tbuckley/cabot-search huggingface dataset:
Principles of Internal Medicine
Authors: Thomas M. Durant
Journal: JAMA (1966)

It was well worth waiting for! The last edition had become superannuated at an age of 6, and academic Harrisonophils had been forced to recommend other tests to their students. No criticism is implied in this, however, since I realize the herculean task involved in bringing a book such as this as nearly up-to-date as possible in an era of such fantastically rapid progress. The editors and authors (increased in number this time from 98 to 136!) have done a magnificent job. Quantitatively, there has been an increase in textual pages from 1782 to 1816. Despite this, the publisher has been able to give us a volume weighing approximately 2 lb less than the previous one, which, in turn weighed a little less than its main competitor This achievement is the result of lighter, yet sufficiently tear-resistant paper. Qualitatively the changes are extensive and excellent. There has been a greater
Supine volume drop and diaphragmatic function in adults with Pompe disease: Table 1–
Authors: Hélène Prigent, David Orlikowski, Pascal Laforêt, Nadège Letilly, Line Falaize, Nadine Pellegrini, Djillali Annane, Jean-Claude Raphael, Frédéric Lofaso
Journal: European Respiratory Journal (2012)

To the Editors:

The onset of the adult form of Pompe disease, also known as acid maltase deficiency or glycogen storage disease type II, is a slow progressive muscular disorder in which little correlation exists between respiratory function and locomotor function [1]. The greater degree of respiratory dysfunction, compared with mobility loss, is mainly ascribable to the predominant and progressive involvement of the diaphragm [1].

The prominent diaphragmatic dysfunction in Pompe disease, together with the recent introduction of enzyme replacement therapy in adults, indicate a need for clarifying respiratory outcomes in adult-onset Pompe disease [2]. An international database of medical information on patients with Pompe disease has been set up by Genzyme Corporation (Cambridge, MA, USA), a manufacturer of replacement enzymes (www.pomperegistry.com). The only parameter recommended in the Genzyme Pompe registry for assessing diaphragmatic function is vital capacity (VC) in the upright position. However, it has been demonstrated in a population of patients with suspected diaphragmatic weakness that the supine VC drop provided a good estimate of diaphragmatic dysfunction [3–5]. The aim of the current study was to determine the relationship between invasive diaphragmatic indices and noninvasive respiratory function variables in patients with adult-onset Pompe disease.

We retrospectively retrieved data from the clinical files of patients with adult-onset Pompe disease at the respiratory laboratory of the Raymond Poincare Teaching Hospital (Garches, France) between 2002 and 2010 for diaphragmatic muscle evaluation. Our study was approved by the French Commission Nationale de l’Informatique et des Libertes in accordance with current French legislation. …
Coexpression of p21<sup>Waf1/Cip1</sup> and p53 in sun-exposed normal epidermis, but not in neoplastic epidermis
Authors: S. INOHARA, K. KITAGAWA, Y. KITANO
Journal: British Journal of Dermatology (1996)

Journal Article Coexpression of p21Waf1/Cip1 and p53 in sun‐exposed normal epidermis, but not in neoplastic epidermis Get access S. INOHARA, S. INOHARA Department of Dermatology Hyogo College of Medicine, Nishinomiya, Hyogo 663, Japan Search for other works by this author on: Oxford Academic Google Scholar K. KITAGAWA, K. KITAGAWA Department of Dermatology Hyogo College of Medicine, Nishinomiya, Hyogo 663, Japan Search for other works by this author on: Oxford Academic Google Scholar Y. KITANO Y. KITANO Department of Dermatology Hyogo College of Medicine, Nishinomiya, Hyogo 663, Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 135, Issue 5, 1 November 1996, Pages 717–720, https://doi.org/10.1046/j.1365-2133.1996.d01-1068.x Published: 01 November 1996 Article history Accepted: 21 March 1996 Published: 01 November 1996
Researchers Find Genetic Clues to Chronic Fatigue Syndrome
Authors: Tracy Hampton
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 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
Lymphocyte-depletion Hodgkin's Disease
Authors: G. A. MacGregor
Journal: BMJ (1973)

