tbuckley/cabot-search huggingface dataset:
Sweet's syndrome in chronic myelomonocytic leukemia
Authors: Muntasir Saffie, Dongmei Sun, Cyrus Hsia
Journal: American Journal of Hematology (2013)

A 64-year-old male with a history of resected rectal cancer presented with a 1-week history of fever, chills, myalgias, generalized malaise, and 4-day history of a productive cough with yellow sputum and dyspnea. With the onset of his respiratory symptoms, he had an abrupt appearance of a skin rash on his hands and extremities. On examination, there were multiple violaceous pustular nodules on the dorsum of his hands (Image 1: Panel A) and extremities (Image 1: Panel B). Initial investigations revealed hemoglobin of 117 g/L, platelet count of 401 × 109/L, an elevated leukocyte count of 68 × 109/L with absolute neutrophil count of 60.2 × 109/L, and monocyte count of 5.4 × 109/L. Blood cultures were negative. A chest radiograph showed extensive bilateral patchy airspace opacities compatible with pneumonia (Image 1: Panel C). Skin biopsy revealed neutrophilic dermatosis. No viral inclusions were seen and the Gram stain and fungus stain (GMS) did not demonstrate any organisms. An erythrocyte sedimentation rate (ESR) was elevated at 92 mm/h. His pneumonia was treated and his leukocyte count decreased to 20 × 109/L with persistent skin lesions and monocytosis at discharge 11 days later. A subsequent bone marrow aspirate supported an underlying diagnosis of chronic myelomonocytic leukemia (CMML, Panel D) and normal male karyotype. Two months later, his skin lesions still persisted and only improved with a course of high-dose oral prednisone. The lesions resolved within a few days of starting prednisone and his CMML was managed supportively. Sweet's syndrome, also called acute febrile neutrophilic dermatosis, presents typically with an abrupt onset of rapidly growing erythematous, painful papules, nodules, or plaques over the head, neck, arms, and legs 1. Additionally, vesicles or bullae may appear on top of these lesions 1. Skin biopsy will show papillary and mid-dermal infiltration of neutrophils. This condition is associated with respiratory infections, malignancies, and certain medications. Acute myeloid leukemia has been commonly associated with this conditions but it has been reported with other myeloid malignancies such as myelodysplastic syndrome and CMML rarely 2. In this patient, Sweet's syndrome may be associated with his pneumonia but most likely was due to his underlying CMML as the association with respiratory infections occur mainly in children 3. This case highlights the importance of searching for an underlying cause such as a hematologic malignancy even in the presence of an active infection.
The national curriculum and medical education
Authors: M C Hime
Journal: BMJ (1989)

venous treatment with these agents is a potential cause of fatal pulmonary oedema.'A more rational management plan would be to expedite delivery of the fetus if maternal heart failure occurs during labour,Neven if the fetus is immature, as with developments in neonatal medicine the outcome for infants beyond 28 weeks' gestation is relatively good and beyond 32 weeks should be little worse than that for infants delivered near term, provided that the infant is delivered in good condition and facilities for neonatal intensive care are at hand.Failure of medical treatment is an indication for surgical intervention, the operative mortality being less than 5%.2Although fetal wastage, especially with open heart surgery including cardiopulmonary bypass, may be comparatively high, a substantial proportion of pregnancies will continue and have a successful outcome.
Galactan-binding antibodies. Diversity and structure of idiotypes.
Authors: S Rudikoff, M Pawlita, J Pumphrey, E Mushinski, M Potter
Journal: The Journal of Experimental Medicine (1983)

