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Biomedical subjects

J Court

Publications and source records attributed to J Court.

At least 19 recordsLinked to original sources
PubMed1995

Distribution of nicotinic subtypes in human brain.

The distribution of high-affinity nicotine and alpha-bungarotoxin receptors has been compared in a number of human brain areas and related to the available data on receptor subtype mRNA expression. Nicotine binding is high in the thalamus, striatum, and substantia nigra pars compacta, and although not generally high in the hippocampal formation, it is concentrated in the entorhinal cortex, the subicular complex, and the stratum lacunosum moleculare. Nicotine binding is relatively low in the cerebral cortex, but it demonstrates varied patterns of distribution in different areas. Nicotine binding is also present in the cerebellar cortex and dentate nucleus. Nicotine binding in the thalamus corresponds to alpha 3 expression, but at variance to data from rodents, there is little evidence of beta 2 mRNA in this brain area. By contrast, there is beta 2 mRNA but not alpha 3 mRNA in the striatum. In the hippocampal formation both alpha 3 and beta 2 mRNAs are expressed, but the pattern of distribution does not resemble nicotine binding, only reaching moderate levels in the dentate granule cell layer and in the CA3 region. In the neocortex, alpha 4 expression is more widely distributed than alpha 3, but both are associated with pyramidal neurons. The distribution of nicotine binding, concentrated in brain areas gating multimodal inputs and often uncorrelated with cholinergic innervation, suggests a neuromodulatory role, possibly facilitating glutamatergic transmission. The distribution of alpha-bungarotoxin binding is different from that of nicotine in the hippocampal formation, being highest in the CA1 region and the dentate granule cell layer, but similar to nicotine binding in the substantia nigra pars compacta.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Distribution↗
PubMed1993

HLA-DQ genotypes are associated with autoimmunity to glutamic acid decarboxylase in insulin-dependent diabetes mellitus patients.

This study has investigated the genetic basis of the heterogeneous autoimmune response to glutamic acid decarboxylase (GAD) in 179 Australian patients with IDDM. Antibodies to GAD have been correlated with HLA-DQB1 alleles and genotypes, as determined by sequence-specific oligonucleotide hybridizations after polymerase chain reaction was applied to exon 2 of the DQ beta 1 gene. HLA-DQ2 was significantly increased (p < 0.01) in IDDM patients with antibodies to GAD. Antibodies to GAD were detected in 64% of 72 DQ2.8 patients, in 55% of 29 DQ2.2 or DQ8.8 patients and in 41% of 78 patients with other HLA-DQB1 genotypes. HLA-DQ genotype association with autoimmunity to GAD was statistically significant (p = 0.02) and reflected early formation of antibodies to GAD, rather than an HLA association with persistence of antibodies to GAD, since the genotype effect was more evident (p = 0.02) in those with more recent onset (0-5 years) of IDDM. Also, the HLA-DQ genotype effect was more evident in patients with IDDM onset after the age of 14 years (p = 0.003). Multivariate analysis showed that HLA-DQB1 genotypes had a more significant impact on antibodies to GAD than either duration or age of onset of IDDM. In patients with IDDM in childhood, only a minority had low-risk HLA-DQB1 genotypes (37%) when compared with those with onset in adulthood (62%) (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Neuropsychological functioning in adolescents with diabetes.

Investigated the relationship between disease variables, neuropsychological performance, and psychosocial status in adolescents with Insulin Dependent Diabetes Mellitus (IDDM). The study group consisted of 85 adolescents, aged 14 to 16.5 years who had been diabetic for longer than 12 months. Parameters of both recent and long-term metabolic control were determined, including diabetic incidents such as severe hypoglycemia or ketoacidosis. The mothers completed standardised measures of adolescent adjustment, and the adolescents provided self-reports of psychosocial status. Neuropsychological functioning was evaluated with standardised tests of verbal and nonverbal intelligence, memory and new learning, visuo-graphic skills, mental flexibility, and problem-solving ability. Using retrospective accounts of disease history, there was no relationship between neuropsychological functioning and variables such as age of onset, chronic poor control, or major metabolic crises. The findings emphasise the need for a long-term, prospective study of a cohort of diabetic children from the time of diagnosis to clarify causal relationships, if any, between illness variables, neuropsychological performance, and psychosocial factors.

Adolescent↗
PubMed1992

Delayed cyanide induced dystonia.

A 16 year old man ingested 1 g potassium cyanide in 1969. A few days after an apparently full recovery he developed a severe dystonia syndrome. He had a positive response to an apomorphine test and showed improvement with levodopa treatment. A 21 year follow up showed minimal neurological sequelae; CT showed bilateral putaminal lucencies. Visual and brain stem auditory evoked potentials were normal.

Adolescent↗
PubMed1987

Serum creatine kinase-BB levels and cerebral cortical creatine kinase activity in senile dementia of the Alzheimer type.

