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Biomedical subjects

A Wallin

Publications and source records attributed to A Wallin.

At least 19 recordsLinked to original sources
PubMed1997

Symptomatological characteristics distinguish between frontotemporal dementia and vascular dementia with a dominant frontal lobe syndrome.

OBJECTIVE: Our hypothesis was that patients with vascular dementia and a dominating frontal lobe syndrome have a symptomatology that reflects a more widespread lesion compared with patients with frontotemporal dementia. DESIGN: Patients with vascular dementia and a dominating frontal lobe syndrome (VAD-F; N = 11) were compared with regard to clinical symptoms and imaging features on CT scans of the brain with patients with frontotemporal dementia (FTD; N = 21). SETTING: A neuropsychiatric diagnostic ward. PATIENTS: Thirty-two inpatients, aged 48-78 years, with frontotemporal dementia or vascular dementia. MEASURES: Relatives were questioned about the initial symptoms. At the clinical investigation, mental and neurological symptoms and signs were recorded using the STEP method (stepwise comparative status analysis). CT scan features of the brain were evaluated by a trained neuroradiologist. The GBS-i (Gottfries-Bråne-Steen, intellectual variables) scale was used to measure the degree of dementia. RESULTS: At the onset of dementia, loss of memory (p < 0.001), sudden onset (p < 0.001), confusion (p < 0.05) and unspecified neurological signs (p < 0.05) had been significantly more frequent in the VAD-F group. At the time of the clinical investigation, lack of social awareness and presence of primitive reflexes were more frequent in the FTD group (p < 0.01 and p < 0.05, respectively) and visuospatial deficits more frequent in the VAD-F group (p < 0.05). CT of the brain showed that, apart from brain infarcts (present only in the VAD-F group), paraventricular leukoaraiosis was significantly more pronounced in the VAD-F group (p < 0.05). The groups did not differ with respect to age, age at onset or level of dementia. CONCLUSION: The findings support our hypothesis.

Age of Onset↗
PubMed1996

Monosomy 1p36.31-33-->pter due to a paternal reciprocal translocation: prognostic significance of FISH analysis.

A rare monosomy 1p36.31-33-->pter was found in a child with physical anomalies, psycho-motor retardation, and seizures. Cytogenetic investigation suggested an unbalanced translocation between 1p and an acrocentric chromosome, but the rearrangement was difficult to assess accurately using conventional chromosome banding techniques. The half-cryptic translocation was further characterized using fluorescence in situ hybridization, and the aberrant chromosome 1 was shown to be a derivate of a paternal reciprocal translocation t(1;15) (p36.31-33;p11.2-12). The breakpoints on chromosome 1 and 15 were defined in detail using locus specific probes. The rearrangement did not include the region on chromosome 1p which previously has been suggested to predispose to the development of neuroblastoma in a case with a constitutional translocation. At 3 6/12 years, the patient has no clinical signs of this disease, which illustrates the prognostic significance of this investigation.

Abnormalities, Multiple↗
PubMed1996

A new magnetic resonance imaging analysis method for the measurement of disc height variations.

STUDY DESIGN: A new magnetic resonance image analysis method is proposed which is based on the definition of the borders of the vertebral bodies adjacent to the intervertebral disc and their varying relationships. The reproducibility of this method (the so-called "centroid" method) was assessed by consecutive measurements. Its potential to depict diurnal disc height variations was studied using randomized groups of volunteers. OBJECTIVE: To determine if magnetic resonance imaging can reliably measure disc height variations in the lumbar spine in vivo. SUMMARY OF BACKGROUND DATA: A review of the literature indicates that noninvasive, accurate methods to study the effect of load on intervertebral discs in vivo are needed. METHODS: The reproducibility of the centroid method was assessed in 10 healthy volunteers in 2 consecutive measurements and compared to a conventional method (mean anterior and posterior disc height). To investigate the potential for the depiction of diurnal disc height variations, 10 volunteers were randomized in a study group (1 measurement in the morning, 1 measurement in the evening) and a control group (2 consecutive measurements in the morning). RESULTS: The centroid method allows the depiction of disc height variations as small as 0.85 mm with a 95% confidence (tolerance limits), whereas a conventional method needs variations of at least 1.66 mm. In the study (diurnal) group, the disc height decreased significantly (P < 0.0001) during the day (mean, -0.9 mm), while no variation (P < 0.8) was found in the control group. CONCLUSIONS: These results indicate that the centroid method can reliably detect disc height variations in an experimental setting. The centroid method provides the potential for evaluations of the effects of various work places, work equipment, work tasks, and postures.

