tbuckley/cabot-search huggingface dataset:
VARIATION IN THE ONCOGENIC POTENTIAL OF HUMAN ADENOVIRUSES CARRYING A DEFECTIVE SV40 GENOME (PARA)
Authors: Fred Rapp, Maryann Jerkofsky, Joseph L. Melnick, Barnet Levy
Journal: The Journal of Experimental Medicine (1968)

The acquisition of the defective SV40 genome by a variety of human adenovirus serotypes by the process of transcapsidation has resulted in the addition of oncogenic potential for newborn hamsters to the previously nononcogenic adenovirus types 1, 2, 5, and 6. These serotypes have previously been grouped together by the high GC content of their DNA. Transcapsidation of the SV40 genome to weakly oncogenic adenovirus types 3, 14, 16, and 21 has failed to increase their oncogenic potential although the parent adenovirus type 7 carrying PARA is highly oncogenic. These serotypes belong to the group possessing a DNA of intermediate GC content. All the PARA-adenovirus populations, even those that were nononcogenic, were able to induce SV40 transplantation immunity and therefore carry the SV40 transplantation marker as well as the marker for synthesis of SV40 tumor or T antigen.
FMLP activates Ras and Raf in human neutrophils. Potential role in activation of MAP kinase.
Authors: G S Worthen, N Avdi, A M Buhl, N Suzuki, G L Johnson
Journal: Journal of Clinical Investigation (1994)

Chemoattractants bind to seven transmembrane-spanning, G-protein-linked receptors on polymorphonuclear leuko- cytes (neutrophils) and induce a variety of functional re- sponses, including activation of microtubule-associated pro- tein (MAP) kinase.Although the pathways by which MAP kinases are activated in neutrophils are unknown, we hy- pothesized that activation of the Ras/Raf pathway leading to activation of MAP/ERK kinase (MEK) would be induced by the chemoattractant f-met-leu-phe.Human neutrophils exposed to 10 nM FMLP for 30 s exhibited an MAP kinase kinase activity coeluting with MEK-1.Immunoprecipitation of Raf-1 kinase after stimulation with FMLP revealed an activity that phosphorylated MEK, was detectable at 30 s, and peaked at 2-3 min.Immunoprecipitation of Ras from both intact neutrophils labeled with [32P]orthophosphate and electropermeabilized neutrophils incubated with [32p]_ GTP was used to determine that FMLP treatment was asso- ciated with activation of Ras.Activation of both Ras and Raf was inhibited by treatment of neutrophils with pertussis toxin, indicating predominant linkage to the Gu2 protein.Although phorbol esters activated Raf, activation induced by FMLP appeared independent of protein kinase C, further suggesting that Gu was linked to Ras and Raf independent of phospholipase C and protein kinase C. Dibutyryl cAMP, which inhibits many neutrophil functional responses, blocked the activation of Raf by FMLP, suggesting that interruption of the Raf/MAP kinase pathway influences neutrophil responses to chemoattractants.These data sug- gest that G2-mediated receptor regulation of the Ras/Raf/ MAP kinase pathway is a primary response to chemoattractants.(
Diabetes Mellitus, Clinical and Metabolic: A Shorter Textbook
Authors: Wayne Callaway
Journal: JAMA (1977)

The subtitle A Shorter Textbook aptly describes this compact volume. It stands midway between the single chapter coverage in most texts of general medicine and the multiauthored tomes that serve as standard references. Its major virtue is a pragmatic orientation. Most of the chapters concern patient management: diagnosis; clinical manifestations; complications; diet, drug, and insulin therapy; special circumstances, such as pregnancy and surgery; and personal, social and economic aspects of diabetes mellitus. The authors are obviously familiar with current trends in diabetes research. However, they have filtered their knowledge through the sands of clinical experience. The result is a down-to-earth, conservative approach that should reassure older clinicians and help younger ones establish workable day-to-day practices.  The book is also addressed to students, both undergraduate and postgraduate. Here one can anticipate some minor difficulties. The sections on physiology and metabolism are a bit superficial and even, at times, inaccurate. The accompanying
The Fiction of Bioethics: A Précis
Authors: Tod Chambers
Journal: The American Journal of Bioethics (2001)

