tbuckley/cabot-search huggingface dataset:
Transnasal Gastroscopy Compared to Conventional Gastroscopy: A Randomized Study of Feasibility, Safety, and Tolerance
Authors: R. Campo, A. Montserrat, E. Brullet
Journal: Endoscopy (1998)

Gastroscopy is often an unpleasant procedure for the patient. Sedation improves the tolerance, but it causes inconvenience both for patients and for endoscopy units. The aim of the present study was to compare the feasibility, safety, and tolerance of transnasal gastroscopy using a thin endoscope with conventional oral gastroscopy.One hundred eighty-one consecutive outpatients referred for diagnostic gastroscopy were randomized to undergo transnasal or oral conventional gastroscopy. The tolerance (discomfort, retching, throat pain, and desire for sedation in any further procedures) and examination difficulty (intubation, examination, aspiration, and visibility) were assessed by the patients and the endoscopists, respectively, using visual analogue scales and a questionnaire.Endoscope insertion failed in six patients (four transnasal, two conventional). The tolerance was significantly better with transnasal gastroscopy in comparison to conventional oral gastroscopy. Only 3% of patients undergoing transnasal gastroscopy desired sedation in any further examinations, compared to 15% in the conventional oral gastroscopy group (P = 0.01). The examination time was longer in the transnasal group (5 min 25 sec +/- 1 min 46 sec vs. 3 min 22 sec +/- 1 min 9 sec, P < 0.001). Visualization capability and aspiration using the thin endoscope were considered more difficult by the endoscopists.Nasal introduction of thin endoscopes is better tolerated by patients than conventional gastroscopy, minimizing the need for sedation. However, technical improvements in thin endoscopes (a wider working channel, increased length and better image quality) would increase their usefulness.
CORRELATION BETWEEN FRACTIONAL FLOW RESERVE AND INTRAVASCULAR ULTRASOUND LUMEN AREA IN INTERMEDIATE CORONARY ARTERY STENOSIS
Authors: Itsik Ben-Dor, Michael Mahmoudi, Teshome Deksissa, Anh B. Bui, Michael A. Gaglia, Manuel A. Gonzalez, Gabriel Maluenda, Gabriel Sardi, Rafael Romaguera, Ana Laynez-Carnicero, Rebecca Torguson, Zhenyi Xue, Lowell F. Satler, William O. Suddath, Joseph Lindsay, Augusto D. Pichard, Ron Waksman
Journal: Journal of the American College of Cardiology (2011)
TRANSPOSITION OF THE VISCERA (SITUS TRANSVERSUS).
Authors: W. J. ZALESKY
Journal: JAMA (1905)

Cases of complete transposition of the viscera are still rare enough to be classed as curiosities and each case reported is of interest if only because of that fact. We have the following case to add to the list: <h3>Patient.</h3> —J. W. B., U. S. Navy, native of Texas, aged 18. <h3>History.</h3> —Parents are both living and in good health; two brothers and one sister are living, also in good health, and with all viscera in normal position. The patient has had all the diseases of childhood, from which he made a good recovery. At the present time he is well built, strong and active, and able to do any kind of work and stand any hardship in the curriculum of a naval training. His condition was first noticed by one of the naval medical officers while on recruiting duty, and before whom the patient appeared for physical examination. Being physically strong, and in the best of health, this transposition could in no way interfere with his appointment to the navy.
UV-induction of keratinocyte endothelin-1 downregulates E-cadherin in melanocytes and melanoma cells
Authors: Sumayah Jamal, Robert J. Schneider
Journal: Journal of Clinical Investigation (2002)

Endothelin-1 (ET-1), a peptide that is secreted by keratinocytes in the skin in response to ultraviolet irradiation, is a ligand for the endothelin-B (ETB) receptor. Blockade of this receptor inhibits melanoma cell growth and induces cell death in vivo and in vitro. Additionally, ETB is a melanoma progression marker. These findings suggest that the ET-1/ETB receptor pathway contributes to melanoma development or progression. Here, we demonstrate that activation of the ET-1/ETB pathway downregulates E-cadherin and associated catenin proteins in human melanocytes and melanoma cells. E-cadherin is an established suppressor of melanoma cell invasion in vitro and in vivo. Downregulation of E-cadherin by ET-1/ETB involves the downstream activation of caspase-8 but not of distal, executioner caspases, and does not lead to apoptosis. ET-1 also induces a transient association between caspase-8 and E-cadherin:β-catenin complexes. Hence, activation of the ET-1/ETB pathway promotes molecular events known to promote melanoma invasion.
TRANSFER OF OVINE EXPERIMENTAL ALLERGIC GLOMERULONEPHRITIS (EAG) WITH SERUM
Authors: Richard A. Lerner, Frank J. Dixon
Journal: The Journal of Experimental Medicine (1966)

