tbuckley/cabot-search huggingface dataset:
Bariatric Surgery and the Changing Current Scope of General Surgery Practice
Authors: Rouzbeh Mostaedi, Mohamed R. Ali, Jonathan L. Pierce, Lynette A. Scherer, Joseph M. Galante
Journal: JAMA Surgery (2014)

The scope of general surgery practice has evolved tremendously in the last 20 years. However, clinical experience in general surgery residency training has undergone relatively little change.To evaluate the current scope of academic general surgery and its implications on surgical residency.The University HealthSystem Consortium and Association of American Medical Colleges established the Faculty Practice Solution Center (FPSC) to characterize physician productivity. The FPSC is a benchmarking tool for academic medical centers created from revenue data collected from more than 90,000 physicians who practice at 95 institutions across the United States.The FPSC database was queried to evaluate the annual mean procedure frequency per surgeon (PFS) in each calendar year from 2006 through 2011. The associated work relative value units (wRVUs) were also examined to measure physician effort and skill.During the 6-year period, 146 distinct Current Procedural Terminology codes were among the top 100 procedures, and 16 of these procedures ranked in the top 10 procedures in at least 1 year. The top 10 procedures accounted for more than half (range, 52.5%-57.2%) of the total 100 PFS evaluated for each year. Laparoscopic Roux-en-Y gastric bypass was consistently among the top 10 procedures in each year (PFS, 18.2-24.6). The other most frequently performed procedures included laparoscopic cholecystectomy (PFS, 30.3-43.5), upper gastrointestinal tract endoscopy (PFS, 26.5-34.3), mastectomy (PFS, 16.5-35.0), inguinal hernia repair (PFS, 15.5-22.1), and abdominal wall hernia repair (PFS, 21.6-26.1). In all years, laparoscopic Roux-en-Y gastric bypass generated the highest number of wRVUs (wRVUs, 491.0-618.2), and laparoscopic cholecystectomy was regularly the next highest (wRVUs, 335.8-498.7).A significant proportion of academic general surgery is composed of bariatric surgery, yet surgical training does not sufficiently emphasize the necessary exposure to technical expertise and clinical management of the patient undergoing bariatric surgery. As the scope of general surgery practice continues to evolve, general surgery residency training will need to better integrate the exposure to bariatric surgery.
One giant leap for NASA's public relations
Authors: J. Ciment
Journal: BMJ (1998)

Few NASA observers question that the return of former astronaut John Glenn to space has provided a much needed publicity infusion for the US space agency, which is known for its adeptness at using astronaut heroes and heroines to prise funds from an often reluctant Congress.

With over 250000 spectators–including President Clinton–last week's launch of the space shuttle Discovery was the most watched since the shuttles returned to service in September 1988, after the Challenger disaster.

But questions about the scientific and medical …
US drug industry's guidelines on advertising too limited, say critics
Authors: Bob Burton
Journal: BMJ (2005)

In the face of growing support for tighter regulations on advertising directly to consumers, the US drug industry's trade association has released voluntary guidelines of its own.

However, the guidelines fall short of a proposal by the leader of the Republican Senate majority, Bill Frist, for a two year waiting period before any new drug can be advertised directly to consumers. In July Dr …
Abstract 3300: Estrogen stimulates cell cycle progression dependent on Src kinase activity and IMP1 stabilization of myc mRNA in estrogen receptor-positive breast cancer cells
Authors: Christopher Abdullah, Hasan Korkaya, Sara A. Courtneidge
Journal: Cancer Research (2014)

