tbuckley/cabot-search huggingface dataset:
Gold-mining activities and mercury contamination of native amerindian communities in French Guiana: key role of fish in dietary uptake.
Authors: N Fréry, R Maury-Brachet, E Maillot, M Deheeger, B de Mérona, A Boudou
Journal: Environmental Health Perspectives (2001)

In 1994, the French National Public Health Network reported significant mercury exposure of native Amerindians in French Guiana. In 1997, a study was conducted in the Wayana community to quantify the dietary intake and to identify the fish species contributing the most to the contamination. The study was completed by an impregnation analysis based on Hg determination in hair samples. The methodology used was a detailed familial dietary study associated with Hg measurements in fish and some game. The study was conducted over 7 days in two different seasons in the four most populated Wayana villages on the upper part of the Maroni River (521 people; 70% of the Wayana population in French Guiana). Analysis was based on data on consumption obtained from 165 people in a 1-14 day period (i.e., 940 persons [times] days) and involved 270 fish samples from 48 species. Total Hg and monomethylmercury (MMHg) were also determined in hair samples (235 samples for total Hg). The results confirm mercury exposure of the Wayana population related to a diet rich in fish, which are relatively highly contaminated for certain species (up to 1.62 mg/kg fresh weight or 8.1 mg/kg dry weight in skeletal muscle). Results from hair samples showed that 57% of the Amerindians had Hg levels above the World Health Organization (WHO) safety limit (10 microg/g); all those over 1 year of age had a Hg intake greater than the WHO safety limit (200 microg MMHg/week for a 60-kg male). Hg concentrations in fish muscle were closely linked to the feeding regime and position of fish in the food webs. Overall, 14.5% of the fish collected exceeded the 0.5 mg/kg (fresh weight) safety limit. Four carnivorous species accounted for no less than 72% of the metal ingested by the Wayana families, although these represented only 28% of the consumed fish biomass. In conclusion, this study revealed excessive exposure to mercury in the Wayana population in French Guiana related to the consumption of contaminated fish.
Intravitreal Aflibercept for Macular Edema Following Branch Retinal Vein Occlusion
Authors: Peter A. Campochiaro, W. Lloyd Clark, David S. Boyer, Jeffrey S. Heier, David M. Brown, Robert Vitti, Husain Kazmi, Alyson J. Berliner, Kristine Erickson, Karen W. Chu, Yuhwen Soo, Yenchieh Cheng, Julia A. Haller
Journal: Ophthalmology (2014)
Retinal Lesions in Cytomegalovirus Infection
Authors: STEVEN A. TEICH
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 January 1986Retinal Lesions in Cytomegalovirus InfectionSTEVEN A. TEICH, M.D., JUAN ORELLANA, M.D.STEVEN A. TEICH, M.D.Search for more papers by this author, JUAN ORELLANA, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-104-1-132_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: A recent article by Felsenstein and colleagues (1) concerns the treatment of cytomegalovirus retinitis with 9-[2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine. We have also been using this drug to treat cytomegalovirus retinitis in patients with the acquired immunodeficiency syndrome (AIDS) and concur that many patients have clinical improvement with healing of retinal lesions but that recurrence is virtually universal within a few weeks of stopping therapy.We do, however, disagree with the description of the fundus in these patients for documenting cytomegalovirus retinitis. Patient 1 was described as having "nerve infarcts, compatible with cytomegalovirus retinitis." In fact, nerve infarcts or cotton-wool spots...References1. FELSENSTEIN D, D'AMICO D, and HIRSCH M. Treatment of cytomegalovirus retinitis with 9-[2-hydroxy-(hydroxymethyl) ethoxymethyl] guanine. Ann Intern Med. 1985;103:377-80. LinkGoogle Scholar2. PEPOSE J, HOLLAND G, NESTOR M, COCHRON A, and FOOS R. Acquired immune deficiency syndrome: pathogenic mechanisms of ocular disease. Ophthalmology. 1985;92:472-84. CrossrefMedlineGoogle Scholar3. NEWSOME D, GREEN W, and MILLER E. Microvascular aspects of acquired immune deficiency syndrome retinopathy. Am J Ophthalmol. 1984;98:590-601. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: STEVEN A. TEICH, M.D.; JUAN ORELLANA, M.D.Affiliations: Beth Israel Medical Center New York, NY 10003 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCytomegalovirus infection in acquired immune-deficiency syndrome7 The management of HIV disease in pregnancyThe Diagnosis of Cytomegalovirus RetinitisJeffrey N. Bloom, MD, Alan G. Palestine, MDHerpesvirus Infections (Cytomegalovirus, Herpes Simplex Virus, Varicella-Zoster Virus)Therapy and Prevention of Cytomegalovirus Infections 1 January 1986Volume 104, Issue 1Page: 132-132KeywordsAIDSCytomegalovirus infectionDrug therapyLesionsNervesRetinitis ePublished: 1 December 2008 Issue Published: 1 January 1986 PDF downloadLoading ...
<i>The Aqueduct</i>
Authors: Jeanette M. Smith
Journal: JAMA (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
A New Example of the Rh Antibody, Anti-Cx
Authors: G. Plaut, P. B. Booth, C. M. Giles, A. E. Mourant
Journal: BMJ (1958)

