tbuckley/cabot-search huggingface dataset:
Cumulative inhibitory effect of low-dose aspirin on vascular prostacyclin and platelet thromboxane production in patients with atherosclerosis.
Authors: B B Weksler, K Tack-Goldman, V A Subramanian, W A Gay
Journal: Circulation (1985)

The relationship between the antithrombotic and antiplatelet effects of aspirin is complex, since aspirin influences other systems that protect against thrombosis as well as inhibiting platelet function. We investigated possible cumulative effects of low-dose aspirin on vascular production of prostacyclin in patients with documented atherosclerotic cardiovascular disease. Candidates for coronary artery vein graft bypass ingested 20 mg of aspirin daily during the week before surgery, and platelet aggregation, platelet formation of thromboxane A2 (TXA2), aortic and saphenous vein production of prostacyclin (PGI2), and hemostatic status were measured at the time of the bypass surgery. Low-dose aspirin markedly inhibited platelet aggregation responses and reduced TXA2 generation by greater than 90%, effects similar to those observed with much higher doses of aspirin. Both aortic and saphenous vein production of PGI2 were inhibited by 50% compared with PGI2 produced by vascular tissues of control subjects who received no aspirin preoperatively (51 +/- 10 pg 6-keto-PGF1 alpha/mg aortic wet weight [mean +/- SEM] in aspirin-treated subjects vs 130 +/- 16 pg/mg in control subjects, and 71 +/- 8 pg/mg saphenous vein wet weight vs 131 +/- 17 pg/mg). Blood loss at surgery was not significantly increased by preoperative low-dose aspirin as measured by chest tube drainage (754 +/- 229 ml in aspirin-treated subjects vs 645 +/- 271 ml in control subjects), hematocrit nadir (31.2 +/- 1.9% vs 31.8 +/- 1.7%), or transfusions (2.2 +/- 1.3 units of red blood cells vs 2.2 +/- 1.7 units).(ABSTRACT TRUNCATED AT 250 WORDS)
THE PSYCHOSOMATIC APPROACH IN MEDICINE
Authors: HAROLD I. KAPLAN
Journal: Annals of Internal Medicine (1957)

Article1 June 1957THE PSYCHOSOMATIC APPROACH IN MEDICINEHAROLD I. KAPLAN, M.D., HELEN S. KAPLAN, Ph.D.HAROLD I. KAPLAN, M.D.Search for more papers by this author, HELEN S. KAPLAN, Ph.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-46-6-1063 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFrom a multicausal point of view, psychologic factors play a rôle in all disease processes,1although the importance of this rôle is highly variable. Lewis2estimated, as a result of his evaluation of recent psychomedical surveys, ". . . that psychological disturbances were responsible, wholly or in part, for the illnesses of . . . 47% of . . . medical patients. . . ." The patients he studied were representative of the type usually seen in general practice. The disorders Lewis considered to be psychogenic included those which are wholly psychologic or functional in origin without any demonstrable organic...Bibliography1. Alexander F: Psychosomatic medicine, 1950, W. W. Norton Co., New York. Google Scholar2. Lewis BI: Psychosomatic disorders and the non-psychiatrist, J. A. M. A. 150: 776, 1952. CrossrefMedlineGoogle Scholar3. : Diagnostic and statistical manual: mental disorders, 1952, American Psychiatric Association, Washington, D. C. Google Scholar4. Mahl G: Anxiety, hydrochloric acid secretion, and peptic ulcer etiology, Psychosom. Med. 12: 158, 1950. CrossrefMedlineGoogle Scholar5. Knight J: The story of my psychoanalysis, 1952, Pocket Books, Inc., New York. Google Scholar6. Levine M: Psychotherapy in medical practice, 1949, The Macmillan Company, New York. Google Scholar7. Wolberg L: The technique of psychotherapy, 1954, Grune and Stratton, New York. Google Scholar8. Ebaugh FG: Iatrogenicity in medicine, J. Michigan M. Soc. 49: 79, 1950. MedlineGoogle Scholar9. Kaplan HI: The combined medical-psychiatric treatment of psychosomatic disorders: a collaboration between physicians, Dis. Nerv. System, in press. Google Scholar10. Kaplan HI: The psychosomatic concept of peptic ulcer, J. Nerv. and Ment. Dis. 123: 93, 1956. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, N. Y.*Received for publication June 28, 1956.From the Department of Psychiatry, New York Medical College, Flower and Fifth Avenue Hospitals, New York, N. Y.Requests for reprints should be addressed to Harold Kaplan, M.D., 110 East Eighty-seventh Street, New York 28, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 June 1957Volume 46, Issue 6Page: 1063-1078KeywordsEmotionsPatient advocacyPrimary care Issue Published: 1 June 1957 PDF downloadLoading ...
Silica and Pulmonary Lesions-Reply
Authors: N. V. Vallyathan
Journal: JAMA (1981)

