tbuckley/cabot-search huggingface dataset:
Muscular Dystrophy in Man and Animals
Authors: Raymond D. Adams
Journal: JAMA (1963)

In recent years there has been a flood of new publications on the pathology of skeletal muscle. From a state of relative neglect the whole field of muscle disease has been transformed into one in which there is active investigation of all aspects of processes involving this tissue. This new and attractive publication on muscular dystrophy in man and animal is the most recent addition to this literature. The subject matter of the book is divided into 12 chapters, nine of which are devoted to human muscular dystrophy and three to metabolic and inherited diseases of muscle in animals. The clinical, genetic, biochemical, and pathological changes which have been found in human cases of muscle dystrophy are extensively reviewed by recognized authorities in this field. Professor Carl Pearson introduces the subject with a systematic account of the pathology of muscle dystrophy. Shapiro and Dreyfus follow with a thorough and informative
Antiarrhythmic Classifications in the 2000 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Authors: Michael F. Caron, Jessica Song, C. Michael White
Journal: Circulation (2001)

We read the American Heart Association's Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care with great interest.We think the committee did a thorough and prudent review of the literature and made valid conclusions.However, there are 2 areas of inconsistency that need clarification.The guidelines classified the antiarrhythmic agent lidocaine as Indeterminate (page I-123) for ventricular fibrillation (VF)/ pulseless ventricular tachycardia (VT) that persists after defibrillation and the administration of epinephrine. 1 However, elsewhere in the guidelines 1 and in the 2000 Handbook of Emergency Cardiovascular Care for Healthcare Providers, 2 lidocaine is classified as a Class IIb therapeutic intervention.As stated on page I-87 of the guidelines, "The evidence supporting antiarrhythmics in general is only fair, and this accounts for the fact that all antiarrhythmics are lumped into one class IIb 'consider' category." 1 In addition, on page 67 of the Handbook, lidocaine is again classified as IIb for cardiac arrest from VF/VT. 2 These inconsistencies could lead a clinician to believe that lidocaine and amiodarone have similar proof of benefit in VF/pulseless VT.However, in the committee's review of the Amiodarone in out-of-hospital Resuscitation of REfractory Sustained ventricular Tachyarrhythmias (ARREST) trial, amiodarone had better evidence-based support than other antiarrhythmic drugs in this setting (page I-87). 3econd, the guidelines also state that amiodarone "as currently available, must be drawn up from a 6-mL glass ampule into a
Goitre Plongeant
Authors: HENRY T. PERKINS, HENRY D. MCINTOSH, JOHN P. BOINEAU
Journal: Circulation (1960)

The diagnosis of an intrathoracic goiter can, on occasion, be difficult to confirm. The Valsalva maneuver was found useful in making this diagnosis in 2 patients whose case histories are reported. Such goiters are termed plunging goiters. The phenomenon is discussed and the use of the Valsalva maneuver in demonstrating such lesions is emphasized.
TOTAL THYROIDECTOMY IN THE TREATMENT OF DIABETES INSIPIDUS
Authors: HARRY BLOTNER
Journal: JAMA (1941)

Considerable advance has been made in recent years in the physiology of the thyroid gland in relation to the other organs of internal and of external secretion. However, during the past forty-five years, clinicians have reported improved elimination of water in certain forms of nephritis by the administration of desiccated thyroid and more recently of thyroxine, alone or combined with solution of parathyroid.<sup>1</sup>No explanation for the effects noted has been forthcoming beyond the possibility that these drugs increase the mobilization and excretion of calcium. Early work has shown that there is a definite relation between the thyroid and the pituitary gland. As early as 1889 Rogowitsch<sup>2</sup>found alterations in the pituitary glands of thyroidectomized dogs and rabbits in the nature of an increase in certain elements in the glandular or anterior portion. Shortly afterward, Hofmeister,<sup>3</sup>Gley,<sup>4</sup>Pisenti and Viola,<sup>5</sup>Schönemann<sup>6</sup>and others reported
Dichloroacetate inhibits glycolysis and augments insulin-stimulated glycogen synthesis in rat muscle.
Authors: A S Clark, W E Mitch, M N Goodman, J M Fagan, M A Goheer, R T Curnow
Journal: Journal of Clinical Investigation (1987)

