tbuckley/cabot-search huggingface dataset:
Signorina Galieri's Scleroderma or Scleredema
Authors: GERALD P. RODNAN
Journal: Annals of Internal Medicine (1972)

Letters, Comments, and Corrections1 April 1972Signorina Galieri's Scleroderma or ScleredemaGERALD P. RODNAN, M.D.GERALD P. RODNAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-76-4-673_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Dr. Benedek and I have shared Dr. Capusan's doubts concerning the nature of the illness of the young woman described by Dr. Curzio in 1753 (1) and in a recent chapter on progressive systemic sclerosis. I, too, have suggested that signorina Patrizia Galieri may have had scleredema adultorum of Buschke rather than scleroderma (2). I would take issue, however, with several of the arguments adduced by Dr. Capusan in excluding the diagnosis of scleroderma. Particularly, I do not believe that the absence of Raynaud's phenomenon (point 2) can be regarded as crucial, since a small but significant...References1. CAPUSAN I: Curzio's case of scleroderma (letter). Ann Intern Med 76:146, 1972 LinkGoogle Scholar2. RODNAN G: Progressive systemic sclerosis (scleroderma), in Arthritis and Allied Conditions, 8th ed., edited by HOLLANDER JL. Philadelphia, Lea & Febiger. In press Google Scholar3. MEDSGERRODNANMoossy TGJ: The nature of skeletal muscle involvement in progressive systemic sclerosis (scleroderma). Arthritis Rheum 11:554-568, 1968 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByThe diagnosis of art: Scleroderma in Paul Klee – and Rembrandt's scholar?Bibliography of Secondary Sources on the History of Dermatology.Progressive Systemic Sclerosis: Gastrointestinal InvolvementScleroderma in the child 1 April 1972Volume 76, Issue 4Page: 673-674KeywordsRaynaud syndromeScleroderma Issue Published: 1 April 1972 PDF DownloadLoading ...
Ultrafine particles in alveolar macrophages from normal children
Authors: H J Bunn
Journal: Thorax (2001)

<h3>Objective</h3> To highlight potential epigenetic risk factors for blood pressure (BP) and ischemic stroke (IS) in loci identified by genome-wide association studies (GWASs). <h3>Methods</h3> We detected DNA methylation for BP (317,756 individuals from UK Biobank) and IS (521,612 individuals from MEGASTROKE) in Europeans by using the summary data–based mendelian randomization (SMR) method. We selected the most relevant gene to validate the association in 1,207 patients with hypertensive IS and 1,269 controls from the Chinese populations. <h3>Results</h3> We first identified 173 CpG sites in 90 genes, 337 CpG sites in 142 genes, and 9 CpG sites in 7 genes that were significantly associated with systolic, diastolic BP, and IS, respectively. The methylation level of cg12760995 in <i>CASZ1</i> was associated with systolic (<i>P</i><sub>SMR</sub> = 1.74 × 10<sup>−12</sup>), diastolic BP (<i>P</i><sub>SMR</sub> = 2.48 × 10<sup>−10</sup>), and IS (odds ratio [OR] = 0.92 [95% confidence interval [CI]: 0.91–0.94]; <i>P</i><sub>SMR</sub> = 2.28 × 10<sup>−8</sup>) in Europeans. The methylation levels of 17 sites in the promoter of <i>CASZ1</i> were measured in the Chinese individuals, and 10 of them were significantly associated with IS. The higher methylation level of <i>CASZ1</i> was associated with a lower risk of IS (adjusted OR = 0.97 [95% CI: 0.96–0.99]). <i>CASZ1</i> seemed to be hypomethylated in hypertensive cases, and the level was negatively correlated with BP. Systolic and diastolic BP mediated approximately 61.2% (<i>p</i> = 3.49 × 10<sup>−6</sup>) and 45.0% (<i>p</i> = 0.0029) of the association between <i>CASZ1</i> methylation and IS, respectively. <h3>Conclusions</h3> This study identified DNA methylations that were associated with BP and IS. <i>CASZ1</i> was hypomethylated in Chinese patients with hypertensive IS.
SECONDARY INFECTIONS OF JOINTS IN ACUTE MEDICAL AILMENTS
Authors: G. H. Edington
Journal: BMJ (1916)