A group of eight IgM hybridoma proteins induced with beta(1,6)-D-galactan-containing antigens has been characterized in terms of primary amino acid sequence and idiotype expression. The H chain amino acid sequences reveal very strong homology in the VH segment although several substitutions are seen that suggest the occurrence of somatic mutation in these IgM molecules. Significant sequence variation was observed in CDR-3, the region generated by the D segment, and the two recombination events, VH-D and D-JH. The number of amino acids in this region contributed by the D segment was found to vary from two to six, yet the overall length of CDR-3 was precisely maintained by the addition of amino acids on either side of D during the recombination processes. These additional amino acids are suggested to result from nucleotide addition by repair enzymes. Idiotypic analysis of these proteins, in conjunction with an assessment of the H chain sequences, has permitted an identification of the molecular basis of both cross-reacting and unique idiotypic determinants expressed by these molecules.
Medical Mycology: The Pathogenic Fungi and the Pathogenic Actinomycetes
Authors: Donald G. Ahearn
Journal: JAMA (1988)

This edition retains the classic approach to medical mycology. The first four chapters and part of chapter 5 offer a review of the pathogenic actionomycetes. Chapter 6 provides a general review of the classification and morphology of microfungi with brief summary statements on fungi as animal pathogens and on the principles of antimycotic therapy. The extensive volume reviews, in separate chapters, the principle etiologic agents of cutaneous, subcutaneous, systemic, and opportunistic mycoses. There are comprehensive chapters on histoplasmosis, coccidioidomycosis, and blastomycoses. The major differences between this edition and the second edition, published in 1982, are the additions of chapters on phaeohyphomycosis and hyalohyphomyces. In the latter chapter brief sections are devoted also to pythiosis, algosis, and rare mycoses. Regretfully, the useful separate chapter on culture methods, media, stains, and procedures of the second edition has been omitted. The book is notable for its extensive lists of full references at the
Synoviocyte-packaged Chlamydia trachomatis induces a chronic aseptic arthritis.
Authors: R D Inman, B Chiu
Journal: Journal of Clinical Investigation (1998)

The basic mechanisms underlying reactive arthritis and specifically the joint injury that follows intra-articular Chlamydia trachomatis infection have not been defined. The present study addresses this question through the development of an experimental model. Stable cell lines were generated from synoviocytes harvested from the knee joints of Lewis rats. The synoviocytes were cocultivated with C. trachomatis to allow invasion by the microbe and were then transferred by intra-articular injection into the knee joints of Lewis rats. The ensuing arthritis could be subdivided into an early phase (</= 14 d) and a late phase. The early phase was characterized by intense, primarily neutrophilic, synovitis; accelerated cartilage injury; dissemination of Chlamydia to liver and spleen; and viable Chlamydia in the joints. The late phase was marked by mixed mononuclear lymphocyte infiltration in the joint; dysplastic cartilage injury and repair; absence of viable organisms; and development of a distinctive humoral response. Western blot analysis comparing reactive arthritis patients to the experimental model indicates that candidate arthritogenic chlamydial antigens are comparable between the two. This model demonstrates that an intense synovitis can be induced by this intracellular pathogen, and that chronic inflammation can persist well beyond the culture-positive phase. Furthermore, these data show that the synoviocyte is a suitable host cell for C. trachomatis and can function as a reservoir of microbial antigens sufficient to perpetuate joint injury.
Methyldopa and Positive Coombs' Test
Authors: Martin S. Belle
Journal: JAMA (1967)

<h3>To the Editor:—</h3> Since the report by Cahal<sup>1</sup>of nine cases of hemolytic anemia in patients treated with methyldopa, we have studied patients taking this hypotensive agent to determine the frequency of occurrence of positive Coombs' tests and hemolytic anemia. Carstairs et al<sup>2</sup>studied two patients with hemolytic anemia who had been taking methyldopa for 15 months. They also did a survey on patients attending their hypertensive clinic to determine the incidence of patients having a positive Coombs' test while on a regimen of antihypertensive therapy. They investigated 104 patients, 57 of whom were taking methyldopa (Aldomet), and 47 who were taking other hypotensive drugs. Of the 57 taking methyldopa, five had a positive Coombs' test, whereas none of the other 47 patients did. The difference between these two groups is statistically significant. However, none of the patients in this survey became anemic; all had been receiving methyldopa
Testosterone Increases Human Platelet Thromboxane A <sub>2</sub> Receptor Density and Aggregation Responses
Authors: Adesuyi A. L. Ajayi, Rajesh Mathur, Perry V. Halushka
Journal: Circulation (1995)