Adult↗
PubMed1996

Decreased lumbar cerebrospinal fluid levels of monoamine metabolites in vascular dementia.

The levels of the monoamine metabolites 5-hydroxy-indoleacetic acid (5-HIAA), homovanillic acid (HVA), and 4-hydroxy-3-methoxy-phenylglycol (HMPG) were determined in lumbar cerebrospinal fluid (CSF) of 56 patients with vascular dementia (VAD) and 57 healthy controls. Despite CSF sampling under standardized conditions, the variability in values was wide among both patients and controls. This suggests that yet unknown factors affect the lumbar CSF concentrations of monoamine metabolites. The VAD group showed significantly lower mean concentrations of 5-HIAA (p < .001) and HVA (p < .001) than the control group. These low concentrations appear to be no disease-specific phenomenon, but may be attributable to subcortical white-matter changes or a decreased production of monoamines, which are dependent on oxygen for their synthesis.

Aged↗
PubMed1996

Cell-specific localization of nitric oxide synthases (NOS) in the rat ovary during follicular development, ovulation and luteal formation.

Nitric oxide (NO) has emerged as one of several important intraovarian regulatory factors. In particular, NO has been implicated in the processes of ovulation and atresia-related apoptosis. The aim of the present study was to investigate the presence and distribution of the NO-generating nitric oxide synthase (NOS) enzymes in the ovary during follicular development, ovulation and luteal formation of the equine chorionic gonadotrophin (ECG)/human chorionic gonadotrophin (HCG)-primed rat. NADPH diaphorase activity was used as a histochemical marker for NOS within the ovary. Diaphorase reactivity was most abundant in the stroma (S) of the ovary and in the theca (T) layer of the follicle. In luteinized ovaries, weaker diaphorase reactivity was present within the corpora lutea (CL). Two different isoforms of NOS, the constitutively expressed endothelial NOS (eNOS) and the inducible isoform of NOS (iNOS), were immunolocalized in ovaries of immature rats and in ECG/HCG-primed rats during the periovulatory period from HCG injection until 2 days after ovulation. In addition, ovarian concentrations of eNOS and iNOS were quantified by immunoblotting. Immunoblotting with a monoclonal anti-eNOS antibody demonstrated the presence of eNOS mainly in the residual ovary (ROV) during the periovulatory period. In luteinized ovaries, higher concentrations of eNOS were seen in CL, while those in the ROV at this stage were lower than in the periovulatory ovary. Immature ovaries contained diminutive amounts of eNOS, detectable mostly in the ROV compartment. In contrast, iNOS was barely detectable during follicular development to the preovulatory stage. A slight elevation of iNOS was observed in the granulosa cells at 6 h after the HCG injection. The levels of iNOS during the luteal phase were also low. Immunohistochemical analysis using polyclonal eNOS and iNOS antibodies revealed the localization of these two isoforms primarily in the S and the T of the periovulatory ovary. In luteinized ovaries, positive immunoreactivity was also seen within the CL. With a monoclonal antibody against eNOS, intense immunoreactivity was observed in the S, T and within CL. There was a particularly strong staining in blood vessels. These data demonstrate the presence of an intraovarian NO-generating system. The localization of this system to the S, T and CL suggests a role for NO in the ovulatory process and in the regulation of CL function.

Animals↗
PubMed1996

Current definition and classification of dementia diseases.

