tbuckley/cabot-search huggingface dataset:
Acute Pancreatitis and Steroid Therapy
Authors: Irwin S. Eskwith
Journal: JAMA (1962)

<h3>To the Editor:—</h3> I was one of the earlier authors ( Eskwith, Cacace, and Sollosy, Acute Hemorrhagic Pancreatitis Treatment with Cortisone,<i>New Engl J Med</i><b>252</b>:494,1955) who reported on the therapy of acute pancreatitis with cortisone. There are several commments I should like to make on the editorial "Acute Pancreatitis and Steroid Therapy" that appeared in the Dec. 9, 1961, issue ofThe Journal(<b>178</b>:1005). It is not my opinion that the steroids' principal use is in combating vascular collapse in this disease. In the original and subsequent cases I have treated, rapid relief of pain and abdominal tenderness, and quick defervescence have been equally striking features of this form of treatment. Carone and Liebow's findings of small areas of pancreatic necrosis in patients treated with steroids is an interesting pathological finding, but none of these patients experienced symptoms of pancreatitis. Nelp's finding that long-term steroid therapy of any
The Ventilatory Capacity of Normal Children
Authors: L. B. Strang
Journal: Thorax (1959)

The plasmin/plasminogen system of enzymes may be involved in leukocyte migration through the endothelial cell layer of the vascular wall during inflammatory processes associated with vascular injury, atherosclerosis, and sepsis. Synthesis of plasminogen activator inhibitor type 1 (PAI-1) by the endothelium may protect these cells and the subendothelial cell matrix from excessive degradation and retard leukocyte migration. We report in this work for the first time the down-regulation of both basal and thrombin- or endotoxin-induced PAI-1 in cultured human endothelial cells by the activated T cell product, IFN-gamma. Down-regulation of basal and thrombin- or endotoxin-induced endothelial PAI-1 protein by IFN-gamma was found to be both time and dose dependent. Decreases of up to 71% relative to thrombin- or endotoxin-treated controls, using an optimal IFN-gamma concentration of between 20 and 200 U/ml, were found for human macrovascular and microvascular endothelial cells. However, IFN-gamma did not appear to affect IL-1 alpha- and TNF-alpha-induced levels of PAI-1 protein or mRNA in these cells. Northern blot analysis paralleled protein results, showing decreases in specific endothelial cell thrombin- or LPS-induced PAI-1 mRNA expression, respectively, after incubation with IFN-gamma for 24 h. These results suggest a means by which the migration of circulating leukocytes through endothelial cell layers during inflammation may be facilitated.
400 DOES ACUTE HEAPTITIS C INFECTION AFFECT THE CENTRAL NERVOUS SYSTEM IN HIV INFECTED INDIVIDUALS?
Authors: L. Garvey, A. Winston, E. Scotney, D. Yerrakalva, J. Allsop, E. Thomson, V. Grover, J. Main, J. Cox, M. Wylezinska, S. Taylor-Robinson
Journal: Journal of Hepatology (2009)
Basis for defective responses of rheumatoid arthritis synovial fluid lymphocytes to anti-CD3 (T3) antibodies.
Authors: M Lotz, C D Tsoukas, C A Robinson, C A Dinarello, D A Carson, J H Vaughan
Journal: Journal of Clinical Investigation (1986)

Synovial fluid mononuclear cells (SFMC) from patients with active rheumatoid arthritis characteristically respond poorly to mitogens. In this study, mitogenic antibodies reactive with the CD3(T3) antigen on human T lymphocytes were used to analyze the basis for the deficiency. OKT3-induced proliferation and release of interleukin 1 (IL-1) and interleukin 2 (IL-2) from SFMC were depressed in all patients. Purified IL-1 or recombinant IL-2 restored proliferative responses in SFMC and increased IL-2 receptor density. Exogenous IL-1 also enhanced IL-2 release. Fractionation of SFMC supernatants on phosphocellulose columns revealed the presence of IL-1 and a potent IL-1 inhibitor. The monocyte-derived IL-1 inhibitor blocked IL-1-dependent responses of normal peripheral blood lymphocytes to OKT3, but had no effect on IL-2-dependent events. These results suggest that IL-1 inhibitor(s) in SFMC impair(s) OKT3-induced mitogenesis by interfering with the effects of IL-1 on T lymphocytes. The net result is deficient IL-2 secretion, IL-2 receptor expression, and impaired cellular proliferation. This novel inhibitory circuit provides a rational explanation for the diminished function of synovial fluid T lymphocytes in rheumatoid arthritis patients.
The use of sterile water at colonoscopy--is it money down the drain?
Authors: J. Smith, C. Cross, P. Scott
Journal: BMJ (2014)

