tbuckley/cabot-search huggingface dataset:
Tuberculosis of the Great Trochanter
Authors: C. G. Martin
Journal: BMJ (1948)

<h3>Background:</h3> Coeliac disease is caused by dietary gluten, which triggers chronic inflammation of the small intestine in genetically predisposed individuals. In one quarter of the patients the disease manifests in the skin as dermatitis herpetiformis. Recently, a novel candidate gene, myosin IXB on chromosome 19p13, was shown to be associated with coeliac disease in the Dutch and Spanish populations. The same gene has previously been associated with inflammatory bowel disease, systemic lupus erythematosus and rheumatoid arthritis risk, making myosin IXB a potential shared risk factor in these inflammatory disorders. <h3>Methods:</h3> In this study, previously reported myosin IXB variants were tested for genetic linkage and association with coeliac disease in 495 Hungarian and Finnish families and in an additional 270 patients and controls. <h3>Results and conclusion:</h3> The results show significant linkage (logarithm of odds (LOD) 3.76, p = 0.00002) to 19p13 which supports the presence of a genuine risk factor for coeliac disease in this locus. Myosin IXB variants were not associated with coeliac disease in this study; however, weak evidence of association with dermatitis herpetiformis was found. The association could not explain the strong linkage seen in both phenotypes, indicating that the role of other neighbouring genes in the region cannot be excluded. Therefore, more detailed genetic and functional studies are required to characterise the role of the myosin IXB gene in both coeliac disease and dermatitis herpetiformis.
Deposition of urate crystals in man.
Authors: W A Katz, G E Ehrlich
Journal: Annals of the Rheumatic Diseases (1969)

For more than 60 years the mainstream of investigation into the pathogenesis of gout centred in the mechanism of hyperuricaemia while recently urate crystal-induced arthritis had rekindled interest.Little attention, however, had been drawn to the deposition of these urate crystals in body tissues.It was the purpose of this experimentation to substantiate at a biochemical level heretofore anatomical observations of the predilection of urate crystals to deposit in the connective tissues such as cartilage and synovia.To this end it was demonstrated that an important ground substance com- ponent, PPL, a protein-polysaccharide containing chondroitin sulphate, was capable of augmenting urate solubility and inhibiting urate crystallization at 4°C.A similar substance had been identified in the sera of both normal subjects and those with gout.It travelled electrophoretically with the alpha and beta globulins and was primarily responsible for the ability of serum to hold more urate in solution than buffers of identical molarity and hydrogen ion concentration.Alteration of the urate-bound PPL molecule resulted in precipitation of urate crystals in a manner proposed to occur in vivo.Utilizing this material, a schema was evolved which provided a new concept for the development of gout in man.Discussion.-DR.J. T. Scorr (London) asked if this hypothesis explained the predilection of urates to deposit in the great toe.DR. KATZ felt that it would be interesting to analyse the nature of the polysaccharide in cartilage from various sites.
Prospective study of asymptomatic hbsag carrier children infected in the perinatal period: Clinical and liver histologic studies
Authors: Mei-Hwei Chang, Lu-Yu Hwang, Hey-Chi Hsu, Chin-Yun Lee, R. Palmer Beasley
Journal: Hepatology (1988)

Liver histologic findings were studied in 18 children who were 4 to 9 years old, and who had been HBsAg carriers since having been infected by their mothers in the perinatal period. All were born to HBeAg-HBsAg carrier mothers; the children were followed periodically from birth. Throughout their entire course, none developed symptoms or signs suggestive of liver disease. All of the 18 children showed mild but definite liver histologic changes: 15 had nonspecific histologic changes, and three had chronic persistent hepatitis. In 13 of 18 children, follow-up aminotransferase activities were abnormal, but none exceeded 100 KU. At the time of biopsy, ALTs on four children were above the upper limit of normal. All children were HBeAg-positive in early infancy, but five lost this antigen and developed antibody during follow-up. The histologic findings in HBeAg-positive children did not differ from those in children with antibody. Perinatal hepatitis B virus infection has been thought to play an important role in chronic liver disease, including hepatocellular carcinoma. This study indicates that some pathologic changes following perinatal infection begin very early.
When Potential Does Not Matter: What Developments in Cellular Biology Tell Us About the Concept of Legal Personhood
Authors: Jonathan Will, Eli Y. Adashi, I. Glenn Cohen
Journal: The American Journal of Bioethics (2013)

