tbuckley/cabot-search huggingface dataset:
Familial Clustering of Hepatitis B Antigen: A Study in Relatives of Patients with Liver Diseases and Hepatitis B Antigenaemia
Authors: M. Bruguera, J. Bosch, J. Rodes, J. Pedreira
Journal: BMJ (1974)

Twelve of the 100 family contacts of 29 patients with transient and persistent hepatitis B antigenaemia were found to be positive for hepatitis B antigen (HBAg). No relation was found between familial clustering and the nature of liver disease or the duration of antigenaemia in the index cases. Eight affected relatives were apparently healthy carriers of HBAG, one had cirrhosis, and three (in the same family) developed acute viral hepatitis. The absence of parenteral exposure in the HBA,-positive family contacts and the identity in antigenic determinants d or y with those of the index cases, suggest a non-parenteral spread of HBAg in families of patients with HBAg-associated liver diseases.
Abstract B60: Analysis of the endocytic receptor MRC2 as a target for mesenchymal pancreatic cancer cells
Authors: Arkadeep Sinha, Aprill Watanabe, Jordan Winter, Peter Allen, Galen Hostetter, Brian B. Haab
Journal: Cancer Research (2013)

Abstract The poor outcome of pancreatic cancer is hypothesized to be due to a subset of cancer cells that have elevated propensity to metastasize and are resistant to current chemotherapeutics. In vitro, the process of epithelial to mesenchymal transition (EMT) has been shown to grant cells with the aforementioned properties. Hence, it has been hypothesized that the process of EMT might have answers to controlling the metastatic cascade. Using gene expression microarrays, MRC2 expression was found to be upregulated when cells undergo EMT. MRC2 is a transmembrane protein known for its role in collagen degradation. Its role in the progression of metastatic pancreatic cancer and in vivo expression was assayed for validation as a drug target. MRC2 upregulation by TGF-β1 did not promote increased transition to a mesenchymal phenotype or migratory ability in the absence of a chemotactic gradient. However, using boyden chamber and matrigel invasion assays, it was observed that MRC2 affects chemotactic and invasive ability. Immunohistochemical analysis of over 250 pancreatic tumors revealed that MRC2 is upregulated in the cancer samples especially in the stromal compartment. MRC2 staining patterns were consistent with involvement in invasion, including elevation in individual, invading cancer cells and stromal elevations in peri-tumoral and poorly differentiated regions. Blinded immunohistochemical studies disclosed a correlation between elevated stromal MRC2 levels and poor prognosis. Flow cytometry is being used on primary tumors to confirm the dual stain results hinting towards the elevation of MRC2 on a subset of pancreatic cancer cells in vivo. Dual stains on tissue microarrays are also being used to identify the stromal cell population showing MRC2 elevation. Based on the role of MRC2 in chemotactic invasion and extracellular matrix remodeling, loss of cells expressing MRC2 might be a deterrent for metastasis. Since MRC2 is part of an endocytic pathway,upon confirmation of MRC2 as a marker of the mesenchymal cancer cells, it has the potential for use as an adjuvant targeted therapy for the treatment of pancreatic cancer. Citation Format: Arkadeep Sinha, Aprill Watanabe, Jordan Winter, Peter Allen, Galen Hostetter, Brian B. Haab. Analysis of the endocytic receptor MRC2 as a target for mesenchymal pancreatic cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr B60.
End-Tidal Pco2 During Cardiopulmonary Resuscitation
Authors: Jack Yetiv
Journal: JAMA (1990)

<h3>To the Editor.—</h3> Sanders and colleagues<sup>1</sup>recently showed that during cardiopulmonary resuscitation, an end-tidal PCO<sub>2</sub>measurement of less than 10 mm Hg predicts a uniformly poor outcome (failure to resuscitate). They state that "there is an urgent need for a reliable method of assessing the efficacy of ongoing cardiopulmonary resuscitation." This suggests that end-tidal PCO<sub>2</sub>was used to evaluate the hemodynamic<i>efficacy</i>of cardiopulmonary resuscitation, although the title and the article itself suggest that end-tidal PCO<sub>2</sub>was studied as a<i>prognostic indicator</i>of the likely outcome of the resuscitation. Whereas a technique of assessing the efficacy of ongoing cardiopulmonary resuscitation may indeed be useful, a simple prognostic indicator already exists—namely, the presence of asystole or electromechanical dissociation as the underlying arrest rhythm. The data of Sanders et al show that only 1 of a total of 68 patients who presented with asystole or electromechanical dissociation survived
CELLULAR IMMUNITY IN VITRO
Authors: Harvey B. Simon, John N. Sheagren
Journal: The Journal of Experimental Medicine (1971)

