tbuckley/cabot-search huggingface dataset:
Regulation of expression of M, B, and mitochondrial creatine kinase mRNAs in the left ventricle after pressure overload in rats.
Authors: H L Fontanet, R V Trask, R C Haas, A W Strauss, D R Abendschein, J J Billadello
Journal: Circulation Research (1991)

Pressure overload of the left ventricle induces synthesis of creatine kinase isoenzymes. To determine whether this response is associated with an altered pattern of creatine kinase gene expression, we induced arterial hypertension in rats by suprarenal aortic banding. After 4 days, left ventricular myocardium from hypertensive (n = 7) and normotensive, sham-operated (n = 5) rats was analyzed for isoenzyme activities by chromatography; M and B creatine kinase subunit protein by Western blot; and M, B, and mitochondrial creatine kinase mRNA by Northern blot. Although total creatine kinase activity increased in hypertensive (1,096 +/- 214 IU/g left ventricle) compared with normotensive rats (648 +/- 81 IU/g left ventricle, p less than 0.01), the relative proportions of the cytoplasmic and mitochondrial isoenzymes did not change. The mass of M and B subunits increased 1.9- and 2.7-fold, respectively, in hypertensive compared with control rats. Similarly, the mRNA for M and B subunits as well as mitochondrial creatine kinase increased 2.6-, 1.6-, and 1.8-fold, respectively, in hypertensive rats compared with control rats. Thus, increased energy requirements in acute pressure overload are met by generalized induction of creatine kinase mRNA and subunit protein and not by an isoenzyme switch.
The Efficacy of Optical and Pharmacological Penalization
Authors: Michael X. Repka, Joann M. Ray
Journal: Ophthalmology (1993)

Purpose: Optical and pharmacological penalization of sound eyes are infrequently used alternatives to occlusion for treating amblyopia. The authors evaluated the efficacy of penalization as their primary treatment of amblyopia. Methods: One hundred sixty-six patients underwent penalization treatment for strabismic or anisometropic amblyopia for a minimum of 3 months. Both atropine and optical penalization methods were used. Results: Visual acuity improved in 67 (77%) of 87 patients treated with optical penalization. There was a significant improvement of the geometric mean visual acuity of the amblyopic eyes from 20/38 to 20/28 (P < 0.001). Visual acuity of 60 (76%) of 79 patients treated with pharmacological penalization improved. There was a significant improvement of mean visual acuity of the amblyopic eyes from 20/61 to 20/40 (P < 0.001). Neither therapy produced an instance of occlusion amblyopia. Thirteen patients discontinued therapy because of blur or discomfort. Conclusions: This study demonstrates that penalization methods are effective methods for the treatment of amblyopia, with a low risk of occlusion amblyopia. Patient acceptance of these methods was excellent. Penalization should be considered more often for the primary treatment of amblyopia. Purpose: Optical and pharmacological penalization of sound eyes are infrequently used alternatives to occlusion for treating amblyopia. The authors evaluated the efficacy of penalization as their primary treatment of amblyopia. Methods: One hundred sixty-six patients underwent penalization treatment for strabismic or anisometropic amblyopia for a minimum of 3 months. Both atropine and optical penalization methods were used. Results: Visual acuity improved in 67 (77%) of 87 patients treated with optical penalization. There was a significant improvement of the geometric mean visual acuity of the amblyopic eyes from 20/38 to 20/28 (P < 0.001). Visual acuity of 60 (76%) of 79 patients treated with pharmacological penalization improved. There was a significant improvement of mean visual acuity of the amblyopic eyes from 20/61 to 20/40 (P < 0.001). Neither therapy produced an instance of occlusion amblyopia. Thirteen patients discontinued therapy because of blur or discomfort. Conclusions: This study demonstrates that penalization methods are effective methods for the treatment of amblyopia, with a low risk of occlusion amblyopia. Patient acceptance of these methods was excellent. Penalization should be considered more often for the primary treatment of amblyopia.
What's in the Cards for ARDS?
Authors: Samuel Vaisrub
Journal: JAMA (1976)

