tbuckley/cabot-search huggingface dataset:
Reply
Authors: C.C. Harland, R.P. Whitaker, J.L. Barron, C.A. Holden
Journal: British Journal of Dermatology (1993)

Journal Article Reply Get access C.C. Harland, C.C. Harland Departments of Dermatology, St Helier Hospital, Carshalton, U.K. Search for other works by this author on: Oxford Academic Google Scholar R.P. Whitaker, R.P. Whitaker Chemical Pathology, St Helier Hospital, Carshalton, U.K. Search for other works by this author on: Oxford Academic Google Scholar J.L. Barron, J.L. Barron Chemical Pathology, St Helier Hospital, Carshalton, U.K. Search for other works by this author on: Oxford Academic Google Scholar C.A. Holden C.A. Holden Departments of Dermatology, St Helier Hospital, Carshalton, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 129, Issue 4, 1 October 1993, Pages 498–499, https://doi.org/10.1111/j.1365-2133.1993.tb03184.x Published: 01 October 1993
Researchers Push To Improve Breast Imaging
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Researchers Push To Improve Breast Imaging Get access JNCI: Journal of the National Cancer Institute, Volume 83, Issue 20, 16 October 1991, Pages 1444–1445, https://doi.org/10.1093/jnci/83.20.1444 Published: 16 October 1991
Tugboats
Authors: George N. Braman
Journal: Annals of Internal Medicine (2008)

Ad Libitum7 October 2008TugboatsGeorge N. BramanGeorge N. BramanFrom Bronx, NY 10471.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-149-7-200810070-00012 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail “And sometimes sent my ships in fleets/All up and down among the sheets.”—Robert Louis Stevenson, “The Land of Counterpane”I loved the tugboats when I was a boy;Their strong squat bodies and exotic names—“Ruggieri Brothers,” “Terence B. McCoy,”Their sturdy smokestacks and powerful frames.They'd tow the barges with effortless ease—I watched and wondered where they were headed—To continents beyond the seven seas,Islands where wild tigers were embedded.If tiny tugboats traveled, so could I,Carrying treasured cargo in my wake;No imperious vessel could denyMy access to some small sequestered lake;And like the tugboats I would there unloadMy trailing adventurous episode. Author, Article, and Disclosure InformationAffiliations: From Bronx, NY 10471.Current Author Address: George N. Braman, MD, 5903 Liebig Avenue, Bronx, NY 10471. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 7 October 2008Volume 149, Issue 7Page: 508 ePublished: 7 October 2008 Issue Published: 7 October 2008 Copyright & PermissionsCopyright © 2008 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
From the Secretary of Health and Human Services
Authors: L. W. Sullivan
Journal: JAMA (1991)

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
Adoptive cell transfer of regulatory T cells causes an exacerbation of hepatic steatosis in high-fat high-fructose diet-fed mice
Authors: Mikhail Van Herck, Luisa Vonghia, Wilhelmus Kwanten, Thomas Vanwolleghem, Didier Ebo, Peter Michielsen, Joris De Man, Benedicte De Winter, Sven Francque
Journal: Journal of Hepatology (2020)
Abstract 307: Systemic Deficiency Of The Map Kinase Activated Protein Kinase 2 Reduces Atherosclerosis In Hypercholesterolemic Mice
Authors: Kumaravelu Jagavelu, Uwe F Tietge, Matthias Gaestel, Helmut Drexler, Bernhard Schieffer, Udo Bavendiek
Journal: Circulation (2007)

