An analgesic effect of synthetic human calcitonin in patients with primary osteoporosis.

Examinations were performed in 20 adult male and female patients (pts) suffering from acute back pain due to vertebral compression fracture secondary to osteoporosis proved by lateral X-rays of the dorso-lumbar spine (Th3-L5), and bone mineral density with the method of dual energy X-ray absorptiometry. The synthetic human calcitonin (SUC) (0.5 mg) was injected I.M. every day during 28 days. Analgesic effect was evaluated on 0, 3, 7, 14, 21 and 28th day by patient's assessment of functional capacity, and physician's assessment of pain and mobility. On the same days biochemical variables of Ca-P homeostasis were determined. Treatment with calcitonin resulted in a positive analgesic effect. The functional capacity and mobility of pts increased with diminution of pain. No significant alterations of Ca-P homeostasis was observed. Mild and transient side effects as nausea and tachycardia were negligible. SHC appears to have a significant analgesic effect in treatment of primary osteoporosis.

Brain phagocytes and the microglia of the cerebral cortex of rats following an incident of total ischaemia.

The aim of the study was to point out the presence of phagocytes and active microglial cells in the cerebral cortex of rats that survived from 6 weeks to 12 months after clinical death. The number of perivascular phagocytes increased with the period of time survived after reanimation. These cells were found to be multipotential, they participated in the enzymatic degradation of cellular elements damaged in the course of clinical death. In areas distant from the capillary vessels the presence of many forms of microglial cells was revealed. The majority of them belonged the dendrous microglia. Their numerous cytoplasmic processes proved their ability to migrate. The results of the study show an increase of pathological processes in the brain, which is proportional to the length of time survival after reperfusion following cardiac arrest. The main participants in this process are the perivascular phagocytes and active cells of the dendrous microglia.

Crystalloid structures in the neuronal nuclei of the cerebral cortex of rats following total ischaemia.

The study was concerned with the nuclei of neurons derived from the cerebral cortex of rats that underwent experimental cardiac arrest for a duration of 10 minutes and then, after reanimation, survived from 2 weeks up to 10 months. The animals were divided into two groups: in the first-those specimens that survived from 2 to 6 weeks; in the second-those that survived 8 weeks to 10 months. In the specimens obtained from the first group we observed irregular vesicular structures and bundles of parallel fibrils 8 nm in diameter. In the second group we often observed paracrystalline form resembling "plaited ropes" and tubulous structures linked by a microfibrillar netting. These structures were analysed with a gonyometer. We believe that both the paracrystalline and the irregular vesicular structures that have been observed in the neurons obtained from ischaemic brains appeared due to the alterations in the structure of the karyoskeleton and that the observed intracellular structures are not specific for post-ischaemic alterations.

AXanthomonas maltophilia isolate tolerating up to 1% sodium azide in Tris/HCl buffer.

A bacterium tolerating up to 1% NaN3 found as a contaminant of Sephadex colums being run with Tris/HCl buffer, was identified asXanthomonas maltophilia. It had low nutrient requirements, was strongly proteolytic and interfered with Sephadex columns run with Tris/HCl buffers.

The perivascular fibrotic reaction in rat brain in the late period after experimental clinical death. II. Precapillary vessels.

The aim of the study was to investigate the area surrounding precapillary vessels in the temporal cortex of rat-brains. The material consisted of animals that survived a 10-minute cardiac arrest and then lived on for 10 to 12 months. In the specimens that survived 10 month we observed dilatation of the pericapillary space pervaded with unidentified cells surrounded by multiple collagen fibrils. In the close vicinity of these vessels we often discerned cells participating in the process of phagocytosis. Smooth muscle cells held numerous pinocytic vesicles which contained microfibrillar material. Collagen fibrils were also discerned beneath their basement membrane. In the animals that survived 12 months in many cases the spaces between blood vessel mural myocytes and brain cells were filled with numerous collagen fibrils. In some cases these fibrils formed bridge-like structures between vessel walls and surrounding nerve cells. These compartments were often accompanied by brain phagocytes, the cytoplasm of which contained single fibres or bundles of collagen located in the close proximity of the phagolysosomes. We discussed the role of myocytes, myofibroblasts and phagocytes in the production of reparative collagen following the destruction of precapillary vessels and brain continuity.

The perivascular fibrotic reaction in rat brain in the late period after experimental clinical death. I. Capillary vessels.