SECONDARY INFECTIONS OF JOINTS.-BmFDI(!ALJ*iAS 289 gauze and soloids.On the sixth day the patient was dressed "nder an anaesthetic.The old wotund had been transformed into a granulating,surface,, as mentioned above, but the tern- perature, as is so often the case, rose after the dressing.SECONDARY INFECTIONS O-F JOINTS IN ACUTTE MEDICAL AILMENTS.BY LIEUT.-COLONELG. H
The acute haemodynamic effects of nasal ventilation by CPAP and BiPAP in patients with congestive heart failure
Authors: J.D. Somauroo, M. Wilkinson, J.R. Pyatt, M. Jackson, E. Rodrigues, D.T. Connelly, P.M.A. Calverley, R.M. Angus
Journal: European Journal of Heart Failure (2000)
Mechanisms of persistent airway inflammation in asthma. A role for T cells and T-cell products.
Authors: W W Busse, R L Coffman, E W Gelfand, A B Kay, L J Rosenwasser
Journal: American Journal of Respiratory and Critical Care Medicine (1995)

The role of T cells in human allergic inflammation is just beginning to be understood. However, the data presented indicate how the T cell may be a pivotal cell to direct features of allergic inflammation in asthma, how the T cell may be able to transfer hyperresponsiveness, which is a feature of bronchial asthma, what some of the genetic factors are that may determine this process, and how an important precipitant of asthma, viral respiratory infections, may participate in this process. Its cells are isolated from patients with asthma and studied for their ability to generate proinflammatory failure. An expanded understanding of the chronic, persistent nature of asthma will become apparent.
"SOME NEW LINES OF PROGRESS IN CANCER RESEARCH"
Authors: Montrose T. Burrows
Journal: JAMA (1924)

<h3>To the Editor:</h3> —The editorial entitled "Some New Lines of Progress in Cancer Research" (The Journal, January 5) discusses an article by Dr. J. A. Murray, director of the Imperial Cancer Research Laboratories of London, England. This article appeared in the<i>Lancet</i>, July 28, 1923. Murray attempts to show that cancer is the result of cell injury, that it is a degenerative overgrowth somewhat perhaps in the sense of Thiersch and Benicke and later of Oertel. The growth in cancer he attributes to the presence of a growth stimulus liberated when cells are injured. He cites work with the tissue culture as proof for this deduction. What I wish to point out here is that I do not believe that the work with the tissue cultures carried on in this country justifies this deduction. In Murray's laboratory, Drew has shown that embryonic tissue and malignant tumor tissue contain an extractable
Thoughts for new medical students at a new medical school
Authors: R. Smith
Journal: BMJ (2003)

Giving advice to medical students makes doctors think about what is important in what they do 

Earlier this year I had the privilege of speaking to new medical students at a new medical school—the Hull York Medical School. What should I say? I felt almost overawed. It seemed a major responsibility, although I knew that most of what I said would—thankfully—be forgotten or ignored as the ramblings of yet another “old fart.” Needing help and a method, I started by asking members of our editorial board, doctors from all over the world, what I should say. They responded with enthusiasm, giving me the thought that it might be a good idea to broaden the debate. That's the main reason for this article: it's a preliminary statement in what I hope might be a rich debate. In thinking what we want to say to new entrants to the profession we have to think of what is important about what we do.

What follows is a mixture of my own ideas and those I selected from the responses of the members of the editorial board. Box 1 summarises responses from the BMJ 's editorial board, and box 2 gives the full advice of Dave Sackett, the “father of evidence based medicine” (and a member of the board). I also spent some time exploring advice from literature to young people, not specifically medical students (see boxes 3, 4, 5, 7).