Background: Atherosclerosis is a chronic inflammatory disease and represents the major cause of cardiovascular morbidity and mortality. The mitogen activated protein kinase (MAPK) activated protein kinase 2 (MAPKAP-2, MK2), a direct substrate of the stress activated MAPK p38α/β, critically regulates inflammatory processes such as production of inflammatory mediators (e. g. TNFα, IL-6) as recently demonstrated in vitro and in vivo. Therefore, we investigated the functional role of MK2 in atherogenesis in hypercholesterolemic mice in vivo as well as potentially underlying mechanisms in vitro. Methods &amp; Results: Activation of MK2 (phospho-MK2) was predominantly detected in the endothelium and macrophage-rich plaque areas within aortas of hypercholesterolemic LDL-receptor-deficient mice ( ldlr −/− ). Systemic MK2-deficiency of ldlr −/− -mice ( ldlr −/− /mk2 −/− ) significantly decreased accumulation of macrophages (MOMA-2 staining: −50%, n = 8–10, p &lt; 0.001) and lipids (oil-red-O staining: −55%, n = 8–10, p&lt; 0.001) in the aortic arch (cryo-sections) as well as lipid-depositions in the aorta descendens ( en face , oil-red-O: −70%, n = 8–10, p &lt; 0.001) after feeding an atherogenic diet for 8 or 16 weeks. MK2-deficiency significantly decreased oxLDL-induced foam cell formation in vitro (oil-red-O positive cells, dil-oxLDL-uptake: −50%, n = 3–5, p &lt; 0.01), diet-induced foam cell formation in vivo (16 weeks atherogenic diet, oil-red-O positive cells: −60%, n = 3, p &lt; 0.05) and expression of scavenger receptor A in peritoneal macrophages (qRT-PCR, westernblot: −70%, n = 3–5, p &lt; 0.05). In addition, silencing of MK2-expression in endothelial cells by siRNA markedly and significantly reduced the IL-1β-induced expression of the adhesion molecule VCAM-1 (westernblot, n = 3) and the chemokine MCP-1 (ELISA: −40%, n = 5, p &lt; 0.01). In line, MK2-deficiency significantly reduced VCAM-1 expression in the endothelium of ldlr −/− - mice in vivo (aortic arch, immunhistochemistry, −60%, n = 8, p &lt; 0.01). Conclusions: MK2 critically promotes atherogenesis by fostering foam cell formation and recruitment of monocytes/macrophages into the vessel wall. Therefore, MK2 might represent an attractive novel target for the treatment of atherosclerotic cardiovascular disease.
Personal View
Authors: D. Falconer
Journal: BMJ (1980)

The ATP-gated P2X<sub>7</sub> receptor (P2X<sub>7</sub>R) is a highly unusual calcium-permeable cationic channel in that within seconds of its activation, dramatic and reversible cytoskeletal rearrangements with prominent membrane blebbing occurs. Agonist-induced membrane currents at hyperpolarized potentials show pronounced facilitation during the initial 30–100 s of receptor activation but mechanisms responsible have not been elucidated. We measured facilitation of ATP-gated currents in HEK cells expressing rat P2X<sub>7</sub>R and delineated distinct calcium-dependent and independent processes. The calcium-dependent facilitation was composed of an instantaneous (millisecond time domain) and slowly developing (time constant, 20 s with maximum agonist stimulation) component. Both components were prevented when recording with a highly specific calmodulin (CaM) inhibitory peptide but only the instantaneous component was reduced by expression of the dominant-negative EF-handless CaM mutant. Coimmunoprecipitation assays detected low levels of CaM binding to unstimulated P2X<sub>7</sub>R, and this increased by 50% during 45 s stimulation of the receptor. We identified a novel 1-5-16 Ca<sup>2+</sup>-dependent CaM binding motif in the intracellular C terminus of P2X<sub>7</sub>R; mutations in this domain resulted in the absence of calcium-dependent facilitation and binding of CaM to unstimulated or stimulated receptor. Blockade of CaM binding also delayed membrane blebbing by threefold. Our results demonstrate that CaM binds constitutively to closed P2X<sub>7</sub>R channels and dynamically during channel activation to significantly enhance and prolong calcium entry. This is the first example of CaM deregulating, rather than tightly controlling, calcium entry through an ion channel.
No association between genetic hemochromatosis and alpha1-antitrypsin deficienc
Authors: S Fargion
Journal: Hepatology (1996)

Genetic hemochromatosis and alpha1-antitrypsin (AAT) deficiency are frequent in white populations. Conflicting data on the association of the two conditions and on the severity of the disease in those in whom these disorders coexist have emerged from analyses of small numbers of patients. To determine if the frequency of AAT deficiency is increased in genetic hemochromatosis, we characterized this protein by isoelectric focusing and DNA analysis in 115 Italian patients with the disease and 290 controls. The frequency of AAT deficiency in patients with genetic hemochromatosis was similar to that in controls (10% and 9%, respectively). The prevalence of cirrhosis in patients with genetic hemochromatosis with MM phenotype was 53%, compared with 58% in those with non-MM phenotype; that of hepatocellular carcinoma, occurring only in cirrhotic patients, was 22% and 28%, respectively. In conclusion, the frequency of AAT deficiency was not increased in our large series of Italian patients with genetic hemochromatosis. Patients in whom the two defects coexisted did not appear to have a more severe disease, but the limited number of subjects with non-MM phenotype does not allow a conclusive evaluation of clinical differences between them and patients with genetic hemochromatosis with MM phenotype. (Hepatology 1996 Nov;24(5):1161-4)
Glutamine transport in isolated human hepatocytes and transformed liver cells*1
Authors: B BODE
Journal: Hepatology (1995)

