tbuckley/cabot-search huggingface dataset:
Cigarette Smoking as a Risk Factor in Stroke
Authors: Elizabeth Barrett-Connor
Journal: JAMA (1988)

<h3>To the Editor.—</h3> We were pleased to see that Wolf et al<sup>1</sup>have confirmed our work<sup>2</sup>showing that cigarette smoking is an independent risk factor for stroke, and somewhat surprised that they did not mention our 1984 article.<sup>2</sup>We reported that male cigarette smokers had a twofold and female cigarette smokers a 3.9-fold increased risk of stroke independent of other risk factors.
Long-term outcomes and quality of life in critically ill patients with hematological or solid malignancies: a single center study
Authors: S. G. Oeyen, D. D. Benoit, L. Annemans, P. O. Depuydt, S. J. Van Belle, R. I. Troisi, L. A. Noens, P. Pattyn, J. M. Decruyenaere
Journal: Intensive Care Medicine (2012)
Lavage of a mucinous cystadenoma of the pancreas with povidone iodate
Authors: E Gaia
Journal: Gut (2005)

Mucinous cystadenomas of the pancreas may progress to malignancy. Surgery is the treatment of choice.1,2

An 88 year old man presented with postprandial vomiting and intractable gastric pain due to an 8 cm pancreatic cyst compressing and displacing the pyloric antrum (fig 1). His picture included (inter alia) ischaemic cardiopathy and he …
THE GROWING IMPORTANCE OF PREVENTIVE MEDICINE TO THE GENERAL PRACTITIONER
Authors: JOHN M. DODSON
Journal: JAMA (1923)

No world can indulge in such a frightful orgy of war as that which occupied our world from 1914 to 1918 without paying the penalty in a tremendous burden of grief and wretchedness and a violent disturbance of social and economic conditions. In such a postwar disturbance, some groups are more profoundly and widely affected than others. Among the groups which were most seriously disturbed by the war was that of the medical profession. There are daily evidences of this on every hand, and a feeling of unrest and dissatisfaction. The conviction that "something must be done about it" is all but universal. In the field of medicine, other factors had been at work before the outbreak of the war which, alone, would have been sufficient to bring about a radical change in the economic and social relations of the physician. The triumphs of preventive medicine resulting in a very
Mortality Associated With Congenital Heart Defects in the United States
Authors: Roumiana S. Boneva, Lorenzo D. Botto, Cynthia A. Moore, Quanhe Yang, Adolfo Correa, J. David Erickson
Journal: Circulation (2001)

Surgical series and some population-based studies have documented a decrease in mortality from heart defects. Recent population-based data for the United States are lacking, however. We examined population-based data for patterns, time trends, and racial differences of mortality from heart defects for the United States from 1979 through 1997.We examined the multiple-cause mortality files compiled by the National Center for Health Statistics of the CDC from all death certificates filed in the United STATES: From these data, we derived death rates (deaths per 100 000 population) by the decedent's age, race, year of death, and heart defect type. We also analyzed age at death as an indirect indicator of survival. From 1979 through 1997, mortality from heart defects (all ages) declined 39%, from 2.5 to 1.5 per 100 000 population; among infants, the decline was 39%, or 2.7% per year. In 1995 to 1997, heart defects contributed to 5822 deaths per year. Of these deaths, 51% were among infants and 7% among children 1 to 4 years old. Mortality was on average 19% higher among blacks than among whites; this gap does not appear to be closing. Age at death increased for most heart defects, although less among blacks than among whites.Mortality from heart defects is declining in the United States, although it remains a major cause of death in infancy and childhood. Age at death is increasing, suggesting that more affected persons are living to adolescence and adulthood. The racial discrepancies should be investigated to identify opportunities for prevention.
Coronary occlusion during coronary angiography.
Authors: S B Guss, L M Zir, H B Garrison, W M Daggett, P C Block, R E Dinsmore
Journal: Circulation (1975)

