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Biomedical subjects

A Moon

Publications and source records attributed to A Moon.

16 recordsLinked to original sources
PubMed1995

Allergic gastroenteropathy in children.

OBJECTIVE: To review the pathogenesis, symptoms, and treatment of gastrointestinal disorders linked to immunopathologic reactions associated with the ingestion of food antigens in infancy and childhood. DATA SOURCES: A computerized MEDLINE search was performed for the following topics: allergic colitis, allergic proctitis, eosinophilic gastroenteritis, eosinophilic colitis, cow milk intolerance, protein losing enteropathy, and malabsorption. This search was restricted to the English language and human subjects. Articles published between 1960 and 1993 were included as references. The textbooks which were used as references include: (1) Walker WA, et al, eds. Pediatric gastrointestinal disease; pathophysiology, diagnosis, management, Philadelphia: BC Decker, 1991; (2) Wyllie R, et al, eds. Pediatric gastrointestinal disease; pathophysiology, diagnosis, management, Philadelphia: WB Saunders, 1993; (3) Targan SR, et al, eds. Immunology & immunopathology of liver and gastrointestinal tract. Igaku-Shoin, 1991; (4) Goldman H, et al, eds. Pathology of the gastrointestinal tract. Philadelphia: WB Saunders, 1992. CONCLUSION: The symptoms of allergic gastroenteropathy may be those of classic allergic reactions or present as symptom complexes that may include diarrhea, malabsorption, and protein-losing enteropathy. The immunopathogenesis of allergic gastroenteropathy is complex and is still not clearly understood. As our understanding of the gastrointestinal mucosal system evolves, we should be able to manage and care for the infants and children who suffer from this group of disorders better.

Allergens↗
PubMed1994

Alas, poor title.

Explore the source record for details and available documents.

Periodicals as Topic↗
PubMed1994

Ultrastructure of the yeast actin cytoskeleton and its association with the plasma membrane.

We characterized the yeast actin cytoskeleton at the ultrastructural level using immunoelectron microscopy. Anti-actin antibodies primarily labeled dense, patchlike cortical structures and cytoplasmic cables. This localization recapitulates results obtained with immunofluorescence light microscopy, but at much higher resolution. Immuno-EM double-labeling experiments were conducted with antibodies to actin together with antibodies to the actin binding proteins Abp1p and cofilin. As expected from immunofluorescence experiments, Abp1p, cofilin, and actin colocalized in immuno-EM to the dense patchlike structures but not to the cables. In this way, we can unambiguously identify the patches as the cortical actin cytoskeleton. The cortical actin patches were observed to be associated with the cell surface via an invagination of plasma membrane. This novel cortical cytoskeleton-plasma membrane interface appears to consist of a fingerlike invagination of plasma membrane around which actin filaments and actin binding proteins are organized. We propose a possible role for this unique cortical structure in wall growth and osmotic regulation.

Actins↗
PubMed1994

A radiation hybrid map of human chromosome 18.

A human x Chinese hamster (CH) somatic cell hybrid subclone deficient in HPRT and containing only human chromosome 18 was irradiated with 7000 rad and fused to a thymidine kinase deficient CH cell line. Radiation-rescued hybrid cell lines, selected in HAT medium, were analyzed for human DNA with human interspersed-repeat sequence primers. Size and number of human chromosome fragments retained in a subset of hybrids were determined by FISH. A panel of 98 radiation hybrids (RH) was selected and analyzed for 90 chromosome 18-specific STSs by PCR, and for the D18Z1 centromeric marker by Southern blotting. STSs were developed from previously mapped RFLP loci and from published sequences. In addition, 32 novel STSs were generated from an 18-specific lambda library and from 18-specific YACs previously localized to chromosome bands by FISH. Marker retention frequency varied from 8-65% with an average of 24%. In selected RH the STS typing data were correlated with the chromosome 18 regions retained using 'reverse FISH' of IRS-PCR products from the RH to normal metaphase chromosomes. The order and intermarker distances of loci were determined using two-point and multipoint maximum likelihood methods. The resulting RH map covers most of chromosome 18 with four groups of tightly linked markers and three regions of loosely linked markers, one around the centromere and two on the long arm. More than a third of the markers are polymorphic and allow integration with the linkage map. This RH map provides a framework for establishing a clone contig of the entire chromosome 18.

