tbuckley/cabot-search huggingface dataset:
THE WESTERN ASSOCIATION OF PHYSICAL THERAPY
Authors: Joseph E. G. Waddington
Journal: JAMA (1927)

<h3>To the Editor:</h3> —InThe Journal, September 24, in a query regarding a reprint entitled "Birth Marks" by Dr. Lynne B. Greene read at the Annual Meeting of the Western Physical Therapy Association, the correspondent somewhat implies that the possibly questionable scientific character of such reprint reflects on the possibly scientific and ethical standing of the association. As president of the Western Physical Therapy Association may I have space in your valued columns to state that membership in the association is conditioned on membership in the American Medical Association; that the outgoing president of the American Electrotherapeutic Association is a past president of the Western, and the outgoing and the incoming president of the American College of Physical Therapy is a member of the Western; and lastly, that neither the Western nor the A. M. A. is to be judged solely by the utterances of one of its members.
Primary Lymphomas of the Thyroid Gland
Authors: David King Sirota
Journal: JAMA (1979)

Twelve patients with primary lymphoma of the thyroid gland were reviewed. Based on clinical observations of this group of patients and a review of the literature, a composite clinical picture can be drawn of the patient at high risk of having primary lymphoma of the thyroid gland. This condition should be considered in the differential diagnosis in patients with a history of lymphocytic thyroiditis and an enlarging neck mass, tender or nontender. The mass may be cold or cool with areas of patchy uptake shown on scintillation scanning. The patient has a greater than 50% chance of having hoarseness with or without vocal cord paralysis. We also review the pathogenesis and prognosis of primary lymphoma of the thyroid gland. (<i>JAMA</i>242:1743-1746, 1979)
Spontaneous Regression of an Infantile Scalp Tumor
Authors: Paula Molés-Poveda, Lucero Noguera, Antonio Torrelo
Journal: JAMA Dermatology (2015)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Dermatology journal
Reversal of the Behavioral and Electrophysiological Abnormalities of An Animal Model of Hepatic Encephalopathy by Benzodiazepine Receptor Ligands
Authors: Sergio H. Gammal, Anthony S. Basile, David Geller, Phil Skolnick, Anthony E. Jones
Journal: Hepatology (1990)

Behavioral and electrophysiological evidence implicating the GABA–benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was obtained using an improved rat model of hepatic encephalopathy caused by thioacetamide–induced fulminant hepatic failure. After the administration of thioacetamide together with supportive therapy, acute hepatocellular failure developed in rats as a result of massive hepatocellular necrosis without evidence of renal failure or hypoglycemia. The evolution of hepatic encephalopthy in this model was sufficiently slow to readily permit the staging of the syndrome. Prominent features of the encephalopathy include a marked reduction in open field activity and an abnormal visual evoked response. Both the deficits in spontaneous motor function and visual evoked response abnormalities of rats in stages III to IV hepatic encephalopathy were significantly improved after the administration of the benzodiazepine receptor ligands flumazenil or Ro 15–4513. Doses of flumazenil or Ro 15–4513 that produced these effects in rats with hepatic encephalopathy had no detectable action on either the behavior or the visual evoked responses of normal rats. The ability of benzodiazepine receptor ligands to ameliorate both the behavioral depression and the visual evoked response abnormalities associated with hepatic encephalopathy in the thioacetamide–induced rat model suggest an involvement of the GABA/benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy. In addition, the similarity of these observations to those in rabbits with hepatic encephalopathy caused by galactosamine–induced fulminant hepatic failure is compatible with the hypothesis that the mechanisms of hepatic encephalopathy in these two distinct models share a common final pathway, the allosteric enhancement of GABAergic tone through the benzodiazepine receptor. These observations suggest that increased concentrations or availability of a ligand with agonist properties at the benzodiazepine receptor may be involved in the pathogenesis of hepatic encephalopathy and that administration of benzodiazepine receptor antagonists may be of value in the management of hepatic encephalopathy in man. (Hepatology 1990; 11: 371-378.)
Anti-Inflammatory, Antithrombotic, and Neuroprotective Effects of Activated Protein C in a Murine Model of Focal Ischemic Stroke
Authors: Masayoshi Shibata, S. Ram Kumar, Arun Amar, Jose A. Fernandez, Florence Hofman, John H. Griffin, Berislav V. Zlokovic
Journal: Circulation (2001)