A rise in serum creatine kinase-BB (CK-BB) levels has been reported previously in cases of dementia. In the present study the levels of serum CK-BB have been measured in patients clinically assessed to have senile dementia of the Alzheimer's type (SDAT) and in cognitively intact individuals, matched for age, by a specific two-site monoclonal immunoradiometric assay. No significant difference was found between the 2 groups. Total creatine kinase activity in temporal cortex (Brodmann area 21 and 22) was also found to be similar in brains from SDAT or control cases, obtained at autopsy. These results suggest no major change in the permeability of the blood-brain barrier to this enzyme in SDAT patients.

Alzheimer Disease↗
PubMed1983

Axonal transport dysfunction in dystrophia myotonica.

Axonal transport of acetylcholinesterase (AChE) was measured in the median and sural nerves of a subject who suffered from dystrophia myotonica and in a control subject. It was found that the basal activity of AChE was increased in myotonic nerves while its proximodistal transport was inhibited.

Acetylcholinesterase↗
PubMed1983

[EEG in vasomotor cephalgias and in tension headache].

The EEG examination of 45 patients with vascular headache and 44 patients with tension headache showed abnormal EEG's in 71% of the cases with migraine and 35% of the cases with tension headache. The examination of morphology and topography of alpha-rhythm and driving-effect during photic stimulation showed statistically significant differences between both groups. Applying specific characteristics in the EEG it is possible to differentiate both types of headache.

Adult↗
PubMed1981

Lymphocytotoxic antibodies and histocompatibility antigens in juvenile-onset diabetes mellitus.

Cold-reacting serum lymphocytotoxic antibodies (LCAs) were measured in sera from 230 insulin-dependent juvenile-onset diabetes mellitus (IDDM) patients and from 116 control subjects. LCAs were present in only 4% of control sera compared with 19% in IDDM patients. The most significant determinant of LCAs was time since onset of diabetes; within the first 12 mo, 55% of IDDM sera had LCAs, compared with 25% after one year and 15% after five years of diabetes. LCAs were absent in sera from patients with IDDM for 10 yr or more. Genetic factors were also implicated in susceptibility toi occurrence of LCAs. HLA antigen B8 and B18 were associated with an increased risk for LCAs, whereas HLA-B7 was associated with a decreased risk. The relative risk for LCAs in patients positive for HLA-B8 but not B7 was 2.3, compared with 0.0 in HLA-B7/B8 heterozygotes. In contrast, B7 did not provide protection from LCAs in B18/B7 IDDM patients. Properdin factor B (Bf) alleles, which are in linkage disequilibrium with alleles of the HLA-B locus, were also associated with LCAs, IDDM patients with alleles BfS1 or BfF hd a prevalence of LCAs of 7%, significantly less than the 39% in Bf-F1S or -F1 patients. LCAs were not identical or closely correlated to pancreatic islet cell antibodies. Our findings indicate genetic heterogeneity in, yet, another autoimmune process in IDDM.

Adolescent↗
PubMed1980

Distribution of complement C'2 and C'6 types in Australian cases of diabetes mellitus.

A series of patients with juvenile onset diabetes (IDDM) and mature onset diabetes (NIDDM) have been typed for genetic variants of two sets of complement factors. For the HLA-linked C'2 system, there was found a significant increase of the C'2 2-1 type in IDDM compared with NIDDM patients or healthy controls. No such increase in any phenotype was observed for the non-HLA-linked C'6 system. These observations emphasize again the genetic distinction between IDDM and NIDDM, and the role of chromosome 6 in controlling susceptibility to the insulin-dependent form of the disease.

Alleles↗
PubMed1980

HLA studies in Australian multiple-case families of juvenile onset diabetes mellitus.

The pathogenesis of insulin-dependent diabetes mellitus (IDDM) will remain obscure until the number of genetic mechanisms contributing to susceptibility can be clarified. Australian multiple-case families of IDDM have been examined for concordance in IDDM and HLA haplotypes and analysed for goodness-of-fit to hypotheses of one or two high-risk susceptibility genes. Diabetic siblings are HLA-identical in 75% of cases, confirming the association between HLA and IDDM, and suggesting recessively in inheritance of IDDM susceptibility. However, the most striking finding is that 52% of IDDM offspring are positive for both HLA-DRW3 and DRW4, compared with only 8% of their non-diabetic sibs and 1% of the general population. The risk for IDDM for the HLA-DRW3/DRW4 heterozygote is 37.2, and the chance that a child from a multiple-case family of IDDM will himself develop the disease is 6.5 times as great if he is a HLA-DRW3/DRW4 heterozygote than if he is not positive for both antigens. Possible genetic mechanisms are discussed, but the present data strongly support the interaction of two HLA-DR associated susceptibility genes in IDDM and rejects the hypothesis of a single autosomal recessive susceptibility gene.

Australia↗
PubMed1979

HLA patterns in Australian patients with insulin dependent diabetes mellitus (IDDM).

HLA antigens were determined in 169 Australian patients with insulin dependent diabetes mellitus (IDDM). HLA-B8 (47.9% v. 23.8%) and B15 (18.9% v. 8.2%) were significantly more frequent in the IDDM patients than in 1460 controls. The relative risks for developing IDDM in people carrying these antigens were 2.94 and 2.59 respectively. Carriers of the B8/B15 genotype had a relative risk of 5.48. These HLA associations in Australian IDDM patients are similar to those reported in other predominantly Caucasian populations.

Adolescent↗