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The purpose of this paper is to inquire into the relationship between Al Eskan disease and the probable exposure to chemical warfare agents by Persian Gulf War veterans. Al Eskan disease, first reported in 1991, compromises the body's immunological defense and is a result of the pathogenic properties of the extremely fine, dusty sand located in the central and eastern region of the Arabian peninsula. The disease manifests with localized expression of multisystem disorder. Signs and symptoms of Al Eskan disease have been termed by the news media "Persian Gulf syndrome." The dust becomes a warfare agent when toxic chemicals are microimpregnated into inert particles. The "dirty dust" concept, that the toxicity of an agent could be enhanced by absorption into inactive particles, dates from World War I. A growing body of evidence shows that coalition forces have encountered Iraqi chemical warfare in the theater of operation/Persian Gulf War to a much greater extent than early U.S. Department of Defense information had indicated. Veterans of that war were exposed to chemical warfare agents in the form of direct (deliberate) attacks by chemical weapons, such as missiles and mines, and indirect (accidental) contamination from demolished munition production plants and storage areas, or otherwise. We conclude that the microimpregnated sand particles in the theater of operation/Persian Gulf War depleted the immune system and simultaneously acted as vehicles for low-intensity exposure to chemical warfare agents and had a modifying-intensifying effect on the toxicity of exposed individuals. We recommend recognition of a new term, "dirty sand," as a subcategory of dirty dust/dusty chemical warfare agents. Our ongoing research efforts to investigate the health impact of chemical warfare agent exposure among Persian Gulf War veterans suggest that Al Eskan disease is a plausible and preeminent explanation for the preponderance of Persian Gulf War illnesses.

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This article examines the potential relationship between Al Eskan disease and the Persian Gulf syndrome. Al Eskan disease, reported in Military Medicine in 1992, is a novel and previously unreported condition triggered by the exceptionally fine sand dust of the Central and Eastern Saudi Arabian peninsula. We repeat our study of the pathogenesis of Al Eskan disease to include the ultrastructural and microanalytical study of the sand, aerobiological studies of the Kingdom of Saudi Arabia, and the etiology, symptoms, and prevalence of the disease. We conclude that immunodepression resulting from the continued presence of sand particles less than 1 micron in diameter in the lungs and bodies of Persian Gulf veterans explains not only the symptoms of the hyperegic lung condition of phase I and the symptoms of phase II of Al Eskan disease, but also provides an important clue to a common factor in most cases of Persian Gulf illnesses. We include a discussion of most of the commonly suspected agents in the Persian Gulf syndrome. In this case, we conclude that each of these factors, such as oil well fires, old-world diseases, or depleted uranium, are probably adjuvant or contributing causes. The only common exposure that would lead to recognition of the Persian Gulf syndrome as a single medical condition, rather than a catch-all phrase for unrelated conditions, appears to be exposure to the ubiquitous, fine sand of the area, and a resulting immunosuppression that is aggravated by opportunistic infections and other nonmicrobial ailments.

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The author describes the structure and organization of the Health Service Support of the Hungarian Armed Forces. The differences and similarities between the U.S. and the Hungarian Military Medical Services are highlighted. The potential for inter-operability is examined. The importance of such considerations is marked by the ongoing hostilities in the former Yugoslav Republic.

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The authors observed an acute desert-related disease when the mixture of the fine Saudi sand dust and pigeon droppings triggered a hyperergic lung condition. It was further aggravated by various kinds of organic pathogenic components contributing to an opportunistic infection of the lung. These all lead to the recognition of a new clinicopathological entity, Desert Storm pneumonitis or Al Eskan disease. For the first time, the Saudi sand dust's elemental composition was studied by ultrastructural and microanalytical means. The authors concluded that, contrary to previous beliefs, sand particles less than 1 microns (0.1 microns to 0.25 microns) in diameter are present in substantial quantities in the Saudi sand and are pathogenic, causing hyperergia. Pathogenesis of the sand dust, induced hyperergia, and its immunopathologic background are highlighted.

