tbuckley/cabot-search huggingface dataset:
631 IFN-A/B TARGET GENES REPERTOIRES MODULATED BY EXOGENOUS TYPE I IFN AND BY THE ENDOGENOUS HBV-INDUCED IFN-RESPONSE IN LIVER CELLS
Authors: B. Testoni, J. Lucifora, L. Belloni, C. Scisciani, D. Durantel, F. Zoulim, M. Levrero
Journal: Journal of Hepatology (2010)
THE RÔLE OF OBSTETRICS IN PREVENTIVE MEDICINE
Authors: W. P. MANTON
Journal: JAMA (1910)

With rare humor Dr. Oliver Wendell Holmes once wrote a prescription for longevity. Arriving at 60, to attain the ripe age of 80 "become the subject of a mortal disease," he says; but he fails to enlighten us as to how we may reach the year at which to begin his remedy. It is the object of every living being to lengthen life to the utmost, and in this prolongation of existence lies, with qualifications; the success of the state and the race. But as from the intervention of disease, few attain to that period when "every man with his staff in his hand for very age" marks the decline of usefulness, it is the object of preventive medicine to attempt so to safeguard life that it may be lengthened out to four-score years and ten of normal existence. Every century sees improvement along these lines, for increasing knowledge of
Heart Rate Variability in Diabetes: Relationship to Age and Duration of the Disease
Authors: Shirley Masaoka, Arye Lev-Ran, L Robert Hill, Gita Vakil, Edward H G Hon
Journal: Diabetes Care (1985)

Heart rate variability (HRV) during deep breathing was studied with a neonatal heart monitor in 143 control subjects and 218 patients with diabetes (102 with IDDM and 116 with NIDDM). In the control group HRV decreased after age 20 by 4–5 beats per decade (from 29.7 ±5.8 beats at age 20–29 to 11.8 ± 5.4 beats at age 60 +). In all age groups HRV in IDDM was lower than in the controls, and both age and duration of diabetes played a role in the decrease of HRV (from 21.5 ± 5.3 beats at age 20–29 to 6.3 ± 5.4 at age 60 +). In NIDDM aging seemed to play a less important role, and the influence of the duration of the disease was not statistically significant. In both groups of patients the frequency of HRV below the 2.5th percentile was 82% in those with symptoms and/or signs of autonomie neuropathy, 64% in patients with peripheral neuropathy only, and 36% in those who had no obvious signs or symptoms of neuropathy. Interindividual variability was pronounced, and age and duration of the disease together accounted for only 36% of the observed differences between IDDM and the controls. Determination of HRV with a standard neonatal heart monitor presents an easy, simple, and nonstressful test of cardiac autonomie neuropathy. The norms of the test are age related.
New Guidelines Established for Comprehensive Cancer Centers
Authors: Michael E. Newman
Journal: JNCI Journal of the National Cancer Institute (1990)

Journal Article New Guidelines Established for Comprehensive Cancer Centers Get access Michael E. Newman Michael E. Newman Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 82, Issue 1, 3 January 1990, Pages 14–15, https://doi.org/10.1093/jnci/82.1.14 Published: 03 January 1990
Endothelin-Converting Enzyme Expression in the Rat Vascular Injury Model and Human Coronary Atherosclerosis
Authors: Tohru Minamino, Hiroki Kurihara, Masaaki Takahashi, Kohei Shimada, Koji Maemura, Hideaki Oda, Takatoshi Ishikawa, Takashi Uchiyama, Kazuhiko Tanzawa, Yoshio Yazaki
Journal: Circulation (1997)

