tbuckley/cabot-search huggingface dataset:
Late deaths and survival after childhood cancer: implications for cure
Authors: C M Robertson, M M Hawkins, J E Kingston
Journal: BMJ (1994)

<h3>Abstract</h3> <b>Objectives</b>: To investigate causes of death and survival in subjects who had survived at least five years after diagnosis of childhood cancer; to compare observed mortality with that expected in the general population; and to compare results with a corresponding cohort diagnosed earlier. <b>Design</b> : Retrospective cohort study. <b>Setting</b> : Population based National Register of Childhood Tumours. <b>Subjects</b> : 9080 five year survivors of childhood cancer diagnosed in Britain during 1971-85, of whom 793 had died. Comparison with corresponding cohort diagnosed during 1940-70. <b>Main outcome measures</b> : Cause of death established from all available sources of information (including hospital and general practitioner records and postmortem reports) and underlying cause of death coded on death certificate. <b>Results</b> : Of the 781 deaths for which sufficient information was available, death was attributed to recurrent tumour in 578 (74%) cases, treatment related effect in 121 (15%), second primary tumour in 52 (7%), and other causes in 30 (4%). Comparison of observed mortality with that expected in the general population indicated a fourfold excess of deaths from non-neoplasic causes. The risk of dying of recurrent tumour in the next 10 years after surviving five years from diagnosis during 1940-70 and 1971-85 fell from 12% to 8%. The risk of dying from a treatment related effect increased slightly from 1% to 2%. <b>Conclusion</b> : Improvements in five year survival after childhood cancer have been accompanied by a reduction in risk of dying from recurrent tumour during the subsequent 10 years and by a slight increase in risk of dying from treatment related effects. The results provide information relevant to decisions concerning balance between effective treatments and their potentially harmful effects.
A BILATERAL HERPES ZOSTER
Authors: HENRY ROCKWELL VARNEY
Journal: JAMA (1910)

The unusual rarity of recorded cases of bilateral zoster makes them worth reporting; though such cases are scattered throughout the literature, they have been very infrequent when compared with the number of cases of the unilateral variety. The relative proportion will never be known, as the ordinary "shingles" is too common to be reported or recorded, in that a large percentage is seen by the general practitioner or not at all. The grandmother, as in ringworm and boils, often makes the diagnosis, and says that if the lesions do not girdle t[ill] patient he will recover; if they girdle or meet he will die. The cases of bilateral zoster reported by observers from different parts of the world are, without doubt, only a small percentage of the number that really occur, as many cases are not reported and probably are not diagnosed properly. While bilateral zoster is generally supposed by
A Short History of Clinical Pathology
Authors: John H. Raach
Journal: JAMA (1962)

This very short book is the result of some painstaking and laborious research into the development of clinical pathology. The chapters are composed of short biographical sketches of the men who were influential in the techniques and phases of clinical pathology as we know them today. While this book deals primarily with the English contribution to the field, it does serve as a useful reference point for those interested in the development of this Cinderella of medicine. There is an interesting final chapter on the organization of the International Society of Clinical Pathologists.
Allergen stimulates bone marrow CD34<sup>+</sup> cells to release IL‐5 <i>in vitro</i>; a mechanism involved in eosinophilic inflammation?
Authors: A.‐K. Johansson, M. Sjöstrand, M. Tomaki, A.‐M. Samulesson, J. Lötvall
Journal: Allergy (2004)

