[Improvement of the system of medical equipmet rationing for military units during the wartime].

The authors analyze new legal regulatory document--Medical equipment and reserves supply rate for military units and organisations of the Armed Forces of the Russian Federation, developed in the process of modernization of the system of medical equipment rationing for military units. New legal regulatory document was developed with the aim to replace the similar document d.d 1996-1997. The authors came to conclusion that costs of new medical equipment and reserves supply rates are similar to previous rates. At the same time costs new medical equipment supply rates for medical service increased more than 25%. It is related to change of the role of medical service in the system of medical supply of the Armed Forces of the Russian Federation. Modernization of the system of medical equipment supply rates for military unit of the Armed Forces of the Russian Federation, performed for the purpose of medical supplement for military unit in accordance with new state of the Armed Forces of the Russian Federation, allowed to actualize the regulatory framework of medical supply by means of development and adoption of new Supply and reserves rates be the Ministry of defence. Use if these rates will increase effectiveness and quality of medical supply during the wartime, provide a commonality of reserves of medical equipment and maintenance of established level of combat readiness of medical service of the Armed Forces of the Russian Federation.

[Carotid sinus atherosclerosis].

A morphological study of 200 atherosclerotic carotid sinus (CS) plaques obtained at carotid endarterectomy revealed the structural components and processes characteristic for severe atherosclerosis (foci of atheromatosis and edema, necrosis of collagen and elastic fiber, newly formed vessels and hemorrhages of various duration, lipophages and lymphocytes, portions of fibrosis and calcification, covering thinning and ulceration, thrombi, and the contents of plagues (atheromatous masses, cholesterol crystals, lipophages, calcificates) on their surface). Clinical and morphological comparisons indicated that patients with stroke had a history of signs of severer atherosclerosis than those with asymptotic CS stenosis. They were found to have more commonly vulnerable atherosclerotic plaques that showed a predominance of atheromatosis foci over the portions of fibrosis and calcification, covering thinning and destruction, formation of thrombi onto its surface. It was ascertained that concomitant arterial hypertension might play a crucial role in the pathogenesis of hemorrhages into the atherosclerotic plague.

[Electron microscopy and hystology of the third ventricle ependyma of rat's brain after repeated simulation of the effects of microgravity].

Scanning electron and light microscopy were applied to study the third ventricle ependyma in rat's brain after 30-d tail-suspension, 30-d readaptation to the horizontal position, and repeated 14-d suspension in parallel with another group of rats exposed to a single 14-d suspension. Despite the repeated blood redistribution toward the head, the second tail-suspension produced significantly less grave destruction of the ependymal cell structure and cilia ultrastructure than the single 14-d or previous 30-d one, which suggests that simulation of microgravity repeated after substantial delay imparts much more persistence to the cerebrospinal fluid outflow from the brain ventricles into the saggital sinus.

Ultrastructure of ependyma in brain third ventricle of the rats exposed to repeated tail-suspension. Scanning electron microscopical study.

By means of scanning electron microscopy the ultrastructure of ependyma was studied in the brain third ventricle of the rats repeatedly exposed to 14-day tail-suspension (TS). Animals were subjected to TS for 30 days, then readapted to horizontal position during 30 days and again, repeatedly subjected to TS for 14 days simultaneously with the rats which were in TS for the first time during 14 days. Repeated TS of rats, inspite of repeated redistribution of body liquid mediums in cranial direction, results in considerably less expressed destructive changes in ultrastructure of ependymocyte cilia, then after primary 14- and 30-day TS, showing much greater cerebrospinal fluid (CSF) outflow from brain ventricles into sagittal venous sinus at postponed for a long time, repeated simulation of weightlessness effects in comparison with CSF outflow at primery one.

[Diagnosis of sarcoidosis of the brain].

Based on 15 years' their own experience and clinical observations of 65 patients with sarcoidosis of the brain, the authors have formulated diagnostic algorithms and a battery of studies that can suspect this disease. Since the clinical manifestations of sarcoidosis of the brain are non-specific, particularly at the early stages of its development, the condition of its recognition is the application of all required high-informative diagnostic neuroimaging techniques that are available to a neurological clinic. Nevertheless, sarcoidosis cannot be timely and correctly recognized in all cases. Diagnostic errors in its recognition are caused by the fact that X-ray computed tomography and/or magnetic resonance imaging is untimely made, tomographic changes are erroneously interpreted, and the studies are conducted improperly.