Serum globulin from donor sheep made nephritic by immunization with glomerular basement membrane and subsequently nephrectomized contained specific kidney-fixing antibody and was capable of inducing an immediate, although transient, glomerulonephritis when injected into unilaterally nephrectomized lambs. This nephritis was characterized by immediate proteinuria, PMN infiltration into the glomerulus, and localization of gammaG- and beta1C-globulins in a linear fashion along the recipients' glomerular capillary walls. The nephritogenic property of the serum could be absorbed in vitro with isolated sheep glomerular basement membranes.
Isoniazid-Related Hepatotoxicity
Authors: LAURENCE S. FARER
Journal: Annals of Internal Medicine (1977)

Comments1 January 1977Isoniazid-Related HepatotoxicityLAURENCE S. FARER, M.D., M.P.H., JEFFREY L. GLASSROTH, M.D., DIXIE E. SNIDER JR., M.D.LAURENCE S. FARER, M.D., M.P.H.Search for more papers by this author, JEFFREY L. GLASSROTH, M.D.Search for more papers by this author, DIXIE E. SNIDER JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-1-114_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The letter from Drs. Moulding, Iseman, and Sbarbaro (Ann Intern Med85:398-399, 1976) contains some misinformation concerning Public Health Service data on isoniazid-related hepatotoxicity. Using criteria established by a panel of experts in hepatic disease, the Public Health Service study showed that the incidence of hepatotoxicity was 2.3% per year for persons 50 to 64 years of age and 0.8% for persons over 64 years of age (1). Therefore, the statement ". . . the incidence of hepatotoxicity . . . for persons above 50 years, 2.3% per year" is incorrect. The rate for all persons 50...Reference1. Isoniazid-associated hepatitis: summary of the report of the Tuberculosis Advisory Committee and Special Consultants to the Director, Center for Disease Control. Morbid Mortal Weekly Rep 23:97-98, 1974 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Tuberculosis Control Division Bureau of State Services Center for Disease Control Atlanta, GA 30333 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrugs used in tuberculosis and leprosy 1 January 1977Volume 86, Issue 1Page: 114-115KeywordsMedical services Issue Published: 1 January 1977 PDF downloadLoading ...
Endoscopic drainage of a post-cholecystectomy biloma with biloma-gastric stenting
Authors: S. Somani, A. Somani, V. Singh
Journal: Endoscopy (2013)

A 56-year-old woman was admitted with a 2-week history of non-radiating severe upper abdominal pain associated with vomiting. She had developed mild jaundice 1 week prior to admission. She had a history of laparoscopic cholecystectomy 3 months previously with an uneventful postoperative recovery. Her serum bilirubin was 5.9 mg/dL (normal range 0.30 – 1.20), predominantly direct bilirubin, and her alkaline phosphatase was 484 IU/L (normal range 42 – 128). Her blood counts were normal.
EXECUTIVE FUNCTIONING, GROSS MOTOR ABILITY AND MOOD ARE KEY DRIVERS OF POORER QUALITY OF LIFE IN CHILD AND ADOLESCENT SURVIVORS WITH COMPLEX CONGENITAL HEART DISEASE
Authors: Bradley S. Marino, Dean Beebe, Amy Cassedy, Melanie Riedel, Mary Burger, Sara Medek, Susan Finan, Charlotte Andersen, Karen Uzark, Joseph Ross, Richard F. Ittenbach, Dennis Drotar
Journal: Journal of the American College of Cardiology (2011)
Effect of 17q21 Variants and Smoking Exposure in Early-Onset Asthma
Authors: Emmanuelle Bouzigon, Eve Corda, Hugues Aschard, Marie-Hélène Dizier, Anne Boland, Jean Bousquet, Nicolas Chateigner, Frédéric Gormand, Jocelyne Just, Nicole Le Moual, Pierre Scheinmann, Valérie Siroux, Daniel Vervloet, Diana Zelenika, Isabelle Pin, Francine Kauffmann, Mark Lathrop, Florence Demenais
Journal: New England Journal of Medicine (2008)