At a time of protracted economic difficulty, hospital trusts are being forced to focus on cost saving measures across the network. This has involved reduction in bed numbers, job cuts, and a restriction on finite resources. With financial constraints ever present in a clinician’s mind, we consider the use of sterile water at colonoscopy and whether this is a necessary expenditure or an unnecessary luxury we can ill afford.

In our …
Abortion must not be advocated as preventive solution to unwanted pregnancy
Authors: S. Ross
Journal: BMJ (1997)

Editor—Jacqui Wise's coverage of the MORI survey on abortion was biased, mainly because of her misleading interpretation of the findings but also because the survey was commissioned by and commented on only by proabortion groups.1

The title and article gave the impression that the public supports all abortions carried out in Britain. The figures given show that …
Clonidine Effect on Diabetic Gustatory Sweating
Authors: H. U. JANKA
Journal: Annals of Internal Medicine (1979)

Letters and Corrections1 July 1979Clonidine Effect on Diabetic Gustatory SweatingH. U. JANKA, M.D., E. STANDL, M.D., H. MEHNERT, M.D.H. U. JANKA, M.D.Search for more papers by this author, E. STANDL, M.D.Search for more papers by this author, H. MEHNERT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-91-1-130_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We have read with interest the recent report by Dr. Stuart on diabetic gustatory sweating (1). Anticholinergic drugs have been recommended for control of this symptom of diabetic autonomic neuropathy, but such treatment has often been limited because of unpleasant side effects. We wish to report a similar case of diabetic gustatory sweating and to propose an alternative therapy.A 39-year-old musician was treated in Schwabing City Hospital, Munich, for juvenile diabetes mellitus of 18 years' duration, diabetic proliferative retinopathy, and diabetic nephropathy (serum creatinine level of 5.8 mg/dL). His chief complaint was severe diffuse sweating of...References1. STUART D. Diabetic gustatory sweating. Ann Intern Med. 1978;89:223-4. LinkGoogle Scholar2. RANDRUSHWILSON MMJ. Some observations of the inhibition of salivation by St 155 [2 - (2, 6 - dichlorophenylamine) - 2 - imidazoline hydrochloride, Catapres, Catapresan] Eur J Pharmacol. 1969;5:168-72. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Schwabing City Hospital Munich West Germany PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByGustatory sweating in people with type 1 and type 2 diabetes mellitus: Prevalence and risk factorsFrey's SyndromeSchlussbetrachtungHyperhidrosisDifferenzialtherapie der fokalen und generalisierten HyperhidrosisClonidine in the management of asymmetrical gustatory facial sweating: An N-of-1 trialGustatory facial sweating subsequent to upper thoracic sympathectomyFREY'S SYNDROME FOLLOWING PAROTID SURGERYAntisympathetic ganglia antibodies in a patient with gustatory sweatingBiology of sweat glands and their disorders. II. Disorders of sweat gland functionProblems+SolutionsEndocrine-skin interactionsClonidine in Neuropsychiatric Disorders: A ReviewClonidine inhibits nicotinic effects in ganglia of the cholinergic-sympathetic systemClonidine and HyperhidrosisFRIEDRICH CONRAD, M.D., HOLGER BAUMGARTNER, M.D., CHRISTIAN WIEDERMANN, M.D., GEORG KLEIN, M.D.An unusual case of gustatory sweatingTreatment of Frey’s Syndrome 1 July 1979Volume 91, Issue 1Page: 130-130KeywordsAdverse reactionsCreatinineDiabetic retinopathyDrug regulationNeuropathyRetinopathyType 1 diabetes Issue Published: 1 July 1979 PDF DownloadLoading ...
Piperacetazine and Chlorpromazine: A Comparison
Authors: ALONZA C. JOHNSON, A. S. KULKARNI
Journal: American Journal of Psychiatry (1973)

