tbuckley/cabot-search huggingface dataset:
Cytotoxin-Associated Gene A Strains of<i>Helicobacter Pylori</i>Represent a Risk Factor for the Development of Microalbuminuria in Type 2 Diabetes
Authors: Antonio Pietroiusti, Maria Giuliano, Andrea Magrini, Antonio Bergamaschi, Alberto Galante
Journal: Diabetes Care (2006)

The reasons why diabetic patients with microalbuminuria have marked endothelial damage (1,2) and an increased risk of atherosclerosis (3,4) are unclear. Infection with Helicobacter pylori , especially with strains carrying the cytotoxin-associated gene A (CagA), might represent a causal factor, since anti-CagA antibodies elicited by infection may cross-react with endothelial antigens (5), increasing the vascular damage associated with diabetes itself and consequent albumin leakage. Furthermore, infection might induce a persistent systemic inflammatory response, which is a recognized risk factor for atherosclerosis (6). In this study, we investigated the possible pathogenetic role of CagA-positive H. pylori strains in type 2 diabetic patients with microalbuminuria.

Consecutive ambulatory patients with a known history of type 2 diabetes who were ≥40 years of age were considered. Data on age, sex, BMI, smoking habit, history of hypertension or hyperlipidemia, disease duration, previous myocardial infarction, previous stroke, and HbA1c (A1C) were collected. Serum level of C-reactive protein (CRP), a marker of systemic inflammation, was measured only in patients without obvious inflammatory conditions. Exclusion criteria were presence of renal failure (creatinine >133 μmol/l), previous H. pylori eradication, and evidence of connective tissue, neoplastic, or hematological disease. Since virtually all peptic ulcers are due to H. pylori (7), and most of them to CagA-positive strains (8), a history of …
Fluticasone propionate aqueous nasal spray compared with terfenadine tablets in the treatment of seasonal allergic rhinitis†
Authors: E BRONSKY, R DOCKHORN, E MELTZER, G SHAPIRO, H BOLTANSKY, C LAFORCE, J RANSOM, J WEILER, M BLUMENTHAL, S WEAKLEY
Journal: Journal of Allergy and Clinical Immunology (1996)
Fraud and Irresponsible Authorship
Authors: L. A. HEALEY
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 June 1986Fraud and Irresponsible AuthorshipL. A. HEALEY, M.D.L. A. HEALEY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-6-886 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo The Editor: To the discussion of fraud and irresponsible authorship by academicians and publishers, I would like to add another point of view: that of a reader. Although irresponsible authorship may facilitate fraud, I disagree that it is the more damaging offense. It is a nuisance to a reader, but fraud is destructive.The escalation of multiple authors and bibliographic items in academic medicine seems, to an outsider, to be a charade that could be stopped without much difficulty. Petersdorf (1) is right that counting papers is easier than reading them, but the papers can be read. If Angell's...References1. PETERSDORF R. The pathogenesis of fraud in medical science. Ann Intern Med. 1986;104:252-4. LinkGoogle Scholar2. ANGELL M. Publish or perish: a proposal. Ann Intern Med. 1986;104:261-2. LinkGoogle Scholar1. PETERSDORF R. The pathogenesis of fraud in medical science. Ann Intern Med. 1986;104:252-4. LinkGoogle Scholar2. WOOLF P. Pressure to publish and fraud in science. Ann Intern Med. 1986;104:254-6. LinkGoogle Scholar3. HUTH E. Irresponsible authorship and wasteful publication. Ann Intern Med. 1986;104:257-9. LinkGoogle Scholar4. BAILAR J. Science, statistics, and deception. Ann Intern Med. 1986;104:259-60. LinkGoogle Scholar5. ANGEL M. Publish or perish: a proposal. Ann Intern Med. 1986; 104:261-2. LinkGoogle Scholar6. HUTH E. Abuses and uses of authorship [Editorial]. Ann Intern Med. 1986;104:266-7. LinkGoogle Scholar7. HUTH E. Guidelines on authorship of medical papers. Ann Intern Med. 1986;104:269-74. LinkGoogle Scholar1. PETERSDORF R. The pathogenesis of fraud in medical science. Ann Intern Med. 1986;104:252-4. LinkGoogle Scholar2. WOOLF P. Pressure to publish and fraud in science. Ann Intern Med. 1986;104:254-6. LinkGoogle Scholar3. HUTH E. Irresponsible authorship and wasteful publication. Ann Intern Med. 1986;104:257-9. LinkGoogle Scholar4. BAILAR J. Science, statistics, and deception. Ann Intern Med. 1986;104:259-60. LinkGoogle Scholar5. ANGEL M. Publish or perish: a proposal. Ann Intern Med. 1986;104:261-2. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: L. A. HEALEY, M.D.Affiliations: The Mason Clinic Seattle, WA 98111-0900 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byEthical Responsibilities in Scientific Publication 1 June 1986Volume 104, Issue 6Page: 886-887KeywordsAcademic medicine ePublished: 1 December 2008 Issue Published: 1 June 1986 PDF downloadLoading ...
Defibrination in Acute Pancreatitis
Authors: PHILIP R. GREIPP
Journal: Annals of Internal Medicine (1972)