Perhaps the most famous advice to young people in the English language is the speech of Polonius—a tiresome old windbag—to his departing son Laertes in Shakespeare's Hamlet (box 3). The speech contains much excellent advice, but perhaps the quintessence is, “To thine own self be true.” Everybody—but perhaps especially medical students—experiences pressure to be somebody else. In the competitive world of medicine there …
Abstract 3450: Growth-inhibitory effect of neurotrophin-3-secreting adipose tissue-derived mesenchymal stem cells on the D283-MED human medulloblastoma cell line
Authors: Young-Hoon Kim, Chae-Yong Kim, Byung-Kyu Cho, Kyu-Chang Wang, Seung-Ki Kim, Ji Hoon Phi, Seung Hee Cho, Soo Jung Lee, Seung Ah Choi, Jin Wook Kim, Chul-Kee Park
Journal: Cancer Research (2011)

Abstract Medulloblastoma (MBL), the most common malignant pediatric brain tumor, is incurable in about one-third of patients and can lead to long-term disabilities despite current multimodal treatments. We evaluate the in vitro, growth-inhibitory effect of neurotrophin-3 (NT-3)-secreting stem cells on an MBL cell line and propose that this cell therapy may have therapeutic effects for MBL. NT-3-secreting stem cells were produced by nucleofecting pIRES2.EGFP-NT3 into human adipose tissue-derived mesenchymal stem cells (hAT-MSCs). Double-layered co-culture experiments with the NT-3-secreting hAT-MSCs and D283-MED MBL cells were performed, and NT-3-induced apoptosis was studied by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) test. The growth-inhibitory effects of these stem cells on human MBL in vitro were confirmed by 3-(4, 5-dimethylathiazol-2-yl)-2, 5-dephenyl-tetrazolium bromide (MTT) assay. We confirmed by western blotting that D283-MED cells express tyrosine kinase C, a specific receptor for NT-3, and we showed by fluorescence microscopy and RT-PCR that transfected hAT-MSCs express NT-3. The double-layered co-culture of D283-MED with NT-3-secreting hAT-MSCs induced a concentration-dependent increase in apoptosis in the tumor cell line. Consequently, the high concentrations of NT-3-secreting hAT-MSCs significantly (P &amp;lt; 0.001) increased the death of D283-MED cells in vitro. The present studies demonstrate the potential of NT-3-secreting hAT-MSCs as an effective therapeutic cell therapy for human MBL in vitro, but in vivo experiments and clinical studies will be required in the future. 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 3450. doi:10.1158/1538-7445.AM2011-3450
Occurrence screening as a method of audit.
Authors: J Bennett, K Walshe
Journal: BMJ (1990)

Although surveillance programmes may need to vary a little between districts to take account of local needs, there are several advantages in a core programme: the training of doctors and nurses could be standardised across the country, the surveillance of children who moved to another health district would not be affected, and primary health care teams who look after children from more than one health district would not have to vary their programme to suit the child's district of residence.
Thiazolidinediones block tumor necrosis factor-alpha-induced inhibition of insulin signaling.
Authors: P Peraldi, M Xu, B M Spiegelman
Journal: Journal of Clinical Investigation (1997)

TNF-alpha has been shown to be an important mediator of insulin resistance linked to obesity. This cytokine induces insulin resistance, at least in part, through inhibition of the tyrosine kinase activity of the insulin receptor. Recently, a new class of compounds, the antidiabetic thiazolidinediones (TZDs), has been shown to improve insulin resistance in obesity and non-insulin-dependent diabetes mellitus in both rodents and man. Here we show that TZDs have powerful effects on the ability of TNF-alpha to alter the most proximal steps of insulin signaling, including tyrosine phosphorylation of the insulin receptor and its major substrate, IRS-1, and activation of PI3-kinase. Troglitazone or pioglitazone essentially eliminate the reduction in tyrosine phosphorylation of IR and IRS-1 caused by TNF-alpha in fat cells, even at relatively high doses (25 ng/ml). That this effect of TZDs operates through activation of the nuclear receptor PPARgamma/ RXR complex is shown by the fact that similar effects are observed with other PPARgamma/RXR ligands such as 15 deoxy Delta12,14PGJ2 and LG268. The TZDs do not inhibit all TNF-alpha signaling in that the transcription factor NF-kB is still induced well. These data indicate that TZDs can specifically block certain actions of TNF-alpha related to insulin resistance, suggesting that this block may contribute to their antidiabetic actions.
Letter Regarding Article by Connolly et al, “Challenges of Establishing New Antithrombotic Therapies in Atrial Fibrillation”
Authors: Michael D. Ezekowitz, Rangadham Nagarakanti
Journal: Circulation (2008)

