tbuckley/cabot-search huggingface dataset:
Skin pigmentation due to minocycline treatment of facial dermatoses
Authors: C.M. DWYER, A.M. CUDDIHY, R.E.I. KERR, R.S. CHAPMAN, B.F. ALLAM
Journal: British Journal of Dermatology (1993)

Fifty‐four patients taking minocycline for acne or rosacea were assessed for adverse effects. Their mean duration of treatment was 17 months, and their average cumulative dose was 47 g. No symptoms attributable to the therapy were reported. Biochemistry and haematology profiles were normal. There was no evidence of an adverse effect on thyroid function. Skin pigmentation was detected in eight patients (14.8%1. Five patients had diffuse facial pigmentation, and three patients had localized pigmentation at the site of a scar or injury. Diffuse pigmentation occurred only in patients who had been on treatment for 3 years or more; 50% of such patients were affected. Age and solar damage may also have been factors in this type of pigmentation. Localized pigmentation occurred at sites of previous tissue damage, and was not directly related to the duration of therapy. Patients who receive long‐term minocycline therapy should be regularly monitored for the development of pigmentation.
IgE-mediated release of leukotriene C4, chondroitin sulfate E proteoglycan, beta-hexosaminidase, and histamine from cultured bone marrow-derived mouse mast cells.
Authors: E Razin, J M Mencia-Huerta, R L Stevens, R A Lewis, F T Liu, E Corey, K F Austen
Journal: The Journal of Experimental Medicine (1983)

Mouse bone marrow-derived mast cells differentiated in vitro and sensitized with monoclonal IgE respond to antigen-initiated activation with the release of histamine, beta-hexosaminidase, chondroitin sulfate E proteoglycan, and leukotriene C4 (LTC4). The chondroitin sulfate E nature of the glycosaminoglycan side chain was established by demonstrating that the chondroitinase ABC disaccharide digestion products were composed of equal quantities of 4-sulfated and 4,6-disulfated N-acetyl-galactosamine. The single immunoreactive sulfidopeptide leukotriene, released and quantitated with a class-specific antibody, was identified as LTC4 by its retention time on reverse-phase high-performance liquid chromatography and by its specific spasmogenic activity on the guinea pig ileum. The release of the preformed mediators, as well as of LTC4, was related in a dose-response fashion to the concentration of monoclonal IgE used during the sensitization step and to the concentration of specific antigen used to initiate the activation-secretion response. The optimal concentrations of IgE for sensitization and of antigen for challenge were the same for the release of preformed mediators and of LTC4. In addition, the time courses of their release were superimposable, with a plateau at 5 min after antigen challenge. The release of three preformed mediators and of LTC4 after fixation of IgE, washing of the sensitized cells, and antigen challenge unequivocally indicates a bone marrow-derived mast cell origin for these products. Linear regression analyses of the net percent release of beta-hexosaminidase to histamine and of 35S-chondroitin sulfate E to beta-hexosaminidase yielded straight lines that intersected at the origin, which indicates that the three preformed mediators are localized in the secretory granules of the bone marrow-derived mast cells. The concomitant generation of 23 ng of LTC4/10(6) sensitized bone marrow-derived mast cells represents the first example of IgE-dependent release of substantial amounts of LTC4, a component of slow reacting substance of anaphylaxis, from a mast cell population of greater than 95% purity. The IgE-dependent generation of LTC4, rather than prostaglandin D2, by the chondroitin sulfate E proteoglycan-containing bone marrow-derived mast cells contrasts with the predominant generation of prostaglandin D2 by heparin proteoglycan-containing mast cells. These differences together support the existence of two phenotypically different mast cell subclasses.
Mutations of CLCN5 in Japanese children with idiopathic low molecular weight proteinuria, hypercalciuria and nephrocalcinosis
Authors: Naoko Akuta, Sarah E. Lloyd, Takashi Igarashi, Hiroshi Shiraga, Takeshi Matsuyama, Seitarou Yokoro, Jeremy P.D. Cox, Rajesh V. Thakker
Journal: Kidney International (1997)
The History of Ophthalmology, vol 1: Antiquity
Authors: Heinrich König
Journal: JAMA (1984)