Coagulation abnormalities in clinical and experimental pancreatitis have been described. The release of proteolytic enzymes from the inflamed pancreas has been postulated as the cause of observed coagulation abnormalities. This report describes a patient who developed acute pancreatitis with severe coagulation abnormalities. Increased proteolytic activity was shown in the patient's serum and plasma and was associated with defibrination, accelerated use of fibrinogen, and other coagulation factors. The coagulation abnormalities improved as the proteolytic activity declined, and the pancreatitis abated.
THE SIGNIFICANCE OF EDEMA OF THE SOFT PALATE
Authors: LEWIS S. SOMERS
Journal: JAMA (1910)

Not infrequently an apparently trivial symptom may be the expression of a serious affection, and if it is unheeded and the opportunity for active treatment allowed to pass it may lead to a fatal termination before its true significance has been appreciated. Such a symptom is edema of the soft palate, and especially the uvula. When observed its possible gravity must be seriously considered. Edema of the soft palate chiefly involves the uvula, but may affect the faucial pillars, especially the posterior, or even the lateral pharyngeal wall. The uvular swelling may be slight, appearing as a glistening drop at its tip, or may be so massive that the faucial isthmus is occluded and breathing becomes impeded.
Constitutively active Stat5b in CD4+ T cells inhibits graft-versus-host disease lethality associated with increased regulatory T-cell potency and decreased T effector cell responses
Authors: Christine Vogtenhuber, Christoph Bucher, Steven L. Highfill, Lisa K. Koch, Emily Goren, Angela Panoskaltsis-Mortari, Patricia A. Taylor, Michael A. Farrar, Bruce R. Blazar
Journal: Blood (2010)
Physical Rehabilitation of the Injured Athlete
Authors: Rose Macdonald
Journal: British Journal of Sports Medicine (1994)

Iron deficiency, defined as a serum ferritin level less than or equal to 50 micrograms/l was found in 28 (11%) of 252 consecutive elderly in-patients (mean age 81 years). Sixteen among them were anaemic and only five had a microcytic anaemia. In a separate study, 15 anaemic and 13 non-anaemic iron-deficient elderly in-patients were investigated in order to evaluate the prevalence of gastrointestinal symptoms and lesions in both groups. In nine of the anaemic and seven of the non-anaemic patients a potential cause for the iron deficiency was established. Most anaemic and non-anaemic patients lacked the symptoms described as suggestive of underlying gastrointestinal pathology. Thus, a ferritin level less than or equal to 50 micrograms/l justifies a gastrointestinal investigation if the general condition allows for it as well in anaemic as in non-anaemic elderly hospitalized patients. Therefore, serum ferritin should be part of the routine biochemical investigation of elderly in-patients.
Clinical Study of Twenty-Three Cases of Ebstein's Anomaly of the Tricuspid Valve
Authors: GEROLD L. SCHIEBLER, PAUL ADAMS, RAY C. ANDERSON, KURT AMPLATZ, RICHARD G. LESTER
Journal: Circulation (1959)

The clinical findings in 23 cases of Ebstein's anomaly are presented, together with a discussion of the diagnostic and surgical aspects of this defect. Attention is again drawn to the frequent occurrence of the Wolff-Parkinson-White electrocardiographic pattern in this anomaly.
Stress Changes in the Ribs Associated With Ballet Dancing
Authors: ZVI BAR-SEVER, LEONARD P. CONNOLLY, S. TED TREVES
Journal: Clinical Nuclear Medicine (1997)

