tbuckley/cabot-search huggingface dataset:
Chronic lymphocytic leukemia and regulatory B cells share IL-10 competence and immunosuppressive function
Authors: D J DiLillo, J B Weinberg, A Yoshizaki, M Horikawa, J M Bryant, Y Iwata, T Matsushita, K M Matta, Y Chen, G M Venturi, G Russo, J P Gockerman, J O Moore, L F Diehl, A D Volkheimer, D R Friedman, M C Lanasa, R P Hall, T F Tedder
Journal: Leukemia (2012)
GLP-1 Provoked Severe Hypoglycemia in an Individual With Type 2 Diabetes and a Benign Insulinoma
Authors: Ronald J. Ruby, John P. Armato, Charles Pyke, Anne L. Peters
Journal: Diabetes Care (2014)

This is a case of a severe hypoglycemia caused by an excess of GLP-1 receptors on a benign insulinoma in an individual with type 2 diabetes. The hypoglycemia was likely induced by a GLP-1 receptor agonist. The patient is a 54-year-old Caucasian female evaluated for “reactive” hypoglycemia that had worsened over the past 10 years. She had gained 20 pounds and reported intermittent episodes of “lightheadedness and shakiness,” which she treated with carbohydrates. One morning after a breakfast of pancakes and syrup, her husband described an episode that required him to feed her “a lot of orange juice to keep her awake.”

She had no pertinent past medical history and a normal physical exam. Diabetes was diagnosed based on an oral glucose tolerance test with a fasting plasma glucose of 7.05 mmol/L, a 120-min value of …
Thrombin-Induced Increase in Intracellular Cyclic 3′,5′-Adenosine Monophosphate in Human Platelets
Authors: Michael J. Droller, Sidney M. Wolfe
Journal: Journal of Clinical Investigation (1972)

The present data disagree with earlier suggestions that thrombin's effect on platelets is to cause a decrease in intracellular cyclic 3',5'-adenosine monophosphate. Washed human platelets or platelet-rich plasma were incubated at 37 degrees C with human thrombin. After centrifugation, the supernates were assayed for nucleotides and calcium released. The platelet pellets, and in some experiments the supernates as well, were assayed by radioimmunoassay for intracellular cyclic AMP. In the washed platelet system, increasing doses of thrombin to 0.5 U/cc induced increasing release of nucleotides and calcium. This was accompanied by an average twofold increase in intracellular cyclic AMP levels. Prostaglandin E(1), which inhibited 30-50% of release, induced a four- to fivefold increase in cyclic AMP levels that was additive to the cyclic AMP-stimulatory effect of thrombin. Theophylline, which inhibited only 20-40% of nucleotide release, was synergistic with thrombin in the intracellular accumulation of cyclic AMP. The time-course of cyclic AMP accumulation in response to thrombin was slower than thrombin-induced nucleotide release. Similar findings were made in the platelet-rich plasma system where thrombin stimulation of nucleotide release also resulted in a marked accumulation of intracellular cyclic AMP. Thrombin did not appear to stimulate the release of intracellular cyclic AMP. The mechanism underlying these observations was not apparent. The thrombin had no measurable inhibitory effect on platelet phosphodiesterase activity in either intact washed cells or the platelet homogenate supernates. Furthermore, thrombin inhibited, rather than stimulated, platelet adenyl cyclase activity in both intact washed cells and washed platelet particulate fractions. Of note, however, was the finding that thrombin did not completely inhibit the adenyl cyclase activity of prostaglandin-stimulated cells. Further work is needed to clarify the significance of this observation.Nonetheless, the accumulation of intracellular cyclic AMP in response to thrombin observed in the present study suggests that the antagonistic actions of various agents on the platelet release reaction, thought to underlie platelet function, may depend upon a mechanism more intricate than a straightforward mediation through directly opposite effects on platelet cyclic AMP.
New Rules Extinguish 'Smoking Lamp' in Growing Number of Public Places
Authors: Charles Marwick
Journal: JAMA (1988)