<h3>In Reply.—</h3> The comments of Dr Jones are, at least in part, correct, and we appreciate his interest. Unfortunately, he would have us attempt to make more of our findings than the observations permit. In our article we attempted to question contemporary concepts rather than to provide definitive answers. We concur with Dr Jones that retrospective autopsy studies are subject to limitations and uncontrolled selective influences. Unfortunately, studies to permit the accumulation of appropriate information are not now possible, because antemortem and postmortem data have never been accumulated in an organized fashion. Indeed, our article closed with a plea for carefully designed correlative studies to relate postmortem findings to environmental dust exposure during life. Experimental studies in animals have shown that "nonspecific" fibrotic lesions develop in animals experimentally exposed to silica. Parkes<sup>1</sup>suggests that "when the proportion of free silica to nonfibrogenic dust in the total dust inhaled is low,
Proposed single budget for health and social care has faced "institutional resistance," MPs are told
Authors: M. Limb
Journal: BMJ (2014)

An independent commission that called for radical reform of health and social care and more funding has faced “institutional resistance,” its leader had told MPs.

Kate Barker, a business economist at the King’s Fund, chaired a review published in September1 that said England should move to a single ringfenced budget for health and social care, with a single commissioner to simplify procedures and rescue a social care system in danger of collapse. She was questioned about the commission’s findings by the Commons health select committee on 18 November.

The independent commission recommended that social care should be provided free at the point of use for more people and paid for by tax and welfare changes that would affect middle aged and elderly people. It estimated that providing free social care for all people whose needs …
654 A RETROSPECTIVE STUDY ON INTRAHEPATIC CHOLESTASIS OF PREGNANCY: MARKERS OF PREMATURE DELIVERY
Authors: F. Alessandrelli, F. Azzaroli, V. Feletti, A. Lisotti, F. Buonfiglioli, M. Montagnani, A. Colecchia, D. Festi, F. Lodato, E. Roda, G. Mazzella
Journal: Journal of Hepatology (2009)
THE INFLUENCE OF THE FOODSTUFFS UPON THE SUSCEPTIBILITY OF THE LIVER TO INJURY BY CHLOROFORM, AND THE PROBABLE MECHANISM OF THEIR ACTION 12
Authors: Samuel Goldschmidt, Harry M. Vars, Isidor S. Ravdin
Journal: Journal of Clinical Investigation (1939)

In a previous publication, data were presented which show that anesthesia produced by the in- halation of chloroform or divinyl ether, volatilized by a stream of oxygen, results in much less dam- age to the liver of the dog than when air is used as the volatilizing agent (1).Evidence already presented (2) reveals, in the dog, no difference in the rate or the degree of discharge of hepatic glvcogen, or the height to which the blood sugar rises, or the amount of fatty infiltration, when the chloroform is volatilized with air or with oxygen, provided a very marked anoxemia does not exist.The protective action of oxygen appears not to be associated with these metabolic changes.In the course of this work our attention was directed to the relation of the dietary to the susceptibility of the animals to liver damage by chloroform, and thus to the present investigation.That a diet high in carbohydrate is protective, and that a diet high in fat induces maximal susceptibility of the hepatic cells, when the liver is exposed to chloroform, has received much con- firmatory support since first reported by Opie and Alford in 1914 (3, 4, 5, 1 ).Diets rich in protein have, also, been found to be protective against the necrotizing action of chloroform.Its value has been regarded as either inferior (3, 4), or at least equal to (5) a carbohydrate diet, in ameliorating the deleterious effects of chloroform.Fasting also intensifies to a great degree the susceptibility of the hepatic cells to injury by chloroform, comparable to (4), or exceeding (5) that which results from a high fat intake.It should be emphasized that our present stud- ies and discussion do not include the late effects
Mammary Gland Selective Excision of <i>c-Jun</i> Identifies Its Role in mRNA Splicing
Authors: Sanjay Katiyar, Xuanmao Jiao, Sankar Addya, Adam Ertel, Yolanda Covarrubias, Vanessa Rose, Mathew C. Casimiro, Jie Zhou, Michael P. Lisanti, Talat Nasim, Paolo Fortina, Richard G. Pestell
Journal: Cancer Research (2011)