Background Endothelin 1 has been implicated in various human diseases, including atherosclerosis. In this study, we examined the expression and localization of endothelin-converting enzyme-1 (ECE-1), the final key enzyme of endothelin 1 processing, in rat carotid arteries after balloon injury and in human coronary atherosclerotic lesions. Methods and Results ECE-1 mRNA levels and ECE activity in rat balloon-injured arteries started to increase between 2 and 5 days after injury. The endothelin 1 content of tissue in injured arteries was concomitantly increased. Immunohistochemical staining located ECE-1 signals in endothelial cells in uninjured arteries, whereas ECE-1 immunoreactivity was detected in neointimal smooth muscle cells in injured arteries 5 to 14 days after balloon denudation. The size of the neointima was effectively reduced by phosphoramidon, an inhibitor of neutral metalloproteases, including ECE-1. In human coronary atherosclerotic lesions, intense ECE-1 immunoreactivity was detected in subsets of cells embedded in atheromatous plaque that correspond to smooth muscle cells and macrophages, as identified by staining for smooth muscle α-actin and CD68 surface marker, respectively. Conclusions The present study ascertained that ECE-1 is expressed in neointimal smooth muscle cells in rat balloon-injured arteries and in both smooth muscle cells and macrophages in human coronary atherosclerotic lesions. Blockade of ECE-1 was effective in reducing neointimal formation after balloon injury. Thus, ECE-1 may contribute to the process of injury-induced neointimal formation and atherosclerosis through the autocrine/paracrine effects of endothelin 1.
274 TACE/TAE in the treatment of early hepatocellular carcinoma (HCC) in patients not suitable for local regional ablation therapy
Authors: G.B. Vizzini, A. Luca, A. D'Antoni, R. Miraglia, U. Palazzo, M.P. Milazzo, S. Caruso, R. Volpes, G. Ferrandelli, A. Arcadipane, B. Gridelli
Journal: Journal of Hepatology (2004)
The Deprofessionalization of Medicine
Authors: Mark E. Reinecke
Journal: JAMA (1988)

To the Editor.  —The article by Drs Reed and Evans 1 in the Dec 11, 1987, issue of JAMA accurately portrays the condition that the profession finds itself in, that is, a state of progressive loss of professional autonomy. The authors propose the development of physiciandriven organizations, primarily in the form of group practices, as a partial or temporary solution to deprofessionalization. Having spent a number of years in group practice as well as health maintenance organization management, I could not agree more. A number of barriers lie in the way, but they are the sort of problems that can be overcome.  Capital formation is no problem for the medical profession due to its earning power. The problem is that in private practice the revenues above office expenses are typically retained as income. In industry it is not unusual for 10% to 15% of revenues to go to research, development,
Simultaneous study of the metabolic turnover and renal excretion of salivary amylase-125I and pancreatic amylase-131I in the baboon
Authors: William C. Duane, Roger Frerichs, Michael D. Levitt
Journal: Journal of Clinical Investigation (1972)

The metabolic turnover of salivary and pancreatic amylase was studied in the baboon, an animal with a serum amylase level and renal clearance of amylase similar to man. Purified amylase was electrolytically iodinated. Although iodinated and uniodinated amylase had similar gel filtration, electrophoretic, enzymatic, glycogen precipitation characteristics, the labeled enzyme was cleared less rapidly by the kidney than was the unlabeled material. However, urinary iodinated amylase which had been biologically screened by the kidney had a renal clearance and serum disappearance rate indistinguishable from unlabeled amylase and thus can serve as a tracer in metabolic turnover studies. Administration of a mixture of salivary amylase-(125)I and pancreatic amylase-(131)I made it possible to simultaneously measure the serum disappearance and renal clearance of these two isoenzymes. The metabolic clearance of both isoenzymes was extremely rapid with half-times of about 130 min. This rapid turnover of serum amylase probably accounts for the transient nature of serum amylase elevation which frequently occurs in pancreatitis. Pancreatic amylase-(131)I was consistently cleared more rapidly (mean clearance ratio: 1.8) by the kidney than was salivary amylase-(125)I. This more rapid renal clearance of pancreatic amylase may help to explain the disproportionate elevation of urinary amylase relative to serum amylase observed in pancreatitis.
Complete Mitochondrial Genome Sequence of the Polychaete Annelid Platynereis dumerilii
Authors: Jeffrey L. Boore
Journal: Molecular Biology and Evolution (2001)