INTRODUCTION: Current clinical diagnosis of dementia diseases mostly relies exclusively on the symptom picture, but there is no clear dividing line between the symptoms per se and the pathological changes. DISCUSSION: The above indistinctness characterizes the current most widely used definitions and classification systems for dementia diseases. There is also a lack of integration, as different categories of doctors conceptualize the dementia syndrome differently, and the various existing classification systems put the emphasis on different aspects of dementia diseases. CONCLUSION: As a first step towards an up-to-date classification of dementia diseases, a distinction between symptoms and pathological changes should be made. A second step is to find patterns both of biological markers and of neuropsychiatric symptoms that are linked to the various pathological changes of the disease.

Aged↗
PubMed1996

Clinical subgroups of the Alzheimer syndrome.

During the last decade, senile dementia and the presenile disease that was named after Alois Alzheimer have been considered a single entity called Alzheimer's disease (AD). This same decade has witnessed the development of many diagnostic tools, such as CT, MRI, and SPECT imaging, that have made possible the systematic analysis of symptoms of brain disorders. With the aid of these sophisticated techniques, it is possible to divide the disorder into clinically relevant subgroups, one of which corresponds to the disease first described by Alzheimer. The disease exists in sporadic and familial forms, and in subgroups of these two basic types. Because the heterogeneity of AD is incontestable, it is time to reconsider the current use of the term "Alzheimer's disease." Because it labels different subgroups whose characteristics are often markedly different, the term "Alzheimer syndrome" appears to be more appropriate.

Alzheimer Disease↗
PubMed1996

The apolipoprotein E allele epsilon 4 does not correlate with the number of senile plaques or neurofibrillary tangles in patients with Alzheimer's disease.

BACKGROUND AND OBJECTIVES: Apolipoprotein E (apoE) has been implicated in regenerative processes in the brain after trauma, as well as in the pathogenesis of Alzheimer's disease. Inheritance of a specific apo epsilon allele (apo epsilon 4) determines in part the risk and the mean age at onset of Alzheimer's disease. ApoE has been found to bind isoform specifically to beta-amyloid protein, the major component of senile plaques, and to the microtubule associated protein tau, which forms paired helical filaments and neurofibrillary tangles. The aim was to further examine the relation between apo epsilon alleles, especially apo epsilon 4, and the development of neuropathological changes associated with Alzheimer's disease. METHODS: Brains of patients with Alzheimer's disease (n = 44) and vascular dementia (n = 11) and of age matched controls (n = 29) were studied. Senile plaques and neurofibrillary tangles in the hippocampus and frontal cortex were quantified. RESULTS: No correlation was found between the number of apo epsilon 4 alleles and the number of senile plaques and neurofibrillary tangles in the hippocampus or the frontal cortex of patients with Alzheimer's disease, or vascular dementia, or control groups. No significant differences in duration or severity of dementia were found between patients with or. without the apo epsilon 4 allele. No increased frequency of apo epsilon 4 was found in vascular dementia. CONCLUSION AND COMMENT: Although the apo epsilon genotype clearly affects whether Alzheimer's disease will develop or not, the present study suggests that it has no influence on pathology or clinical intellectual status, once the dementia has manifested itself. No increased apo epsilon 4 allele frequency was found in neuropathologically diagnosed patients with vascular dementia in whom concomitant Alzheimer's disease can be excluded.

Aged↗
PubMed1996

Immunoglobulin M in cerebrospinal fluid: reference values derived from 111 healthy individuals 18-88 years of age.

The importance of immunoglobulin M (IgM) determination in cerebrospinal fluid (CSF) has increased parallel to the need for early diagnosis of infectious and inflammatory disorders of the central nervous system. Current reference values are based on analysis of CSF from 'reference groups' consisting of patients with psychiatric and/or neurological symptoms but without positive clinical findings. Therefore, accurate reference values for CSF IgM are of utmost importance. The present study presents reference values for IgM in CSF in a large sample (n = 111) of healthy individuals with an age span of 18-88 years. The upper reference limit, calculated as the 0.95 fractile, was 0.36 mg/l for CSF IgM, 0.40 for CSF/serum IgM ratio, and 0.045 for the IgM index. These parameters showed no significant difference between sexes nor any significant correlations with age. The correlations between CSF/serum albumin ratio and CSF/S IgM ratio were linear and statistically highly significant, suggesting that the IgM index values do not depend on the blood-CSF barrier function within the normal range of the CSF/serum albumin ratio.