The c-jun gene regulates cellular proliferation and apoptosis via direct regulation of cellular gene expression. Alternative splicing of pre-mRNA increases the diversity of protein functions, and alternate splicing events occur in tumors. Here, by targeting the excision of the endogenous c-jun gene within the mouse mammary epithelium, we have identified its selective role as an inhibitor of RNA splicing. Microarray-based assessment of gene expression, on laser capture microdissected c-jun(-/-) mammary epithelium, showed that endogenous c-jun regulates the expression of approximately 50 genes governing RNA splicing. In addition, genome-wide splicing arrays showed that endogenous c-jun regulated the alternate exon of approximately 147 genes, and 18% of these were either alternatively spliced in human tumors or involved in apoptosis. Endogenous c-jun also was shown to reduce splicing activity, which required the c-jun dimerization domain. Together, our findings suggest that c-jun directly attenuates RNA splicing efficiency, which may be of broad biologic importance as alternative splicing plays an important role in both cancer development and therapy resistance.
New pharmacological models needed to care for dying patients at home
Authors: S. Head
Journal: BMJ (2013)

<h3>Background</h3> Severe hemorrhagic transformation (HT) after mechanical thrombectomy predicts a poor clinical outcome in acute ischemic stroke. To better understand the mechanism of HT, we investigated the role of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) in HT after reperfusion during acute stroke and whether NOX2/4 inhibitor VAS2870 reduces reperfusion-induced HT after mechanical recanalization. <h3>Methods</h3> A model of reperfusion-induced HT was established in rats (n=182) with hyperglycemic challenge and 5 h middle cerebral artery occlusion followed by 19 h reperfusion. NOX inhibitor VAS2870 was delivered intravenously 30 min before reperfusion. Infarct volume, brain water content, HT, neurological score, mortality rate, blood–brain barrier (BBB) damage, neuronal apoptosis, and reactive oxygen species were determined at 24 h after cerebral ischemia. The expressions of NOX1, NOX2, NOX4, and BBB-associated proteins were measured. <h3>Results</h3> NOX2 and NOX4 upregulation and severe HT were observed in hyperglycemic rats after cerebral ischemia/reperfusion. VAS2870 suppressed oxidative stress, neuronal apoptosis, and NOX2/4 upregulation in the ischemic hemisphere. VAS2870 reduced infarct volume (17.2±5.3% vs 37.4±9.2%, p&lt;0.01) and the frequency of reperfusion-induced parenchymal hematoma (29.7% vs 59.5%, p&lt;0.05) at 24 h after ischemia compared with the ischemia/reperfusion group. VAS2870 attenuated brain edema and reduced reperfusion-induced BBB breakdown, resulting in improved neurological outcome (neurological deficit score 1.43±0.50 vs 2.43±0.93, p&lt;0.001) and reduced mortality (11.9% vs 64.1%, p&lt;0.001). <h3>Conclusions</h3> NOX2 and NOX4 may mediate HT in rats with large vessel stroke after mechanical reperfusion. Infusion of NOX inhibitor VAS2870 before mechanical thrombectomy represents a novel adjunctive therapeutic strategy to prevent reperfusion-induced HT and improve outcome of acute stroke treatment.
Ethical, social and legal implications of genetic testing in liver disease
Authors: Dirk J. van Leeuwen, James L. Bernat
Journal: Hepatology (2006)

Advances in molecular genetics challenge the hepatology community to understand and implement genetic knowledge. Despite excitement about the potential benefits of new genetic information, concerns have been raised about the inappropriate use of genetic testing, clinicians' incorrect ordering and misinterpretation of test results, and discrimination in employment and insurability based on tests results. Among the public there is fear and mistrust, in part based on horrifying historical events that were gross violations of medical ethical standards. Clinicians, scientists, patient advocacy groups, and government agencies worldwide are debating the optimal legal protections to prevent abuse. In addition, these groups are developing clinical guidelines for optimal use. Traditional ethical and legal standards of confidentiality between physicians and their patients are under scrutiny. A new principle, "the duty to warn," is emerging that has applications specific to genetic testing and may conflict with the duty to maintain patient confidentiality. Emerging ethical, legal, and social issues involve the appropriate use and protection of confidential data in tissue and serum banks. Education of the profession and the public at many levels will increase the likelihood that the unraveling of the human genome will maximally benefit society. If fear of genetic testing can be alleviated, selection bias in research could be reduced. Professional and lay organizations concerned with liver disease should consider a more active role in the public and professional debate, and foster education at all levels.
Mechanical aids to ventilation for use in the field.
Authors: M G Harries
Journal: BMJ (1980)