In their excellent article “The Argument from Potentiality in the Embryo Protection Debate: Finally ‘Depotentialized’?” Marco Stier and Bettina Schoene-Seifert (2013) make use of developments in ce...
Principles and Practice of Dialysis
Authors: Hariprasad Trivedi
Journal: JAMA (2011)

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
NF-κB: a key role in inflammatory diseases
Authors: Paul P. Tak, Gary S. Firestein
Journal: Journal of Clinical Investigation (2001)

NF-κB in defense and diseaseActivation of the NF-κB/Rel transcription family, by nuclear translocation of cytoplasmic complexes, plays a central role in inflammation through its ability to induce transcription of proinflammatory genes (1).This pathway is activated upon appropriate cellular stimulation, most often by signals related to pathogens or stress.Here we will discuss the specificity of various NF-κB proteins, their role in inflammatory disease, the regulation of NF-κB activity by IκB proteins and IκB kinase (IKK), and the development of therapeutic strategies aimed at inhibition of NF-κB. Functions of individual NF-κB proteins in immune cellsThe NF-κB/Rel family includes NF-κB1 (p50/p105), NF-κB2 (p52/p100), p65 (RelA), RelB, and c-Rel (2).Most members of this family (RelB being one exception) can homodimerize, as well as form heterodimers with each other.The most prevalent activated form of NF-κB is a heterodimer consisting of a p50 or p52 subunit and p65, which contains transactivation domains necessary for gene induction.Studies in knockout mice have shown distinct functions for different members of the NF-κB/Rel family.Various NF-κB proteins play a pivotal role in defense of the host against certain pathogens.Furthermore, lack of RelA leads to embryonic lethality and liver degeneration in knockout mice, whereas mice lacking p50 or RelB are immunodeficient but otherwise develop normally to adulthood.B cells from p50 knockout mice show abnormal mitogen responses and antibody production.RelB plays a role in the development and differentiation of dendritic cells, and a mutation disrupting relB impairs antigen presentation.Other NF-κB proteins, including C-Rel and p52, are also essential for normal immune function.Of interest, unlike either of the corresponding single knockout mice, p50/p52 double knockout mice exhibit impaired development of osteoclasts and B cells (3).The expression of NF-κB proteins can provide siteand event-specificity in response to a particular stimulus.For instance, IL-1-induced collagenase expression in synoviocytes is primarily activated by p50 homodimers that bind to a critical NF-κB-like binding site (4).Both p50 and p65 play a role in constitutive IL-6 pro-duction in rheumatoid arthritis (RA) synovial fibroblasts (5), whereas p65 activation by thrombin regulates ICAM-1 expression in endothelial cells (6).p50 and p65 heterodimers are intimately involved in activation of inflammatory genes by IL-1 or TNF-α in human monocytes, and these effects are blocked by the anti-inflammatory cytokine IL-10 (7).Additional specificity is provided by the expression patterns of other regulatory molecules, including surface receptors to proinflammatory cytokines as well as the hierarchy of IKK and IκB isotypes in each cell lineage (see below).These differences, along with multiple variations in NF-κB-like binding sites that interact with certain NF-κB hetero-and homodimers, permit cells to respond to the external environment at the appropriate time with the correct genes.
Peutz-Jeghers Syndrome
Authors: P J Morrison, N C Nevin
Journal: New England Journal of Medicine (1993)