The transport of l-glutamine was examined in isolated adult and fetal human hepatocytes as well as in the human hepatoma cell lines HepG2 and SK-Hep. In all cells studied, glutamine uptake was at least 85% Na+-dependent. Kinetic analysis of the Na+-dependent component indicated mediation by a single transporter in three human hepatocyte preparations and in SK-Hep cells, whereas two transporters appeared to be responsible for glutamine uptake in HepG2 cells and in hepatocytes from the liver of one male patient. Amino acid inhibition analysis showed primary mediation by System N in fetal and adult hepatocytes, whereas System ASC was principally responsible for glutamine uptake in transformed cells. Similar to the rat transporter, human System N was pH-sensitive, stereospecific, and responsive to treatment with steroid hormones. Although the human carrier was less tolerant of Li+- for Na+ substitution, glutamine transport in primary human hepatocytes was stimulated by treatment with hypotonic buffer (cell swelling), as reported in rat parenchymal cells. In contrast, glutamine transport in hepatoma cells was relatively insensitive to changes in extracellular pH and failed to show enhanced activity in response to hypoosmotic challenge. Collectively, the data suggest that markedly distinct plasma membrane transporters mediate the concentrative uptake of glutamine in normal and transformed human hepatocytes, and that the salient properties of System N have been largely conserved from rat to man.
Clinical activity and immune modulation in cancer patients treated with CP-870,893, a novel CD40 agonist monoclonal antibody
Authors: R. H. Vonderheide, K. T. Flaherty, M. Khalil, M. S. Stumacher, D. L. Bajor, M. Gallagher, P. Sullivan, J. J. Mahaney, P. J. O’Dwyer, R. D. Huhn, S. J. Antonia
Journal: Journal of Clinical Oncology (2006)

2507 Background: The cell-surface molecule CD40 plays a critical role in activating antigen presenting cells (APC) and mediates upregulation of costimulatory and MHC molecules, cytokine release, and enhancement of tumor immunity. CD40 is also expressed by 30%-70% of solid tumors, and engagement of CD40 on tumor cells results in apoptosis. CP-870,893 - a fully human and selective CD40 agonist monoclonal antibody - activates human APC in vitro and inhibits growth of human tumors in immune-deficient and immune-reconstituted SCID-beige mice. Methods: A phase 1, dose-escalation study of CP-870,893 was designed to characterize the safety and maximum tolerated dose (MTD) of single doses of CP-870,893 in patients (pts) with advanced solid tumors. CP-870,893 was administered i.v. on day 1 and pts were followed for 43 days. Results: Twenty-nine pts received CP-870,893 in doses ranging from 0.01 to 0.3 mg/kg. Dose limiting toxicity was observed in 2 of 7 pts at the 0.3 mg/kg dose level (venous thromboembolism and grade 3 headache). The MTD was defined as 0.2 mg/kg. The most common adverse event was dose-related cytokine release syndrome (grade 1 to 2). Abnormal lab findings included dose-related and transient elevations in liver transaminases (grade 1 to 2; one pt with grade 3). Modest elevations in serum D-dimer were observed in pts treated at the highest dose levels. Four pts with melanoma (14% of all pts and 27% of pts with melanoma) had objective partial responses (PR) at day 43 evaluation (one PR sustained at 7+ months and 3 unsustained on follow-up scans). Each pt with a PR received 0.2 or 0.3 mg/kg of antibody. To assess pharmacodynamic actions of CP-870,893, flow cytometry was performed on peripheral blood B cells, which uniformly express CD40. CP-870,893 infusion resulted in depletion of peripheral CD19+ B cells (&gt;80% depletion at the highest dose levels). Among B cells remaining in blood, we found a marked, dose-related upregulation of costimulatory and MHC molecules after treatment. Conclusions: Clinical and laboratory findings demonstrate biological activity of CP-870,893. Antitumor activity was observed in 4 pts with melanoma. Further studies of repeated doses of CP-870,893, and CP-870,893 in combination with other antineoplastic agents, are warranted. [Table: see text]
Associations of renal function with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase genes in Korean lead workers.
Authors: Virginia M Weaver, Brian S Schwartz, Kyu-Dong Ahn, Walter F Stewart, Karl T Kelsey, Andrew C Todd, Jiayu Wen, David J Simon, Mark E Lustberg, Patrick J Parsons, Ellen K Silbergeld, Byung-Kook Lee
Journal: Environmental Health Perspectives (2003)