Twenty-six agitated acute schizophrenic patients in a state hospital received intramuscular injections of either piperacetazine or chlorpromazine. Three rating scales were used to assess the effects of the drugs. Both drugs were found to be effective in producing significant improvement in the patients. Piperacetazine appeared to be more potent than chlorpromazine. No side effects were observed.
MID-TERM OUTCOMES OF PERCUTANEOUS CORONARY INTERVENTIONS FOR ESTABLISHED SURGERY CLASS I INDICATIONS AT A NON-CARDIAC SURGERY CENTER
Authors: Roberto Del Castillo Medina, Lorenzo Hernando Marrupe, Maria Luisa Salto Camacho, Gemma Montalvo, Fatima Perez Gonzalez, Javier Botas Rodriguez
Journal: Journal of the American College of Cardiology (2011)
Abstract A31: Roles of Nogo-B receptor (NgBR) in regulating Ras translocation and modulating breast cancer cell sensitivity to chemotherapeutic drug and irradiation
Authors: Baofeng Zhao, Zhong Liu, Suresh Kumar, Robert Q. Miao
Journal: Clinical Cancer Research (2012)

Abstract Ras, a critical oncogene, is one of small GTPase family members. It is active when bound to GTP and inactive when bound to GDP. The activation process needs membrane translocation of Ras because its activators are recruited by membrane receptors, such as EGF receptors. In addition, appropriate localization of activated Ras also is critical for interacting with the downstream effectors. Therefore, regulation of Ras membrane translocation is very important for Ras function. Nogo-B receptor (NgBR) is a type I receptor with a single transmembrane domain. Our previous work has shown that axon guidance gene family Nogo-B and its receptor (NgBR) are essential for chemotaxis and morphogenesis of endothelial cells in vitro and blood vessel formation in Zebrafish. Here, we demonstrate that NgBR can bind and recruit farnesylated Ras to plasma membrane, which results in the activation of PI3K-Akt and Raf-MEK-ERK signaling pathways in human breast cancer cells. Direct interaction between NgBR and farnesylated Ras has been demonstrated by co-immunoprecipitation of MBP-NgBR from incubation of purified recombinant farnesylated Ras and MBP-NgBR protein. Knockdown of NgBR in MDA-MB-231 human breast cancer cells remarkably reduces the amount of membrane-associated Ras. These results suggest that NgBR is a potential modulator for Ras translocation. Knockdown of NgBR expression in MDA-MB-231 breast cancer cells decreases cancer cell colony formation, and abolishes EGF-stimulated Ras activation and phosphorylation of Akt in MDA-MB-231 cells. In addition, overexpression of NgBR caused the transformation of NIH-3T3 cells via increasing Ras plasma membrane translocation and enhancing EGF-stimulated Ras signaling. Knockdown of NgBR decreases the survival and colony formation of MDA-MB-231 cells after irradiation and increases the cisplatin-induced apoptosis and Caspase-3 activity of MDA-MB-231 Cells. These results suggest that NgBR can increase MDA-MB-231 breast cancer cell sensitivity to chemotherapeutic drug and irradiation. Consequently, our preliminary results further demonstrated that inducible knockdown of NgBR in tumor xenograft of MDA-MB-231 cells in nude mice significantly retards tumor growth. Thus, these data demonstrate that NgBR is a unique receptor that recruits farnesylated Ras to the plasma membrane via its hydrophobic cytoplasmic domain and then activates both PI3K-Akt and Raf-MEK-ERK pathways in human breast cancer cells. Collectively, it is the first study to demonstrate that NgBR is a potential therapeutic target for inhibiting Ras-dependent growth of breast cancer and decreasing the sensitivity of breast cancer cells to chemotherapeutic drug and irradiation.
Rescue of Obesity-Induced Infertility in Female Mice due to a Pituitary-Specific Knockout of the Insulin Receptor
Authors: Kathryn J. Brothers, Sheng Wu, Sara A. DiVall, Marcus R. Messmer, C. Ronald Kahn, Ryan S. Miller, Sally Radovick, Fredric E. Wondisford, Andrew Wolfe
Journal: Cell Metabolism (2010)
A proline-rich peptide improves cell transfection of solid lipid nanoparticle-based non-viral vectors
Authors: A. del Pozo-Rodríguez, S. Pujals, D. Delgado, M.A. Solinís, A.R. Gascón, E. Giralt, J.L. Pedraz
Journal: Journal of Controlled Release (2008)
DIAGNOSTIC AND PROGNOSTIC VALUE OF THE ELECTROENCEPHALOGRAM
Authors: FREDERIC A. GIBBS
Journal: JAMA (1942)