The decrease in plasma lactate during dichloroacetate (DCA) treatment is attributed to stimulation of lactate oxidation. To determine whether DCA also inhibits lactate production, we measured glucose metabolism in muscles of fed and fasted rats incubated with DCA and insulin. DCA increased glucose-6-phosphate, an allosteric modifier of glycogen synthase, approximately 50% and increased muscle glycogen synthesis and glycogen content greater than 25%. Lactate release fell; inhibition of glycolysis accounted for greater than 80% of the decrease. This was associated with a decrease in intracellular AMP, but no change in citrate or ATP. When lactate oxidation was increased by raising extracellular lactate, glycolysis decreased (r = - 0.91), suggesting that lactate oxidation regulates glycolysis. When muscle lactate production was greatly stimulated by thermal injury, DCA increased glycogen synthesis, normalized glycogen content, and inhibited glycolysis, thereby reducing lactate release. The major effect of DCA on lactate metabolism in muscle is to inhibit glycolysis.
TRANSMISSION OF AGENT OF POST-TRANSFUSION NON-A, NON-B HEPATITIS BY CRYOPRECIPITATE PREPARED FROM PLASMA OF SYMPTOMLESS CHRONIC CARRIER
Authors: Edward Tabor, Philip Snoy, RobertJ. Gerety, Milan Wickerhauser, Doris Menache, LeonardB. Seeff
Journal: The Lancet (1983)
Malaria Is Not a Disease.
Authors: None Zeta.
Journal: JAMA (1898)

New York, July 25, 1898. <h3>To the Editor:</h3> —I note that in your items for your issue of the 16th inst. Dr. Koch is represented as speaking of "tropical malaria" as if the cause and effect were the same. That is to say, if my view is correct, malaria is a "bad air" or other bad influence that begets a certain disease, namely, malarial fever. I would like to ask you to turn to Dr. Koch's own writing in the<i>Deutsche Med. Woch.</i>, June 16, and tell your readers if he has fallen into the error of lumping cause and effect, or whether the<i>lapsus</i>has occurred in the course of transcribing his valuable observations into the English. By giving your readers a little light on this subject, you will, no doubt, confer a favor on others beside Yours faithfully,
P4-14-02: Risk Factors for Early Lymphoedema Do Not Predict Late Development of Lymphoedema.
Authors: SL Kilbreath, J Beith, KM Refshauge, M-J Lee, LC Ward
Journal: Cancer Research (2011)

Abstract Background: Previously, we investigated whether an upper limb 8 week exercise program commencing 1 month after surgery was associated with higher incidence of LE. As part of that study, we investigated the risk factors for development of LE at 12 month follow-up, which was equivalent to 15 m post surgery. As LE fluctuates during the first year, our secondary aim was to identify risk factors for LE at the conclusion of the intervention and at 6 m follow-up. Methods: Women (n=160) were recruited who had undergone breast and axillary surgery within the previous month for unilateral early stage breast cancer. Potential predictors were measured at approximately one month postoperatively after which women were randomised to the exercise or control group. Possible predictors of LE included age, BMI, side of surgery, treatments for breast cancer, physical measures of shoulder range of motion and strength, inter-limb bioimpedance ratio at each previous measurement occasion and the treatment group to which women were randomised. The outcome measure for LE was based on the inter-limb impedance ratio. Presence of LE was determined using established cut-offs for LE. The relationship of each variable to the outcome measures (i.e. presence of LE) was assessed using t-tests and correlations. Significant variables (P &amp;lt; 0.25) were further examined with a multivariate logistic regression model. Results: At least 10% of women developed LE: following intervention (N=15), and at 6m (N=15) and 12 m (N=20) follow-up. Risk factors for LE varied across the 3 time points (Table 1). At 12 m follow-up, the only significant risk factor was surgery on the non-dominant side. In contrast, the risk factors for LE following the intervention were allocation to the control group and commencement of taxane-based chemotherapy. At 6 m follow-up, risk factors for LE were having LE following the intervention and receiving taxane-based chemotherapy. Conclusion: Fluctuation of LE over the first year is associated with different risk factors. For example, fluid accumulation is a common side effect of taxanes and it was therefore not surprising that there was a transient increase in LE. However, overall, we speculate that the higher risk for LE after 1 year is because of lack of use of the non-dominant affected arm. It is use of the upper limb which is likely the critical issue in this first year. Exercise was preventative while it was being undertaken; we question whether women maintained the level of exercise once the intervention concluded. Acknowledgement: Cancer Council NSW; NBCF Australia Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-14-02.
Active Tetanus Immunization-Reply
Authors: George C. Kaiser
Journal: JAMA (1962)

