tbuckley/cabot-search huggingface dataset:
Serum concentration of intercellular adhesion molecule–1 in patients with hepatocellular carcinoma is a marker of the disease progression and prognosis
Authors: Yukihiro Shimizu, Masami Minemura, Takashi Tsukishiro, Yoshirou Kashii, Megumi Miyamoto, Hiroshi Nishimori, Kiyohiro Higuchi, Akiharu Watanabe
Journal: Hepatology (1995)

Serum levels of soluble forms of intracellular adhesion molecule-1 (sICAM-1) and lymphocyte function-associated antigen-3 (sLFA-3) in 122 patients with chronic liver disease including hepatocellular carcinoma (HCC) were measured by enzyme-linked immunosorbent assays. Serum levels of sICAM-1 in patients with HCC were significantly higher than those of chronic hepatitis (CH) and cirrhosis. On the other hand, serum levels of sLFA-3 in patients with HCC were almost the same as those of cirrhosis. Western blot analyses showed that molecular sizes of sICAM-1 and sLFA-3 detected in the sera were 90 kd and 50 kd, respectively, indicating that both molecules include whole extracellular domains. In patients with HCC, circulating sICAM-1 levels were significantly (P < .001) correlated with tumor volume (r = .50), total bilirubin (r = .38), serum aspartate aminotransferase levels (r = .51), and gamma-globulin (r = .63). Furthermore, serum sICAM-1 levels were significantly elevated in patients with multiple HCC (tumor number > 3) or HCC with tumor embolus in the first branch or trunk of portal vein. Survival periods were analyzed in relation to serum sICAM-1 levels in patients with HCC who had been treated by transcatheter arterial chemoembolization. The HCC patients with < 1,000 ng/mL of serum ICAM-1 showed significantly (P = .0005) longer survival than those with higher levels of the molecule. The same results were obtained when only patients with moderately differentiated HCC were analyzed (P = .02). Analyses by Cox's proportional hazard model showed that sICAM-1 is a significant (P = .032) prognostic factor for patients with HCC.(ABSTRACT TRUNCATED AT 250 WORDS)
Use and Interpretation of the Fantus Estimation of Urinary Chloride
Authors: W. H. Taylor
Journal: BMJ (1951)

The immunosuppressive drug cyclosporin A (CsA) frequently induces hypertension, but the mechanism(s) is unknown. Thus, we examined the mechanism(s) by which CsA increases arterial blood pressure (MAP) in the normotensive rat. Three different treatment modalities were used. First, chronic CsA treatment (20 mg/kg/day, s.c., for 1 week) significantly increased MAP from 109.6 +/- 2.3 mm Hg to 125.8 +/- 2.9 mm Hg (P less than .05). Second, subacute i.v. infusion of CsA (20 mg/kg daily for 3 days) increased MAP to even higher values (140.5 +/- 2.3 mm Hg), which correlated significantly with the highest circulating values of the drug. The pressor effect after i.v. infusion appears to be unrelated to endogenous release of catecholamines, because phentolamine, which abolishes the response to exogenous norepinephrine, failed to prevent the CsA-induced pressor response. Third, i.v. bolus injections of CsA (10-20 mg/kg) evoked immediate, dose-dependent and short-lasting increases in MAP (+15-25 mm Hg) in both anesthetized and conscious rats. Ganglionic blockade did not prevent this effect, rather, a 2- to 3-fold increase in amplitude (+40-60 mm Hg) and duration (+30-45 min) of the CsA-induced pressor response was observed in anesthetized rats. Heart rate was not increased significantly by either acute or chronic administration of CsA. Our results suggest that both CsA-induced pressor responses and hypertension are due to a peripheral action unrelated to sympathetic outflow. Furthermore, CsA9s hypertensive effect is accompanied by severe morphological changes in the vascular endothelium and smooth muscle cells. In addition, CsA-treated rats showed significantly attenuated vasodilatory responses to prostacyclin and sodium nitroprusside, and increased pressor responses to norepinephrine. Thus, a direct vascular action of CsA is likely to contribute to the alterations on systemic vascular responsiveness, as well as to the hypertensive effect of the drug.
Attenuation of the reflex pressor response to muscular contraction by an antagonist to somatostatin.
Authors: K W McCoy, D M Rotto, K J Rybicki, M P Kaufman
Journal: Circulation Research (1988)

