tbuckley/cabot-search huggingface dataset:
An Outbreak of Mycobacterial Furunculosis Associated with Footbaths at a Nail Salon
Authors: Kevin L. Winthrop, Marcy Abrams, Mitchell Yakrus, Ira Schwartz, Janet Ely, Duncan Gillies, Duc J. Vugia
Journal: New England Journal of Medicine (2002)

In September 2000, a physician in northern California described four patients with persistent, culture-negative boils on the lower extremities. The patients had received pedicures at the same nail salon. We identified and investigated an outbreak of Mycobacterium fortuitum furunculosis among customers of this nail salon.Patients were defined as salon customers with persistent skin infections below the knee. A case-control study was conducted that included the first 48 patients identified, and 56 unaffected friends and family members who had had a pedicure at the same salon served as controls. Selected M. fortuitum isolates, cultured from patients and the salon environment, were compared by pulsed-field gel electrophoresis.We identified 110 customers of the nail salon who had furunculosis. Cultures from 34 were positive for rapidly growing mycobacteria (32 M. fortuitum and 2 unidentified). Most of the affected patients had more than 1 boil (median, 2; range, 1 to 37). All patients and controls had had whirlpool footbaths. Shaving the legs with a razor before pedicure was a risk factor for infection (70 percent of patients vs. 31 percent of controls; adjusted odds ratio, 4.8; 95 percent confidence interval, 2.1 to 11.1). Cultures from all 10 footbaths at the salon yielded M. fortuitum. The M. fortuitum isolates from three footbaths and 14 patients were indistinguishable by electrophoresis.We identified a large outbreak of rapidly growing mycobacterial infections among persons who had had footbaths and pedicures at one nail salon. Physicians should suspect this cause in patients with persistent furunculosis after exposure to whirlpool footbaths.
Occupancy of platelet receptors for platelet-activating factor in patients with septicemia.
Authors: F Lopez Diez, M L Nieto, S Fernandez-Gallardo, M A Gijon, M Sanchez Crespo
Journal: Journal of Clinical Investigation (1989)

The possible involvement of platelet-activating factor (PAF) in the pathogenesis of endotoxemia, was investigated by using a binding assay to patients' platelets, complemented with the extraction and chemical characterization of PAF obtained from patients' platelets. Platelets from 12 human volunteers had 281 +/- 63 freely accessible high affinity binding sites (PAF-receptors) per platelet; whereas this number was of 49 +/- 37 PAF-receptors per platelet, n = 14 samples, P less than 0.01, in a group of 13 patients with positive blood culture. A group of patients with respiratory or cardiovascular disturbances and negative blood culture had 253 +/- 74, accessible receptors per platelet (n = 19 samples from 16 patients, P less than 0.01 as compared to septic patients, which was not significantly different when compared to control individuals). Patients with sepsis possessed significant amounts of PAF associated to their platelets, whereas this mediator could not be isolated from platelets of patients with respiratory or cardiovascular disturbances and negative blood culture, nor from platelets of control individuals. PAF was also assayed in whole blood samples and found at high concentrations in sepsis patients. These data indicate that occupancy of PAF receptors in combination with high amounts of platelet-associated PAF, is a common finding in patients with sepsis.
Adrenal Suppression with Dry Powder Formulations of Fluticasone Propionate and Mometasone Furoate
Authors: Tom C. Fardon, Daniel K. C. Lee, Kay Haggart, Lesley C. McFarlane, Brian J. Lipworth
Journal: American Journal of Respiratory and Critical Care Medicine (2004)