Background —Activated protein C (APC) contributes to systemic anticoagulant and anti-inflammatory activities. APC may reduce organ damage by inhibiting thrombin generation and leukocyte activation. Neutrophils and cerebrovascular thrombosis contribute to ischemic neuronal injury, suggesting that APC may be a potential protective agent for stroke. Methods and Results —We examined the effects of APC in a murine model of focal ischemia. After middle cerebral artery occlusion/reperfusion, the average survival time in controls was 13.6 hours. Animals that received purified human plasma–derived APC 2 mg/kg IV either 15 minutes before or 10 minutes after stroke induction survived 24 hours and were killed for neuropathological analysis. APC 2 mg/kg given before or after onset of ischemia restored cerebral blood flow, reduced brain infarct volume (59% to 69%; P &lt;0.003) and brain edema (50% to 61%; P &lt;0.05), eliminated brain infiltration with neutrophils, and reduced the number of fibrin-positive cerebral vessels by 57% ( P &lt;0.05) and 25% (nonsignificant), respectively. The neuroprotective effect of APC was dose-dependent and associated with significant inhibition of ICAM-1 expression on ischemic cerebral blood vessels (eg, 61% inhibition with 2 mg/kg APC). Intracerebral bleeding was not observed with APC. Conclusions —APC exerts anti-inflammatory, antithrombotic, and neuroprotective effects in stroke. Central effects of APC are likely to be related to improved maintenance of the blood-brain barrier to neutrophils and to reduced microvascular obstructions and fibrin deposition.
Flame Retardants in Placenta and Breast Milk and Cryptorchidism in Newborn Boys
Authors: Katharina Maria Main, Hannu Kiviranta, Helena Eeva Virtanen, Erno Sundqvist, Jouni Tapio Tuomisto, Jouko Tuomisto, Terttu Vartiainen, Niels Erik Skakkebæk, Jorma Toppari
Journal: Environmental Health Perspectives (2007)

Polybrominated diphenyl ethers (PBDEs) are widely used in Western countries.Because the prevalence of cryptorchidism appears to be increasing, we investigated whether exposure to PBDEs was associated with testicular maldescent.In a prospective Danish-Finnish study, 1997-2001, all boys were examined for cryptorchidism. We analyzed whole placentas (for 95 cryptorchid/185 healthy boys) and individual breast milk samples (62/68) for 14 PBDEs and infant serum samples for gonadotropins, sex-hormone binding globulin, testosterone, and inhibin B.In 86 placenta-milk pairs, placenta PBDE concentrations in fat were lower than in breast milk, and a larger number of congeners were nondetectable. There was no significant difference between boys with and without cryptorchidism for individual congeners, the sum of 5 most prevalent, or all 14 congeners. The concentration of PBDEs in breast milk was significantly higher in boys with cryptorchidism than in controls (sum of BDEs 47, 153, 99, 100, 28, 66, and 154: median, 4.16 vs. 3.16 ng/g fat; p < 0.007). There was a positive correlation between the sum of PBDEs and serum luteinizing hormone (p < 0.033). The sum of PBDEs in breast milk did not differ between Denmark and Finland (median, 3.52 vs. 3.44 ng/g fat), but significant differences in some individual congeners were found.Two different proxies were used for prenatal PBDE exposure, and levels in breast milk, but not in placenta, showed an association with congenital cryptorchidism. Other environmental factors may contribute to cryptorchidism. Our observations are of concern because human exposure to PBDEs is high in some geographic areas.
Nitric Oxide Regulates Monocyte Chemotactic Protein-1
Authors: Philip S. Tsao, Bing-yin Wang, Ricardo Buitrago, John Y.-J. Shyy, John P. Cooke
Journal: Circulation (1997)