Although group III and IV fibers are known to compose the afferent pathway of the reflex arc causing the pressor response to static muscular contraction, little is known about the neurotransmitters released by these muscle afferents. Somatostatin might be one of these neurotransmitters because this peptide is found in the terminals of fine afferent fibers ending in the dorsal horn of the lumbar spinal cord. Therefore, in chloralose-anesthetized cats, the reflex pressor response to static contraction was examined before and after subarachnoid injections onto the lumbosacral cord of a peptide antagonist to somatostatin. We found that before giving the antagonist, the pressor response to contraction of the triceps surae muscles in 12 cats averaged 33 +/- 4 mm Hg, while 37 +/- 7 minutes after giving the antagonist, the pressor response averaged only 18 +/- 3 mm Hg (p less than 0.001). In contrast, the antagonist to somatostatin had no effect on either the pressor response to electrical stimulation of the cut central end of the sciatic nerve or the pressor response to stimulation of the posterior diencephalon. Furthermore, subarachnoid injection of a peptide antagonist to luteinizing hormone-releasing hormone had no effect on the reflex pressor response to static contraction. Our findings are consistent with the hypothesis that somatostatin plays a role in the spinal transmission of the contraction-induced pressor reflex arising from hind limb skeletal muscle.
Aspirin and Hemophilia
Authors: HARRY M. BAUER
Journal: Annals of Internal Medicine (1977)

Letters and Corrections1 December 1977Aspirin and HemophiliaHARRY M. BAUER, M.D.HARRY M. BAUER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-87-6-795_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The review of acetaminophen by Ameer and Greenblatt (1) contains what appears to be a typographical error, the implication of which is seriously misleading. The authors state on p. 205, "Hemophilic patients receivingaspirin(my italics) or multiple doses of acetaminophen showed no significant changes in bleeding time." The reference given for that statement, in fact, is quite clear in stating that acetaminophen only was given to hemophiliac persons, not aspirin (2). Although the use of aspirin might not cause significant changes in the bleeding time of patients with mild bleeding disorders, in severe hemophilia the results...References1. AMEERGREENBLATT BD: Acetaminophen. Ann Intern Med 87:202-209, 1977 LinkGoogle Scholar2. MIELKEBRITTEN CA: Use of aspirin or acetaminophen in hemophilia (letter). N Engl J Med 282:1270, 1970 CrossrefMedlineGoogle Scholar3. KANESHIROMIELKEKASPERRAPAPORT MCCS: Bleeding time after aspirin in disorders of intrinsic clotting. N Engl J Med 281:1039-1042, 1969 CrossrefMedlineGoogle Scholar4. RAPAPORT S: Introduction to Hematology. New York, Harper and Row, 1971, p. 352 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1977Volume 87, Issue 6Page: 795-795KeywordsAspirinHemophiliaHemorrhage Issue Published: 1 December 1977 PDF DownloadLoading ...
Risks of Imbalanced Information on US Hospital Websites
Authors: Yael Schenker, Alex John London
Journal: JAMA Internal Medicine (2015)

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 Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast 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 Internal Medicine journal
Effects of a cardio-selective beta-adrenergic blocking agent on the heart and coronary circulation
Authors: G. Ross, C. R. Jorgensen
Journal: Cardiovascular Research (1970)

Journal Article Effects of a cardio-selective beta-adrenergic blocking agent on the heart and coronary circulation Get access Gordon Ross, Gordon Ross 2 From the Departments of Physiology and Medicine, UCLA School of Medicine, Los Angeles, California, U.S.A. 2This work was done during the tenure of an Established Investigatorship of the American Heart Association. Search for other works by this author on: Oxford Academic PubMed Google Scholar Charles R. Jorgensen Charles R. Jorgensen From the Departments of Physiology and Medicine, UCLA School of Medicine, Los Angeles, California, U.S.A. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 4, Issue 2, April 1970, Pages 148–153, https://doi.org/10.1093/cvr/4.2.148 Published: 01 April 1970 Article history Accepted: 24 October 1969 Published: 01 April 1970
The Experimental Use of Psychedelic (LSD) Psychotherapy
Authors: Walter N. Pahnke, Albert A. Kurland, Sanford Unger, Charles Savage, Stanislav Grof
Journal: JAMA (1970)