Recently, bioethics has become interested in engaging with narrative, but in this engagement, narrative is usually viewed as a mere helpmate to philosophy. In this precis to his book The Fiction of Bioethics, Tod Chambers argues that narrative theory should not be simply a helpful addition to medical ethics but instead should be thought of as being as vital and important to the discipline as moral theory itself. The reason we need to rethink the relationship of medical ethics to narrative is that ethicists test their ideas by applying them to cases, and cases are a narrative genre. Recognizing the importance that cases have for the way medical ethicists do ethics is essential in order to appreciate the field as a form of applied philosophy. Like other forms of representation, narrative has distinct and defining features, which ethicists, in order to understand the data of their field, must learn to recognize and differentiate. Ethicists need to attend to the way decisions about the discourse of a narrative influences the kind of moral theories judged relevant to it. The author briefly examines six features of narrative discourse that rhetorically condition the way we understand medical ethics cases: filter, reportability, closure, characters, chronotope, and gender.
Myocardial reinfarction after anesthesia and surgery
Authors: P. A. Steen
Journal: JAMA (1978)

During the years 1974 and 1975 at our institution, 587 patients who had suffered previous myocardial infarctions underwent anesthesia and surgery. Thirty-six (6.1%) had a reinfarction and 25 (69%) died. Patients operated on within three months of the previous infarction had a 27% reinfarction rate. This decreased to 11% if the infarct had occurred three to six months previously and stabilized at 4% to 5% if the interval was more than six months. Risk factors associated with significantly increased reinfarction rates included preoperative hypertension, intraoperative hypotensive episodes, and noncardiac thoracic or upper abdominal operations of more than three hours' duration. Time under anesthesia was strikingly correlated with reinfarction rates in the entire group. Postoperative intensive care unit admission did not significantly affect the reinfarction rate, nor did diabetes, angina, patient age or sex, or site of the previous myocardial infarction. (<i>JAMA</i>239:2566-2570, 1978)
Estimation of 24-Hour Thyroid Uptake of 1-131 Sodium Iodide Using a 5-Minute Uptake of Technetium-99m Pertechnetate
Authors: JOHN J. SMITH, BARBARA Y. CROFT, VALERIE A. BROOKEMAN, CHARLES DAVID TEATES
Journal: Clinical Nuclear Medicine (1990)

The authors have developed a method to estimate the 24-hour sodium iodide thyroid uptake based on a 5-minute Tc-99m pertechnetate thyroid uptake using the equation: Estimated Iodide Uptake = 17.72*In(Pertechnetate Uptake) + 30.40. This estimation has a correlation coefficient of 0.90. It is based on a data pool of 44 patients who underwent I-131 and Tc-99m studies within 2 weeks of each other from 1978-1988, with established diagnoses as follows: 12 euthyroid, 6 hyperthyroid with multinodular goiters, 15 hyperthyroid with diffuse goiters, 4 with subacute thyroiditis, and 7 unknown. The population consisted of 30 women and 14 men with a mean age of 52.0 +/- 17.5 years; this sample was screened for use of thyroid hormone, propylthiouracil, and radiographic contrast. The authors believe this estimation method is of value whenever a 24-hour iodide uptake is desired, and where speed and minimizing radiation dose are factors. This method is strongly recommended for thyroid uptake evaluation before I-131 therapy.
An Alarming History of Famous and Difficult! Patients: Amusing Medical Anecdotes From Typhoid Mary to FDR
Authors: Joseph B. Vander Veer
Journal: JAMA (1997)

I suspect that within most of us there is a fascination with the peculiarities of other people's lives: witness the popularity of television shows depicting the lifestyles of the rich and  and supermarket tabloids.  Such fascination—served up with greater sophistication and historical accuracy—is the fare of Richard Gordon's latest book, an account of the maladies of 39 famous patients throughout history, each of whom has a chapter in this slender volume. The chapters stand alone, making it a good  book.  That said, I doubt that Sir William (Osier) would have included it in his bedside library for medical students,1 the intent of which was to impart to the student the education, if not of a scholar, at least of a gentleman. Nevertheless, it's a good read.  Gordon is a British physician who has published two score books, including the famous Doctor in the House series, adapted for stage
Subacute prurigo variant of bullous pemphigoid: Autoantibodies show the same specificity compared with classic bullous pemphigoid
Authors: Enno Schmidt, Cassian Sitaru, Barbara Schubert, Ulrich Wesselmann, Arno Kromminga, Eva-Bettina Bröcker, Detlef Zillikens
Journal: Journal of the American Academy of Dermatology (2002)
Biochemistry of Viral Infection
Authors: Morton N. Swartz, John W. Littlefield
Journal: New England Journal of Medicine (1960)

