tbuckley/cabot-search huggingface dataset:
Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations.
Authors: B G Brown, C A Gallery, R S Badger, J W Kennedy, D Mathey, E L Bolson, H T Dodge
Journal: Circulation (1986)

Thrombolytic recanalization of the obstructed coronary lumen was studied in 32 patients receiving intracoronary streptokinase for 60 to 90 min during acute myocardial infarction. The process was viewed at high arteriographic magnification and was quantified with computer-assisted measurements from repeated single-plane views. The variability of the method for this application was 0.15 to 0.18 mm on minimum diameter estimates. Structural details were seen that are not commonly appreciated at conventional magnification. The recanalized lumen appears to form along an interface between the thrombus and the vessel wall, progressively enlarging its minimum arteriographic diameter to 0.65 +/- 0.24 mm (+/- 1 SD) at the end of the short-term infusion of streptokinase reflecting a final percent stenosis of 77 +/- 10%. In nine infarct lesions found patent 5 +/- 3 weeks later, the recanalized lumen further improved an average of 0.34 mm in minimum diameter (p less than .005) and 13% stenosis (p less than .01). A thin film of contrast medium surrounding the obstructing thrombus faintly defined the boundaries of the original atherosclerotic lumen in all but two cases. The "original stenosis" measured 1.25 +/- 0.32 mm in minimum diameter and 56 +/- 14% stenosis when first visualized; it was unchanged throughout the course of infusion of streptokinase. In five patients catheterized 10 +/- 12 weeks before their infarction, the original stenosis averaged 1.15 +/- 0.22 mm in the preinfarct angiogram, as compared with 1.17 +/- 0.23 mm in its faintly defined form during thrombolytic therapy (p = NS). In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.(ABSTRACT TRUNCATED AT 250 WORDS)
Afterload induced changes in myocardial relaxation A mechanism for diastolic dysfunction
Authors: A Leite-Moreira
Journal: Cardiovascular Research (1999)

Background: Diastolic left ventricular (LV) dysfunction manifests as an upward shift of the diastolic pressure–volume relation. One of the possible causes of diastolic LV dysfunction is incomplete myocardial relaxation. It is well known that high afterload slows myocardial relaxation. This contribution investigated to what extent afterload elevation could also affect LV filling pressures including end-diastolic LV pressure (LVP). Methods: Selective, beat-to-beat elevations of afterload were induced in anaesthetised open-chest rabbits (n=9) by abrupt narrowing of the ascending aorta during the diastole of the preceding heartbeat. This was performed with physiological heart rate and blood pressure. Results: These interventions increased systolic LVP from 90±3 mm Hg at baseline to 103±4, 123±5, 139±5 and 154±6 mm Hg. The last intervention was a total aortic occlusion inducing a first beat isovolumetric contraction. Smaller afterload elevations decreased τ (accelerated LVP fall) and did not elevate diastolic pressure-internal diameter relation (P-ID). Larger afterload elevations increased τ (decelerated LVP fall), induced an upward shift of the diastolic P-ID and increased end-diastolic LVP. Effects of afterload on end-diastolic LVP were correlated with effects on τ (r=0.89; P<0.01). Incomplete relaxation or load-dependent residual active state appeared to be the mechanism for this diastolic dysfunction. Similar findings were made retrospectively in dogs instrumented with circumferential segment length gauges (n=16). Conclusions: Diastolic LV dysfunction was induced by elevated afterload in healthy hearts of rabbits and dogs. If this mechanism could be shown to be operative in the failing heart, reversal of diastolic dysfunction should contribute to the beneficial effects of vasodilating and inotropic therapy on pulmonary congestion.
Action of sodium aurothiomalate on erythrocyte membrane.
Authors: J M Campbell, J Reglinski, W E Smith, D Porter, R D Sturrock
Journal: Annals of the Rheumatic Diseases (1992)

The number of sulphydryl groups on the erythrocyte membrane has been assessed as a function of nutritional status for two groups of patients, one receiving non-steroidal anti-inflammatory drugs (NSAIDs) and the other receiving sodium aurothiomalate (Myocrisin). The patients receiving NSAIDs had a significantly higher number of sulphydryl groups in both the glucose depleted and glucose activated states than the patients receiving sodium aurothiomalate. The study focuses on the hexose transport protein where there is a specific binding site for gold using the two sulphydryl residues on helices 11 and 12 of the protein. The data suggest that the strong binding of gold to the erythrocyte membrane occurs via thiol pairs rather than by isolated sulphydryl groups and that there are possibly two further binding sites for gold on the membrane, the identities of which are still unclear.
Lasker awards honored long-term achievers
Authors: C. Marwick
Journal: JAMA (1984)