The history of research with psychedelic drugs has produced a variety of methods for their use and conflicting claims about results. First came the wave of excitement among experimentalists in the 1950s when it was claimed that lysergic acid diethylamide (LSD) could produce a model psychosis which might be useful in understanding schizophrenia. While this promise was fading, enthusiastic reports about the possibility of LSD as an aid to psychotherapy in the treatment of alcoholism and other psychiatric disorders appeared. All these approaches were represented in 1959 at the first international conference devoted entirely to LSD. 1 Since then, there have been at least five more published proceedings of such conferences on various aspects of psychedelic drugs. 2-6 The most recent conference on various means of producing states of consciousness was sponsored by the Menninger Foundation and the American Association of Humanistic Psychology on April 7 to 11, 1969, in
Refrigeration preserves synovial fluid cytology.
Authors: S T Jones, J Denton, P J Holt, A J Freemont
Journal: Annals of the Rheumatic Diseases (1993)

Refrigeration preserves synovial fluid cytologySir: We recently published an algorithm based on combinations of synovial fluid (SF) cell number thresholds and types which should considerably extend the diagnostic use of SF cytology in non-septic/crystal
Book Review Contagious: Cultures, Carriers, and the Outbreak Narrative (A John Hope Franklin Center Book.) By Priscilla Wald. 373 pp., illustrated. Durham, NC, Duke University Press, 2008. $84.95 (cloth); $23.95 (paper). 978-0-8223-4128-4 (cloth); 978-0-8223-4153-6 (paper).
Authors: Suok Kai Chew
Journal: New England Journal of Medicine (2008)
PCSK9 inhibitors reduce cardiovascular events, preliminary data show
Authors: S. Mayor
Journal: BMJ (2015)

Two investigational drugs from a new class of lipid lowering agents—the proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors—significantly reduce cardiovascular events, new exploratory analyses have shown.

PCSK9 promotes the degradation of low density lipoprotein (LDL) receptors, so blocking its action increases the levels of receptor, which facilitates the clearance of LDL cholesterol. 

The studies, reported in the New England Journal of Medicine , investigated the efficacy and safety of two monoclonal antibodies that inhibit PCSK9 and showed that they …
Foreign Body in a Meckel's Diverticulum
Authors: Arindam Purkayastha
Journal: JAMA (1984)

<h3>To the Editor.—</h3> A 19-month-old girl infant was seen because of abdominal pain and discomfort. Her mother stated that approximately six weeks ago she had swallowed a penny. Roentgenograms revealed the coin in the right lower quadrant. The patient continued to have intermittent bouts of abdominal pain and vomiting. Serial roentgenograms taken once a week showed no progression of the coin. Exploration was undertaken when the coin was found in a Meckel's diverticulum. The diverticulum, along with the coin, was excised. Postoperative recovery was uneventful except for a wound abscess, which resolved with drainage.
Herpesvirus-based infectious titering of recombinant adeno-associated viral vectors
Authors: Imran Mohiuddin, Scott Loiler, Irina Zolotukhin, Barry J. Byrne, Terence R. Flotte, Richard O. Snyder
Journal: Molecular Therapy (2004)

Studies in animals and human clinical trials demonstrate the safety and persistence of recombinant adeno-associated viral (rAAV) serotype 2 vectors in a variety of tissues. rAAV vectors of other serotypes are also being developed for efficient gene transfer. To date, the literature describing these vectors has relied on physical or transducing titers to determine dose, but few, if any, infectious titers have been presented. This is due in large part to the lack of reagents and methods that would facilitate the infectious titering of vectors other than serotype 2. Here, we describe reagents and methods for infectious titering of AAV2 ITR-containing vectors pseudotyped with other AAV capsid serotypes and demonstrate their utility by titering pseudotyped rAAV1 or rAAV5 vectors. Cell lines are screened for optimal transduction using a vector of a particular serotype that expresses a marker transgene. Once a cell line and vector serotype are matched, a recombinant herpes simplex virus vector expressing AAV2 rep and cap genes provides helper functions that amplify the rAAV vector genome. The vector genomes are then detected and a titer is calculated. These methods generate reliable infectious titers for AAV vectors of different serotypes, thus enhancing product characterization and reducing risk in future clinical applications.
Reactions to Nickel
Authors: Herman Solomon
Journal: JAMA (1973)