We present a case of a ballet dancer who was referred for skeletal scintigraphy because of bilateral leg pain. In addition to diffuse stress changes in the legs and feet, skeletal scintigraphy showed bilateral focal uptake in posterolateral lower ribs. The patient had not experienced rib pain. These scintigraphic abnormalities can be attributed to frequent dancing routines in which the patient was held by the sides of the thorax and lifted, causing microtrauma to the ribs.
Surgical management of metastatic inguinal lymphadenopathy: Sentinel node biopsy has cost implications for the NHS
Authors: Negin Shamsian, Stephen Hamilton, Apul Parikh, Peter E M Butler
Journal: BMJ (2005)

Electronic data protection: procedures need drastic improvementEditor-Gulena et al are correct to challenge overzealous interpretation of data protection law in their questionnaire survey of patients' and visitors' views about having their names displayed in hospital. 1Measures taken by doctors to safeguard patient confidentiality, especially electronic records, are, however, severely deficient and fuel the concerns of those entrusted to police data security.We invited 32 surgical trainees to complete a questionnaire regarding their Data Protection Act registration and electronic data confidentiality practices.Of 29 responders, 26 trainees regularly computerised and stored patients' data.One person was registered with the Data Protection Act.Only three of 14 desktops, eight of 19 laptops, and three of 14 handheld computers forced a password logon.Sixteen of 29 trainees used the same password for all machines, and 25 of 27 passwords were less than eight characters long.All desktops, 16 of 19 laptops, and five of 14 handhelds were routinely connected to the internet, and half of these had not had their online security settings adjusted.Of 29 trainees, 28 did not encrypt their sensitive data files.Ten trainees had sent patients' data unencrypted over the internet, using a non-secure server.Electronic data confidentiality practices among surgical trainees are unsafe, and this is unlikely to be confined to our study population.A breach in confidentiality would have widespread implications for public trust.][4] Existing passwords should be improved, and biometric logon systems (fingerprint scanning) considered.Files containing sensitive data should be routinely encrypted.Magnetic and solid state computer storage devices (including hard disks, floppy disks, CD Roms, DVD Roms, and memory sticks) should undergo routine physical or electronic data shredding after their final use. 5 We are implementing medical information technology security training for this particu-lar group of doctors and would urge others to initiate similar programmes before a serious breach occurs.
Budget Reconciliation
Authors: Stephan E. Lawton
Journal: New England Journal of Medicine (1981)

IN recent months, persons seeking to understand and influence health legislation in Washington have encountered a bewildering maze created by the Congressional Budget Act. Most major actions in Congress this year have been taken through recisions, deferrals, and reconciliation bills. The result for legislators and lobbyists alike has been an unfamiliar, unpredictable, and all but uncontrollable legislative process.Budgetary procedures now serve as the means for determining not only the extent of federal financial commitment to health programs but also the substance of legislation that puts these programs in place. This fact has not been lost on a new, immensely . . .
Effect of ischaemic preconditioning on vascular dysfunction induced by ischaemia and reperfusion in rat hindquarters
Authors: K LOKE, O WOODMAN
Journal: Cardiovascular Research (1996)

