tbuckley/cabot-search huggingface dataset:
P244 Characteristics And Outcomes In Lung Transplant Recipients Aged 65 And Over
Authors: S. Isse, R. Hackett, D. Thomas, P. Catarino, S. Tsui, J. Parmar
Journal: Thorax (2014)

<h3>Rationale</h3> Lung transplantation has become an accepted treatment option in a select group of patients with end-stage lung disease. The current International Society for Heart and Lung Transplantation (ISHLT) guidelines suggest age above 65 is a relative contraindication. However, increasingly patients with COPD and IPF are being referred for consideration after this age. The outcomes in this group (above 65) are not well described. We have studied the characteristics and outcomes of patients aged 65 and over, offered lung transplantation in our institution. <h3>Method</h3> Retrospective review from the transplant database and patient records. We examined the Age, Sex, Indication for transplant and cause of death in all transplant recipients aged 65 and over from 1991 to July 2013. As a control group we compared them with 50 single lung transplant recipients front the same era and institution who were under 65. We used SPSS to generate the survival curves. <h3>Results</h3> In total we had 19 lung transplant recipients aged 65 and over who all had a single lung transplant, with a mean survival of 1600 days post-transplant. 13/19 were male recipients. The indication for transplantation was COPD and IPF in all. The cause of death was BOS in 9/14, malignancy in 2/14 and pulmonary embolism, stroke and bleeding in the others. When compared with 50 single lung transplant recipients aged 60–64, we did not find any statistically significant differences in survival (p value 0.158) (see figure 1), cause of death and reason for transplantation. <h3>Conclusion</h3> We have shown from our limited data that patients aged 65 and over have very similar outcomes to their younger counterparts. Hence, age whilst still important should not be a deterring factor when referring patients for lung transplant assessment. It would also be important to examine longer term outcomes and complications such as rates of renal dysfunction, hypertension, rejection and admissions into hospital. As the number of patients aged 65 and older receiving lung transplant increases, we should be able to gather more effective data.
Points: Clinical algorithms: infertility
Authors: D Carr-Locke, P Bannister, G T Watts
Journal: BMJ (1985)

The chance of a dialysis patient in France receiving a transplant in 1983 was 1:13, in Italy it was 1:29, while in the United Kingdom it was greater than 1:4.Surely the way to increase the number of patients being treated (Mrs Elizabeth Ward's leading article, 22-29 December, p 1712) is to inform our colleagues of the successful parts of our renal failure programme while working hard to improve those areas in which we are deficient.
Self-portrait of Frida Kahlo
Authors: Peter Glusker
Journal: JAMA (1994)

To the Editor.  —Dr Southgate comments on the self-portrait of Frida Kahlo on the cover of your October 27,1993, issue.1While some of the main points are accurate enough, there are a number of details of her interpretation that astonish me. Some are taken from Herrera's book,2and say much more about Ms Herrera than about Frida Kahlo.  Frida Kahlo and Diego Rivera were close friends of my family, and I grew up seeing Frida several times a month for years. Her home was very familiar to me, as were her monkeys, Diego's hairless dogs, and the rest of the archaeological and botanical panoply of their home. Based on this knowledge, and my own background growing up in Mexico, as well as my mother's (Anita Brenner) known expertise on Mexico, I take issue with Dr Southgate's comments and suggest your readers may want to consider some other ideas.
Platelet-activating factor effects on bovine pulmonary artery endothelial cells.
Authors: G Y Grigorian, U S Ryan
Journal: Circulation Research (1987)