Less than two months ago, the Albert Lasker Medical Research Awards were presented for the 38th time in New York City. Herewith, an account of the work, part of it done some time ago, for which these three $15,000 prizes were awarded: In less than three decades, from the mid-1950s to the present day, pediatric practice has undergone a revolution. The<b>Public Service Award</b>recognized two leaders of the revolution,<b>Saul Krugman</b>, MD, and<b>Maurice R. Hilleman</b>, PhD. When Krugman became an instructor in pediatrics at New York University School of Medicine in 1948, measles, diphtheria, pertussis, and poliomyelitis were major viral diseases of childhood, causing permanent aftereffects in all too many cases. But it was only a year later, in 1949, that John Enders, PhD, showed it was possible to cultivate polio virus, and the golden age of clinical virology essentially began. With the ability to manipulate viruses in
The effect of amino acids and dipeptides on sodium and water absorption in man
Authors: M. D. Hellier, C. Thirumalai, C. D. Holdsworth
Journal: Gut (1973)

A perfusion technique has been used to quantitate the effect of the amino acids glycine and alanine and the dipeptides glycyl-glycine and glycyl-L-alanine on sodium and water absorption from the human jejunum. Although no net absorption of sodium and water was seen in the absence of non-electrolytes, a significant stimulation occurred in the presence of both free amino acids and dipeptides. In the case of glycine and alanine, sodium and water absorption increased linearly with increasing concentration of the amino acid and saturation was not demonstrated over the range of concentrations studied. Molar ratios for net absorption of free amino acid and sodium were approximately 1:1 for all but the highest concentration of alanine. In contrast, the corresponding molar ratios for the two dipeptide solutions and sodium were approximately 1:2. Possible explanations for these observations are discussed.
SHIP-1 inhibits CD95/APO-1/Fas-induced apoptosis in primary T lymphocytes and T leukemic cells by promoting CD95 glycosylation independently of its phosphatase activity
Authors: E Charlier, C Condé, J Zhang, L Deneubourg, E Di Valentin, S Rahmouni, A Chariot, P Agostinis, P-C Pang, S M Haslam, A Dell, J Penninger, C Erneux, J Piette, G Gloire
Journal: Leukemia (2010)
Screening and Accountability-Reply
Authors: Barbara Woo
Journal: JAMA (1986)

In Reply.—  We certainly agree that there are practical, low-technology maneuvers to ensure that physicians provide the services that they would like to provide. Regardless of whether the proposed solution includes nurses or computer-generated reminders, 1-3 our data 1-3 emphasize that since well-intentioned physicians may not live up to their own expectations, they should welcome approaches to narrowing the gap between intentions and actual performance.
Premorbid Diet and the Prognosis of Women With Breast Cancer
Authors: M. Jain, A. B. Miller, T. To
Journal: JNCI Journal of the National Cancer Institute (1994)

Consumption of a high-fat diet has been associated with poor survival in breast cancer patients. However, studies examining this association are limited and have not used adjustment of energy in their estimates.The effect of usual diet before diagnosis of breast cancer on the risk of dying of breast cancer was examined in a cohort of women with breast cancer from the National Breast Screening Study (NBSS) in Canada.From a cohort of 89,835 women in the NBSS, a total of 1270 histologically confirmed cases of invasive carcinoma of the breast were identified by active follow-up, supplemented by passive follow-up involving record linkage to provincial cancer registries. Of these, 678 case patients who had completed a diet history and were diagnosed from January 1982 up to June 1992 formed the cohort for this investigation. Diet was ascertained from a self-administered diet-history questionnaire. Mortality data were obtained by linkage to the Canadian Mortality Data Base of Statistics Canada, provincial cancer registries, and annual follow-up of cases through physicians. Risk of dying and survival probabilities were estimated by the Cox proportional hazards method and the actuarial life-table method.There were 83 deaths in this study cohort of 678 women; 76 deaths were due to breast cancer, and the remaining seven resulted from other causes. The 5-year survival rate was 90%. For every 5% increase in energy from saturated fat, the risk of dying of breast cancer increased by 50% (hazard ratio = 1.50; 95% confidence interval [CI]: 1.08-2.08). No significant increase in risk was seen with total fat intake (hazard ratio = 1.21; 95% CI = 0.91-1.61) or oleic acid intake (hazard ratio = 1.25; 95% CI = 0.90-1.74). There was a lower risk of dying of breast cancer in the highest quartiles of beta carotene intake (hazard ratio = 0.48; 95% CI = 0.23-0.99) and vitamin C intake (hazard ratio = 0.43; 95% CI: 0.21-0.86); both vitamins showed a significant dose-response relationship (P for trend, < or = .05). These effects varied with menopausal status at diagnosis and tumor characteristics.These results suggest an increased risk of dying of breast cancer with higher intakes of saturated fat before diagnosis and slightly reduced risk with higher intakes of beta carotene and vitamin C.More attention should be paid to premorbid dietary habits in relation to breast cancer prognosis. Further studies, however, need to be done with full ascertainment of dietary changes prior to and subsequent to diagnosis.
Interferon decreases expression of human scavenger receptor class BI, a possible HCV receptor in hepatocytes
Authors: K. Murao, H. Imachi, X. Yu, W. M. Cao, T. Nishiuchi, K. Chen, J. Li, R. A. M. Ahmed, N. C. W. Wong, T. Ishida
Journal: Gut (2007)

