Biomedical subjects

J Rafałowska

Publications and source records attributed to J Rafałowska.

At least 19 recordsLinked to original sources

PubMed2001

Are all new data referring to amyotrophic lateral sclerosis certain? Some doubts.

Progress in molecular investigations presents new data facilitating the recognition of pathogenic mechanisms of numerous nervous system diseases, among them amyotrophic lateral sclerosis (ALS). Molecular studies of ALS are mainly concentrated on genetic search, excitotoxicity and astrocytic participation, pathology of neurofilaments, apoptosis, trophic factors, and selective motoneurone degeneration. In literature part of the results of these investigations are presented as certainty but some doubts exist. Problems of the role of the superoxide dismutase (SOD-1) mutation gene and free radical scavenging and selective vulnerability and death of motor neurone cells in ALS are mentioned.

Amyotrophic Lateral Sclerosis↗

PubMed2000

Paraneoplastic syndrome in the course of lung adenocarcinoma: morphological picture and immunohistochemical analysis of the inflammatory infiltrates and PECAM-1 expression.

We examined sections of brain, spinal cord, spinal roots, and peripheral nerves from a patient with paraneoplastic syndrome in the course of lung adenocarcinoma. Morphological examination showed marked loss of myelin fibers in peripheral nerves, severe brain tissue edema, and paraneoplastic degeneration involving cerebrum and cerebellum with inflammatory components. Inflammatory infiltrates examined immunohistochemically using antibodies against antigens CD 3, CD 4, CD 8, and CD 20 turned out to be composed of cytotoxic T lymphocytes. The expression of platelet-endothelial cell adhesion molecule-1 (PECAM-1) in blood vessels was increased in comparison with control material, which may facilitate transendothelial lymphocyte migration triggering a cascade of biochemical and morphological reactions observed in paraneoplastic syndrome.

Adenocarcinoma↗

PubMed2000

Astrogliosis and blood vessel development during human spinal cord myelination.

The aim of our study was to investigate a relationship between vessel development, astrogliosis and myelination in humans. We examined spinal cords of human fetuses and infants using immunohistochemical methods with antibodies against Myelin Basic Protein (MBP), Glial Fibrillary Acidic Protein (GFAP) and lectin Ulex Europaeus Type 1 (UEA-1). Our investigation showed that in parallel to the increase of MBP reactivity in the spinal cord white matter more GFAP-immunoreactive astrocytes appeared. Reaction of vessel endothelium with lectin UEA-1 revealed the temporal increase of vascularization in the course of the spinal cord tracts myelination in fetuses. In the postnatal period when the myelination is nearly morphologically completed, the spinal cord white matter was poorly vascularized although GFAP-immunoreactive cells were still relatively numerous. We suggested that the increase of vascularization and astrogliosis observed during spinal cord tracts myelination may be connected with their participation in process of myelin sheath formation via, among others, local secretion of growth factors necessary for normal myelin development.

Astrocytes↗

PubMed2000

Correlative ultrastructural and immunohistochemical study of developing vascular basement membrane in postnatal rat spinal cord.

We investigated the development of vascular basement membrane in immature spinal cord vessels during rat spinal cord myelination. Correlative ultrastructural and immunohistochemical study indicated that fibronectin was the first component of extracellular matrix. Then, on the 9th postnatal day, laminin appeared. At that time, lamina lucida of vascular basement membrane was not detectable. On the 15th day, when collagen IV was visible, lamina densa and lamina lucida were occasionally observed. All components of basement membrane--fibronectin, laminin, collagen IV, alpha-2 laminin (merosin)--and ultrastructural division into two layers were detected on the 25th postnatal day. The results of this study indicates that a gradual development of endothelium in immature rat spinal cord blood vessels leads to a gradual increase of synthesis of extracellular matrix components.

Animals↗

PubMed1999

Do astrocytes participate in rat spinal cord myelination?