Background The incidence of thrombotic cardiovascular disease is greater in men than in premenopausal women. Testosterone has been implicated as a significant risk factor for cardiovascular disease and for acute myocardial infarctions and strokes in young male athletes who abuse anabolic steroids. Thromboxane A 2 (TXA 2 ) is a vasoconstrictor and platelet proaggregatory agent that has been implicated in the pathogenesis of cardiovascular disease. We therefore tested the hypothesis that testosterone regulates the expression of human platelet TXA 2 receptors. Methods and Results In a double-blind, placebo-controlled, randomized, parallel-group study, we determined the effects of testosterone cypionate 200 mg IM given twice, 2 weeks apart, or saline placebo in 16 healthy men. Platelet TXA 2 receptor density (B max ) and dissociation constant ( K d ) were measured by use of the TXA 2 mimetic 125 I-BOP. Platelet aggregation responses to I-BOP and to thrombin and plasma testosterone concentrations were measured before treatment (pretreatment phase), at 2 and 4 weeks (active phase), and again at 8 weeks (recovery phase). Treatment with testosterone was associated with an increase in the B max value from 0.95±0.13 to 2.10±0.4 pmol/mg protein (n=9), with a peak effect at 4 weeks ( P =.001), returning to baseline by 8 weeks. There was no significant change in B max values in the saline-treated group. The K d values were unchanged. Testosterone treatment was associated with a significant increase in the maximum platelet aggregation response to I-BOP ( P &lt;.001) at 4 weeks and returned to baseline at 8 weeks. The EC 50 values were not significantly changed. Platelet TXA 2 receptor density was positively correlated ( r =.56, P &lt;.001, n=32 measurements) with pretreatment (endogenous) plasma testosterone levels (range, 215 to 883 ng/dL) but not K d . Conclusions Testosterone regulates the expression of platelet TXA 2 receptors in humans. This may contribute to the thrombogenicity of androgenic steroids.
RELATIONSHIP BETWEEN PLATELET REACTIVITY AND CULPRIT AND NON–CULPRIT LESION MORPHOLOGY: THE ADAPT–DES IVUS SUBSTUDY
Authors: Kyeong Ho Yun, Gary Mintz, Bernhard Witzenbichler, Christopher Metzger, Michael Rinaldi, Ernest Mazzaferri, Peter Duffy, Giora Weisz, Thomas Stuckey, Bruce Brodie, Roxana Mehran, Gregg Stone, Akiko Maehara
Journal: Journal of the American College of Cardiology (2013)
Incontinentia pigmenti in male patients
Authors: Theresa R. Pacheco, Moise Levy, James C. Collyer, Nelida Pizzi de Parra, Cristobal A. Parra, Marisel Garay, Gabriela Aprea, Silvia Moreno, Anthony J. Mancini, Amy S. Paller
Journal: Journal of the American Academy of Dermatology (2006)
Prediction of Diabetic Foot Ulcer Occurrence Using Commonly Available Clinical Information
Authors: Edward J. Boyko, Jessie H. Ahroni, Karin M. Nelson
Journal: Diabetes Care (2006)

We appreciate the interest of Leese and Morris (1) in our article and enjoyed reading their publication (2), which was published 1 month before our own and hence was not cited by us (3). We wish to point out that their characterization of our population as having been “recruited from a hospital diabetes clinic” is not correct, as we clearly describe that our subjects were recruited from a general internal medicine clinic (3). With regard to the generalizability of our findings, they should be applicable to the ∼25 million U.S. …
TUBERCULOSIS AND SYPHILIS
Authors: EDWARD VON ADELUNG
Journal: JAMA (1918)