Abstract Estrogen (E2) stimulation promotes proliferation in estrogen receptor-positive (ER+) breast cancer, which accounts for 60-75% of all breast cancer. E2 signals through the ER via three pathways: the classical genomic pathway involving transcriptional activation of the ER, crosstalk between ER and other transcription factors, and “non-genomic” signaling cascades, which do not involve the transcriptional activity of the ER. This “non-genomic” pathway likely involves Src family kinases (SFKs) and has been implicated in cell cycle progression in fibroblasts engineered to express the ER (Castoria 1999). While not typically amplified or mutationally activated in ER+ breast cancer, Src is hyperactive in most breast cancers. To test whether SFK activity is required for G1/S cell cycle progression in breast cancer cells, we pretreated quiescent ER+ MCF7 cells with a selective SFK inhibitor (SU11333) prior to stimulation with E2. Inhibition of SFK activity blocked progression from G1 to S phase. Previous data from our laboratory has demonstrated that G1/S progression in response to peptide growth factor stimulation of quiescent fibroblasts is dependent upon SFK-mediated stabilization of myc mRNA (Bromann 2005). We therefore tested whether SFK activity also regulates myc expression in breast cancer cells. Our data suggest that SFK activity is required for accumulation of myc mRNA in quiescent MCF7s after E2 stimulation, and that E2 stimulated stabilization of myc mRNA is dependent on SFK activity. One potential myc mRNA stabilizer is IMP1 (IGF2BP1, ZBP1, CRDBP) an RNA binding protein that is primarily expressed during development and in stem cells, and re-expressed in some cancer types, including breast cancer. IMP1 has previously been shown to stabilize myc mRNA in stem cells as well as osteosarcoma cells. While the signaling pathways that mediate this stabilization have not been well studied, previous work has identified a Src phosphorylation site on IMP1 which regulates IMP1 function (Sasaki 2010). We hypothesized that IMP1 may play a role in E2-mediated stabilization of myc mRNA. Indeed, MCF7 cells require IMP1 to accumulate myc mRNA after E2 stimulation. In summary, E2 stimulation activates SFKs, which then promote G1/S cell cycle progression in part by stabilizing myc mRNA levels, through the activity of IMP1. Bromann et al JBC, 2005 Castoria et al. EMBO J, 1999 Sasaki et al. J Neurosci, 2010 Citation Format: Christopher Abdullah, Hasan Korkaya, Sara A. Courtneidge. Estrogen stimulates cell cycle progression dependent on Src kinase activity and IMP1 stabilization of myc mRNA in estrogen receptor-positive breast cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3300. doi:10.1158/1538-7445.AM2014-3300
Talc Granuloma Identified by X-ray Microanalysis
Authors: John A. Terzakis, Sandra R. Shustak, Elyse G. Stock
Journal: JAMA (1978)

SOPHISTICATED analytical techniques now available may solve problems in the differential diagnosis of reactive and neoplastic diseases. An example is provided by the discovery of talc in an axillary granuloma of an unknown cause. A 34-year-old man had had a skin biopsy of an axillary lesion five years earlier. This was seen at another institution and diagnosed as compound nevus. Two months before his present biopsy, he had noticed several redbrown papules in the region of the first biopsy site. His concerns were that either the first diagnosis was in error and that he might have a recurrent malignant neoplasm, or that the papules were a result of using a popular deodorant. Results of an examination by the electron microscope showed these ideas to be incorrect. <h3>Materials and Methods</h3> The specimen was received in formalin and was said to be from the axilla. It consisted of a piece of firm,
RADIOLABELED METAIODOBENZYLGUANIDINE (MIBG) IN THE DIAGNOSIS OF PHEOCHROMOCYTOMA (PHEO)
Authors: A. N. Ansari, M. E. Siegel, V. DeQuattro, T. L. Ebenkamp
Journal: Clinical Nuclear Medicine (1984)

Most PHEOs are located in the adrenals (A), but up to 30% may be found in extraadrenal (EA) locations. We studied 21 patients suspected of PHEO with MIBG and correlation was made with transmission computerized tomography (TCT). MIBG scans were graded 0 to 4 as reported in the literature. Nineteen of 21 patients had TCT and all patients had plasma and/or urine catecholamines (CA). Nine of 21 patients had venous sampling and 7 had angiograms. Patients with positive (+) MIBG, TCT, or angiogram and high CA were operated upon. Eleven were normal by MIBG, TCT and our laboratory criteria. In the remaining 10 patients, MIBG localized 10 sites, 7 A and 3 EA, with only one false +. This was an A site with 3+ uptake. In 8 patients, TCT localized 9 sites, 7 A and 2 EA. Both MIBG and TCT had one false negative (-) at the same EA site. Two of 7 angiograms were false+. Results of MIBG and TCT are as follows: Scan True+ False+ False - A EA A EA EA MIBG 6 3 1 0 1 TCT 5 0 2 2 1 The false + MIBG had a normal adrenal at surgery. False + TCT images were found to be various unrelated pathologies. Two plus or > uptake was seen in all proven PHEOs. In summary, MIBG appears useful in the detection of PHEO especially EA in comparison to TCT. False + can occur with MIBG. Mild focal uptake (2+) is significant when CA level is diagnostic of PHEO.
Recognition of clonogenic leukemic cells, remission bone marrow and HLA-identical donor bone marrow by CD8+ or CD4+ minor histocompatibility antigen-specific cytotoxic T lymphocytes.
Authors: L M Faber, J van der Hoeven, E Goulmy, A L Hooftman-den Otter, S A van Luxemburg-Heijs, R Willemze, J H Falkenburg
Journal: Journal of Clinical Investigation (1995)

