tbuckley/cabot-search huggingface dataset:
Malondialdehyde-Modified LDL as a Marker of Acute Coronary Syndromes
Authors: Paul Holvoet
Journal: JAMA (1999)

SCHEMIC INJURY OF ENDOTHELIUM ISassociated with prostaglandin synthesis and platelet adhesion and aggregation, which may be associated with the release of aldehydes that substitute the lysine residues in the apolipoprotein B-100 moiety of lowdensity lipoprotein (LDL) in the absence of lipid peroxidation. 1,2This type of oxidatively modified LDL is referred to as malondialdehyde (MDA)modified LDL. 3 Plasma levels of MDAmodified LDL are increased in patients with acute coronary syndromes, ie, unstable angina or acute myocardial infarction (AMI). 3,4Previously, Creactive protein 5 and cardiac troponins [6][7][8][9] have been proposed as diagnostic markers of acute coronary syndromes.In this study, we compared the usefulness of MDA-modified LDL as a marker of acute coronary syndromes with that of C-reactive protein and troponin I. METHODSA total of 168 patients were studied, including 104 consecutive patients admitted to the emergency department of the University Hospital of Leuven, Belgium, because of an acute coronary syndrome and 64 patients with stable, angiographically documented coronary artery disease (CAD) without clinical signs of ischemia.Patients with stable CAD were treated with aspirin, ␤-blockers, nitrates, and, in a great majority, angiotensin-converting enzyme inhibitors.Patients with acute coronary syndromes had ischemic chest discomfort with transient ST-segment elevation or persistent ST-segment depression of more than 0.5 mm, or T-wave inversion of more than 1 mm.Blood samples for MDA-modified LDL assay from patients with acute coronary syndromes were collected at admission, within 6-8 hours of onset of chest pain, and before therapy was started.Blood samples for total creatine kinase (CK) and for CK isoenzyme MB mass assay were obtained at entry, 6 to 8 and then 12 to 16 hours after admission.Enzyme evidence of AMI was defined as CK-MB elevation above the normal range and at least 3% of total CK.All patients with acute coronary syndromes received oral aspirin, intravenous nitrates, and heparin for 48 to 72 hours.Most of these patients underwent coronary angiography and revascularization within the first 3 to 5 days after hospital admission.Blood samples were collected in
Florbetapir PET analysis of amyloid-β deposition in the presenilin 1 E280A autosomal dominant Alzheimer's disease kindred: a cross-sectional study
Authors: Adam S Fleisher, Kewei Chen, Yakeel T Quiroz, Laura J Jakimovich, Madelyn Gutierrez Gomez, Carolyn M Langois, Jessica BS Langbaum, Napatkamon Ayutyanont, Auttawut Roontiva, Pradeep Thiyyagura, Wendy Lee, Hua Mo, Liliana Lopez, Sonia Moreno, Natalia Acosta-Baena, Margarita Giraldo, Gloria Garcia, Rebecca A Reiman, Matthew J Huentelman, Kenneth S Kosik, Pierre N Tariot, Francisco Lopera, Eric M Reiman
Journal: The Lancet Neurology (2012)
Blockade of Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Kinase and Murine Double Minute Synergistically Induces Apoptosis in Acute Myeloid Leukemia via BH3-Only Proteins Puma and Bim
Authors: Weiguo Zhang, Marina Konopleva, Jared K. Burks, Karen C. Dywer, Wendy D. Schober, Jer-Yen Yang, Teresa J. McQueen, Mien-Chie Hung, Michael Andreeff
Journal: Cancer Research (2010)