The specific mechanisms that alter bone marrow (BM) eosinophilopoiesis in allergen‐induced inflammation are poorly understood. The aims of this study were to evaluate (a) whether the number of BM CD34 + cells is altered due to allergen sensitization and exposure in vivo and (b) whether BM CD34 + cells produce and release interleukin (IL)‐5, IL‐3 and granulocyte macrophage‐colony stimulating factor (GM‐CSF) after stimulation in vitro . A mouse model of ovalbumin (OVA)‐induced airway inflammation was used. Bone marrow CD34 + cells were cultured in vitro and the cytokine release was measured by enzyme‐linked immunosorbent assay. The IL‐5‐production from CD34 + cells was confirmed by immunocytochemistry. Airway allergen exposure increased the number of BM CD34 + cells ( P = 0.01). Bone marrow CD34 + cells produced IL‐5 when stimulated with the allergen OVA in vitro , but not IL‐3 or GM‐CSF. Nonspecific stimulus with calcium ionophore and phorbol‐myristate‐acetate of BM CD34 + cells caused release of IL‐5, IL‐3 and GM‐CSF. The induced release of IL‐5 was increased in alum‐injected vs naive mice ( P = 0.02), but was not affected by allergen sensitization and exposure. The release of IL‐3 and GM‐CSF was increased after allergen sensitization and exposure ( P &lt; 0.02). In conclusion, allergen can stimulate BM CD34 + cells to produce IL‐5 protein. It is likely that the CD34 + cells have autocrine functions and thereby regulate the early stages of BM eosinophilopoiesis induced by airway allergen exposure. Alum, a commonly used adjuvant, enhances the release of IL‐5 and may thereby enhance eosinophilopoiesis.
Changes in the Postdoctoral Education of Internists?
Authors: LAWRENCE E. YOUNG
Journal: Annals of Internal Medicine (1975)

Editorials1 November 1975Changes in the Postdoctoral Education of Internists?LAWRENCE E. YOUNG, M.D., M.A.C.P.LAWRENCE E. YOUNG, M.D., M.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-83-5-728 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptIf the internist is to serve as personal physician for adults, providing both primary and secondary care by current definitions, what are his educational needs? My answers focus on the first three or four postdoctoral years, but many of the principles underlying them apply to the earlier years of medical education as well as to the initial preparation of the medical subspecialist.Care of Ambulatory PatientsA major need for change in the education of internists is in the provision of adequate experience with ambulant patients in settings in which ready access to comprehensive care is assured. Continuity of contact...References1. BERRY M: Internal medicine, 1973, in The Third Trimester. Kansas City, Missouri, Maxwell G. Berry, 1973, p. 72 Google Scholar2. YOUNG L: The broadly based internist as the backbone of medical practice, in Controversy in Internal Medicine II, edited by INGELFINGER FJ, EBERT RV, FINLAND M, et al. Philadelphia, W. B. Saunders Co., 1974, pp. 15-63 Google Scholar3. ENGEL G: The best and the brightest. The missing dimension in medical education. Pharos 36:129-133, 1973 Google Scholar4. ATCHLEY D: Science and medical education. JAMA 164:541-544, 1957 CrossrefMedlineGoogle Scholar5. GRAVES R: A System of Clinical Medicine, Introductory Lecture, Session 1837-38. Dublin, Fannin and Co., 1843, pp. 22-41 Google Scholar6. OSLER W: After twenty-five years, in Aequanimitas. Philadelphia, P. Blakiston, 1932, p. 210 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: The University of Rochester Associated Hospitals Program in Internal Medicine Rochester, New York PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByThe Need for a New Medical Model: A Challenge for BiomedicineCurrent successes in medical education beyond the bedsideThe Need for a New Medical Model: A Challenge for BiomedicineDevelopment of an academic section of general internal medicineThe Book of Job and the Modern View of DepressionMORTON ALLAN KAPUSTA, M.D., F.R.C.P.(C), F.A.C.P., SOLOMON FRANK, M.A., Ph.D., LL.B.The Need for a New Medical Model: A Challenge for BiomedicineThe general internist an academic viewpointPrimary medical care and training programs in general internal medicineInternal Medicine 1976: Consequences of Subspecialization and TechnologyROBERT G. PETERSDORF, M.D., F.A.C.P. 1 November 1975Volume 83, Issue 5Page: 728-730KeywordsMedical educationSub-specialty care Issue Published: 1 November 1975 PDF DownloadLoading ...
Carcinoma in Situ of the Uterine Cervix: A Study of 235 Cases from the Free Hospital for Women
Authors: M. Edward Davis
Journal: JAMA (1961)

The authors present a comprehensive story of carcinoma in situ. The case histories were presented previously in two published reports in 1949 and 1951. In that this is a retrospective study, it was not possible to obtain new pathologic material, although new and serial sections were cut from existing blocks and old tissue was reblocked. A diagnosis of carcinoma in situ was made in 127 of the 235 patients in the series, and the tumors were classified as carcinoma in situ with (1) surface involvement, (2) glandular involvement, and (3) stromal invasion. These lesions are described in great detail and illustrated in numerous excellent photographs. Short abstracts of typical histories are presented. A diagram illustrates the interrelationships of the various benign and malignant prickle cell hyperplasias. The clinical findings concerning age, symptoms, appearance of cervix, location of lesion, results of Schiller tests, findings on colposcopy, marital history, racial incidence, and
Insulin as a Vascular and Sympathoexcitatory Hormone
Authors: Urs Scherrer, Claudio Sartori
Journal: Circulation (1997)

