tbuckley/cabot-search huggingface dataset:
AB0024 Genetic Signatures May Be Associated with Vascular Pathology in Rheumatoid Arthritis
Authors: S. Poliska, E. Végh, A. Váncsa, N. Bodnár, S. Szamosi, M. Csumita, G. Kerekes, Z. Szabό, G. Szücs, S. Szántό, G. Zahuczky, P. Soltész, L. Nagy, Z. Szekanecz
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> Accelerated atherosclerosis, increased cardiovascular (CV) morbidity and mortality have been associated with rheumatoid arthritis (RA). In single SNP studies, <i>CD40, HLADRB1, MTHFR, SMAD3</i> and possibly other alleles have been associated with cardiovascular disease (CVD) or vascular pathophysiology in RA. Endothelial dysfunction, carotid atherosclerosis and arterial stiffness that may predict the development of CVD are assessed by bracial artery flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and arterial pulse-wave velocity (PWV), respectively. <h3>Objectives</h3> In this study, we wished to determine expression profiles of multiple genes that may differentiate between physiological and pathological vascular function in RA. <h3>Methods</h3> Altogether 16 RA patients were recruited. FMD, ccIMT and PWV were assessed in all patients using standard B-mode ultrasound techniques. FMD &lt;6%, ccIMT &gt;0.6mm and PWV &gt;9 m/sec were considered abnormal. Peripheral blood mononuclear cell samples were obtained and used in microarray. The signature of those genes were determined by principal component analysis (PCA) and hierarchic clustering (GeneSpring software), which significantly differentiated patient subsets with normal vs abnormal FMD, ccIMT and PWV. <h3>Results</h3> Among RA patients, 11 had low (impaired) and 5 had normal FMD, 11 had high (increased) and 5 had normal ccIMT and 9 had high (increased) and 7 had normal PWV. Altogether 20 genes differentiated patients with low vs normal FMD. Altogether 33 genes separated high vs normal PWV. Finally, 240 genes differentiated increased vs normal ccIMT. <h3>Conclusions</h3> Using microarray, genetic signatures may differentiate RA patients with and without vascular pathology. <h3>Disclosure of Interest</h3> None declared
The Continuing Paradoxes of Nursing Home Policy
Authors: Bruce C. Vladeck
Journal: JAMA (2011)

FEW INDIVIDUALS CHOOSE TO LIVE IN A NURSING HOME rather than in their own home. Many older people and their families fear nursing homes; advocates for younger disabled people lobby for alternatives. Only a small fraction of practicing physicians and nurses work in nursing homes, not all as a first choice. Hospital administrators, who rely on nursing homes as a destination for patients who cannot be discharged to home—and in many instances, as a source of admissions as well—tend to not understand them very well. State and federal budgetmakers believe they cannot live without nursing homes, yet fund them reluctantly. For 30 years, public policy toward long-term care has attempted to minimize the number of people residing in nursing homes. Yet every day 1.5 million individuals in the United States are living in nursing homes, half of whom will never again live anywhere else. More than 1 in 3 US residents who reach age 65 years will spend some time in a nursing home before they die. Nobody, it seems, loves nursing homes very much, but nursing homes are as necessary as they are misunderstood. The confusion about nursing homes arises because many clinical practices and public policies about long-term care are unclear and frustrating. In the patchwork of US health care delivery and financing, nursing homes sit squarely atop 2 of the most problematic seams: the disjunction between Medicare and Medicaid and the disjunction between episodic acute care and long-term care. As a result, facilities referred to as “nursing homes” are generally individual facilities with 2 entirely separate—and often conflicting— clinical missions, serving 2 very different kinds of patients (or, as Zweig et al demonstrate with the case of Mrs R when she begins her nursing home stay for rehabilitation and continues as a long-term stay resident, the same person under very different clinical and financial circumstances), under radically different sets of payment rules and incentives of Medicare and Medicaid.
We Have Went Astray
Authors: Harry S. Grannatt
Journal: JAMA (1964)

<h3>To the Editor:—</h3> Regarding the last line of "Just Words" in the Feb 8 issue (<i>JAMA</i><b>187</b>:403, 1964): I thought good grammar Might prevent Constructions like "He has just went." At least it seems That way to me, But then I ain't No PhD.
Progress in myasthenia gravis.
Authors: C W Havard
Journal: BMJ (1973)