Adolescent↗
PubMed1996

Stepwise comparative status analysis (STEP): a tool for identification of regional brain syndromes in dementia.

A method for clinical examination of patients with dementia, stepwise comparative status analysis (STEP), is presented. It combines psychiatric and neurologic status examination methods to identify certain common dementia symptoms by which the patient's regional brain symptom profile can be determined. Fifty status variables (items) are estimated with respect to occurrence and severity. The analysis is performed in three steps. The scores on the 'primary' variables reflect observations of single dementia symptoms. These scores form the basis for the assessment of the 'compound' variables, which in turn form the basis for evaluation of the 'complex' variables, one of which describes the patient's regional (predominant) brain syndrome (subcortical, frontosubcortical, frontal, frontoparietal, parietal, or global). In 96 mildly and moderately demented inpatients, the global (42%) and frontosubcortical (31%) were the most common. Ninety-one percent of the patients with vascular dementia had a predominant frontal and/or subcortical symptomatology.

Aged↗
PubMed1995

Direct exposure to nitrogen dioxide fails to induce the expression of some inflammatory cytokines in an IC-21 murine macrophage cell model.

Biologically-active molecules secreted from alveolar macrophages, such as cytokines, have been proposed to be involved in the induction of pulmonary toxicity and inflammation in response to the inhalation of oxidant gas pollutants such as NO2 and O3. Despite this, mechanistic studies are hampered by the difficulty in obtaining control macrophages from human subjects, and the intrinsic variability of such primary cells. It is, thus, of importance to develop alternative models for such studies. Here, we have characterised expression kinetics of the mRNAs for tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), macrophage inflammatory protein-1 alpha (MIP-1 alpha) and macrophage inflammatory protein-1 beta (MIP-1 beta) in confluent cultures of the murine IC-21 macrophage line in response to LPS. The secretion of TNF-alpha protein into the medium, assayed by L-929 cell bioassay, closely followed the expression of its mRNA in response to the LPS stimulus. In contrast to LPS, the exposure of IC-21 cells to either air or various concentrations of NO2 in air between 2 and 20 ppm, in an inverted plate exposure model, failed to induce the expression of any of the cytokine mRNAs probed. We conclude that the IC-21 cell line may represent a suitable model for studying the role of stimulated cytokine gene expression in inflammation and that the early events in the pulmonary inflammatory response to the inhalation of NO2 do not involve stimulated release of TNF-alpha, IL-1 beta or MIP-1 alpha/MIP-1 beta from macrophages.

Actins↗
PubMed1995

[Subtype identification in vascular dementia. An important step towards more precise diagnosis and improved treatment].

Until 1970, the definition of vascular dementia was unspecific and resulted in overdiagnosis of "atherosclerosis". It was replaced by an oversimplified definition based on the notion that vascular dementia is practically always a result of infarctions. However, since the beginning of the 1990s, the concept of vascular dementia has undergone re-evaluation. With the aid of brain imaging, the existence has been demonstrated of circulation-related cerebral tissue changes other than infarcts. It is now clear that vascular dementia is a heterogeneous entity possible to subtype. One of the subtypes is subcortical white-matter dementia, which is perhaps more common than multi-infarct dementia. Subtype identification is a useful aid to reliable diagnosis, and in the long run it may prove helpful in improving treatment.

Aged↗
PubMed1995

Cerebrospinal fluid neuropeptides in Alzheimer's disease and vascular dementia.