Astrocytes play an important role in CNS development phenomena, such as neuron migration and blood-brain barrier formation, but only a little is known of their role in the process of myelination. The aim of our investigation was to examine the relationship between astrocytes and myelin formation. We evaluated rat spinal cords using hematoxylin-eosin and Klüver-Barrera staining methods as well as immunohistochemical methods with antibodies against myelin basic protein (MBP), glial fibrillary acidic protein (GFAP) and lamins A/C and B2. Our investigation revealed that myelination in the rat spinal cord tracts began between the 6th and 9th postnatal day involving the anterior funiculi, then the lateral funiculi and later the posterior ones. The process of myelination finished about the 25th postnatal day. More GFAP immunoreactive astrocytes were detected in parallel to the increase of MBP reactivity. We suggest that the temporary increase of GFAP positive cells accompanying the process of myelination is necessary for normal myelin development and may be connected with local secretion of growth factors by astrocytes.

Animals↗

PubMed1999

Genetically determined vascular diseases.

Review of literature data concerning genetically determined blood vessel diseases is presented. These disorders are a cause of a process similar to Binswanger's disease but occurring familial. Recurrent TIA, ischemic strokes and other kind of blood supply disturbances lead to numerous and various intensity vasogenic brain tissue damage, particularly in the white matter. Progressive neurological symptoms and dementia form the picture of subcortical leukoencephalopathy in several members of family. Moyamoya disease, fibromuscular dysplasia, hereditary hemorrhagic telangiectasia, hereditary cerebral hemorrhage with amyloidosis, pseudoxanthoma elasticum, two types of subcortical encephalopathy in Japan, HERNS and CADASIL are described.

Brain Diseases↗

PubMed1999

Ultrastructural features of immaturity in blood vessels of neonatal rat spinal cord.

Ultrastructural study was carried out on the lumbo-sacral segment of the spinal cord in 1, 3, 6, 9, 12, 15, 18, 21 and 25-day-old rats. Unusual features of blood vessels in postnatal life of rats were observed: capillaries with abundant endothelial cells, numerous invaginations and narrow lumen. In addition, microvilli of diverse size and number on the luminal surface of capillaries as well as larger vessels were present. They were more numerous in younger animals. An intriguing finding, not observed in older animals, was the appearance of abluminal protrusions projecting into surrounding tissue. Closed endothelial junctions were noted in all the investigated vessels. The above mentioned ultrastructural features indicate an immature character of blood vessels. The presence of this kind of vessels during the postnatal period may be connected with vascularisation of spinal cord due to the myelination process.

Age Factors↗

PubMed1998

HIV-1-infection in the CNS. A pathogenesis of some neurological syndromes in the light of recent investigations.

The main factors in the pathogenesis of AIDS-dementia complex (ADC) are analyzed. The author suggests that these factors can be divided into two groups. The "nonspecific" factors present in every immunologic processes manifested by inflammation compose the first group. They are cytotoxic lymphocytes T, the immunoactivation of infected macrophages, cytokines, NO, NOS and iNOS, the increase of the BBB permeability, the accumulation of beta-amyloid precursor protein, excitotoxic amino acids, various and numerous cells adhesion molecules. The second group may contain factors connected with HIV-1 infection of CNS. In the pathogenesis of AIDS an important role is played by toxic glycoproteins gp 120 and gp 41 which are in the coat of HIV-1 virus, nucleotide sequences variability, possibility of various virus replication in various parts of CNS, the participation of lymphokines IL-4 and IL-10, and presence of co-receptors to HIV-1 virus on lymphocytes, macrophages, neurons and microglial cells.

AIDS Dementia Complex↗

PubMed1998

Vascular changes in tuberculous meningoencephalitis.

Our report refers two cases of tuberculous encephalomeningitis which differ in the course and pathological changes. In case 1 blood vessels showed features of peri, endo-, or panvasculites. In some vessels endothelium proliferation leading to the stenosis or obliteration of the vascular lumen was observed. Necrosis was an effect of vessels occlusion. In case 2 many fewer vessel were involved in onflammation process. Vascular changes were also less extensive and were observed more rarely. Tuberculous infection often caused less tissue lesions than vascular changes. Different pathological changes probably depend on the type and virulence of Myobacterium tuberculosis and on the host immune response to the infection.

Adult↗

PubMed1998

Tumor necrosis factor-alpha induced pathology in the rat brain: characterization of stereotaxic injection model.