Complete mitochondrial genome sequences are now available for 126 metazoans (see Boore 1999; Mitochondrial Genomics link at http://www.jgi.doe.gov), but the taxonomic representation is highly biased. For example, 80 are from a single phylum, Chordata, and show little variation for many molecular features. Arthropoda is represented by 16 taxa, Mollusca by eight, and Echinodermata by five, with only 17 others from the remaining {approx}30 metazoan phyla. With few exceptions (see Wolstenholme 1992 and Boore 1999) these are circular DNA molecules, about 16 kb in size, and encode the same set of 37 genes. A variety of non-standard names are sometimes used for animal mitochondrial genes; see Boore (1999) for gene nomenclature and a table of synonyms. Mitochondrial genome comparisons serve as a model of genome evolution. In this system, much smaller and simpler than that of the nucleus, are all of the same factors of genome evolution, where one may find tractable the changes in tRNA structure, base composition, genetic code, gene arrangement, etc. Further, patterns of mitochondrial gene rearrangements are an exceptionally reliable indicator of phylogenetic relationships (Smith et al.1993; Boore et al. 1995; Boore, Lavrov, and Brown 1998; Boore and Brown 1998, 2000; Dowton 1999; Stechmann and Schlegel 1999; Kurabayashi and Ueshima 2000). To these ends, we are sampling further the variation among major animal groups in features of their mitochondrial genomes.
THE EFFECT OF VARIED OXYGEN SUPPLY AND OF FOOD INTAKE ON WATER MOVEMENT IN SURVIVING LIVER TISSUE
Authors: Eugene L Opie
Journal: The Journal of Experimental Medicine (1961)

Water movement in liver slices has been measured in the presence of varied oxygen supply and during the progress of gastrointestinal digestion. Maximum water intake occurs both with anoxia and with exposure to oxygen when animals have received no food during 20 to 24 hours. It diminishes almost immediately after the ingestion of food and is least after 8 to 10 hours when digestion is nearly complete. These changes coincide with the passage of amino acids from the gastrointestinal tract to the liver by way of the blood. Movement of water into the liver cells is favorable to the entrance of dissolved substances and when it is greatest with approaching anoxia the movement promotes the diffusion of oxygen into the cells.
Clinical Outcome of a Large-Scale Multi-Institutional Retrospective Study for Locally Advanced Bladder Cancer: A Survey Including 1131 Patients Treated during 1990–2000 in Japan
Authors: Hiroyuki Nishiyama, Tomonori Habuchi, Jun Watanabe, Satoshi Teramukai, Harue Tada, Yoshinari Ono, Shinichi Ohshima, Kiyohide Fujimoto, Yoshihiko Hirao, Masanori Fukushima, Osamu Ogawa
Journal: European Urology (2003)
Rare Pediatric Diseases
Authors: Mike Mitka
Journal: JAMA (2010)

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
Dreaming and REM sleep are controlled by different brain mechanisms
Authors: Mark Solms
Journal: Behavioral and Brain Sciences (2000)

The paradigmatic assumption that REM sleep is the physiological equivalent of dreaming is in need of fundamental revision. A mounting body of evidence suggests that dreaming and REM sleep are dissociable states, and that dreaming is controlled by forebrain mechanisms. Recent neuropsychological, radiological, and pharmacological findings suggest that the cholinergic brain stem mechanisms that control the REM state can only generate the psychological phenomena of dreaming through the mediation of a second, probably dopaminergic, forebrain mechanism. The latter mechanism (and thus dreaming itself) can also be activated by a variety of nonREM triggers. Dreaming can be manipulated by dopamine agonists and antagonists with no concomitant change in REM frequency, duration, and density. Dreaming can also be induced by focal forebrain stimulation and by complex partial (forebrain) seizures during nonREM sleep, when the involvement of brainstem REM mechanisms is precluded. Likewise, dreaming is obliterated by focal lesions along a specific (probably dopaminergic) forebrain pathway, and these lesions do not have any appreciable effects on REM frequency, duration, and density. These findings suggest that the forebrain mechanism in question is the final common path to dreaming and that the brainstem oscillator that controls the REM state is just one of the many arousal triggers that can activate this forebrain mechanism. The “REM-on” mechanism (like its various NREM equivalents) therefore stands outside the dream process itself, which is mediated by an independent, forebrain “dream-on” mechanism.
Comparison between two fludarabine-based reduced-intensity conditioning regimens before allogeneic hematopoietic stem-cell transplantation: fludarabine/melphalan is associated with higher incidence of acute graft-versus-host disease and non-relapse mortality and lower incidence of relapse than fludarabine/busulfan
Authors: A Shimoni, I Hardan, N Shem-Tov, A Rand, C Herscovici, R Yerushalmi, A Nagler
Journal: Leukemia (2007)
A de novo Philadelphia chromosome-positive acute mixed-lineage leukemia with both major and minorBCR/ABL mRNA transcripts
Authors: Takahisa Tarumoto, Shigehiko Imagawa, Ken Ohmine, Atsushi Mano, Tadashi Nagai, Masaaki Takatoku, Kazuo Muroi, Kiyohiko Hatake, Keiya Ozawa
Journal: American Journal of Hematology (2000)

