Journal: JAMA (1960)

Being so far, and relatively speaking, only occasionally involved with the law, pediatricians will probably find but occasional use for this particular reference-source. The present edition of this interesting and compact volume includes a number of cases decided in the four-year interval since the first edition and properly stresses the alarming nationwide increase in malpractice claims. Three chapters might be considered to have particular pediatric interest. Chapter 7 deals with responsibility of the physician in sudden and unexpected deaths, but it contains relatively little information pertinent to those most commonly encountered among infants and children. Chapter 9, "Blood Group Tests and Blood Transfusions," contains some interesting records concerning disputed parentage and several anecdotes dealing with negligence in transfusion procedures—particularly as to concepts concerning "calculated risks"—when these are followed by hepatitis. Chapter 11, "Adoption of a Baby," very briefly emphasizes the remarkable variations in state statutes and the consequent understandable confusion,
Endothelin-1 Inhibits the Slow Component of Cardiac Delayed Rectifier K <sup>+</sup> Currents via a Pertussis Toxin–Sensitive Mechanism
Authors: Takashi Washizuka, Minoru Horie, Masato Watanuki, Shigetake Sasayama
Journal: Circulation Research (1997)

Abstract Endothelin-1 (ET-1) is a 21–amino acid peptide hormone released from myocardial and endothelial cells, whose receptors (both ET A and ET B ) are expressed in the myocardium. We report here that ET-1 inhibits the cardiac delayed rectifier K + current (I K ) via a pertussis toxin (PTX)–sensitive mechanism. Ventricular myocytes enzymatically isolated from guinea pig hearts were voltage-clamped by the conventional whole-cell and nystatin–perforated patch technique (intrapipette and extrapipette K + concentrations, 150 and 5.4 mmol/L, respectively) in the presence of nifedipine (2 μmol/L). Amplitudes of tail and steady state (2-second pulse) currents were measured as I K . ET-1 suppressed the basal I K by 20.9±2.3% in a concentration-dependent manner, with an IC 50 of 1.1±0.3 nmol/L (n=19), although it did not suppress the basal I K using the nystatin method. E-4031 (5 μmol/L), a blocker of the rapid component of I K (I Kr ), did not prevent the inhibitory action of ET-1. ET-1 reduced by 63.4±6.5% the slow component of I K (I Ks ) that had been enhanced to ≈2-fold by isoproterenol (ISO, 20 nmol/L). The action was concentration dependent, with an IC 50 of 0.7±0.4 nmol/L (n=22), and was also observed using the nystatin method. The effect of ET-1 appeared to be mediated by an ET A receptor, because it was prevented by FR139317, an ET A -selective antagonist (1 μmol/L, n=4), and sarafotoxin S6c, an ET B -selective agonist (100 nmol/L, n=4), could not inhibit the ISO-enhanced I K . ET-1 antagonized I Ks enhanced by histamine (250 nmol/L, n=7) and forskolin (500 nmol/L, n=7) but did not inhibit I Ks enhanced by the internal application of cAMP (100 μmol/L, n=6). Preincubation of myocytes with PTX (5 μg/mL for &gt;60 minutes at 36°C) completely abolished the inhibitory action of ET-1 on the ISO-enhanced I Ks (n=4). Thus, nanomolar ET-1 inhibits I Ks via the ET A receptor/PTX–sensitive G protein/PKA pathway.
Expression of inducible nitric oxide synthase and formation of nitric oxide by alveolar macrophages: an interspecies comparison.
Authors: N K Jesch, M Dörger, G Enders, G Rieder, C Vogelmeier, K Messmer, F Krombach
Journal: Environmental Health Perspectives (1997)

Nitric oxide (NO) is suggested to play a role in mediating pulmonary injury. However, interspecies differences appear to exist in the ability of alveolar macrophages (AM) to express the inducible nitric oxide synthase (iNOS) and to generate NO. The purpose of this study was to compare iNOS expression and NO production by rat, hamster, monkey, and human AM using the identical experimental conditions in vitro. As AM donors, CD rats, Syrian golden hamsters, cynomolgus monkeys, and nonsmoking, healthy human volunteers were used. The AM were obtained by bronchoalveolar lavage and stimulated in vitro with various concentrations and combinations of lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). The oxidation product of NO, nitrite, was measured in the AM supernatant by the Griess reaction. The expression of iNOS in AM was detected using immunocytochemistry and immunoblotting. The expression of iNOS mRNA was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR). Rat AM, stimulated with either LPS or IFN-gamma, produced nitrite in a time- and dose-dependent manner. Combination of LPS and IFN-gamma resulted in a significantly enhanced nitrite formation. However, none of the treatments was able to induce hamster, monkey, or human AM to release measurable amounts of nitrite. Whereas expression of iNOS protein was only detected in stimulated rat AM, expression of iNOS mRNA was found in unstimulated and stimulated rat AM, slightly in stimulated hamster AM, but not in monkey and human AM. In conclusion, our findings point to distinct regulatory mechanisms of the NO pathway in AM from these four different species.
Letter: Plagiarism in medicine.
Authors: D Perrins
Journal: BMJ (1974)

would like to add one more consideration.I have recently observed two cases of post- anaesthetic jaundice in which halothane was employed.On careful investigation these were proved to be due to Gilbert's disease (congenital hyperbilirubinaemia). Starvation precipitates icterus in these cases, causing a raised plasma unconjugated bilirubin level, usually within 48 hours.The incidence of Gilbert's disease may be as high as 5% and it should therefore be a consideration in the differential diagnosis of cases of post- anaesthetic jaundice.-Iam, etc.,
Sarcoidosis presenting as gingivitis
Authors: J P Hayter, J M Robertson
Journal: BMJ (1988)

Sarcoidosis presenting as gingivitisSarcoidosis is a systemic granulomatous disease of unknown cause that may affect any tissue in the body.In the head and neck the most common signs, together with widespread systemic disease, are cervical lymphadenopathy and swelling ofthe parotid glands.' Gingival symptoms at any stage are rare,2 and patients who have them usually present with other clinical features ofthe disease23 or with gross gingival hyperplasia.45We describe a patient whose sole presenting complaint was persistent soreness and ulceration ofthe gums and who was subsequently found to have systemic sarcoidosis. Case reportA 34 year old man was referred by his dentist with a two month history of soreness and ulceration of the gums; he had no other symptoms.There had been no improvement after scaling and courses ofmetronidazole and penicillin.He was taking no drugs although he had taken phenytoin and phenobarbitone for childhood epilepsy until he was 18.He had no history ofallergy.No abnormality was found on general physical examination; in particular there was no lymphadenopathy or visceromegaly.On examination of his mouth the attached gums looked granulomatous with superficial ulceration and bled readily when probed.
Bristol inquiry appoints doctor to its panel
Authors: A. Ferriman
Journal: BMJ (1999)

Sir Brian Jarman, emeritus professor at Imperial College School of Medicine at St Mary's Hospital, London, has been appointed medical member of the inquiry into the deaths of children who had heart surgery at Bristol Royal Infirmary.

Other members of the panel, which is chaired by Ian Kennedy, professor of health law, ethics, and policy at University College London, are Mavis Maclean, …