Search PubMed⌕ Search

Biomedical subjects

A Wallin

Publications and source records attributed to A Wallin.

At least 145 records · Page 8Linked to original sources
PubMed1990

Intra-blood-brain-barrier synthesis of immunoglobulins in patients with dementia of the Alzheimer type.

Serum and cerebrospinal fluid (CSF) of 56 patients with dementia of the Alzheimer type (DAT) and 33 healthy controls were examined in order to investigate intra-blood-brain-barrier (intra-BBB) synthesis of immunoglobulins. Intra-BBB immunoglobulin G (IgG) synthesis was defined as an elevated IgG index (greater than 0.7) and/or presence of oligoclonal IgG in CSF but not in serum on isoelectric focusing, and intra-BBB immunoglobulin M (IgM) synthesis as an elevated IgM index (greater than 0.06). In total, 10 (18%) DAT patients displayed an intra-BBB immunoglobulin synthesis--five (9%) an IgG and five (9%) an IgM synthesis--but none among the controls. Also, the DAT patient group showed higher mean IgG and IgM indexes than the control group. These findings support the hypothesis that immunological mechanisms may play a role in the etiology and/or pathogenesis of Alzheimer disease, at least in a subgroup of patients.

Aged↗
PubMed1989

Lidocaine treatment of neonatal convulsions, a therapeutic dilemma.

Three infants with neonatal convulsions were given lidocaine infusions for three days, three weeks and three months, respectively, and the plasma concentrations of lidocaine and its metabolites were analyzed by HPLC. After a prolonged infusion there was considerable accumulation of the metabolites. This may account for the difficulty of stopping the infusion without relapse of the seizures.

Female↗
PubMed1989

Monoamine metabolites in cerebrospinal fluid and behavioral ratings in patients with early and late onset of Alzheimer dementia.

Patients with Alzheimer disease (AD, onset less than 65 years of age, n = 13) and senile dementia of the Alzheimer type (SDAT, onset greater than or equal to 65 years of age, n = 28) were investigated for cerebrospinal fluid (CSF) content of homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxy-phenylglycol (MHPG) and compared with a group of controls (n = 26). A geriatric rating scale, the Gottfries-Bråne-Steen scale, was used to assess impairment of motor performance, intellectual and emotional functioning, and symptoms common in dementia disorders. The HVA levels in CSF were significantly lower in the AD group than in the SDAT group and controls. MHPG was slightly but significantly increased in the SDAT group when compared with the controls. The HVA and 5-HIAA concentrations were correlated negatively with impairment of motor performance in the SDAT group; 5-HIAA correlated positively with impaired performance in the AD group; and 5-HIAA/HVA ratios were correlated positively with the performance variables. HVA correlated significantly and negatively with "impaired wakefulness" and "inability to increase tempo" in the SDAT group. 5-HIAA and the ratio 5-HIAA/HVA correlated significantly and positively with some items measuring intellectual and emotional impairment. In the AD group, "anxiety" and "fear-panic" correlated positively with 5-HIAA and "restlessness" with MHPG. The data indicate qualitative differences in the CSF monoamine pattern between AD and SDAT.

Aged↗
PubMed1989

Neurotransmitter deficits in a non-multi-infarct category of vascular dementia.

Brain tissue from 9 severely demented patients cared for in psychiatric long-term wards and with records of stroke episodes, macroscopic signs of brain infarcts and with no clinical evidence of senile dementia of the Alzheimer type was investigated and compared with control material. The mean volume of the brain infarcts in this vascular dementia group was only 6.8 ml. Pronounced disturbances of the serotoninergic and cholingergic systems were found in subcortical and cortical grey matter. These widespread neurotransmitter changes can hardly be explained by the localized brain infarcts per se, but suggest the existence of another category of vascular dementia. Since the neurotransmitter disturbances were found to be similar to those of Alzheimer's disease and senile dementia of the Alzheimer type, it seems more likely that they indicate a common pathway for dementia disorders than that they serve as markers of different dementia categories.

Aged↗
PubMed1989

Decreased myelin lipids in Alzheimer's disease and vascular dementia.