<h3>To the Editor:—</h3> The problem of tetanus prophylaxis is an important and intriguing experimental and clinical problem, and is a long way from being solved. We, too, were concerned about the method of comparison of our results with those of others. We realized the deficiencies in comparing our study with the groups studied by Banton and Miller, and Turner, Stafford, and Goldman. We utilized the concept of a "significant response" proposed by Miller, Ryan, and Beard as a method of comparison primarily to attempt to relate the serum antitoxin level and the response of the patient to possible clinical application. The difficulties in deciding upon a method of comparison were also referred to in the paper. The absolute titer of tetanus antitoxin in the serum which is necessary for tetanus prophylaxis is unknown. Certainly if a specific serum level could be accepted as protective, comparison of absolute levels would have
Abstract 822: The molecular diversity of Luminal A breast cancer.
Authors: Ciriello Giovanni, Charles M. Perou, Chris Sander, Nikolaus Schultz
Journal: Cancer Research (2013)

Abstract Breast cancer is a collection of diseases with distinct molecular traits, prognosis, and therapeutic options. Luminal A breast cancer is the most heterogeneous, both molecularly and clinically. Using genomic data from nearly 1000 Luminal A tumors from multiple studies, we identified at least four major subtypes defined by distinct copy-number and mutation profiles. Here we show an atypical Luminal A subtype characterized by high genomic instability, TP53 mutations, and increased Aurora kinase signaling. These genomic alterations lead to a worse clinical prognosis. Copy number heterogeneity comes in tandem with distinct mutation spectra. We find a prevalence of PIK3CA, GATA3, and AKT1 mutations in the subtypes characterized by relatively diploid genomes subtypes. Moreover, we highlight a strong association between MAP3K1 mutations and gains and losses of chromosomes 8 and 16. Finally, an unbiased pathway analysis revealed multiple rare, but mutually exclusive, alterations linked to loss of activity of co-repressor complexes N-Cor and SMRT. These rare alterations are prevalent in Luminal A tumors and may predict response to endocrine therapy. Our work shows how comprehensive genomic characterization of tumor subtypes is fundamental to inform clinical trials and to move towards personalized therapies. Figure 1: Luminal A subtypes as determined by copy-number clustering. Citation Format: Ciriello Giovanni, Charles M. Perou, Chris Sander, Nikolaus Schultz. The molecular diversity of Luminal A breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 822. doi:10.1158/1538-7445.AM2013-822 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Carcinoma of the Right Colon
Authors: Bentley P. Colcock
Journal: New England Journal of Medicine (1952)

THIS study is based on 242 patients who were operated on between 1930 and 1950 for carcinoma of the right colon. This group includes patients with carcinoma of the cecum, the ascending colon and the hepatic flexure. Judging from a previous study1 of 1457 patients with cancer of the large bowel and rectum, this group represents approximately 12.76 per cent of all patients with cancer of the colon and rectum. Carcinomas at any point in the ascending colon, including the hepatic flexure, may properly be grouped with carcinomas of the cecum, as all these lesions tend to metastasize to lymph . . .
Clinical Problems, Injuries, and Complications of Gynecologic Surgery
Authors: Ralph C. Benson
Journal: JAMA (1984)