IN ABOUT two weeks, New York City begins strict enforcement of what has been called "the most sweeping nonsmoking law in the United States." It is just one of a growing number of indications that those Americans who continue to smoke in the months and years ahead will find fewer public places to do so. That eventually may include more of those who can't even go home to smoke—the inmates of the nation's jails and prisons. In Utah, for example, the Davis County Jail now is smoke free. The National Commission on Correctional Care, Chicago, says the Davis County sheriff made the decision after studying the experience of the smoke-free jail in Orchard Cove, Wash, noting the legislature's prohibiting of smoking in any general public place, realizing his jail is poorly ventilated, and arranging counseling and medical service for inmates addicted to tobacco. The commission says complaints "have been minimal."
Abstract 1119: The oxidation of proline by proline oxidase provides a regulated source of ROS for mitochondria derived cellular signaling
Authors: Chad N. Hancock, James Phang
Journal: Cancer Research (2012)

Abstract A role for reactive oxygen species (ROS) in intracellular signaling has been generally accepted, but the organellar localization, the enzymatic source and the regulation of ROS generation are not well understood. Recent work by others has focused on mitochondria as a source of ROS and specifically on the reduction of oxygen by electrons from complex III to form superoxide. The accessibility of complex III to the mitochondrial intermembrane space and cytosol provides an attractive hypothesis for mitochondrial ROS as regulators of cellular redox signaling. We now report that the regulated metabolism of proline makes it a special substrate for this process. Proline oxidase (POX) is an inner mitochondrial membrane protein that oxidizes proline to generate superoxide as well as ATP. Work in our laboratory has documented that POX activity is highly regulated during genotoxic and metabolic stress. Inducers of POX include p53, and proline-dependent ROS play a role in mitochondrial apoptosis. PPAR-γ and its ligands also induce POX but depending on the metabolic context, POX initiates autophagy as well as apoptosis. Mechanistic models for ROS generation by POX have come from microorganisms. PutA, the prokaryotic homolog of POX can generate ROS by electrons reducing oxygen directly from its catalytic center. On the other hand, in S. cerevisiae, the POX homolog, Put1, has been shown to directly interact with ubiquinone, thereby contributing electrons derived from proline oxidation into the electron transport chain. In this work, we now report that human POX interacts directly with ubiquinone and that POX activity is markedly increased by the presence of ubiquinone. In addition, by using selective inhibitors of electron transport, we demonstrate that electrons derived from proline can be converted to superoxide by complex III of the electron transport chain. These radicals are directed into both the mitochondrial matrix as well as into the intermembrane space and the cytosol. Thus, POX is not only specifically regulated but also specially located and coupled to the mitochondrial electron transport chain to mediate ROS signaling. These POX- mediated mechanisms provide important insights into its novel apoptotic and metabolic tumor suppressive functions. 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 1119. doi:1538-7445.AM2012-1119
1009-169 Cardiovascular variability in hypertensive subjects with and without obstructive sleep apnea
Authors: Maria do Socorro Brasileiro Santos, Maria Ångela Casas Coelho, Sonia Togeiro, Rodrigo D.M Plentz, Fernanda Marciano Consolim-Colombo, Maria Claudia Irigoyen, Nicola Montano, Eduardo Moacir Krieger
Journal: Journal of the American College of Cardiology (2004)
Very Low-Calorie Diets for Obesity-Reply
Authors: Susan Zelitch Yanovski
Journal: JAMA (1994)