During platelet biogenesis, microtubules (MTs) are arranged into submembranous structures (the marginal band) that encircle the cell in a single plane. This unique MT array has no equivalent in any other mammalian cell, and the mechanisms responsible for this particular mode of assembly are not fully understood. One possibility is that platelet MTs are composed of a particular set of tubulin isotypes that carry specific posttranslational modifications. Although β1-tubulin is known to be essential, no equivalent roles of α-tubulin isotypes in platelet formation or function have so far been reported. Here, we identify α4A-tubulin as a predominant α-tubulin isotype in platelets. Similar to β1-tubulin, α4A-tubulin expression is up-regulated during the late stages of megakaryocyte differentiation. Missense mutations in the α4A-tubulin gene cause macrothrombocytopenia in mice and humans. Defects in α4A-tubulin lead to changes in tubulin tyrosination status of the platelet tubulin pool. Ultrastructural defects include reduced numbers and misarranged MT coils in the platelet marginal band. We further observed defects in megakaryocyte maturation and proplatelet formation in <i>Tuba4a</i>-mutant mice. We have, thus, discovered an α-tubulin isotype with specific and essential roles in platelet biogenesis.
Arylsulfatase B activities and glycosaminoglycan levels in retrovirally transduced mucopolysaccharidosis type VI cells. Prospects for gene therapy.
Authors: C Fillat, C M Simonaro, P L Yeyati, J L Abkowitz, M E Haskins, E H Schuchman
Journal: Journal of Clinical Investigation (1996)

Mucopolysacchariodosis type VI (MPS VI) is the lysosomal storage disorder caused by the deficient activity of arylsulfatase B (ASB; N-acetylgalactosamine 4-sulfatase) and the subsequent accumulation of the glycosaminoglycan (GAG), dermatan sulfate. In this study, a retroviral vector containing the full-length human ASB cDNA was constructed and used to transduce skin fibroblasts, chondrocytes, and bone marrow cells from human patients, cats, or rats with MPS VI. The ASB vector expressed high levels of enzymatic activity in each of the cell types tested and, in the case of cat and rat cells, enzymatic expression led to complete normalization of 35SO4 incorporation. In contrast, overexpression of ASB in human MPS VI skin fibroblasts did not lead to metabolic correction. High-level ASB expression was detected for up to eight weeks in transduced MPS VI cat and rat bone marrow cultures, and PCR analysis demonstrated retroviral-mediated gene transfer to approximately 30-50% of the CFU GM-derived colonies. Notably, overexpression of ASB in bone marrow cells led to release of the enzyme into the media and uptake by MPS VI cat and rat skin fibroblasts and/or chondrocytes via the mannose-6-phosphate receptor system, leading to metabolic correction. Thus, these studies provide important rationale for the development of gene therapy for this disorder and lay the frame-work for future in vivo studies in the animal model systems.
Assessing Predictive Performance Beyond the Framingham Risk Score—Reply
Authors: Ioanna Tzoulaki
Journal: JAMA (2010)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Plan for General Practice
Authors: J. G. Ball, J. S. Price, M. H. Aylward, A. A. Walker, R. F. Lurring, H. H. B. Lamb, J. M. Elliott, M. Molony, P. Molony, S. C. Harper, H. M. Buchanan, P. J. Chaudoir, D. E. Sargent, M. A. Young, W. T. Mackie
Journal: BMJ (1965)
The neutrophil serine protease inhibitor <i>serpinb1</i> preserves lung defense functions in <i>Pseudomonas aeruginosa</i> infection
Authors: Charaf Benarafa, Gregory P. Priebe, Eileen Remold-O'Donnell
Journal: The Journal of Experimental Medicine (2007)