Mometasone furoate (MF) and fluticasone propionate (FP) are high potency inhaled corticosteroids. The systemic bioavailability of MF is claimed to be negligible, leading to a minimal potential for systemic adverse effects. We assessed the overnight urinary cortisol/creatinine as the primary outcome of adrenal suppression in 21 patients with persistent asthma (mean FEV1 = 91%). Patients were randomized in a crossover fashion to receive 2 weekly consecutive doubling incremental doses of either FP Accuhaler (500, 1,000, and 2,000 μg/day) or MF Twisthaler (400, 800, and 1,600 μg/day). For the 21 per protocol completed patients, there was significant suppression of overnight urinary cortisol/creatinine with high and medium doses of both drugs—as geometric mean fold suppression (95% confidence interval) from baseline: FP 2,000 μg, 1.85 (1.21–2.82, p = 0.002); FP 1,000 μg, 1.45 (1.07–1.96, p = 0.02); MF 1,600 μg, 1.92 (1.26–2.93, p = 0.001); and MF 800 μg, 1.39 (1.04–1.88, p = 0.02). For secondary outcomes of 8:00 A.M. plasma cortisol, serum osteocalcin, and early morning urinary cortisol/creatinine, there was significant suppression with MF and FP at the highest dose. Our data refute the assertion that MF has negligible systemic bioavailability and a lower potential for systemic adverse effects compared with FP.
American Medical Malpractice Litigation in Historical Perspective
Authors: James C. Mohr
Journal: JAMA (2000)

Medical malpractice and the problems associated with it remain an important issue in the US medical community. Yet relatively little information regarding the long-term history of malpractice litigation can be found in the literature. This article addresses 2 questions: (1) when and why did medical malpractice litigation originate in the United States and (2) what historical factors best explain its subsequent perpetuation and growth?Medical malpractice litigation appeared in the United States around 1840 for reasons specific to that period. Those reasons are discussed in the context of marketplace professionalism, an environment that provided few quality controls over medical practitioners. Medical malpractice litigation has since been sustained for a century and a half by an interacting combination of 6 principal factors. Three of these factors are medical: the innovative pressures on American medicine, the spread of uniform standards, and the advent of medical malpractice liability insurance. Three are legal factors: contingent fees, citizen juries, and the nature of tort pleading in the United States. Knowledge of these historical factors may prove useful to those seeking to reform the current medical malpractice litigation system.
Structure of an Alanine Transfer Ribonucleic Acid
Authors: Robert W. Holley
Journal: JAMA (1965)

The structures of nucleic acids are especially interesting and important because they provide specificity and enable nucleic acids to carry out many vital functions. Recently, work in our laboratories has led to the first determination of the chemical structure of a nucleic acid.<sup>1-4</sup>A brief summary of the work is given in this paper. The structure that was determined was that of an alanine transfer ribonucleic acid (RNA). Transfer RNAs function as specific carriers of activated amino acids, and during protein synthesis they interact with other cellular components (ribosomes and messenger RNA) to determine the structure of the protein that is being synthesized. (For a review of protein synthesis, see Moldave.<sup>5</sup>) In comparison with other nucleic acids, transfer RNAs are relatively small molecules. It seemed possible, therefore, some seven years ago, when our work was undertaken, that transfer RNAs might be amenable to detailed structural analysis. <h3>Isolation of</h3>
Association of estrogen receptor gene alpha polymorphisms with postmenopausal mammary density.
Authors: EH Ramos, G Facina, ID Silva, AM Costa, AC Nazario, C Kemp
Journal: Cancer Research (2009)

Abstract Abstract #5003 Background: With the human genome studies, knowledge about polymorphisms started raising interest in a variety of fields and, in medicine, the evidence of direct action of polymorphisms on the arising and progression of diseases, disclosing the possibility of using them as disease predisposition markers. Substitutions, insertions or deletions which are transmitted through generations and reach frequencies equal or superior to 1% in the population are named polymorphisms. Knowing that the mammographic pattern is a multifactorial character, the objectives of this study were to evaluate a possible association of clinical characteristics and polymorphisms HaeIII, MspI and XbaI of the estrogen receptor gene alpha with postmenopausal mammary density. Materials and Methods: A prospective evaluation was made of 120 women who were not hormone therapy users and had no clinically or mammographically identified breast lesions. All of them underwent bilateral mammography, and the radiological density was determined by three independent observers, with two subjective evaluations based on the ACR-BIRADS® classification of mammographic patterns, 2003, and one computerized evaluation – the grey-scale histogram tool of the Adobe Photoshop® 7.0 software. Peripheral blood samples were obtained for DNA extraction, performed according to the GFX® Kit protocol from Amersham-Pharmacia. After DNA extraction, PCR-RFLP (Polymerase Chain Reaction - Restriction Fragment Length Polymorphism) was carried out for an analysis of the polymorphisms present in intron 1 (HaeIII and XbaI) and in exon 1 (MspI) of the estrogen receptor gene. Results: There was a high degree of concordance among the observers in the determination of mammary density (Kappa, Pearson and Spearman - p&amp;lt;0.001). The associations of clinical characteristics with mammary density were: age (p=0.04), body mass index (p&amp;lt;0.0001), age at menarche (p=0.02), age at menopause (p=0.120), age at first delivery (p=0.120), parity (p=0.09). The relation between the allele distribution of the polymorphisms and the density was: XbaI (p=0.02), HaeIII (p=0.65), and MspI (p=0.65). Conclusion: Polymorphism XbaI and the clinical factors age, menarche and body mass index showed to be associated with postmenopausal mammary density. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 5003.
Psychotherapeutic Approach to the Management of the Severely Injured Patient
Authors: J.C.C. Badenhorst
Journal: Psychotherapy and Psychosomatics (1990)