For the purpose of impressing the necessity of applying the Wassermann test to tuberculous patients, and thus avoiding a considerable percentage of common error, a tabulation of the cases seen in the Alameda County Tuberculosis Clinic during the past four years is here presented. The data were gathered in the course of regular examinations of patients in the Clinic of the Alameda County Society for the Study and Prevention of Tuberculosis—a society financed by annual appropriations from the treasuries of Alameda County and Oakland City, supplemented by contributions from private purses. In this work, I have been greatly assisted by Dr. Philip F. Abbott and Dr. V. O. Saphro. The Wassermann tests were made at the California State Hygienic Laboratory, Berkeley, Calif. In 1914, of thirty-four cases of tuberculosis confirmed by the finding of tubercle bacilli in the sputum, eight yielded positive Wassermann tests. This means that 23.5 per cent,
Abstract 2806: Inactivation of PBRM1, a gene frequently mutated in clear cell renal carcinoma, suppresses tumor growth
Authors: Huang Dachuan, Ong Choon Kiat, Teh Bin Tean, Bernice Wong Huimin, Waraporn Chan-on, Chutima Subimerb, Kyle Furge, Andrew Futreal
Journal: Cancer Research (2011)

Abstract The genetics of renal cancer is dominated by inactivation of the VHL tumour suppressor gene in clear cell renal carcinoma (ccRCC), the commonest histological subtype. However, our previous work has demonstrated that VHL loss alone is insufficient for ccRCC tumourigenesis arguing the need for additional genetic events. Recently, we have sequenced of the protein coding exome in 257 cases of primary renal carcinoma (RCC) and reported the identification of the SWI/SNF chromatin remodeling complex gene Polybromo 1 (PBRM1) as a second major RCC cancer gene with truncating mutations in 41% (85/257) of cases. In particular, all 9 cases with a SETD2 mutation have a mutation in either PBRM1 or VHL, with 7 of 9 cases having mutations in all three genes. The concomitant VHL, PBRM1 and SETD2 mutations, with all three genes mapping to chromosome 3p, suggest that the mutations are non-redundant functionally. To obtain further evidence that PBRM1 can act as a cancer gene, transcriptional profiling before and after PBRM1 knockdown was performed using gene expression microarrays. The results showed that PBRM1 activity regulates pathways associated with chromosomal instability and cellular proliferation. Consistently, knockdown of PBRM1 RNA resulted in a significant increase in proliferation 4/5 RCC lines. No effect was seen, however, in A704 cell, which carries a homozygous truncating PBRM1 mutation, confirming the specificity of the assay. Further, knockdown of PBRM1 resulted in significantly increased colony formation in soft-agar and increased cell migration indicative of an increase in transformed phenotype. Taken together, these data support PBRM1 having a tumor suppressor role in ccRCC. Therefore, understanding the contribution of PBRM1 mutation to clinical disease progression and outcome as well the potential for exploiting SWI/SNF complex abrogation therapeutically are important future areas of renal cancer research. 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 2806. doi:10.1158/1538-7445.AM2011-2806
A Phoenix of Peace Rises From the Ashes
Authors: Michael B. Heisler
Journal: JAMA (1989)

At 11:41 AM on December 7, 1988, an earthquake of massive proportions, measuring 6.9 on the Richter scale, struck northern Armenia. The shifting of tectonic plates created a cataclysmic force that erupted near the city of Spitak. The destructive energy was focused on a quiet, wind-swept valley that sits against the shoulder of the Caucasus Mountains. A deafening rumble rose from deep in the earth and the valley floor began to sway violently. The shock continued for 30 seconds. When it stopped, the cities of Spitak, Leninakan, Kirovakan, and Stepanavan and more than 150 villages lay demolished. Eight million square meters of dwelling space had been destroyed, including 35 000 homes. Schools serving 63 000 pupils, hospitals containing 5000 beds, and polyclinics providing services for 8900 patients per day were all destroyed (George Reid, Director, Red Cross Relief Operations, Yerevan, Soviet Armenia, oral communication, December 19, 1988).  We were three of
Managerial Structure of a Neighborhood-Based Health-Maintenance Organization.
Authors: Herbert A. Lints
Journal: Annals of Internal Medicine (1972)