Abstract The past several years have witnessed a major surge of interest in the cardiovascular actions of insulin. This interest has stemmed on the one hand from epidemiological studies that demonstrated an association between obesity, insulin resistance, and hypertension, leading to the so-called insulin hypothesis of hypertension. On the other hand, this interest has been stimulated by experimental evidence suggesting that the vascular actions of insulin may play a role in its main action, namely the promotion of glucose uptake in skeletal muscle tissue. Two tenets have emerged about how insulin may exert its cardiovascular actions. First, it is now firmly established that acute insulin administration stimulates sympathetic nerve activity in both animals and humans. Second, there is increasing evidence that insulin stimulates muscle blood flow, an effect that appears to be mediated at least in part by an endothelium-dependent mechanism. This review summarizes the current understanding and gaps in knowledge on cardiovascular actions of insulin in humans and pathophysiological consequences of derangements of such actions.
EXERCISE TRAINING REVERSES DYSFUNCTION OF EARLY ENDOTHELIAL PROGENITOR CELLS IN PATIENTS WITH CHRONIC HEART FAILURE.
Authors: Emeline M. Van Craenenbroeck, Paul Beckers, Nadine Possemiers, Kurt Wuyts, Vicky Hoymans, Geert Frederix, Christiaan Vrints, Viviane Conraads
Journal: Journal of the American College of Cardiology (2010)
PLATINUM NEEDLES FOR ELECTROLYSIS.Read before the Section of Surgery and Anatomy, at the Forty-second Annual Meeting of the American Medical Association, held at Washington, D. C., May, 1891.
Authors: ROBERT NEWMAN
Journal: JAMA (1891)

It is at present difficult to procure a small sized platinum needle, which is in every respect satisfactory to the operator. The needles on the market are deficient: for instance, the insulation is rough, uneven, and not smooth on an equal plane from the non-insulated point, to and over the beginning of the insulation, the point is too dull, and will not readily pass through cuticle and fascia; the non-insulated part is weak, and breaks off easily; the shaft, or the whole needle is not stiff enough to be easily pushed into the tissues, and on any attempt at use will bend. The shape of the point is also objectionable, and makes a hole at the point of entrance, instead of cutting evenly and pushing through the tissues more by dilatation, than in such a manner, so that on withdrawal of the needle the point of entrance contracts again, without
Evidence for a role of iron-catalyzed oxidants in functional and metabolic stunning in the canine heart.
Authors: N E Farber, G M Vercellotti, H S Jacob, G M Pieper, G J Gross
Journal: Circulation Research (1988)

Brief (15-minute) coronary occlusion and subsequent reperfusion lead to prolonged functional and metabolic abnormalities (stunned myocardium). Previous work suggests that one factor responsible for this phenomenon is oxygen-derived free radicals. The formation of the highly reactive hydroxyl radical requires the presence of metal ions, most importantly iron. In the present study, the effect of the iron-chelator deferoxamine on the recovery of segment shortening (%SS) in the stunned myocardium was compared with a control group in barbital anesthetized dogs. Deferoxamine (500 mg intra-atrially) was administered 15 minutes prior to and throughout 15 minutes of coronary occlusion. %SS, regional myocardial blood flow, hemodynamics, and myocardial high-energy phosphates were measured. Areas at risk, collateral blood flow, and all hemodynamic parameters were similar between control and deferoxamine-treated animals. While deferoxamine did not prevent the loss of systolic wall function that occurred during ischemia, deferoxamine significantly improved the recovery of %SS at all times throughout reperfusion (3-hour %SS of pretreatment: control, 12 +/- 11; deferoxamine, 65 +/- 12), normalized endocardial ATP (percent of nonischemic area: control, 79 +/- 3%, deferoxamine, 93 +/- 6%), attenuated the reperfusion-induced rebound increase in phosphocreatine and prevented the increase in tissue edema at 3 hours after reperfusion. Thus, deferoxamine exhibited a cardioprotective action both metabolically and functionally in the stunned myocardium presumably by decreasing the redox cycling, and hence, the availability of catalytic iron for use in hydroxyl radical formation and for the initiation of lipid peroxidation. These data suggest a possible role for the hydroxyl radical as a mediator of postischemic abnormalities in reversibly injured tissue.
Phenotypic and functional activation of alveolar macrophages, T lymphocytes and NK cells in patients with systemic sclerosis and primary Sjogren's syndrome.
Authors: B Gudbjornsson, R Hallgren, O Nettelbladt, R Gustafsson, A Mattsson, E af Geijerstam, T H Totterman
Journal: Annals of the Rheumatic Diseases (1994)