We investigated whether minor histocompatibility (mH) antigen-specific cytotoxic T lymphocytes (CTL) can discriminate between leukemic hematopoietic progenitor cells (leukemic-HPC) from AML or CML patients, the HPC from their remission bone marrow (remission-HPC), and normal HPC from their HLA-identical sibling bone marrow donor (donor-HPC). Specific lysis by CD8+ CTL clones was observed not only of the leukemic-HPC but also of the donor-HPC in 3/4 patient/donor combinations expressing mH antigen HA-1, 3/5 combinations expressing mH antigen HA-2, 2/3 combinations expressing mH antigen HA-3, and 2/2 combinations expressing mH antigen HY-A1. In four patient/donor combinations the recognition of the donor-HPC was clearly less than of the leukemic-HPC, indicating differential susceptibility to lysis by these mH CTL clones. In addition, differential recognition of leukemic-HPC and remission-HPC within seven patients was analyzed. In one patient expressing the HA-2 antigen on the leukemic cells the recognition of the remission-HPC was clearly less than of the leukemic-HPC. One CD4+ CTL clone showed specific lysis of the leukemic-HPC from an AML patient and a CML patient as well as of normal remission-HPC and donor-HPC. These results illustrate that in general CD8+ and CD4+ mH antigen specific CTL clones do not differentially recognize leukemic-HPC and normal-HPC. However, differences in susceptibility to lysis of malignant versus normal cells may contribute to a differential GVL effect.
ULERYTHEMA SYCOSIFORME (LUPOID SYCOSIS) WITH REPORT OF TWO CASES.
Authors: J. ABBOTT CANTRELL
Journal: JAMA (1898)

The following report is deemed worthy of presentation on occount of the rarity of the disease and the obscurity that has until recently surrounded it. About 1865 the disease was described by Milton under the name "lupoid sycosis." This author says "I have seen in some rare cases (of sycosis) a slow superficial form of ulceration beginning with minute tubercles and attacking the hair follicles causing falling of the hair and slight though indelible cicatrices, a disorder which seems to me to be nothing more than lupus non-exedens." Unna, in 1889, described a disease which he terms<i>ulerythema sykosiforme</i>and reports a case in considerable detail. By ulerythema the latter writer means a pathologic process which goes on to the formation of atrophic scars without intermediate suppuration or ulceration; in other words, through the resorption of the cellular infiltrate. We append a full record of the case reported by Unna
Child and Adolescent Psychiatry: A Comprehensive Textbook
Authors: Helen R. Beiser
Journal: JAMA (1996)

This is a massive book by 171 contributors in 127 chapters. Rather than a textbook, it is more of a reference library of the field. As in other such books with multiple contributors, it does not have a unifying perspective, and there are many overlaps and repetitions. Certainly, any information in the field could be found, if not in a chapter itself, in the long list of references following each chapter. The first section is on normal development, including eight chapters on biological development. Although there is heavy emphasis on the biological, psychological theories are not neglected. There are expected sections on clinical syndromes, etiology, treatment, and the relationship of child psychiatry to education, pediatrics, the law, and public health. The last section is a grab bag of chapters on training, research, ethics, and history. In a book of this sort, besides repetitions, there are bound to be contradictions. It
Pathology of Tumours of the Nervous System
Authors: Kyung-Whan Min
Journal: JAMA (1990)

This is a much-awaited new edition of<i>Pathology of Tumours of the Nervous System</i>. The last, published in 1977, served as an authoritative reference for those dealing with the title subject. The new edition has increased its volume by 564 pages, better than twice the length of the previous edition, to provide the coverage of ever-expanding knowledge. Two new chapters have been added, one presenting an extensive and authoritative compilation of information on experimental tumors and the other on the dysgenetic syndromes associated with tumors and hamartomas of the nervous system; the latter represents a systematic reorganization of information spread in bits through many different chapters in the previous edition. The "Introduction" in the previous edition has been changed to "Incidence, Pathogenesis and Other General Aspects" and contains extensive and up-to-date material on the role of oncogenes, cytogenetics, immunocytochemistry, and modern molecular biologic techniques in the understanding of the pathogenesis
Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle. Implications for catheter ablation.
Authors: S Nath, C Lynch, J G Whayne, D E Haines
Journal: Circulation (1993)

