tbuckley/cabot-search huggingface dataset:
Endometrial and Ovarian F-18 FDG Uptake in Serial PET Studies and the Value of Delayed Imaging for Differentiation
Authors: Zhaohui Zhu, Bocheng Wang, Wuying Cheng, Xin Cheng, Ruixue Cui, Li Huo, Yonghong Dang, Zhe Fu
Journal: Clinical Nuclear Medicine (2006)

Purpose: This study was designed to characterize the physiological endometrial and ovarian F-18 FDG uptake through analysis of clinical patients with serial PET follow ups (group 1) or who underwent delayed imaging (group 2). Methods: Group 1 had 24 patients (14 premenopausal and 10 postmenopausal). Each patient underwent 2 to 4 serial FDG PET studies and summed to 57 studies. Group 2 included 15 premenopausal patients with delayed imaging 3 hours after injection. Ten of them showed endometrial uptake, and 8 showed intense uptake in 10 ovaries. Visual and semiquantitative methods were applied for analysis. Results: By analysis of serial PET studies, endometrial and ovarian uptake showed some specific characteristics. Surrounded by a relatively low-uptake uterine wall, the inverted cone-shaped endometrium showed 2 peaks of uptake, one in early menstruation and the other in midcycle. The ovarian uptake was more prominent in the midcycle, and the foci of uptake had an ovoid shape and located at the left and/or right side superior–posterior to the bladder. For the postmenopausal and amenorrhea women (35 studies), only one study in a woman within 1 year of menopause showed mild endometrial and ovarian uptake. Compared with the imaging 1 hour after injection, the standardized uptake value increased in 2 of 10 endometria and 4 of 10 ovaries in the delayed imaging. Conclusion: Physiological endometrial and ovarian uptake can be identified on PET alone by their specific shape and position as well as their relation to the menstrual state, whereas delayed imaging was of little value for differentiation in this preliminary study.
On Reading Walt Whitman’s “The Wound Dresser”
Authors: Jack Coulehan
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 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
Intensive-Care Units: Who Needs Them?
Authors: Arnold S. Relman
Journal: New England Journal of Medicine (1980)

The intensive-care unit originated as a postoperative recovery room. Then, in the early 1960's, it rapidly gained favor on medical services when electro-cardiographic monitoring of patients with acute coronary-artery disease came into vogue and relatively effective treatment of life-threatening cardiac arrhythmias became possible. At first, medical ICU's were reserved largely for patients with known or suspected myocardial infarction, but soon they were expanded to include patients with serious arrhythmias or heart failure even when not associated with acute myocardial infarction, as well as patients with pulmonary insufficiency, coma, sepsis, gastrointestinal bleeding, acute renal failure, and many other kinds of urgent . . .
Spontaneous HBsAg loss in Korean patients: relevance of viral genotypes, S gene mutations, and covalently closed circular DNA copy numbers
Authors: Kyun-Hwan Kim, Hye-Young Chang, Jun Yong Park, Eun-Sook Park, Yong Kwang Park, Kwang-Hyub Han, Sang Hoon Ahn
Journal: Clinical and Molecular Hepatology (2014)

Background/Aims Occult HBV infection can persist following HBsAg loss and be transmitted, but the virological features are not well defined. Methods Here we investigated 25 Korean patients who lost HBsAg during follow up, either spontaneously or subsequent to therapy. Results Whereas subtype adr (genotype C) was found in 96% of HBsAg positive patients, 75 % of patients who lost HBsAg spontaneously were seemed to be infected with the ayw subtype with sequence similar to genotype D. Mutations in the major hydrophilic region (MHR) of HBsAg were found in 7 patients who lost HBsAg spontaneously. The mutations include T123S, M125I/N, C139R, D144E, V177A, L192F, and W196L, some of which have not been reported before. Functional analysis via transfection experiments indicate that the C139R and D144E mutations drastically reduced HBsAg antigenicity, while the Y225del mutation found in one interferon-treated patient impaired HBsAg secretion. Conclusions Lack of detectable HBsAg in patient serum could be explained by low level of ccc DNA in liver tissue, low antigenicity of the surface protein, or its secretion defect. Keywords: Hepatitis B virus; HBsAg loss; ccc DNA; Mutation
Hyperkalemic hypertension–associated cullin 3 promotes WNK signaling by degrading KLHL3
Authors: James A. McCormick, Chao-Ling Yang, Chong Zhang, Brittney Davidge, Katharina I. Blankenstein, Andrew S. Terker, Bethzaida Yarbrough, Nicholas P. Meermeier, Hae J. Park, Belinda McCully, Mark West, Aljona Borschewski, Nina Himmerkus, Markus Bleich, Sebastian Bachmann, Kerim Mutig, Eduardo R. Argaiz, Gerardo Gamba, Jeffrey D. Singer, David H. Ellison
Journal: Journal of Clinical Investigation (2014)