OBJECTIVES--Attempts to differentiate between the pathogenesis of the severe pulmonary manifestations observed in systemic sclerosis (SSc) and the mild form in primary Sjögren9s syndrome (pSS) were performed by studying cell populations recovered during bronchoalveolar lavage (BAL). METHODS AND RESULTS--Two-colour flow cytometric analysis of BAL fluid lymphocytes showed a similar degree of phenotypic activation (DR+) of CD4+ and CD8+ T lymphocyte subsets and CD16+ NK cells in patients with SSc (n = 13) and pSS (n = 11) groups and healthy controls (n = 11). Alveolar macrophages expressed the CD14 antigen at significantly increased densities in patients with SSc. Alveolar macrophage activation in SSc was also suggested by increased IL-6 concentrations in neat BAL fluid and increases in macrophage production of TNF alpha and EGF in vitro. SSc patients also had increased proportions of neutrophils and eosinophils in BAL fluid. No correlations were found between any cellular subsets or cytokine levels in BAL fluid and lung status at the time of lavage in SSc or pSS patients or the subsequent course of the pulmonary function in SSc patients. CONCLUSION--It is concluded that the phenotypical activation of alveolar helper/inducer (DR+CD4+) and suppressor/cytotoxic (DR+CD8+) T lymphocytes and NK (DR+CD16+) cells is not a prerequisite for the development of lung fibrosis in SSc or bronchial hyper-responsiveness in pSS. Alveolar macrophage activation may contribute to the development of lung fibrosis in SSc.
An analysis of the autonomic control of gastrointestinal motility in the cat.
Authors: J Neely, B N Catchpole
Journal: Gut (1967)

EDITORIAL COMMENT These observations in the cat show that the stomach has a high level of extrinsic, and a low level of intrinsic, cholinergic control, but this is reversed in the small intestine.Similar studies are clearly needed in man to provide us with logical tests for the management of motility disorders.
Increasing coronary perfusion pressure on diastolic and systolic performance is less pronounced in right ventricle than in left ventricle
Authors: A. Fukui, S. Yamaguchi, Y. Tamada, H. Miyawaki, M. Shirakabe, G. Baniya, H. Tomoike
Journal: Cardiovascular Research (1996)

Objective: Little is known as to whether an increase in coronary perfusion pressure can alter the right ventricular (RV) distensibility and the contractile function as it does in the case of the LV. Methods: In eight isolated isovolumically contracting canine hearts, RV and LV volumes and coronary perfusion were independently controlled. Effects of an increase in coronary perfusion pressure (from 73 ± 1 to 152 ± 6 mmHg) on the end-diastolic and end-systolic pressure-volume relations in both RV and LV were assessed. Results: Following an increase in coronary perfusion, and at a similar volume of the ventricles, end-diastolic pressure was elevated by 2.8 ± 0.8 mmHg in RV and 8.9 ± 2.0 mmHg in LV (P < 0.01; RV vs LV), and the slope of RV end-systolic pressure-volume relation, Ees, increased by 11 ± 6% (P < 0.05) and that of the LV Ees by 21 ± 5% (P < 0.01). The percent change of RV pressure-volume area (PVA) was less than that in LV-PVA (26 ± 9 vs 48 ± 11%; P < 0.05). Conclusions: Accordingly, increases in coronary perfusion pressure and/or flow decreased the RV distensibility and enhanced the RV contractile function, the extent of which, however, was less than that in the LV.
Prognostic Value of Multidetector Coronary Computed Tomography Angiography in Relation to Exercise Electrocardiogram in Patients With Suspected Coronary Artery Disease
Authors: Iksung Cho, Jaemin Shim, Hyuk-Jae Chang, Ji Min Sung, Youngtaek Hong, Hackjoon Shim, Young Jin Kim, Byoung Wook Choi, James K. Min, Ji-Ye Kim, Chi-Young Shim, Geu-Ru Hong, Namsik Chung
Journal: Journal of the American College of Cardiology (2012)
Hypertrophic osteoarthropathy: four early reports by British authors (1889-97).
Authors: L Doyle
Journal: Thorax (1987)