histological picture was characterized by a massive, almost syncytial growth of reticulum cells with many Reed-Stemnberg cells, severe lymphocyte depletion, and albsence of eosinophils, plasma cells, or fiibrinoid necrosis.This picture was completely differ- ent from the entity described as Hodgkin's sarcoma.Deelmant and I concluded that this disease could be described, both on clinical and on pathological grounds, as a separate entity.I had the opportunity to discuss these cases personally in 1955 with both Dr.F. Parker and Dr. R. J. Lukes, who were at that time rather sceptical about my pro- posal to mark off this disease from classic Hodgkin's disease as a separate subgroup.However, it should be borne in mind that in 1955 discussions about the immunological nature of Hodgkin's disease were still un- heard of.A good account of identical cases had already been given in 1953 by Miss
Smoking and cardiovascular outcomes in dialysis patients: The United States Renal Data System Wave 2 Study1,21The interpretation and reporting of the data presented here are the responsibility of the authors, and in no way should be seen as an official policy or interpretation of the United States government.2See Editorial by Orth and Uehlinger, p. 1580.
Authors: Robert N. Foley, Charles A. Herzog, Allan J. Collins
Journal: Kidney International (2003)
Pennyroyal Oil Poisoning and Hepatotoxicity
Authors: John B. Sullivan
Journal: JAMA (1979)

PENNYROYAL oil has been used in folklore medicine for many years as an abortifacient and as a means to induce menstruation.<sup>1</sup>Herbal medicine books currently in health food stores mention its use as an abortifacient and recommend its use for various minor ailments. We report two recent cases of pennyroyal oil ingestion for the purpose of abortion. One of these cases resulted in shock, disseminated intravascular coagulation (DIC), massive hepatic nercrosis, and death. <h3>Report of Cases</h3><h3>Case 1.—</h3> An 18-year-old girl came to the Denver General Hospital emergency department on Nov 15,1978, with abdominal pain, nausea, vomiting, and vascilating between lethargy and agitation. She gave a history of having ingested two one-half ounce bottles of pennyroyal oil two hours earlier to abort a suspected pregnancy. She was very depressed, and the ingestion could also have been a suicide attempt. She had drunk pennyroyal tea made from the leaves of
Bronchopleural fistula following intrauterine transfusion
Authors: H. V. Price, J. Andrews, K. M. Laurence
Journal: Thorax (1972)

An infant developed a bronchopleural fistula following intrauterine transfusion given for severe haemolytic disease of the newborn. The fistula was shown to be due to the transfusion being given into the right pleural cavity and lung. Initial treatment along conservative lines is suggested, reserving thoracotomy and lobectomy for use if these simple measures fail. Hypocalcaemia was a complicating feature.
Cadmium Impairs Albumin Reabsorption by Down-regulating Megalin and ClC5 Channels in Renal Proximal Tubule Cells
Authors: Patrizia Gena, Giuseppe Calamita, William B. Guggino
Journal: Environmental Health Perspectives (2010)