An in vitro model of cellular immunity in the guinea pig was established. Animals were immunized with tubercle bacilli, bovine gamma globulin, or picrylated human serum albumin in complete Freund's adjuvant. Oil-induced peritoneal exudates from immune and control animals were cultured overnight with and without specific antigen. The cultures were washed and the macrophage monolayers were infected with Listeria monocytogenes. At intervals the monolayers were lysed and the numbers of viable intracellular bacteria were quantitated by pour plate cultures. Random monolayers were also evaluated in sequence by visually counting the intracellular bacteria on Gram-stained plates. Both methods demonstrated that the macrophages from immune animals had markedly enhanced listericidal activity when the peritoneal exudates were cultured with antigen before infection. Macrophage migration inhibition was also demonstrated under these conditions. The experiments reported here describe an in vitro model of cellular immunity which will allow separation and recombination of cell types and direct assay of cell products in efforts to elucidate further the mechanisms of the immunologically mediated enhancement of macrophage bactericidal capacity.
THE SPECIFICITY OF THE MINOT-MURPHY DIET IN PERNICIOUS ANEMIA
Authors: I. C. BRILL
Journal: JAMA (1927)

During the past year, I have treated by the Minot-Murphy method ten cases of pernicious anemia and four cases of severe secondary anemia. In the latter series were included two cases in which the anemia was the result of more or less continuous bleeding, over a long period of time, from the uterus and the rectum, respectively. In both instances the lesions were benign and were removed by operation before the special diet was commenced. The third case was one in which the anemia was apparently due to syphilis, and treatment for the latter was carried out, together with the application of the dietary measures. In the fourth case the anemia resulted from a gastric carcinoma. The growth was confined to the greater curvature of the stomach, about two-thirds up on the cardiac end, and although it was large and deemed inoperable, it did not cause obstruction and did not
Polymorphism of the<i>N</i>-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatitis
Authors: Yi-Shin Huang, Herng-Der Chern, Wei-Juin Su, Jaw-Ching Wu, Shinn-Liang Lai, Shi-Yi Yang, Full-Young Chang, Shou-Dong Lee
Journal: Hepatology (2002)

Antituberculosis drug-induced hepatitis is one of the most prevalent drug-induced liver injuries. Isoniazid is the major drug incriminated in this hepatotoxicity. Isoniazid is mainly metabolized to hepatotoxic intermediates by N -acetyltransferase (NAT). However, the association of polymorphic NAT acetylator status and antituberculosis drug-induced hepatitis is debatable. To determine whether acetylator status is a risk factor for antituberculosis drug-induced hepatitis, we genotyped NAT2 in 224 incident tuberculosis patients who received antituberculosis treatment. Antituberculosis drug-induced hepatitis was diagnosed based on a positive isoniazid rechallenge test and exclusion of viral hepatitis. Acetylator status was determined by genotyping NAT2 in patients using a polymerase chain reaction with restriction fragment length polymorphism. Univariate analysis and logistic regression analysis were used to evaluate the risk factors of isoniazid-induced hepatitis. Thirty-three patients (14.7%) were diagnosed with antituberculosis drug-induced hepatitis. Slow acetylators had a higher risk of hepatotoxicity than rapid acetylators (26.4% vs. 11.1%, P = .013). Among patients with hepatotoxicity, slow acetylators had significantly higher serum aminotransferase levels than rapid acetylators. Logistic regression showed that slow-acetylator status (odds ratio [OR], 3.66; 95% CI, 1.58-8.49; P = .003) and age (OR, 1.09; 95% CI, 1.04-1.14; P &lt; .001) were the only 2 independent risk factors for antituberculosis drug-induced hepatitis. In conclusion, slow-acetylator status of NAT2 is a significant susceptibility risk factor for antituberculosis drug-induced hepatitis. Additionally, slow acetylators are prone to develop more severe hepatotoxicity than rapid acetylators. Regular monitoring of serum aminotransferase levels is mandatory in patients receiving antituberculosis treatment, especially in slow acetylators.
Evolving Research and Stakeholder Perspectives on Pharmacogenomics
Authors: Amber L. Beitelshees, David L. Veenstra
Journal: JAMA (2011)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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
Infections Caused by Haemophilus influenzae Type b
Authors: Eugene D. Shapiro
Journal: JAMA (1993)

