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Biomedical subjects

P Helén

Publications and source records attributed to P Helén.

At least 19 recordsLinked to original sources
PubMed2002

Vertebral epidural arteriovenous fistula and radicular pain in neurofibromatosis type I.

A minor trauma caused opening of an arteriovenous fistula between the right vertebral artery and cervical spinal epidural venous plexus in a patient with neurofibromatosis Type I. Subsequent dilation of the plexus caused compression of the spinal cord and radicular symptomology of the right upper extremity. The single-hole fistula and its arterial feeder were filled with electrodetachable coils via an intra-arterial approach. This lead into shrinkage of the plexus, reformation of the cord caliber and full and stable clinical recovery. The achieved endovascular occlusion of the fistula proved to be permanent on follow-up.

Adult↗
PubMed2001

Microglial response to the neurotoxicity of 6-hydroxydopamine in neonatal rat cerebellum.

Depletion of noradrenaline in newborn rats by 6-hydroxydopamine (6-OHDA) affects the postnatal development and reduces the granular cell area in the neocerebellum (lobules V-VII). During the first postnatal month, Bergmann glial fibers guide the migration of immature granule cells to the internal granule cell layer. Microglia and Bergmann glia may play an important role in this process, but the exact mechanism behind this phenomenon is not known. We studied the effect of systemic administration of 6-OHDA on the expression and localization on microglia and Bergmann glia in the neonatal cerebellum by immunohistochemistry. In the neocerebellum, 6-OHDA treatment caused a significant increase in the number of activated microglia. The increase was observed mainly in the granule cell layer and the cerebellar medulla. Bergmann glial cells in treated brains were abnormally located, did not form intimate associations with Purkinje cells, and the glial fibers were structurally different. Our findings indicate that a noradrenergic influence may be necessary for the normal maturation and migration of granule cells, and abnormal migration may be the result of Bergmann glia destruction and the activation of microglia. Activated microglia in the granule cell layer may be used as a marker for an injured cerebellar area.

Age Factors↗
PubMed2001

Analysis of p53 tumor suppressor gene in families with multiple glioma patients.

The high incidence of gliomas in Li-Fraumeni families and the high frequency of somatic p53 mutations in sporadic glial tumors have raised the possibility that germline p53 mutations could play an important role in familial aggregation of gliomas. In the present study, 18 families with two or more gliomas were screened for germline p53 mutation. The families were identified through questionnaires sent to 369 consecutive glioma patients operated at Tampere University Hospital during 1983-1994. In these families, a family history of cancer was verified through the Finnish Cancer Registry. Interestingly, the questionnaires reveled only 15 of 57 cancers (index gliomas excluded) retrieved through the Cancer Registry. None of the 18 families fufilled the criteria for classic Li-Fraumeni syndrome. Immunostaining analysis of p53 protein accumulation suggested that alterations of the p53 gene are as common in familial as in sporadic gliomas. Sequencing analysis of exons 4-10 of the p53 gene revealed no germline mutations in any of the 18 families. Thus, although occasional glioma families carrying germline p53 mutations have been identified in earlier studies, systematic evaluation of familial glioma patients suggests that the p53 gene is not a common susceptibility gene in case of familial gliomas. The p53 tumor suppressor gene seems to have a similar role in the tumorigenesis of most familial and sporadic gliomas.

Adult↗
PubMed2000

Chromosome imbalances in familial gliomas detected by comparative genomic hybridization.

