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Biomedical subjects

M Rogers

Publications and source records attributed to M Rogers.

At least 217 records · Page 12Linked to original sources
PubMed1989

Screening for Duchenne muscular dystrophy.

A programme was introduced in Wales to screen all 18 month old boys who were not yet walking for raised creatine kinase activity within the existing community developmental screening programme. During an 18 month period 25 229 such boys were identified of whom 19 930 (79%) had a Denver developmental screening test and 338 (1.7%) of these were not walking. Two hundred and five of those who did not walk (61%) had creatine kinase activity assayed and two cases of Duchenne muscular dystrophy were detected. We conclude that screening boys of 18 months who do not walk is worthwhile if the opportunity arises, but that a population based screening programme of this type is not justified as detection rates will be unacceptably low.

Child Development↗
PubMed1989

Serology of acute and chronic type B hepatitis.

Hepatitis B infection remains a clinically important cause of acute and chronic hepatitis worldwide. New information, based on the detection in serum of HBV markers has allowed new insight into the behavior of the virus in acute and chronic infection. The serology of an acute, self-limited infection remains relatively simple and is based on a typical rise and fall in HBsAg and IgM anti-HBc levels with subsequent production of anti-HBs. A better understanding of viral behavior in chronically infected individuals has led to the designation of replicative and nonreplicative phases. If used in conjunction with liver biopsy findings, these newer divisions allow a clearer understanding of variations in serology, clinical course and ultimate outcome than was possible previously. Finally, with the introduction of hepatitis B vaccines and promising early results from studies designed to treat chronic infection, we may at last be making progress in this major health problem.

Acute Disease↗
PubMed1989

The narcotic bowel syndrome.

In this editorial, we review the narcotic bowel syndrome, its etiology, presentation, and treatment. We suggest this is an often overlooked diagnosis in many clinical settings.

Abdomen↗
PubMed1989

Heterotropic brain tissue presenting as bald cysts with a collar of hypertrophic hair. The 'hair collar' sign.

We report the cases of two children who were each noted at birth to have a single bald compressible nodule on the scalp that was surrounded by a collar of hypertrophic hair. One of the mothers had taken doxylamine succinate during pregnancy. Extensive investigations and, finally, surgery revealed that the lesions were heterotropic brain tissue without connection to the brain. Encephaloceles may also have a "hair collar." The presence of a hair collar around any cutaneous lesion should alert the clinician to the possibility of a neuroectodermal defect. All procedures on these lesions should be delayed until appropriate investigations have excluded any connection with the underlying nervous system.

Brain↗
PubMed1989

Occurrence of platelet-activating factor (PAF) and an endogenous inhibitor of platelet aggregation in diffuse cutaneous mastocytosis.

We have identified PAF in the blister fluid from a patient with bullous mastocytosis, a rare form of mast-cell disease. We have found a novel endogenous inhibitor of platelet aggregation which obscured the presence of the PAF in unprocessed blister fluid and in ethanol or lipid extracts. The PAF was characterized by the demonstration of chromatographic, mass spectral and biological properties identical to those of authentic PAF. Thus this is the first demonstration of PAF in biological fluid from a patient with mastocytosis. High levels of immunoreactive prostaglandin D2 (PGD2) and histamine were also present in the blister fluid. The interaction between PAF and the inhibitor of platelet aggregation in patients with systemic mastocytosis may provide an explanation for some of the manifestations of the disease, in particular the episodic hypotension, cutaneous flushing and pallor.

Blister↗
PubMed1988

Canine alpha-L-fucosidase in relation to the enzymic defect and storage products in canine fucosidosis.

Canine liver alpha-L-fucosidase was purified to apparent homogeneity by affinity chromatography on agarose-epsilon-aminohexanoyl-fucopyranosylamine. It is composed of multiple forms of a common active subunit of 45-50 kDa, which can aggregate in different combinations to form polymers, predominantly dimers. Antiserum was raised against the purified enzyme. There is negligible residual alpha-L-fucosidase in the tissues of English springer spaniels with the lysosomal storage disease fucosidosis. Although no alpha-L-fucosidase protein was detected by Western blotting or by the purification procedure in the affected tissues, some enzymically inactive cross-reacting material was detected in both normal and affected tissues. This suggests that another protein without alpha-L-fucosidase activity was co-purified with the enzyme. Dog liver alpha-L-fucosidase was precipitated by goat anti-(human liver alpha-L-fucosidase) IgG, indicating homology between the enzymes in the two species. Two purified storage products isolated from the brain of a dog with fucosidosis were used as natural substrates for various preparations of canine liver alpha-L-fucosidase. Analysis of the digestion mixtures by t.l.c. and fast-atom-bombardment mass spectrometry suggests that canine alpha-L-fucosidase acts preferentially on the alpha-(1-3)-linked fucose at the non-reducing end and that removal of alpha-(1-6)-linked asparagine-linked N-acetylglucosamine is rate-limiting in the lysosomal catabolism of fucosylated N-linked glycans.

Animals↗
PubMed1988

Structural studies of the O-antigen polysaccharide of Salmonella thompson, serogroup C1 (6,7).