Julius Hirschberg's well-known<i>History of Ophthalmology</i>was written in German and appeared in 1918 in the<i>Graefe-Saemisch Handbuch der Gesamten Augenheilkunde</i>. For more than 60 years it has been the essential source of medicohistorical information in ophthalmology, but because it has long been out of print, a new edition is overdue. Professor Frederick C. Blodi, MD, head of the Department of Ophthalmology at the University of Iowa and an experienced multilingual ophthalmologist, has now undertaken the monumental task of translating Hirschberg's comprehensive work into English. The first of the 11 volumes to be published has recently been issued. For anyone familiar with the German edition, browsing in the first volume of the translated work is a unique experience. It begins with ophthalmology in ancient Egypt and elucidates the fact that true insight into the medicine of ancient Egypt only dates back to the unfinished contributions of Georg Eber (Eber's Papyrus)
"COARCTATION OF THE AORTA"-Reply
Authors: Wilmot F. Pierce
Journal: JAMA (1934)

<h3>To the Editor:—</h3> The correspondent is justified in criticizing the expression "absolutely irregular" as applied to the heart rhythm. It would have been better to say "quite irregular from numerous extrasystoles." "Perpetual arrhythmia," "complete irregularity," if used at all nowadays are usually meant to imply auricular fibrillation. I have no quarrel with him over his contention that an "irregularity" can generally be diagnosed without the electrocardiogram. This should be attempted always. The electrocardiogram should be confirmatory or corrective. This was the procedure in the case reported and I regret that there was not greater care in the use of terms.
Cadmium and Breast Cancer: Exposure Associated with Basal-Like Phenotype
Authors: Julia R. Barrett
Journal: Environmental Health Perspectives (2009)

Nanotechnology holds the promise of vastly expanding our ability to clean up hazardous waste sites and decontaminate polluted groundwater in situ.Polychlorinated biphenyls, organic solvents, petroleum products, arsenic, and many more contaminants are on the list that specifically engineered nanoparticles could rapidly remove from contaminated soil and water, saving billions of dollars that would have been spent on more expensive conventional remediation methods.These possibilitites are discussed in a review of field tests using nanomaterials [EHP 117:1823-1831; Karn et al.].However, the authors caution, our knowledge of the potential environmental and health hazards posed by these nanomaterials is in its infancy.In the United States alone there are hundreds of thousands of sites contaminated with hazardous wastes, with more than 1,200 requiring priority attention.Using traditional remediation technologies, such as pumping out and treating contaminated groundwater and removing contaminated soil, the job of cleaning up U.S. hazardous waste sites could take 35 years and $250 billion.The authors of this review, however, report on results showing that nanoscale zero-valent iron (nZVI) nanoparticles could dramatically reduce the time required to remediate soil and water as well as, according to one report, save 80-90% compared with conventional methods.Although tiny in diameter, the surface area of these iron-based nanoparticles reaches 20-40 m 2 /g.This relatively large surface area can greatly increase the particles' reactivity.Flowing with the groundwater they can spread out to react with pollutants, transforming them into safer compounds, including compounds that bacteria can break down.The authors provide many examples of how nZVIs, currently the nano materials most widely used for in situ remediation, produced measurable effects within days or, in some cases, hours.However, the authors also emphasize that we do not know much about the potential adverse effects of nanoparticles deployed into the environment-agents that could, for example, end up in our drinking water.Some nanomaterials have already been found to enter organisms.Might some be toxic or transport bound pollutants to places they might not other wise have gone?Can they be biomagnified?How do they affect living organisms?The authors point out that, although the environment is full of naturally occurring nanoparticles, manufactured nanoparticles may behave in unpredictable ways.They recommend that while we improve engineering applications using nanoparticles for in situ remediation, we also develop the analytical tools to enable the study of manufactured nanoparticles in the environment and increase research on the ecosystem effects of these materials.
Complementary Medicine and the Cochrane Collaboration
Authors: Jeanette Ezzo
Journal: JAMA (1998)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Development of Reticulum-Cell Sarcoma at the Site of Antilymphocyte Globulin Injection in a Patient with Renal Transplant
Authors: Sharad D. Deodhar, Arlington G. Kuklinca, Donald G. Vidt, Abel. L. Robertson, John B. Hazard
Journal: New England Journal of Medicine (1969)