Monocyte chemotactic protein-1 (MCP-1) is a 76-amino-acid chemokine thought to be the major chemotactic factor for monocytes. We and others have demonstrated that NO inhibits monocyte-endothelial cell interactions and atherogenesis. We hypothesize that the antiatherogenic effect of NO may be due in part to its inhibition of MCP-1 expression.Smooth muscle cells (SMCs) were isolated from normal rabbit aortas by the explant method. Cells were then exposed to LPS (10 microg/mL), native LDL, or oxidized LDL (30 microg/mL) for 6 hours. The expression of MCP-1 in SMCs and chemotactic activity in the conditioned medium were induced by lipopolysaccharide (LPS) or by oxidized LDL but not native LDL. The induction of MCP-1 by cytokines or oxidized lipoproteins was associated with an increased generation of superoxide anion by the SMCs and increased activity of the transcriptional protein nuclear factor-kappaB (NFkappaB). The induced expression of MCP-1 and activation of NFkappaB were reduced by previous exposure of the SMCs to the NO donor DETA-NONOate (100 micromol/L) (P<.05). To determine whether NO exerted its effect at a transcriptional level, SMCs and COS cells were transfected with a 400-bp fragment of the MCP-1 promoter. Promoter activity was enhanced by oxidized LDL, and LPS was inhibited by DETA-NO. Nuclear run-on assays confirmed that the effect of NO occurred at a transcriptional level. To investigate the role of endogenous NO in the regulation of MCP-1 in vivo, New Zealand White rabbits were fed normal chow, normal chow plus nitro-L-arginine (LNA), high-cholesterol diet (Chol), or high-cholesterol diet supplemented with L-arginine (Arg). After 2 weeks, thoracic aortas were harvested and total RNA was isolated. Northern analysis using full-length MCP-1 cDNA demonstrated increased expression in Chol and LNA aortas; this expression was decreased in aortas from Arg animals.These studies indicate that the antiatherogenic effect of NO may be mediated in part by its inhibition of MCP-1 expression.
Effect of bile acid on anorectal function in man.
Authors: C A Edwards, S Brown, A J Baxter, J J Bannister, N W Read
Journal: Gut (1989)

The effects of rectal infusions (500 ml) of deoxycholic acid (1 mmol/l, 3 mmol/l) or normal saline on basal anorectal motility and responses to rectal distension were studied in 11 normal volunteers. Deoxycholic acid (1 mmol/l) did not alter anorectal motor patterns under basal conditions but reduced the rectal volumes required to induce a desire to defecate (deoxycholic acid 76 (12) ml v saline 123 (12) ml; mean (SEM) p less than 0.01), and to produce anal relaxation (deoxycholic acid 83 (14) ml v saline 152 (24) ml; p less than 0.05) and perception of the rectal balloon (deoxycholic acid 56 (10) ml v saline 104 (17) ml; p less than 0.01) that were sustained for the period of distension (1 min). Seven of 10 subjects could not tolerate an infusion of 3 mmol/l deoxycholic acid. Between two and 30 minutes after the start of the infusion they experienced an extreme urge to defecate which was associated with large amplitude pressure waves in the rectal channels (amplitude 30 (5) mmHg, duration 0.7 (0.1) min, frequency 1.7 (0.4)/min). Such contractions were never seen during saline infusion. Thus, rectal infusion of deoxycholic acid at physiological concentrations increases the sensitivity of the rectum to distension, and promotes an urgent desire to defecate in normal subjects.
Toward a Molecular Understanding of Congenital Heart Disease
Authors: R. Mark Payne, Mark C. Johnson, James W. Grant, Arnold W. Strauss
Journal: Circulation (1995)