We analyzed data from 798 lead workers to determine whether polymorphisms in the genes encoding delta-aminolevulinic acid dehydratase (ALAD), endothelial nitric oxide synthase (eNOS), and the vitamin D receptor (VDR) were associated with or modified relations of lead exposure and dose measures with renal outcomes. Lead exposure was assessed with job duration, blood lead, dimercaptosuccinic acid (DMSA)-chelatable lead, and tibia lead. Renal function was assessed with blood urea nitrogen (BUN), serum creatinine, measured creatinine clearance, calculated creatinine clearance and urinary N-acetyl-beta-D-glucosaminidase (NAG), and retinol-binding protein. Mean (+/- SD) tibia lead, blood lead, and DMSA-chelatable lead levels were 37.2 +/- 40.4 microg/g bone mineral, 32.0 +/- 15.0 microg/dL, and 767.8 +/- 862.1 microg/g creatinine, respectively. After adjustment, participants with the ALAD(2) allele had lower mean serum creatinine and higher calculated creatinine clearance. We observed effect modification by ALAD on associations between blood lead and/or DMSA-chelatable lead and three renal outcomes. Among those with the ALAD(1-2) genotype, higher lead measures were associated with lower BUN and serum creatinine and higher calculated creatinine clearance. Participants with the eNOS variant allele were found to have higher measured creatinine clearance and BUN. In participants with the Asp allele, longer duration working with lead was associated with higher serum creatinine and lower calculated creatinine clearance and NAG; all were significantly different from relations in those with the Glu/Glu genotype except NAG (p = 0.08). No significant differences were seen in renal outcomes by VDR genotype, nor was consistent effect modification observed. The ALAD findings could be explained by lead-induced hyperfiltration.
Travel-associated Legionnaires’ disease in Europe in 2009
Authors: C A Joseph, K D Ricketts, R Yadav, S Patel, None on behalf of the European Working G
Journal: Eurosurveillance (2010)

A total of 818 cases of Legionnaires&apos; disease with onset of illness in 2009 were reported from 22 European and two non-European countries to the European Surveillance Scheme for Travel-Associated Legionnaires&apos; Disease (EWGLINET). This is a decrease of 52 cases compared with 2008 and 129 fewer than in 2007 - the peak year of reporting to date. A total of 794 (97.1%) cases were reported as confirmed and 24 as presumptive cases. Outcome of illness was reported for 561 (68.6%) cases. Of these cases 28 (5%) were reported to have died. More than half, of the cases in 2009 (n=469, 57.3%) were reported within 20 days of symptom onset. Cases visited 53 countries and were infected in all months of the year, with a peak in September (n=146). By country of residence of the cases, the United Kingdom (UK) reported the highest number of cases (n=173). Italy reported the second highest number of cases (n=169) and was also the country associated with the most cases by country of infection (n=209). A total of 88 new clusters (75 in Europe and 13 outside Europe) were detected in 2009 and were associated with 196 cases. The largest cluster occurred in Italy and involved seven cases. Without the scheme&apos;s international database, thirty three (37.5%) of the newly detected clusters would not have been identified. In 49 of the accommodation sites with clusters of cases, environmental samples were found to be positive for Legionella spp. Details of 10 sites were published on the European Working Group for Legionella Infections (EWGLI) website for failure to return information on the status of environmental .
Lymphedema, lymphocytic myocarditis, and sarcoidlike granulomatosis. Manifestations of Whipple's disease
Authors: J. F. Southern
Journal: JAMA (1989)