Neutrophil serine proteases (NSPs; elastase, cathepsin G, and proteinase-3) directly kill invading microbes. However, excess NSPs in the lungs play a central role in the pathology of inflammatory pulmonary disease. We show that serpinb1, an efficient inhibitor of the three NSPs, preserves cell and molecular components responsible for host defense against Pseudomonas aeruginosa. On infection, wild-type (WT) and serpinb1-deficient mice mount similar early responses, including robust production of cytokines and chemokines, recruitment of neutrophils, and initial containment of bacteria. However, serpinb1−/− mice have considerably increased mortality relative to WT mice in association with late-onset failed bacterial clearance. We found that serpinb1-deficient neutrophils recruited to the lungs have an intrinsic defect in survival accompanied by release of neutrophil protease activity, sustained inflammatory cytokine production, and proteolysis of the collectin surfactant protein–D (SP-D). Coadministration of recombinant SERPINB1 with the P. aeruginosa inoculum normalized bacterial clearance in serpinb1−/− mice. Thus, regulation of pulmonary innate immunity by serpinb1 is nonredundant and is required to protect two key components, the neutrophil and SP-D, from NSP damage during the host response to infection.
Dr. Scheppegrell's Book.
Authors: W. SCHEPPEGRELL
Journal: JAMA (1898)

New Orleans, Sept. 6, 1898. <h3>To the Editor:</h3> —On my return to the city, a few days ago, I noted the reference to my recently published work on "Electricity in the Diagnosis and Treatment of Diseases of the Nose, Throat and Ear," among the Book Notices in your issue of August 20. An author naturally expects various kinds of criticisms, but the writer in medical literature has reason to believe that his work will receive fair attention at the hands of the more important medical journals, and that the criticisms will be made by some one competent to judge of the merits or defects of his work. In the case of theJournal of the American Medical Association, there is, according to my opinion, more than the usual relation between subscriber and editor. This journal is the official organ, in fact the mouth-piece, of theAmerican Medical Association. In other
Teenagers, sex, and risk taking.
Authors: R Kaul, S Kaul
Journal: BMJ (1993)

400 mg, 800 mg, and 1200 mg groups were 87, 88, and 95, respectively, corresponding to death rates of.54%, 56%, and 61% (p-0-65, log rank test).Ten patients (2%) were lost to follow up.On the basis of this and other randomised dose studies, in which the doses of the drug were 500 mg v 1500 mg' and 600 mg v 1200 mg,3 it may be concluded that to obtain the maximum effect on survival rates the dose of zidovudine need not exceed 400 mg daily.
A Mechanism-Driven Treatment for Chronic Lymphocytic Leukemia?
Authors: Robin Foà, Anna Guarini
Journal: New England Journal of Medicine (2013)

Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in the Western world. Its prevalence is increasing largely because of extended life expectancies. CLL has a highly heterogeneous clinical course: some patients live for years or decades, never require treatment, and eventually die from a cause other than CLL, whereas others have a slowly progressive clinical picture and others have an aggressive disease course of 2 years or less.Since 1975, clinicians have relied on clinical staging systems to define prognosis and make treatment decisions. Over the past 12 years, a number of biologic markers have allowed a . . .
1021 CARDIAC DIASTOLIC DYSFUNCTION IS ASSOCIATED WITH IMPAIRED NATRIURESIS IN PATIENTS WITH DECOMPENSATED CIRRHOSIS AND ASCITES
Authors: E. Cholongitas, J. Goulis, D. Ekklisiarchos, C. Birtsou, T. Nakouti, P. Chalevas, D. Paulou, M. Ioannidou, E. Akriviadis
Journal: Journal of Hepatology (2013)
Carbapenem-resistant Klebsiella pneumoniae is associated with poor outcome in hemodialysis patients
Authors: Dina Bleumin, Matan J. Cohen, Olivier Moranne, Vincent L.M. Esnault, Shmuel Benenson, Ora Paltiel, Keren Tzukert, Irit Mor-Yosef Levi, Iddo Z. Ben-Dov, Ronen Levi, Aharon Bloch, Yosef S. Haviv
Journal: Journal of Infection (2012)
Systemic Arterial Patterns in the Lung and Clubbing of the Fingers
Authors: M. Turner-Warwick
Journal: Thorax (1963)