[Functioning of the brain vessels in rats after repeated simulation of some effects of microgravity (histological analysis)].

Histological methods were employed to investigate brain vessels of rats subjected to 30-d tail-suspension and 30-d readaptation in the horizontal position afterwards, and suspended again for 14 days simultaneously with other rats that had no such experience in the past. Repeated suspension produced, although there was blood redistribution to the cranial end, much less profound changes in brain vessels as compared with the previous 30-d suspension and the first-time suspended mates. This suggests an unknown arterial mechanism triggered in the region forward of the extracerebral arteries of the brain surface which hampered an excess blood flow to the brain during repeated suspension.

[Morphology of vessels and vascular plexus in the rat's brain following 93-day simulation of the effects of microgravity].

Results of the histological analysis of the brain of rats subjected to 93-d tail-suspension reveal morphological changes occurred to the arteries, veins and capillaries, ependymal cells of the ventricles and epithelium of the vascular plexus, and nervous and glial cells. On the one hand, these suggest venostatis and brain edema, impaired liquor production and liquor dynamics and increase in intracranial pressure and, on the other hand, adaptive processes in the arterial walls preventing the excess blood flow to the brain.

Brain vessels in the rats exposed to primary and repeated tail-suspension. Minimization of structural changes after repeated exposure.

The aim of study was histological examination of brain vessels in the rats exposed to repeated tail-suspension (TS). The rats were subjected to 30-day TS, then readapted to horizontal position for 30 days and again exposed to 14-day TS simultaneously with the rats which were underwent to 14-day TS for the first time. 30-day TS induced in brain vessels the adaptive changes hindering the excessive blood inflow to brain--spasm and hypertrophy of muscle-elastic valves in extra- and intracerebral arteries and also the destructive changes--loss of vascular tone in extra- and intracerebral arteries, plethora in extra- and intracerebral veins, intracerebral venules and capillaries, conglutination of erythrocytes in capillaries, plasmatization of veins and capillaries and edema of brain tissue pointing out in total the increase in blood inflow to the brain and difficulty of blood outflow. After 30-day readaptation of TS-rats to horizontal position only adaptive changes in extracerebral arteries and intracerebral capillaries (cell proliferation) and edema of brain tissue were revealed. After repeated, 14-day TS in spite of new redistribution of blood to the head, in contrast to the vessel alterations after primary 14-day TS, the adaptive and destructive changes in brain vessels were lack, excluding only moderate plethora of intracerebral veins, cell proliferation in capillaries and weak signs of edema.

[Recurrent brain infarctions in atherosclerosis and arterial hypertension]. / Povtornye infarkty golovnogo mozga pri ateroskleroze i arterial'noi gipertonii.

In 100 cases of brain infarctions of different size and time caused by atherosclerosis and arterial hypertension, the infarctions were located in the territory of carotid arteries (44 cases), of vertebro-basilar system arteries (18 cases) and of both the systems (38 cases). The infarctions were repeated, multiple in 82 cases, single--in 18 cases. Atherothrombosis and atherostenosis, thromboembolism of the brain arteries from the heart are main pathogenetic factors. The phenomenon of "infarction in the infarction" is observed in the limits of one arterial pool.

[Morphological features of atherosclerotic plaques of internal carotid artery sinus (biopsy data from carotid endarterectomy)]. / Morfologicheskie osobennosti sosudov ateroskleroticheskikh bliashek sinusa vnutrennei sonnoi arterii (na materiale bioptatov, poluchennykh pri karotidnoi éndarteréktomii).

A histological study was made of 140 atherosclerotic plaques in the sinus of the internal carotid artery (ICA) removed at carotid endarterectomy. New formed thin-walled vessels of various diameter having the structure of arteries, blocking arteries and, presumably, arteriolo-venous anastomoses were found in 112 plaques. The majority of the vessels were oriented along the ICA this indicating blood circulation parallel to that in ICA. It is assumed that deficiency of blocking arteries results in the development of intraplaque hemorrhages from thin-walled vessels.

[Cerebral sarcoidosis diagnosed by biopsy]. / Tserebral'nyi sarkoidoz, diagnostirovannyi s pomoshch'iu biopsii.

Space-occupying lesion was found by head computer tomography in the left brain hemisphere of the patients with lung and lymph node sarcoidosis. Neurologic symptoms and clinical course did not allow to exclude brain tumour. Granulomas typical for sarcoidosis were found in the stereotaxis biopsy of the parietal brain region.