Circulation 1 have clearly defined the important challenges we face in evaluating antithrombotic drugs for stroke prevention in atrial fibrillation (AF).We are in general agreement with the authors.However, we differ on the advisability of conducting a superiority trial of a new, presumably effective antithrombotic agent against aspirin in patients at high risk for stroke.The only evidence supporting the benefit of aspirin against the placebo for stroke prevention in AF is from the Stroke Prevention in Atrial Fibrillation (SPAF) I trial. 2 The relative risk reduction of stroke and systemic embolism was 42%.The confidence interval was wide (95% confidence interval, 9% to 63%).Other trials, such as the Copenhagen AF, Aspirin, and Anticoagulation Study (AFASAK) and European AF Trial (EAFT), showed a nonsignificant risk reduction of 17% and 11%, respectively.The EAFT included high-risk patients and had an annual stroke rate of 12%, 10%, and 4% in patients assigned to placebo, aspirin, and anticoagulation, respectively. 3 The SPAF III trial reported an annual stroke rate of 7.9% and 1.9% in high-risk patients randomized to aspirin plus low-dose warfarin (international normalized ratio, 1.2 to 1.5) and adjusted-dose warfarin (international normalized ratio, 2 to 3), respectively. 4The Birmingham AF Treatment of the Aged (BAFTA) study of high-risk patients reported annual stroke rates of 3.8% and 1.8% in patients assigned to aspirin and warfarin, respectively. 5Thus, with the exception of the SPAF I study, the evidence is overwhelming that stroke rates on aspirin approximate placebo rates in high-risk patients.A second consideration is the definition of warfarin ineligibility.Definition of warfarin ineligibility in the SPAF I study included patients aged Ͼ75 years, now considered a risk factor for stroke prevention and an inclusion factor for current trials.Patients with uncontrolled hypertension or at high risk for bleeds were also excluded.These represent exclusions for any anticoagulant.In the Atrial Fibrillation Clopidogrel Trial With Irbesartan for Prevention of Vascular Events (ACTIVE) A trial, warfarin ineligibility is defined as contraindication to or unwillingness (subjective) to take "oral anticoagulation therapy."ACTIVE A compares reduction in
Porcine xenograft valves. Long-term (60-89-month) follow-up.
Authors: J B Lakier, F Khaja, D J Magilligan, S Goldstein
Journal: Circulation (1980)

An analysis of 211 patients who had porcine xenograft valve replacements at Henry Ford Hospital between October 1971 and March 1974, was accomplished, with 100% follow-up. The follow-up period extended from 60-89 months after implantation. One hundred sixty-seven patients with 192 valves survived the perioperative period and were subjected to life table analysis. Hemodynamically significant porcine xenograft degeneration that required reoperation occurred in 18 patients, two of whom had infective endocarditis. Only four valves failed within 48 months of surgery. Ten of 42 (23.8%) patients with isolated aortic valve replacement and eight of 102 patients (7.8%) patients with isolated mitral valve replacement required reoperation (p < 0.01). In patients under 25 years of age, six of nine surviving patients had repeat operations. Our data indicate that porcine xenograft degeneration is related to the duration of implantation and the age of the patient at the time implantation was performed. In addition, porcine xenograft valves in the aortic position are more likely to degenerate than are those in the mitral position.
Neutrophil derived human S100A12 (EN-RAGE) is strongly expressed during chronic active inflammatory bowel disease
Authors: D Foell
Journal: Gut (2003)

<b>Background:</b> Intestinal inflammation in Crohn’s disease (CD) and ulcerative colitis (UC) is characterised by an influx of neutrophils into the intestinal mucosa. S100A12 is a calcium binding protein with proinflammatory properties. It is secreted by activated neutrophils and interacts with the multiligand receptor for advanced glycation end products (RAGE). Promising anti-inflammatory effects of blocking agents for RAGE have been reported in murine models of colitis. <b>Aims:</b> To investigate expression and serum concentrations of S100A12 in inflammatory bowel disease (IBD). <b>Methods:</b> We performed immunohistochemical studies and immunofluorescence microscopy in biopsies from patients with CD and UC. S100A12 serum concentrations were analysed using a sandwich ELISA. <b>Results:</b> Immunohistochemical studies revealed profound expression of S100A12 in inflamed intestinal tissue from IBD patients whereas no expression was found in tissue from healthy controls. Staining for S100A12 during chronic active CD and UC was restricted to infiltrating neutrophils. Serum S100A12 levels were significantly elevated in patients with active CD (470 (125) ng/ml; p&lt;0.001, n=30) as well as those with active UC (400 (120) ng/ml; p&lt;0.01, n=15) compared with healthy controls (75 (15) ng/ml; n=30). Even in inactive disease, elevated serum concentrations were found, at least in CD. S100A12 levels were well correlated with disease activity in CD and UC. <b>Conclusions:</b> We demonstrated that neutrophil derived S100A12 is strongly upregulated during chronic active IBD, suggesting an important role during the pathogenesis of IBD. Serum S100A12 may serve as a useful marker for disease activity in patients with IBD.
Defending the NHS with poorly reasoned rhetoric won't save it
Authors: S. Black
Journal: BMJ (2013)