Between January 1, 1970, and December 31, 1974, 2981 patients underwent coronary arteriography. Twelve acute coronary dissections or embolizations occurred, an incidence of 0.4%. The incidences of acute occlusions for the Sones and Judkins techniques were 0.19% (4/2077 studies) and 0.88% (8/940), respectively. No instance of acute occlusion has occurred during the past 490 studies performed by the Judkins technique. Eight patients with right coronary artery dissections or circumflex emboli were treated medically. All survived, but in seven a myocardial infarction evolved. Four patients underwent emergency saphenous venous bypass grafting because of refractory ventricular fibrillation (two patients) or because large amounts of myocardium were thought jeopardized (two patients). All patients in this group had interruption of flow supplying the left anterior descending coronary artery. Despite surgical intervention in less than three hours in all patients, survivors all sustained transmural myocardial infarctions. Three patients survived surgery and were discharged home.
Desloratadine prevents compound 48/80‐induced mast cell degranulation: visualization using a vital fluorescent dye technique
Authors: Y. H. Wang, Y. Taché, A. G. Harris, W. Kreutner, A. F. Daly, J. Y. Wei
Journal: Allergy (2004)

Background: Desloratadine is a selective H 1 ‐antihistamine used in the treatment of allergic rhinitis and chronic idiopathic urticaria. Desloratadine inhibits the release of allergic inflammatory mediators in vitro . We studied the impact of desloratadine on mast cell degranulation due to activation and re‐activation by the secretagogue, compound 48/80. Methods: Rat peritoneal eluate containing 5–6% mast cells were activated by a low concentration of compound 48/80 in a medium containing the vital fluorescent dye, Sulforhodamine‐B (SFRM‐B, 200 μ g/ml), which is engulfed by activated mast cells. The fluorescent image of activated mast cells was captured digitally and the total fluorescent area was analyzed when desloratadine was applied before or after compound 48/80. Results: Mast cells were not activated by desloratadine (10 −4 M), SFRM‐B (200 μ g/ml), or diluent alone. A low concentration of compound 48/80 (0.125 μ g/ml) induced fluorescence, while mast cells lost fluorescent images due to further degranulation on re‐exposure to compound 48/80. Desloratadine (10 −8 –10 −4 M), inhibited compound 48/80‐induced mast cell degranulation in a concentration‐dependent manner. Desloratadine also reduced the loss of fluorescent images due to re‐exposure to compound 48/80. Conclusions: Desloratadine may have a mast cell stabilizing effect at low concentrations in response to repeated mast cell activation in vitro .
Long term potentiation: Attending to levels of organization of learning and memory mechanisms
Authors: Matthew Shapiro, Eric Hargreaves
Journal: Behavioral and Brain Sciences (1997)

Shors &amp; Matzel set up a straw man, that LTP is a memory storage mechanism, and knock him down without due consideration of the important relations among different levels of organization and analysis regarding LTP, learning, and memory. Assessing these relationships requires analysis and hypotheses linking specific brain regions, neural circuits, plasticity mechanisms, and task demands. The issue addressed by the authors is important, but their analysis is off target.
Pulmonary function in asthmatic patients in remission.
Authors: K N Palmer, G R Kelman
Journal: BMJ (1975)

Thirty-five asthmatic patients (average age 28 years) who attended a pulmonary function laboratory when their mean ratio of forced expiratory volume in one second: forced vital capacity was 81 per cent (within the normal range for their age group) had arterial hypoxaemia and hypocapnia. These were probably secondary to lung hyperinflation and pulmonary ventilation/perfusion imbalance. The pulmonary abnormalities of bronchial asthma are not always detected by simple spirometric tests and the results of such tests should be interpreted cautiously.
Mechanism of augmented rate of left ventricular filling during exercise.
Authors: C P Cheng, Y Igarashi, W C Little
Journal: Circulation Research (1992)

