Biomedical subjects

J Rafałowska

Publications and source records attributed to J Rafałowska.

At least 37 records · Page 2Linked to original sources

PubMed1994

Morphological picture in paroxysmal nocturnal hemoglobinuria. Case report.

25-year-old woman with paroxysmal nocturnal hemoglobinuria was admitted to the hospital because of headache, progressing right hemiparesis and speech disorders. Several days later patient lost consciousness. Cerebrospinal fluid was xanthochromic with increased pleocytosis and protein level. CT-scan revealed ischemic area with hemorrhagic focus within left cerebral hemisphere. Patient died 3 weeks after the admission. Brain section revealed hemorrhagic infarct in the cortex of the left parietal lobe, thrombosis of the superior sagittal sinus and "respiratory brain" changes. Microscopic examination revealed meningeal venous thrombosis, hemorrhagic infarct, vasculitis, abundant accumulation of bacteria within blood vessels, and other pathological changes such as petechiae, perivascular exudates and small, round areas composed of acellular fibrillary network. There were no macrophages and GFAP-positive astrocytes in any of these areas. Authors suggest that weak cell reactivity may be connected with alterations in cell membranes, mainly low phosphatidylinositol (GPI) content.

Adult↗

PubMed1993

Ammon's horn changes in focal brain ischemia in humans.

Neuronal changes in Ammon's horn were examined immunocytochemically in 20 patients aged from 51 to 101 years, deceased in the course of ischemic lesions localized within the area supplied by vessels derived from other then Ammon's horn vascularization (middle cerebral artery). Numerous neurons within various sector of the pyramidal layer, in the dentate gyrus, subiculum and entorhinal cortex were immunopositive in reaction with antibodies to serum proteins (albumin, IgG, alpha-1-antitrypsin), indicating their damage. The distribution of damaged Ammon's horn pyramidal cells differed from the location of injured Ammon's horn neurons in experimental investigations of brain ischemia and did not indicate a selective vulnerability of pyramidal cells in the human h1 area, corresponding to the CA1 sector in animals. Contrary to experimental material, changes in the human Ammon's horn are caused by numerous overlapping factors.

Age Factors↗

PubMed1993

Rare coexistence of congenital malformations in adult.

Coexistence of several developmental abnormalities in adults is very rare and often asymptomatic. In many instances appearance of clinical symptomatology is evoked by some additional factors, not related directly with the basic pathological process. In a 21-year-old oligophrenic man a progressive paresis of inferior limbs appeared in the course of the upper respiratory tract infection. During 5 days of hospitalization transient peripheral paresis of the right facial nerve, tetraplegia, sphincter and respiratory disturbances occurred. Guillain-Barré syndrome and subarachnoid hemorrhage were diagnosed. On autopsy hemorrhagic focus in the medulla and in the cervical and upper thoracic parts of the spinal cord was found. Microscopic examination revealed hypocellularity of the 2nd and 4th layers of the temporal cortex, presence of the central canal within the brain stem, and hemorrhagic focus in the medulla. Two malformations in spinal cord were revealed: intraspinal angioma extending from the C2 to the Th6 segments and diastematomyelia within Th11 and lumbar segments. Diastematomyelia, cortical hypocellularity and angioma composed of fetal, lacunar artery- and vein-like vessels, are related with different periods of the ontogenic development. Coexistence of these malformations indicates prolonged action of the pathogenic factor(s), both in the embryonic and fetal life.

Adult↗

PubMed1993

Morphological changes in the peripheral nervous system in the case of congenital malformations of the spinal cord.

A 21-year-old oligophrenic man developed after upper respiratory tract infection, quadriplegia with sphincter and respiratory disturbances. Lumbar punction revealed subarachnoid bleeding and elevated cerebrospinal protein level. Guillain-Barré syndrome and subarachnoid hemorrhage were diagnosed. At autopsy intraspinal angioma (C2-D6) and diastematomyelia (D11-lumbar segments) were found. Beside, intraspinal hemorrhage was present. Morphological examination of posterior and anterior spinal roots as well as peripheral nerves was done. Spheroids, axonal degeneration and prominent loss of myelinated fibers were observed in the proximal parts of the spinal roots. Axonal degeneration of myelinated fibers and regenerated fibers were noted in the distal parts of spinal roots and in peripheral nerves. Abnormal, fetal-like vessels were present in the spinal roots. Two mechanisms of acute and chronic changes (transneuronal and Wallerian degeneration) are discussed.