Background This review discusses the incidence and importance of congenital heart disease (CHD), the reasons that investigation of causative mechanisms for human CHD has been slow, and the limitations of the multifactorial theory for the etiology of CHD. Methods and Results The molecular defects underlying three vasculopathies—Marfan’s syndrome (fibrillin), supravalvar aortic stenosis, and Williams’ syndrome (elastin)—and hereditary telangiectasia are presented to emphasize the role of microfibrils and extracellular matrix in the pathophysiology of these vascular defects. Animal models of CHD, including situs inversus, canine conotruncal malformations, and chick neural crest ablation, are examined to emphasize how such studies relate to human CHD, especially by pointing to single-gene defects for conotruncal malformations, candidate loci for situs inversus, and phenotypic variability caused by neural crest lesions. The crucial role of cardiac transcription factors in heart morphogenesis is emphasized by review of gene knockout studies of these factors, which cause fetal death secondary to heart maldevelopment. Several lines of evidence demonstrating genetic etiologies of human CHD are also presented, including the mapping of familial atrial septal defects, to prove that one anatomic type of CHD may be due to single-gene defects at different loci. Review of atrioventricular canal, both secondary to trisomy 21 and as an autosomal-dominant familial defect, reiterates this conclusion. The evidence that monosomy on chromosome 22 causes multiple types of CHD, including aortic arch and conotruncal defects as part of the CATCH-22 syndrome, is presented, with results supporting the idea that deletions at this site alone may cause 5% of surgically treated CHD. Conclusions We conclude that (1) human CHD is frequently due to single-gene defects and that even sporadic defects may arise from a single-gene abnormality; (2) a common genetic defect may cause several apparently different forms of CHD; (3) elucidation of the genetic basis of CHD provides clues to normal cardiovascular developmental biology; (4) the same cardiac malformation can be caused by mutant genes at different loci; and (5) interactions of clinical investigators (cardiologists and cardiothoracic surgeons) with basic scientists should allow more rapid progress in defining the genetic basis of CHD.
Medical Technology Policies and Computed Tomography
Authors: HARVEY V. FINEBERG
Journal: Annals of Internal Medicine (1979)

Editorials1 January 1979Medical Technology Policies and Computed TomographyHARVEY V. FINEBERG, M.D.HARVEY V. FINEBERG, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-90-1-114 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptComputed tomography (CT) has been a cause célèbre in the American health care community since it was introduced into the United States in 1973. The CT scanner was then a dramatically new and expensive imaging device. Like a seed crystal dropped into a supersaturated solution, it became the focus of a rapidly expanding controversy over the value and cost of new medical technology.In August 1978, the Office of Technology Assessment (OTA) of the Congress of the United States published its report on the policy implications of computed tomography (1). This wide-ranging and well-organized document describes the principles of computed...References1. : Policy Implications of the Computed Tomography (CT) Scanner. Washington, D.C.; U.S. Government Printing Office, August 1978. Google Scholar2. : Assessing the Efficacy and Safety of Medical Technologies. Washington, D.C.; U.S. Government Printing Office, September 1978. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: HARVEY V. FINEBERG, M.D.Affiliations: Center for the Analysis of Health Practices Harvard School of Public Health Boston, Massachusetts PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byReferences 1 January 1979Volume 90, Issue 1Page: 114-115KeywordsComputed axial tomographyHealth careHealth care policyPrevention, policy, and public health ePublished: 1 December 2008 Issue Published: 1 January 1979 Copyright & Permissions© 1979 American College of PhysiciansPDF downloadLoading ...
Abstract 3405: Caveolin-1 modulates the metastatic ability of Ewing's sarcoma
Authors: Miguel Sainz-Jaspeado, Laura Lagares-Tena, Jaime Lasheras, Fariba Navid, Carlos Rodriguez-Galindo, Silvia Mateo-Lozano, Vicente Notario, Xavier Sanjuan, Xavier Garcia del Muro, Angels Fabra, Oscar M. Tirado
Journal: Cancer Research (2010)