Endothelial cells (ECs) were isolated from bovine pulmonary artery and maintained in long-term culture. On reaching confluency, ECs formed a characteristic "cobblestone" monolayer. One hour after addition of 1 nM platelet-activating factor (PAF) to the growth medium, ECs underwent dramatic changes in shape from their normal polygonal morphology to more elongated spindle-shaped forms. More pronounced effects were evident in the presence of 0.1 nM phorbol-12-myristate-13-acetate (PMA), a potent activator of C kinase. It was found that at concentrations from 10(-11)-10(-7) M, PAF stimulates the phosphoinositide turnover in EC. The half-maximal activation in the release of inositol phosphates was at 10(-9) M. This finding suggested that an increase in intracellular Ca2+ concentration and activation of protein kinase C were involved in the mechanism of action of PAF on EC. The metabolic responses of EC were evaluated by measuring the activity of beta-adrenergic receptor-coupled adenylate cyclase (AC) in a crude membrane fraction and by assay of prostacyclin and thromboxane released by cultured EC. AC from control membranes was activated by isoproterenol in a dose-dependent manner (EC50 = 30 nM) from 0.8-5.5 pmol cAMP/min/mg protein. If the membranes were isolated after preincubation of ECs with 1 nM PAF or 0.1 nM PMA, the AC activity was decreased by 70 and 90%, respectively; in both cases, affinity for isoproterenol was lowered threefold (EC50 = 100 nM). Our data suggest that PAF interaction with EC leads to an apparent beta-adrenergic receptor desensitization that probably acts via a phosphorylation mechanism involving C kinase.(ABSTRACT TRUNCATED AT 250 WORDS)
NOTE ON SEA-SICKNESS
Authors: M. Flack
Journal: BMJ (1931)

ANALYSIS OF SECONDARY REACTIONSIn order to analyse the secondary reactions it was decided to record the results from eight continuous rota- tions on fifty-two volunteers, as offering a wider field for research, only eight having consented to the variant of two-minute interrupted rotations.The subjects were all healthy.All but twelve were betweenthe ages of 17 and 30.Of the twelve, the ages ranged between 40 and 52, ten of these with a long sea service, and two *with air service.The primary reactions, being irrelevant, were not recorded.The results were those usually found in sea-sickness, the blood pressure taken for convenience as the chief vaso- motor reaction, and the symptoms and signs were tabulated alongside as follows: Systolic Blood Symptoms Nil Pressure and Signs Rise ... ... .
Abstract 3531: Functional characterization of genes that sensitize pancreatic cancer cells to gemcitabine
Authors: Vikram Bhattacharjee
Journal: Cancer Research (2011)

Abstract Pancreatic cancer has been one of the most aggressive cancers to date. At the point of diagnosis, most patients’ life expectancies are measured in months. While several chemotherapeutic agents have been used to treat pancreatic cancer, none have been very successful in prolonging a patient's lifespan in a major way. Pancreatic adenocarcinoma, the major form of pancreatic cancer, has several risk factors including chronic pancreatitis, advanced age, smoking, obesity, diabetes, and genetic predispositions. Chronic pancreatitis has been thought to promote tumorigenesis ultimately resulting in pancreatic adenocarcinoma. Presently, several classes of drugs (anti-proliferative agents, platanating agents, fluoropyrimidines, and taxanes) are used in the clinic to treat pancreatic cancer, but patient response is very poor when compared to other cancers. Therefore, there is an urgent need to identify novel molecular targets that sensitize pancreatic cancer cells to chemotherapeutic agents. Gemcitabine (an inhibitor of DNA replication) is of particular interest to us because it remains the drug of choice in the treatment of pancreatic cancer. We have completed a genome wide RNA interference (RNAi) screen and have identified numerous targets that greatly sensitize pancreatic cancer cells to gemcitabine. In the screen, every gene in the human genome was ablated individually via RNAi, so we can identify gene candidates that negatively affect cell survival following drug treatment. We have finalized our validated gene target list. We have utilized automated microscopy tools in addition to molecular biological approaches that are established in our lab in order to chronicle in real time how these pancreatic cancer cells are being sensitized to gemcitabine either via aberrant mitotic processes, direct induction of apoptosis, or other forms of cell death. Indeed, we have found two distinct stages of the cell cycle where death is prevalent. We have the capacity to observe the cells at every stage of the cell cycle before, during, and after the addition of drug. We have established pancreatic cancer cells lines that stably express fluorescent marker proteins that enable us to observe and get a handle on how these cancer cells are surviving drug treatment and how coupling siRNA treatment with chemotherapy sensitizes these cells. We have focused on two major pathways that are aiding cell survival in order to characterize major players that help pancreatic cancer cells survive drug treatment. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3531. doi:10.1158/1538-7445.AM2011-3531
High-Dose Epinephrine During Resuscitation
Authors: Joseph P. Ornato
Journal: JAMA (1991)