Infections caused by<i>Haemophilus influenzae</i>type b (Hib) have been a deadly scourge of children for many years. Until recently Hib was the most common cause of bacterial meningitis in the United States (most of which occurred in children less than 2 years of age).<sup>1</sup><i>Haemophilus influenzae</i>type b has been responsible for death or severe permanent neurologic damage in tens of thousands of children in the United States and throughout the world.<sup>1,2</sup>The morbidity and mortality of Hib infections in the United States in the early 1980s were comparable to the morbidity and mortality of poliomyelitis during the great polio epidemics of the 1950s.<sup>3</sup>Three articles in the current issue ofThe Journalreport that in recent years the incidence of Hib infections in the United States has fallen by 85% to 90%.<sup>4-6</sup>Is this occurring throughout the See also pp 221, 227, and 246.
Hyperosmotic Coma Complicating Peritoneal Dialysis with Sorbitol Dialysate
Authors: RASIB M. RAJA
Journal: Annals of Internal Medicine (1970)

A uremic and severely edematous patient with diabetic nephropathy underwent peritoneal dialysis with hypertonic sorbitol dialysate. Although azotemia and edema improved, he became comatose after 72 hr of continuous dialysis and died in an advanced hyperosmolar state.
AINHUM, A FAMILY DISEASE
Authors: K. M. B. Simon
Journal: JAMA (1921)

Ainhum is fairly common in British Honduras. It has been described as a chronic dystrophy of the fifth or fourth toe in native races, characterized by the formation of a furrow at the digitoplantar fold. This fibrosis extends, injuring the vessels, and producing an endarteritis obliterans and a rarefying osteitis. I have noticed a similar dystrophy in the little finger of an Indian. That the disease is inherited is proved by the fact that the father and brother of the patient, the condition of whose foot is illustrated herewith, suffered from the same condition, all ending in loss of the toe. The cause of this disease is unknown; but the theories that it is due to leprosy or self-mutilation are untenable. The condition resembles ground itch, except that in ground itch there is ulceration under every toe; in ainhum, under only one toe The treatment consists of an incision
Effects of Administration of an Organo-phosphorus Compound as an Antibilharzial Agent, with Special Reference to Plasma Cholinesterase
Authors: S. Hanna, K. Basmy, O. Selim, S. M. Shoeb, A. Y. Awny
Journal: BMJ (1966)

The organo-phosphorus compound Dipterex1 (trichlorphon ; 00-dimethyl-2,2,2,-trichlorethyl phosphonate) has attracted considerable attention during the past few years. Besides its use as an insecticide, an attempt has been made to employ this substance for the treatment of intestinal parasites (Beheyt, Lebrun, Cerf, Dierickx, and Degroote, 1961 ; Cerf, Lebrun, and Dierickx, 1962). Schistosomiasis is a very common condition in the United Arab Republic and a simplified course of treatment given by mouth would be a great improvement on the treatment in use. Hence a trial experiment was carried out to evaluate the efficacy of Dipterex in treating bilharziasis.
Enhanced T-cell immunogenicity of plasmid DNA vaccines boosted by recombinant modified vaccinia virus Ankara in humans
Authors: Samuel J McConkey, William H H Reece, Vasee S Moorthy, Daniel Webster, Susanna Dunachie, Geoff Butcher, Jenni M Vuola, Tom J Blanchard, Philip Gothard, Kate Watkins, Carolyn M Hannan, Simone Everaere, Karen Brown, Kent E Kester, James Cummings, Jackie Williams, D Gray Heppner, Ansar Pathan, Katie Flanagan, Nirmalan Arulanantham, Mark T M Roberts, Michael Roy, Geoffrey L Smith, Joerg Schneider, Tim Peto, Robert E Sinden, Sarah C Gilbert, Adrian V S Hill
Journal: Nature Medicine (2003)
The Use of Fresh-Frozen Plasma in Hereditary Angioedema
Authors: Allen Lieberman
Journal: JAMA (1994)