Cerebrospinal fluid (CSF) levels of several neuropeptides have been suggested as candidate markers in neurodegenerative disorders. We have examined the levels of corticotropin-releasing hormone (CRH), beta-endorphine (BEND), delta sleep-inducing peptide (DSIP), somatostatin (SRIF), and neuropeptide Y (NPY) in CSF samples obtained under highly standardized conditions from healthy aged controls and from patients suffering from Alzheimer's disease (AD) or vascular dementia (VAD). The influence of some potentially confounding factors was evaluated. CRH and BEND were markedly decreased in both AD and VAD patients, and BEND levels correlated negatively with degree of dementia within the patient population. SRIF was decreased in both AD and VAD patients. DSIP was slightly increased in AD, but not in VAD. NPY did not differ between groups. For none of the peptides did CSF concentrations correlate significantly with duration of illness, nor, with the exception of BEND, with its degree. Present data do not support the hypothesis that specific neuropeptide changes occur in different neurodegenerative disorders, but are in agreement with previous reports suggesting that neuropeptide systems are differentially affected by neurodegeneration.

Aged↗
PubMed1995

The cytoprotective roles of ascorbate and glutathione against nitrogen dioxide toxicity in human endothelial cells.

The depletion of human umbilical vein endothelial (HUVE) cell glutathione with buthionine sulfoximine or with sulfur amino acid-free medium potentiated the sub-lethal (3H-deoxyglucose release) and lethal (lactate dehydrogenase release) cytotoxicity responses of the cells to direct exposure to NO2 over the range 2-20 ppm. When control cells, or glutathione-depleted cells, were either pre-loaded with ascorbate (intracellular ascorbate), or washed with ascorbate-containing medium just before exposure (extracellular ascorbate), the cells were fully protected from NO2-dependent toxicity. Concomitant with these exposures, NO2 caused dose-dependent depletions of both glutathione and ascorbate. Further, it was noted that the depletion of the intracellular ascorbate pool was accelerated in these glutathione depleted cells. Conversely, loading ascorbate into the cells significantly diminished NO2-dependent depletion of intracellular GSH. In contrast to affecting the acute cytotoxicity response of the HUVE cells to NO2, ascorbate supplementation of the medium of cells exposed to NO2 at clonal density facilitated considerable protection to the colony-forming efficiency of the cells. We conclude that both ascorbate and glutathione play important protective roles in defending HUVE cells from the toxicity of NO2 under direct exposure conditions. The results also strengthen the premise that ascorbate and glutathione co-operate in the antioxidative protection of cellular viability.

Antioxidants↗
PubMed1995

Cytotoxicity of NO2 gas to cultured human and murine cells in an inverted monolayer exposure system.

We report the development of an optimised exposure system for the exposure of inverted cell cultures to NO2, which presents several advantages over conventional, right-side-up exposure systems. Firstly, the cells may be directly exposed to NO2 in the gas phase for up to 1 h, without the interposition of an aqueous layer. Secondly, the chamber system allows simple and precise control of the gas concentration during the exposure. Finally, the system allows the simultaneous exposure of large numbers of cells under sterile conditions, facilitating further culture of the cells after the exposure period. We report the application of this system to a comparative study of the toxicity of NO2 in three different cell types involved in the circuit of the inflammatory response, the IC-21 murine macrophage line, the A-549 human pulmonary type II-like epithelial cell line and human umbilical vein endothelial cells. As little as 2 ppm NO2 for 20 min reduced colony-forming efficiency of HUVE cells and A-549 cells and A-549 cells to 35% and 78% of their air controls, respectively. Exposure to 5 ppm NO2 for 1 h increased lactate dehydrogenase release of HUVE cells, IC-21 macrophages and A-549 cells from 7.9% to 21.6%, 5.7% to 10.9% and 2.0% to 3.4%, respectively, whilst 10 ppm NO2 for 1 h lowered cellular glutathione in HUVE cells, IC-21 cells and A-549 cells from 35.2 nmol/mg to 23.3 nmol/mg, from 45.0 nmol/mg to 31.0 nmol/mg and from 86.4 nmol/mg to 69.2 nmol/mg, respectively. Of the cell types tested it was shown that HUVE cells and IC-21 cells were equally sensitive to the toxicity of NO2, whilst A-549 cells displayed considerable resistance, perhaps due to the considerably higher levels of glutathione in this cell line. Further, a comparison of the sensitivity of HUVE cells to NO2, using several modes of exposure (inverted and right-side-up (either rocked or static)) and the assay of lactate dehydrogenase and [3H]deoxyglucose release, revealed that the present inverted exposure technique potentiated the acute cytotoxicity of the gas.

