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Contributors
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- By Jennifer Alvarez, Ananda B. Amstadter, Metin Başoğlu, David M. Benedek, Charles C. Benight, George A. Bonanno, Evelyn J. Bromet, Richard A. Bryant, Barbara Lopes Cardozo, M. L. Somchai Chakkraband, Claude Chemtob, Roman Cieslak, Lauren M. Conoscenti, Joan M. Cook, Judith Cukor, Carla Kmett Danielson, JoAnn Difede, Charles DiMaggio, Anja J.E. Dirkzwager, Cristiane S. Duarte, Jon D. Elhai, Diane L. Elmore, Yael L.E. Errera, Julian D. Ford, Carol S. Fullerton, Sandro Galea, Freya Goodhew, Neil Greenberg, Lindsay Greene, Linda Grievink, Michael J. Gruber, Sumati Gupta, Johan M. Havenaar, Alesia O. Hawkins, Clare Henn-Haase, Kimberly Eaton Hoagwood, Christina W. Hoven, Sabra S. Inslicht, Krzysztof Kaniasty, Ronald C. Kessler, Rachel Kimerling, Richard V. King, Rolf J. Kleber, Jessica Mass Levitt, Brett T. Litz, Maria Livanou, Katelyn P. Mack, Paula Madrid, Shira Maguen, Paul Maguire, Donald J. Mandell, Charles R. Marmar, Andrea R. Maxwell, Shannon E. McCaslin, Alexander C. McFarlane, Thomas J. Metzler, Summer Nelson, Yuval Neria, Elana Newman, Thomas C. Neylan, Fran H. Norris, Carol S. North, Lawrence A. Palinkas, Benjaporn Panyayong, Maria Petukhova, Betty Pfefferbaum, Marleen Radigan, Beverley Raphael, James Rodriguez, G. James Rubin, Kenneth J. Ruggiero, Ebru Şalcıoğlu, Nancy A. Sampson, Arieh Y. Shalev, Bruce Shapiro, Laura M. Stough, Prawate Tantipiwatanaskul, Warunee Thienkrua, Phebe Tucker, J. Blake Turner, Robert J. Ursano, Bellis van den Berg, Peter G. van der Velden, Frits van Griensven, Miranda Van Hooff, Edward Waldrep, Philip S. Wang, Simon Wessely, Leslie H. Wind, C. Joris Yzermans, Heidi M. Zinzow
- Edited by Yuval Neria, Columbia University, New York, Sandro Galea, University of Michigan, Ann Arbor, Fran H. Norris
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- Book:
- Mental Health and Disasters
- Published online:
- 07 May 2010
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- 20 July 2009, pp xi-xvi
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VI.15 - Food as Aphrodisiacs and Anaphrodisiacs?
- from Part VI - History, Nutrition, and Health
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio, Kriemhild Coneè Ornelas
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- Book:
- The Cambridge World History of Food
- Published online:
- 28 March 2008
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- 07 December 2000, pp 1523-1534
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Summary
According to the first edition of the Encyclopaedia Britannica (1771), aphrodisiacs are “medicines which increase the quantity of seed, and create an inclination for venery.” Since the twentieth-century advent of sexual endocrinology, the definition of an aphrodisiac has become restricted to “a substance which excites sexual desire” (Steadman’s Medical Dictionary, 25th edition, 1990).The search for aphrodisiacs is rooted in universal anxieties about sexual performance and fertility. In many instances since ancient times, a distinction has been made between substances that were alleged to improve fertility (quantity of seed) and those that only stimulate the sex drive (inclination to venery). Some authorities held that the latter could only be achieved by achieving the former.
The scope of this essay is limited geographically to Europe and the Near East and, so far as possible, to foods and their preparation. Adequate nourishment has always been recognized as a requirement for health and a normal level of sexual activity, although the norm for the latter undoubtedly varies somewhat among cultures.
In ancient medical practices, when and by what indications nutritive and medicinal qualities of foods were differentiated is uncertain. A rather clear distinction, however, was made by Heracleides of Tarentum, a Greek physician in the first century B.C. In writing about aphrodisiacs, he said that “bulbs, snails, eggs and the like are supposed to produce semen, not because they are filling, but because their very nature in the first instance has powers related in kind to semen” (Athenaeus 1951: 275).
VIII.31 - Cystic Fibrosis
- from Part VIII - Major Human Diseases Past and Present
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- Book:
- The Cambridge World History of Human Disease
- Published online:
- 28 March 2008
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- 29 January 1993, pp 657-658
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Summary
Cystic fibrosis, also called fibrocystic disease of the pancreas, and mucoviscidosis, is a genetically determined disease of infants, children, and young adults. Most of its many manifestations result from the abnormally viscous mucus, which interferes with pulmonary function, and the insufficient production of pancreatic digestive enzymes, which causes nutritional deficiencies and developmental retardation.