IMMUNOLOGIC mechanisms have an important surveillance role in detecting and destroying abnormal, potentially malignant cells arising either spontaneously or through the effect of various agents. The enhancing effect of various immunosuppressive measures on oncogenesis induced by various agents in laboratory animals and also the well known clinical association between immunologic deficiency syndromes and malignant processes, especially of the lymphoid system, are consistent with this hypothesis. One would expect clinical immunosuppressive therapy to lead to a similar increased occurrence of malignant tumors in man; however, such a result has not been demonstrated in a definitive manner. Recently, five cases of malignant . . .
Mitochondrial protection by the JNK inhibitor leflunomide rescues mice from acetaminophen-induced liver injury
Authors: Calivarathan Latchoumycandane, Catherine W. Goh, Michie M.K. Ong, Urs A. Boelsterli
Journal: Hepatology (2007)

Acetaminophen (APAP) is a widely used analgesic and antipyretic drug that is safe at therapeutic doses but which can precipitate liver injury at high doses. We have previously found that the antirheumatic drug leflunomide is a potent inhibitor of APAP toxicity in cultured human hepatocytes, protecting them from mitochondria-mediated cell death by inhibiting the mitochondrial permeability transition. The purpose of this study was to explore whether leflunomide protects against APAP hepatotoxicity in vivo and to define the molecular pathways of cytoprotection. Male C57BL/6 mice were treated with a hepatotoxic dose of APAP (750 mg/kg, ip) followed by a single injection of leflunomide (30 mg/kg, ip). Leflunomide (4 hours after APAP dose) afforded significant protection from liver necrosis as assessed by serum ALT activity and histopathology after 8 and 24 hours. The mechanism of protection by leflunomide was not through inhibition of cytochrome P450 (CYP)–catalyzed APAP bioactivation or an apparent suppression of the innate immune system. Instead, leflunomide inhibited APAP-induced activation (phosphorylation) of c-jun NH2-terminal protein kinase (JNK), thus preventing downstream Bcl-2 and Bcl-XL inactivation and protecting from mitochondrial permeabilization and cytochrome c release. Furthermore, leflunomide inhibited the APAP-mediated increased expression of inducible nitric oxide synthase and prevented the formation of peroxynitrite, as judged from the absence of hepatic nitrotyrosine adducts. Even when given 8 hours after APAP dose, leflunomide still protected from massive liver necrosis. Conclusion: Leflunomide afforded protection against APAP-induced hepatotoxicity in mice through inhibition of JNK-mediated activation of mitochondrial permeabilization.
P145 Thrombolysis of Acute PE Patients Reduces Subsequent Development of CTEPH
Authors: D C Thomas, R M Limbrey
Journal: Thorax (2012)