A genomewide association study has shown an association between variants at chromosome 17q21 and an increased risk of asthma. To elucidate the relationship between this locus and disease, we examined a large, family-based data set that included extensive phenotypic and environmental data from the Epidemiological Study on the Genetics and Environment of Asthma.We tested 36 single-nucleotide polymorphisms (SNPs) in the 17q21 region in 1511 subjects from 372 families for an association with asthma. We also tested for genetic heterogeneity according to the age at the onset of asthma and exposure to environmental tobacco smoke in early life.Eleven SNPs were significantly associated with asthma (P<0.01), of which three (rs8069176, rs2305480, and rs4795400) were strongly associated (P<0.001). Ordered-subset regression analysis led us to select an onset at 4 years of age or younger to classify patients as having early-onset asthma. Association with early-onset asthma was highly significant (P<10(-5) for four SNPs), whereas no association was found with late-onset asthma. With respect to exposure to environmental tobacco smoke in early life, we observed a significant association with early-onset asthma only in exposed subjects (P<5x10(-5) for six SNPs). Under the best-fitting recessive model, homozygous status (GG) at the most strongly associated SNP (rs8069176) conferred an increase in risk by a factor of 2.9, as compared with other genotypes (AG and AA) in the group exposed to environmental tobacco smoke (P=2.8x10(-6); P=0.006 for the test for heterogeneity of the SNP effect on early-onset asthma between groups with tobacco exposure and those without such exposure).This study shows that the increased risk of asthma conferred by 17q21 genetic variants is restricted to early-onset asthma and that the risk is further increased by early-life exposure to environmental tobacco smoke. These findings provide a greater understanding of the functional role of the 17q21 variants in the pathophysiology of asthma.
Reply to Krüger et al.: Intramucosal Adenocarcinoma of the Appendix
Authors: I. Sakamoto
Journal: Endoscopy (2004)

We are grateful to Krüger et al. for their interest in our article [1]. Their report is quite interesting and suggestive. As Nitecki et al. reported, second primary malignancies were encountered in 35 % of patients with surgically treated primary adenocarcinoma of the appendix and synchronous lesions in 18 % - usually in the large intestine (59 %), as well as the pancreas, ovary, uterus, breast, kidney, prostate, and lung [2]. This incidence of secondary neoplasms is much higher than that for colonic cancer in general. In 30 cases of carcinoma metastatic to the appendix reported by Burney et al., the primary lesion was in the breast in 12 cases (40 %), in the lung in five cases, and in the stomach in three cases [3]. In 33 cases reported in Japan, the primary lesion was in the stomach in 25 cases (76 %), in the gallbladder in four cases, and in the lung and breast in two cases each [4]. We diagnosed our case as a primary adenocarcinoma of the appendix firstly because, as shown in Figure 3 in the article, the well-differentiated adenocarcinoma was adjacent to normal glandular structures, and secondly the lesion was an intramucosal adenocarcinoma with no vascular involvement and no metastases to the lymph nodes.
Synovial fluid neutrophils of patients with rheumatoid arthritis have membrane antigen changes that reflect activation.
Authors: P Emery, A.F Lopez, G.F Burns, M.A Vadas
Journal: Annals of the Rheumatic Diseases (1988)

The level of expression of surface antigens was studied on neutrophils from paired samples of blood and synovial fluid of patients with rheumatoid arthritis (RA). By measuring the immunofluorescence of labelled monoclonal antibodies it was shown that on joint neutrophils there was an increase in expression of complement receptor 3 (CR3) and granulocyte functional antigens 1 and 2 compared with blood neutrophils, whereas the expression of GpIIb-IIIa was reduced. The pattern of expression was the same as that seen with in vitro activation and strongly suggest that activation is occurring within the joint.
Gene Expression Profiling of Familial and Sporadic Interstitial Pneumonia
Authors: Ivana V. Yang, Lauranell H. Burch, Mark P. Steele, Jordan D. Savov, John W. Hollingsworth, Erin McElvania-Tekippe, Katherine G. Berman, Marcy C. Speer, Thomas A. Sporn, Kevin K. Brown, Marvin I. Schwarz, David A. Schwartz
Journal: American Journal of Respiratory and Critical Care Medicine (2006)