Cadmium (Cd) is a potent nephrotoxicant that impairs the reabsorptive and secretory functions of the renal proximal tubule, leading to albuminuria.To gain insights into the mechanisms of Cd-induced albuminuria, we investigated effects of Cd on the expression of megalin and chloride channel 5 (ClC5), two key players in albumin-receptor-mediated endocytosis.We used quantitative polymerase chain reaction, Western blotting, the albumin endocytosis assay, and confocal microscopy to evaluate effects of Cd on the expression and regulation of megalin and ClC5 in cultured LLC-PK1 cells, a pig proximal tubular cell model.Ten micromolar cadmium chloride (CdCl2) caused a significant time- and dose-dependent decrease in both mRNA and protein levels of megalin and ClC5, whereas no changes resulted from exposure to other divalent metals (zinc chloride, manganese chloride, magnesium chloride, and nickel chloride). After inhibiting protein synthesis using cycloheximide (CHX), we found that levels of both megalin and ClC5 were lower in Cd-challenged cells than in cells treated with Cd or CHX only, which is consistent with reduced translation and/or posttranslational down-regulation. Moreover, Cd-induced degradation of megalin and ClC5 was abolished by the lysosomal pathway inhibitor bafilomycin A-1 but not by the proteasome system blocker MG-132, suggesting that the enhanced proteolysis was occurring via lysosomes. Using confocal microscopy, we observed a remarkable reduction of fluoroisothiocyanate (FITC)-labeled albumin uptake after Cd exposure.We found that Cd reduced the transcriptional expression of megalin and ClC5 and, at the same time, increased the degradation of megalin and ClC5 proteins via the lysosomal pathway in an in vitro model of renal proximal tubular cells. Overall, these results provide valuable insights into the molecular mechanisms by which Cd impairs luminal protein reabsorption by renal proximal tubules.
EVALUATION OF TECHNETIUM-99m-(Tc-99m)-LABELED LIPOSOMES VERSUS Tc-99m-SULFUR COLLOID (SC) AND Tc-99m-HUMAN SERUM ALBUMIN (HSA) FOR LYMPHOSCINTIGRAPHY IN A RABBIT MODEL.
Authors: W. T. Phillips, T. Andrews, H. L. Liu, R. Klipper, A. Landry, R. Blumhardt, B. Goins
Journal: Clinical Nuclear Medicine (1999)

Scientific Abstracts And Posters From The 44Th Annual Meeting Of The Southwestern Chapter Of The Society Of Nuclear Medicine, And From The 12Th Northeastern Regional Scientific Meeting Of The New England And New York Chapters Of The Society Of Nuclear Medicine
Quantitative analysis of IgM anti-HBc in chronic hepatitis B patients using a new “gray-zone” for the evaluation of “borderline” values
Authors: Guido Colloredo, Giorgio Bellati, Gioacchino Leandro, Piero Colombatto, Anna Rho, Franco Bissoli, Maurizia Rossana Brunetto, Giovanni Angeli, Gaetano Ideo, Ferruccio Bonino
Journal: Journal of Hepatology (1996)
The pressure of time
Authors: Douglas Kamerow
Journal: BMJ (2005)

The pressure of timePrimary care is a busy place.We don't limit what our patients can talk about.We don't have the luxury of saying this or that part of the body or disease is not our business.We don't just deal with prevention or diagnosis or treatment.Anything's fair game.This takes a lot of time.Most primary care doctors are paid by the visit.More visits and more complex visits mean more income.Time is limited.Everyone wants to be a member of the "good doctor club," doing the right thing for our patients at the right time, but time is often a barrier-to taking a complete history, performing a complete physical, providing needed counseling.How much health care is enough?How much is too much?These are crucial questions in all of medicine.Should we take the time to check the fundi of all our patients with hypertension?We were all taught to do this in medical school.The guidelines say so.But a systematic review by Bert-Jan van den Born and colleagues (p 411) finds that there isn't much evidence that funduscopy provides additional value in the management of hypertensive patients.Should we counsel our older patients about the risks and benefits of prophylactic aspirin, recommending it for those without contraindications?Peter Elwood and colleagues (p 423) say yes, that the possibility of benefits (protection from cardiovascular events and maybe cancer and dementia as well) outweighs the risk of bleeding.Colin Baigent (p 425) disagrees, finding the evidence not persuasive that this intervention makes sense on a population basis.Should we make time to screen our patients for increased intraocular pressure to prevent decreased vision from glaucoma?A systematic review by Philip Maier et al (p 389), finding that lowering intraocular pressure reduces visual field loss, seems to support such screening.But Russell Harris, a member of the US Preventive Services Task Force, argues (p 381) that the case for screening in primary care is far from settled.It may be that investing the time to do this screening will not pay off in clinical benefit.Everyone agrees that we shouldn't waste time on unproven tests, treatments, and preventive maneuvers.There isn't enough time in the day or money in anyone's budget to do everything.One purpose of a medical journal is to publish papers and editorials like these to help us sort things out.If we abandon the unproven, maybe that will leave us just enough time to do things that really make a difference.
ELEVATED BNP PREDICTS NEW ONSET ATRIAL FIBRILLATION COMPLICATING ACUTE MYOCARDIAL INFARCTION: ANALYSIS OF THE TRIUMPH REGISTRY
Authors: Susmita Parashar, Jonathan J. Langberg, Viola Vaccarino, Kimberly J. Reid, John Spertus, Michael S. Lloyd
Journal: Journal of the American College of Cardiology (2010)
Estimation of the conduction time of the baroreceptor-cardiac reflex in man
Authors: T. G. PICKERING, J. DAVIES
Journal: Cardiovascular Research (1973)