Familial occurrence of gliomas, in the absence of well-defined hereditary multisystem disorders, is reported occasionally. We describe 17 families that have been afflicted with two or more gliomas but do not raise suspicion of other inheritable syndromes. The families were identified among 369 consecutive glioma patients operated at the Tampere University Hospital during 1983-1994. We applied comparative genomic hybridization (CGH) analysis on 21 gliomas occurring in these 17 families. The most frequent genetic alterations, detected in over 20% of the tumors, were losses of 6q, 10, 4q, 9p and gains of 7, 19, 20q, 1p. We compared the chromosomal alterations detected in the familial gliomas to those reported previously on 209 sporadic gliomas in nine different CGH studies. In this comparison, the familial gliomas more often showed losses of chromosome arms 4q and 6q and gains of 1p and 22q. The most frequent losses (9/21 tumors) in the familial gliomas resided on chromosome arm 6q (P = 0.005, Fisher's exact test; with Bonferroni correction, P = 0.04). The loss of 6q was also the most common intrafamilial aberration, present in four separate gliomas belonging to two families. The minimal common area of loss on this chromosome resided at 6q14-16. In conclusion, we have found several characteristic aberrations by CGH in the familial gliomas and we present new chromosomal regions possibly involved in the familial predisposition to gliomas.

Adult↗
PubMed2000

Neonatal 6-hydroxydopamine treatment affects GABA(A) receptor subunit expression during postnatal development of the rat cerebellum.

Neurotoxic elimination of noradrenergic terminals by 6-hydroxydopamine (6-OHDA) leads to alteration of the granule cell layer formation. We have studied the developmental expression of GABA(A) receptor subunits in rat cerebellum after neonatal administration of 6-OHDA during the first postnatal month of life. 6-OHDA was injected subcutaneously. The expression of GABA(A) receptor subunits was studied by in situ hybridization and immunohistochemistry. The alterations were observed in the neocerebellum - the part of the cerebellum which starts development postnatally. The migration of granule cells was delayed, and the total area of the granule cell layer in the neocerebellum from 6-OHDA-treated rats was reduced to 22.6+/-5% of the corresponding area from control rats. In situ hybridization with subunit-specific antisense oligonucleotide probes was performed for alpha1, alpha2, alpha3, alpha5, alpha6, beta1, beta2, gamma1 and gamma2 subunits of the GABA(A) receptor. In neocerebellum, 6-OHDA treatment caused a significant reduction in the alpha1, alpha6 and gamma2 subunit mRNA levels. The expression of the other subunits was not changed. It has been shown that in the postnatal cerebellum alpha1 and alpha6 subunits can be detected in granule cells only when the cells had migrated to their final destination. Our findings indicate that a noradrenergic influence may be necessary for the normal maturation and migration of cerebellar granule cells.

Adrenergic Agents↗
PubMed1999

Increased expression of peripheral benzodiazepine receptors and diazepam binding inhibitor in human tumors sited in the liver.

The peripheral benzodiazepine receptor system triggers intracellular metabolic events and has been associated with cell proliferation. Its endogenous ligand, the diazepam binding inhibitor, contributes to steroidogenesis by promoting cholesterol delivery to the inner mitochondrial membrane. The present study was undertaken to verify whether this system is altered in tumors sited in the liver. Peripheral benzodiazepine receptors and diazepam binding inhibitor were studied using immunocytochemistry and in situ hybridization in 9 human tumors sited in the liver, in liver hyperplasia, cirrhotic nodular regeneration, intestinal adenocarcinoma and in surrounding non-tumoral tissue. Immunocytochemical staining and in situ hybridization demonstrated that peripheral benzodiazepine receptors and diazepam binding inhibitor were more prominently expressed in neoplastic cells than in non-tumoral tissue. They were present in the same cells, suggesting that diazepam binding inhibitor may act in an intracrine manner in these cells. Higher peripheral benzodiazepine receptors and diazepam binding inhibitor expression in tumor cells suggest an implication of this system in the metabolism of neoplastic cells. Furthermore the evaluation of peripheral benzodiazepine receptor and diazepam binding inhibitor expression might be useful in evaluating malignancy and in diagnostic approaches of tumors in liver tissue.

Aged↗
PubMed1999

Clinicopathological correlation of cell proliferation, apoptosis and p53 in cerebellar pilocytic astrocytomas.