Twelve years have passed since Berger<sup>1</sup>first described the electrical beat of the brain in man. In these twelve years workers all over the world have studied intensively the anatomic, physiologic and psychic correlates of the electroencephalogram.<sup>2</sup>More than six hundred articles dealing with this subject have been published and sufficient evidence has been accumulated to indicate the general significance of this new phenomenon and to show that it has practical value for the solution of clinical problems, and also that it has certain definite limitations. Before proceeding further, I shall define electroencephalography: It is the technic of recording the electrical beat of the brain. As Berger pointed out, this beat is analogous to the beat of the heart as it appears in the electrocardiogram. The brain beat is entirely electrochemical, however; it has no appreciable mechanical component. In the normal waking state the brain does not beat
Medical research in Australia. The nitty gritty: funding, reviewing, training, and communicating.
Authors: R Smith
Journal: BMJ (1991)

About 16% of Australia's research effort is devoted to medical research, and yet medical researchers produce almost half of Australia's research publications.'Medical research has until recently done much better than non-medical research in increasing its funding in the past 10 years, and government funding of medical research more than doubled in real terms between 1980 and 1988.'This was a faster rate of growth than in any other country in the Organisation for Economic Cooperation and Development.'Yet in 1988, a recent Australian study shows, the Australian government was still spending a smaller proportion of its gross domestic product (0-02%) on medical research than was Britain (0 03%) or the United States (0-13%) (table I).These international comparisons are difficult and must be treated cautiously, but the Australian study also shows that roughly two thirds of the funds for medical research in Australia come from the government compared with about one third in Britain (table II).The box describes the peer review system of the Medical Research Committee (MRC), which is distinguished by its openness and by the interaction among
Assessing Normal Growth of Hepatic Hemangiomas During Long-term Follow-up
Authors: Hani Y. Hasan, J. Louis Hinshaw, Edward J. Borman, Alison Gegios, Glen Leverson, Emily R. Winslow
Journal: JAMA Surgery (2014)

Few long-term data describe the natural history of hepatic hemangiomas. Because these lesions are frequently imaged repetitively on studies performed for other indications, health care professionals are commonly confronted with the problem of a growing hemangioma. Because the rate and magnitude of normal growth is not well characterized, it is difficult to recognize lesions growing at an abnormal rate, which may require further evaluation or intervention.To establish quantitatively the expected growth rate of hepatic hemangiomas and to define a measure of hemangioma growth that could be used clinically to help identify hemangiomas for which growth is more than expected.Retrospective cohort study at an academic hospital tertiary referral center evaluating the growth rate of hepatic hemangiomas on cross-sectional imaging studies during a 10-year period (1997-2007). The mean (SD) follow-up time was 3.7 (1.9) years. The radiology information system was searched in a 10-year period for hemangioma. Patients with hepatic hemangiomas that were 1 cm or larger as seen on cross-sectional imaging (computed tomography or magnetic resonance imaging), and 1 year or more apart were selected. Images with the longest interval between studies were selected for further review. Each study was rereviewed for diagnostic confirmation and to ensure consistency in measurement technique. Lesions were remeasured in 3 dimensions, and volumes were calculated using 3-dimensional software.Primary outcomes include the fraction of hepatic hemangiomas that demonstrated growth during long-term follow-up and the annual growth rate of those lesions.A total of 163 hemangiomas were identified in 123 patients. The mean (SD) initial size was 3.2 (3.1) cm. During follow-up, 39.3% of hemangiomas grew 5% or more in mean linear dimension. The mean (SD) annual linear growth rate was 0.03 (0.21) cm for all lesions and 0.19 (0.23) cm for those that grew 5% or more. By volume, 44.7% of lesions grew 5% or more. The mean (SD) annual volumetric growth rate was 2.8% (21.0%) for all lesions and 17.7% (22.8%) in those that grew 5% or more. The initial size predicted the growth in linear dimension and volume (P < .001). There was no significant change in growth rate over time, indicating uniform growth (R = 0.00843; P = .92).Nearly 40% of hepatic hemangiomas grow over time. Although the overall rate of growth is slow, hemangiomas that exhibit growth do so at a modest rate (2 mm/y in linear dimension and 17.4% per year in volume). Further research is needed to determine how patients with more rapidly growing hemangiomas should be treated.
Acyclovir Prophylaxis Against Herpes Simplex Virus Infection in Patients with Leukemia
Authors: Rein Saral, Richard F. Ambinder, William H. Burns, Chris M. Angelopulos, Diane E. Griffin, Philip J. Burke, Paul S. Lietman
Journal: Annals of Internal Medicine (1983)