A patient with a Philadelphia chromosome (Ph)-positive acute mixed-lineage leukemia (AMLL) expressing both major and minor BCR/ABL mRNA transcripts is described. Phenotypic analysis of the leukemic blasts revealed positivity for both myeloid and B-cell lineages. Southern blot analysis showed a rearrangement of the immunoglobulin heavy chain (IgH) gene. Reverse transcriptase polymerase chain reaction (RT-PCR) analysis showed the expression of both major and minor BCR/ABL mRNA transcripts. To our knowledge, this is the first report of AMLL expressing both major and minor BCR/ABL mRNA transcripts and rearrangement of the IgH gene. Am. J. Hematol. 65:72–74, 2000. © 2000 Wiley-Liss, Inc.
MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment
Authors: Jürgen Bernhagen, Regina Krohn, Hongqi Lue, Julia L Gregory, Alma Zernecke, Rory R Koenen, Manfred Dewor, Ivan Georgiev, Andreas Schober, Lin Leng, Teake Kooistra, Günter Fingerle-Rowson, Pietro Ghezzi, Robert Kleemann, Shaun R McColl, Richard Bucala, Michael J Hickey, Christian Weber
Journal: Nature Medicine (2007)
Serotonin promotes tumor growth in human hepatocellular cancer
Authors: Christopher Soll, Jae Hwi Jang, Marc‐Oliver Riener, Wolfgang Moritz, Peter Johannes Wild, Rolf Graf, Pierre‐Alain Clavien
Journal: Hepatology (2009)

In addition to its function as a neurotransmitter and vascular active molecule, serotonin is also a mitogen for hepatocytes and promotes liver regeneration. A possible role in hepatocellular cancer has not yet been investigated. Human hepatocellular cancer cell lines Huh7 and HepG2 were used to assess the function of serotonin in these cell lines. Characteristics of autophagy were detected with transmission electron microscopy, immunoblots of microtubule-associated protein light chain 3(LC3) and p62 (sequestosome 1). Immunoblots of the mammalian target of rapamycin (mTOR) and its downstream targets p70S6K and 4E-BP1 were used to investigate signaling pathways of serotonin. Two different animal models served as principle of proof of in vitro findings. Clinical relevance of the experimental findings was evaluated with a tissue microarray from 168 patients with hepatocellular carcinoma. Serotonin promotes tumor growth and survival in starved hepatocellular carcinoma cells. During starvation hepatocellular carcinoma cells exhibited characteristics of autophagy, which disappeared in serotonin-treated cells. Rapamycin, an inhibitor of mTOR, is known to induce autophagy. Serotonin could override rapamycin by an mTOR-independent pathway and activate common downstream signals such as p70S6K and 4E-BP1. In two tumor models of the mouse, inhibition of serotonin signaling consistently impaired tumor growth. Human biopsies revealed expression of the serotonin receptor HTR2B, correlating with downstream signals, e.g., phosphorylated p70S6K and proliferation. Conclusion: This study provides evidence that serotonin is involved in tumor growth of hepatocellular cancer by activating downstream targets of mTOR, and therefore serotonin-related pathways might represent a new treatment strategy. (HEPATOLOGY 2010.)
CD4 Augments the Response of a T Cell to Agonist but Not to Antagonist Ligands
Authors: Johannes Hampl, Yueh-hsiu Chien, Mark M Davis
Journal: Immunity (1997)