[Small brain infarcts in arterial hypertension and atherosclerosis (pathogenesis and criteria of morphologic diagnosis]. / Malye glubinnye infarkty golovnogo mozga pri arterial'noi gipertonii i ateroskleroze (patogenez i kriterii morfologicheskoi diagnostiki).

Small infarcts, few millimeters in size, localized in the deep regions of brain hemispheres, cerebellum and pons were found in 36 patients with arterial hypertension and atherosclerosis. These infarcts develop in the intracerebral arteries having the diameter up to 500 microns. Two types of these infarcts are distinguished: hypertensive and atherosclerotic. Arterial stenosis and obliteration are at the basis of hypertensive infarcts. Reduction of circulation due to the atherosclerotic stenosis is the cause of the atherosclerotic infarcts.

[Hypertensive angio-encephalopathy and vascular dementia]. / Gipertonicheskaia angioéntsefalopatiia i sosudistaia dementsiia.

A clinicomorphological analysis of 60 postmortem cases with brain circulation disturbances against the background of arterial hypertension (AH) is performed. Lacunar infarcts, areas of incomplete necrosis and perivascular encephalolysis, small hemorrhages, criblures, persistent oedema and widespread spongiosis are found in the white matter (WM) of the brain in cases of AH of long duration with dementia. An important role in the WM lesions belongs to its ischemia due to hypertension angiopathy and disturbances of hemodynamics and liquor circulation. Complex of these lesions is called "hypertension leucoencephalopathy".

[Angiodysgenetic necrotizing myelopathy (the Foix-Alajouanine syndrome)]. / Angiodisgeneticheskaia nekrotiziruiushchaia mielopatiia (sindrom Fua--Alazhuanina).

One observation of a rare disease--angiodysgenetic necrotizing myelopathy--in a 50-year-old patient is described. The diagnosis was established at necropsy and did not confirm suspected spinal cord tumor and myelitis. The disease is angiodysplasia with resulting necrotizing myelopathy. Large dysplastic intra- and extramedullary vessels with a disturbed wall permeability, vascular malformations and necrotic foci in the spinal cord are characteristic for this condition.

[Pathogenesis and etiology of amyotrophic lateral sclerosis (clinico-morphological research)]. / K patogenezu i étiologii bokovogo amiotroficheskogo skleroza (kliniko-morfologicheskoe issledovanie).

The authors describe a 22-year-long course of lateral amyotrophic sclerosis; 14 of these years the patient was maintained by artificial ventilation of the lungs. Total paralysis was associated with intact consciousness and the function of the eye-moving muscles. According to morphological findings the death of motoneurons of the spinal cord and brain stem, as well as of corticospinal tracts was combined with signs of slowly progressive inflammatory process. Virus-like inclusions detected in the cytoplasm of neurons and astrocytes point to a possible infectious nature of the disease.

[Hypertensive angiopathy of the brain]. / Gipertonicheskaia angiopatiia golovnogo mozga.

Cerebral vessels were studied by light microscopy in 20 autopsies after hemorrhagic stroke from arterial hypertension. Primary (acute), secondary (reparative) changes, as well as changes reflecting compensatory-adaptive processes, were found in the intracerebral and superficial arteries of the brain. The whole complex of these vascular changes was defined as hypertonic angiopathy. The usage of such terms as "angiopathy" and "combined angiopathy" were discussed. Criteria of morphologic diagnosis of angiopathies were proposed.

[Lacunar infarct--special form of focal vascular pathology of the brain in arterial hypertension]. / Lakunaryi infarkt--osobaia forma ochagovoi sosudistoi patologii golovnogo mozga pri arterial'noi gipertonii.

Lacunar infarctions were studied morphologically in 22 subjects who died of a cerebral hemorrhage associated with arterial hypertension. It has been established that lacunar infarctions developed in the intracerebral arteries 100-500 microns in diameter. Narrowing or obliteration of these arteries are brought about by the changes associated with arterial hypertension. An analysis of clinical and computer-tomographic data obtained from 32 patients with lacunar infarction showed that characteristic of these patients were the following features: 1) elevated arterial pressure, often without any cephalgia; 2) gradually developing (over a period of several hours or days) focal neurologic symptomatology; 3) the absence of either higher cortical dysfunctions or psychopathologic symptomatology with infarctions localized in the left or the right cerebral hemisphere respectively; and 4) considerable recovery of impaired functions.