Objective: The aim of this study was to examine the effect of ischaemia on vascular responses to endothelium-dependent and endothelium-independent vasodilators and on vasoconstrictor responses. Furthermore, the ability of preconditioning to prevent ischaemia-induced changes in vascular reactivity was examined in the rat hindquarters. Methods: The abdominal aortae of anaesthetized rats were cannulated for hindquarters perfusion with Krebs bicarbonate solution containing phenylephrine to induce vasoconstrictor tone. Responses of the hindquarters to endothelium-dependent and endothelium-independent vasodilators were examined. Hindquarters responses to neuronal release of the vasodilator acetylcholine (ACh) induced by peri-aortic nerve stimulation were also examined. Results: Ischaemia with 2 h aortic occlusion prior to Krebs perfusion attenuated vasodilator responses to the neuronal release of ACh [10 Hz; decrease in perfusion pressure (ΔPP) control: − 18(s.e.m. 3) mmHg, ischaemic: − 13(3) mmHg], exogenous ACh [10 ng; ΔPP control: − 22(2) mmHg, ischaemic: − 17(2) mmHg] and carbachol [1.0 μg; ΔPP control: − 21(3) mmHg, ischaemic: − 12(3) mmHg]. Responses to other endothelium-dependent vasodilators bradykinin and histamine or the endothelium-independent vasodilator, sodium nitroprusside, were not impaired by ischaemia. Similarly vasoconstriction to noradrenaline and serotonin was not affected. Ischaemia preceded by preconditioning with 5 min aortic occlusion and 10 min reperfusion prevented impairment of vasodilatation to nerve stimulation [10 Hz; ΔPP preconditioned: − 20(1) mmHg], ACh [10 ng; ΔPP preconditioned: − 22(1) mmHg] and carbachol [1.0 μg; ΔPP preconditioned: mn 24(3) mmHg] caused by ischaemia. Conclusions: These data indicate that hindquarters ischaemia causes selective impairment of dilator responses to muscarinic agonists and ischaemic preconditioning prevents that impairment.
Co-delivery of PDTC and doxorubicin by multifunctional micellar nanoparticles to achieve active targeted drug delivery and overcome multidrug resistance
Authors: Li Fan, Fei Li, Haitao Zhang, Yukun Wang, Chong Cheng, Xiaoye Li, Chun-hu Gu, Qian Yang, Hong Wu, Shengyong Zhang
Journal: Biomaterials (2010)
Protein S and C alterations in acutely III patients
Authors: S. B. Sheth, A. C. Carvalho
Journal: American Journal of Hematology (1991)

Abstract Protein C, a potent vitamin K‐dependent protein activated by an endothelial cell cofactor, thrombomodulin, has anticoagulant and profibrinolytic activity. Free protein S, a cofactor for protein C, potentiates protein C activity at the endothelial cell surface. Pulmonary thromboemboli are a consistent finding in adult respiratory distress syndrome (ARDS). To determine if protein S or protein C were affected by widespread endothelial cell damage in ARDS, we measured bound and free protein S levels and protein C antigenic and functional levels in 18 patients with acute lung injury, 6 critically ill patients without lung history, and 22 normal subjects. Free (PS:F) and bound (PS:Ag) protein S and protein C antigen (PC:Ag) levels were measured using an enzyme‐linked immunoassay and protein C function (PC:Fn) by measuring its anticoagulant activity. We found a significant decrease in bound and free protein S levels of both patient groups in comparison to normal and a shift toward the inactive, bound protein S form. In addition, a significant decrease in free protein S compared to bound protein S in both patient groups was observed. While both PC:Ag and PC:Fn were significantly reduced compared to normal, the PC:Fn was significantly and severely decreased out of proportion to the PC:Ag in both patient groups. There was no difference between those with and without lung injury for both protein S and protein C. Analyzed according to etiology of lung injury, there was no difference in the bound and free protein S, nor in PC:Ag and PC:Fn levels between patients with sepsis and trauma. However, there were significant decreases in both protein S and protein C levels compared with normal subjects. Levels of both PS and PC levels in patients who survived did not differ from those who died. In summary, our data show that both protein S and C are markedly deranged in acutely ill patients who suffered from either sepsis or trauma, and these changes are independent of lung injury. The marked reductions in functional activity of PS and PC may be contributing factors to the thromboembolic complications often observed in these patients.
Atrial Fibrillation in Flying Personnel
Authors: LAWRENCE E. LAMB, LAWRENCE W. POLLARD
Journal: Circulation (1964)

Sixty cases of atrial fibrillation from the USAF flying population are reported. Follow-up information in 59 subjects averaged 41.2 months. Only three cases of persistent atrial fibrillation were detected and two of these had normal sinus rhythm prior to the onset of atrial fibrillation. There were 21 cases of recurrent paroxysmal atrial fibrillation and 36 cases of isolated acute atrial fibrillation associated with a variety of precipitating factors. Thyrotoxicosis was notable by its absence in any of these cases of atrial fibrillation. Symptomatology either related to the primary disorder precipitating atrial fibrillation or secondary to the arrhythmia itself was frequently observed. The hemodynamic effects of atrial fibrillation on cardiac output, and cerebral artery spasm with diminished cerebral blood flow are important aeromedical considerations.
Abstract PR3: The cholesterol metabolite 27-hydroxycholesterol increases breast cancer tumor growth and metastasis
Authors: Erik Russell Nelson, Suzanne E. Wardell, Matthew K. Howe, Nicole J. Carver, Michihisa Umetani, Donald P. McDonnell
Journal: Cancer Research (2013)