Myasthenia is a syndrome of increased fatigability in striated muscle. It may occur with lesions of the central nervous system or with lesions of muscle. The muscle weakness in these dis orders is usually persistent and unrelenting. Myasthenia gravis, however, is a disorder of neuromuscular function due to a reduction of available acetylcholine (AC) receptors at the neuro muscular junction. The muscle weakness is characteristically worse after effort and improved by rest. The patient starts to comb her hair and is unable to finish, or halfway through a meal finds that she can chew no longer. The muscle weakness has a characteristic distribution, the extraocular, bulbar, neck, limb girdles, distal limbs, and trunk muscles being affected in that order. The myasthenia responds to cholinesterase inhibitors, which enhance the effects of the limited supply of AC at the neuromuscular junctions, and the quick-acting anticholinesterase edrophonium (Tensilon) provides a useful diagnostic test for myasthenia gravis. The diagnosis is not difficult so long as the possibility is kept in mind. When the distribution of muscle weakness is atypical psychiatric disease is commonly and erroneously diagnosed. The incidence of myasthenia gravis is about 1 in 30 000. There is a tendency to early remission but complete remissions are not prolonged and are rarely repeated. They usually occur in those patients with the ocular forms of the disease and within two years of its onset. Patients with the purely ocular form of myasthenia gravis do not commonly develop generalised myasthenia if symptoms remain confined to the extraocular muscles for more than a year, and this may be a distinct variety of the disease.
Shared Decision Making in Cancer Care
Authors: Sarah T. Hawley, Reshma Jagsi
Journal: JAMA Oncology (2015)

Kenneth L. Kehl, MD; Mary Beth Landrum, PhD; Neeraj K. Arora, PhD; Patricia A. Ganz, MD; Michelle van Ryn, PhD, MPH; Jennifer W. Mack, MD, MPH; Nancy L. Keating, MD, MPH
The bacterial effector protein YopM is a selfdelivering immune therapeutic agent that reduces inflammation in rheumatoid arthritis
Authors: J. Bertrand, C. Ruther, J. Scharnert, M. Niedermeier, A. Schmidt, T. Pap
Journal: Annals of the Rheumatic Diseases (2010)

Synovial fibroblasts (RASF) are active drivers of joint destruction in rheumatoid arthritis (RA) through the production of cytokines that maintain the inflammatory process. The Yersinia outer protein M (YopM) is an effector protein of pathogenic Yersinia and is able to enter host cells by membrane penetration and subsequent downregulation of inflammatory responses. Here, we investigated whether YopM has the potential to act as a ‘self-delivering’ immune therapeutic agent by exhibiting a beneficial effect on inflammation and joint destruction …
TCT-206 Angiographic efficacy of Resolute Zotarolimus- or Everolimus- Eluting Stent versus Sirolimus-Eluting Stent Implantation in Long or Diabetic Coronary Artery Disease: Result from LONG-DES III, IV, and ESSENCE-DIABETES trials
Authors: Seung-Whan Lee, Jung-Min Ahn, Young-Rak Cho, Seungbong Han, Jeong Yoon Jang, Soo-Jin Kang, Won-Jang Kim, Young-Hak Kim, Chang Hee Kwon, Jong-Young Lee, Cheol Whan Lee, Woo Seok Lee, Nae Hee Lee, Duk-Woo Park, Gyung-Min Park, Seong-Wook Park, John Seo, Seung-Jung Park
Journal: Journal of the American College of Cardiology (2013)
Metabolic stress–induced activation of FoxO1 triggers diabetic cardiomyopathy in mice
Authors: Pavan K. Battiprolu, Berdymammet Hojayev, Nan Jiang, Zhao V. Wang, Xiang Luo, Myriam Iglewski, John M. Shelton, Robert D. Gerard, Beverly A. Rothermel, Thomas G. Gillette, Sergio Lavandero, Joseph A. Hill
Journal: Journal of Clinical Investigation (2012)