<h3>To the Editor.—</h3> Recent letters by Fisher and Kellum, "Safety of Stainless Steel in Nickel Sensitivity" (221:1279, 1972) in response to our article "Eczematous Dermatitis From Nickel," (220:1244, 1972) seem to cast some doubt on the ability of nickel in stainless steel surgical implants to cause "internal" allergic contact dermatitis. Fisher states that positive results of patch tests to a hard metal like stainless steel may represent only an irritant reaction. As stated in our article, the patient also had a positive result in a patch test for chemical nickel in petrolatum. Fisher also apparently ignored that this patient's unrelenting dermatitis cleared completely and promptly only when the stainless steel screws were removed. He further states that he had never heard of allergic reactions to stainless steel. One of the references in our article<sup>1</sup>presented two documented cases of widespread eczematous dermatitis from internal exposure to nickel in stainless steel
Multi-locus models of genetic risk of disease
Authors: Naomi R Wray, Michael E Goddard
Journal: Genome Medicine (2010)

Evidence for genetic contribution to complex diseases is described by recurrence risks to relatives of diseased individuals. Genome-wide association studies allow a description of the genetics of the same diseases in terms of risk loci, their effects and allele frequencies. To reconcile the two descriptions requires a model of how risks from individual loci combine to determine an individual's overall risk. We derive predictions of risk to relatives from risks at individual loci under a number of models and compare them with published data on disease risk. The model in which risks are multiplicative on the risk scale implies equality between the recurrence risk to monozygotic twins and the square of the recurrence risk to sibs, a relationship often not observed, especially for low prevalence diseases. We show that this theoretical equality is achieved by allowing impossible probabilities of disease. Other models, in which probabilities of disease are constrained to a maximum of one, generate results more consistent with empirical estimates for a range of diseases. The unconstrained multiplicative model, often used in theoretical studies because of its mathematical tractability, is not a realistic model. We find three models, the constrained multiplicative, Odds (or Logit) and Probit (or liability threshold) models, all fit the data on risk to relatives. Currently, in practice it would be difficult to differentiate between these models, but this may become possible if genetic variants that explain the majority of the genetic variance are identified.
T lymphocytes in atherogenesis?functional aspects and antigenic repertoire
Authors: O DEBOER, A BECKER, A VANDERWAL
Journal: Cardiovascular Research (2003)

Atherosclerosis represents an inflammatory and reparative response to chronic or episodic injury of arterial intima [1]. During the longstanding process of plaque formation a myriad of secretory products of inflammatory cells is released in the plaque, likely connected to the nature and extent of injury to the vessel wall. These inflammatory mediators do not only have profound effects on growth and morphologic differentiation of plaques, but eventually may also initiate plaque rupture, and thus life threatening complications such as myocardial infarction and stroke [2]. Such insights have led to intense investigations over the past years tempting to unravel molecular and cellular basis of plaque inflammation, which include also factors that initiate or sustain the inflammatory response. Cell types that take part in plaque inflammation are macrophages, T-lymphocytes, mast cells and dendritic cells. Among these, the participation of T cells in atherogenesis is relevant for several reasons. First, T-cells are immune regulatory cells, which, once activated, are able to secrete cytokines or express surface molecules with bioactive potential. These receptors and cytokines are capable of modulating the type and intensity of the inflammatory response, and also influence the microenvironment (growth behavior of vascular smooth muscle cells, synthesis and degradation of extracellular matrix proteins), implying that they may affect the stability of the plaque. Second, T-lymphocytes are cells with an immunological memory; they are genetically programmed to respond only to a very specific sequence of peptides (antigens), which is unique for each T-cell. Such antigenic recognition leads to activation, clonal expansion and/or cytokine production; in other words, initiating a cell mediated inflammatory response. Knowing the antigen specificity of T cells in plaques could thus provide information about the causes of plaque inflammation, and such information can be considered pivotal to develop treatment modalities that interfere with the process of plaque … 