Familial hyperkalemic hypertension (FHHt) is a monogenic disease resulting from mutations in genes encoding WNK kinases, the ubiquitin scaffold protein cullin 3 (CUL3), or the substrate adaptor kelch-like 3 (KLHL3). Disease-associated CUL3 mutations abrogate WNK kinase degradation in cells, but it is not clear how mutant forms of CUL3 promote WNK stability. Here, we demonstrated that an FHHt-causing CUL3 mutant (CUL3 Δ403–459) not only retains the ability to bind and ubiquitylate WNK kinases and KLHL3 in cells, but is also more heavily neddylated and activated than WT CUL3. In cells, activated CUL3 Δ403–459 depleted KLHL3, preventing WNK degradation, despite increased CUL3-mediated WNK ubiquitylation; therefore, CUL3 loss in kidney should phenocopy FHHt in murine models. As predicted, nephron-specific deletion of Cul3 in mice did increase WNK kinase levels and the abundance of phosphorylated Na-Cl cotransporter (NCC). Over time, however, Cul3 deletion caused renal dysfunction, including hypochloremic alkalosis, diabetes insipidus, and salt-sensitive hypotension, with depletion of sodium potassium chloride cotransporter 2 and aquaporin 2. Moreover, these animals exhibited renal inflammation, fibrosis, and increased cyclin E. These results indicate that FHHt-associated CUL3 Δ403–459 targets KLHL3 for degradation, thereby preventing WNK degradation, whereas general loss of CUL3 activity — while also impairing WNK degradation — has widespread toxic effects in the kidney.
US comes last in international comparison of health systems
Authors: Janice Hopkins Tanne
Journal: BMJ (2007)

A meta-analysis of 42 trials of the type 2 diabetes drug rosiglitazone (Avandia) has shown a significantly raised risk of myocardial infarction and an increase in cardiovascular deaths that did not quite reach statistical significance (New England Journal of Medicine 2007 May 21 doi: 10.1056/ NEJMoa072761).The analysis by Steven Nissen and Kathy Wolski, of the Cleveland Clinic, Cleveland, Ohio, included 15 560 patients randomly assigned to regimens that included rosiglitazone, and 12 283 patients assigned to regimens that did not.The mean age of patients was 56 years, and the mean baseline glycated haemoglobin concentration was about 8.2%.Patients receiving rosiglitazone had an odds ratio for myocardial infarction of 1.43 (95% confidence interval 1.03 to 1.98, P=0.03).The odds ratio for death from cardiovascular causes was 1.64 (0.98 to 2.74, P=0.06).An editorial (doi: 10.1056/NEJMe078099) criticised the Food and Drug Administration for approving the drug on the basis of only its efficacy in glycaemic control in short term studies and also for a poor system for reporting adverse events after marketing.Bruce Psaty of the University of Washington in Seattle and Curt Furberg of Wake Forest University in Winston-Salem, North Carolina, also say that the Food and Drug Administration Revitalization Act, now moving through Congress, should be strengthened so that the FDA can follow a drug through its life cycle, with new emphasis on postmarketing.The FDA posted a safety alert on its website, cautioning patients taking the drug who have heart disease or are at high risk of a heart attack to talk to their doctors (www.fda.gov).GlaxoSmithKline said it "strongly disagrees" with the findings (www.gsk.com). Study links diabetes drug to heart deathsUK
Inhibition of aldehyde dehydrogenase-2 suppresses cocaine seeking by generating THP, a cocaine use–dependent inhibitor of dopamine synthesis
Authors: Lina Yao, Peidong Fan, Maria Arolfo, Zhan Jiang, M Foster Olive, Jeff Zablocki, Hai-Ling Sun, Nancy Chu, Jeongrim Lee, Hee-Yong Kim, Kwan Leung, John Shryock, Brent Blackburn, Ivan Diamond
Journal: Nature Medicine (2010)
Association of Parkinson Disease Risk Loci With Mild Parkinsonian Signs in Older Persons
Authors: Joshua M. Shulman, Lei Yu, Aron S. Buchman, Denis A. Evans, Julie A. Schneider, David A. Bennett, Philip L. De Jager
Journal: JAMA Neurology (2014)