The leading cause of death in diabetic patients is cardiovascular disease; diabetic cardiomyopathy is typified by alterations in cardiac morphology and function, independent of hypertension or coronary disease. However, the molecular mechanism that links diabetes to cardiomyopathy is incompletely understood. Insulin resistance is a hallmark feature of diabetes, and the FoxO family of transcription factors, which regulate cell size, viability, and metabolism, are established targets of insulin and growth factor signaling. Here, we set out to evaluate a possible role of FoxO proteins in diabetic cardiomyopathy. We found that FoxO proteins were persistently activated in cardiac tissue in mice with diabetes induced either genetically or by high-fat diet (HFD). FoxO activity was critically linked with development of cardiomyopathy: cardiomyocyte-specific deletion of FoxO1 rescued HFD-induced declines in cardiac function and preserved cardiomyocyte insulin responsiveness. FoxO1-depleted cells displayed a shift in their metabolic substrate usage, from free fatty acids to glucose, associated with decreased accumulation of lipids in the heart. Furthermore, we found that FoxO1-dependent downregulation of IRS1 resulted in blunted Akt signaling and insulin resistance. Together, these data suggest that activation of FoxO1 is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease.
Common variants in the GDF5-UQCC region are associated with variation in human height
Authors: Serena Sanna, Anne U Jackson, Ramaiah Nagaraja, Cristen J Willer, Wei-Min Chen, Lori L Bonnycastle, Haiqing Shen, Nicholas Timpson, Guillaume Lettre, Gianluca Usala, Peter S Chines, Heather M Stringham, Laura J Scott, Mariano Dei, Sandra Lai, Giuseppe Albai, Laura Crisponi, Silvia Naitza, Kimberly F Doheny, Elizabeth W Pugh, Yoav Ben-Shlomo, Shah Ebrahim, Debbie A Lawlor, Richard N Bergman, Richard M Watanabe, Manuela Uda, Jaakko Tuomilehto, Josef Coresh, Joel N Hirschhorn, Alan R Shuldiner, David Schlessinger, Francis S Collins, George Davey Smith, Eric Boerwinkle, Antonio Cao, Michael Boehnke, Gonçalo R Abecasis, Karen L Mohlke
Journal: Nature Genetics (2008)
AMPHETAMINE (BENZEDRINE) SULFATE AS A CORRECTIVE FOR THE DEPRESSION OF SEDATIVE MEDICATION IN EPILEPSY
Authors: LEON J. ROBINSON
Journal: American Journal of Psychiatry (1941)

Amphetamine ( benzedrine) sulfate, (5-30 mgm.) was given to 58 epileptic patients with toxic manifestations as a result of increased anti-convulsant medication, the latter consisting mainly or in part of phenobarbital in all but one case, (receiving mebaral alone). The toxic effects of the anti-convulsant medication consisted of drowsiness, ataxia, irritability, aggressiveness, anorexia, vertigo, nystagmus and tremor. Amphetamine (benzedrine) sulfate was notably of value in combating the drowsiness (64.2 per cent of cases); and secondarily of value in relieving ataxia, irritability, aggressiveness and anorexia, associated with the drowsiness. Amphetamine was effective in 39 cases, ineffective in 18 cases. When effective, amphetamine was constantly necessary in 18 patients, and only temporarily necessary (7 days to 2 months) in 21 patients. In itself, amphetamine (benzedrine) sulfate did not affect the incidence of epileptic seizures. By counteracting toxic effects amphetamine (benzedrine) sulfate made it possible, in many cases, to reduce seizures by giving adequate anti-convulsant medication, and in this respect proved of appreciable importance as an adjunct in the therapy of epilepsy.
Hypnotic drug use among the elderly living at home
Authors: R. Rozzini, A. Bianchetti, G. Binetti, M. Trabucchi
Journal: BMJ (1988)

like Zimbabwe, India,5 and Egypt,6 where the widespread use of home remedies has reduced mortality from acute diarrhoeal disease.The principles of oral rehydration in acute gastro- enteritis should be common knowledge among parents in Britain (as it is in Zimbabwe) and they should be encouraged to make up solutions as a first aid measure before seeking medical advice.
Differences in innate immune function between allergic and nonallergic children: New insights into immune ontogeny
Authors: Meri K. Tulic, Megan Hodder, Anna Forsberg, Suzi McCarthy, Tara Richman, Nina D’Vaz, Anita H.J. van den Biggelaar, Catherine A. Thornton, Susan L. Prescott
Journal: Journal of Allergy and Clinical Immunology (2010)
CURE OF APLASTIC ANÆMIA IN PAROXYSMAL NOCTURNAL HÆMOGLOBINURIA BY MARROW TRANSFUSION FROM IDENTICAL TWIN: FAILURE OF PERIPHERAL-LEUCOCYTE TRANSFUSION TO CORRECT MARROW APLASIA
Authors: C. Hershko, R.P. Gale, W.G. Ho, M.J. Cline
Journal: The Lancet (1979)
Abstract 784A: Profiling pancreatic cancer metabolism and tumor microenvironment for therapy
Authors: Sminu Bose, Takashi Tsukamoto, Barbara Slusher, Robert E. Royer, David L. Vander Jagt, Anne Le
Journal: Cancer Research (2012)