A late arrival to receive due recognition as a catastrophic aftermath of shock and shock-like states, the adult respiratory distress syndrome (ARDS) is now receiving the kind of attention that had previously been accorded to acute tubular necrosis and disseminated intravascular coagulopathy—the two other cataclysmic complications with which it shares a number of characteristics. Like the renal and the coagulation disorders, the pulmonary syndrome has gone—in fact, is still going—through labor pains of terminology. Not to be outdone by the "crush-kidney," "low nephron nephrosis," "vasomotor nephropathy," and others of the former and the "defibrination syndrome," "consumption coagulopathy," and others of the latter, ARDS sports many synonyms of its own—"shock lung," "wet lung," "DaNang lung," "pump lung"—that are vying for acceptance. More important than the terminologic similarity is that of prognosis. It is nearly hopeless in all three disorders, if they are left untreated. Only after scrupulous application of the therapeutic
Assisted dying bill passes second reading in Lords, as support and opposition seem equally divided
Authors: C. Dyer
Journal: BMJ (2014)

The Assisted Dying Bill was given a second reading in the House of Lords on 18 July and will go on to its committee stage, after peers who oppose it accepted that it should be scrutinised further.

Among more than 120 peers who spoke in the marathon second reading debate, opposition and support for the bill were split roughly 50:50.

The bill’s sponsor, the former Labour lord chancellor Charles Falconer, feared that peers who are against it would put down a wrecking amendment to derail it. But no one did, and it could complete its remaining stages in the Lords by the end of the year, although attempts to wreck it could still come at committee or …
Phagocytosis of codeveloping megakaryocytic progenitors by dendritic cells in culture with thrombopoietin and tumor necrosis factor-α and its possible role in hemophagocytic syndrome
Authors: Kunie Saito, Makoto Hirokawa, Kayo Inaba, Hiroshi Fukaya, Yoshinari Kawabata, Atsushi Komatsuda, Junsuke Yamashita, Kenichi Sawada
Journal: Blood (2005)
The Circulating Thyroid Hormones in Thyrotoxicosis
Authors: M. L. Wellby, B. S. Hetzel, B. F. Good
Journal: BMJ (1963)

The application of the technique of paper chromato- graphy and the use of radioactive iodine resulted in the demonstration of thyroxine (T4) as the major iodine-containing component in the plasma (Laidlaw, 1949; Taurog et al., 1950).Thyroxine was also found to be the major circulating iodine compound in thyrotoxicosis by Rosenberg (1951).In 1952 Gross and Pitt-Rivers demonstrated the presence of 3-5-3'-L triiodothyronine (T.) in the serum of four thyrotoxic patients and two patients with thyroid carcinoma.They suggested that there was no qualitative difference beween the iodine compounds present in the circulation of normal and thyrotoxic subjects.Subsequent studies (Benua and Dobyns, 1955; Dingledene et al., 1955; Arons and Hydovitz, 1959) have confirmed the findings of Gross and Pitt-Rivers in thyrotoxicosis.T4 was found to be the major component, while T3 was detected in a variable proportion of thyrotoxic patients after radio- active iodine (1: 1l) administration.The presence of triiodothyronine in the plasma of both normal and thyrotoxic subjects was confirmed by Maclagan et al. (1957) using a chemical method of detection.This method made use of the very sensitive ceric-sulphate-arsenious-acid catalytic system for detecting iodine.Their finding eliminated the
Abstract 5401: The influences of morphine on dendritic cell-mediated immunity
Authors: Ming-Cheng Chang, Yu-Li Chen, Ching-Ting Huang, Ying-Cheng Chiang, Chia-Yen Huang, Wen-Fang Cheng, Tzer-Ming Chen
Journal: Cancer Research (2012)