Abstract Metastasis is the final stage of tumor progression and is thought to be responsible for up to 90% of deaths associated with solid tumors. Caveolin-1 (CAV1) regulates multiple cancer-associated processes including cellular transformation, tumor growth, cell death and survival, multidrug resistance, angiogenesis, cell migration and metastasis. Although CAV1 was previously identified as a metastasis-associated gene that is a transcriptional target of EWS/FLI1 as well as an important determinant of Ewing's sarcoma family of tumors (ESFT) malignant phenotype, the possible involvement of CAV1 in regulating the ability of ESFT to metastasize has not been established. Therefore, in the present study we tested the hypothesis that CAV1 modulates the metastatic ability of ESFT cells. First, we analyzed the expression of CAV1 by immunostaining a tissue microarray (TMA) containing 43 paraffin-embedded ESFT tumors with known EWS translocations. Even though no evidence was found for a significant association between CAV1 expression with stage, size or tumor site, all metastatic samples (10/10) had significantly high CAV1 expression, suggesting that high CAV1 content makes it easier for ESFT cells to metastasize. To determine the effect of CAV1 on the migratory and invasive capabilities of ESFT cells, we knocked down CAV1 expression in TC252 and A673 cells by stably transfecting a previously validated shRNA construct. In vitro, wound healing and transwell migration and invasion assays showed that, in both cell lines. CAV1 knocked-down cells migrated significantly less (p≤0.01) than parental and vector-transfected control cells. Moreover, control transfected A673 cells introduced into balb/c nude mice by tail vein injection strongly colonized the lungs. In contrast, about 40% of animals injected with low CAV1 cells had no incidence of metastasis to any organ, and the other 60% suffered a significant delay in lung colonization (P=0.0005). These data demonstrate that CAV1 plays a key role in regulating the ability of ESFT cells to metastasize. Ongoing experiments are designed to elucidate the CAV1-regulated signalling pathways responsible for the development of ESFT metastases. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3405.
Prognostic Factors for Children With Hodgkin’s Disease Treated With Combined-Modality Therapy
Authors: Ron S. Smith, Qing Chen, Melissa M. Hudson, Michael P. Link, Larry Kun, Howard Weinstein, Amy Billett, Karen J. Marcus, Nancy J. Tarbell, Sarah S. Donaldson
Journal: Journal of Clinical Oncology (2003)

Evaluation of pretreatment factors to identify children at high risk for relapse after combined-modality therapy for Hodgkin's disease.From 1990 to 2000, 328 pediatric patients with clinical stage I to IV Hodgkin's disease were treated with chemotherapy and low-dose involved-field radiotherapy on prospective, collaborative, risk-adapted protocols at three institutions. Pretreatment factors were analyzed by univariate and multivariate analysis for prognostic significance for 5-year disease-free survival (DFS) and overall survival (OS).With a median follow-up of 59 months (range, 8 to 125 months), the 5-year DFS and OS for all patients were 83% and 93%, respectively. Several factors were associated with inferior DFS and OS by univariate analysis. By multivariate analysis, male sex; stage IIB, IIIB, or IV disease; bulky mediastinal disease; WBC more than 13.5 x 10(3)/mm3; and hemoglobin less than 11.0 g/dL were significant for inferior DFS. A prognostic index was developed incorporating the five significant factors from the multivariate analysis, assigning each a score of 1. The 5-year DFS and OS for children with a prognostic score of 0 to 1 were 94% and 99%; score 2, 85% and 96%; score 3, 71% and 92%; and score 4 or 5, 49% and 72%, respectively. There was a significant difference in DFS among each of these groups, with significantly worse OS in those with a score of 4 to 5.A prognostic index that was based on five pretreatment factors correlated with inferior DFS by multivariate analysis stratified patients by outcome; this may be useful in assigning children with Hodgkin's disease to risk-adapted therapy.
Preliminary Observations of the Effects on Breast Adenocarcinoma of Plasma Perfused over Immobilized Protein A
Authors: David S. Terman, James B. Young, William T. Shearer, Carlos Ayus, Daniel Lehane, Carlos Mattioli, Rafael Espada, Jimmy F. Howell, Tsuyoshi Yamamoto, Henry I. Zaleski, Lisa Miller, Peter Frommer, Louis Feldman, Joseph F. Henry, Richard Tillquist, Gary Cook, Yerach Daskal
Journal: New England Journal of Medicine (1981)

PROTEIN A, a constituent of the cell wall of Staphylococcus aureus Cowans 1 (SpA), reacts with the Fc region of immunoglobulins from many mammalian species and combines with immune complexes in serum.1 2 3 4 Previously, tumoricidal effects were observed in a patient with cancer of the colon after administration of autologous plasma that had been circulated over immobilized SpA.5 This approach was extended to dogs with spontaneous breast adenocarcinoma, and rapid and extensive tumor necrolytic reactions were noted after plasma perfusion over SpA but not over protein A-deficient staphylococcus.6 , 7 These findings were confirmed in an independent study.8 Similar tumor necrolytic responses were . . .