Adult↗

PubMed1992

Influence of aging on the protein profile of myelin isolated from human brain white matter.

Myelin proteins composition was examined in material of 20 autoptic cases at ages from 20 to 97 years. The technique of polyacrylamide gel electrophoresis and isotachophoresis was applied. In polyacrylamide gel electrophoresis a progressive increase starting at the age of 60 years of Wolfgram protein at the expense of Folch-Lees proteolipid protein and DM-20 protein was observed. The myelin-associated protein started to increase in the 4th and 5th decade of life, returning thereafter to values observed in younger cases. The isotachophoretic technique did not differentiate the changes observed in myelin protein in the course of aging.

Adult↗

PubMed1992

The breakdown process of human brain infarction in middle-aged and senile cases.

The material comprised 15 cases of ischemic brain stroke at the age of 45 to 101 years. Six brain of subjects deceased at the age of 45 to 57 years and 9 brains of those deceased at the age of 80 to 101 years were studied. Phagocytic cell immunoreactivity in both age groups during the first 5 days and on the 11th and 12th were compared. Phagocytic reactivity in cases of patients who died on the 6th, 15th and 35th days after stroke onset was also estimated. Colliquative necrosis with cavitation was observed in middle-aged cases from the 3rd infarction day. In the senile group the beginning of tissue breakdown was noted on the 5th day, but colliquative necrosis with cavitation was found on the 11th infarction day. Senile alterations in the biochemical components in various brain tissue elements are probably the cause of the different course and dynamics of the pathological process.

Aged↗

PubMed1992

Blood-cerebrospinal fluid barrier integrity in cerebral infarction.

Using a sensitive isotachophoretic technique total cerebrospinal fluid protein, CSF-serum albumin and CSF-serum IgG ratios as indicators of blood-CSF barrier integrity were determined in 35 cases of ischemic cerebral infarction. Since it proved to be changed in about 57% of these patients, the CSF-serum albumin ratio was found to be the most sensitive parameter in evaluating the blood-CSF barrier disturbances. No clear-cut correlation was found between the age of patients, the clinical course of the disease, different periods after onset of the illness nor the size of the infarction and CSF-blood barrier permeability.

Aged↗

PubMed1992

Does damage of perivascular astrocytes in multiple sclerosis plaques participate in blood-brain barrier permeability?

In six young and two senile MS cases perivascular astrocytes within demyelination lesions were evaluated immunocytochemically. The peroxidase-antiperoxidase method of Sternberger et al. (1970) was used for visualization of glial fibrillary acidic protein (GFAP). In all cases very weak immunoreactivity of perivascular astrocytes was noted. Accumulation of perivascular glial fibers, and infrequently their fragmentation were observed both within active and old demyelination plaques. Clasmatodendrosis, Rosenthal's fibers and prominent regressive changes of astrocyte perikarya were found only in old plaques. A lack of immunoreactivity of perivascular astrocytes was noted within old demyelination lesions. The background of the latter was often immunonegative to GFAP. It is suggested that secondary damage of perivascular astrocytes influences vascular permeability within demyelination lesions including old plaques.

Adult↗

PubMed1990

[Brain infarcts in humans during middle age and senility. I. Defects of blood-brain barrier permeability in immunocytochemical studies].

Brains of the deceased in the age from 45 to 57 years (6 cases) and from 80 to 101 years (9 cases) with ischemic brain damage were studied. Technique of the peroxidase-antiperoxidase (Sterberger et al. 1970) was used for visualization of the brain tissue reactivity for albumin, IgG, alpha 1-antitrypsin and alpha 2-macroglobulin. In all cases the disturbances of the blood vessels permeability were found. The BBB deterioration within the first days of brain infarct seems to be smaller in senile age than in middle age. However, after some days senile blood vessels permeability increases and become similar in both age groups.

Aged↗

PubMed1990