In this modern day and age, severe injury has become the dire consequence of an ever-increasing number of motor vehicle, industrial and mining accidents as well as sport-, military- and terror-related incidents that occur. The management of the severely injured patient is mostly directed on an exclusively physical level. Often, very little attention is afforded to the psychosocial factors that prevail following physical trauma. The author describes and discusses how holistic multidisciplinary intervention within the medical milieu facilitates a more psychotherapeutic approach to the management of severely injured patients. This approach facilitates physical recovery and increases the rate of readjustment and reintegration into society, of those who have sustained severe injury.
Emotional Impairment in Internal Medicine House Staff
Authors: Gary Anderson
Journal: JAMA (1986)

<h3>To the Editor.—</h3> I found the article "Emotional Impairment in Internal Medicine House Staff"1 both interesting and disturbing. It has been nine months since my residency in family practice, which included five months of first-year medicine. I would like to make some observations based on my own experiences. I was very disturbed that only one third of the directors thought that the work load or working conditions might be a factor in emotional impairment. My feelings are that it is one of the major causes of impairment or "resident burnout." I performed my residency in an urban private medical center of about 500 beds. A typical on-call schedule is being on call every third day. The day started at 7 AM and would be over by 6 PM, if it was a quiet day and the resident was efficient. We were required to come in every Saturday for about four
Cytokines Production, Expression of CD40/CD40L and Correlation with Immunoglobulins in Patients with Ataxia-Telangiectasia
Authors: Camila T.M. Pereira, Beatriz T.C. Carvalho, Nadijane V.S. Ferreira, Milena K.C. Brunialti, Reinaldo Salomao, Danielle Bichueti Silva
Journal: Journal of Allergy and Clinical Immunology (2015)
Transferable Vancomycin Resistance in a Community-Associated MRSA Lineage
Authors: Flávia Rossi, Lorena Diaz, Aye Wollam, Diana Panesso, Yanjiao Zhou, Sandra Rincon, Apurva Narechania, Galen Xing, Thais S R Di Gioia, André Doi, Truc T Tran, Jinnethe Reyes, Jose M Munita, Lina P Carvajal, Alejandra Hernandez-Roldan, Denise Brandão, Inneke Marie van der Heijden, Barbara E Murray, Paul J Planet, George M Weinstock, Cesar A Arias
Journal: New England Journal of Medicine (2014)