We have analysed 78 cerebellar pilocytic astrocytomas to assess whether histopathology, cell proliferation, apoptosis rate, p53 immunoreactivity, or flow cytometry could predict their long-term behaviour. Classic pilocytic/microcystic pattern was seen in 62 patients and 16 patients had mixed pattern with an additional non-pilocytic glial component. The overall 5-year survival was 93%, complete resection providing 100% survival. The four patients who died during the follow-up were more than 14 years of age, their primary operation had been incomplete and three of them were mixed variants. In 15 cases the tumour recurred giving a recurrence-free 5-year survival of 77%. The proliferation indices were low: Ki-67MIB-1 (median 2.0%), PCNA (1.2%) and S-phase fraction (4.4%). The Ki-67MIB-1-labelling index was significantly higher in young patients, but did not differ between the classic and mixed variants. Twenty-two per cent of the tumours were aneuploid with a significantly higher S-phase fraction than in diploid tumours. p53 seems to act as ardian of the genome' in pilocytic astrocytomas, because aberrant/increased expression of p53 and aneuploidy associated with enhanced apoptosis. Only patient age (P = 0.01), radicality of the primary operation (P = 0.0001) and histology (classic vs mixed, P=0.008) significantly correlated with survival. The poorer prognosis of the mixed variant suggests that this may represent a distinct entity. Although none of the novel parameters significantly predicted recurrence or survival, they indicate substantial biological variation among cerebellar pilocytic astrocytomas.

Adolescent↗
PubMed1997

Accumulation of genetic changes is associated with poor prognosis in grade II astrocytomas.

Unexpectedly aggressive clinical course of some grade II astrocytomas is a diagnostic dilemma for routine histopathology. Because increasing tumor malignancy is a consequence of progressive accumulation of chromosomal alterations, we investigated whether aggressive behavior of grade II astrocytomas could be predicted by the number and type of gross chromosomal aberrations. We used comparative genomic hybridization to analyze 11 grade II astrocytomas with typical (good, n = 7) or poor (n = 4) prognosis. The results were also compared with a reference material of 13 grade III-IV astrocytomas and nine established cell lines. We found a median of two aberrations (range 0 to 4) in tumors with good prognosis and of 15.5 changes (range 8 to 28) in tumors with poor prognosis. Chromosomal gains were present in both groups, whereas chromosomal losses were frequent in tumors with poor prognosis (median 9.5, range 3 to 14) but rare in tumors with good prognosis (range 0 to 2). All chromosomal gains were also found in the high-grade astrocytoma group and the majority of them in cell lines. Chromosomal losses in grade II astrocytomas with poor prognosis were very similar to those in grade III-IV astrocytomas and cell lines. We conclude that an early accumulation of genetic changes in grade II astrocytomas is closely associated with poor patient prognosis, suggesting diagnostic use for comparative genomic hybridization in characterization of grade II astrocytomas.

Adolescent↗
PubMed1995

Expression of peripheral-type benzodiazepine receptor and diazepam binding inhibitor in human astrocytomas: relationship to cell proliferation.

The expression of peripheral-type benzodiazepine receptor (PBR) and diazepam binding inhibitor (DBI) were studied in human astrocytic tumors using immunocytochemistry and in situ hybridization. Both PBR and DBI were prominently expressed in neoplastic cells, whereas in normal brain their amount was low or undetectable. Immunocytochemical double staining demonstrated that PBR and DBI were present in the same cells, suggesting that DBI may act in an autocrine manner in these cells. Analysis of 86 cases showed that PBR expression was statistically significantly associated with tumor malignancy grade (P = 0.004) and the proliferative index as determined by immunocytochemistry with the MIB-1 antibody (P = 0.004). Patients having tumors with high levels of PBR-immunoreactive cells had a shorter life expectancy than patients whose tumors showed lower PBR contents (P = 0.024). In conclusion, these results show that PBR expression is higher in neoplastic cells than in normal brain tissue. They also suggest that PBR immunocytochemistry might be useful in evaluating malignancy in brain tumors.

Adolescent↗
PubMed1995

Increased expression of diazepam binding inhibitor in human brain tumors.