At rest, most of left ventricular (LV) filling occurs early in diastole. This LV filling occurs in response to the pressure gradient produced as LV pressure falls below left atrial (LA) pressure. Because mitral valve flow occurs in response to an LA to LV pressure gradient, augmented diastolic mitral valve flow during exercise may be due to an increased mitral valve pressure gradient resulting from a rise in LA pressure and/or a fall in LV early diastolic pressure. Accordingly, we studied 13 conscious dogs, instrumented to measure micromanometer LV and LA pressures, and determined LV volume from three ultrasonic dimensions during exercise. The animals ran on a treadmill for 8-15 minutes at 5-8 miles/hr. With reflexes intact, during exercise, the heart rate increased from 116 +/- 20 to 189 +/- 24 beats per minute (mean +/- SD, p less than 0.01), the maximum rate of change of LV volume (dV/dtmax) increased from 185 +/- 44 to 282 +/- 76 ml/sec (p less than 0.01), the ejection fraction and cardiac output increased, and the duration of diastole decreased from 296 +/- 83 to 162 +/- 71 msec (p less than 0.01). Mitral valve opening pressure, mean LA pressure (10.9 +/- 4.4 versus 10.2 +/- 3.9 mm Hg, p = NS), and LV end-diastolic pressure (12.8 +/- 4.8 versus 13.1 +/- 3.3 mm Hg, p = NS) were all relatively unchanged. The time constant of the fall of isovolumic LV pressure decreased from 28 +/- 3.3 to 21 +/- 4.4 msec (p less than 0.05). The early diastolic portion of the LV pressure-volume loop was shifted downward during exercise, with the minimum LV pressure decreasing from 3.3 +/- 2.8 to -2.8 +/- 3.4 mm Hg (p less than 0.05) and the maximum mitral valve pressure gradient increasing from 5.5 +/- 1.7 to 11.8 +/- 3.5 mm Hg (p less than 0.01). A similar downward shift of the early diastolic portion of the LV pressure-volume loop was produced by infusion of dobutamine (6 micrograms/kg/min i.v.) at rest, as well as by exercise when the heart rate was held constant by right ventricular pacing at 190-210 beats per minute. The downward shift during exercise was prevented by beta-blockade (metoprolol, 0.5 mg/kg i.v.). We conclude that during exercise, sympathetic stimulation and tachycardia produce a downward shift of the early diastolic portion of the LV pressure-volume loop.(ABSTRACT TRUNCATED AT 400 WORDS)
Primary varicella-zoster infection in patients on biologic therapies for psoriasis
Authors: C.B. Hackett, B. Kirby
Journal: British Journal of Dermatology (2010)

Journal Article Primary varicella‐zoster infection in patients on biologic therapies for psoriasis Get access C.B. Hackett, C.B. Hackett Department of Dermatology, St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland E‐mail: c.hackett@svuh.ie Search for other works by this author on: Oxford Academic Google Scholar B. Kirby B. Kirby Department of Dermatology, St Vincent’s University Hospital, Elm Park, Dublin 4, Ireland E‐mail: c.hackett@svuh.ie Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 163, Issue 5, 1 November 2010, Page 1122, https://doi.org/10.1111/j.1365-2133.2010.09938.x Published: 01 November 2010
Mitral valve prolapse in sickle cell disease: Manifestation of a generalized connective tissue disorder
Authors: Scott M. Lippman, R. Patrick Abergel, Leonard E. Ginzton, Jouni Uitto, Kouichi R. Tanaka, Eric K. Miyamoto, Michael M. Laks
Journal: American Journal of Hematology (1985)

Abstract Previous studies have shown an association of sickle cell disease with generalized connective tissue disorders such as pscudoxanthoma elasticum. We recently documented an unexpectedly high prevalence of mitral valve prolapse, a connective tissue disorder, in sickle cell discase. To investigate this association, skin biopsies were analyzed from 32 sickle cell disease patients, 11 of whom had mitral prolapse. Total and type III collagen, collagen solubility, and uronic acid were not different between the patients with or without mitral prolapse (p &gt; 0.05). Computerized morphometric quantitation of the volume fraction of elastic fibers was greater in sickle cell disease patients than in 10 normals (3.1 ± 0.1 mean ± SEM vs 2.0 ± 0.3%; p &lt; 0.01) but less than in three patients with pseudoxanthoma elasticum (9.7 0.6%; p &lt; 0.001). Desmosine radioimmunoassay (an index of elastic fibers) was greater in sickle cell disease patients with mitral prolapse than those without (239.3 ± 9.3 vs 171.7 ± 25.4 ng/mg wet weight; p &lt; 0.02). Histopathologic grading showed a similar trend (p = 0.07). The combined probabilities of these three independent tests of elastic fiber quantity showed an increased elastic fiber concentration in mitral prolapse patients compared to those without mitral prolapse (p &lt; 0.02). Thus, there is no evidence for a specific collagen defect; rather, sickle cell disease appears to be associated with a spectrum of elastic tissue disorders, a feature that could predispose to mitral valve prolapse.
Abstract 231: Development of an ELISA for quantification of in vitro and cellular PTEN phosphatase activity
Authors: Michael B. Landward, Kimberly K. Ehrmantrout, Xin Chen Morrow, Angie M. Branch, Colin G. Ferguson
Journal: Cancer Research (2012)