Molecular aberrations of the Ras/Raf/mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK) kinase (MEK)/ERK and/or Murine double minute (MDM2)/p53 signaling pathways have been reported in 80% and 50% of primary acute myeloid leukemia (AML) samples and confer poor outcome. In this study, antileukemic effects of combined MEK inhibition by AZD6244 and nongenotoxic p53 activation by MDM2 antagonist Nutlin-3a were investigated. Simultaneous blockade of MEK and MDM2 signaling by AZD6244 and Nutlin-3a triggered synergistic proapoptotic responses in AML cell lines [combination index (CI) = 0.06 +/- 0.03 and 0.43 +/- 0.03 in OCI/AML3 and MOLM13 cells, respectively] and in primary AML cells (CI = 0.52 +/- 0.01). Mechanistically, the combination upregulated levels of BH3-only proteins Puma and Bim, in part via transcriptional upregulation of the FOXO3a transcription factor. Suppression of Puma and Bim by short interfering RNA rescued OCI/AML3 cells from AZD/Nutlin-induced apoptosis. These results strongly indicate the therapeutic potential of combined MEK/MDM2 blockade in AML and implicate Puma and Bim as major regulators of AML cell survival.
Peripheral Autoantigen Induces Regulatory T Cells that Prevent Autoimmunity
Authors: Benedict Seddon, Don Mason
Journal: The Journal of Experimental Medicine (1999)

Previous studies have shown that autoimmune thyroiditis can be induced in normal laboratory rats after thymectomy and split dose γ-irradiation. Development of disease can be prevented by reconstitution of PVG rats shortly after their final irradiation with either peripheral CD4+CD45RC− T cells or CD4+CD8− thymocytes from syngeneic donors. Although the activity of both populations is known to depend on the activities of endogenously produced interleukin 4 and transforming growth factor β, implying a common mechanism, the issue of antigen specificity of the cells involved has not yet been addressed. In this study, we show that the regulatory T cells that prevent autoimmune thyroiditis are generated in vivo only when the relevant autoantigen is also present. Peripheral CD4+ T cells, from rats whose thyroids were ablated in utero by treatment with 131I, were unable to prevent disease development upon adoptive transfer into thymectomized and irradiated recipients. This regulatory deficit is specific for thyroid autoimmunity, since CD4+ T cells from 131I-treated PVG.RT1u rats were as effective as those from normal donors at preventing diabetes in thymectomized and irradiated PVG.RT1u rats. Significantly, in contrast to the peripheral CD4+ T cells, CD4+CD8− thymocytes from 131I-treated PVG donors were still able to prevent thyroiditis upon adoptive transfer. Taken together, these data indicate that it is the peripheral autoantigen itself that stimulates the generation of the appropriate regulatory cells from thymic emigrant precursors.
Deaths from Asthma in England and Wales
Authors: D. A. Williams
Journal: Thorax (1953)

It is known and accepted that asthma is a very common condition, and from a stirvey of the ill- nesses of the adult population of England and Wales (1944-7) by Stocks (1949) it has been esti- mated that asthma occurs in one in every 110 of the adult population, or, more correctly, in 904 per 100,000 of the adult population.The frequency of death from status asthmaticus in this common condition is, however, uncertain, and opinions differ.Witts (1936) has written: "When status asthmaticus persists for two days, the risk of sudden death should be seriously con- sidered.Experience of a large clinic at which several hundred patients are in regular attendance suggests that one or two of these patients may be expected to die of asthma each year."Coope (1948) writes: *' The prognosis of the acute attack is usually good.It is sometimes said that no one ever dies of asthma, but this is not entirely true."Young and Beaumont (1950) in Price's textbook of medicine write: ". . .Although in a severe attack of asthma the aspect of the patient may be so alarming that a fatal issue appears imminent, death rarely occurs."From the United States we read:" Traditionally, asthma is a disease causing pro- longed and recurrent disability, but not death....Many physicians of wide experience in the field have expressed the opinion that death from asthma is the result of mistreatment or even of the medication rather than the disease itself.For example, a recent textbook states that 'death in uncomplicated asthma is rare unless morphine has been used.' . . .In con- sidering fatalities from asthma it is at once apparent that the prognosis is very different in asthma due to demonstrable external allergens and in so-called ' intrinsic' asthma. . . .Patients with 'intrinsic' asthma, possibly resulting from infection, are more apt to develop symptoms in middle age and may succumb within ten years " (Sherman, 1952).From Canada Walton, Penner, and Wilt (1951) have written: " . . .It does not appear to be suffi- ciently widely appreciated that bronchial asthma is a disease which may be fatal in itself."
The Management of Pathologic Interdependency in Drug Addiction
Authors: RALPH B. LITTLE, MANUEL M. PEARSON
Journal: American Journal of Psychiatry (1966)