<h3>In Reply.</h3> —We thank Drs Kaplan and Stifler for their comments regarding our article on VLCDs. We agree, as we stated in our article, that VLCDs are clearly effective in promoting short-term weight loss. Unfortunately, no short-term nonsurgical intervention for obesity has been shown to provide long-term maintenance of lost weight for the majority of patients. Obesity is a chronic condition, and as such, any treatments developed need to be continued indefinitely in order to maintain their effectiveness. Without ongoing support or intervention, lifetime changes in diet, behaviors, and— perhaps most important—physical activity are difficult if not impossible for most individuals to sustain. Health care professionals play an important role in determining which patients will benefit medically from weight loss, as well as identifying psychological and social factors that may impact on the type and intensity of any treatment provided. Adjunctive treatments, including anorectic medications<sup>1</sup>or surgical treatment in
420 INFLUENCE OF GENDER ON VIRAL LOAD ACCORDING TO AGE IN PATIENTS WITH CHRONIC HEPATITIS C: A POSSIBLE EFFECT OF HORMONAL FACTORS
Authors: C. Stern, R. Moucari, A.-C. Cardoso, M. Martinot-Peignoux, N. Boyer, M.-P. Ripault, P. Bedossa, P. Marcellin
Journal: Journal of Hepatology (2009)
Abstract 3033: NKX2-5, a potential tumor suppressor gene in prostate cancer
Authors: Mohammad Daremipouran, Song Ping Wang, Alexander Ellis, Zebalda Bamji, Bernard Kwabi-Addo
Journal: Cancer Research (2011)

Abstract Background: Prostate cancer (PCa) is a common malignancy and a leading cause of cancer deaths among men in the United States. Abundant evidence has accumulated to suggest that epigenetic DNA methylation changes may appear earlier during PCa development than genetic changes, as well as more commonly and consistently suggesting that DNA methylated genes can be explored as DNA-based biomarker for PCa disease detection. Recently, we have identified NKX2-5 as a novel that is hypermethylated in prostate cancer. However, there is little information about the biological significance of this gene in prostate carcinogenesis. We hypothesize that NKX2-5 is a potential tumor suppressor gene that is frequently inactivated in prostate cancer. Methods: We carried out gain-and-loss functional studies of NKX2-5 in prostate cancer cell lines and validated expression at the RNA transcript level using quantitative RT-PCR. Protein expression was analyzed by western blotting and cell cycle analysis investigated by flow cytometer. Results: Over-expression of NKX2-5 was detrimental to prostate cancer cell proliferation as evidenced by significant inhibition of prostate cancer cell proliferation in comparison to control (vector only transfection) and this was due to cell arrest in Go/G1 phase and increase apoptosis. In contract, successful knockdown of NKX2-5 by shRNA transfection increased prostate cancer cell proliferation. Western blot analysis demonstrated that NKX2-5 plays a key regulatory role in the expression of several genes including p53, PTEN, Histone H1 and the androgen receptor. Conclusion: Our observation suggests that NKX2-5, a member of the homeobox gene family of plays an important tumor suppressor activity in prostate carcinogenesis. Because this gene plays important role in several signal transduction pathways, this gene can be exploited as potential biomarker for the early detection of prostate cancer and could be an attractive target to explore for drug investigation or gene therapies of prostate cancer. 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 3033. doi:10.1158/1538-7445.AM2011-3033
A Better Treatment of Pneumonia Wanted—The "Galbraith Quinin-Iron Method."
Authors: J. E. Summers
Journal: JAMA (1906)

Omaha, Neb., April 3, 1906. <h3>To the Editor:</h3> —Recently, after having a chill and feeling badly I wondered, should my case develop into a pneumonia, whether my physician would give me the best chance to live by employing the modern treatment indicated in your recent editorial. It has been disappointing not to have learned more about the "Galbraith quinin-iron treatment" of pneumonia from those in a position to try and better their statistics. The death rate from acute lobar pneumonia is high, and hospital statistics during many years show no great improvement in its treatment. Every one acquainted with Dr. Galbraith knows him as an experienced and exceedingly practical "allaround" man; his diagnosis in a case or series of cases of pneumonia can be as absolutely relied on as that of any physician, wherever located. It is this knowledge of the man that leads me to have faith in what
Improvement of Cardiac Function During Enzyme Replacement Therapy in Patients With Fabry Disease
Authors: Frank Weidemann, Frank Breunig, Meinrad Beer, Joern Sandstede, Oliver Turschner, Wolfram Voelker, Georg Ertl, Anita Knoll, Christoph Wanner, Jörg M. Strotmann
Journal: Circulation (2003)