Infection with the hepatitis C virus (HCV) causes acute hepatitis. This disease has a high probability of becoming chronic and leading to cirrhosis, but a more deadly consequence is hepatocellular carcinoma. Interferon alpha (IFN alpha)-based treatment combined with ribavirin is the major therapeutic choice available for the treatment of chronic HCV infection.The scavenger receptor class B type I (SR-BI) or its human homologue CD36 and LIMPII Analogous-1 (hSR-BI/CLA-1) has recently been shown to interact with HCV envelope glycoprotein E2, thus suggesting that it might participate in entry of the virus into host cells. This rationale underlies current interest in the potential role of IFN alpha in hSR-BI/CLA-1 expression in HepG2 cells.It was shown that endogenous hepatocyte expression of hSR-BI/CLA-1 was suppressed by exposure to IFN alpha. Decreased hSR-BI/CLA-1 expression in IFN alpha-treated cells was due to lower transcriptional activity of the promoter. A potential pathway for the effect of IFN alpha on hSR-BI/CLA-1 promoter activity was identified when the inhibitory action of IFN was abrogated in signal transducer and activator of transcription 1 (STAT1)/STAT2 knocked-down cells. Exposure of HepG2 cells to IFN alpha elicited a rapid phosphorylation of STAT1/STAT2, a known target of IFN alpha signalling. In addition, the mutagenesis of a STAT1/STAT2 response element in the hSR-BI/CLA-1 promoter abolished the ability of IFN alpha to suppress promoter activity.Together, these results indicate that the STAT1/STAT2 pathway participates in IFN alpha inhibition of hSR-BI/CLA-1 expression, and raise the possibility that lowering the expression of this gene may be of therapeutic value for treating HCV infections.
An Obscure Case
Authors: W. Sankey
Journal: BMJ (1860)

this plan does not answer very satisfactorily, for, independently of the escape of the fluid from the edges of the cell, a few of the largest crystals grow still larger at the expense of the smaller ones, adtd the beauty of the specimen is destroyed.The different forms of these crystals, as they appear in the microscope, are given in the Illustrations of Urine, Urinary Deposits, and Calculi.(Urine, plates i to Ix.) See also TIhe Microscop)e in its Application to Practical MUedicinie, chapter ix, page 292.
Molecular prognosticators of complex karyotype soft tissue sarcoma outcome: a tissue microarray-based study
Authors: G. Lahat, D. Tuvin, C. Wei, W.L. Wang, R.E. Pollock, D.A. Anaya, B.N. Bekele, L. Corely, A.J. Lazar, P.W. Pisters, D. Lev
Journal: Annals of Oncology (2009)
Early primary biliary cirrhosis: Just delayed or different?
Authors: K D Lindor
Journal: Hepatology (1997)