Tumor necrosis factor alpha (TNF-alpha) is a cytokine of cytotoxic and proinflammatory properties. It is believed to play an important role in inflammatory and demyelinization processes in the central nervous system (CNS). The aim of this study was to investigate what pathological changes could be produced by a stereotaxic administration of TNF-alpha in vivo into rat brain. Specimens were evaluated after staining with hematoxylin and eosin (H & E), Kluver-Barrera staining and using immunocytochemical methods. Disturbances of the blood-brain barrier (BBB) were analyzed as well as inflammatory infiltrates, changes in neurons, astrocytes and myelin. TNF-alpha injected in vivo into a rat brain caused a prominent inflammatory reaction in the cerebral meninges and a local cytotoxic brain edema when compared with the control group. Moreover, disturbances of the BBB premeability, infiltration of blood-borne macrophages in the area of the cytokine injection and early arising astrogliosis were observed. These results suggest that TNF-alpha can be an important mediator of inflammatory processes in the CNS.

Animals↗

PubMed1998

Does the pathological factor in amyotrophic lateral sclerosis (ALS) damage also astrocytes?

Introduction of immunocytochemical reaction to glial fibrillary acidic protein (GFAP) made possible more accurate estimation of astrocytes reactivity in various diseases of CNS, among others, in amyotrophic lateral sclerosis (ALS). Lack of present studies concerning reactive astroglia in spinal cord, inclined us to examine the reaction of astrocytes in cervical, thoracic and lumbar spinal cord. Material included 11 sporadic ALS patients. Sections of formalin-fixed, paraffin-embedded tissue were stained with hematoxylin and eosin, Kluver-Barrera method and with antibody against GFAP. In all cases various degree of nerve cells loss in the anterior horn, pigmentary degeneration of remaining neurons, the pallor of myelin in the white matter of anterior and lateral columns were observed. In a part of cases background tissue rarefaction within anterior horn was seen. Intensity of morphological changes within anterior horns made possible to divide material into two groups and separate one senile case. Very intensive neuronal changes associated with weak reaction of astrocytes in the anterior horn allow us to pose the hypothesis of influence of an unknown pathological factor on both anterior horn neurons and astrocytes.

Adult↗

PubMed1997

Obstructive sleep apnea syndrome in patient with Creutzfeldt-Jakob disease. Clinical and morphological report.

We report a case of Creutzfeldt-Jakob disease (CJD) which at the beginning of the disease presented clinical syndrome of progressive supranuclear palsy. Rapid intellectual deterioration, supranuclear palsy, postural instability and myoclonic jerks suggested clinical diagnosis of CJD. After five months suffering from the disease patient developed obstructive sleep apnea syndrome (OSAS) confirmed by serial polysomnograms. OSAS is discussed in the context of the localization of histopathological findings and possible involvement of central autonomic structures. The main structures affected by spongiosis and astrogliosis were cortex, thalamus, basal ganglia and midbrain. OSAS was found as another sleep disturbance in CJD apart from insomnia and sleep-wake cycle abnormalities.

Brain↗

PubMed1996

White matter injury in amyotrophic lateral sclerosis (ALS).

Microscopic examination of 6 brains and spinal cords of patients deceased of amyotrophic lateral sclerosis reveals as follows: 1) White matter changes considerably exceeding those found in motor neurons structures. 2) They involve white matter of frontal, temporal and parietal lobes including long association fibers. 3) Pyramidal tracts are extremely damaged within spinal cord and medulla. 4) Within spinal cord besides pyramidal tracts majority of ascending and descending pathways are damaged. 5) Pathomechanism of white matter changes seems to be complex. Within brain hemispheres predominate nonspecific changes, 6) Imaging methods in ALS bring a diagnostic progress but at present the conclusions on specificity of changes encountered in various imaging methods in different diseases seem to be precautions.

Adult↗

PubMed1996

Neuroacanthocytosis. Review of literature and case report.