This paper draws attention to the substantial contribution made by British authors to the early reports on hypertrophic osteoarthropathy, or osteo-arthro- pathy as it was written in the period under review.A short account of the original papers by Marie and Bamberger is followed by discussion of four reports of special interest.In 1886 Revue de Medecine published Pierre Marie's classic memoire "Sur deux cas d'acrom6galie."1In addition to his two cases, he included an abridged description of five other cases in the literature which he considered to be of the same nature as his own two cases (acromegaly).Four years later (1890) the same journal published another classic metmoire: "De l'osteo-arthropathie hyper- trophiante pneumique."2In his introduction he wrote: "Je desire d'abord debarrasser le champ de l'acromegalie de faits qui l'encombraient en pure perte puisqu'ils ne lui appartiennent pas, et qui ris- quaient ainsi de creer une confusion regrettable ... Later he gave an account of one case of hypertrophic osteoarthropathy associated with chronic intra- thoracic sepsis and, as previously, he added abridgments of four similar case histories, two from his 1886 article and two that had been reported sepa- rately in Britain.Clearly, by 1890 Marie had appre- ciated the cardinal points in the history and clinical findings whereby acromegaly and hypertrophic osteoarthropathy might be differentiated.Bamberger (1889) in a short report described bone changes asso- ciated with bronchiectasis3 and two years later (1891) reported in full a series of cases with similar changes.4The first report of hypertrophic osteoarthropathy in Britain was by Saundby from the General Hospi- tal, Birmingham.'The report, entitled "A case of acromegaly," was
P479Extracellular S100A4 induces arterial smooth muscle cell activation in a RAGE-dependent manner
Authors: C Chaabane, CW Heizmann, ML Bochaton-Piallat
Journal: Cardiovascular Research (2014)

Background: It has been proposed that smooth muscle cells (SMCs) from the arterial wall are heterogeneous and that only a subset of medial SMCs are prone to accumulate into the intima leading to atheromatous plaque formation. We isolated 2 distinct SMC phenotypes from porcine coronary artery: spindle-shaped (S) and rhomboid (R). Biological features of R-SMCs (i.e. enhanced proliferative and migratory activities as well as poor level of differentiation) explain their capacity to accumulate into the intima. We identified S100A4 as being a marker of the R-SMCs in vitro and of intimal SMCs, both in pig and human. S100A4 is a Ca2+-binding protein that can also be secreted; it has extracellular functions probably via the receptor for advanced glycation end products (RAGE). Purpose: Explore the role of S100A4 in SMC phenotypic change, a phenomenon characteristic of atherosclerotic plaque formation. Methods and Results: Transfection of a human S100A4-containing plasmid in spindle-shaped (S) SMCs (devoid of S100A4) led to approximately 10% of S100A4-overexpressing SMCs, S100A4 release, and a transition towards a R-phenotype of the whole SMC population. Furthermore treatment of S-SMCs with S100A4-rich conditioned medium collected from S100A4-transfected S-SMCs induced a transition towards a phenotype typical of the R-SMCs, which was associated with decreased SMC differentiation markers, increased proliferation and migration, as well as induced proteolytic activity through activation of urokinase-type plasminogen activator (uPA), matrix metalloproteinases (MMP-1,-2, -3, and -9) and their inhibitors (TIMP-1). Furthermore, extracellular S100A4 yielded activation of NF-kB in a RAGE-dependent manner. Blockade of extracellular S100A4 in R-SMCs with S100A4 neutralizing antibody induced a transition from R- to S-phenotype, decreased proliferative activity and upregulation of SMC differentiation markers. In contrast, silencing of S100A4 mRNA in R-SMCs did not change the level of extracellular S100A4 nor SMC morphology in spite of decreased proliferative activity. Conclusions: Our results indicate that SMC phenotypic changes are essentially dependent on extracellular S100A4 activity. It could be a new target to prevent SMC accumulation during atherosclerosis and restenosis.