Etiology
Among Caucasians, cystic fibrosis (CF) is the most common fatal disease having an autosomal recessive inheritance. Despite the primary involvement of several organs, the disease is caused by a single defective gene that is located on chromosome 7 and is carried by about 4 percent of the Caucasian population. Its expression is similar in both sexes.
Clinical Manifestations
CF manifests itself at birth in about 8 percent of cases through mechanical obstruction of the small intestine by the secretion of abnormally viscous mucus (meconium ileus). Symptoms of insufficient secretion of exocrine (noninsulin) digestive enzymes by the pancreas appear during the first year of life in 90 percent of cases. The development of such symptoms indicates that pancreatic function is less than 10 percent of normal; and the more severe the deficiency of pancreatic enzymes, the more severe the fecal excretion of undigested fat, usually as diarrhea. As much as 80 percent of dietary fat may be lost, thus partially explaining malnutrition. Loss of undigested nutrients can be corrected only partially by treatment with pancreatic enzyme tablets. Pulmonary disease is responsible for most of the debility and mortality. Onset occurs in the first 2 years of life in at least 75 percent of cases, and by the age of 6 years in most of the remaining cases.
VIII.83 - Lupus Erythematosus
- from Part VIII - Major Human Diseases Past and Present
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- The Cambridge World History of Human Disease
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- 28 March 2008
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- 29 January 1993, pp 848-852
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Summary
Lupus erythematosus (LE) is a clinical syndrome that has multiple, but largely unknown causes. It exhibits an extremely broad spectrum of symptoms, and it can range in severity from being potentially fatal within a few weeks to eliciting minor indolent symptoms which, prior to immunologic testing, are virtually undiagnosable. When limited to the skin, it is called discoid lupus erythematosus (DLE); when the viscera are symptomatically affected, it is termed systemic lupus erythematosus (SLE). The inciting causes activate immunologic mechanisms that mediate the pathological, predominantly inflammatory, tissue responses.
History
Medical use of the term lupus has been traced to the fifteenth century, when it designated a variety of cancer. The term was reintroduced by London physician Robert Willan in 1808 to designate cutaneous tuberculosis, particularly when it affected the face. Cutaneous tuberculosis eventually received the synonym lupus vulgaris. In 1851 P. L. Alphée Cazenave of Paris used the term lupus erythemateaux to describe the condition that came to be called discoid lupus erythematosus (DLE) by Vienna’s Moriz Kaposi in 1872 (Jarcho 1957). During 1866–70, Kaposi diagnosed this disease in 22 patients and concluded that it was more common and more severe in women. All 3 deaths occurred among his 15 female patients. Although one of these had pulmonary tuberculosis, and cutaneous tuberculosis was common, Kaposi believed that DLE is not related to tuberculosis. Such a causal relationship, however, came to be advocated, particularly by French dermatologists, and remained under discussion until the 1930s. During the 5 years in which Kaposi saw 22 cases of DLE, 279 cases of lupus vulgaris were seen in the same department (Kaposi 1872).
II.6 - Concepts of Cancer
- from Part II - Changing Concepts of Health and Disease
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- The Cambridge World History of Human Disease
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- 28 March 2008
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- 29 January 1993, pp 102-110
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Summary
In past centuries people feared epidemic diseases with their sudden onset, ghastly symptoms, agonizing death for many, and sometimes disfigurement or physical impairment for survivors. Today, especially in the developed world (with a few notable exceptions), the dread of epidemic contagion seems almost as anachronistic as the burning of witches. It has been replaced by the dread of cancer. As with the epidemics of yesterday, the basic causes of cancer remain shrouded in mystery, while its effects in terms of human suffering are all too well known.
Cancer is a process whereby a loss of control of normal cell division and multiplication produces a tumor that can invade adjacent tissues and metastasize, that is, implant cancerous cells at a site that is noncontiguous to their origin, where abnormal multiplication continues. When cancer originates in connective tissues (mainly bone or muscle), it is called sarcoma; when it originates in epithelial tissues (lining tissues and organs such as the breast, lungs, or stomach), it is called carcinoma. The latter is by far more common. Invasive tumors occur in all complex species and probably antedate the advent of vertebrates. The oldest paleopathological evidence is limited to lesions that affected bones, such as those found in dinosaurs. Tumors have been found in Egyptian mummies dating from 2000 to 3000 b.c., and physicians of that ancient land knew of and treated patients for cancers of several sites.
