ABSTRACT
The British Journal of Hospital Medicine is 50 years old. This article takes a look back at articles published during the year of its inception from the British Medical Journal, the Lancet and the Journal of the American Medical Association.
Subject(s)
Periodicals as Topic/history , Abortion, Induced/history , Acetaminophen/history , Acetaminophen/toxicity , Adrenocortical Adenoma/history , Allopurinol/history , Allopurinol/therapeutic use , Analgesics/history , Analgesics/toxicity , Antineoplastic Agents/history , Antineoplastic Agents/therapeutic use , Attitude of Health Personnel , Attitude to Health , Bird Fancier's Lung/history , Celiac Disease/complications , Celiac Disease/history , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/history , Dermatitis Herpetiformis/complications , Dermatitis Herpetiformis/history , Drug Discovery/history , Gout/drug therapy , Gout/history , Gout Suppressants/history , Gout Suppressants/therapeutic use , Graft Rejection/history , Graft Rejection/immunology , Granulomatous Disease, Chronic/history , History, 20th Century , Humans , Medicare/history , Publishing/history , United Kingdom , United StatesABSTRACT
Bruton's XLA and DiGeorge syndrome patients show that two basic immune systems are distinct from each other in humans - thymus-dependent cell-mediated immunodeficiencies vs. antibody-based immunodeficiencies. The appendix-sacculus lymphoid organ of rabbits, like the bursa of Fabricius, represents a central lymphoid organ. Chronic granulomatous disease of childhood (CGD) revealed that phagocytosis killing of catalase-positive microorganisms employ oxidative burst. Bone marrow transplantation (BMT) proved life saving in severe combined immunodeficiency (SCID). The first BMT cured XSCID and the second BMT cured a complicating aplastic anemia launching BMT as a treatment of many diseases. Now 75 fatal diseases have been cured by myeloablative BMT. BMT also cured experimental autoimmune diseases. BMT alone did not cure lupus with polyarthritis in MRL/lpr mice or polyarthritis in NZB/KN mice, but BMT plus bone (stromal cell) transplants cured these diseases. Autoimmune diseases and lethal glomerulonephritis were prevented or cured in BXSB mice by mixed allogeneic plus syngeneic BMT. X-linked Hyper IgM syndrome (XHIM) was also cured by BMT from a 2-year-old MHC-matched sibling donor. Nonmyeloablative BMT plus mesenchymal stem cells (stromal cells) was effective treatment for a form of collagen-vascular disease and also a lethal form of hypophosphatasia. Mannan-binding lectin, an opsonin that activates the complement system when mutated and at low levels in blood, opens a door to frequent infections throughout childhood and adult life. This new immunodeficiency is based on genetic mutations that involve a native defense system.
Subject(s)
Immune System Diseases/history , Immunity, Cellular/immunology , Agammaglobulinemia/history , Agammaglobulinemia/immunology , Allergy and Immunology/history , Animals , Bone Marrow Transplantation/history , Bursa of Fabricius/growth & development , Bursa of Fabricius/immunology , Chickens , Cricetinae , DiGeorge Syndrome/history , DiGeorge Syndrome/immunology , Granulomatous Disease, Chronic/history , Granulomatous Disease, Chronic/immunology , History, 20th Century , Humans , Immune System Diseases/immunology , Mice , Rabbits , Thymoma/history , Thymoma/immunologySubject(s)
Immunologic Deficiency Syndromes/history , Agammaglobulinemia/genetics , Agammaglobulinemia/history , Animals , Complement System Proteins/deficiency , Complement System Proteins/genetics , Female , Genes, Recessive , Genetic Linkage , Granulomatous Disease, Chronic/history , History, 20th Century , Humans , Immunologic Deficiency Syndromes/genetics , Immunologic Deficiency Syndromes/immunology , Leukocyte-Adhesion Deficiency Syndrome/history , Male , X Chromosome/geneticsABSTRACT
Investigando-se como e quando a hanseníase foi introduzida no Brasil, verifica-se que a moléstia jamais foi descrita pelos navegadores ou pelos padres que vieram catequizar os silvícolas. Há inúmeros argumentos a favor da ausência da hanseníase entre os índios. Tem-se considerado o elemento europeu como uma das causas do aparecimento da hanseníase no país, introduzindo a doença provavelmente por diversos pontos da costa brasileira. Aqui, a moléstia deve ter trilhado a rota da colonizaçäo e transmitida pelo contágio. A introduçäo do elemento africano, sob o regime de escravidäo, segundo a maioria dos estudiosos, deve ter representado papel importante na origem da hanseníase no Brasil. Porém, alguns autores argumentam que nenhum comprador de escravos, quando se tratava do próprio interesse, haveria de aceitar em sua casa, lavoura ou engenho, um negro em que a doença se manifestasse. Há mais concordância entre os autores em atribuir a origem da hanseníase aos portugueses. Näo falta base histórica a esta afirmaçäo: enquanto a doença se extinguira no continente no século XVI, época da primeira colonizaçäo deste país, ela existia na Ilha da Madeira, nas Indias Portuguesas, nos Açores e nas possessöes marroquinas, de onde vinham os colonos, dentre os quais, certamente, muitos doentes de hanseníase