The lipid composition of white matter and myelin from the semioval centre was studied in autopsy material from cases with Alzheimer's disease (AD) (n = 11), vascular dementia (VD) (n = 7), and age-matched controls (n = 11). In AD and VD the white matter content of phospholipids and cholesterol was reduced to 72-76% of the control values (P less than 0.01), the diminution of cerebrosides and sulphatides was more pronounced (55-69%) (P less than 0.001) while the concentration of gangliosides did not change significantly (87-90%). The myelin composition was the same in the 3 groups, suggesting that the white matter involvement is not caused by alteration of the myelin structure. The altered lipid composition in white matter in AD and VD suggests that the myelin sheath is the primary lesion site.

Aged↗
PubMed1989

White matter low attenuation on computed tomography in Alzheimer's disease and vascular dementia--diagnostic and pathogenetic aspects.

Demented patients with early-onset Alzheimer's disease (AD) (n = 17), late-onset Alzheimer's disease (n = 30) and vascular dementia (VD) (n = 20) were studied with computed tomography of the brain. Semiquantitative evaluation of white matter low attenuation (WMLA) and central and cortical atrophy was performed without knowledge of the clinical diagnosis. In early onset AD there was almost complete absence of WMLA and central atrophy compared with the other groups, which showed moderate to severe changes. This suggests that early-onset AD should be separated from the late-onset form. The increased systolic blood pressure found in the WMLA group supports the opinion that WMLA has a vascular origin. The high percentage of WMLA in VD and late-onset AD indicates that subcortical factors have to be considered in the pathogenesis of these disorders.

Aged↗
PubMed1989

Regulation of protein binding from 35S-(pentachlorobutadienyl)-L-cysteine in renal epithelial cells and mitochondria.

The protein binding rate of the reactive metabolite formed from the beta-lyase-mediated cleavage of S-(1,2,3,4-pentachloro-1,3-butadienyl)-L-cysteine was determined in rat kidney fractions and isolated renal epithelial cells. The binding was highest in mitochondria and localized to the outer membrane/intermembrane space and matrix. The matrix activity was stimulated by an alpha-keto acid. Soluble thiols and anoxia inhibited the protein binding.

Animals↗
PubMed1988

Features of microsomal and cytosolic glutathione conjugation of hexachlorobutadiene in rat liver.

Hepatic GSH conjugation is the initial step in the mammalian biotransformation of hexachloro-1,3-butadiene (HCBD) and analogous haloalkenes. The present paper reports an in vitro investigation of the glutathione-dependent conversion of HCBD to water-soluble products, i.e. the enzyme-catalyzed conjugation of HCBD with GSH. The method employed avoids artifacts due to the volatility, low solubility and hydrophobic nature of the chloro-carbon substrate. In order to assess the relative importance of membrane-bound and cytosolic glutathione S-transferase in the conjugation process, microsomal and cytosolic fractions from adult rat liver were tested separately for their ability to promote water solubilisation of the substrate. In addition, microsomal purified and liposomally reconstituted glutathione S-transferase, were tested. The reaction exhibited Michaelis-Menten kinetics, and conjugation rates were linear for at least 20 min. The hepatic microsomal fraction metabolized HCBD 116 times faster than the cytosolic fraction when substrate saturated. Both mono- and bis-substituted conjugates were formed by microsomal as well as by the cytosolic fraction. Treatment of animals with inducers and the use of specific inhibitors indicated absence of cytochrome P-450 involvement in the formation of water soluble HCBD metabolites and supported the view that microsomal glutathione S-transferase is more important in catalyzing GSH conjugation of this haloalkene than the cytosolic forms of transferases.

Animals↗
PubMed1988

CT evaluation of coverage and congruency of the hip prior to osteotomy.

A computer-assisted model has been developed to improve the results of surgical techniques for reconstruction of hip dysplasia. This method assesses the coverage and congruency of the femoral head by evaluating multiple factors that may influence surgical planning. It achieves a more reliable image because the measurements are based on a three-dimensional representation, and attention is focused on the cartilaginous coverage of the femoral head. A method to simulate the operative correction helps the surgeon in planning osteotomies of the femur and pelvis. This technique clearly establishes both deficiencies of coverage and congruency of pathologic hips and thus may be used to create a more precise definition and treatment of multiple congenital abnormalities.

Hip↗
PubMed1987

Toxicity of S-pentachlorobutadienyl-L-cysteine studied with isolated rat renal cortical mitochondria.