Many clinicians have begun to use high-dose epinephrine (HDE) rather than standard-dose epinephrine (SDE) during cardiopulmonary resuscitation.<sup>1-6</sup>(HDE is usually defined as an intravenous bolus of &gt;1 mg, often 0.2 mg/kg, and SDE is usually defined as a 0.5- to 1.0-mg intravenous bolus.) In animal models, HDE improves measurements of hemodynamics, enhances blood flow in the coronary and cerebral circulation during resuscitation, and brings a higher rate of return of spontaneous circulation than SDE.<sup>7-10</sup>Anecdotal case reports<sup>2-6</sup>and preliminary hemodynamic results in humans are consistent with the observations in animals,<sup>11</sup>but no prospective, controlled study has yet proved that higher doses of epinephrine improve survival or other measures of outcome from cardiac arrest in humans. Other clinicians and scientists have voiced a concern that HDE may be detrimental, especially during ischemia and ventricular fibrillation. Since a fibrillating heart consumes oxygen at a rapid rate,<sup>12-16</sup>HDE
Undue Inducement: Nonsense on Stilts?
Authors: Ezekiel J. Emanuel
Journal: The American Journal of Bioethics (2005)

Keywords: Undue inducementcoercionexploitationresearch ethicspaymentOpen Peer Commentaries: Norman Fost, p. 14Howard Brody, p. 15Harold Y. Vanderpool, p. 16Robert Klitzman, p. 19Toby L. SchonfeldJoseph S. BrownBruce G. Gordon, p. 22Joan McGregor, p. 24Ari VanderWalde, p. 25Lynette Reid, p. 27Alex John, p. 29
Tranilast Suppresses Vascular Chymase Expression and Neointima Formation in Balloon-Injured Dog Carotid Artery
Authors: Naotaka Shiota, Hideki Okunishi, Shinji Takai, Imao Mikoshiba, Hiroshi Sakonjo, Nobuo Shibata, Mizuo Miyazaki
Journal: Circulation (1999)

Background —Activation of vascular chymase plays a major role in myointimal hypertrophy after vascular injury by augmenting the production of angiotensin (ANG) II. Because chymase is synthesized mainly in mast cells, we assumed that the chymase-dependent ANG II formation could be downregulated by tranilast, a mast cell–stabilizing antiallergic agent. We have assessed inhibitory effects of tranilast on neointima formation after balloon injury in the carotid artery of dogs, which share a similar ANG II–forming chymase with humans, and further explored the pathophysiological significance of vascular chymase. Methods and Results —Either tranilast (50 mg/kg BID) or vehicle was orally administered to beagles for 2 weeks before and 4 weeks after balloon injury. Four weeks after the injury, remarkable neointima was formed in the carotid arteries of vehicle-treated dogs. Chymase mRNA levels and chymaselike activity of vehicle-treated injured arteries were increased 10.2- and 4.8-fold, respectively, those of uninjured arteries. Angiotensin-converting enzyme (ACE) activity was slightly increased in the injured arteries, whereas ACE mRNA levels were not. Tranilast treatment completely prevented the increase in chymaselike activity, reduced the chymase mRNA levels by 43%, and decreased the carotid intima/media ratio by 63%. In vehicle-treated injured arteries, mast cell count in the adventitia showed a great increase, which was completely prevented by the tranilast treatment. Vascular ACE activity and mRNA levels were unaffected by tranilast. Conclusions —Tranilast suppressed chymase gene expression, which was specifically activated in the injured arteries, and prevented neointima formation. Suppression of the chymase-dependent ANG II–forming pathway may contribute to the beneficial effects of tranilast.
Proteasome-dependent autoregulation of Bruton tyrosine kinase (Btk) promoter via NF-κB
Authors: Liang Yu, Abdalla J. Mohamed, Oscar E. Simonson, Leonardo Vargas, K. Emelie M. Blomberg, Bo Björkstrand, H. Jose Arteaga, Beston F. Nore, C. I. Edvard Smith
Journal: Blood (2008)
Sternal Infection and Retrosternal Abscess Shown on Tc-99m HMPAO-Labeled Leukocyte Scintigraphy
Authors: Jean Robert Hauet, Marie Luce Barge, Odile Fajon, Frederic Comte, Denis Mariano Goulart
Journal: Clinical Nuclear Medicine (2004)