The primary mechanism of tissue injury by radiofrequency catheter ablation is presumed to be thermally mediated. However, the myocardial cellular electrophysiological effects of hyperthermia are not well characterized. We used an in vitro model of isolated guinea pig right ventricular papillary muscle to investigate the acute cellular electrophysiological effects of hyperthermia.Excised guinea pig right ventricular papillary muscles were pinned in a high-flow tissue bath and superfused with Tyrode's solution at 37.0 +/- 0.5 degrees C. The superfusate temperature was rapidly changed to 38.0 to 56.0 degrees C for 60 seconds and then returned to 37.0 degrees C. Conventional microelectrodes were used to measure membrane potential (Vm), maximum rate of rise of the action potential (dV/dtmax), and action potential (AP) amplitude and AP duration at 50% (APD50) and 90% (APD90) repolarization. Hyperthermia resulted in (1) a progressive depolarization of Vm at temperatures > or = 40.0 degrees C, which became more prominent at temperatures > or = 45.0 degrees C; (2) changes in the AP characterized by a temperature-dependent increase in dV/dtmax and a temperature-dependent decrease in AP amplitude, APD50, and APD90; (3) reversible loss of cellular excitability within a temperature range of 42.7 to 51.3 degrees C (median, 48.0 degrees C); (4) irreversible loss of cellular excitability and tissue injury at temperatures > or = 50.0 degrees C; and (5) the development of abnormal automaticity at temperatures > 45.0 degrees C.Hyperthermia causes significant changes in myocardial cellular electrophysiological properties that include membrane depolarization, reversible and irreversible loss of excitability, and abnormal automaticity. There appear to be specific temperature ranges for reversible and irreversible electrophysiological changes. These observations may have important implications for tissue temperature monitoring during radiofrequency catheter ablation.
Decreasing the Risk of Diabetic Retinopathy in a Study of Case Management
Authors: David J. Pettitt, Alison Okada Wollitzer, Lois Jovanovic, Guozhong He, Eli Ipp
Journal: Diabetes Care (2005)

OBJECTIVE—Diabetic retinopathy affects &amp;gt;60% of people with type 2 diabetes during the first 2 decades of the disease and is ameliorated by good glycemic control. This study tested whether intensive diabetes case management could prevent or delay diabetic retinopathy in patients with established type 2 diabetes. RESEARCH DESIGN AND METHODS—This study was part of a randomized, controlled clinical trial of diabetes case management in type 2 diabetes in southern California counties serving low income ethnic minority populations. Subjects were randomized to intervention (diabetes case management) or control (traditional treatment) groups. Subjects with at least two retinal photographs (n = 149) were included in this analysis to assess the effect of intervention on development or progression of diabetic retinopathy. RESULTS—Progression of retinopathy in the intervention group was not significantly less than in the control group (P = 0.226). However, those in the intervention group with no evidence of retinopathy at baseline were less likely to develop diabetic retinal changes (5/48) during a mean follow-up of 23.1 months than those in the control group (10/34, χ2 = 4.805, P = 0.028). This difference remained significant in a logistic regression model that controlled for potential confounders (odds ratio 5.35 [95% CI 1.14–25.12]). CONCLUSIONS—This study shows that a relatively short duration of case management instituted before the onset of clinically identifiable retinopathy significantly diminished the risk of developing retinopathy in patients with type 2 diabetes. The findings also emphasized the retinal disease burden in this population, with development and progression of retinopathy occurring in &amp;lt;2 years.
Interatrial septum pacing guided bythree-dimensional intracardiac echocardiography
Authors: Tamas Szili-Torok, Geert-Jan P Kimman, Marcoen F Scholten, Jurgen Ligthart, Nico Bruining, Dominic A.M.J Theuns, Peter J Klootwijk, Jos R.T.C Roelandt, Luc J Jordaens
Journal: Journal of the American College of Cardiology (2002)
Requirement of Analgesia for Extracorporeal Shock Wave Lithotripsy and Efficacy of a Nonsteroidal Antiinflammatory Drug: Piroxicam
Authors: Zafer Aybek, Tahir Turan, Tarik Yongu&ccedil;, Cihad Bozbay, &Ouml;zcan Atahan, O. Levent Tuncay
Journal: European Urology (1998)
THE METABOLISM OF CREATINE-1-C14 BY MICE WITH HEREDITARY MUSCULAR DYSTROPHY*
Authors: Coy D. Fitch, James D. Oates, James S. Dinning
Journal: Journal of Clinical Investigation (1961)