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At the conclusion of 4 years' careful study of the health services support of a separate infantry brigade (mechanized) during the unit's annual training periods, the authors report on the effectiveness of a support team consisting of Army Reserve medical elements, an Active Army field unit, and a Public Health Service Clearing/Staging unit joining forces in a field environment to provide real world medical care to the same unit in a follow-on annual training period. The emphasis of the team created was on validating the forward care concept of field medical support. The result of this effort was "state of the art" medical service to the troops in the most forward areas, and a savings of 0.66 training days per soldier out of 10 days possible field training time. The cross-training of joint elements was enhanced by providing hands-on treatment of soldiers in a tactical environment, training that cannot be adequately replaced by simulated training.

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The authors have combined their experience of recent changes in the Health Service Support of a separate mechanized infantry brigade during 10-day field training exercises conducted by the same population, in the same geographical area, and in the same season in 4 consecutive years. The development of Health Service Support and the reasons necessitating its evolution are discussed. The impact of MedForce activities on training effectiveness is highlighted. The intensive use of health care providers in the most forward field medical treatment facilities, to include the nursing pool from the training support reserve hospital and Army Medical Department augmentation pool doctors, can alleviate unit medical staff shortfalls and provide exceptional training for unit medics "in house." The deployment of medical assets far forward and the maximization of "in situ" treatment of casualties prevents significant loss of training time and can prevent loss of life in combat. The authors recommend changing the medical care doctrine of Vietnam, from the life-threatening "scoop and run" doctrine to the life-preserving "doc in the box" doctrine presented in this article.

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Approximately 1,500 reserve soldiers conducted annual training in the same geographical location and in the same season during 4 consecutive years. This unique situation allowed the authors to collect data on the incidence of illnesses and injuries, and assess environmental and weather influences on readiness and training effectiveness during 10 days of field training exercises. The authors demonstrate that the health of the force and medical preventive countermeasures are decisive contributors to military success or failure.

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The authors have reviewed the present system of graduate medical education, including independent, affiliated, and integrated residency training programs. Advantages and disadvantages are considered in light of recent changes in health-care delivery systems. Structure, historical development, present status, and limitations of the programs are discussed. Personnel resources of the residency program are classified as United States citizens and non-citizens, American medical school graduates, United States citizen graduates of foreign medical schools, and alien foreign medical school graduates, and their different educational backgrounds are compared. Financial aspects of these programs are considered, and the need to increase university control over residency programs, especially in multi-institutional affiliated residency training programs is discussed. The authors recommend upgrading the status of residents from that of student to that of full-fledged medical doctor with concomitant authority and responsibility.

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This addition to the classification of myopathies is a result of the improved diagnostic techniques in muscle pathology in recent years, largely through the application of electronmicroscopy and histochemistry. After summarizing the clinical picture, the authors call for classification: (1) Congenital myopathies due to developmental arrest: myotubular myopathy, congenital fiber type disproportion. (2) Congenital myopathies due to persistent organellar regression: focal loss of cross striation, myopathy with lysis of myofibrils, nemaline body myopathy, zebra body myopathy, spheroid body myopathy, myopathy with tubular aggregates, satellite cell myopathy. (3) Congenital myopathies due to metabolic errors: mitochondrial myopathy, mitochondria-lipid-glycogen disease. (4) Congenital myopathies due to the lack of the trophic influence of innervation: central core disease, multicore, minicore disease. These congenital myopathies have been taken from the ill-defined heterogeneous conglomeration known as amyotonia congenita or floppy infant syndrome and given a place of their own.

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The authors condensed their knowledge of physical injuries of skeletal muscle, particularly injuries caused by mechanical energy, atmospheric pressure, radiation, extremes of temperature and electricity. The possible perils, outcomes and consequences are discussed. Special attention is given to the military medical projections.

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A 40-year-old black man developed the primary features of Kawasaki disease, along with a pronounced distal motor and sensory neuropathy, abnormal electromyograms, and elevated creatine kinase levels. Results of the biopsy of a distal muscle showed myonecrosis, some type II grouping, immunoglobulin deposition in the sarcolemma, and disordered sarcomeric alignment with dilated T-tubules and terminal cisternae. Immunologic evaluation showed high concentrations of cryoglobulins and circulating immune complexes. It is possible that several manifestations of Kawasaki disease are mediated by immune complex deposition in vessels and tissues.