Abstract Morphine is a widely-used drug for analgesics and drug abuse. Previous studies have also demonstrated that the widely used as an anesthetic agent as well as adjuvant for the treatment of cancer pain and neuropathic pain, will bring harmful effects on specific immune system. Furthermore, the suppressed immune function may lead to postoperative infection and postoperative dissemination of carcinoma. Our research team has confirmed that morphine could promote tumor growth in naïve immunocompromised mice in our previous project, and morphine could suppress the proliferative ability of T lymphocytes even erased the tumor protection effects enhanced by tumor vaccines in vivo. However, these apoptotic phenomena could not explain the complete reasons that morphine induced tumor progression. The antigen processing and presenting activity enhanced by antigen presenting cells is the main cause in tumor development, especially in dendritic cells. The tumorgenesis is always associated with the low antigen presentation activity, and it results the poor recognization by cytotoxic T cells even causes the immuno-escape responses. In the present study, we confirmed that the efficiency of bone marrow monocytes differentiate into dendritic cells was significantly decreased after morphine stimulation. Under high dose morphine treatment, more than 30 % of differentiation efficiency was eliminated in 6 days incubation. Besides, the expression of co-stimulation factor CD80 and CD86 were both decrease after morphine treatment. Furthermore, cytokine expression including IL-6 and TNF-α were both inhibited, however, only IL-10 was slightly increase after morphine stimulation. Besides, the antigen processing and presenting activity of ex-vivo bone marrow-derived dendritic cells were reduced after morphine stimulation. These results suggested that morphine might reduce the process of dendritic cells maturation. These results provided the complete molecular mechanism and the correlation between morphine and immunity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5401. doi:1538-7445.AM2012-5401
710 DIFFERENTIAL TLR RESPONSES IN HBEAG SERCONCONVERTERS WITHIN 4 WEEKS OF PEGYLATED IFN THERAPY
Authors: K. Visvanathan, N.A. Skinner, A.J.V. Thompson, F. Weilert, E. Gane, W. Abbott, P. Desmond, S.A. Locarnini
Journal: Journal of Hepatology (2008)
Severe thrombocytopenia following oral cholecystography with iocetamic acid
Authors: Carmen L. G. Insausti, Fuad Lechin, Bertha van der Dijs
Journal: American Journal of Hematology (1983)

Abstract We report the first case of severe thrombocytopenia occurring after ingestion of a widely used cholecystographic medium, iocetamic acid. The patient had not been given any treatment before he received the gallbladder contrast medium. Onset of symptoms was acute, and the clinical course was benign with complete recovery after one week. Bone marrow aspiration showed increased numbers of megakaryocytes, suggesting that platelets were rapidly removed from circulation. In vitro tests for antiplatelet antibodies were not performed because iocetamic acid is insoluble in aqueous solutions. Since only a few cases of thrombocytopenia following ingestion of iodine‐compounds have been reported, it seems highly unlikely that purpura will be, in the future, a major hazard in cholecystography. However, it would be wise to question patients as to any prior sensitivity to iodine before proceeding with oral cholecystography.
Ventrosuspension of Uterus.
Authors: Thor Moeller
Journal: JAMA (1899)

Hillsboro, N. D., Aug. 8, 1899. <h3>To the Editor.</h3> —In connection with the recommendation of Dr. J. Wesley Bovee, to utilize a bundle of the rectus for ventrosuspension of the uterus, I wish to draw your attention to the successful performance and result of this idea in a case operated on by me in 1896, reported to the last meeting of the North Dakota State Medical Society and printed in the<i>Northwestern Lancet</i>for June 15, 1899. This patient was well one year after. I have endeavored to get the subsequent history as to conceptions, labors, etc., but have not yet succeeded. Yours very truly, [All the mention we find in the paper referred to is contained in the following very brief report of a case: "Case 15.—Mrs. S., March 19, 1896. Ventrosuspension of the uterus by a bundle of the rectus muscle and fascia for retroflexion. Discharged in three
Dilated Cardiomyopathy in Transgenic Mice With Cardiac-Specific Overexpression of Tumor Necrosis Factor-α
Authors: Toru Kubota, Charles F. McTiernan, Carole S. Frye, Susan E. Slawson, Bonnie H. Lemster, Alan P. Koretsky, A. Jake Demetris, Arthur M. Feldman
Journal: Circulation Research (1997)

Abstract The failing human heart expresses tumor necrosis factor-α (TNF-α). However, its pathophysiological significance is not clear. We previously reported that robust overexpression of TNF-α in the murine heart causes lethal myocarditis. In this study, we modified the transgene to reduce the production of TNF-α by preserving the destabilizing sequence in TNF-α cDNA. Expression was driven by the murine α-myosin heavy chain promoter. Use of this modified construct allowed us to establish a murine transgenic line (TG). TG offspring were examined at 6, 12, and 24 weeks. All showed a significantly higher heart weight–to–body weight ratio. Northern blot analysis confirmed the expression of transgene in the heart, and enzyme-linked immunosorbent assay demonstrated the presence of TNF-α protein. The TG heart demonstrated a mild, diffuse, lymphohistiocytic interstitial inflammatory infiltrate. Cardiomyocyte necrosis and apoptosis were present but not abundant. Magnetic resonance imaging showed that the TG heart was significantly dilated with reduced ejection fraction. Although the left ventricular dP/dt max was not different at baseline, its responsiveness to isoproterenol was significantly blunted in TG. Atrial natriuretic factor was expressed in the TG ventricle. A group of TG died spontaneously, and subsequent autopsies revealed exceptional dilatation of the heart, increased lung weight, and pleural effusion, suggesting that they died of congestive heart failure. The cumulative mortality rate at 6 months was 23%. In conclusion, the mouse overexpressing TNF-α recapitulated the phenotype of congestive heart failure. This provides a novel model to elucidate the role of this cytokine in the development of congestive heart failure.
Epitope Landscape in Breast and Colorectal Cancer
Authors: Neil H. Segal, D. Williams Parsons, Karl S. Peggs, Victor Velculescu, Ken W. Kinzler, Bert Vogelstein, James P. Allison
Journal: Cancer Research (2008)