The subcellular mechanism of alkenyl halide S-conjugate-induced nephrotoxicity was studied in mitochondria isolated from rat kidney cortex in vitro using the cysteine conjugate of hexachloro-1,3-butadiene, i.e., S-pentachlorobutadienyl-L-cysteine (PCBC) as a model substrate. Respiring mitochondria exposed to various concentrations of PCBC exhibited a dose-dependent loss of ability to retain calcium. This phenomenon was associated with a sudden collapse of the mitochondrial membrane potential. PCBC caused a slow nonenzymatic depletion of mitochondrial glutathione. This was not due to oxidation or formation of mixed disulfides, and was efficiently counteracted by preincubation with aminooxyacetic acid, an inhibitor of cysteine-conjugate beta-lyase activity. PCBC inhibited state 3 respiration in the presence of succinate as substrate, which indicates that the activity of succinate dehydrogenase was affected. Thus, the present data confirm that impairment of mitochondrial function is a feature of nephrotoxicity mediated by alkenyl halide S-conjugates. We suggest a pathway involving interaction of beta-lyase-dependent reactive metabolite with the mitochondrial inner membrane, loss of membrane potential, disturbance of Ca2+ homeostasis, and subsequent respiratory insufficiency as a mechanism for renal tubular cytotoxicity.

Aminooxyacetic Acid↗
PubMed1987

Enzymatic hydrolysis of leukotriene A4 into 5,6-dihydroxy-7,9,11,14-eicosatetraenoic acid and LTB4 by mammalian kidney.

Homogenates from rat and pig kidney converted leukotriene A4 to 5,6-dihydroxy-7,9,11,14-eicosatetraenoic acid as well as leukotriene B4. Both hydrolyses were enzymatic as judged by the effects of heat treatment and proteolytic digestion. Upon subcellular fractionation, conversion of leukotriene A4 to 5,6-dihydroxy-7,9,11,14-eicosatetraenoic acid occurred both in the 105,000xg supernatant and the 20,000xg pellet from rat kidney, whereas conversion to leukotriene B4 was confined to the 105,000xg supernatant. We also found production of 5,6-dihydroxy-7,9,11,14-eicosatetraenoic acid and leukotriene B4 in isolated rat renal epithelial cells, either from exogenous leukotriene A4 or from this substrate supplied by human leukocytes.

Animals↗
PubMed1987

Antibodies in cerebrospinal fluid of some Alzheimer disease patients recognize cholinergic neurons in the rat central nervous system.

The etiology of Alzheimer disease is unclear. However, immunological aberrations have been suggested to be critical factors in the pathogenesis of this neurodegenerative disease. This study was carried out to investigate if cerebrospinal fluid (CSF) from Alzheimer disease patients contains antibodies that recognize specific neuronal populations in the rat central nervous system. The results indicate that in a subgroup of patients this is indeed the case. The antibodies reported in this study have the following properties: (i) they recognize neuronal populations and components in the medial septum and spinal motor neurons in rats perfused with a mixture that fixes small neurotransmitter molecules; (ii) adsorption of the patient CSF with staphylococcal protein A-Sepharose and using a polyclonal antiserum against human IgG3 indicates that the immunocytochemical reaction in these brain regions is mainly due to the subclass IgG3; and (iii) the CSF immunocytochemical reaction is blocked by preincubation of the sections with a rabbit anti-acetylcholine antiserum. These results provide evidence that antibodies in the CSF of some, but not all, Alzheimer disease patients recognize acetylcholine-like epitopes in cholinergic neurons in the rat central nervous system.

Acetylcholine↗
PubMed1987

A double-blind evaluation of electroconvulsive therapy in Parkinson's disease with "on-off" phenomena.

Eleven patients with severe Parkinson's disease and on-off-phenomena were included in a controlled double-blind study on the effect of electroconvulsive therapy (ECT). Pharmacological treatment was optimally adjusted before the trial. The severity of extrapyramidal symptoms was measured before, during and after the treatment. The patients were randomly allocated into one group, receiving active ECT and another, receiving sham treatment. The patients given active ECT showed significantly (P less than 0.05) prolonged duration of "on"-phases after ECT, in comparison to the sham-treated group. When collecting data from the controlled part of the study and the subsequent with open administration of ECT, the treatment was in addition found to significantly decrease the time and number of steps required to walk 10 meters. Moreover it reduced the severity of parkinsonian symptoms according to the Webster scale. The improvement induced by ECT was generally short-lasting. Lumbar punctures were performed before and after ECT. The concentrations of monoamine metabolites in cerebrospinal fluid were not affected by the treatment. The results indicate that ECT has an antiparkinsonian effect which probably is mediated via changed responsiveness of dopamine receptors and that further improvement is possible in patients, therapy resistant to the presently available medication.