Neuroacanthocytosis is a rare disease of nervous system with multisystem pathology. This review presents clinical syndromes and morphological changes of sporadic and familial forms of neuroacanthocytosis and is illustrated by the case of a 27-year-old man. Progressive extrapyramidal syndrome appeared at the age of 22. Dementia preceded by behavioral changes observed since childhood, was noticed when he was 24 years old. Gross examination of the brain showed atrophy of the brain and caudatum. In microscopic examination most intensive changes were manifested by caudate nucleus atrophy of its head and body, loss of small neurons and extensive astrocytic reaction in dorso-lateral part of the putamen. Within the pallidum similar but less intensive pathological changes were visible. These data are in accordance with those found in literature, but in contrary to the authors who gave attention to spared cerebral cortex which distinguishes neuroacanthocytosis from Huntington's chorea. In the examined case hypocellularity of the cerebral mainly frontal cortex with lamina disorganization but without glial reaction was noted. Moreover, in frontal cortex especially within layer III, differently oriented pyramidal cells its conglomerates and very large neurons were observed. Authors suggest that these alterations are probably manifestations of developmental failures of the cerebral cortex. They concluded that anatomical studies support the possibility that lesions of basal ganglia lead to abnormal intellectual functions.

Acanthocytes↗

PubMed1995

Developmental failures of blood vessels within central nervous system.

Basing on the literature and her own material the author considers some of developmental vessel malformations: aneurysms, teleangiectases, angiomas and cavernous angiomas. The author pays attention to difficulties in classifying of developmental vascular malformations and choice of terminology. Presumable etiopathogenesis of some malformations with particular regard to role of viral oncogenes is taken into account.

Adult↗

PubMed1995

Coexistence of various vascular malformations within the brain.

Authors present two cases of basilar artery aneurysm accompanied by different development failures of blood vessels. In both cases anomaly in formation of brain base vessels, angioma consisted of different size thin-walled vessels and arterio-venous angioma within brain stem were stated. Besides, conglomerates of abnormal vessels, angiosis within pia matter, diffused lacunar and fetal as well as thin-walled venous vessels were found. Pathological vessels, their conglomerates were present in brain stem, cerebellum and cerebral hemispheres. The variability of vascular malformations seems to point at long-lasting action pathogenic factor during ontogenesis. Authors try to refer particular developmental anomalies to proper stage of ontogenesis.

Aged↗

PubMed1994

Pre- and postnatal blood vessel development of the human spinal cord: association with myelination.

The material comprised spinal cord segments C8 or Th1 of 5 human fetuses aged from 18 up to 34 weeks and 6 infants aged from one day to 3 years. On formalin-fixed paraffin-embedded sections, peroxidase-antiperoxidase Sternberger's et al. (1970) method for visualization of blood vessels endothelium (lectin Ulex europeus and Factor VIII) and myelin basic protein (MBP) was used. A distinct F VIII immunoreactivity of vessels endothelium was recorded since a 1 day old newborn. Lectin immunoreactivity suggested the increased vascularization of the undergoing myelination spinal cord tracts. In the postnatal period, which was characterized morphologically by the nearly completed myelination, the spinal white matter appeared poorly vascularized. A temporary increase of spinal cord tract vascularization during myelination is probably caused by local secretion of angiogenic factors. It is possible that their source might be young developing myelin.

Animals↗

PubMed1994

Immunochemical analysis of some proteins in cerebrospinal fluid and serum of patients with ischemic strokes.

Immunochemical studies of gamma gamma-neuron specific enolase (NSE), parvalbumin (PV), S-100 protein (S-100) and acidic fibrillary glial protein (GFAP) were studied in the cerebrospinal fluid and blood serum in 7 patients with ischemic cerebral stroke, aged 57 to 81 years. Cerebrospinal fluid and the first blood sample were taken on the first or second day of the disease. Further blood samples were taken once a week till the end of patients hospitalization, ending by patients discharge or death. Immunochemical identification of proteins under study were performed with Western-blotting technique. It was found that all proteins studied were present in both cerebrospinal fluid and blood serum on the first two days of the disease in small quantities. The blood content of both NSE and PV increased significantly during the first week of the disease. Both proteins disappeared from the blood serum between the second and fourth disease weeks. S-100 protein and GFAP contents in the blood reached significantly high level within the time interval between second and fifth disease weeks, and remained at a relatively high level till patients' death. In all cases computed tomography study and/or brain autopsy revealed extensive ischemic foci localized within areas supplied by the middle cerebral artery. No clear-cut correlation between extensiveness of the ischemic cerebral damage and the content of the proteins studied in both cerebrospinal fluid and blood serum was found. However, our data indicate that serial studies of the above proteins in patients with ischemic stroke may be useful in monitoring the progress of the disease, and occasionally in the prognosis at least in some cases.

Aged↗