<h3>Introduction</h3> Pulmonary Embolism (PE) is a frequent diagnosis and the incidence of Chronic Thromboembolic pulmonary hypertension (CTEPH) after a single acute episode of PE is higher than expected – in one prospective long-term study 3.8% at 2 years <i>(Pengo et al 2004).</i> A diagnosis of CTEPH carries a 30% 5 year mortality and early diagnosis is vital if treatment is to be of success although successful treatment options remain limited. We hypothesized that by following up all new diagnoses of PE we would pick up early cases of CTEPH and identify risk factors for those developing CTEPH. We also hypothesized that thrombolysis as per the BTS guidelines would reduce the subsequent incidence of CTEPH. <h3>Methods</h3> A retrospective study of all patients referred to a PE clinic over a 2 year period was performed. Initial and follow up echocardiograms were examined, provoking factors and treatment identified with a primary end point of development of CTEPH at 2 years. <h3>Results</h3> Of the first 50 patients presenting with an acute PE 12% (n=6) had evidence of CTEPH on echocardiogram after 2 years. The major risk factor for the development of CTEPH was an initial echocardiogram demonstrating a RVSP&gt;50mmHg which conferred a 5-fold increase in persistent pulmonary hypertension on echocardiogram at 2 years (36% versus 7%). None of the thrombolysed patients went on to develop CTEPH despite having in 50% an RVSP&gt;50mmHg and all had a normal early (within six months) repeat echocardiogram. <h3>Conclusions</h3> Patients who present with an acute PE and have an initial RVSP of &gt;50mmHg on echocardiogram have a 5 fold increase in developing persistent pulmonary hypertension at 2 years. However patients who had a RVSP&gt;50mmHg at diagnosis and are thrombolysed do not appear to develop CTEPH and have normal echocardiography at 2 years. Bearing in mind the mortality CTEPH carries and the difficulty in treating it, patients presenting with an acute significant PE and a RVSP&gt;50mmHg should be considered for thrombolysis regardless of haemodynamic compromise. <h3>Reference</h3> Pengo V, Lensing AWA, Prins MH, et al., Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism, N Engl J Med, 2004; 350:2257–64.
Mortality and Morbidity Associated With Body Weight in People With IDDM: The WHO Multinational Study of Vascular Disease in Diabetes
Authors: Nishi Chaturvedi, Lynda K Stevens, John H Fuller
Journal: Diabetes Care (1995)

OBJECTIVE Strict glycemic control in people with insulin-dependent diabetes mellitus (IDDM) reduces the risk of microvascular complications, but improvementsin control are also associated with weight gain. Fears about the mortality risks of obesity may limit the acceptability of tight control. Therefore, we examined morbidity and mortality risks associated with body weight in people with IDDM. RESEARCH DESIGN AND METHODS This was a cohort study of 644 men and 576 women with IDDM from nine centers worldwide. Baseline examinations were performed in 1975–1977, and mortality follow-up continued until 1988. RESULTS Body weight was positively associated with blood pressure and, in men, with cholesterol. Fasting blood glucose was higher in the most obese groups in women only. There were 204 deaths among the men and 148 among the women. There was a reverse J-shaped relationship between body weight and all-cause mortality, with the highest mortality rates occurring in the leanest body mass index (BMI) category. The age-, duration-, and center-adjusted mortality rate ratio (95% confidence interval) comparing BMI category &amp;lt; 20 kg/m2 with BMI category ≥22 and &amp;lt;24 kg/m2 was 2.64 (1.59–4.38) in men and 1.54 (0.77–3.06) in women. Additional adjustment for smoking, blood pressure, glucose, cholesterol, and proteinuria did not qualitatively alter these findings. CONCLUSIONS We conclude that except in very lean people with IDDM, body weight is not significantly associated with mortality. Thus, efforts to improve glycemic control should not be restricted by concerns about the effects of weight gain on mortality.
MEDIASTINAL LIPOMA SIMULATING CARDIAC ENLARGEMENT
Authors: A. M. Gottlieb
Journal: JAMA (1953)