VIII.93 - Muscular Dystrophy
- from Part VIII - Major Human Diseases Past and Present
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- Book:
- The Cambridge World History of Human Disease
- Published online:
- 28 March 2008
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- 29 January 1993, pp 890-891
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Summary
The muscular dystrophies are a group of genetically determined, almost exclusively pediatric diseases. Generally, the earlier the age at which symptoms begin, the poorer is the prognosis. Because of a considerable overlap of manifestations and rates of progression and, until recently, the lack of any biochemical test, their classification is still unsettled. As a group, the principal differential diagnosis of the muscular dystrophies is from the muscular atrophies. In the former, the primary defect is in the voluntary muscle fibers; in the latter, it is in the innervation of muscles.
Classification
The most common of the dystrophies and the first to be described was that delineated by Guillaume B. A. Duchenne, a French neurologist, in 1868. Duchenne muscular dystrophy (DMD) is a sex-linked recessive disorder. Consequently, it clinically affects only males and is inherited through female carriers of the gene. Although affected boys have abnormally elevated concentrations of muscle cell enzymes such as creatine phosphokinase in their blood, this abnormality is also found in about three-fourths of the asymptomatic female carriers. DMD appears to have a rather uniform incidence worldwide, with a mean incidence estimated to be about 1 case per 4,000 live male births, or 15 to 33 cases per 100,000. Most surveys have been of predominantly Caucasian populations, but the results of a study in Japan were consistent with the others. A family history of DMD can be obtained in only about one-third of cases. The others are attributed to either a previously unexpressed carrier state or to a new mutation.
VIII.117 - Rheumatic Fever and Rheumatic Heart Disease
- from Part VIII - Major Human Diseases Past and Present
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- Book:
- The Cambridge World History of Human Disease
- Published online:
- 28 March 2008
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- 29 January 1993, pp 970-977
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Summary
Acute rheumatic fever is a noncontagious disease characterized by febrile, nonsuppurative inflammation, primarily of articular and cardiac tissues, less frequently affecting the skin and brain. The cerebral manifestation – Sydenham’s chorea – and the superficial manifestations – subcutaneous nodules and erythema marginatum – are limited to children and young adults.
Etiology and Treatment
The disease is caused by infection, most often of the throat, with type A beta-hemolytic strains of streptococcus. Fever, migratory joint pains and tachycardia, the most frequent symptoms, typically begin 1 to 3 weeks after the onset of untreated streptococcal pharyngitis. However, only 0.1 to 3.0 percent of untreated bouts of this infection result in a first attack of rheumatic fever. Consequently, various largely unidentified permissive factors must participate in initiating the immunologic pathogenesis of the disease.
First attacks of acute rheumatic fever can be prevented by timely treatment of the streptococcal infection with penicillin or another appropriate antibiotic, but such treatment does not influence the course of the disease once it has begun. Rheumatic fever recurs only as a result of a new infection with a pathogenic strain of streptococcus. Prophylactic antibiotic treatment diminishes, but does not eradicate recurrences (Taranta et al. 1964). The shorter the interval since the previous bout of rheumatic fever, the greater is the likelihood that a new attack will be elicited. An infection that occurs within 2 years of an attack has a 20 to 25 percent chance of inducing a recurrence. If the first attack does not affect the heart, a recurrence usually spares it as well, but if the heart has been involved, a second bout it likely to result in greater damage (Spagnuolo, Pasternack, and Taranta 1971).
VIII.63 - Gout
- from Part VIII - Major Human Diseases Past and Present
- Edited by Kenneth F. Kiple, Bowling Green State University, Ohio
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- The Cambridge World History of Human Disease
- Published online:
- 28 March 2008
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- 29 January 1993, pp 763-772
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Summary
Gout is a chronic, intermittently symptomatic disease. It is manifested primarily by small numbers of acutely painful swollen joints that result from an inflammatory reaction to the precipitation of crystals of monosodium urate.
Etiology
The predisposing metabolic factor for primary gout is an abnormally high or rapidly changing concentration of uric acid in the blood. Hyperuricemia may result from an accelerated synthesis of uric acid, or decreased excretory capacity for uric acid in otherwise normal kidneys as a result of unidentified but probably heritable causes. Hyperuricemia leading to secondary gout occurs particularly (1) in diseases of the blood-forming tissues that increase the availability of precursors of uric acid; (2) in kidney failure, which limits the excretion of uric acid; or (3) as a result of medications that either accelerate the breakdown of purine-rich cells (e.g., antineoplastic drugs) or interfere with the renal excretory mechanism (e.g., some diuretics). Dissolved in the serum, uric acid is harmless. However, because of unidentified local circumstances it may leak from capillaries and crystallize. The crystals of monosodium urate elicit the inflammatory reaction, which is the gouty attack, and the microscopic identification of the crystals in synovial fluid confirms the diagnosis. Why this inflammation occurs predominantly in joints, and why much more commonly in some joints (such as those of the feet or in the knee) than in others (such as the hip or those of the vertebral column) are unexplained characteristics.