Twenty-nine adult patients with acute leukemia receiving timed sequential chemotherapy participated in a randomized, double-blind, placebo-controlled trial of acyclovir prophylaxis against reactivated herpes simplex virus infection. Patients with pretreatment antibody titers of 1:16 or greater received acyclovir or placebo starting 4 days after their initial chemotherapy. Treatment was given either for 32 days or until the patients were discharged from the hospital or until a culture-positive herpes simplex virus infection was found. Culture-positive herpes simplex virus infection developed in 11 of 15 patients who received placebo. No infection appeared in 14 patients who received acyclovir (p < 0.00005). No obvious acute drug toxicity was seen. Recurrent infection was seen in 6 of 14 patients after cessation of acyclovir when retreated with chemotherapy, suggesting no effect on viral latency in these 6 patients. Acyclovir provided highly effective prophylaxis against reactivated herpes simplex virus infections in adult patients with acute leukemia receiving timed sequential chemotherapy.
French authorities raid drug company offices to investigate collusion over eye drug
Authors: N. Hawkes
Journal: BMJ (2014)

Competition authorities in France have raided the offices of Roche and Novartis and confiscated material in connection with an investigation into alleged collusion over treatment for age related macular degeneration (AMD).

The raids are the latest stage in an investigation begun in 2012 at the prompting of the health minister, Marisol Touraine. Novartis markets ranibizumab (Lucentis) in Europe for the treatment of wet AMD, while Roche sells the related cancer drug, bevacizumab (Avastin). The complaint being investigated is that the two companies colluded to prevent the use of the much cheaper Avastin to treat the eye condition. …
Abstract A39: The novel atypical retinoid ST1926 is active against rhabdomyosarcoma and induces cell cycle arrest in S and G2/M phases
Authors: Hussein Basma, Loai Dweik, Nadine Darwiche, Claudio Pisano, Raya Saab
Journal: Cancer Research (2014)

Abstract Rhabdomyosarcoma (RMS) is the most common soft tissue sarcoma in children with two subtypes: embryonal rhabdomyosarcoma (ERMS) and alveolar rhabdomyosarcoma (ARMS). With current treatment strategies, most children with recurrent or high-risk disease fare poorly, identifying a need for novel therapeutic approaches. The novel retinoid, ST1926, is an orally available compound belonging to the class of synthetic atypical retinoids and is currently in clinical trials. ST1926 is showing promise because of its increased specificity and reduced toxicity and its unique antitumor mechanism of action that appears different from that of classical all-trans retinoic acid (ATRA). We are investigating the therapeutic potential of this novel synthetic retinoid ST1926, in treatment of RMS. Cell viability assessed by MTT assay showed that ST1926 was a much more potent inhibitor of cell proliferation than ATRA, in both ERMS and ARMS cell lines in vitro. In fact, ST1926 effectively inhibited cell proliferation in all tested cell lines, at concentrations as low as 0.5 micromolar, which is easily achievable in vivo. Unlike ATRA, ST1926 did not induce morphological differentiation in RMS cells. Further analysis showed that ST1926 induced accumulation of cells in S and/or in G2/M phases of the cell cycle, as well as induction of apoptosis in some cell lines, in a p53-independent manner. We are currently investigating the mechanistic details of the cell cycle inhibitory activities of ST1926 in RMS cells. This data identifies ST1926 as an interesting possible therapeutic agent in RMS, and in vivo preclinical studies utilizing this agent are currently underway. Citation Format: Hussein Basma, Loai Dweik, Nadine Darwiche, Claudio Pisano, Raya Saab. The novel atypical retinoid ST1926 is active against rhabdomyosarcoma and induces cell cycle arrest in S and G2/M phases. [abstract]. In: Proceedings of the AACR Special Conference on Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; Nov 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;74(20 Suppl):Abstract nr A39.