*Corresponding author. Tel.: +31-20-566-4369; fax: +31-20-691-4738. Email address: o.j.deboer{at}amc.uva.nl
OBSERVATIONS ON THE PRODUCTION OF PYROGENIC SUBSTANCES BY RABBIT AND HUMAN LEUCOCYTES
Authors: J. H. Fessler, K. E. Cooper, W. I. Cranston, R. L. Vollum
Journal: The Journal of Experimental Medicine (1961)

1. The mechanism of release of a pyrogen from leucocytes has been studied in cells obtained from sterile rabbit peritoneal exudates and from rabbit blood. Attempts were made to induce human leucocytes-from blood-to release a pyrogen. 2. Rabbit leucocytes, kept below 4 degrees C., were not pyrogenic and did not release any pyrogen when disintegrated. Incubating such cells, in various media, at 37 degrees C. led to the formation of a pyrogen which was heat-labile. The maximum yield was attained after 1(1/2) hours' incubation. 3. The formation of rabbit leucocytic pyrogen was prevented by freezing and thawing the leucocytes, by heating them to 56 degrees C. for half an hour before incubation, and by ageing them in the cold. 4. Nitrofurazone (5-nitro-2-furaldehyde semicarbazone) prevents the formation of leucocytic pyrogen when given by mouth to the cell-donor animals, or when added to leucocytes in intro. 5. Leucocytes from rabbit blood formed leucocytic pyrogen, on incubation in saline, and this formation was also inhibited by nitrofurazone. 6. No leucocytic pyrogen was released from human leucocytes subjected to mechanical, osmotic, or thermal damage, and it was not formed when the cells were incubated in saline. 7. The source of rabbit leucocytic pyrogen, the action of nitrofurazone on leucocytes, and the supposed role of leucocytic pyrogen in fever are discussed.
Successful Endoscopic Removal of a Common Bile Duct Foreign Body
Authors: P.F.B. O'Regan, F. Shanahan, J.R. Lennon, J. Crowe
Journal: Endoscopy (1982)

See also: Endoscopic Removal of an Atypical Common Bile Duct Foreign BodyEndoscopy 1990; 22(02): 93-93DOI: 10.1055/s-2007-1012806
Primary disease recurrence after liver transplantation for alveolar echinococcosis: Long-term evaluation in 15 patients
Authors: Solange Bresson-Hadni, St�phane Koch, Isabelle Beurton, Dominique-Ang�le Vuitton, Brigitte Bartholomot, Stephan Hrusovsky, Bruno Heyd, Dani�le Lenys, Anne Minello, Marie C. Becker, Claire Vanlemmens, Georges-Andr� Mantion, Jean-Philippe Miguet
Journal: Hepatology (1999)

Between 1986 and 1991, 21 patients received liver grafts in our center for incurable alveolar echinococcosis (AE). The aim of this study was to analyze the long-term results in 15 of these 21 patients who survived more than 1 year after undergoing a liver transplantation (LT). The follow-up, mainly aimed at the diagnosis of recurrence, consisted of repeated radiological and specific immunological investigations. The role of pre- and post-LT benzimidazole (BZM) therapy was also evaluated. Among the 15 patients, 8 patients had a palliative LT related to previously known pulmonary AE metastases and/or inextirpable abdominal parasitic foci. In the 7 remaining patients, LT was considered curative. In June 1998, the mean follow-up duration was 96 months (range: 28-138 months). Five late deaths occurred, 2 of them were directly related to residual AE. A reinfection of the graft was observed in 4 patients. Preoperative BZM therapy seemed useful in preventing or delaying the parasitic recurrence. Post-LT BZM was able to stabilize and even to reduce residual AE. The anti-Em2 enzyme-linked immunosorbent assay (ELISA), which is the standard test used in patient follow-up after partial liver resection for AE, did not appear useful in detecting recurrence here; however, an ELISA, using a crude heterologous antigen (Echinococcus granulosus) allowed early diagnosis of residual AE. In conclusion, primary disease recurrence is not rare after LT for AE. Immunosuppressive therapy may favor larval growth in extrahepatic sites; therefore, an extensive extrahepatic radiological check-up has to be performed before LT. BZM therapy seems to stabilize residual foci. Anti-Eg immunoglobulin G (IgG) follow-up is the most useful test for early diagnosis of parasite recurrence.