The NHS reforms initiated by Andrew Lansley deserve much criticism, but David Hunter’s opposition to reform is ineffective because it appeals to emotions and doesn’t draw on credible evidence.1 

For example, rather than discuss the evidence about whether competition among providers is good for patients,2 Hunter goes straight to the easy rhetorical point that this will lead to a system governed by “naked greed,” as in the …
Embryology for Surgeons: The Embryological Basis for the Treatment of Congenital Anomalies
Authors: Stanley W. Jacob
Journal: JAMA (1995)

Nature is nowhere accustomed more openly to display her secret mysteries than in cases where she shows traces of her workings apart from the beaten path; nor is there any better way to advance the proper practice of medicine than to give our minds to the discovery of the usual law of nature, by careful investigation of cases of rarer forms of disease. For it has been found in almost all things, that what they contain of useful or of applicable, is hardly perceived unless we are deprived of them, or they become deranged in some way. This excerpt from a 1657 letter by William Harvey begins the preface to the second edition of Skandalakis and Gray's massive achievement,<i>Embryology for Surgeons</i>, and sums up the approach of the book. This quote from a more humanistic age is especially appropriate because the authors, while admirably meeting their declared first edition
Demonstration of a critical role for free fatty acids in mediating counterregulatory stimulation of gluconeogenesis and suppression of glucose utilization in humans.
Authors: C Fanelli, S Calderone, L Epifano, A De Vincenzo, F Modarelli, S Pampanelli, G Perriello, P De Feo, P Brunetti, J E Gerich
Journal: Journal of Clinical Investigation (1993)

In vitro studies indicate that FFA compete with glucose as an oxidative fuel in muscle and, in addition, stimulate gluconeogenesis in liver. During counterregulation of hypoglycemia, plasma FFA increase and this is associated with an increase in glucose production and a suppression of glucose utilization. To test the hypothesis that FFA mediate changes in glucose metabolism that occur during counterregulation, we examined the effects of acipimox, an inhibitor of lipolysis, on glucose production and utilization ([3-3H]glucose), and incorporation of [U-14C]-alanine into glucose during insulin-induced hypoglycemia. Eight normal volunteers were infused with insulin for 8 h to produce modest hypoglycemia (approximately 3 mM) on two occasions, first without acipimox (control) and then with acipimox administration (250 mg per os at 60 and 240 min). Despite identical plasma insulin concentrations, glucose had to be infused in the acipimox experiments (glucose-clamp technique) to maintain plasma glucose concentrations identical to those in control experiments. Acipimox completely prevented counterregulatory increases in lipolysis so that during the last 4 h plasma FFA were below baseline values and averaged 67 +/- 13 vs. 725 +/- 65 microM in control experiments, P < 0.001. Concomitantly, overall glucose production was reduced by 40% (5.5 +/- 11 vs. 9.3 +/- 0.7 mumol/kg per min, P < 0.001), and gluconeogenesis from alanine was reduced by nearly 70% (0.32 +/- 0.09 vs. 1.00 +/- 0.18 mumol/kg per min, P < 0.001), while glucose utilization increased by 15% (10.8 +/- 1.4 vs. 9.3 +/- 0.7 mumol/kg per min). We conclude that FFA play a critical role in mediating changes in glucose metabolism during counterregulation, and that under these conditions, FFA exert a much more profound effect on hepatic glucose production than on glucose utilization.