The recognition of peptide variants by the T cell receptor (TCR) has revealed a wide range of possible responses. Here, using a series of CD4+ and CD4− variants of the same T cell hybridoma, we find that while the expression of CD4 converts weak agonists into full agonists, none of the antagonist peptides are efficiently recognized as agonists. Furthermore, in antagonist assays, little difference can be seen in the response of CD4+ and CD4− T cells. Together with previous work showing a marked difference in stability between TCR binding to agonist versus antagonist ligands, these data suggest that CD4 engagement occurs after a TCR-peptide/MHC complex has formed and that it requires a certain minimal half-life of the ternary complex to be fully engaged in signaling.
Evaluation of two immunochromatographic tests (ImmunoCard Toxins A&amp;B, Xpect C. difficile Toxin A&amp;B) and PCR for the detection of Clostridium difficile toxins in faecal samples
Authors: Bram M.W. Diederen, Harold Verbakel, Anneke Bergmans, Marcel F. Peeters
Journal: Journal of Infection (2007)
Secondary prevention of venous thromboembolism
Authors: S. Schulman, J. Douketis
Journal: BMJ (2013)

Emerging anticoagulation treatments not more effective but safer than warfarin

The seemingly endless debate on the optimal duration of anticoagulation after unprovoked venous thromboembolism has been accorded another dimension. With the addition of new oral anticoagulants (NOACs) and aspirin being evaluated for extended duration prophylaxis after three to six months of anticoagulant therapy for venous thromboembolism, there are now alternatives to treatment with vitamin K antagonists. But this has come at the cost of increased uncertainty among physicians who are less familiar with the recent trials of different agents and the interpretation of these results. Adding to the murkiness is the paucity of head to head comparisons between the NOACs and comparisons of each compound to vitamin K antagonists, administered to achieve an international normalised ratio (INR) of 2.0 to 3.0, which has been the reference standard. So far, only one such trial has been performed—dabigatran versus warfarin.1 To clarify the relative benefits and harms of emerging treatments for extended prophylaxis against disease recurrence in patients with unprovoked venous thromboembolism, Castellucci and colleagues (doi:10.1136/bmj.f5133) present a network meta-analysis of 13 randomised trials, totalling 12 000 patients.2

Studies in atrial fibrillation have shown that NOACs are at least as efficacious (dabigatran 110 mg twice daily, rivaroxaban 20 mg daily, apixaban 5 mg twice daily)3 4 5 or more efficacious (dabigatran 150 mg twice daily) as warfarin for ischaemic stroke prevention.3 However, warfarin remains the best treatment for …
PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditioning
Authors: J BOPASSA, R FERRERA, O GATEAUROESCH, E COUTURELEPETIT, M OVIZE
Journal: Cardiovascular Research (2005)

We investigated whether phosphatidylinositol 3-kinase (PI3K) might regulate mitochondrial permeability transition pore (mPTP) opening in hearts reperfused with either low pressure or postconditioning.Male Wistar rat hearts (n=72) were perfused according to the Langendorff technique, exposed to 30 min of ischemia, and assigned to one of the following groups: (1) reperfusion with normal pressure (NP; 100 cm H2O), (2) reperfusion with low pressure (LP; 70 cm H2O), or reperfusion with postconditioning, i.e. 3 episodes of 30 s reperfusion followed by 30 s of ischemia (PostC). Hearts received either the PI3K inhibitors wortmannin or LY294002, or vehicle at the onset of the 60 min reperfusion. Postischemic functional recovery was assessed by rate-pressure product (RPP), and irreversible injury by lactate dehydrogenase (LDH), creatine kinase (CK) and troponin I (TnI) release. Mitochondria were isolated from the reperfused myocardium, and Ca2+-induced mPTP opening was measured using a potentiometric method.Functional recovery was significantly improved in LP and PostC hearts with RPP averaging 13,880+/-810 (LP) and 17,130+/-900 mm Hgxbeats/min (PostC) versus 6450+/-500 mm Hgxbeats/min in NP hearts (p<0.01). LDH release averaged 230+/-30 and 145+/-15 IU/h/g of myocardial tissue in LP and PostC versus 340+/-10 IU/h/g in NP (p<0.05). Wortmannin and LY294002 prevented both RPP improvement and decrease in LDH, CK, and TnI release in LP and PostC groups. The Ca2+ load required to induce mPTP opening averaged 58+/-3 and 52+/-1 nmol/mg mitochondrial proteins in LP and PostC groups, respectively, versus 35+/-4 nmol/mg in the NP group (p<0.01). Wortmannin and LY294002 prevented the beneficial effect in both the LP and PostC groups.These results suggest that PI3K regulates the opening of the mitochondrial permeability transition pore in rat hearts reperfused with low pressure or postconditioning.