The concept of the addictor has been formulated to describe a person who finds relief from his emotional tensions by unconsciously encouraging and/or perpetuating the drug addiction of another individual. The authors point out that understanding of the pathological interdependency which may exist between the addict and a significant other person in his environment can facilitate the psychiatrist's treatment of drug addiction and may determine its success or failure.
K <sub>ATP</sub> Channel Activation Induces Ischemic Preconditioning of the Endothelium in Humans In Vivo
Authors: M.W. Broadhead, R.K. Kharbanda, M.J. Peters, R.J. MacAllister
Journal: Circulation (2004)

Endothelial dysfunction contributes to ischemia-reperfusion injury (IRI) and is reduced by ischemic preconditioning (IPC). IPC may involve activation of ATP-sensitive potassium channels (K(ATP)). We determined whether modulation of K(ATP) channels occurs in endothelial IPC in humans.IRI of the forearm was induced by inflating a blood pressure cuff to 200 mm Hg for 20 minutes in healthy volunteers. K(ATP) activation was modulated by intra-arterial glibenclamide (blocker) and diazoxide (opener). Endothelial function (response to intra-arterial acetylcholine) was assessed with forearm plethysmography before and after (1) 15-minute reperfusion, (2) IRI preceded by IPC (3 five-minute periods of ischemia), (3) IRI preceded by IPC with glibenclamide, (4) IPC followed by glibenclamide before IRI, (5) IRI preceded by diazoxide, and (6) IRI preceded by coinfusion of glibenclamide with diazoxide. IRI caused endothelial dysfunction (P=0.002), which IPC prevented (P=0.40). Glibenclamide abolished IPC when given contemporaneously with (P=0.003) or during IRI (P=0.0005). Diazoxide prevented endothelial dysfunction after IRI (P=0.68) but not when coinfused with glibenclamide.Glibenclamide abolishes and diazoxide mimics endothelial IPC in humans. The time course of the effect of glibenclamide suggests involvement of K(ATP) channels as effectors of endothelial IPC in vivo. These data may have implications for understanding the therapeutic role of agents that modulate K(ATP) channel function.
Principal Component Analysis under Population Genetic Models of Range Expansion and Admixture
Authors: O. Francois, M. Currat, N. Ray, E. Han, L. Excoffier, J. Novembre
Journal: Molecular Biology and Evolution (2010)

In a series of highly influential publications, Cavalli-Sforza and colleagues used principal component (PC) analysis to produce maps depicting how human genetic diversity varies across geographic space. Within Europe, the first axis of variation (PC1) was interpreted as evidence for the demic diffusion model of agriculture, in which farmers expanded from the Near East ∼10,000 years ago and replaced the resident hunter-gatherer populations with little or no interbreeding. These interpretations of the PC maps have been recently questioned as the original results can be reproduced under models of spatially covarying allele frequencies without any expansion. Here, we study PC maps for data simulated under models of range expansion and admixture. Our simulations include a spatially realistic model of Neolithic farmer expansion and assume various levels of interbreeding between farmer and resident hunter-gatherer populations. An important result is that under a broad range of conditions, the gradients in PC1 maps are oriented along a direction perpendicular to the axis of the expansion, rather than along the same axis as the expansion. We propose that this surprising pattern is an outcome of the "allele surfing" phenomenon, which creates sectors of high allele-frequency differentiation that align perpendicular to the direction of the expansion.
Expansion of Secretin-Like G Protein-Coupled Receptors and Their Peptide Ligands via Local Duplications Before and After Two Rounds of Whole-Genome Duplication
Authors: Jong-Ik Hwang, Mi Jin Moon, Sumi Park, Dong-Kyu Kim, Eun Bee Cho, Nui Ha, Gi Hoon Son, Kyungjin Kim, Hubert Vaudry, Jae Young Seong
Journal: Molecular Biology and Evolution (2013)