We report the case of a patient from Brazil with a bloodstream infection caused by a strain of methicillin-resistant Staphylococcus aureus (MRSA) that was susceptible to vancomycin (designated BR-VSSA) but that acquired the vanA gene cluster during antibiotic therapy and became resistant to vancomycin (designated BR-VRSA). Both strains belong to the sequence type (ST) 8 community-associated genetic lineage that carries the staphylococcal chromosomal cassette mec (SCCmec) type IVa and the S. aureus protein A gene (spa) type t292 and are phylogenetically related to MRSA lineage USA300. A conjugative plasmid of 55,706 bp (pBRZ01) carrying the vanA cluster was identified and readily transferred to other staphylococci. The pBRZ01 plasmid harbors DNA sequences that are typical of the plasmid-associated replication genes rep24 or rep21 described in community-associated MRSA strains from Australia (pWBG745). The presence and dissemination of community-associated MRSA containing vanA could become a serious public health concern.
AlaSOPro mutation in the gene encoding α-synuclein in Parkinson's disease
Authors: Rejko Krüger, Wilfried Kuhn, Thomas Müller, Dirk Woitalla, Manuel Graeber, Sigfried Kösel, Horst Przuntek, Jörg T. Epplen, Ludger Schols, Olaf Riess
Journal: Nature Genetics (1998)
Association of myeloperoxidase promotor polymorphism with cirrhosis in patients with hereditary hemochromatosis
Authors: Christoph H. Österreicher, Christian Datz, Felix Stickel, Claus Hellerbrand, Melitta Penz, Harald Hofer, Fritz Wrba, Edward Penner, Detlef Schuppan, Peter Ferenci
Journal: Journal of Hepatology (2005)
A novel laboratory technique demonstrating the influences of <i>RHD</i> zygosity and the RhCcEe phenotype on erythrocyte D antigen expression
Authors: Patrick T. McGann, Jenny M. Despotovic, Thad A. Howard, Russell E. Ware
Journal: American Journal of Hematology (2011)

D antigen is the most immunogenic and clinically relevant antigen within the complex Rh blood group system. Variability of D antigen expression was first described decades ago but has rarely been investigated quantitatively, particularly in the context of RHD zygosity along with RhCcEe serological phenotype. With IRB approval, 107 deidentified blood samples were analyzed. Rh phenotypes were determined serologically by saline technique using monoclonal antibodies against D, C, c, E, and e antigens. RHD zygosity was determined using both PCR-restriction fragment length polymorphisms and quantitative real-time PCR techniques. A novel and robust method was developed for quantitation of erythrocyte D antigen sites using calibrated microspheres and flow cytometry, allowing correlation of D antigen density with RHD zygosity and expression of Rh CcEe antigens. Subjects homozygous for RHD expressed nearly twice the number of D antigen sites compared with RHD hemizygotes (33,560 ± 8,222 for DD versus 17,720 ± 4,471 for Dd, P < 0.0001). Expression of c or E antigens was associated with significantly increased erythrocyte D antigen expression, whereas presence of C or e antigens reduced expression. These data and this novel quantitation method will be important for future studies investigating the clinical relevance of D antigen variability.
THE INDUCED DEVELOPMENT AND HISTOGENESIS OF PLASMA CELLS
Authors: Franklin R. Miller
Journal: The Journal of Experimental Medicine (1931)

As result of finding numerous plasma cells in the omenta of rabbits injected with tuberculo-protein, a method to induce the production of large numbers of these cells has been discovered. The tissues in which they were pronouncedly increased were the subserosal connective tissues of the omentum, body wall, and intestinal wall. The precursor of the plasma cells is a primitive connective tissue cell. As this cell develops into the typical Marshalkó plasma cell there is a progressive increase in the basophilia of the cytoplasm, the nucleus becomes eccentric, a condensation of the chromatin occurs near the nuclear membrane, and there is a loss of the nucleoli. At the time when the nucleus assumes the eccentric position, the clear area appears in the center of the cytoplasm. The early cells are capable of reproducing themselves by mitosis, while the typical mature cells divide by amitosis. The mature plasma cells often have muddy, spongy cytoplasm which contains acidophilic or hyaline granules as the cells grow old or begin to degenerate. The cells with granules or hyaline bodies usually have pycnotic or fragmented nuclei. These cells are the final stage reached by some plasma cells. Others, when degenerating, show vacuoles and signs of senility. Those with the granules and hyaline bodies are the so called Russell body cells. Plasma cells developed in greatest numbers after our largest injections of tuberculo-protein. The differentiation into young, mature, and senile forms was most clearly recognizable when some days had been allowed to elapse after the last large injection of the stimulating agent. A description of the plasma cell as viewed supravitally has been given. The cells are met in the blood stream as well as in the tissues. They are characterized by their deep yellowish gray cytoplasm, indistinct eccentrically placed nuclei, and large numbers of mitochondria. The plasma cells differ from lymphocytes, in that they did not develop in large numbers after direct stimulation of the lymph nodes with tuberculo-protein. The young plasma cells also differ in morphology from the young lymphocytes. When plasma cells were found in the lymph nodes they were in the connective tissue cords. The plasma cell is a definite entity, having a maturation cycle. It is stimulated to great proliferation by certain toxic irritants.
Primary extramedullary leukemia of the prostate: Case report and review of the literature
Authors: Emmanuel T. Quien, Bruce Wallach, Linda Sandhaus, Pamela Kidd, Roger Strair, Parvin Saidi
Journal: American Journal of Hematology (1996)