Many gynecologic rocks and shoals are identified in this small book. Exciting reading is scattered here and there and feelings of déjà vu or "there but for the grace of God go I" are recurrent. Important do's and don'ts are emphasized by acclaimed contributing authors. This book should be a valuable reference source for residents and practitioners. However, the pace is uneven; some sections are short and succinct, others are long, even rambling. More basically, one wonders what the true purpose of this text is. The most valuable portion is about gynecologic surgery and operative injuries. However, numerous topics seem to have been tacked on, almost as an afterthought. Some topics are uncommon, others too common for inclusion. Surely, the resident likely to encounter massive prolapse will know what to do when the patient has an abnormal papanicolaou smear, postmenopausal endometrial hyperplasia, or when endocrine problems of acute surgical menopause
Abstract P1-03-06: Population Based In Vivo Biomarker Discovery Using Engineered Human Tumors
Authors: M Wu, K Clark, N Deng, Z Cai, R Nicoletti, K Sun, B Feng, J Heyer, I Chiu, M. Robinson
Journal: Cancer Research (2010)

Abstract Background: Tumors from patients exhibit significant inter-tumor variation, where each tumor harbors a unique set of genetic alterations that impact prognosis and response to treatment. Unfortunately, this variation contributes to low response rates in the clinic and creates significant challenges for treating patients with appropriate drugs. Cancer cell line based xenografts have traditionally been the preclinical model of choice to assess the efficacy of clinical compounds; however, such in vitro models exhibit inherent artifacts, and are unable to adequately capture natural variation seen in human tumor populations. It has therefore become a priority in oncology and personalized medicine to match patients to drugs that will result in a favorable treatment outcome. In this report, we describe a population based approach for response prediction featuring naturally occurring variation in tumors derived from genetically defined human-in-mouse models of cancer. Materials and Methods: A population of De novo human breast tumors were generated by genetically engineering normal primary human breast epithelial cells with HER2 and SV40 early region (HER2/SV40er) or KRAS and SV40 early region (KRAS/SV40er) in an in vivo Human-In-Mouse (HIM) tissue transgenic model (Wu et al, Proc Natl Acad Sci U S A 2009, 106: 7022-2027). Each tumor of the population has been comprehensively characterized histopathologically, and at the RNA and DNA level. Furthermore, the population has been adapted to conduct quantitative efficacy studies of anti-cancer agents and combinations. Results: The HER2/SV40er and the KRAS/SV40er HIM tumors develop as invasive human breast adenocarcinoma that are histologically similar to those observed in patients. Microarray and CGH profiling demonstrated significant inter-tumor variation among the established tumors, as has been reported for patient tumors. Moreover, the KRAS/SV40er tumors clustered with basal type breast cancers from patients, a poor prognosis human breast cancer subtype. Both HER2/SV40er and KRAS/SV40er tumors exhibited variable responses to treatments with the potent selective triple VEGFR inhibitor, tivozanib. Further characterization of those tumors, both pre-and post-treatment, identified potential biomarkers for tumor response to tivozanib. Discussion: The genetically defined human-in-mouse tumors exhibited natural variations similar to that occurs in human cancer. This population-based HIM system enables us to identify and validate biomarkers of therapeutic response in an in vivo human tumor model. Figure available in online version. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-03-06.
Brown Tumor in End-Stage Renal Disease
Authors: G M Nassar, J C Ayus
Journal: New England Journal of Medicine (1999)

Figure 1. A 62-year-old man with end-stage renal disease from hypertensive nephrosclerosis that had been treated by hemodialysis for 14 years presented to the emergency room with a productive cough and fever, from which he recovered. A chest film showed right hilar prominence and pleural-based masses (arrows in Panel A), with destructive changes in the adjacent ribs on the left. The cardiac silhouette, pulmonary vasculature, and position of a LeVeen shunt placed for recurrent dialysis-associated ascites were unchanged from a previous chest film. Computed tomography of the chest showed mild mediastinal adenopathy and multiple expansile lytic lesions of the ribs . . .
Chronic β-Adrenergic Stimulation Induces Myocardial Proinflammatory Cytokine Expression
Authors: David R. Murray, Sumanth D. Prabhu, Bysani Chandrasekar
Journal: Circulation (2000)