babies) given infusions of the drug for preeclampsia.7It therefore seems possible, but is not proved, that therapeutic doses of chlormethiazole may predispose old people to hvpothermia.However, wvhether chlormcthiazole is any better or worse than other hypnotics in this respect is not known, and somc research is needed.
Heparin rescues factor V Leiden–associated placental failure independent of anticoagulation in a murine high-risk pregnancy model
Authors: Jianzhong An, Magarya S. Waitara, Michelle Bordas, Vidhyalakshmi Arumugam, Raymond G. Hoffmann, Brian G. Petrich, Uma Sinha, Paula E. North, Rashmi Sood
Journal: Blood (2013)
Phakomatosis pigmentokeratotica associated with hypophosphataemic vitamin D-resistant rickets: improvement in phosphate homeostasis after partial laser ablation
Authors: A. Saraswat, S. Dogra, A. Bansali, B. Kumar
Journal: British Journal of Dermatology (2003)

Sir, The term epidermal naevus syndrome (ENS) is applied to a group of phenotypically distinct syndromes having an association of an epidermal naevus with various neurological, ophthalmological and skeletal anomalies. A relatively recent addition to this group has been named phakomatosis pigmentokeratotica (PP), which comprises a sebaceous naevus (SN), speckled and lentiginous naevi, hemiatrophy and neurological defects.1 Rarely, vitamin D‐resistant rickets has been described in association with the ENS.2–5 It has been proposed that this is a type of tumour‐induced osteomalacia, which is a rare association of a mesenchymal neoplasm with vitamin D‐resistant rickets. We report the first case of PP with associated hypophosphataemic vitamin D‐resistant rickets (HVRR). Carbon dioxide (CO2) laser ablation of the SN resulted in improvement of phosphate homeostasis, confirming the lesion as the cause of the hypophosphataemia. A 22‐year‐old man, born at term to nonconsanguineous parents, presented with multiple pigmented skin lesions and bony deformities. Since birth, he had numerous, light brown areas of speckled pigmentation, mostly localized to the left side of the body, on the neck, shoulder, arm, lower back and thigh. Several 0·2–5 cm deeply pigmented papules and plaques, some with overlying coarse hair, were also present. A large brownish lesion on the left cheek was observed at the age of 3 years, which became corrugated and reddish‐tan in colour at puberty (Fig. 1a). There was no relevant family history. A biopsy from a hairy pigmented lesion revealed the characteristic histopathology of a congenital melanocytic naevus, and the facial lesion was confirmed to be an SN.
Reduced positive inotropic effects in diseased human ventricular myocardium
Authors: L. BROWN, B. LORENZ, E. ERDMANN
Journal: Cardiovascular Research (1986)

In isolated contracting human ventricular myocardium taken from patients undergoing mitral valve replacement the positive inotropic effects of calcium, isoprenaline, dobutamine, dopamine, histamine, milrinone, isobutylmethylxanthine, and theophylline were determined. Calcium (15 mmol·litre−1) produced an increase in force of contraction similar to that of a maximal effective concentration of ouabain (1 × 10−7 mol·litre−1); significantly lower maximal effects were measured with all the other positive inotropic compounds tested. The addition of these positive inotropic substances after a stable maximum effect with ouabain (1 × 10−7 mol·litre−1) had been reached increased the incidence of toxicity without producing any further inotropic effects. These results suggest that inotropic substances acting through cyclic adenosine monophosphate give less than the maximum inotropic response in isolated muscle from diseased human hearts, which is not additive to the maximal ouabain induced inotropy.
CINCA syndrome (chronic infantile neurological cutaneous articular syndrome). A case report of a superficial resemblance to systemic-onset JRA with mutation in CIAS 1 gene from Thailand*1
Authors: K. Kittisarapong, N. Thavonpanich, S. Benjapolpitak, G. Basile
Journal: Journal of Allergy and Clinical Immunology (2004)
EXPERIENCE WITH CHOLECYSTOGRAPHY IN CASES COMING TO OPERATION
Authors: C. C. McCOY
Journal: JAMA (1926)