Enzyme replacement therapy (ERT) has been shown to enhance microvascular endothelial globotriaosylceramide clearance in the hearts of patients with Fabry disease. Whether these results can be translated into an improvement of myocardial function has yet to be demonstrated.Sixteen patients with Fabry disease who were treated in an open-label study with 1.0 mg/kg body weight of recombinant alpha-Gal A (agalsidase beta, Fabrazyme) were followed up for 12 months. Myocardial function was quantified by ultrasonic strain rate imaging to assess radial and longitudinal myocardial deformation. End-diastolic thickness of the left ventricular posterior wall and myocardial mass (assessed by magnetic resonance imaging, n=10) was measured at baseline and after 12 months of ERT. Data were compared with 16 age-matched healthy controls. At baseline, both peak systolic strain rate and systolic strain were significantly reduced in the radial and longitudinal direction in patients compared with controls. Peak systolic strain rate increased significantly in the posterior wall (radial function) after one year of treatment (baseline, 2.8+/-0.2 s(-1); 12 months, 3.7+/-0.3 s(-1); P<0.05). In addition, end-systolic strain of the posterior wall increased significantly (baseline, 34+/-3%; 12 months, 45+/-4%; P<0.05). This enhancement in radial function was accompanied by an improvement in longitudinal function. End-diastolic thickness of the posterior wall decreased significantly after 12 months of treatment (baseline, 13.8+/-0.6 mm; 12 months, 11.8+/-0.6 mm; P<0.05). In parallel, myocardial mass decreased significantly from 201+/-18 to 180+/-21 g (P<0.05).These results suggest that ERT can decrease left ventricular hypertrophy and improve regional myocardial function.
Heart of the athlete.
Authors: A J Ryan
Journal: British Journal of Sports Medicine (1991)

When sports medicine was in its infancy in the early 1900s, and before anyone had heard of an exercise physiologist, some physicians had been concerned about the effects of vigorous exercise on the heart.Among them where Schott', Henschen2, Kienbock3, Barach, and Lee5 who had made and recorded observations on swimmers, cross-country skiers and wrestlers.With the general increase in sports activity that followed World War I, many physicians expressed concerns about the long-term effects of sports participation on the adolescent heart.Their apprehension was embodied in a concept of 'athlete's heart' that stemmed back to an erroneous calculation of the German cardiologist Beneke6, published in 1879, that resulted in his statement that the growth of the left ventricle was disproportionate to the increase in diameter of the ascending aorta during adolescence.This error was pointed out by Karpovich7, but the concept and the term lingered on.Studies of the trainability of athletes by cardiologists and physiologists following World War II demonstrated the relationships between the heart rate attained during exercise and oxygen consump- tion, giving rise to the concept of maximal oxygen consumption V62, max8* Aerobic and anaerobic per-
Antitrust Implications of Medical Technology Assessment
Authors: Martin Rose, Robert F. Leibenluft
Journal: New England Journal of Medicine (1986)

AS the pressure to control health care costs has grown, third-party payers and others have increasingly undertaken to assess the merits of procedures and equipment used in patient care. Interest in such assessment is strong in both the public and private sectors and shows no signs of waning.1 2 3 In assessing medical technology, organizations typically consult medical experts or medical specialty societies. Some assessments, especially those by payers or influential professional organizations, can have profound implications in the marketplace. An assessment that is unfavorable or inconclusive may substantially reduce the sale or use of a medical device or procedure or may . . .
Determinants of Successful Selective Tracheobronchial Suctioning
Authors: Paul B. Haberman, Joseph P. Green, Carol Archibald, Deon L. Dunn, Sheldon R. Hurwitz, William L. Ashburn, Kenneth M. Moser
Journal: New England Journal of Medicine (1973)