The close association between clubbing of the fingers and some forms of heart and lung disease have been reviewed fully by Mendlowitz (1942).The frequent association of clubbing of the extremities with cyanotic heart disease led to the suggestion that hypoxia was an important causal factor (Mendlowitz, 1942), but hypoxia alone does not account for the presence of finger clubbing in many types of lung disease.Cudkowicz and Wraith (1957a) could find no single clinical common factor in 27 patients with finger clubbing and various pulmonary disorders.From the anatomical standpoint, Cudkowicz and Armstrong (1953) suggested that the essential feature in the lungs of patients with clubbing was the presence of precapillary communications between the bronchial and pulmonary arteries.Later they supported this suggestion with right heart catheterization studies in 28 patients with finger clubbing and various lung disorders; they found high oxygen saturations in the pulmonary artery branch to the diseased lobe and concluded that there must be a left to right shunt at pulmonary artery level.More recently Cudkowicz, Calabresi, Nims, and Gray (1959) have shown in four patients with clubbing that the output of the left ventricle exceeded that of the right, and they regarded this on July 25, 2023 by guest.
Per oral dual-scope rendezvous technique for endoscopic bridging of complete pancreatic duct disruption
Authors: M. Ergun, C. Descamps, P. Deprez
Journal: Endoscopy (2010)

A 43-year-old man with a history of heavy alcohol consumption and recent acute pancreatitis was admitted for recurrent epigastric pain and diagnosed as having a 4-cm pancreatic pseudocyst. Endoscopic retrograde cholangiopancreatography (ERCP) showed a pancreas divisum with total obstruction of the main pancreatic duct (MPD) in the mid-pancreas and no communication with the fluid collection. Minor papilla sphincterotomy was performed with placement of a 7-Fr plastic stent (Zimmon, Wilson-Cook, Winston-Salem, North Carolina, USA) in the pancreatic duct. Endoscopic ultrasound-guided cystogastrostomy was carried out (Pentax EG3860UT, Hamburg, Germany) and a single, 10-Fr double-pigtail stent was placed ([Fig. 1]).
Results of Rhegmatogenous Retinal Detachment Repair in Cytomegalovirus Retinitis with and without Scleral Buckling
Authors: Roberto F. García, Marisa Flores-Aguilar, Jose I. Quiceno, Edmund V. Capparelli, David Munguia, Baruch D. Kuppermann, Fernando Arevalo, William R. Freeman
Journal: Ophthalmology (1995)
Enhanced bone regeneration via multimodal actions of synthetic peptide SVVYGLR on osteoprogenitors and osteoclasts
Authors: Hiroshi Egusa, Yoshitoshi Kaneda, Yoshihiro Akashi, Yoshinosuke Hamada, Takuya Matsumoto, Makio Saeki, Devang K. Thakor, Yasuhiko Tabata, Nariaki Matsuura, Hirofumi Yatani
Journal: Biomaterials (2009)
SCHIZOPHRENIA ASSOCIATED WITH ADDISON'S DISEASE
Authors: HAROLD D. WOLFF, P. E. HUSTON
Journal: American Journal of Psychiatry (1959)

A patient is presented who showed an acute schizophrenic reaction. Treated with ECT, there was marked improvement. Four weeks later the schizophrenic symptoms returned accompanied by signs and symptoms of Addison's disease. Treated with hormones, there was a remission of both the Addison's disease and the mental symptoms. After one year of maintenance on cortisone, the patient is without evidence of schizophrenia or Addison's disease.
Symptomatic Coronary Artery Disease in a Marathon Runner
Authors: Claus A. Pierach
Journal: JAMA (1983)