A patient with Whipple's disease presented with a long prodromal period characterized by granulomatous lymphadenitis and progressive lymphedema of the extremities. No gastrointestinal tract symptoms were present and a small bowel biopsy sample was normal. His clinical condition deteriorated with the onset of lymphocytic myocarditis. At autopsy, intestinal involvement with macrophages that stained positively with periodic acid—Schiff was limited primarily to the submucosa. Diffuse fibrous effacement of lymph nodes with afferent lymphangiectasia seemed to be the mechanism of diffuse lymphedema, protein-losing enteropathy, and hypoproteinemia. Whipple's disease, therefore, should be considered in the differential diagnosis of patients presenting with granulomatous disease, lymphocytic myocarditis, or unusual lymphedema. (<i>JAMA</i>1989;261:1467-1470)
The pledge
Authors: Wladyslaw Essigman
Journal: BMJ (2005)

trichotillomania. 9 Similar factors, such as violence between parents or siblings, disturbed parent-child interaction, recent death, or illness in the family have been well described as criteria for suspecting child abuse. 10 A child with this background who presents with mechanical hair loss, may have either condition.Without witnesses to confirm hair pulling by the child, the possibility of child abuse should be kept in mind and initial assessment should aim to confirm only the diagnosis of mechanical alopecia.Other causes of mechanical alopecia-traction alopecia due to unusual hairstyles or hair accessories 11 or localised hair shaft abnormalities 12 -should then be ruled out.Subsequently, attempts to find the person responsible for pulling the hair should be made with the objective of getting disclosure by the child.This may require collaboration with the family doctor or pediatrician.The case exemplifies the need to keep a high index of suspicion not to miss child abuse.In cases of localised hair loss in children, especially if a mechanical alopecia-trichotillomania or traction alopecia-is being considered, the possibility of child abuse should also be kept in mind while examining the patient.
In-Vitro Efficacy of the Deoxyguanoside Analogs Forodesine (BCX-1777) and ARA-G in Pediatric Acute Lymphoblastic Leukemia.
Authors: Irene Homminga, Michel C. Zwaan, Amel Seghouani, Chantal Y. Manz, Shanta Bantia, Wilco Smits, Rob Pieters, Jules P.P. Meijerink
Journal: Blood (2009)
The Role of Data Audits in Detecting Scientific Misconduct
Authors: Stuart L. Nightingale
Journal: JAMA (1990)

<h3>To the Editor.—</h3> The article by Dr Shapiro and Mr Charrow<sup>1</sup>usefully high-lighted a major program that the Food and Drug Administration (FDA) operates to ensure that valid and reliable data are submitted to the agency and that the rights of human subjects of research are protected. It should be emphasized, however, that the focus of the FDA's program is not on "scientific misconduct" per se; rather, it reviews the work of clinical investigators to ascertain compliance with FDA investigational new drug regulatory requirements. The authors state that some investigators were able to continue to conduct drug trials after what is described as flagrant violations of recognized norms of research, and they decry the fact that it takes so long for the FDA to "discipline" investigators who are negligent or who have submitted false data. While it is true that the disqualification process can be protracted, largely to
(26) Blepharochalasis
Authors: C.D. Calnan
Journal: British Journal of Dermatology (1974)

Journal Article (26) Blepharochalasis Get access C.D. Calnan C.D. Calnan St John's Hospital, London Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 91, Issue s10, 1 July 1974, Page 78, https://doi.org/10.1111/j.1365-2133.1974.tb12528.x Published: 01 July 1974
Pulmonary Cryptococcosis
Authors: Sam J. Kuykendall, F. Henry Ellis, Lyle A. Weed, F. Edmund Donoghue
Journal: New England Journal of Medicine (1957)

CRYPTOCOCCOSIS, also known as torulosis and European blastomycosis, is a subacute or chronic mycotic infection caused by Cryptococcus neoformans (Torula histolytica, Cryptococcus hominis). Cryptococci have been found occurring as saprophytes in every part of the world, and pathogenic strains of the organism have been recovered from the nasopharynx, skin, gastrointestinal tract and vagina of human beings, from milk, from peaches, from soil and from various animals.1 Although evidence exists that the skin and mucous membranes may be sites of primary inoculation, most authorities agree that the respiratory tract is probably the most common portal of entry of the organisms in . . .