Parkinsonian motor signs are common in the aging population and are associated with adverse health outcomes. Compared with Parkinson disease (PD), potential genetic risk factors for mild parkinsonian signs have been largely unexplored.
ETME, a novel β-elemene derivative, synergizes with arsenic trioxide in inducing apoptosis and cell cycle arrest in hepatocarcinoma cells via a p53-dependent pathway
Authors: Zhiying Yu, Fangling Wu, Liang Chen, Qian Li, Chaojie Wang, Jinhua Dong, Song-qiang Xie
Journal: Acta Pharmaceutica Sinica B (2014)

Arsenic trioxide (ATO) has been identified as an effective treatment for acute promyelocytic leukemia (APL) but is much less effective against solid tumors such as hepatocellular carcinoma (HCC). In the search for ways to enhance its therapeutic efficacy against solid tumors, we have examined its use in combination with a novel derivative of β-elemene, N-(β-elemene-13-yl)tryptophan methyl ester (ETME). Here we report the effects of the combination on cell viability, apoptosis, the cell cycle and mitochondria membrane potential (MMP) in HCC SMMC-7721 cells. We found that the two compounds acted synergistically to enhance antiproliferative activity and apoptosis. The combination also decreased the MMP, down-regulated Bcl-2 and pro-proteins of the caspase family, and up-regulated Bax and BID, all of which were reversed by the p53 inhibitor, pifithrin-α. In addition, the combination induced cell cycle arrest at the G2/M phase and reduced tumor volume and weight in an xenograft model of nude mice. Overall, the results suggest that ETME in combination with ATO may be useful in the treatment of HCC patients particularly those unresponsive to ATO alone.
Chemoprevention by lipoxygenase and leukotriene pathway inhibitors of vinyl carbamate-induced lung tumors in mice.
Authors: William T Gunning, Paula M Kramer, Vernon E Steele, Michael A Pereira
Journal: Cancer Research (2002)

5-Leukotriene pathway inhibitors, Accolate, MK-886, and Zileuton, were evaluated as chemopreventive agents in female strain A mice. The mice were administered by injection vinyl carbamate (2 x 16 mg/kg) to induce lung tumors. Two weeks later, they received in their diet Accolate (270 and 540 mg/kg), MK-886 (30 mg/kg), Zileuton (600 and 1200 mg/kg), or combinations containing the lower concentration of two agents. Thirteen weeks later, Accolate, Zileuton (only the high concentration), and combinations of Zileuton with either Accolate or MK-886 reduced lung tumor multiplicity. At week 43, MK-886, Accolate, and Zileuton reduced lung tumor multiplicity by 37.8, 29.5, and 28.1%, respectively. They also decreased the size of the tumors and the yield of carcinomas. These results demonstrate that leukotriene inhibitors prevent lung tumors and slow the growth and progression of adenomas to carcinoma; leukotriene inhibitors warrant further consideration for potential use in humans.
IN SUPPORT OF HYGEIA
Authors: Arthur F. Greenwald
Journal: JAMA (1949)