The time relation between the rise of arterial pressure provoked by phenylephrine and the resulting reflex bradycardia was examined in a group of young healthy subjects studied at rest and during exercise. When systolic pressure is related to pulse interval on a beat to beat basis during the pressure rise the best correlation is obtained if each beat is related to the pulse interval immediately following, provided the heart rate is less than 75/min. For faster heart rates the correlation is better if each pressure is related to the next-but-one pulse interval. Similar findings were obtained in a group of older subjects with higher arterial pressures. These results suggest that the conduction time of the whole reflex loop is about 775 msec, or 475 msec from the baroreceptors to the effect on the heart.
P93 NF B activation by TLR agonists is deficient in macrophages lacking STAT2
Authors: W. Alazawi, A. Gamero, H. Heath, P. Smith, M. Jacobs, J. Waters, G. R. Foster
Journal: Gut (2011)

<h3>Introduction</h3> Engagement of Toll-like receptors (TLRs) is an important initiator of the innate immune response in inflammatory liver diseases and leads to release of a range of inflammatory cytokines. TLRs signal through divergent signal transduction pathways but the majority lead to activation of members of the NFκB family. STAT2 is an essential component of canonical signalling through the type I and type III interferon (IFN) receptor but, unlike other members of the Stat family, is not believed to be involved in other signal transduction pathways. <h3>Aim</h3> We examined the role of STAT2 on inflammatory signalling. <h3>Results</h3> Loss of STAT2 markedly reduced immortalised macrophages’ response to a range of TLR agonists (lipopolysaccharide (LPS), poly I:C and IL-1)—production of TNFα and RANTES proteins and a range of inflammatory mRNAs were decreased. The reduction in inflammatory cytokine production could be reversed by reconstitution with STAT2 but blockade of type I IFN signalling did not reproduce the phenotype. Restoration of the normal response to LPS could be achieved with tyrosine phosphorylation defective STAT2 indicating that STAT2 interacts with these signalling pathways without phosphorylation on Tyr690. The multiplicity of STAT2′s effect suggests a common defect to these signalling pathways. There were no abnormalities in the activation of early signalling components in the absence of STAT2, however, levels of phosphorylated IκB, although not total IκB, were reduced in STAT2<sup>−/−</sup> cells. Phosphorylation of this inhibitor of NFκB leads to its degradation and release of NFκB proteins into the nucleus. We found that translocation of the NFκB protein p65 into the nucleus and its subsequent binding to DNA was impaired in STAT2 deficient cells. <h3>Conclusion</h3> These data suggest that STAT2 is a critical component of the TLR signalling response to early inflammatory stimuli, in particular through maintaining the normal phosphorylation of IκB.
Mitochondrial reactive oxygen species and c-Src play a critical role in hypoxic response in vascular smooth muscle cells
Authors: H SATO, M SATO, H KANAI, T UCHIYAMA, T ISO, Y OHYAMA, H SAKAMOTO, J TAMURA, R NAGAI, M KURABAYASHI
Journal: Cardiovascular Research (2005)