Aged↗
PubMed1987

Biochemical and functional evidence for nerve sprouting in the decentralized, hypertrophied rat urinary bladder.

The preganglionic nerves of the rat urinary bladder were cut. The decentralized bladders gained markedly in weight. Both one and four weeks post-operatively, transmural nerve stimulation evoked contractile responses of the muscle strips of the decentralized bladders, that were of the same magnitude as those of the control bladders. However, four weeks post-operatively, the atropine resistant fraction of the response was decreased; consequently, the atropine sensitive (cholinergic) fraction was increased. The activity of the acetylcholine synthesizing enzyme, choline acetyltransferase, was increased at the late time of observation. The present biochemical and functional findings may suggest outgrowth of branches from the decentralized post-ganglionic cholinergic nerves.

Animals↗
PubMed1986

The mechanism of pentachlorobutadienyl-glutathione nephrotoxicity studied with isolated rat renal epithelial cells.

Isolated renal epithelial cells were used to study the mechanism of toxicity of pentachlorobutadienyl-glutathione (PCBG), a nephrotoxic glutathione conjugate of hexachlorobutadiene. The cytotoxicity of PCBG displayed a very steep dose-response relationship; at 10 microM PCBG no toxicity was observed whereas 25, 50, and 100 microM PCBG all resulted in a similar degree of toxicity. In all cases, loss of cell viability was observed only after a 30-min lag period and reached a plateau of 50 to 60% nonviable cells between 90 and 100 min. Toxic doses of PCBG also resulted in the depletion of cellular thiols. Blocking PCBG metabolism by inhibition of gamma-glutamyl transpeptidase [1-gamma-L-glutamyl-2-(2-carboxyphenyl)hydrazine (anthglutin), 2 mM] or renal cysteine conjugate beta-lyase (aminooxyacetic acid, 0.5 mM) resulted in complete protection against PCBG-induced cell damage. Exposure of isolated renal epithelial cells to 100 microM PCBG resulted in the rapid formation of plasma membrane blebs which appeared to be associated with a loss of Ca2+ from the mitochondrial compartment and an elevation of cytosolic Ca2+ concentration as measured by Quin-2. PCBG treatment also resulted in the inhibition of cell respiration and a marked depletion of cellular ATP content, indicating additional mitochondrial effects of the toxin. Our results support a role for renal cysteine conjugate beta-lyase in the metabolic activation of PCBG and suggest that PCBG-induced renal cell injury may be the result of selective effects on mitochondrial function.

Adenosine Triphosphate↗
PubMed1986

Prediction of hearing loss from acoustic-reflex thresholds in the older adult population.

The clinical applicability of prediction of hearing loss in 126 ears of 83 adults more than 44 years of age was investigated. The method of hearing-loss prediction was based on that proposed by Silman, Silverman, Showers, and Gelfand (J Speech Hear Res 1984;27:12-9). This method, which utilized the acoustic reflex thresholds for hearing-loss prediction, was modified to create a more clinically feasible procedure; 5 dB rather than 1 dB intensity increments and visual monitoring of needle deflection rather than the use of a graphic level recorder were used. This modified method yielded a high predictive accuracy for at least mild and/or high-frequency hearing impairment. Criteria based on acoustic-reflex threshold levels were developed to identify the presence of significant hearing loss (pure-tone average = or greater than 30 dB HL) in adults more than 44 years of age. The results have implications for hearing screenings for the difficult-to-test population such as the elderly.

Aged↗
PubMed1986

Transient supersensitivity in the hypertrophied rat urinary bladder.

The presence of a paraffin bolus intravesically for 1 or 4 weeks was accompanied by an approximate three-fold increase in bladder weight. A supersensitivity to methacholine was demonstrated in these hypertrophied bladders at 1 week but not at 4 weeks. At the earlier time of observation, the contractile responses in vitro to nerve stimulation were reduced, while at the later time of observation the responses were the same as those of controls; the atropine-sensitive fraction of the response was entirely responsible for the recovery. The concentration of choline acetyltransferase, indicating cholinergic nerve density and initially reduced by about 50%, rose in course of time. It is suggested that in the beginning of the experimental period, the muscle cells of the hypertrophied bladders in situ are exposed to 'subnormal' transmitter concentration. An extension of the field of innervation of the cholinergic nerves may explain the disappearance of the supersensitivity.

Animals↗