<h3>To the Editor:—</h3> Although I have been out of medical school for more than five years, I have only recently become acquainted with<i>Hygeia</i>magazine. The attention of all doctors should be called to the valuable service this periodical can perform for them if their patients read it. The articles give the patients the sort of knowledge we find in our medically well educated patients and try to impart with considerable pains to our less well educated patients; yet the information given never invades the doctor's province—unlike medical articles in almost all other periodicals. We doctors can save ourselves much time and energy and facilitate instruction in health preservation by urging all our patients to subscribe to and read<i>Hygeia</i>thoroughly.
Morphometric Analysis of Insulin-like Growth Factor-I Localization in Lung Tissues of Patients with Idiopathic Pulmonary Fibrosis
Authors: SOO-TAEK UH, YOSHIKAZU INOUE, TALMADGE E. KING, EDWARD D. CHAN, LEE S. NEWMAN, DAVID W. H. RICHES
Journal: American Journal of Respiratory and Critical Care Medicine (1998)

Insulin-like growth factor-I (IGF-I) has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) through its ability to stimulate fibroblast proliferation and collagen synthesis. However, although alveolar macrophages (AM) have been shown to express this growth factor, it is likely to also have other cellular sources. We sought to determine the distribution of cells expressing IGF-I in lung tissues obtained from 10 patients with IPF and 10 control subjects. We evaluated the levels of IGF-I and of a macrophage/monocyte-specific marker, CD68, by immunocytochemistry and quantified by morphometry. In control subjects, IGF-I was localized principally to AM. In contrast, in IPF patients IGF-I was localized to AM, interstitial macrophages, alveolar epithelial cells, and ciliated columnar epithelial cells. The normalized volume density (Vv) of IGF-I-positive (IGF-I+) interstitial macrophages (Vv of IGF-I+ interstitial macrophages/Vv of lung × 100) was increased in patients with IPF as compared with control subjects, and the ratio of Vv of IGF-I+ to CD68+ interstitial macrophages correlated with: (1) the degree of clinical impairment in patients with IPF as measured by their clinical–radiologic–physiologic (CRP) score; and (2) the degree of collagen deposition in the interstitium. These findings support a role for interstitial macrophages as a source of IGF-I in IPF.
Glutathione Peroxidase 4 Senses and Translates Oxidative Stress into 12/15-Lipoxygenase Dependent- and AIF-Mediated Cell Death
Authors: Alexander Seiler, Manuela Schneider, Heidi Förster, Stephan Roth, Eva K. Wirth, Carsten Culmsee, Nikolaus Plesnila, Elisabeth Kremmer, Olof Rådmark, Wolfgang Wurst, Georg W. Bornkamm, Ulrich Schweizer, Marcus Conrad
Journal: Cell Metabolism (2008)
Narrowing of knee joint space in patients with pseudogout.
Authors: M H Ellman, N L Brown, B Levin
Journal: Annals of the Rheumatic Diseases (1981)

Abnormalities of joint space in knee roentgenograms were compared among 28 symptomatic patients with pseudogout and 2 control groups consisting of spouses of patients and hospital based patients with knee pain. Joint space narrowing was significantly more frequent in the pseudogout patients than in the 2 control groups. Division of patients and controls into 3 age groups revealed a striking degree of joint space narrowing in the youngest patients with pseudogout. Our study suggests that symptomatic patients with pseudogout have joint destruction beginning at a relatively early age. We speculated that this may reflect concurrence of chondrocalcinosis and another disease such as osteoarthritis.
WHO at the crossroads.
Authors: F Godlee
Journal: BMJ (1993)

mic control should be agreed between patient and doctor.Although many elderly diabetic patients can be managed in primary care, closer liaison between general practitioners and hospital doctors is likely to be beneficial.In each locality or district, guidelines for managing diabetes should be agreed between interested parties, and these should be supported by adequate documentation, computerisation of information, and clinical audit.A simple mechanism should exist to ensure that elderly diabetic patients who require consultation with a consultant (for example, those with serious diabetic complications or those requiring insulin) receive it.Geriatricians can manage many elderly diabetic patients, especially those with increasing dependency and multiple medical problems, but they will require training in diabetes to do this well.Rather than setting up diabetic clinics for elderly patients it may be more appropriate for a geriatrician to join the diabetic team, allowing the concentration of resources and ready access to support services required for the care of elderly patients.These strategies may help to meet the needs of this important sector of the diabetic population, but to be effective they must begin at an early stage of the disease and be adequately funded.It is hoped that the enthusiasm for implementing the St Vincent declaration, which recommends ways of reducing the substantial toll of complications such as amputation, renal failure, and blindness in the diabetic population," 12 will also take on board the special problems of elderly diabetic patients.
Hepatic secretion of phospholipid vesicles in the mouse critically depends on mdr2 or MDR3 P-glycoprotein expression. Visualization by electron microscopy.
Authors: A R Crawford, A J Smith, V C Hatch, R P Oude Elferink, P Borst, J M Crawford
Journal: Journal of Clinical Investigation (1997)