Abstract Pancreatic cancers have one of the highest fatality rates among all cancers and their response to therapies is highly variable. We have recently shown that inhibition of lactate dehydrogenase A (LDHA) and glutaminase (GLS) through small drug-like molecules causes pancreatic tumor regression. These studies indicate that targeting the metabolic reprogramming of cancer cells is a promising new approach to pancreatic cancer therapy. In order to translate these metabolic inhibitors to the clinic, our goal is to characterize and enable targeted selection of patients based on predicted metabolic response. Although genetic mutations may ultimately be the prime causes of early stage cancer, they can also lead to changes in cancer metabolism which enable cancer cells to proliferate and survive even under the hypoxic and nutrient-deprived conditions often encountered in the tumor microenvironment. The biochemical changes in cancer cells, which determine their behavior in terms of growth, survival and mobility, represent a functional readout of responses to external agents. We hypothesize that the metabolites of tumors that are sensitive to metabolic inhibitors are measurably different from those of resistant ones. We can therefore propose these metabolites as potential functional predictors of response. The proposed research will also study the metabolic reprogramming of cancer cells in the tumor microenvironment that can affect pancreatic cancer sensitivity to LDHA and GLS inhibition. The proposed experiments will use Metabolomics technology to trace the metabolic prototypes of pancreatic orthotopic xenografts to identify the metabolic signature of FX11 or BPTES-sensitive tumors as compared to resistant ones. For an analysis of the effects due to the tumor hypoxic microenvironment, we will use our innovative tool, the HypoxCR reporter system, which can simultaneously detect hypoxic cells and proliferating cells to define the effects of the pancreatic cancer tumor microenvironment on their sensitivity to metabolic inhibitors. This will be the first evaluation of the hypoxic tumor microenvironment in regards to how it affects the response of subfractions of pancreatic orthotopic xenograft tumor cells to metabolic inhibitors. 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 784A. doi:1538-7445.AM2012-784A
Harveian Lecture ON THE FUNCTIONAL ANATOMY OF THE HEART
Authors: A. Keith
Journal: BMJ (1918)

78, hie w s the leading lectur6-on a4atomy J London..It was the appli LaSibn.a-rIg t method to tld study) of the Atucture od the hum.body which Bed him to see that vthe -heatt ws du"ble pup forcing' the blood.to circulate throughopt tilie'.qy.. To understand .how;Iareye became an anataoist we must follow hi.m to the, Unitersity of' Padua in Jtie' last year of tlie sixteentlih eiyy,i wlli lie wa4 'in his twenty-second year.It wao a fortunate circumsfince fr Harvey 'that Fabricius,: Prdfaesor of.A:aomy at Padua, was then reinvestigating the occurrence and use of valves in veins.He explained to, hta students that valves did not occur in arteries because in.' thIem.theblood ebbed and flowed;; but they -were .absolutelyessentfal for veins in order that tlhe; venous blood, wlicil was designed for the nourishment of the tissues, miglht be evenly distributed.to all parts of the body.,-.Were the veins of the arms and legs destitute of valves, it was quite clear, he maintained that blood would gravitate to the hands and feet and so rob otier parts of tlhe body of their just share.We see, tlien, that Fabricius was studying the anatomy of the various parts of the human body in order to find ouit the purpose which tlhey served; he was a functional anatomist.We may smiile at his conclusipns, but we could not make a greater mistake tllan to condemn his methods, for it was by followin-g Fabricius's example that Harvey was led to his great discovery.We have no exact information relating to Harvey's investigations between the time of his .return to .England -in 1602 anid his appointmen.tas LumWhian lecturess at the College of Physicians in 1615.During those thirteen years he dissected many kinds,of animals,2 for Harvey was not only a funotiOnal.anatnist, 'a comparative anatomist and en:4ryol6gist a`well."We have '-nly to turn to his introduction to his book on {he motiol of the
Methadone Treatment of Heroin Addicts
Authors: Andrew T. Canada
Journal: JAMA (1972)

<h3>To the Editor.—</h3> I would like to make two comments regarding the article by Dobbs (<b>218</b>:1536, 1971) on problems associated with methadone programs. I would like to comment on two aspects of his article. First, there is generally little, if any, means of forcing a person participating in a methadone program to abstain from heroin. One of the few means is through fair but stringent rules regarding continued treatment in the methadone program. Most methadone programs either do not have such rules or do not enforce them if such exist. Both lay and exaddict counselors tend to avoid any situation where they may have to make a decision to drop a patient from the program. Programs permit continued use of heroin, continued antisocial behavior, and sales of methadone on the street with no disciplinary measures. How these programs think they are going to encourage the addict to remake his heretofore
Relationship between blood flow direction and endothelial cell orientation at arterial branch sites in rabbits and mice.
Authors: B L Langille, S L Adamson
Journal: Circulation Research (1981)