This case of a mediastinal lipoma is reported because, by its location and shape, it so closely simulated cardiac enlargement. Mediastinal tumor is not usually considered in the differential diagnosis of enlargement of the cardiac silhouette. Lipomas are uncommon intrathoracic neoplasms. Thirty-five of the 56 intrathoracic lipomas reported to date were in the mediastinum,<sup>1</sup>and only two of these lipomas were confused with cardiac enlargement. One was in Yater and Lyddane's series,<sup>1f</sup>and the other was presented by Sosman and Levine at a clinic during the annual meeting of the American College of Physicians in Boston in 1949. <h3>REPORT OF A CASE</h3> A 30-year-old white man who was an automobile salesman was admitted to the hospital on Jan. 10, 1952. On admission, the diagnosis cardiac enlargement with cause undetermined was made. The patient had been recalled to active duty as a Navy fighter pilot. During the routine physical
70. Long Term Correction of beta-Thalassemia by Transplantation of Transduced Hematopoietic Stem Cells
Authors: Annarita Miccio, Rossano Cesari, Francesco Lotti, Claudia Rossi, Francesca Tiboni, Francesca Sanvito, Maurilio Ponzoni, Samantha Routledge, Michael Antoniou, Giuliana Ferrari
Journal: Molecular Therapy (2006)

Gene therapy for beta-thalassemia requires stable transfer of the beta-globin gene into hematopoietic stem cells (HSCs) and high and regulated Hb expression in the erythroblastic progeny. We developed a novel high-titer LV to express therapeutic level of Hb in one of the most severe murine model of beta-thalassemia. We cloned the human beta globin gene under the control of a minimal promoter and 2 elements of the LCR (HS2 and HS3), in the context of a SIN-18 LV. We evaluated the efficiency of this LV to correct the thalassemic phenotype in the th3/+ mouse mutant, that exhibit chronic anemia, anomalies in red cell size and shape, splenomegaly, extramedullary hematopoiesis (EMH) and iron accumulation in liver and spleen. The beta globin transgene expression was analyzed in the differentiated progeny of transduced HSCs, after transplantation into lethally irradiated thalassemic mice. Transplantation of LV- transduced HSCs lead to a high proportion (79%–100%) of donor RBCs expressing human beta globin, which remained stable up to 9 months after transplantation. HPLC analysis allowed the detection of the human beta globin chain, accounting for up to 43% of endogenous murine beta globin chains. The hematocrit, red blood cell count and hemoglobin level were markedly improved (HCT 44.90±6.10; RBC 9.15±1.22, HGB 12.07±1.75) in comparison to the hematological parameters in control mice transplanted mock- transduced th3/+ cells (HCT 29.33±2.08; RBC 5.79±0.45, HGB 8.03±1.12). The vector derived beta-globin synthesis was able to strongly reduced abnormalities in RBC morphology in mice transplanted with LV-transduced cells. FACS analysis of the erythroid TER119+ bone marrow subpopulations showed the restoration of normal erythroblastic maturation in the gene therapy- treated mice. Finally, the histopathological analysis demonstrated the correction of splenomegaly, EMH and drastic reduction of iron deposition in the spleen and liver. Quantitative PCR analysis revealed that the average proviral copy number ranged from 0.3 to 2.2, showing a direct correlation with the degree of phenotype correction. Analysis of single erythroid CFU-S, derived from secondary recipients, confirmed that the level of vector-derived human beta-globin was copy number dependent. Moreover, Southern Blot analysis of DNA extracted from transduced bone marrow samples indicated that the engraftment of a relatively small number of transduced HSCs was sufficient to fully correct the thalassemic phenotype in the th3/+ model. Finally, we demonstrated that LV-derived human beta globin expression was persistent and rescued the thalassemic phenotype in secondary transplanted th3/+ mice. Experiments are ongoing to test the therapeutic potential of the described LV to correct thalassemia major.
A Comparison of the Clinical Features of Poliomyelitis in Adults and in Children
Authors: Louis Weinstein, Alexis Shelokov, Raymond Seltser, Gordon D. Winchell
Journal: New England Journal of Medicine (1952)

ONE of the remarkable changes that have occurred in poliomyelitis in many parts of the world in the past twenty years is the rise in its incidence in older age groups.1 Formerly uncommon in others than the pre-school child, the disease has gradually become frequent in those five to nine years old and is, at present, increasing in prevalence in even older persons. As a matter of fact, it is not at all rare today for poliomyelitis to affect patients in the third and fourth decades of life. Because of this changing age frequency, the term "infantile paralysis" is no . . .