In this paper we studied the pericapillary zone of the hypothalamic neurosecretory nuclei and temporal cerebral cortex of rats 6-12 months after experimentally evoked cardiac arrest of 10 minutes duration. The most significant ultrastructural findings were presence of single collagen fibrils and collagen bundles in the compartment between endothelia and pericytes, pericytes and basement membrane and also inside the phagocytic cells. In the animals that survived at least 10 months after resuscitation the capillaries filled with thrombocytes were encountered. Moreover, in the vicinity of these capillaries the dead cells and collagen bundles were observed. We interpret these findings as the evidence of the reparatory process in the border between capillaries and the surrounding brain cells. We discuss the hypothesis that the non-fibroblastic cells present in rat brain are able to synthesize collagen that leads to a process comparable with the fibrosis of parenchymal organs.

Ultrastructure of phagocytizing cells of the rat hypothalamic neurosurgery nuclei in a remote period after the sustained clinical death.

Ultrastructural studies were carried out on neurosecretory nuclei taken from brains of rats which have survived for 16 weeks following clinical death of 5 or 10 min duration. The reported observations indicate that brain lesions were caused by changes due to ischemia and superimposed secondary changes resulting from the maturation of pathological processes. In animals subjected to clinical death for 5 min the observed cells in the perivascular area were integrated in the capillary wall and wrapped by the basement membrane. Sometimes they were accompanied by cells engaged in the process of phagocytosis. Phagocytizing cells were more frequently noted in the animals subjected to clinical death for 10 min and then their cytoplasmic processes were connected with the adjacent capillaries. We assume that these cells, which may represent cerebral macrophages occur by transformation of pericytes or blood derived monocytes.

Ultrastructural changes in the hypothalamic secretory nuclei of rats depending on the duration of clinical death.

The studies were carried out on neurosecretory nuclei of rat hypothalamus following complete circulatory arrest for 5 min (group I) and 10 min (group II). The surviving time of the animals after the experiment was 6 weeks. In group I, the ultrastructural appearance of the perikaryonic areas of the neurons indicates increased metabolic activity of these cells. Crinophagocytic bodies were noted near the Golgi apparatus. In the processes of neurons changes in the structure of the cytoskeletal elements were observed. In group II significant differences were noted, as compared with group I. They consisted in the desolation of the rough endoplasmic reticulum membranes from ribosomes, dilatation of the Golgi area cisternae, and swelling of mitochondria. In the perivascular region cells with the surface of the cytoplasmic processes membranes covered by the product of the Alcian blue reaction were noticed. In our opinion these cells may represent "cerebral macrophages". The ultrastructural changes were more pronounced in animals of group II, as compared with animals of group I.

Studies on the hypothalamus and secretory nuclei of rat in the remote period following clinical death.

Ultrastructural studies of hypothalamic secretory nuclei were carried out on rats which survived 16 weeks after 5- or 10-min-long clinical death. Active neurosecretory cells were noted without any signs of injury. In perikaryonic area numerous polymorphic lysosomes and "nucleolus-like bodies" were observed. Attention was called to significant changes in the structure of cytoskeleton and observations were discussed in relation to biochemical data. In both groups of the studied animals neurosecretory cells with features of apoptosis were found. Apoptotic cells appeared more often in animals which survived 10-min-long clinical death. Characteristic morphological features of the process of apoptosis are shown in illustrations.

[Electron-microscopic changes in neurosecretory nuclei of the rat hypothalamus after total ischemia in short-term clinical death]. / Zmiany mikroskopowo-elektronowe w jadrach neurosekrecyjnych podwzgórza szczura po calkowitym niedokrwieniu w sytuacji krótkotrwalej smierci klinicznej.

Hypothalamic neurosecretory nuclei of rats in which short-term clinical death was experimentally induced, were examined electron-microscopically. Material for studies was taken two weeks after resuscitation of animals following 5 min cardiac and respiratory arrest. Application of aldehyde fixatives with Alcian blue as well as fixatives containing tannic acid revealed numerous additional ultrastructural features not visualized in routine electron microscopy. The obtained results are indicative that short-term cerebral ischemia in rats results in ultrastructural abnormalities in neurosecretory hypothalamic nuclei, which appear after 2 weeks survival. These are electron microscope exponents of reduced secretory function, increased number of lysosomal structures and changes in cytoskeleton organization. They are accompanied by abnormalities in axoplasm and myelin sheaths. The authors consider those structural abnormalities as exponents of delayed irreversible metabolic changes of nerve cells.