The orientation of endothelial cells near arterial branch sites has been compared with flow streamlines near the arterial wall. We detected cell orientation by examining cell impressions in vascular casts of rabbit and mouse arterial branch sites. Flow streamlines were assessed in glass models with flow parameters approximating mean in vivo values. At high Reynolds numbers (large arteries), secondary flow develop near branch sites, and this was reflected in the pattern of streamlines near the vessel wall. At symmetrical Y bifurcations, streamlines originating near the inner wall of the branches are directed toward the lateral wall; thus they appear to wind around the daughter vessels and merge on the lateral wall. A similar phenomenon was observed on a 90 degree side branch. When flow conditions in the Y bifurcation and side branch models approximated those at the iliac bifurcation and renal artery origin, respectively, the streamlines near the walls were almost identical to the patterns of endothelial cell orientation. At very low Reynolds numbers, no secondary flow phenomena occurred and streamlines followed branch geometry. This mimicked endothelial cell orientation in very small vessels. Hence the influence of mean blood flow on endothelial cell was well predicted by the model studies.
microRNA 223 Is Upregulated in the Multistep Progression of Barrett's Esophagus and Modulates Sensitivity to Chemotherapy by Targeting <i>PARP1</i>
Authors: Mirte Mayke Streppel, Shweta Pai, Nathaniel R. Campbell, Chaoxin Hu, Shinichi Yabuuchi, Marcia Irene Canto, Jean S. Wang, Elizabeth A. Montgomery, Anirban Maitra
Journal: Clinical Cancer Research (2013)

Recent microarray and RNA-sequencing studies have uncovered aberrantly expressed microRNAs (miRNA) in Barrett's esophagus-associated esophageal adenocarcinoma. The functional significance of these miRNAs in esophageal adenocarcinoma initiation and progression is largely unknown.Expression levels of miR-199a/b-3p, -199a-5p, -199b-5p, -200b, -200c, -223, and -375 were determined in microdissected tissues from cardiac mucosa, Barrett's esophagus, dysplastic Barrett's esophagus, and esophageal adenocarcinoma using quantitative real-time PCR. miR-223 expression was validated in precursors and esophageal adenocarcinomas from 95 patients with esophageal adenocarcinoma by in situ hybridization (ISH). miR-223 was transfected into two esophageal adenocarcinoma cell lines, and in vitro assays were conducted. Target genes were identified using Illumina microarray, and results were validated in cell lines and human specimens.miR-199 family members and miR-223 were significantly overexpressed in esophageal adenocarcinoma, however, only miR-223 showed a stepwise increase during esophageal adenocarcinoma carcinogenesis. A similar trend was observed by ISH, which additionally showed that miR-223 is exclusively expressed by the epithelial compartment. miR-223-overexpressing cells had statistically significantly more migratory and invasive potential than scramble sequence-transfected cells. PARP1 was identified as a direct target gene of miR-223 in esophageal adenocarcinoma cells. Increased sensitivity to chemotherapy was observed in cells with enforced miR-223 expression and reduced PARP1.miR-223 is significantly upregulated during the Barrett's esophagus-dysplasia-esophageal adenocarcinoma sequence. Although high miR-223 levels might contribute to an aggressive phenotype, our results also suggest that patients with esophageal adenocarcinoma with high miR-223 levels might benefit from treatment with DNA-damaging agents.
SOURCES OF PLAGUE.
Authors: W. J. CALVERT
Journal: JAMA (1904)

This subject involves a discussion of the early and present pandemics, cardinal features of the viability and dissemination of<i>Bacillus pestis</i>and the transmission of plague. <h3>HISTORICAL SKETCH.</h3> While indefinite statements regarding plague are found in the earliest writings, no definite knowledge of this disease has been found until the writings of Rufus of Ephesus regarding plague in Egypt in the second century B. C. At this time the disease was present in lower Egypt, spread along the coast of the Mediterranean and existed as a pandemic for an unknown period. Numerous detailed accounts give positive data that this pandemic was the same disease as that now known as bubonic plague. During this period war, drought and famines were prevalent throughout the world. During the centuries following this pandemic, numerous references to plagues are found, but each is too indefinite to warrant a diagnostication of bubonic plague. In the Justinian
Diagnosis of Autoimmune Pancreatitis vs Neoplasms in Children With Pancreatic Mass and Biliary Obstruction
Authors: Joel Friedlander, J. Antonio Quiros, Terry Morgan, Zili Zhang, Wei Tian, Elizabeth Kehr, Dustin V. Shackleton, Andrew Zigman, Peter Stenzel
Journal: Clinical Gastroenterology and Hepatology (2012)