<h3>To the Editor.</h3> —In a recent article in<i>JAMA</i>, the guidelines for the use of fresh-frozen plasma were reviewed.<sup>1</sup>Although many clinical indications were listed, most for the treatment of coagulopathies, an important omission was made. Not mentioned was the prophylactic use of fresh-frozen plasma in patients with hereditary angioedema before oral surgery. Patients with hereditary angioedema are prone to acute, severe attacks of upper airway edema. Dental procedures are a well-recognized precipitating factor. Prophylaxis with fresh-frozen plasma prior to oral surgery is effective in preventing attacks of angioedema.<sup>2</sup>Therefore, the clinical indications for the use of fresh-frozen plasma should include patients with hereditary angioedema.
Ulcerative colitis and Crohn's disease
Authors: G Hearn, J Maberly, H Anthony
Journal: BMJ (1994)

annually by the Human Fertilisation and Embryology Authority2 included rates of multiple pregnancy and birth rates according to both the woman's age and the number of embryos transferred.Any policy allowing numerous embryos or oocytes to be replaced entails a calculated risk of multiple pregnancy.Our data support the point made by Redgment and colleagues that the principle underlying the present policy leaves room to raise the number of embryos or eggs replaced in women aged 40 and over to try to increase their pregnancy rates while keeping rates of multiple pregnancy down to what is currently acceptable in women under 40.
MECHANISM OF RECOVERY FROM SYSTEMIC VACCINIA VIRUS INFECTION
Authors: M. Worthington, A. S. Rabson, S. Baron
Journal: The Journal of Experimental Medicine (1972)

Administration of Cytoxan in doses capable of inhibiting both humoral and cellular immunity markedly potentiated primary systemic vaccinia virus infection in mice. Immunosuppressed mice did not form neutralizing antibody to vaccinia virus and had a prolonged and more severe viremia than nonimmunosuppressed control mice. Passive transfer of physiologic amounts of neutralizing antibody late in the course of infection, at a time when nonimmunosuppressed mice had similar levels of serum antibody, largely reversed the effect of Cytoxan on vaccinia virus infection. Transfer of 100 million immune spleen cells was much less effective than antibody in reversing the effect of Cytoxan on vaccinia virus infection, and mice receiving these cells did make some antibody. Serum interferon levels were not affected by Cytoxan. The results suggest an essential role for humoral antibody, but not for cellular immunity, in recovery from primary vaccinia virus infection in the mouse.
Abstract 3191: Elevation of tumor-promoting cytokines in mice exposed to the environmental contaminant tributyltin
Authors: Shanieek Lawrence, Samuel Troy Pellom, Tasia Hurd-Brown, Anil Shanker, Margaret Whalen
Journal: Cancer Research (2014)