Idiopathic interstitial pneumonia (IIP) and its familial variants are progressive and largely untreatable disorders with poorly understood molecular mechanisms. Both the genetics and the histologic type of IIP play a role in the etiology and pathogenesis of interstitial lung disease, but transcriptional signatures of these subtypes are unknown.To evaluate gene expression in the lung tissue of patients with usual interstitial pneumonia or nonspecific interstitial pneumonia that was either familial or nonfamilial in origin, and to compare it with gene expression in normal lung parenchyma.We profiled RNA from the lungs of 16 patients with sporadic IIP, 10 with familial IIP, and 9 normal control subjects on a whole human genome oligonucleotide microarray.Significant transcriptional differences exist in familial and sporadic IIPs. The genes distinguishing the genetic subtypes belong to the same functional categories as transcripts that distinguish IIP from normal samples. Relevant categories include chemokines and growth factors and their receptors, complement components, genes associated with cell proliferation and death, and genes in the Wnt pathway. The role of the chemokine CXCL12 in disease pathogenesis was confirmed in the murine bleomycin model of lung injury, with C57BL/6(CXCR4+/-) mice demonstrating significantly less collagen deposition than C57BL/6(CXCR4+/+) mice. Whereas substantial differences exist between familial and sporadic IIPs, we identified only minor gene expression changes between usual interstitial pneumonia and nonspecific interstitial pneumonia.Taken together, our findings indicate that differences in gene expression profiles between familial and sporadic IIPs may provide clues to the etiology and pathogenesis of IIP.
Protective effect of A at position 168 in the type III promoter of the MHCIITA gene in systemic lupus erythematosus
Authors: H. Okamoto, H. Kaneko, C. Terai, N. Kamatani
Journal: Annals of the Rheumatic Diseases (2007)

<h3>Objective.</h3> To assess the frequency of clinical remission in a cohort of patients with systemic juvenile idiopathic arthritis (JIA) who received continuous anti-tumor necrosis factor (TNF) therapy; and to identify potential predictors of remission. <h3>Methods.</h3> Patients with systemic JIA who were treated with anti-TNF agents for &gt; 6 months were studied. Demographic and nosologic variables recorded at the start of anti-TNF therapy were analyzed. Association between early variables and occurrence of remission was evaluated through Cox proportional hazard regression analysis. <h3>Results.</h3> Forty-five patients were included (30 girls), median age 9 years (range 2–17 yrs), age at disease onset 5 years (range 0.5–15), disease duration 3 years (range 0.5–13). Twenty-one (47%) children showed systemic symptoms at the start of anti-TNF therapy. Patients received therapy for 24 months (range 6–88): 45 (100%) were given etanercept, 17 (38%) infliximab, and 5 (11%) adalimumab, in combination with methotrexate. Anti-TNF switching was performed in 22 (49%) children. Eleven (24%) met definition criteria for remission while taking etanercept (n = 8), infliximab (2), or adalimumab (1). Remission occurred following 26 (range 9–65) months of therapy. Flares occurred in 5 (45%) patients 2 to 14 months after remission was first recorded. Absence of systemic symptoms at the start of therapy and fulfilment of improvement criteria at Month 3 were associated with remission in univariate analysis; no variable showed any association in multivariate analysis. <h3>Conclusion.</h3> Twenty-four percent of patients with systemic JIA experienced remission with anti-TNF therapy, but only 13% experienced sustained benefit.
Commensal bacteria–derived signals regulate basophil hematopoiesis and allergic inflammation
Authors: David A Hill, Mark C Siracusa, Michael C Abt, Brian S Kim, Dmytro Kobuley, Masato Kubo, Taku Kambayashi, David F LaRosa, Ellen D Renner, Jordan S Orange, Frederic D Bushman, David Artis
Journal: Nature Medicine (2012)
Hartnup Disease
Authors: Charles R. Scriver
Journal: New England Journal of Medicine (1965)

A SPECIFIC hyperaminoaciduria affecting certain neutral alpha-amino acids is believed to be the one constant finding in all homozygous patients who have the autosomal recessive hereditary condition called Hartnup disease.1 , 2 There are three groups of alpha-amino acids whose transport is not abnormal in Hartnup disease: a neutral group, including the two "imino acids," proline and hydroxyproline, and the amino acid, glycine; the diaminomonocarboxylic amino acids, lysine, orthinine and arginine (cystine, which is a diaminodicarboxylic amino acid, is also included in the group, for reasons still to be clarified, although its excretion in association with the "basic" amino acids is abnormal . . .
Stop Isoniazid Prophylaxis
Authors: HAROLD L. ISRAEL
Journal: Annals of Internal Medicine (1974)