Meeting Abstracts1 May 1972Managerial Structure of a Neighborhood-Based Health-Maintenance Organization.Herbert A. Lints, M.D., F.A.C.P.Herbert A. Lints, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-76-5-856_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe managerial structure of a neighborhood-based health-maintenance organization and its effectiveness in terms of modern industrial management theory are described. The analysis is pertinent because of the impending proliferation of health-maintenance organizations in terms of economics, patient benefit, and employee satisfaction. The health center analyzed was conceived in 1967 as a health-maintenance organization. Enrollment in this health plan began in July 1971. Coverage includes the following: full outpatient, hospital, extended and home care; X ray, laboratory, physical therapy, drugs, glasses, and blood services; and consultative, referral, and short-term inpatient care for emotional and drug abuse problems.The health center serves... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia, Pa. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1972Volume 76, Issue 5Page: 856-856KeywordsBloodDrug abuseDrug therapyEmotionsHealth economicsInpatientsOutpatient clinicsResearch laboratories Issue Published: 1 May 1972 PDF DownloadLoading ...
Assessment of Microvascular Leakage via Sputum Induction
Authors: Elizabeth L. J. Van Rensen, Pieter S. Hiemstra, Klaus F. Rabe, Peter J. Sterk
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Microvascular leakage is an important feature of inflammation. However, the assessment of vascular leakage has seldom been used to monitor airway inflammation in asthma. The aim of this study was to determine the effect of inhaled substance P, a potent neurokinin 1 (NK1) agonist and mediator of plasma extravasation, on markers of microvascular leakage in induced sputum from patients with asthma. In a crossover study, sputum was induced before and 30 minutes after inhalation of substance P or neurokinin A (as control) by 12 subjects with atopic and mild, steroid-naive asthma. The levels of α2-macroglobulin, ceruloplasmin, albumin, and fibrinogen were determined in induced sputum as markers of leakage. Substance P induced a significant increase in the levels of α2-macroglobulin, ceruloplasmin, and albumin in induced sputum (median fold change, 3.1, 2.2, and 2.9, respectively) (p < 0.013), whereas inhaled neurokinin A was not able to induce significant changes (p > 0.31). The increase in sputum leakage markers was not associated with the cumulative dose of substance P (p > 0.12). These results indicate that NK1 receptor stimulation causes a rapid increase in microvascular leakage as shown in induced sputum in patients with asthma. This investigational model of “dual induction” (first leakage, then sputum) may therefore be useful to test the antiexudative effect of newly develop drugs, such as NK1 antagonists.
Zinc in Human Immunodeficiency Virus Infection
Authors: James D. Shoemaker
Journal: JAMA (1988)

<h3>To the Editor.—</h3> In reference to the letters of Falutz et al<sup>1</sup>and Fabris et al,<sup>2</sup>we present the results of a pilot study aimed at revealing nutritional factors involved in the progression of human immunodeficiency virus seropositivity to acquired immunodeficiency syndrome. <h3>Study.—</h3> Mixed leukocyte concentrations of six minerals, major fatty acids, and cholesterol, serum and red blood cell zinc concentrations, and serum cholesterol levels were examined and seven-day dietary diaries were kept by the subjects. The ten human immunodeficiency virus—infected homosexual men and two uninfected homosexual men were classified according to their T4/T8 cell ratio and by the Walter Reed criteria.<sup>3</sup>Diet analysis revealed that all of the men had intakes of zinc greater than 18 mg/d, primarily from self-supplementation. The serum zinc concentration was 14.2 to 14.7 μmol/L in three subjects who had T4/T8 cell ratios of 0.08 to 0.30 and who were clinically well.
When Separate Is More Equal
Authors: Nancy E. Adler
Journal: JAMA (2010)

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Isolated Pneumocystis carinii Infection of Adrenal Glands Causing Addison's Disease in a Non-Immunocompromised Adult
Authors: Jyotsna Agarwal, Gaurav Agarwal, Archana Ayyagari, Dileep K Kar, Saroj K Mishra, Eesh Bhatia
Journal: Endocrine Pathology (2001)