Figure 1 Peutz-Jeghers Syndrome. Striking examples of facial (Panel A) and lip (Panel B) pigmentation are shown in an eight-year-old boy with Peutz-Jeghers syndrome, an inherited disorder characterized by mucocutaneous pigmentation, gastrointestinal polyposis, and occasionally carcinoma of the colon or duodenum. The patient also had smudgy pigmentation of the fingertips and pigmentation of the mucous membranes of the mouth, but no other manifestations. Figure 1 Peutz-Jeghers Syndrome. Striking examples of facial (Panel A) and lip (Panel B) pigmentation are shown in an eight-year-old boy with Peutz-Jeghers syndrome, an inherited disorder characterized by mucocutaneous pigmentation, gastrointestinal polyposis, and occasionally carcinoma of the colon or duodenum. The patient also had smudgy pigmentation of the fingertips and pigmentation of the mucous membranes of the mouth, but no other manifestations. Patrick J. Morrison, M.D.Norman C. Nevin, M.D.Belfast City Hospital, Belfast BT9 7AB, Northern Ireland, United Kingdom
A CASE OF ACUTE MYELOBLASTIC LEUKAEMIA
Authors: R. Hill
Journal: BMJ (1916)

<h3>Background</h3> Echocardiography has been a popular modality used to aid in the diagnosis of infective endocarditis (IE) with the modified Dukes9 criteria. We evaluated the necessity between the uses of either a transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) in patients with a body mass index (BMI) greater than or equal to 25 kg/m<sup>2</sup> and less than 25. <h3>Methods</h3> A single-centered, retrospective study of 198 patients between the years of 2005 and 2012 diagnosed with IE based on modified Dukes9 criteria. Patients were required to be above the age of 18, undergone an echocardiogram study and had blood cultures to be included in the study. This study was conducted at a major hospital in one of the most diverse communities in the United States, providing a cultural and epidemiologically significant advantage. An approved chart analysis using QuadraMed Computerized Patient Record (QCPR) was retrospectively accessed with data-input and calculations formulated in computerized software. <h3>Results</h3> Among 198 patients, two echocardiographic groups were evaluated as 158 patients obtained a TTE, 143 obtained a TEE, and 103 overlapped with TEE and TTE. 167 patients were included in the study as 109 (65%) were discovered to have native valve vegetations on TEE and 58 (35%) with TTE. TTE findings were compared to TEE results for true negative and positives to isolate valvular vegetations Overall sensitivity of TTE was calculated to be 67% with a specificity of 93%. Patients were further divided into two groups with the first group having a BMI less than or equal to 25 kg/m<sup>2</sup> and the subsequent group with a BMI&lt;25. Patients with a BMI less than or equal to 25 that underwent a TTE study had a sensitivity and specificity of 54% and 92, respectively. On the contrary, patients with a BMI&lt;25 had a TTE sensitivity and specificity of 78% and 95, respectively. Furthermore, we obtained the sensitivities of specific valves diseased from vegetations, visualized by TTE (figure&nbsp;1). Lastly, we were able to demonstrate a correlation between the different modalities of echocardiography used to the specific organism identified on blood cultures (figure&nbsp;2). <h3>Conclusion</h3> Calculating a BMI in patients with suspicion for IE may provide benefit in reducing further diagnostic imaging. Our study demonstrated that patients having a BMI &lt;25 kg/m<sup>2</sup> with a negative TTE should refrain from further diagnostic studies with TEE, given the findings of increased sensitivities (figure&nbsp;3). Patients with a BMI less than or equal to 25 may proceed directly to a TEE, possibly avoiding an additional study with a TTE given the low sensitivities identified in this population. Clinicians should be aware that this study has several limitations, one of which a small sample size that may be increased with a multi-centered study. Further investigations with a larger population may improve and possibly provide similar findings, reinforcing the study.
Infectious Mononucleosis: Neurologic and EEG Findings.
Authors: R. G. Schnell
Journal: Annals of Internal Medicine (1965)