Abstract Phosphatase and Tensin Homolog deleted on Chromosome 10 (PTEN) is a 3′ phosphoinositide phosphatase that converts PI(3,4,5)P3 to PI(4,5)P2 thus opposing PKB/Akt activation by PI 3-Kinase. PTEN is involved in neuronal stem cell proliferation and self-renewal, cardiac myocyte hypertrophy and contractility, and a wide range of developmental processes. However, PTEN is best known for its role as a tumor suppressor. Loss of PTEN activity results in accumulation of PI(3,4,5)P3, abnormal activation of PKB/Akt, unregulated cell growth, suppression of apoptosis, and increased tumorigenesis in a number of human tissues. It has also been proposed that PTEN is a candidate for targeted chemotherapy because certain anti-cancer agents preferentially destroy tumors with PTEN mutations. In addition to this direct role in cancer, PTEN has recently been shown to regulate cancer-associated pathways including VEGF-mediated angiogenesis and others. Consequently interest in PTEN as a cancer target is still high. Traditionally, quantification of PTEN phosphatase activity has required the use of radioactivity, organic solvents, and chromatography. In addition, detection of free phosphate released from the PTEN activity is commonly used for quantification. However, this latter method has limited sensitivity and dynamic range, and is susceptible to contamination from other sources of inorganic phosphate which can give incorrect results. To address the need for a better quantification method, we have developed a PTEN activity assay using a standard competitive ELISA format. Rather than detecting free phosphate, the assay detects the PTEN product, PI(4,5)P2, giving much more accurate quantification, improved sensitivity, and eliminates possible errors from phosphate contamination. We have shown that the assay can successfully quantify PTEN activity using both recombinant and immunoprecipitated enzyme. Several cell lines were tested for PTEN activity including the human breast cancer cell lines MDA-MB-231 and MDA-MB-468 (PTEN deficient). 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 231. doi:1538-7445.AM2012-231
Abstract C9: Human melanoma metastasis in NSG mice correlates with clinical outcome in patients
Authors: Elena Piskounova, Elsa Quintana, Mark Shackleton, Timothy M. Johnson, Sean J. Morrison
Journal: Cancer Research (2013)

Abstract Although metastasis is the leading cause of cancer-related deaths, little is known about the molecular mechanisms that enable tumor cells to metastasize. We have recently developed a model in which for the first time human melanomas readily engraft in nonobese diabetic/severe combined immunodeficient interleukin-2 receptor-g chain null (NSG) mice. Melanomas from 25 patients exhibit reproducible differences in the rate of spontaneous metastasis after transplantation into NSG mice. Importantly metastasis in mice is strongly correlated with metastasis, and clinical outcome, in the patients, providing an opportunity to test the mechanisms of metastatic progression of human melanoma in an animal model. In transplanted mice, efficiently metastasizing melanomas have much higher levels of circulating melanoma cells compared to inefficiently metastasizing ones, suggesting that the rate of entry into the blood is one factor that limits the rate of metastasis. In addition, we have profiled both genomic mutations and gene expression in 33 primary human melanomas with varying metastatic potential, in order to gain insight into the key regulatory pathways involved in melanoma metastasis. Using our xenograft model we are currently investigating the role of select genes in enhancing melanoma metastasis, at the level of intravasation into the blood stream, survival in circulation and proliferation in distal organs. Citation Format: Elena Piskounova, Elsa Quintana, Mark Shackleton, Timothy M. Johnson, Sean J. Morrison. Human melanoma metastasis in NSG mice correlates with clinical outcome in patients. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Invasion and Metastasis; Jan 20-23, 2013; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2013;73(3 Suppl):Abstract nr C9.
Detection of Cell-CAM 105 in the pericanalicular domain of the rat hepatocyte plasma membrane
Authors: Jeanette Mowery, Douglas C. Hixson
Journal: Hepatology (1991)