biopsy specimens in 16 of 35 patients.Of note, despite using to be more optimistic about vaccines or immunoadjuvant therapies designed to elicit host anti-HCV specific CTL.vaccinia vectors encoding genotype 1a HCV epitopes in their assays, anti-HCV specific CTL activity was detected in 3 of 9 patients with genotype 1b and 3 of 9 patients with non-DWAIN L. THIELE, M.D. type 1 genotypes as well as in 10 of 17 patients with genotype Liver Unit/Internal Medicine 1a or mixed genotype 1a and 2a infections.Thus despite UT Southwestern Medical Center at Dallas concerns that CTL responses might be underestimated be-Dallas, TX cause of sequence differences between in vivo viral antigens stimulating the response and the recombinant genotype 1a REFERENCES antigens used in in vitro research assays, sufficient CTL re-1.Chisari FV, Ferrari C. Hepatitis B virus immunopathology.Springer sponses appear to be directed against conserved epitopes Semin Immunopathol 1995;17:261-281.derived from the HCV core protein to allow detection in 2. Brook MG, Karayiannis P, Thomas HC. Which patients with chronic hepatitis B virus infection will respond to a-interferon therapy?A statis-such assays of CTL responses in patients with non-type 1a tical analysis of predictive factors.
Screening for Osteoporosis
Authors: Lawrence G. Raisz
Journal: New England Journal of Medicine (2005)

At her annual visit, a 60-year-old woman asks her physician whether she should have a bone-density test to screen for osteoporosis. The patient went through menopause at the age of 52 years and received postmenopausal hormone therapy for four years. She takes 500 mg of calcium twice daily and exercises regularly. She has no personal history of fractures, but her mother had a hip fracture at the age of 82. Her height is 63 in. and her weight is 120 lb. What should her physician advise?
The Effect of a Medicated Wash on Acne, Sebum Excretion Rate and Skin Surface Lipid Composition
Authors: W. J. Cunliffe, J. A. Cotterill, B. Williamson
Journal: British Journal of Dermatology (1972)

Journal Article The Effect of a Medicated Wash on Acne, Sebum Excretion Rate and Skin Surface Lipid Composition Get access W. J. Cunliffe, W. J. Cunliffe Department of Dermatology, The General Infirmary, Leeds, St James' (University) Hospital, Leeds, Harrogate General Hospital Search for other works by this author on: Oxford Academic Google Scholar J. A. Cotterill, J. A. Cotterill Department of Dermatology, The General Infirmary, Leeds, St James' (University) Hospital, Leeds, Harrogate General Hospital Search for other works by this author on: Oxford Academic Google Scholar B. Williamson B. Williamson Department of Dermatology, The General Infirmary, Leeds, St James' (University) Hospital, Leeds, Harrogate General Hospital Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 86, Issue 3, 1 March 1972, Pages 311–312, https://doi.org/10.1111/j.1365-2133.1972.tb02237.x Published: 01 March 1972
A memorable doctor: "We never met"
Authors: N. Wilson
Journal: BMJ (1997)

I never met him, not in person. But I did meet him through his receptionist, his scrambled notes, his scruffy premises, and most of all through his patients.

He was an inner city general practitioner and I was his locum for the day. This was my first experience of a singlehanded practice, having trained and worked in highly thought of group practices. My spirit had been squashed by the transitory life of a locum. The simple problems …
Calsequestrin mutation and catecholaminergic polymorphic ventricular tachycardia: A simulation study of cellular mechanism
Authors: G FABER, Y RUDY
Journal: Cardiovascular Research (2007)

Patients with a missense mutation of the calsequestrin 2 gene (CASQ2) are at risk for catecholaminergic polymorphic ventricular tachycardia. This mutation (CASQ2(D307H)) results in decreased ability of CASQ2 to bind Ca2+ in the sarcoplasmic reticulum (SR). In this theoretical study, we investigate a potential mechanism by which CASQ2(D307H) manifests its pro-arrhythmic consequences in patients.Using simulations in a model of the guinea pig ventricular myocyte, we investigate the mutation's effect on SR Ca2+ storage, the Ca2+ transient (CaT), and its indirect effect on ionic currents and membrane potential. We model the effects of isoproterenol (ISO) on Ca(V)1.2 (the L-type Ca2+ current, I(Ca(L))) and other targets of beta-adrenergic stimulation.ISO increases I(Ca(L)), prolonging action potential (AP) duration (Control: 172 ms, +ISO: 207 ms, at cycle length of 1500 ms) and increasing CaT (Control: 0.79 microM, +ISO: 1.61 microM). ISO increases I(Ca(L)) by reducing the fraction of channels which undergo voltage-dependent inactivation and increasing transitions from a non-conducting to conducting mode of channel gating. CASQ2(D307H) reduces SR storage capacity, thereby reducing the magnitude of CaT (Control: 0.79 microM, CASQ2(D307H): 0.52 microM, at cycle length of 1500 ms). The combined effect of CASQ2(D307H) and ISO elevates SR free Ca2+ at a rapid rate, leading to store-overload-induced Ca2+ release and delayed afterdepolarization (DAD). If resting membrane potential is sufficiently elevated, the Na+-Ca2+ exchange-driven DAD can trigger I(Na) and I(Ca(L)) activation, generating a triggered arrhythmogenic AP.The CASQ2(D307H) mutation manifests its pro-arrhythmic consequences due to store-overload-induced Ca2+ release and DAD formation due to excess free SR Ca2+ following rapid pacing and beta-adrenergic stimulation.
Bilateral Deep Venous Thrombosis in Protein S Deficiency Detection by Radionuclide Venography
Authors: WILLIAM A. WEGENER, SYDNEY HEYMAN
Journal: Clinical Nuclear Medicine (1990)