s1 November 1965Infectious Mononucleosis: Neurologic and EEG Findings.R. G. Schnell, M.D., P. J. Dyck, M.D., E. J. W. Bowie, M.D., D. W. Klass, M.D.R. G. Schnell, M.D.Search for more papers by this author, P. J. Dyck, M.D.Search for more papers by this author, E. J. W. Bowie, M.D.Search for more papers by this author, D. W. Klass, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-63-5-913_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFrom 1950 to 1963 a diagnosis of infectious mononucleosis was made in 1,285 cases at the Mayo Clinic. This is a review of 13 cases with nervous system involvement that had detailed neurologic evaluation and met the hematologic, serologic, and clinical requirements for a diagnosis of infectious mononucleosis. This group included 11 males and 2 females with an age range of 11 to 25 years.Of 13 cases, 8 had an acute meningo-encephalomyelitis of short duration characterized by headache, fever, stiff neck, delirium, and confusion. Additional manifestations in some included combative and irrational behavior, seizures, papilledema, and signs of cerebellar... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Rochester, Minnesota PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 November 1965Volume 63, Issue 5Page: 913-914KeywordsBehaviorDeliriumElectroencephalographyEpileptic seizuresFeversHeadachesNervous system ePublished: 1 December 2008 Issue Published: 1 November 1965 PDF downloadLoading ...
Sciences, Médecine, Pharmacie de la Révolution à l'Empire (1789-1815)
Authors: Lester S. King
Journal: JAMA (1970)

The French Revolution and the Napoleonic era transformed the political and social patterns of the world. And under the stimulus of intense military activity and the problems engendered thereby, the period 1789 to 1815 also produced great changes in the medical sciences and medical practice. In his new book Professor Huard describes medical aspects of this crucial period. This new volume is similar to the others in the series that Dacosta has published. The format is beautiful, the illustrations excellent and abundant. One hundred and fifty-four black-and-white reproductions and 18 color plates furnish a virtual pictorial history that, almost alone, can bring back the flavor and drama of a bygone era. The typography is fully in keeping with the excellence of the pictures. The text, however, appears rather cursory. The greatest emphasis is given to medicine, surgery, and pharmacy, in both the military (and naval) and the civilian environment. Other
Electrophysiologic effects of dipyridamole on atrioventricular nodal conduction and supraventricular tachycardia. Role of endogenous adenosine.
Authors: B B Lerman, R C Wesley, L Belardinelli
Journal: Circulation (1989)

Exogenous adenosine has been shown to have potent electrophysiologic effects and antiarrhythmic properties within the atrioventricular (AV) node. Endogenous adenosine, a nucleoside with an increased release signaled by ischemia and hypoxia, is not believed to exert significant effects during homeostatic conditions. Recent experimental evidence suggests, however, that under normoxic conditions, the amount of adenosine released may be sufficient to mediate some of its physiologic effects. This study was designed to test the hypothesis that in humans the electrophysiologic effects of endogenously released adenosine on AV nodal conduction can be demonstrated under normoxic conditions by inhibiting uptake and degradation of the nucleoside. In the first protocol, the effects of intravenous dipyridamole (0.56 mg/kg bolus i.v., 5 micrograms/kg/minute infusion), a nucleoside-transport blocker that elevates endogenous plasma levels of adenosine, on AV nodal conduction were evaluated in seven patients. At a constant atrial paced cycle length, dipyridamole increased the AH interval from 110 +/- 19 to 164 +/- 26 msec, p = 0.002 (+/- SEM). Aminophylline (5.6 mg/kg i.v.), a competitive antagonist of adenosine, completely reversed the effects of dipyridamole on AV nodal conduction. Similarly, dipyridamole increased the cycle length at which pacing-induced AV nodal Wenckebach occurred, from 348 +/- 31 (control) to 388 +/- 33 msec (dipyridamole) (p = 0.002). In a second protocol, the effects of intravenous dipyridamole were evaluated in another group of six patients who had supraventricular tachycardia (SVT) in which the AV node was part of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
Abstract 607: Enhanced inhibition of prostate cancer xenograft tumor growth by combining quercetin and green tea
Authors: Piwen Wang, David Heber, Susanne M. Henning
Journal: Cancer Research (2012)