Abstract Cytokines are important regulators of immune responsiveness. Alterations of cytokine secretion from immune cells would have the potential to disrupt both immune destruction of cancer cells and to alter the proliferation and invasiveness of tumor cells due to their capacity to act as growth factors, angiogenic factors, and inducers of epithelial-mesenchymal transition. Tributyltin (TBT) is a widespread environmental contaminant having been used in a variety of industrial applications and is found in human blood at levels ranging as high as 261 nM. Studies in human immune cells have shown that secretion of tumor necrosis factor alpha (TNFα) is altered by exposures to TBT. There have been no in vivo studies of the effects of exposure to TBT on the cytokine communication network. As it is not possible to examine alterations of this network in exposed humans, we examined the effects of TBT exposure in a mouse model using Milliplex mouse cytokine/chemokine magnetic bead premixed 32 plex kit. Serum and spleens of TBT-exposed mice were analyzed for changes in cytokine secretion/levels. TBT increased the levels of IL13 in the serum of non-tumor-bearing mice and increased IL1β, IL6, KC, and M-CSF in tumor-bearing mice. The spleens of both non-tumor-bearing and tumor-bearing mice showed increases in Eotaxin when exposed to TBT. Of significant interest is the fact that the presence of tumor causes increases in Eotaxin, IL12p40, M-CSF, and TNFα and exposure to TBT alone can cause increases in these same cytokines. Tumors are known to increase levels of cytokines that enhance their ability to survive. The results showing that TBT can amplify the levels of several cytokines that are increased by tumor suggest that TBT may have tumor-promoting abilities by modulating tumor growth and/or invasiveness. Experiments are under way to dissect cytokine signaling pathways that are affected by TBT. The findings will allow identification of molecular targets that are necessary to intercept the tumor promoting signaling following TBT exposure. Supported by: NIH grant 5U54CA163066-03 Citation Format: Shanieek Lawrence, Samuel Troy Pellom, Tasia Hurd-Brown, Anil Shanker, Margaret Whalen. Elevation of tumor-promoting cytokines in mice exposed to the environmental contaminant tributyltin. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3191. doi:10.1158/1538-7445.AM2014-3191
WAR NEUROSES, SHELL SHOCK AND NERVOUSNESS IN SOLDIERS
Authors: PEARCE BAILEY
Journal: JAMA (1918)

0.01 c.c, and this was the dosage of low virulence adopted for the series of inoculations.In order to get a broader view of the effect of typhoid vaccine on lowering the resistance, it was decided to have three series of mice, inoculated at intervals of several days, in each experiment.Mice were inoculated subcutaneously with the stan- dard triple typhoid lipovaccine used in all the camps.The dosage was sufficiently large to cause all the animals to be sick and quite a high proportion of them to die, the idea being to lower their resistance as much as possible.If proportionate dosage were given man
αKlotho: FGF23 coreceptor and FGF23-regulating hormone
Authors: Harald Jüppner, Myles Wolf
Journal: Journal of Clinical Investigation (2012)

Low levels of phosphate can disrupt bone ossification and predispose to fractures. FGF23 is one of the major determinants of phosphate homeostasis, acting to increase urinary phosphate excretion. However, the regulation of FGF23 is incompletely understood. In this issue of the JCI, Smith et al. show that the cleaved form of αKlotho, the membrane-bound form of which is an FGF23 coreceptor, serves as a novel endocrine regulator of phosphate homeostasis, capable of inducing FGF23 production in osteocytes.
P211Vulnerable index detected by virtual histology intravascular ultrasound (VH-IVUS) in diseased coronary segments in patients with acute myocardial infarction and stable angina pectoris
Authors: N Tagieva, R Shakhnovich
Journal: Cardiovascular Research (2014)

Title: Vulnerable index (VI) detected by virtual histology intravascular ultrasound (VH-IVUS) in diseased coronary segments in patients with acute myocardial infarction and stable angina pectoris. Purpose: The present study examined the relationship between the clinical presentation of coronary artery disease and the plaque characteristics of nonculprit segment assessed by virtual histology intravascular ultrasound (VH-IVUS). Objectives: The aim of this study was to investigate the difference of non-culprit lesion morphologies assessed by VH-IVUS between patients with acute myocardial infarction (AMI) and stable angina pectoris (SAP). Methods: In 38 consecutive AMI and 32 SAP patients the non-culprit artery was analyzed with VH-IVUS. We measured the 4 basic VH-IVUS coronary plaque components: fibrous, fibrofatty, dense calcium (DC), and necrotic core (NC). We calculated vulnerable index - NC/DC ratio. Results: We analyzed 130 plaques. AMI patients showed significantly higher ratio of dense calcium (9,27% +/- 7,5% versus 9.0% +/- 7,15%) and necrotic core plaque (25,4 % +/- 9% versus 23, % +/- 10%) compared with SAP patients. AMI group had greater vulnerable index (4,76 +/- 1,8 versus 4,03 +/- 2,6). VH-IVUS-derived thin-cap fibroatheroma (VH-TCFA) was more frequently observed in AMI patients compared with SA patients (40% versus 24%, p = 0.005). Conclusion: AMI patients presented higher prevalence of VH-TCFA in nonculprit segment. VH-IVUS analysis demonstrated that vulnerable index was associated with more vulnerable plaque components and was higher in AMI group.