Abstract The finding that individual cancers contain many mutant genes not present in normal tissues has prompted considerable interest in the cancer epitope landscape. To further understand such effects, we applied in silico–based epitope prediction algorithms and high throughput post hoc analysis to identify candidate tumor antigens. Analysis of 1,152 peptides containing missense mutations previously identified in breast and colorectal cancer revealed that individual cancers accumulate on average ∼10 and ∼7 novel and unique HLA-A*0201 epitopes, respectively, including genes implicated in the neoplastic process. These data suggest that, with appropriate manipulation of the immune system, tumor cell destruction in situ may provide a polyvalent tumor vaccine without a requirement for knowledge of the targeted antigens. [Cancer Res 2008;68(3):889–92]
An Intact Cuticle in Distal Tissues Is Essential for the Induction of Systemic Acquired Resistance in Plants
Authors: Ye Xia, Qing-Ming Gao, Keshun Yu, Ludmila Lapchyk, DuRoy Navarre, David Hildebrand, Aardra Kachroo, Pradeep Kachroo
Journal: Cell Host & Microbe (2009)
Acute Fluid Replacement in the Therapy of Shock
Authors: Lloyd D. MacLean
Journal: JAMA (1975)

In this multiauthored text, with 38 papers, the presentations range from excellent to irrelevant, but most are in the former category. Varied and frequently opposing arguments appear throughout, especially on appropriate regimens for volume replacement and dangers to pulmonary function. Despite these limitations the volume is an excellent summary of the "state of the art," with particular reference to blood, blood products and other volume replacements that are now or will in the future be useful in the therapy of hypovolemia. The section on clinical implications of severe blood loss is particularly interesting. Surprisingly few controlled clinical studies are available to support therapeutic regimens but, overall, the text is practical and will be useful to clinician and researcher alike. The editors are calm and organized in the summary and imply that several routes to successful therapy are possible, that good patient care need not be a research project, and that
Testing for hepatitis C virus in Italy.
Authors: R M Dorizzi, R Schiavon, A Disperati, E Capuzzo, P Piccoli
Journal: BMJ (1991)

ELISA would have failed to prevent transmission.Interestingly, these donors have given 15, 23, and 27 donations and have never been implicated in any other case of transmission of hepatitis.As far as
P138p66ShcA adaptor protein facilitates heart rupture via activation of MMP-2 in an in vivo model of myocardial infarction in mice.
Authors: A Baysa, A Maghazachi, F Di Lisa, A Carpi, M Giorgio, J Vaage, G Valen
Journal: Cardiovascular Research (2014)

Purpose: Heart failure is a growing problem worldwide. Cardiac remodeling, which features aseptic inflammation, metalloproteinase (MMP) activation and induction of matricellular proteins, contributes to heart failure progression after myocardial infarction (MI). The ShcA gene encodes three isoforms: p46-, p52- and p66ShcA, which are crucial for embryonic development of the heart. The p66ShcA isoform regulates mitochondrial respiration and oxidative stress. p66ShcA deletion protects against acute myocardial ischemia ex vivo. We studied the role of p66ShcA in chronic cardiac ischemia and cardiac remodeling in vivo. We aimed to find whether (a) p66ShcA expression was induced by MI, (b) p66ShcA was involved in cardiac remodeling and (c) to elucidate underlying mechanisms with focus on MMP and inflammation.

Materials and Methods: MI was induced in vivo via occlusion of the left descending coronary artery in C57Bl/6 male mice. Cardiac expression of p66ShcA in wild type mice (WT) was evaluated serially postinfarction (n=105). The functional effects of p66ShcA were evaluated in knockout mice (p66KO) compared to WT (n=72). Hearts from WT and p66KO were harvested three days postinfarction to evaluate infarct size, expression of MMP and matricellular proteins. Simultaneously, spleens were collected for splenocytes isolation (n=5 in each group). Interleukins expression in the splenocytes was assessed by flow cytometry. Six weeks after MI, survival, heart function and cardiac fibrosis were evaluated (n=19 per group). Mouse embryonic fibroblasts with p66ShcA knockdown were used to study MMP-2 expression.