Objective: Thickened atherosclerotic plaques are prone to be hypoxic because of poor perfusion. In this study, we tested (a) whether reactive oxygen species (ROS) and c-Src play roles in hypoxic induction of HIF-1α protein and PAI-1 gene expression in the rabbit aortic smooth muscle cell line C2/2 cells and primary cultures of rat aortic smooth muscle cells, and (b) how mitochondria act on the hypoxia-induced signaling mechanism. Methods and results: Hypoxic exposure of C2/2 cells increased H2O2 generation, c-Src phosphorylation, HIF-1α protein expression, and PAI-1 gene expression. Catalase, a scavenger of H2O2, inhibited the hypoxia-induced ROS generation and PAI-1 gene expression. Src kinase inhibitors PP1 and PP2 inhibited hypoxia-induced HIF-1α protein and PAI-1 gene expression. Ablation of mitochondrial respiration by rotenone abolished hypoxia-induced ROS generation, c-Src phosphorylation, HIF-1α protein expression, and PAI-1 gene expression. Conclusion: Induction of HIF-1α protein and PAI-1 gene expression in response to hypoxia was regulated by ROS production and c-Src activation in vascular smooth muscle cells. Mitochondria linked the hypoxic signal to c-Src, which in turn led to HIF-1α protein and PAI-1 gene expression. These results provide evidence that hypoxia induces the ROS-mediated and c-Src-dependent signaling cascades which are closely associated with angiogenesis and thrombosis in atherosclerotic vasculature.
THE THERAPEUTIC VALUE OF TYPE I ANTIPNEUMOCOCCUS SERUM
Authors: ARTHUR L. BLOOMFIELD
Journal: JAMA (1923)

Despite the excellent results of treatment of Type I lobar pneumonia with antipneumococcus serum which have been reported by Cole,<sup>1</sup>no final agreement as to the value of the procedure has been reached by clinicians. Approximately 1,000 treated cases are now on record in the literature.<sup>2</sup>They have been reported, for the most part, in small groups, and the mortality rates have varied from 0 to 27 per cent. Each observer is naturally influenced by his own series, and, in fact, in certain quarters skepticism seems to exist as to the real value of the serum. It is obvious that with the criterion of success which has hitherto been relied on, namely, the degree of reduction in the gross mortality of treated Type I infections, a huge number of cases will have to be collected before the matter will be settled to the satisfaction of every one. At
Doctors, Drug Companies, and Gifts
Authors: Howard Gelbart
Journal: JAMA (1990)

To the Editor.—  In a recent article, Chren et al 1 presented the practical and ethical considerations associated with physicians accepting gifts from pharmaceutical companies. Two issues, the educational efforts regarding gifts within medical schools and residency programs and the actual importance of many new medications, deserve further emphasis.  The offering of gifts such as a stethoscope, medical bag, or textbook begins in medical school. As mentioned in the article 1 and as illustrated by the findings of Palmisano and Edelstein, 2 the ethical issues of accepting gifts from pharmaceutical companies should be discussed very early. In a survey of 100 third-year medical students, Palmisano and Edelstein 2 reported that more than 85% of the students believed it inappropriate for a public official to accept a $50 gift from a contractor, while fewer than half responded similarly in reference to accepting a gift of equal value from a pharmaceutical company.
Effects of cimetidine on the healing and recurrence of duodenal ulcers and gastric ulcers.
Authors: M Tatsuta, H Iishi, S Okuda
Journal: Gut (1986)

The effects of cimetidine on the healing and recurrence of duodenal ulcers and gastric ulcers were compared. The extent of the acid secreting areas was examined by the endoscopic Congo red methylene blue test. Using the extent of acid secreting areas gastric ulcers were classified into ulcers with and without extensive acid secreting areas. Duodenal ulcers were all associated with extensive acid secreting areas. The gastric acid outputs in the basal state and after maximal stimulation with gastrin were highest in duodenal ulcers, and lowest in gastric ulcers without extensive acid secreting areas. Cimetidine treatment significantly promoted the healing of duodenal ulcers and gastric ulcers with extensive acid secreting areas when compared with placebo, but not of the gastric ulcers without extensive acid secreting areas. Cimetidine also significantly diminished the recurrence of duodenal ulcers, but not gastric ulcers with and without extensive acid secreting areas. These findings indicate that in Japan cimetidine promotes the healing of duodenal and gastric ulcers associated with high gastric acid production and prevents recurrence of duodenal ulcers, but has little or no influence on the healing and recurrence of gastric ulcers associated with low acid secretion.
Rare Disease Research Gets Boost
Authors: Tracy Hampton
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 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