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Proximal myopathy and different types of neuromuscular syndromes are frequently observed in hyperthyroid patients with complicated thyrotoxicosis. Conflicting reports on the changes seen in muscle biopsies range from no abnormalities to muscle necrosis with the fibers being replaced by connective tissue and fat. On the basis of 21 skeletal muscle biopsies from chronic thyrotoxic myopathic patients, coupled with studies in experimentally induced triiodothyronine myopathy in rats, the histological, histochemical, immunofluorescent, and electron-microscopic findings diagnostic for thyrotoxic myopathy are defined. These criteria include: clumping of nuclei, loss of cross-striation, vacuolar degeneration, and fatty infiltration of endo- and perimysium, presence of giant mitochondria, increased number of mitochondria, disorganization of contractile elements, swelling of transverse tubules, presence of microtubular aggregations, and a significant increase of lipofuscin granules. Both muscle fiber types or in some cases selective type II fibers display atrophy with signs of reinnervation. These alterations are polyfocal and polyphasic and, therefore, polychronous and stereotyped rather than pathognomonic. However, they are related to the severity of thyrotoxic myopathy and the duration of disease. The results of muscle biopsies have a predictive value in determining the reversibility of irreversibility of pathologic changes with therapeutic consequences.

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A case of chronic anterior tibial compartment syndrome is reported where the entity was accompanied with a primary neurogenic type of muscle atrophy. Histology, histochemistry and electronmicroscopy indicated the diagnosis. The authors concluded that in a moderate case of leg trauma with peroneal nerve involvement, when it is complicated by intermittent arterial spasm, the anterior tibial compartment syndrome may develop chronically.

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Skeletal muscle samples from the upper and lower extremities of 38 human fetuses (6 to 18 weeks' gestation) of both sexes were studied by histologic, histochemical, and electron microscopic methods. Ultrastructural morphometry was applied. In the different stages of normal development are found regressive changes, ranging from reversible dystrophic to irreversible necrotic alterations, which are characteristic of either primary myogenic myopathies or primary neurogenic muscle atrophies in older age. Several pathologic patterns of so-called congenital myopathies also presented. On the basis of their findings, the authors conclude that in a certain group of congenital myopathies full normal development of muscle is hindered or blocked and that groups of muscles or the whole voluntary musculature is arrested at certain stages of maturation. For example, insufficient or absent innervation of the fetal muscle may be a factor in Werdnig-Hoffmann or Kugelberg-Welander syndromes. The authors' findings suggest that pathologic patterns in muscle diseases have been used physiologically in fetal development to eliminate unnecessary overproduction of muscle fibers.

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Chronic brucellosis was produced in the rabbit by parental and penicillin-induced L-phase revertant of Brucella canis. Animals in the experimental groups were injected with 1.2 x 10(8) organisms/ml of appropriate strains by specified routes at intervals. At a maximum of 12 weeks postinfection, animals were killed and samples were taken for bacteriology, serology, histology, immunofluorescent and electron microscopy. Results revealed faecal shedding in some animals from 72 hours up to three weeks postinfection. High agglutinating antibody titres of 1:1280 were sustained in all infected animals. Histopathological and ultrastructural changes attributed to the invading organisms were apparent and evidence of mitochrondriopathic changes are provided. The implication and indirect role of L-phase in brucellosis are discussed.

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Lithopedions are very rare; the medical literature mentions 330 cases. In the present case, a calcified lithopedion was found in the abdominal cavity of a 69-year-old woman who had died of unrelated causes. In general, the different organs of the lithopedion were easily distinguishable macroscopically. Microscopic examination detected reasonably well preserved structure only in skeletal muscle. Dry weight studies showed a definite dehydration (mummification) had taken place. Chemical analysis revealed a shell consisting mostly of inorganic constituents. Quantitative inorganic analysis of tissues was done and results compared to normal tissues. These results showed significant decrease of K and Cl, significant increase in Mg, P, Na and enormous increase in Ca. These data are compatible with the histologically observed calcification of the tissues. Under proper conditions, presumably dormant enzymes were reactivated in brain, liver, and muscle, although the total activity was low. Discernible LDH isoenzymes were found in liver and muscle. Discernible CK isoenzymes were found in brain and muscle.

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