Benzodiazepines, which are in extensive clinical use, can regulate neoplastic growth via benzodiazepine receptors. We have studied the expression of the diazepam binding inhibitor (DBI) polypeptide, a putative endogenous ligand for benzodiazepine receptors in normal and pathological human brain. In normal brain, DBI immunoreactivity (IR) and mRNA were detected in all brain areas, with the highest levels in the cerebellum, amygdala, and hippocampus. In light and electron microscope immunohistochemistry, DBI-IR was only detected in glial and ependymal cells. In brain tumors, such as astrocytomas, glioblastomas and medulloblastomas, a much higher content of DBI-IR and -mRNA was found in normal tissues. The highest level of DBI expression was found in the most anaplastic tumors. DBI-IR was virtually undetectable in meningiomas and pituitary adenomas. The high expression of DBI in brain tumors might play a role in the neoplastic growth of glial cells via the mitochondrial benzodiazepine receptor, or it may be involved in the regulation of the high energy consumption of these tumors via acyl-CoA metabolism.

Adolescent↗
PubMed1991

[Brain abscess].

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Adult↗
PubMed1986

Neuropeptide Y (NPY)-like immunoreactivity in rat sympathetic neurons and small granule-containing cells.

The distribution of neuropeptide Y-like immunoreactivity (NPY-LI) was examined in the rat superior cervical and hypogastric ganglia. NPY-LI was localized in the majority of the sympathetic neurons, a few small granule-containing (SGC) cells and nerve terminals. Most of the NPY-immunoreactive sympathetic neurons were also tyrosine hydroxylase (TH)-immunoreactive but in hypogastric ganglia few neurons with NPY-LI were devoid of TH-immunoreactivity. Electron microscopically NPY-LI was found in the Golgi complexes of sympathetic neurons, in large cytoplasmic granules (100-150 nm in diameter) of the SGC cells and in large dense-cored vesicles (80-100 nm in diameter) of the nerve terminals. NPY-LI coexists mainly with noradrenaline in sympathetic neurons, and may have regulatory functions in sympathetic ganglia and in target organs.

Animals↗
PubMed1986

Bleeding of a venous hemangioma inside the filum terminale.

Spinal vascular malformations can present with acute symptoms suggesting spinal cord or nerve root compression. We describe a case of bleeding from a venous hemangioma within the filum terminale. This malformation caused acute compression of the lumbar spinal roots. Thus, vascular malformations may exist behind the symptoms of acute radiating pain and lower extremity weakness. They can be treated by total extirpation, when possible, by resection or by decompressive laminectomy alone.

Cauda Equina↗
PubMed1984

Bombesin/gastrin-releasing peptide (GRP)- and Met5-enkephalin-Arg6-Gly7-Leu8-like immunoreactivities in small intensely fluorescent (SIF) cells and nerve fibers of rat sympathetic ganglia.

Superior cervical and hypogastric ganglia were removed from rats that had been perfused with a mixture of 4% paraformaldehyde and 0.25% glutaraldehyde. Specific antisera against Met5-enkephalin-Arg6-Gly7-Leu8 (MEAGL) and bombesin/gastrin-releasing peptide (BN/GRP) were used in the immunofluorescence procedure. In hypogastric ganglia, a subpopulation of small intensely fluorescent (SIF) cells, as identified by their aqueous aldehyde (Faglu)-induced fluorescence, showed MEAGL- and BN/GRP-like immunolabeling. SIF cells in the superior cervical ganglia were unlabeled. In both ganglia, varicose nerve fiber networks and nerve terminals surrounding principal ganglion cells showed MEAGL- and BN/GRP-like immunoreactivities. Unlabeled SIF cells often were in close contact with nerve fibers that had MEAGL-like immunolabeling. Immunoreactivities against MEAGL- and BN/GRP-like neuropeptides in nerve fibers and terminals suggest a neurotransmitter or neuromodulator role for these peptides. In addition, labeling in SIF cells implies their possible endocrine function.

Animals↗