Since the introduction of cholecystography by Graham and Cole of St. Louis, numerous articles have appeared paying tribute to it as a measure of great value in the diagnosis of gallbladder disease. There have been, however, relatively few reports of series of consecutive cases coming to operation in which the cholecystographic diagnoses have been correlated with the findings at the operating table and in the pathologic laboratory. On this account, it has seemed to us that it might be of some value to present these correlations for our patients who have been operated on, and to tabulate, so far as it seems feasible, the similar reports found in the literature. It is perhaps advisable to preface the presentation of our own cases by a brief summary of the technic and point of view in interpretation that we have followed, although these have been copied in all essential features from the
The challenge of preventing spree killings
Authors: J. H. M. Crichton
Journal: BMJ (2012)

We know something about who perpetrates them and why, but not how to prevent them

The tragic shooting in Newtown, Connecticut on 14 December raises recurring questions. Who commits such atrocities and why? How can they be prevented? Despite their seemingly regular occurrence in the United States, the relative rarity of spree killings challenges attempts to understand them scientifically. Yet broad themes emerge if we examine published non-randomized samples that may help answer such questions.

Mass, or multiple, homicide has been defined as a single incident in which five or more victims are injured, at least three of them fatally.1 Mass murderers have been categorized according to their style: family annihilators, disciple murders, pseudo-commanders, disgruntled employees, and set and run killers.2 The events themselves can be divided into instrumental killings, victim specific killings, and massacres.3 Massacres are indiscriminate killings where victims are chosen by chance, situation, or peripheral affiliation. The autogenic massacre, which is distinct from the civil or military massacre, is carried out by an individual (or very occasionally more than one individual), serves …
CEREBRAL VASCULAR LESION
Authors: Meyer Naide
Journal: JAMA (1960)

<h3>To the Editor:—</h3> I would like to comment on the editorial on cerebral vascular accidents inThe Journal, Aug. 6, page 1584. The word "accidents" should be dropped when referring to cerebral vascular occlusions or hemorrhage. A cerebral vascular incident is no more an accident than is a coronary artery occlusion. This comment is prompted by a death certificate in which a resident in a hospital wrote as the cause of death "cerebral vascular accident." It is just as easy to use the term "cerebral vascular lesion," if one does not have a more specific diagnosis. The implication of the word "accident" is such that we should drop the use of this term, since it serves no useful purpose in this connection.
289. Highly Inducible and Prostate Specific Oncolytic Adenovirus with E1A-AR Chimera
Authors: Ying Li, Chien-Lun Chen, David C. Johns, Ronald Rodriguez
Journal: Molecular Therapy (2005)

Top of pageAbstract
Previously, we demonstrated prostate-specific replication and passive cell lysis using E1A driven by a prostate-specific antigen promoter (PSA) and enhancer (PSE). However, the expression of E1A relies on promoters that utilize the androgen receptor (AR) for optimal function. Recently we have discovered that E1A and AR are mutually antagonistic in their transcriptional regulation. We demonstrate that a chimeric fusion of AR with the E1A converts an androgen receptor repressor to a co-activator. Here, we describe the features of conditionally replication-competent adenoviruses (CRADs) with E1A-AR chimeric expression in prostate cancer cells and non-prostate cancer cells.

We constructed a series of recombinant chimeric E1A-AR viruses including wild type AR (E1A-ARwt), transactivation domain (E1A-TAD), and a full-length AR with a point mutation in the ligand binding domain (E1A-ARC685Y), under the control of the prostate-specific enhancer (PSE) and rat probasin promoter (PBN). The E1A function of these viruses was evaluated in prostate cancer cells and non-prostate cancer cells using an adenovirus with Fiber-IRES-GFP lacking E1A as a reporter.

The wild type Ad5 with an E3-deletion replicates in both prostate cancer cells and non-prostate cancer cells. Replication of this virus is decreased by 50% by activated androgen receptors in the LNCaP cell line. The CRAD Ad5PSE-PBN-E1A displayed a rapidly inducible replication in prostate cancer cells in the presence of R1881, however, it had a delayed and relatively high expression in the absence of R1881. The chimeric CRADs Ad5PSE-PBN-E1A-AR and Ad5PSE-PBN-E1A-C685Y displayed marked induction of E1A in LNCaP (AR+), no induction in PC3 (AR-), and non-prostate cancer cells Hela in the presence of hormone, and no expression in any cell line in the absence of hormone. The cytopathic effect (CPE) of these chimeric viruses was also confirmed using crystal violet staining.

Our highly engineered E1A-AR chimeras not only convert a negative regulatory process into a positive regulatory process, but also greatly enhance the tissue specificity and the regulation of viral replication in the prostate. This strategy dramatically reduces toxicity in non-prostate tissue, while maintaining prostate specificity.