Animals↗
PubMed1993

Perceptions of elder abuse and help-seeking patterns among African-American, Caucasian American, and Korean-American elderly women.

Thirteen scenarios were used to measure and compare the perceptions of elder abuse and help-seeking behaviors of African-American, Caucasian American, and Korean-American elderly women. Significant group differences existed in their perceptions of elder abuse with regard to six scenarios, and the Korean-American women were substantially less likely to perceive a given situation as abusive than the other groups. The three groups also showed significant differences in their intended use of formal and informal sources of help in the case of elder abuse.

Black or African American↗
PubMed1993

Promoting the health promoting school.

The Health of the Nation strategy commits the government to establishing a national network of health-promoting schools. Alysoun Moon describes an independent pilot project in Wandsworth, south London which is pioneering the concept in ten selected primary schools.

Child↗
PubMed1992

Sural nerve conduction parameters in normal subjects related to age, gender, temperature, and height: a reappraisal.

Failure to take body height into considerations in the evaluation of nerve conduction velocities (CV) has recently been deemed unacceptable. This statement prompted the present study. Besides height, the influence of age, gender, and temperature was studied in 92 normal subjects, half of whom were females. The CV decreased 0.9 m/s per 10 years increase in age, the same in women and men aged 15 to 44 years. Mean temperature between distal and proximal ends of the nerve segment examined increased 6.1 +/- 0.3 degree C after heating followed by a CV increase of 7.0 +/- 0.5 m/s. The CV decreased 0.15 m/s per 100-mm increase in heights. When considering 37 individuals aged 25 to 34 years only, the CV increased 0.34 m/s per 1-m increase in height. In both instances, the changes were within the experimental error (2.3%) of the method.

Action Potentials↗
PubMed1988

Long-chain acyl-coenzyme A dehydrogenase deficiency: biochemical studies in fibroblasts from three patients.

We studied fibroblasts from three patients with long-chain acyl-coenzyme A dehydrogenase (LCADH) deficiency; siblings H.C. and J.C. had milder clinical phenotypes than unrelated patient R-1. In H.C., J.C., and R-1 oxidation of [9,10(n)-3H]palmitate was 50, 48, and 28% of control, respectively, with R-1 having significantly less activity than H.C. and J.C. (p less than 0.05). Assays of mitochondrial short-chain and medium-chain acyl-coenzyme A dehydrogenases were normal in H.C. and J.C. However, mitochondrial LCADH activities in all three ranged from 17 to 21% of control. Flavin adenine dinucleotide addition increased LCADH activities in all three to 27-36% of control. In the presence of monospecific medium-chain acyl-coenzyme A dehydrogenase antiseria, LCADH activity decreased 17% in controls, and fell to less than or equal to 11% of control in J.C. and R-1. The heterogeneity observed in the [3H]palmitate oxidation studies was not explained by differences in LCADH activities under any assay condition.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed1987

Complementation analysis of fatty acid oxidation disorders.

We assayed [9,10(n)-3H]palmitate oxidation by fibroblast monolayers from patients with fatty acid oxidation disorders. Activities in the different disorders were (percent control): short-chain acyl-coenzyme A (CoA) dehydrogenase deficiency (115%), medium chain acyl-CoA dehydrogenase deficiency (18%), long-chain acyl-CoA dehydrogenase deficiency (28%), multiple acyl-CoA dehydrogenation disorder, mild and severe variants (49% and 7%), and palmityl-carnitine transferase deficiency (4%). Multiple acyl-CoA dehydrogenation disorder, medium chain acyl-CoA dehydrogenase-deficient lines, and long-chain acyl-CoA dehydrogenase-deficient lines all complemented one another after polyethylene glycol fusion, with average activity increases of 31-83%. We detected two complementation groups in the severe multiple acyl-CoA dehydrogenation disorder lines, consistent with deficiencies of either electron transfer flavoprotein or electron transfer flavoprotein:ubiquinone oxidoreductase. The metabolic block in the latter cell lines is threefold more severe than in the former (P less than 0.001). No intragenic complementation was observed within either group. We assigned two patients with previously unreported severe multiple acyl-CoA dehydrogenation disorder to the electron transfer flavoprotein:ubiquinone oxido-reductase-deficient group.