SIXTY years have passed since the initial classic experiments of Beijerinck, demonstrating the serial transmission of mosaic disease of tobacco plants with cell-free filtrates, offered the first substantial evidence of the existence of filtrable viruses.1 In the ensuing years, hundreds of viral agents, producing diseases in man, animals, insects, plants and even bacteria, have been described. Very little was known, however, of the chemical composition of viruses or of the biochemical changes produced in host cells as a consequence of infection, until the crystallization of tobacco mosaic virus and its identification as a ribonucleoprotein by Stanley2 twenty-four years ago.The . . .
Clinical Outcomes and Adherence to Medications Measured by Claims Data in Patients With Diabetes
Authors: Manel Pladevall, L. Keoki Williams, Lisa Ann Potts, George Divine, Hugo Xi, Jennifer Elston Lafata
Journal: Diabetes Care (2004)

OBJECTIVE—Although poor medication adherence may contribute to inadequate diabetes control, ways to feasibly measure adherence in routine clinical practice have yet to be established. The present study was conducted to determine whether pharmacy claims-based measures of medication adherence are associated with clinical outcomes in patients with diabetes. RESEARCH DESIGN AND METHODS—The study setting was a large, integrated delivery and financial system serving the residents of southeastern Michigan. The study population consisted of 677 randomly selected patients aged ≥18 years with a diagnosis of diabetes, hypercholesterolemia, and hypertension and who filled at least one prescription for either an antidiabetic, lipid-lowering, or antihypertensive drug in each of the 3 study years (1999–2001). The main outcome measures were HbA1c, LDL cholesterol levels, and blood pressure. RESULTS—Nonadherent patients had both statistically and clinically worse outcomes than adherent patients. Even after adjusting for demographic and clinical characteristics, nonadherence was significantly associated with HbA1c and LDL cholesterol levels. A 10% increase in nonadherence to metformin and statins was associated with an increase of 0.14% in HbA1c and an increase of 4.9 mg/dl in LDL cholesterol levels. Nonadherence to ACE inhibitors was not significantly associated with blood pressure. CONCLUSIONS—Claims-based measures of medication adherence are associated with clinical outcomes in patients with diabetes and may therefore prove to be useful in clinical practice. More research is needed on methods to introduce claims-based adherence measurements into routine clinical practice and how to use these measurements to effectively improve adherence and health outcomes in chronic care management.
Chromosome territories reposition during DNA damage-repair response
Authors: Ishita S Mehta, Mugdha Kulashreshtha, Sandeep Chakraborty, Ullas Kolthur-Seetharam, Basuthkar J Rao
Journal: Genome biology (2013)

Abstract Background Local higher-order chromatin structure, dynamics and composition of the DNA are known to determine double-strand break frequencies and the efficiency of repair. However, how DNA damage response affects the spatial organization of chromosome territories is still unexplored. Results Our report investigates the effect of DNA damage on the spatial organization of chromosome territories within interphase nuclei of human cells. We show that DNA damage induces a large-scale spatial repositioning of chromosome territories that are relatively gene dense. This response is dose dependent, and involves territories moving from the nuclear interior to the periphery and vice versa. Furthermore, we have found that chromosome territory repositioning is contingent upon double-strand break recognition and damage sensing. Importantly, our results suggest that this is a reversible process where, following repair, chromosome territories re-occupy positions similar to those in undamaged control cells. Conclusions Thus, our report for the first time highlights DNA damage-dependent spatial reorganization of whole chromosomes, which might be an integral aspect of cellular damage response.
Zoledronic Acid Is Effective against Experimental Malignant Pleural Effusion
Authors: Georgios T. Stathopoulos, Charalampos Moschos, Heleni Loutrari, Androniki Kollintza, Ioannis Psallidas, Sophia Karabela, Sophia Magkouta, Zongmin Zhou, Spyros A. Papiris, Charis Roussos, Ioannis Kalomenidis
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Rationale: Aminobiphosphonates, such as zoledronic acid (ZA), exert potent indirect antitumor effects and are currently being tested against human solid tumors. The antitumor actions of aminobiphosphonates, including angiostasis, are relevant to the pathogenesis of malignant pleural effusion (MPE), but no study has addressed the efficacy of these compounds against malignant pleural disease.Objectives: Here we hypothesized that treatment of immunocompetent mice with ZA would halt tumor progression in a mouse model of adenocarcinoma-induced MPE.Methods: To induce MPE in mice, Lewis lung carcinoma cells were delivered directly into the pleural space. Subsequently, animals were treated with ZA in both a prevention and a regression protocol.Measurements and Main Results: ZA treatment resulted in significant reductions in pleural fluid accumulation and tumor dissemination, while it significantly prolonged survival. These effects of ZA were linked to enhanced apoptosis of pleural tumor cells, decreased formation of new vessels in pleural tumors, and reduced pleural vascular permeability. In addition, ZA was able to inhibit the recruitment of mononuclear cells to pleural tumors, with concomitant reductions in matrix metalloproteinase-9 release into the pleural space. Finally, ZA limited the expression of proinflammatory and angiogenic mediators, as well as the activity of small GTP proteins Ras and RhoA, in tumor cells in vivo and in vitro.Conclusions: ZA is effective against experimental MPE, suggesting that this intervention should be considered for testing in clinical trials.
Updates from the British Association of Dermatologists 89th Annual Meeting, 7-10 July 2009, Glasgow, U.K.
Authors: A.B. Alexandroff, C. Flohr, G.A. Johnston
Journal: British Journal of Dermatology (2010)