In humans, the secretin-like G protein-coupled receptor (GPCR) family comprises 15 members with 18 corresponding peptide ligand genes. Although members have been identified in a large variety of vertebrate and nonvertebrate species, the origin and relationship of these proteins remain unresolved. To address this issue, we employed large-scale genome comparisons to identify genome fragments with conserved synteny and matched these fragments to linkage groups in reconstructed early gnathostome ancestral chromosomes (GAC). This genome comparison revealed that most receptor and peptide genes were clustered in three GAC linkage groups and suggested that the ancestral forms of five peptide subfamilies (corticotropin-releasing hormone-like, calcitonin-like, parathyroid hormone-like, glucagon-like, and growth hormone-releasing hormone-like) and their cognate receptor families emerged through tandem local gene duplications before two rounds (2R) of whole-genome duplication. These subfamily genes have, then, been amplified by 2R whole-genome duplication, followed by additional local duplications and gene loss prior to the divergence of land vertebrates and teleosts. This study delineates a possible evolutionary scenario for whole secretin-like peptide and receptor family members and may shed light on evolutionary mechanisms for expansion of a gene family with a large number of paralogs.
Tourette's syndrome and homozygosity for the dopamine D3 receptor gene
Authors: Johannes Hebebrand, MarkusM Nöthen, Gerd Lehmkuhl, Fritz Poustka, Martin Schmidt, Peter Propping, Helmut Remschmidt, DavidE Comings, Donn Muhleman, George Dietz, Micaela Dino, Rick Legro, Radhika Gade
Journal: The Lancet (1993)
STUDIES IN EDEMA
Authors: Moyer S. Fleisher, Leo Loeb
Journal: The Journal of Experimental Medicine (1909)

1. In non-nephrectomized animals the addition of adrenalin to sodium chloride solutions or to mixtures of sodium chloride and calcium chloride solutions increases the amount of urine and of ascites, and diminishes the intestinal fluid (this diminution takes place only with mixtures of solutions of sodium chloride and calcium chloride, the quantity of intestinal fluid remaining approximately unchanged in the sodium chloride series). 2. In nephrectomized animals the addition of adrenalin to sodium chloride solutions or to mixtures of sodium chloride and calcium chloride solutions again increases the ascites and diminishes the amount of intestinal fluid in both sodium chloride and sodium chloride plus calcium chloride series. 3. We find, therefore, a summation of the action of calcium chloride and adrenalin in regard to their influence upon the formation of ascites, an antagonistic action in regard to the elimination of urine; here the influence of calcium chloride in diminishing the urine is more potent than is the action of adrenalin in increasing the amount of urine. The adrenalin decreases the elimination of fluid into the intestines and in this case we note a summation of the actions of calcium chloride and of adrenalin. 4. We see, therefore, that adrenalin and calcium chloride influence the amount of ascitic fluid and of intestinal fluid in the same direction. The amount of urine is, however, decreased by calcium chloride and increased by adrenalin. 5. If we increase the rapidity of inflow of the solutions and simultaneously decrease proportionately the time of the infusion, the amount of ascites and intestinal fluids in nephrectomized animals remains approximately unchanged, as compared with the amounts obtained at the usual rate of inflow.
An excess of widespread pain among South Asians: are low levels of vitamin D implicated?
Authors: G J Macfarlane
Journal: Annals of the Rheumatic Diseases (2005)