Background —The sympathetic nervous system and proinflammatory cytokines are believed to play key roles in the pathophysiology of congestive heart failure. To evaluate a possible relationship between these neurohormonal systems, we studied the effects of chronic β-adrenergic stimulation on the myocardial and systemic elaboration of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Methods and Results —Male rats received either L-isoproterenol (2.4 mg · kg −1 · d −1 , n=8) or saline (n=7) via miniosmotic pumps for 7 days. Myocardial cytokine expression was analyzed by both Northern and Western blotting and localized in the tissue using immunohistochemistry. ELISA was performed to measure circulating levels of cytokines. In myocardium from control animals, neither TNF-α nor IL-1β were detected, whereas IL-6 was present at very low levels. Isoproterenol led to a significant ( P &lt;0.01) increase in mRNA and protein expression of all 3 cytokines. Immunohistochemistry did not detect immunoreactivity for either cytokine in myocardium from controls; however, all 3 cytokines were readily detected ( P &lt;0.05) throughout the myocardium, localized to resident cells and vessels, in animals treated with isoproterenol. Neither treatment group had detectable levels of cytokines in the serum. Conclusions —Chronic β-adrenergic stimulation induces myocardial, but not systemic, elaboration of TNF-α, IL-1β, and IL-6.
MicroRNA silencing of tumor suppressor DLC-1 promotes efficient hepatitis C virus replication in primary human hepatocytes
Authors: Krishna Banaudha, Michael Kaliszewski, Tamara Korolnek, Liliana Florea, Man Lung Yeung, Kuan-Teh Jeang, Ajit Kumar
Journal: Hepatology (2010)

MicroRNAs (miRNAs) are approximately 22-nucleotide noncoding RNAs that constitute silencers of target gene expression. Aberrant expression of miRNA has been linked to a variety of cancers, including hepatocellular carcinoma (HCC). Hepatitis C virus (HCV) infection is considered a major cause of chronic liver disease and HCC, although the mechanism of virus infection–associated hepatocarcinogenesis remains unclear. We report a direct role of miRNAs induced in HCV-infected primary human hepatocytes that target the tumor suppressor gene DLC-1 (a Rho GTPase-activating protein), which is frequently deleted in HCC, and other solid human tumors. MicroRNA miR-141 that targets DLC-1 was accentuated in cells infected with HCV genotypes 1a, 1b, and 2a. We present several lines of evidence that efficient HCV replication requires miR-141–mediated suppression of DLC-1. An increase in miR-141 correlated with the inhibition of DLC-1 protein in HCV-infected cells. Depletion of miR-141 with oligonucleotides complementary to the miRNAs inhibited virus replication, whereas artificially increased levels of intracellular miR-141 enhanced HCV replication. HCV-infected hepatocytes showed enhanced cell proliferation that can be countered by overexpression of DLC-1. Conclusion: The collective results of this study suggest a novel mechanism of HCV infection–associated miRNA-mediated regulation of a tumor suppressor protein that has the ability to influence cell proliferation and HCV infection–mediated liver cancer. (Hepatology 2011)
Assessment of mycobacterial DNA in cells and tissues of mycobacterial and sarcoid lesions.
Authors: E Richter, U Greinert, D Kirsten, S Rüsch-Gerdes, C Schlüter, M Duchrow, J Galle, H Magnussen, M Schlaak, H D Flad, J Gerdes
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

In this study we applied a polymerase chain reaction (PCR) assay for the detection and species-specific identification of mycobacteria to samples from patients with sarcoidosis and mycobacterial infections and from control patients. The PCR-technique is based on the amplification of mycobacterial DNA coding for 16S rRNA, which is present in all mycobacterial species, and on the additional sequencing of the PCR fragment to determine the species. Mycobacterial DNA could be detected in lung tissues and bronchoalveolar lavage cells from cases of tuberculosis and infections with atypical mycobacteria. On the other hand, mycobacterial DNA was amplified only in lung tissue from one patient with sarcoidosis. Twenty-three samples from patients with sarcoidosis were negative for mycobacterial DNA. From our results we conclude that the granulomatous lesions in sarcoidosis may not be due to mycobacterial infections.