This is a synopsis of the significant research and clinical papers presented at the British Association of Dermatologists meeting held during 7-10 July 2009 in Glasgow, U.K. The conference and satellite symposia highlighted the recent biological, epidemiological and therapeutic advances in dermatology. This report is not meant as a substitute for reading the conference proceedings and related references quoted in this article.
Myocardial Infarction and Erythema Multiforme
Authors: Carl G. Kardinal
Journal: JAMA (1968)

<h3>To the Editor:—</h3> Since the original description of erythema multiforme by von Hebra in 1860, this skin reaction has been reported to be associated with a variety of seemingly unrelated conditions such as viral, bacterial, or mycotic infection, collagen disease, occult malignancy, deep x-ray therapy, severe sunburn, and hypersensitivity reactions to numerous drugs, contactants, and foods. The common denominator, however, does seem to be hypersensitivity. In addition to the cutaneous manifestations erythema multiforme exudativum (Stevens-Johnson syndrome), may have associated systemic manifestations including fever, dehydration, arthralgias, cardiac arrhythmias, pericarditis, lymphadenopathy, pneumonitis, nephritis, and transient myocarditis. The histopathology of erythema multiforme is that of an allergic vasculitis with a perivascular inflammatory exudate composed mainly of mononuclear cells, but also neutrophils, eosinophils, scattered nuclear fragments, and at times extravasated erythrocytes. <h3>Report of a Case:—</h3> A 65-year-old retired warrant officer with a long standing history of angina pectoris was seen in the Surgical Outpatient
Abstract 1130: AKT-mediated phosphorylation is responsible for TWIST1-mediated tumor growth and metastasis
Authors: Osman N. Ozes, Suray Pehivanoglu, Gokhan Ertosun, Gokhan Gorgisen, Nuray Erin, Duygu Unal, Gamze Tanriover
Journal: Cancer Research (2014)

Abstract Cancer cells show epithelial-mesenchymal transition (EMT) during cell migration, invasion and dissemination. Although it has been shown by numerous publications that the evolutionary conserved basic helix-loop-helix (b-HLH) transcription factor TWIST1 plays pivotal role during EMT the molecular mechanism responsible for TWIST1 function is not fully understood. Here we show that Twist1 binds to and phosphorylated by AKT/protein kinase-B at S42, T121 and S123. While conversion of S42, T121 and S123 to phosphorylation-mimicking Aspartic or glutamic acids created active Twist1, Alanin mutants of the same sites diminished the DNA-binding and transctivating functions of Twist1. In line with this, Glutamic Acids mutants suppressed the expression of E-Cadherin, whose expression is negatively regulated by active TWIST1, Alanin mutants induced the expression of E-Cadherin. Similarly, we tested the impact of above mentioned mutants on cell migration and proliferation. Our results demonstrated that while Glutamic acid mutants accelerated, Alanin mutants suppressed the migration and proliferation of 293T cells. Our in vitro results prompted us to test our mutants under in vivo conditions using breast cancer as a model. We transfected non-metastatic mouse mammary tumor cell line, 67NR, with Glutamic acid mutants, and metastatic mouse mammary tumor cell line, 4T1, with Alanin mutants of mouse TWIST1 and selected the Neo-resistant populations. We injected 1 million 67NR cells over-expressing wild type or Glutamic acid mutants of Twist1, and 100.000 4T1 cells over-expressing wild type or Alanin mutants of Twist1 into the breast tissue of female inbred BalBC mice, and animals were monitored for metastasis. At the end of the 4th week, we sacrifised and examined the animals for tumor growth and metastasis. Although 67NR cells over-expressing wild type Twist1 did not show any metastasis, cells over-expressing 1E (S42E) and 2E (S42E, T121E) mutants of Twist1 showed 15-20 macroscopic metastasis to liver and Lungs. Paralel to this, 4T1 cells expressing 1A (S42A) and 2A (S42A, T121A) mutants of TWIST1 showed no macroscopic metastasis. Our results clearly indicate that phosphorylation of S42 and T121 by AKT is essential for TWIST1-mediated tumor growth and metastasis. Citation Format: Osman N. Ozes, Suray Pehivanoglu, Gokhan Ertosun, Gokhan Gorgisen, Nuray Erin, Duygu Unal, Gamze Tanriover. AKT-mediated phosphorylation is responsible for TWIST1-mediated tumor growth and metastasis. [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 1130. doi:10.1158/1538-7445.AM2014-1130
Evidence shows that cyclists should wear helmets
Authors: R. M Davis, B. Pless
Journal: BMJ (1996)