Results: p66ShcA expression increased transiently during the first weeks postinfarction. p66KO mice had increased survival after MI (p=0,005) and reduced occurrence of heart rupture (p=0,04). Three days postinfarction, cardiac MMP-2 and matricellular proteins, such as connective tissue growth factor and thrombospondin-1, were down-regulated in the hearts of p66KO compared to WT mice. After MI, p66KO splenocytes had a lower expression of IL-17 and IL-4 than WT mice. Six weeks after MI, p66KO mice had attenuated both fibrosis and left ventricular dilatation. At the same time, p66ShcA depletion in vitro attenuated activation of MMP-2.

Conclusions: The p66ShcA isoform is involved in adverse cardiac remodeling after myocardial infarction. Deletion of p66ShcA prevented cardiac rupture and improved survival. The underlying mechanism was partly elucidated: p66ShcA activates MMP-2 and regulates expression of IL-4 and IL-17. The p66ShcA can be a potential target for preventing adverse cardiac remodeling postinfarction.
Tuberculosis Case-Finding Study
Authors: William E. Mosher
Journal: JAMA (1963)

The usefulness of routine tuberculin testing as a case-finding technique was evaluated in a joint study by the Buffalo and Erie County Tuberculosis and Health Association and the Erie County Department of Health. Meticulous follow-up study of all household contacts of positive reactors to tuberculin was carried out. Six infants in this study were found to be positive reactors and were later confirmed as having primary tuberculosis. In addition, three adult contacts were found to have active disease, and one sibling was diagnosed as having primary tuberculosis. The rate of active disease, including primary tuberculosis and that in adults found directly or indirectly as a result of this program, was 5.9 cases/1,000 infants tested with tuberculin. The tuberculin reactor rate was 3.6 cases/1,000. The cost of finding an active case of tuberculosis was approximately $501 per case, which is considerably below that of mass x-ray programs.
"MALARIA TREATMENT OF PARESIS"
Authors: Watson W. Eldridge
Journal: JAMA (1925)

To the Editor:  —I have read the letter of Dr. M. K. Amdur of Cleveland (The Journal, May 2, p. 1375) commenting on my article inThe Journal, April 11, on the malaria treatment of paresis. Since my article was written, a second group of forty-seven patients with paresis, has been treated, and the inoculations were made practically as described by Dr. Amdur, except that none were made intravenously. In addition, those who failed of inoculation in the first group reported and those who were still living were reinoculated. In spite of this there were thirteen patients who failed to develop malaria. Of the second group mentioned, two were inoculated with infected mosquitoes. Of these two, one had malaria and the other did not.  I differ with Dr. Amdur's statement about the nontransmissibility of artificial malaria. It is not uncommon for asexual forms of the parasite in the human blood
REPORT ON AN EPIDEMIC OF CEREBRO-SPINAL MENINGITIS.Read in the Section of the Practice of Medicine and Physiology, at the Forty-second Annual Meeting of the American Medical Association, held at Washington, D. C., May, 1891.
Authors: J. S. NOWLIN
Journal: JAMA (1891)

In presenting the subject of Cerebro-Spinal Meningitis, the first thought I offer is that our nomenclature in this as in many other diseases leads to an erroneous view of the pathology and treatment. Our authors have almost universally written as though the inflammatory action found in the coverings of the brain and spinal column was the original lesion to be combated. It will not be necessary, for the purposes designed in this paper, to deny the fact that an inflammatory action may be found in many cases. The error, as I conceive it to be, and to which I would direct attention, is that the inflammation, if it does exist, in a given case, is not the disease to be treated, but a sequence. It is only necessary to call attention to the great number of deaths occurring within five days, with no exudation in these tissues evincing inflammation. It
A prospective randomized trial between the prophylactic endoscopicvariceal ligation and propranolol administration for prevention offirst bleeding in cirrhotic patients with high-risk esophageal varices
Authors: I.H. Song, J.W. Shin, I.H. Kim, J. Choi, C.Y. Lim, J.W. Kim, I.H. Roe
Journal: Journal of Hepatology (2000)