The chemopreventive activity of green tea (GT) and green tea polyphenols (GTPs) in prostate cancer has been demonstrated in preclinical cell culture and animal models. However, extensive methylation of GTPs in vivo to less active methyl-metabolites may be limiting the anti-cancer activity of GT. The objective of the present study was to investigate whether quercetin (Q), a natural inhibitor of catechol-O-methyltransferase (COMT), will increase tissue concentrations of non-methylated GTPs and enhance the inhibition of xenograft tumor growth in severe combined immune deficient (SCID) mice. Androgen-sensitive LAPC-4 prostate cancer cells were injected subcutaneously into SCID mice (n=12 per group). SCID mice were randomly assigned to four groups: control, GT, Q, and GT + Q treatment. The interventions were initiated when tumors reached volume of 10mm3. The final concentration of GTPs in brewed tea administered as drinking water was 0.07% and Q was supplemented in AIN-93G diet at a concentration of 4g/kg diet. There were no differences in food intake, body weight or water consumption during the intervention. Tissue bioavailability of GTPs was increased significantly by 2 to 3-fold in lung, kidney and xenograft tumors and showed a trend to increase by 1.3-fold in liver tissue by GT and Q treatment compared to GT alone. Methylation of epigallocatechin gallate (EGCG), the main polyphenol in green tea, was decreased in tissues from mice in the GT+Q group. After 6 weeks, tumor growth was inhibited by 16% (Q alone), 21% (GT alone), and 45% (GT+Q) compared to the control group. Western blot analysis demonstrated a significant inhibition of methyl transferases such as COMT (31%) and DNA methyltransferase (DNMT) (52%) in tumors from the GT+Q group compared to the control. It has been demonstrated previously that EGCG can act as androgen receptor (AR) antagonist as well as inhibit angiogenesis via inhibition of the vascular endothelial growth factor (VEGF). Together Q+GT inhibited protein expression of AR (35%), prostate-specific antigen (PSA) (39%), and VEGF (25%) more than either GT or Q alone. This study demonstrates an enhanced inhibition of prostate tumor growth when GT and Q are co-administered and this is likely due to inhibition of methylation resulting in enhanced anti-tumor activity of EGCG via effects on angiogenesis, and androgen-mediated tumor growth. This study sets the stage for future human interventions to confirm the increase in bioavailability and chemoprevention using GT in combination with Q. This project was supported by DOD grant W81XWH-10-1-0298 and NIH grant RO3 CA150047-01.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 607. doi:1538-7445.AM2012-607
Response of secondary amyloidosis in psoriasis to treatment with etretinate and ultraviolet light.
Authors: E af Ekenstam, G Michaelsson, R Hallgren
Journal: BMJ (1986)

Quarter: 3 4 1 2 3 4 1 2 3 4 1 2 3 4 1 2 1981 1982 1983 1984$985 Seasonal mortality among people in warm housing (deaths/106 housing units containing 12 people/unit) and among general population of England and Wales aged 65 and over (deaths/IO' population) related to mean minimum temperature at London (Kew), Birmingham, and Bradford.Q-Q =People in warm housing.*-*=General population.exposure to cold.The simplest explanation is that though the quality of life was higher with heated housing, the beneficial effects on mortality of the high indoor temperatures were balanced by the adverse effects of increased exposure to cold outdoors.The results therefore suggest that the traditional tendency of the British to expose themselves to fresh air may be as important as poor heating in causing excess mortality during the winter.They also support previous evidence that cold weather causes death mainly by means other than hypothermia.4This study was