Hepatocellular secretion of bile salts into the biliary space induces phospholipid and cholesterol secretion, but the mechanism for integrated lipid secretion is poorly understood. Knockout mice unable to make the canalicular membrane mdr2 P-glycoprotein exhibit normal rates of bile salt secretion, yet are virtually incapable of secreting biliary phospholipid and cholesterol. As the mdr2 P-glycoprotein is thought to mediate transmembrane movement of phospholipid molecules, this mouse model was used to examine the mechanism for biliary phospholipid secretion. In wild-type mdr2 (+/+) mice, ultrarapid cryofixation of livers in situ revealed abundant unilamellar lipid vesicles within bile canalicular lumina. Although 74% of vesicles were adherent to the external aspect of the canalicular plasma membrane, bilayer exocytosis was not observed. Vesicle numbers in mdr2 (+/-) and (-/-) mice were 55 and 12% of wild-type levels, respectively. In a strain of mdr2 (-/-) mice which had been "rescued" by heterozygous genomic insertion of the MDR3 gene, the human homologue of the murine mdr2 gene, vesicle numbers returned to 95% of wild-type levels. Our findings indicate that biliary phospholipid is secreted as vesicles by a process largely dependent on the action of the murine mdr2 P-glycoprotein or human MDR3 P-glycoprotein. We conclude that mdr2-mediated phospholipid translocation from the internal to external hemileaflet of the canalicular membrane permits exovesiculation of the external hemileaflet, a vesiculation process promoted by the detergent environment of the bile canalicular lumen.
Peter David Phelps
Authors: S. Phelps
Journal: BMJ (2002)

Former consultant radiologist (b 1939; q Charing Cross Hospital 1962; MD, FRCR, FRCS), d 7 February 2002.

Peter trained in otorhinolaryngology but as a result of deteriorating hearing retrained in radiology, which he initially hated. He became an international authority in his field and lectured and published widely. His main hobby was vintage cars and he owned three at the time of his death. He was a canal enthusiast, and had been on every canal in England and Wales. He leaves a wife, Susan; and two children
Prostaglandin H Synthase and Xenobiotic Oxidation
Authors: T E Eling, D C Thompson, G L Foureman, J F Curtis, M F Hughes
Journal: The Annual Review of Pharmacology and Toxicology (1990)

Due to the massive data sets available for drug candidates, modern drug discovery has advanced to the big data era. Central to this shift is the development of artificial intelligence approaches to implementing innovative modeling based on the dynamic, ...Read More
REGRESSION OF CORONARY ATHEROSCLEROSIS IN DIABETIC PATIENTS WITH HIGH INTESITY STATIN REGIMENS: INSIGHTS FROM SATURN
Authors: Brian Stegman, Leslie Cho, Steven Nissen, Mingyuan Shao, Christie Ballantyne, Phillip Barter, M. Chapman, Peter Libby, Joel Raichlen, Kiyoko Uno, Yu Kataoka, Rishi Puri, Stephen Nicholls
Journal: Journal of the American College of Cardiology (2013)
Association between sensitization to specific dust mites allergens and manifestation of allergic diseases in four different populations
Authors: A.C. Angus, X.S. Wang, A. Mari, V. Mahakittikun, C. Bunnag, P. Vichyanond, Y.S. Sew, H. Kulaveerasingam, S.H. Tan, S.C. Chua, S.T. Wun, S.T. Ong, K.T. Kuay, W.L. Wang, X.Z. Bi, H.S. Shang, F.T. Chew
Journal: Journal of Allergy and Clinical Immunology (2003)