Acyl-CoA Dehydrogenase, Long-Chain↗
PubMed1987

Short-chain acyl-coenzyme A dehydrogenase deficiency. Clinical and biochemical studies in two patients.

We describe two patients with short-chain acyl-coenzyme A (CoA) dehydrogenase (SCADH) deficiency. Neonate I excreted large amounts of ethylmalonate and methylsuccinate; ethylmalonate excretion increased after a medium-chain triglyceride load. Neonate II died postnatally and excreted ethylmalonate, butyrate, 3-hydroxybutyrate, adipate, and lactate. Both neonates' fibroblasts catabolized [1-14C]butyrate poorly (29-64% of control). Neonate I had moderately decreased [1-14C]octanoate catabolism (43-60% of control), while neonate II oxidized this substrate normally; both catabolized radiolabeled palmitate, succinate, and/or leucine normally. Cell sonicates from neonates I and II dehydrogenated [2,3-3H]butyryl-CoA poorly (41 and 53% of control) and [2,3-3H]octanoyl-CoA more effectively (59 and 95% of control). Mitochondrial acyl-CoA dehydrogenase (ADH) activities with butyryl- and octanoyl-CoAs were 37 and 56% of control in neonate I, and 47 and 81% of control in neonate II, respectively. Monospecific medium-chain ADH (MCADH) antisera inhibited MCADH activity towards both butyryl- and octanoyl-CoAs, revealing SCADH activities to be 1 and 11% of control for neonates I and II, respectively. Fibroblast SCADH and MCADH activities were normal in an adult female with muscular SCADH deficiency.

3-Hydroxybutyric Acid↗
PubMed1987

Clinical and biochemical variation and family studies in the multiple acyl-CoA dehydrogenation disorders.

We report clinical and biochemical studies in patients with multiple acyl-CoA dehydrogenation disorders (MAD) and their parents. A severely affected (MAD:S) patient presented with neonatal acidosis leading to death and excreted a wide range of straight- and branched-chain acyl CoA derivatives. Two patients with mild variants of the same disorder (MAD:M) presented with neurologic abnormalities, acidotic coma, and/or poor growth; they primarily excreted ethylmalonate and variable amounts of adipate. Fibroblasts from the MAD:S patient demonstrated severely defective radiolabeled substrate oxidation, while the MAD:M cells had milder oxidative defects. Fibroblasts from two other MAD:M and six other MAD:S patients demonstrated analogous defects in substrate oxidation. As a group, MAD:S cells deficient in electron transfer flavoprotein:ubiquinone oxidoreductase had significantly lower residual oxidative activities than did MAD:S cells deficient in electron transfer flavoprotein. Fibroblasts from the parents of four MAD:S patients oxidized radiolabeled substrates significantly less effectively than did normal infant controls but were indistinguishable from normal adult cells. We found relatively higher residual oxidative activities in maternal than in paternal cells. Amniocytes from a fetus at risk for MAD:S catabolized labeled substrates normally; the infant has been clinically and biochemically normal up to 30 months of age.

Acyl-CoA Dehydrogenase↗
PubMed1985

14C-labeled substrate catabolism by human diploid fibroblasts derived from infants and adults.

Untransformed diploid skin fibroblasts from eight normal adults, aged 24 to 74 years, catabolized several 14C-labeled substrates less effectively than cells from ten normal male infants. 14C-labeled substrate metabolism was quantitated either by measuring the evolution of 14CO2 from the 14C-labeled compounds or the incorporation of 14C into cellular protein via transamination of tricarboxylic acid cycle intermediates derived from the 14C-labeled substrates. With these methods, adult cells catabolized [1-14C]butyrate, [1-14C]octanoate, and 1-[2-14C]leucine at rates 44 to 64% of those found in infant cells. The oxidation of [1,4-14C]succinate and [U-14C]malate was identical in both infant and adult cells, while [2,3-14C]succinate catabolism was mildly decreased in adult cells (65-80% of control). These observations parallel those made in rat tissues and confirm that the same phenomenon occurs in cultured human fibroblasts.

Adult↗