Patients with primary hypercoagulopathies often present with recurrent, spontaneous deep venous thrombosis and pulmonary embolism. An adolescent eventually diagnosed with protein S deficiency presented with unilateral deep venous thrombosis documented ultrasonographically. Scintigraphic studies showed no evidence of pulmonary embolism but revealed a complete absence of and the abdoment. Subsequent ultrasonography and CT Radionuclide scintigraphy may play an important role in the serial evaluationof primary hypercoagulable states, particularly when pulmonary scintigraphy is combined with bilateral, lower extremity venography.
A Survey of Hospital Pharmacists' Knowledge of the Content of Drug Combinations
Authors: Jacques Gagné, Pierre Biron, Richard Moisan
Journal: Annals of Internal Medicine (1975)

Letters1 May 1975A Survey of Hospital Pharmacists' Knowledge of the Content of Drug CombinationsJACQUES GAGNÉ, PH.D., PIERRE BIRON, M.SC., RICHARD MOISAN, M.SC.JACQUES GAGNÉ, PH.D.Search for more papers by this author, PIERRE BIRON, M.SC.Search for more papers by this author, RICHARD MOISAN, M.SC.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-82-5-680 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTwo years ago, one of us reported the results of a preliminary survey suggesting that the knowledge of physicians about the exact content of the drug combinations they are prescribing is somewhat limited (1). The purpose of the present study was to find out hospital pharmacists' knowledge concerning the content of the same drug combinations that the physicians were previously asked to identify.During the semiannual meeting of the Quebec Hospital Pharmacists Association held in September 1973 in Trois-Rivières, Quebec, the 71 pharmacists present in the conference room were asked, without warning, to fill out the questionnaire, whose answers appeared...References1. BIRON P: A hopefully biased pilot survey of physicians knowledge of the content of drug combinations. Can Med Assoc J 109:35-39, 1973 MedlineGoogle Scholar2. Quebec Health Insurance Board List of Drugs, 4th ed., 1974 Google Scholar3. MACCANNELL K: The case against combination drugs, in Proceedings of the 5th International Congress of Pharmacology, vol. 3. Basel, S. Karger AG, 1973, pp. 18-22 Google Scholar4. CARR E: Report of the discussion on combination drug therapy—good or bad. See Reference 3, pp. 28-32 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: JACQUES GAGNÉ, PH.D.; PIERRE BIRON, M.SC.; RICHARD MOISAN, M.SC. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byTrade Names and Generic Names Problems for Prescribing Physicians 1 May 1975Volume 82, Issue 5Page: 680-682KeywordsDrugsPharmacistsQuestionnaires ePublished: 1 December 2008 Issue Published: 1 May 1975 PDF downloadLoading ...
DEATH FROM EMBOLISM AFTER INJECTION OF VARICOSE VEINS
Authors: H. I. Biegeleisen
Journal: JAMA (1941)

To the Editor:—  The article entitled Death from Pulmonary Embolism Following the Injection of Varicose Veins (The Journal, August 2, p. 347) requires comment. Nunn and Harrison draw attention to a mortality from pulmonary embolism following what they term  injection  for varicose veins. From time to time I have emphasized in the literature the dangers of so-called routine treatment in such cases, but evidently these warnings have gone unheeded. The authors are apparently unable to explain the fatality after having carefully studied the case and performed a detailed autopsy.  After reading this report inThe Journal, I find the following significant points in the history: The patient was treated with 2 cc. of sodium morrhuate as the first injection. The authors state that there was no decided reaction after this treatment and a satisfactory thrombosis followed. Yet six weeks later, on admission to the hospital, which was two