Abstract Breast cancer remains the most common cancer and is the second leading cause of cancer death in women. The magnitude of this problem provides strong rationale for studies that may lead to the development of new chemopreventative strategies and/or lifestyle changes that reduce cancer incidence. It is of significance, therefore, that circulating cholesterol has been correlated to the development of breast cancer, and patients taking lipophilic inhibitors of 2-hydroxy-3-methylglutaryl coenzyme A (statins) demonstrate significantly lower breast cancer incidence, and decreased breast cancer recurrence. Therefore, our recent finding that 27-Hydroxycholesterol (27HC), a primary metabolite of cholesterol, exerts partial agonist activity on both the estrogen receptors (ERs) and liver X receptors (LXRs) suggests a potential, mechanistic link between hypercholesterolemia and breast cancer incidence. Importantly, the enzyme responsible for the conversion of cholesterol to 27HC (CYP27A1) is primarily expressed in macrophages, and it is well established that tumor infiltrating macrophages are associated with more aggressive tumors and worse patient outcome. Therefore, we initiated a series of studies to determine the impact of 27HC on breast cancer pathophysiology. Here, we demonstrate that (1) macrophage produced 27HC increases breast cancer cell proliferation, (2) elevation of exogenous 27HC increases in vivo tumor growth and lung metastases, and (3) genetic ablation of the enzyme responsible for 27HC synthesis increases latency, and reduces tumor growth and metastasis. Our ongoing work is aimed at identifying the mechanisms responsible for the 27HC induced increase in metastasis. In summary, our data thus far strongly indicate a role for macrophage produced 27HC in breast cancer pathophysiology and metastasis. The results provide additional support for the exploration of potential chemopreventative benefits of lower cholesterol diets, pharmacological inhibitors of HMG-CoA reductase or CYP27A1, and macrophage ablative strategies. DOD Postdoctoral Award BC085585 (ERN), NIH 5R37DK048807 (DPM). This abstract is also presented as Poster B50. Citation Format: Erik Russell Nelson, Suzanne E. Wardell, Matthew K. Howe, Nicole J. Carver, Michihisa Umetani, Donald P. McDonnell. The cholesterol metabolite 27-hydroxycholesterol increases breast cancer tumor growth and metastasis. [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 PR3.
Pure RBC Aplasia and Diphenylhydantoin
Authors: Yune-Gill Jeong
Journal: JAMA (1974)

Two patients developed pure red blood cell (RBC) aplasia while taking diphenylhydantoin sodium; one had concurrent acute viral hepatitis. Whether these patients had pure RBC aplasia secondary to diphenylhydantoin use or whether viral hepatitis or drugs other than diphenylhydantoin played a role cannot be decided. The facts that (1) the cases reported in association with acute viral hepatitis have all been a true aplastic anemia, (2) the drugs other than diphenylhydantoin used in these patients have never been reported to cause pure RBC aplasia, and (3) our patients recovered completely with cessation of diphenylhydantoin therapy and initiation of steroid therapy, led us to believe that diphenylhydantoin was the most likely cause. (<i>JAMA</i>229:314-315, 1974)
Newer Respiratory Disease Viruses
Authors: HARRY F. DOWLING
Journal: Annals of Internal Medicine (1964)

Editorials1 March 1964Newer Respiratory Disease VirusesHARRY F. DOWLING, M.D.HARRY F. DOWLING, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-60-3-528 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptProgress in the understanding of a disease is often like a forest fire; it creeps along for a while in the underbrush so that only a few specially knowledgeable people are aware of it, then suddenly it bursts into flame for the whole world to see. The field of the respiratory viruses has recently caught fire, and a Committee headed by Dr. Clayton Loosli have taken us on a trip to see the site. The occasion was the Conference on the Newer Respiratory Viruses held at the National Institutes of Health in October, 1962; the proceedings have been published as...1 Newer Respiratory Diseases: Amer. Rev. Resp. Dis. 88: 1-419 (Sept., Part 2), 1963. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: HARRY F. DOWLING, M.D.Affiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 March 1964Volume 60, Issue 3Page: 528-529KeywordsPulmonary diseases ePublished: 1 December 2008 Issue Published: 1 March 1964 PDF downloadLoading ...