We present the case of a 67-year-old male with primary extramedullary leukemia of the prostate gland, the first reported case in the literature to the best of our knowledge. His initial symptoms consisted of episodes of urinary retention. He underwent transurethral resection of the prostate, and a diagnosis of high-grade lymphoma was rendered. He then received a course of doxorubicin-based lymphoma chemotherapy regimen. However, based on a panel of immunocytochemical stains, a diagnosis of extramedullary leukemia or chloroma was confirmed. His bone-marrow examination at this point was normal. He underwent radiation therapy to the prostate with a total dose of 3960 cGy. Seven months after his initial presentation, he progressed to acute nonlymphocytic leukemia (ANLL), M2 by FAB classification. He was successfully treated with induction and consolidation chemotherapy with Ara-C and idarubicin, and was maintained in complete remission up to 19 months of follow-up. Eight other cases of prostatic leukemia reported in the literature are presented. Five cases occurred in association with ANLL, 2 cases as sites of ANLL relapse, and 1 case in association with myelodysplasia. The use of immunohistochemical stains has aided us in diagnosis of extramedullary leukemia. Surgery, radiation therapy, and chemotherapy play complementary roles in the treatment of prostatic extramedullary leukemia. © 1996 Wiley-Liss, Inc.
313 DYNAMIC FLUCTUATION OF VIROLOGICAL MARKERS DURING THE NATURAL COURSE OF HEPATITIS DELTA
Authors: B. Calle Serrano, B. Heidrich, J. Jaroszewicz, B. Bremer, K. Deterding, I. Mederacke, R. Raupach, M. Cornberg, M.P. Manns, H. Wedemeyer
Journal: Journal of Hepatology (2010)
Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic β cells recapitulates neonatal diabetes
Authors: Christophe A. Girard, F. Thomas Wunderlich, Kenju Shimomura, Stephan Collins, Stephan Kaizik, Peter Proks, Fernando Abdulkader, Anne Clark, Vicky Ball, Lejla Zubcevic, Liz Bentley, Rebecca Clark, Chris Church, Alison Hugill, Juris Galvanovskis, Roger Cox, Patrik Rorsman, Jens C. Brüning, Frances M. Ashcroft
Journal: Journal of Clinical Investigation (2008)

Neonatal diabetes is a rare monogenic form of diabetes that usually presents within the first six months of life. It is commonly caused by gain-of-function mutations in the genes encoding the Kir6.2 and SUR1 subunits of the plasmalemmal ATP-sensitive K+ (KATP) channel. To better understand this disease, we generated a mouse expressing a Kir6.2 mutation (V59M) that causes neonatal diabetes in humans and we used Cre-lox technology to express the mutation specifically in pancreatic beta cells. These beta-V59M mice developed severe diabetes soon after birth, and by 5 weeks of age, blood glucose levels were markedly increased and insulin was undetectable. Islets isolated from beta-V59M mice secreted substantially less insulin and showed a smaller increase in intracellular calcium in response to glucose. This was due to a reduced sensitivity of KATP channels in pancreatic beta cells to inhibition by ATP or glucose. In contrast, the sulfonylurea tolbutamide, a specific blocker of KATP channels, closed KATP channels, elevated intracellular calcium levels, and stimulated insulin release in beta-V59M beta cells, indicating that events downstream of KATP channel closure remained intact. Expression of the V59M Kir6.2 mutation in pancreatic beta cells alone is thus sufficient to recapitulate the neonatal diabetes observed in humans. beta-V59M islets also displayed a reduced percentage of beta cells, abnormal morphology, lower insulin content, and decreased expression of Kir6.2, SUR1, and insulin mRNA. All these changes are expected to contribute to the diabetes of beta-V59M mice. Their cause requires further investigation.