Cell-CAM 105 has been identified as a cell adhesion molecule based on the ability of anti-cell-CAM 105 monospecific Fab fragments to inhibit the reaggregation of rat hepatocytes. Because of its adhesive properties, it was expected that cell-CAM 105 would be present on the lateral cell surface where adhesive interactions predominate. Paradoxically, however, immunofluorescence analysis of frozen sections of rat liver using specific monoclonal antibodies indicated that cell-CAM 105 was present exclusively in the bile canalicular domain of the rat hepatocyte where there is no intercellular adhesion. To more precisely define the in situ localization of cell-CAM 105, immunoperoxidase labeling and electron microscopy were used to examine intact and mechanically dissociated liver tissue. Results showed that when accessibility was provided by mechanical dissociation of perfusion fixed liver tissue, cell-CAM 105 could be detected in the pericanalicular region of lateral membranes. In contrast, when hepatocytes were labeled after incubation in vitro under conditions used during adhesion assays to induce reaggregation, cell-CAM 105 rapidly redistributed to all areas of the plasma membrane. Immunofluorescence analysis of primary hepatocyte cultures further revealed that cell-CAM 105 and two other bile canalicular proteins relocalized to discrete domains reminiscent of bile canaliculi, whereas cell-CAM 105 was also present in areas of intercellular contact. Serial section electron microscopy analysis of well-defined, cross-sectional profiles of bile canaliculi suggested the presence of cell-CAM 105—positive membrane folds that extended along the length of the bile canalicular border. In sections from livers in which calcium-dependent adhesive contacts had been disrupted by treatment with ethylenediamine tetraacetate, intact bile canaliculi were found that remained attached only by these border folds. The implications of these results are discussed with regard to a possible role for cell-CAM 105 in bile canalicular formation. (HEPATOLOGY 1991; 13:47–56).
Intravenous Radionuclide Diffusion Hepatography in Hepatic Abscesses and Congenital Solitary Cysts
Authors: SHIN-HWA YEH
Journal: Clinical Nuclear Medicine (1976)

Intravenous diffusion hepatography with 99mTc-pertechnetate was used to evaluate the diffusion patterns of solitary hepatic masses which had little or no perfusion demonstrable by the 113mIn perfusion study. The scintiphotos of 21 proven cases were analyzed. The results indicate that the diffusion study may help to differentiate hepatic abscesses, especially amebic abscesses, from congenital solitary cysts. This simple and innocuous approach would be another step toward increasing the specificity and accuracy of the nuclear diagnosis of hepatic mass lesions.
Signaling from toxic metals to NF-kappaB and beyond: not just a matter of reactive oxygen species.
Authors: Fei Chen, Xianglin Shi
Journal: Environmental Health Perspectives (2002)

The nuclear factor kappa B (NF-kappaB) family of transcription factors controls expression of a number of early response genes associated with inflammatory responses, cell growth, cell cycle progression, and neoplastic transformation. These genes include a multitude of cytokines, chemokines, adhesion molecules, immune receptors, stress proteins, apoptotic or anti-apoptotic regulators, and several oncogenes. Accumulating evidence indicates that a variety of toxic metals are able to affect the activation or activity of NF-kappaB, but the molecular mechanisms involved in this process remain largely unknown. The signaling pathways mediating cytokine- or microorganism-induced NF-kappaB activation have been well established recently. Whether the same signaling systems are involved in metal-induced NF-kappaB activation, however, is unclear. In the present review, we have attempted to evaluate and update the possible mechanisms of metal signals on the activation and function of NF-kappaB.
Diagnostic Errors and Patient Safety—Reply
Authors: David E. Newman-Toker
Journal: JAMA (2009)

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Authors' reply to Turner and colleagues
Authors: I. Abubakar, S. Sridhar, M. Eisenhut, A. Roy, R. J. Harris, L. C. Rodrigues, P. Mangtani, I. Adetifa, A. Lalvani
Journal: BMJ (2014)

Turner and colleagues do not accept our conclusion that BCG prevents Mycobacterium tuberculosis infection without a valid mechanism and propose an alternative hypothesis for an apparent effect.1 2 We presented the consistent epidemiological finding of a protective effect of BCG against tuberculosis infection rather than speculating on a mechanism of action for this …