Creatinuria, diminished urinary creatinine ex- cretion and low concentrations of creatine in skele- tal muscle are characteristic findings in progressive muscular dystrophy in man (1).These abnormalities of creatine metabolism are sometimes thought to be nonspecific changes secondary to a smaller muscle mass (2), but this has not been proven; and, because of the probable importance of phosphocreatine to energy metabolism in skele- tal muscle (3), it is possible that an abnormality of creatine metabolism would contribute to the weakness if not to the actual damage of muscle fibers in muscular dystrophy.It is therefore im- portant to establish the nature of the defect in creatine metabolism in muscular dystrophy.Since the hereditary myopathy of mice de- scribed by Michelson, Russell and Harman (4) resembles progressive muscular dystrophy, an in- vestigation of creatine metabolism in these mice was undertaken.It was found that the muscle creatine of the dystrophic mouse has a shortened turnover time1 which suggests that the low con- centration of creatine in the skeletal muscle in this condition is due to an impaired ability to retain creatine. METHODSStrain 129 dystrophic mice and their normal litter mates, approximately 8 weeks of age and of both sexes, were obtained from the Roscoe B. Jackson Memorial Laboratory.
The Mitral Apparatus
Authors: JOSEPH K. PERLOFF, WILLIAM C. ROBERTS
Journal: Circulation (1972)

This review deals with the functional anatomy of the six components of the mitral apparatus, namely, the left atrial wall, annulus, leaflets, chordae tendineae, papillary muscles, and left ventricular wall. Each component is considered individually, in the context of the apparatus as a whole, in relation to the mode of closure of the normal mitral valve, and in the light of many acquired and congenital disorders that disturb the harmony of the finely coordinated mitral mechanism and render it incompetent. The left atrium is related to mitral valve competence in terms of contraction and relaxation and in terms of dilatation of its posterior wall. The annulus not only serves as a fulcrum for the leaflets but exhibits sphincteric contraction in systole that decreases the size of the orifice. The two leaflets differ in shape but are nearly identical in area, and together are about two and one half times the area of the orifice that they are required to close. Leaflet abnormalities causing acquired or congenital mitral regurgitation result from deficient leaflet tissue, excessive leaflet tissue, or restricted leaflet mobility. Chordae tendineae are considered according to their leaflet attachments, ventricular attachments, thicknesses, lengths, and arborization patterns. Mitral regurgitation due to chordal abnormalities results from chordae that are abnormally long, abnormally short, ectopically inserted, or ruptured. In this context, systolic clicks and late systolic murmurs are discussed, and severe acute mitral regurgitation is contrasted with severe chronic mitral regurgitation. The papillary muscles and the left ventricular wall represent the two muscular components of the mitral apparatus. An appraisal of papillary muscle dysfunction includes dysfunction with loss in continuity (rupture) and dysfunction without loss in continuity (fibrosis, ischemia, replacement). Finally, the role of altered left ventricular shape is discussed in the context of mitral regurgitation, and the effect of dilatation is ascribed chiefly to alterations in the position of papillary muscles and their directional axes of tension.
Inorganic Phosphate Treatment of Hypercalcemia of Diverse Etiologies
Authors: Ralph S. Goldsmith, Sidney H. Ingbar
Journal: New England Journal of Medicine (1966)

HYPERCALCEMIA occurs in a wide variety of diseases (for example, hyperparathyroidism, hypervitaminosis D, sarcoid, cancer, hyperthyroidism and poliomyelitis)1 and is often responsible for many of the symptoms associated with them. Most often, these symptoms are more distressing than disabling and include such nonspecific complaints as constipation, dyspepsia, lassitude, easy fatigability and polyuria. Underlying these mild symptoms, however, is a process that may lead to nephrolithiasis and nephrocalcinosis. Of even more serious import2 is the usually fatal syndrome that has been called hypercalcemic crisis — intractable nausea and vomiting, dehydration, stupor, coma and azotemia. Since this constitutes a true medical emergency . . .