<h3>To the Editor.—</h3> A recent article by Handler et al described a 48-year-old man who had trained in a vigorous running program for approximately eight years and then experienced angina pectoris. Angiography demonstrated a 90% to 99% stenosis of his proximal left anterior descending coronary artery. The authors concluded that "a long distance marathon runner's life-style is not necessarily protective against the progression of coronary atherosclerosis." This may be correct, but a single, probably very rare, case can hardly be considered as sufficient evidence or proof. We do not know if this patient previously had rather extensive coronary atherosclerosis that may have regressed. It is also possible that the isolated high-grade stenosis represented a spasm rather than atherosclerosis. Although nobody should claim running to be a panacea, one could still argue in this well-verified case that the vigorous exercise program may have prolonged this patient's life already. Who knows what
Myosin filament assembly onto myofibrils in live neonatal cardiomyocytes observed by TPEF-SHG microscopy
Authors: Honghai Liu, Yonghong Shao, Wan Qin, Raymond B. Runyan, Meifeng Xu, Zhen Ma, Thomas K. Borg, Roger Markwald, Bruce Z. Gao
Journal: Cardiovascular Research (2012)

Understanding myofibrillogenesis is essential for elucidating heart muscle formation, development, and remodelling in response to physiological stimulation. Here, we report the dynamic assembly process of contractile myosin filaments onto myofibrils in a live cardiomyocyte culture during myofibrillogenesis. Utilizing a custom-built, two-photon excitation fluorescence and second harmonic generation imaging system equipped with an on-stage incubator, we observed new sarcomere additions in rat neonatal cardiomyocytes during 10 h of on-stage incubation. The new sarcomere additions occurred at the side of existing myofibrils, where we observed mature myofibrils acting as templates, or at the interstice of several separated myofibrils. During sarcomeric addition, myosin filaments are assembled onto the premyofibril laterally. This lateral addition, which proceeds stepwise along the axial direction, plays an important role in the accumulation of Z-bodies to form mature Z-disks and in the regulation of sarcomeric alignment during maturation.
Benign sixth-nerve palsy.
Authors: K. P. Dawson
Journal: BMJ (1970)

MBDICALIOURNAL 177 account of a painful hip owing to ischaemic necrosis complicating an old fracture of the femoral neck.During the operation of McKee-Farrar total hip replacement con- siderable osteoporosis was encountered, and insertion of the femoral component required twice the usual amount of cement.Immedi- ately following reduction of the hip, profound hypotension and bradycardia occurred.There were no warning signs on the E.C.G.Cardiac arrest ensued, and attempts at resuscitation were unsuccessful.Necropsy showed air and fat in the pelvic veins on the side of the operation, right heart, and in the coronary vessels.There was marked myocardial degeneration.The cause of death was considered to be air embolism acting on a previously defective myocardium.It would seem possible that air (or fat) embolism might account for some of the cases of transient hypotension with recov- ery.We now use a polythene tube while inserting the cement and note the consider- able quantities of fat and air which are expelled through it.We also feel that we should use an oesophageal stethoscope and a central venous pressure line (for diagnosis and treatment) as recommended recently by O'Higgins.'-We are, etc.,
Tietz Textbook of Clinical Chemistry
Authors: None David
Journal: JAMA (1994)

For years and through two editions, Tietz's<i>Fundamentals of Clinical Chemistry</i>served as one of the major references in the field. In 1986, a closely related book, the first edition of<i>Textbook of Clinical Chemistry</i>, was published, followed by the third edition of<i>Fundamentals of Clinical Chemistry</i>in 1987. The major difference between these two versions—<i>Textbook</i>and<i>Fundamentals</i>—lies in the discussion of pathophysiology found in<i>Textbook</i>, while<i>Fundamentals</i>retained a more analytical laboratory- and methods-oriented approach. Eight years later and with the second edition of the<i>Textbook</i>, Dr Tietz has passed his editorship to two new and very capable successors. Although a good number of the chapter authors have changed, the book retains many of its important characteristics. In the new edition of<i>Textbook</i>, the editors have made some minor revisions in organization. The 20 chapters of the previous edition have been expanded to 41, and the book