Anecdotal reports from rheumatologists in the United Kingdom suggest that patients from South Asian backgrounds are more likely to report widespread body pain.To confirm the presence of an excess of widespread pain in South Asians, and to evaluate the relationship of their symptoms with levels of 25-OH vitamin D.Two population studies involving over 3135 subjects were carried out in the North West and Midlands areas of England.The first study confirmed an excess of widespread pain among South Asians (OR = 1.6, 95% CI 1.3 to 2.1). The second smaller study conducted only among young women also showed a similar excess of widespread pain among South Asians (OR = 1.8, 95% CI 0.7 to 4.7) and found that low levels of 25-OH vitamin D (<10 ng/ml) were more common among those with widespread pain (OR = 3.5, 95% CI 0.4 to 31.0).Owing to the small numbers, the relationship between 25-OH vitamin D and widespread pain must be considered preliminary and requires further investigation. However, it may be one potentially treatable cause of widespread pain.
High Perioperative Oxygen Fraction for Abdominal Surgery and Risk of Surgical Site Infection
Authors: Hai Yu
Journal: JAMA (2010)

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The key or just a cog in the wheel to operability assessment?
Authors: Nick H. Kim
Journal: European Respiratory Journal (2012)

The ability to measure the hydrostatic pressure in a capillary bed ( P c) was an impetus for the development of the arterial occlusion method [1]. The relevance of P c in pulmonary circulation is its role in pulmonary oedema formation. In order to accurately measure P c, the isogravimetric method and the double occlusion technique have served as standards [2, 3]. However, both techniques require surgical isolation of the organ. The pulmonary artery occlusion technique was developed for in vivo use with a standard fluid-filled pulmonary artery catheter. When incorporated, the technique enabled P c measurements as part of a standard right heart catheterisation procedure. But interest in this technique appeared to wane after discovering that the pulmonary artery occlusion technique, rather than measuring P c, was measuring a pre-capillary pressure in the >80–100 μm calibre range [1, 4]. Although this limited its application in pulmonary oedema research, the technique would later find renewed interest in the field of pulmonary hypertension (PH) [4, 5].

Of the …
Nitric oxide may mediate the hemodynamic effects of recombinant growth hormone in patients with acquired growth hormone deficiency. A double-blind, placebo-controlled study.
Authors: R H Böger, C Skamira, S M Bode-Böger, G Brabant, A von zur Muhlen, J C Frolich
Journal: Journal of Clinical Investigation (1996)

We studied the effects of recombinant growth hormone on systemic nitric oxide (NO) formation and hemodynamics in a double-blind, placebo-controlled trial in adult patients with acquired growth hormone deficiency. 30 patients were randomly allocated to either recombinant human growth hormone (r-hGH; 2.0 IU/d) or placebo for 12 mo. In the subsequent 12 mo, the study was continued with both groups of patients receiving r-hGH. In months 1, 3, 6, 9, and 12 of each year, urine and plasma samples were collected for the determination of urinary nitrate and cyclic GMP as indices of systemic NO production, and of plasma IGF-1 levels. Cardiac output was measured in months 1, 12, and 24 by echocardiography. r-hGH induced a fourfold increase in plasma IGF-1 concentrations within the first month of treatment. Urinary nitrate and cyclic GMP excretion rates were low at baseline in growth hormone-deficient patients (nitrate, 96.8+/-7.4 micromol/mmol creatinine; cyclic GMP, 63.6+/-7.1 nmol/mmol creatinine) as compared with healthy controls (nitrate, 167.3+/-7.5 micromol/mmol creatinine; cyclic GMP, 155.2+/-6.9 nmol/mmol creatinine). These indices of NO production were significantly increased by r-hGH, within the first 12 mo in the GH group, and within the second 12 mo in the placebo group. While systolic and diastolic blood pressure were not significantly altered by r-hGH, cardiac output significantly increased by 30-40%, and total peripheral resistance decreased by approximately 30% in both groups when they were assigned to r-hGH treatment. In the second study year, when both groups were given r-hGH, there were no significant differences in plasma IGF-1, urinary nitrate, or cyclic GMP excretion, or hemodynamic parameters between both groups. In conclusion, systemic NO formation is decreased in untreated growth hormone-deficient patients. Treatment with recombinant human growth hormone normalizes urinary nitrate and cyclic GMP excretion, possibly via IGF-1 stimulation of endothelial NO formation, and concomitantly decreases peripheral arterial resistance. Increased NO formation may be one reason for improved cardiovascular performance of patients with acquired hypopituitarism during growth hormone therapy.