Comments1 May 1974Stop Isoniazid ProphylaxisHAROLD L. ISRAEL, M.D., F.A.C.P.HAROLD L. ISRAEL, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-5-672_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Having been an early advocate (1) of isoniazid prophylaxis, I feel an obligation to urge termination of this practice. In 1960 isoniazid seemed to be an innocuous and inexpensive drug, and tuberculosis was still a major problem. Now, because of outbreaks of hepatitis in many parts of the country, it is clear that close and costly surveillance of isoniazid users is mandatory, and even this may not avert severe or chronic hepatic damage. Dr. Murphy (2) has raised the proper issue by asking whether tuberculosis today causes "enough morbidity and mortality to justify the use of prophylactic...References1. ISRAEL H: The next step in the campaign against tuberculosis. Am Rev Resp Dis 81:581-584, 1960 MedlineGoogle Scholar2. MURPHY D: Isoniazid hepatitis (letter). Ann Intern Med 80:113-114, 1974 LinkGoogle Scholar3. EDWARDSACQUAVIVALIVESAY LFV: Identification of tuberculous infected. Dual tests and density of reaction. Am Rev Resp Dis 108:1334-1339, 1973 MedlineGoogle 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 byHepatotoxicity Associated With Acetaminophen Usage in Patients Receiving Multiple Drug Therapy for TuberculosisTwo different mechanisms in Isoniazid-induced hepatitisChemoprophylaxis of pulmonary tuberculosisManagement of tuberculosisHazards and Complications of BCG ImmunotherapyInfectious diseases: fortieth and final annual review of significant publications. 1 May 1974Volume 80, Issue 5Page: 672-673KeywordsDrugsHepatitisIsoniazidMorbidityMortalityProphylaxis Issue Published: 1 May 1974 PDF downloadLoading ...
Adjuvant Chemotherapy for Invasive Bladder Cancer: A 2013 Updated Systematic Review and Meta-Analysis of Randomized Trials
Authors: Jeffrey J. Leow, William Martin-Doyle, Padma S. Rajagopal, Chirayu G. Patel, Erin M. Anderson, Andrew T. Rothman, Richard J. Cote, Yuksel Urun, Steven L. Chang, Toni K. Choueiri, Joaquim Bellmunt
Journal: European Urology (2013)
Battling with motor neurone disease.
Authors: B Wilson
Journal: BMJ (1982)

My husband Geoffrey died a few weeks ago, and my children and I are just surfacing from the emotional trauma of watching our beloved husband and Dad go down with the relentless progress of the disease that caused his demise?amyotrophic lateral sclerosis (motor neurone disease). Roger Carus's article on this disease1 was found among Geoff's personal effects, and he had been working to organise a New Zealand register of those with the disorder. Clearly urgent research into the cause of the disease has been going on in many areas. After our marriage 25 years ago we had an interesting life in different lands?general practice in the United Kingdom and in Canada, where he had trained in the Air Force during the second world war, then to the Northern Territory of Australia Medical Services, to New Zealand as an anaesthetist, and, finally, as a casualty officer at the Southland Hospital, Invercargill, New Zealand. During most of this period I worked as a nurse, in my capacity as a camp follower, except when our sons, now 14 and 13 were too young for school.
Should we sequence everyone's genome? No
Authors: F. Flinter
Journal: BMJ (2013)

This is an exciting time to work in medicine. The enormous advances in our understanding of inherited diseases that have flowed from sequencing the human genome mean that many patients benefit from faster, more accurate diagnoses, targeted screening, cascade testing for relatives, and the availability of prenatal diagnosis and pre-implantation genetic diagnosis. Clinicians see patients, take a family history, examine them, and then decide which tests will confirm or exclude specific diagnoses.

Sequencing the first human genome took 13 years and cost $3bn (£2bn; €2.3bn); today we can sequence a complete human genome in a few days for a few thousand pounds. The price will fall further; however, the cost and challenges of analysing, interpreting, and storing the data are substantial.1 2

Mutation screening within a single gene is rapidly being replaced by targeted screening of a relevant panel of genes known to be implicated in particular phenotypes, and whole exome or whole genome sequencing is likely to become the preferred approach in these situations over the next few years.3 Sequencing data can be filtered so that only variants in relevant genes are analysed; variants that might cause disease can then be validated by functional studies before their pathogenicity is confirmed. …