EDITOR,—We are disappointed to read that “Minerva is a keen cyclist but does not like wearing her helmet.”1 This is hardly the attitude towards injury prevention that we would expect from one who is such a proficient reader of the medical literature. We are concerned that this negative view might infect many of Minerva's loyal readers. Minerva expresses interest in an article from the Journal of Medical Ethics that argued that helmets should not be made mandatory until their use …
Molecular cloning and chromosomal mapping of DNA rearranged with the parathyroid hormone gene in a parathyroid adenoma.
Authors: A Arnold, H G Kim, R D Gaz, R L Eddy, Y Fukushima, M G Byers, T B Shows, H M Kronenberg
Journal: Journal of Clinical Investigation (1989)

Parathyroid adenomas are common benign neoplasms for which no chromosomal defects have been described. We recently found two parathyroid adenomas bearing clonal restriction fragment abnormalities involving the PTH locus, and now show that in one of these tumors: (a) a DNA rearrangement occurred at the PTH locus; (b) the rearrangement separated the PTH gene's 5' flanking region from its coding exons, conceivably placing a newly adjacent gene under the influence of PTH regulatory elements; (c) the DNA that recombined with PTH normally maps to 11q13, the known chromosomal location of several oncogenes and the gene for multiple endocrine neoplasia type I; and (d) the rearrangement was a reciprocal, conservative recombination of the locus on 11q13 (Human Gene Mapping Library assignment D11S287) with PTH (on 11p15). These data provide molecular cytogenetic evidence for the clonal occurrence of a major chromosome 11 aberrancy in this benign parathyroid tumor. The D11S287 clone could prove useful in genetic linkage analyses, in determining precise 11q13 breakpoints in other neoplasms, and in identifying a gene on chromosome 11 that may participate in parathyroid tumor development.
Letter: Effect of natural oestrogens on coagulation.
Authors: M Notelovitz, H B Greig
Journal: BMJ (1974)

with oral conitraceptives.Without being able categorically to deny this possibility I think it unlikely for the following reasons.Retinol in human blood is predominantly bound to a specific transport-protedin known as the retinol-binding protein (RBP).Under physiological conditions RBP ibinds to pre- albumin.4The amount of free retinol is very small, indeed.Using a fluorescence assay5 measurements have been made of the amoun-t of RBP,in plasma from 10 women before starting to take a combined oral con- traceptive (Minovlar: 1 mg nocethisterone acetate and 50 ,ug ethynylestradiol) and again after three months' treatment.The mean pretreatment level of RBP was 42±8 (S.D.) ,ug/ml, but this rose to 75 ± 10 ug/ml during treatmenrt.This finding indicates that the rise in iseruum vitamin A level during the taking of oral contraceptives is due to an increased concentrtion of RBP.The amount of free retinod is unchanged.Hypervitaminosis A and the teratogeic effects of the vitamnm in pregnant animls are seen with doses which far exceed the binding capacty of RBP.I,t seems unlikely that an increase in protein-bound retinol is hazadous.A very analogous isiituation occurs with coricosterodds, where plasma levels are very high in women taking oral cotraceptives owng to an increase in,transcartin.6The increase in plasma RBP seen in women taking oral contraceptives is prob- ably due to the oestirogen component, for plasma retinol is not increased by progestogens alone.2Serum vitamin A is also raised in volunteers exposed to DDT,7 for this compound yields oestrogenic mexa-