We report a case of a 61-year-old man who underwent coronary artery bypass grafting in 1975 and progressively developed chronic sternal osteomyelitis. He was examined for fever with an increase of pain and swelling of the sternal scar. Computed tomographic scan performed 2 weeks before was normal. The patient was referred to the nuclear medicine department for a bone scan. There was a high level of blood-pool activity in the lower thorax in the blood-pool phase, and intense linear midline uptake was observed extending from the lower thorax into the upper abdomen in the late phase. Anterior and posterior Tc-99m HMPAO-labeled leukocyte images of the chest and abdomen obtained approximately 24 hours after injection demonstrated major accumulation in the same location extending to the anterior mediastinum. A control computed tomographic scan for comparison obtained 1 day later demonstrated a large retrosternal abscess with sternal osteomyelitis. This was confirmed at surgery with drainage of pus. Staphylococcus aureus was isolated. The patient was treated with appropriate antibiotics with good effect.
Risk assessment of low-level chemical exposures from consumer products under the U.S. Consumer Product Safety Commission chronic hazard guidelines.
Authors: M A Babich
Journal: Environmental Health Perspectives (1998)

The U.S. Consumer Product Safety Commission (CPSC) is an independent regulatory agency that was created in 1973. The CPSC has jurisdiction over more the 15,000 types of consumer products used in and around the home or by children, except items such as food, drugs, cosmetics, medical devices, pesticides, certain radioactive materials, products that emit radiation (e.g., microwave ovens), and automobiles. The CPSC has investigated many low-level exposures from consumer products, including formaldehyde emissions from urea-formaldehyde foam insulation and pressed wood products, CO and NO2 emmissions from combustion appliances, and dioxin in paper products. Many chemical hazards are addressed under the Federal Hazardous Substances Act (FHSA), which applies to acute and chronic health effects resulting from high- or low-level exposures. In 1992 the Commission issued guidelines for assessing chronic hazards under the FHSA, including carcinogenicity, neurotoxicity, reproductive/developmental toxicity, exposure, bioavailability, risk assessment, and acceptable risk. The chronic hazard guidelines describe a series of default assumptions, which are used in the absence of evidence to the contrary. However, the guidelines are intended to be sufficiently flexible to incorporate the latest scientific information. The use of alternative procedures is permissible, on a case-by-case basis, provided that the procedures used are scientifically defensible and supported by appropriate data. The application of the chronic hazard guidelines in assessing the risks from low-level exposures is discussed.
Cationic drug-derived nanoparticles for multifunctional delivery of anticancer siRNA
Authors: Rae Sung Chang, Min Sung Suh, Sunil Kim, Gayong Shim, Sangbin Lee, Sung Sik Han, Kyung Eun Lee, Hyesung Jeon, Han-Gon Choi, Yongseok Choi, Chan-Wha Kim, Yu-Kyoung Oh
Journal: Biomaterials (2011)
The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart.
Authors: E Downar, M J Janse, D Durrer
Journal: Circulation (1977)

Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.
Tubercular Abscess of Spine—Incision and Irrigation—Drainage with Iodoform Gauze-Recovery.
Authors: A. C. Harrison
Journal: JAMA (1894)

from which is derived etiology, is compounded of \ g=a\ \ g=i \ \ g=t \ \ g=i \ \ g=a\ a cause and \ g=l \ \ g=o\ \ g=g\ \ g=o\ \ g=f s\ , which taken in composition signifies a study or science.The whole means the study or science of causes.A\ g=i \ \ g=t \ \ g=i \ \ g=o\ \ g=l \ \ g=o\ \ g=g\ \ g=i \ \ g=kschr \ \ g=f s\ , from which comes etiologic, means a person skilled in the study of causes, and may mean any person or thing pertaining to the science of causation.Factor is a Latin word lugged in to mix with the Greek, and signifies a person doing or producing anything.It has also a mathematical use.When two quantities are multiplied together and bring out a product, they are called factors, that is producers.Putting it all together, an "etiologic factor" should be some person or thing producing some other person or thing skilled in, or related to the science of causes ;or in other words a causative-science-maker ; or a maker of something or of somebody pertaining to the science of causes.
SHOULD THE MEDICAL UNDERGRADUATE BE INSTRUCTED IN THE PRINCIPLES OF DENTISTRY?
Authors: M. L. RHEIN
Journal: JAMA (1900)

It is, at the outset, necessary that the term "principles of dentistry," as used in this paper, should be specifically defined. Such a definition is required, both because there should be a definite understanding of the points that the discussion should embrace, and because, mindful of the fact that the path of the medical student already bristles with subjects, we should be loath to add an unnecessary amount of work to his daily routine. A requisite knowledge of the shape and uses of the various dental instruments can not be expected of the general practitioner; indeed, all the variations in dental technique as applied both to laboratory and operating-room are distinctively beyond the scope of dental principles, in their relation to general medical education. The question at issue then narrows itself down to the advisability of the medical undergraduate being acquainted with principles of dentistry as they bear on general
Increased Sympathetic Nervous Activity and the Effects of Its Inhibition with Clonidine in Alcoholic Cirrhosis
Authors: Murray Esler, Frank Dudley, Garry Jennings, Henry Debinski, Gavin Lambert, Penelope Jones, Brendan Crotty, John Colman, Ian Willett
Journal: Annals of Internal Medicine (1992)

Objective: To study disturbances in sympathetic nervous system function in patients with alcoholic cirrhosis and the effect of Clonidine on such disturbances. Design: Cross-sectional physiologic and neurochemical evaluation of patients with cirrhosis and of healthy controls; an uncontrolled trial of intravenous Clonidine in the cirrhotic patients. Patients: Forty-four hospitalized patients with biopsy-proven alcoholic cirrhosis and 31 healthy controls. Interventions: Intravenous clonidine. Main Outcome Measures: Radiotracer-derived measures of norepinephrine release to plasma, central hemodynamics, wedge hepatic vein pressure, and measures of renal function. Main Results: In patients with cirrhosis, clonidine reduced previously elevated norepinephrine overflow rates for the whole body, kidneys, and hepatomesenteric circulation. This sympathetic inhibition was accompanied by the following potentially clinically beneficial effects: the lowering of renal vascular resistance (median reduction, 24%; 95% Cl, 14% to 31%), the elevation of glomerular filtration rate (median increase, 27%; Cl, 14% to 39%), and the reduction of portal venous pressure (median reduction, 25%; Cl, 18% to 32%). The norepinephrine and hemodynamic responses to graded clonidine dosing (1, 2, and 3 µg/kg body weight intravenously) indicated that the sympathetic outflow to the hepatomesenteric circulation was more sensitive to pharmacologic suppression with clonidine than was the sympathetic outflow to the systemic circulation. Conclusions: The sympathetic nerves to the kidneys, heart, and hepatomesenteric circulation are stimulated in patients with cirrhosis. Clonidine inhibits these activated sympathetic outflows differentially, which could possibly provide a basis for the selective pharmacologic treatment of portal hypertension in patients with cirrhosis.