Animals↗
PubMed1995

Cerebrospinal fluid 'neuronal thread protein' comes from serum by passage over the blood-brain barrier.

Cerebrospinal fluid (CSF) biochemical markers for Alzheimer's disease (AD) would be of great value, both to improve clinical diagnostic accuracy and to increase our knowledge of the pathogenesis of the disorder. An increase in the CSF-level of 'neuronal thread protein' (pancreatic thread protein (PTP) immunoreactive material in the brain) has been suggested to be just such a biochemical marker. We have studied CSF 'neuronal thread protein'-like immunoreactivity (NTPLI) using a microparticle enzyme immunoassay. CSF-NTPLI did not differ significantly between AD type I (pure AD) and controls, but was significantly higher in AD type II (senile dementia) and vascular dementia (VAD) as compared with controls. Signs of blood-brain barrier (BBB) damage (elevated CSF/S albumin ratio) were found in both AD type II and in VAD, but not in AD type I. In a multiple ANOVA, with age and CSF/S albumin ratio as covariates, no significant difference in CSF-NTPLI between diagnostic groups was noted though both CSF/S albumin ratio and age (P < 0.0001 and P < 0.001 respectively) were found to influence the CSF-NTPLI level. Since BBB function was found to influence the CSF-NTPLI level, we examined whether NTPLI was present in serum. Indeed, serum NTPLI was about 40 times higher than CSF-NTPLI in neurological patients. Moreover, there was a statistically significant correlation between S-NTPLI and CSF-NTPLI. Taken together, present findings suggest that most of NTPLI in CSF comes from the serum, by passage over the BBB.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Tau protein in cerebrospinal fluid: a biochemical marker for axonal degeneration in Alzheimer disease?

Cerebrospinal fluid (CSF) biochemical markers for Alzheimer disease (AD) would be of great value to improve the clinical diagnostic accuracy of the disorder. As abnormally phosphorylated forms of the microtubule-associated protein tau have been consistently found in the brains of AD patients, and since tau can be detected in CSF, two assays based on several well-defined monoclonal tau antibodies were used to study these proteins in CSF. One assay detects most normal and abnormal forms of tau (CSF-tau), while the other is highly specific for phosphorylated tau (CSF-PHFtau). A marked increase in CSF-PHFtau was found in AD (2230 +/- 930 pg/mL), as compared with controls (640 +/- 230 pg/mL; p < 0.0001), vascular dementia, VAD (1610 +/- 840 pg/mL; p < 0.05), frontal lobe dementia, FLD (1530 +/- 1000 pg/mL; p < 0.05), Parkinson disease, PD (720 +/- 590 pg/mL; p < 0.0001), and patients with major depression (230 +/- 130 pg/mL; p < 0.0001). Parallel results were obtained for CSF-tau. No less than 35/40 (88%) of AD patients had a CSF-PHFtau value higher than the cutoff level of 1140 pg/mL in controls. The present study demonstrates that elevated tau/PHFtau levels are consistently found in CSF of AD patients. However, a considerable overlap is still present with other forms of dementia, both VAD and FLD. CSF-tau and CSF-PHFtau may therefore be useful as a positive biochemical marker, to discriminate AD from normal aging, PD, and depressive pseudodementia. Further studies are needed to clarify the sensitivity and specificity of these assays, including follow-up studies with neuropathological examinations.

Aged↗