In 24 patients with nasotracheal, orotracheal and tracheostomy tubes in place, a scintigraphic technic was used to monitor attempts to cannulate selectively the right and left main-stem bronchi by suction catheters. Regardless of catheter type and patient positioning, the left main-stem bronchus was more difficult to enter (46 per cent success rate) than the right (75 per cent success). Angle-tipped suction catheters were more successful than straight catheters In cannulating both right and left mainstem bronchi. Catheters packed in straight, rather than coiled, configurations were more successful In achieving left-main-stem bronchus cannulation. The left main-stem bronchus was particularly difficult to enter through nasotracheal tubes. Turning the head to the right improved the success of left-main-stem-bronchus catheterization. Turning the head to the left or shoulder positioning did not assist in selective bronchial cannulation. (N Engl J Med 289:1060–1063, 1973)
Abstract 2737: Anti-proliferative action of metformin on various types of human lung cancer cell lines
Authors: Hironori Ashinuma, Yuichi Takiguchi, Satoru Kitazono, Miyako Kitazono-Saitoh, Atsushi Kitamura, Yuji Tada, Katsushi Kurosu, Emiko Sakaida, Ikuo Sekine, Nobuhiro Tanabe, Koichiro Tatsumi
Journal: Cancer Research (2012)

Abstract [Background] Metformin has a potential to inhibit tumor growth in various cancer cell lines in vitro and in vivo. [Purpose] To elucidate anti-proliferative actions of the agent on various types of human lung cancer cell lines, and to evaluate combined effects with cisplatin. [Methods] Cell lines used consisted of four human lung cancer cell lines, RERF-LC-AI (squamous cell carcinoma), A549 (adenocarcinoma), IA-5 (large cell carcinoma) and WA-hT (small cell carcinoma). Colonogenic assay was employed to evaluate colonogenicity with exposure to metformin for 1, 24 hours and 10 days. In cell surviving assay, 100,000 cells per plate were cultured for 4 days with metformin and/or cisplatin, and survived cells were counted. [Results] Metformin inhibited colonogenecity in every cell line in a dose-dependent manner when cells were exposed to the agent for 10 days, whereas 1- and 24-hour exposure yielded not significant or only mild effects, with the degree varied depending on cell lines. With cell surviving assay at the metformin concentrations where 70% (IC70) and 30% (IC30) of the cells survived for each cell line, apoptosis was not increased over control groups in every cell line except for WA-hT that showed significant increase in apoptosis with metformin. Significant alteration in cell cycle distribution with the agent was not observed in all of the 4 cell lines. For evaluating combination treatment consisting of metformin and cisplatin, cisplatin at doses of IC50 and IC10 was combined with metformin. Inhibitory effects of metformin on cell proliferation were slightly suppressed with cisplatin at its dose of IC50 in all except for in A549. High dose (IC10) of cisplatin almost completely countervailed or even reversed the metformin effects in all cell lines, again except for A549 where a modest but significant sub-additive effect was observed. [Conclusions] Metformin has anti-proliferative effects on various types of human lung cancer cell lines. Although apoptosis was observed only in a small-cell lung cancer cell line, its effects may not depend on apoptosis in other 3 cell lines. Alteration of cell cycle distribution was not observed in all cell lines. Metformin and cisplatin were antagonistic especially with higher dose cisplatin. 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 2737. doi:1538-7445.AM2012-2737
The States' Next Challenge — Securing Primary Care for Expanded Medicaid Populations
Authors: Leighton Ku, Karen Jones, Peter Shin, Brian Bruen, Katherine Hayes
Journal: New England Journal of Medicine (2011)

Many of the U.S. states with the largest anticipated Medicaid expansions are also the ones that have less primary care capacity. These states could face surging demand from the newly insured population without having sufficient primary care resources available.
Circulatory and Renal Effects Following Transfusion of Human Blood and its Components to Dogs
Authors: HADLEY L. CONN, JOHN C. WOOD, JOHN C. ROSE
Journal: Circulation Research (1956)

The cardiovascular effects of the transfusion of human blood and of some of its components were studied in dogs. Human blood, hemoglobin, globin and red cell stroma produced significant circulatory depression. The reaction to stromal materials was considered to represent a combination of peripheral pooling and myocardial depression. The reactions to human hemoglobin and globin indicated primary vasoconstriction as the initial abnormality. The reaction to human blood, apparently, was a combination of the reactions to stroma and hemoglobin, with an anaphylactoid response after second blood transfusions.