The structure of the O-antigen polysaccharide of Salmonella thompson, serogroup C1 (6,7) has been investigated mainly by methylation analysis, n.m.r. spectroscopy, specific degradations by a phage-associated enzyme, N-deacetylation-deamination, and f.a.b.-m.s. It is concluded that the structure involves the following repeating unit. (formula; see text) There are two populations of chains, with and without alpha-D-glucopyranosyl groups, 3-linked to an alpha-D-Manp residue, and only the latter type is hydrolysed by the phage enzyme. The alpha linkage of the third Manp residue is cleaved by the O14 phage enzyme. The structure, with or without the alpha-D-glucopyranosyl group, represents the biological repeating-unit.

Carbohydrate Conformation↗
PubMed1988

Bryostatin 1, an activator of protein kinase C, mimics as well as inhibits biological effects of the phorbol ester TPA in vivo and in vitro.

The macrocyclic lactone bryostatin 1 activates protein kinase C as effectively as the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Nevertheless, there are only certain TPA-effects that can be induced by bryostatin 1. These include stimulation of epidermal DNA synthesis and alkaline phosphatase activity in vivo as well as activation of the Ca2+-independent, phospholipid-requiring phosphorylation of an epidermal protein in a cell-free system. Various other TPA-effects in vivo and in vitro, which are not mimicked by bryostatin 1 can be inhibited by applying bryostatin 1 30 min prior to TPA. TPA-effects suppressible by bryostatin 1 include the Ca2+-dependent stimulation of arachidonic acid and prostaglandin E2 release, of ornithine decarboxylase (ODC) activity and ODC-mRNA expression and of transglutaminase activity in keratinocytes in vivo and/or in vitro and, in addition, Epstein-Barr virus induction in Raji cells. The same is true for the conversion step (first stage of promotion) of multistage carcinogenesis. In contrast to the TPA induction of arachidonic acid and prostaglandin E2 release and of transglutaminase activity, induction by the Ca2+-ionophore and by high Ca2+-shift, respectively, are not significantly inhibited by bryostatin 1. We suggest that bryostatin 1 might inhibit a specific 'Ca2+-component' of TPA action.

Animals↗
PubMed1987

A three-year study of impetigo in Sydney.

Two hundred and forty-three cases of impetigo, which were seen in children in Sydney in the three-year period from July, 1983 to June, 1986, were studied. The great majority of cases was seen in summer and autumn, and over half the cases occurred in the preschool age group. Staphylococcus aureus was grown from 86% of the cases; in 69% of cases it was the only organism to be found, indicating the predominant importance of this organism in impetigo in Sydney in the 1980s. Antibiotic-sensitivity testing of the staphylococci that were cultured demonstrated that fewer than 2% of strains were sensitive to penicillin and fewer than 50% of strains were sensitive to erythromycin. Our experience suggests that flucloxacillin is the antibiotic agent of choice in the treatment of impetigo in children in Sydney.

Adolescent↗
PubMed1987

Unusual skin rash following withdrawal of oral 6-mercaptopurine in children with leukemia.

Sixteen episodes of a distinctive, papular rash occurred in eight patients following withdrawal of 6-mercaptopurine (6MP) and methotrexate (MTX) used as maintenance therapy for acute lymphoblastic leukemia (ALL). The rash also developed in one of the eight patients when only 6MP was discontinued. The eruption occurred mainly on the face, and in this site resembled the perioral dermatitis seen following withdrawal of topical fluorinated steroids. The rash generally began within 3 weeks of stopping 6MP and lasted 3 to 4 weeks. It failed to improve with the use of topical corticosteroid. We conclude that this rash is caused by the withdrawal of oral 6MP.

Child↗
PubMed1987

Effects of the phorbolester TPA and of the ionophore A 23187 on phospholipase A2 and C activities in the mouse epidermal cell line HEL-30.

The 12-O-tetradecanoylphorbol-13-acetate (TPA)- or ionophore A 23187-induced release of 14C-arachidonic acid from prelabeled murine HEL-30 keratinocytes was studied in vitro. Starting 8 min after drug treatment, a linear increase in the arachidonic acid content in the extracellular medium was observed with a concomitant loss of label in cellular phosphatidylcholine and phosphatidylinositol, but not in phosphatidylethanolamine and phosphatidylserine. No increase in intracellular diacylglycerol and phosphatidic acid was observed. The TPA-induced arachidonic acid release was inhibited by fluocinolone acetonide. The results indicate a direct activation of phosphatidylcholine- and phosphatidylinositol-specific phospholipases A2 by TPA and A23187. Cells prelabeled with 3H-choline released choline, choline phosphate and CDP-choline upon TPA but not upon A 23187 treatment. This could indicate activation of a phospholipase C-type enzyme by the phorbol ester. However, concomitant generation of diacylglycerol and phosphatidic acid was not detected.

Animals↗
PubMed1987

Neutrophilic dermatosis of myeloproliferative disease in a 10-year-old.

The initial features of acute myeloid leukemia in a previously well 10-year-old girl consisted of cellulitic lesions on the face and limbs. These lesions subsequently progressed, with superimposed blistering and pustulation. They were painful and tender. The condition did not respond to systemic broad-spectrum antibiotic therapy. Skin biopsy showed an intense, dermal neutrophilic infiltrate without additional evidence of infection or leukemic deposits. The cutaneous lesions responded promptly to high-dose systemic corticosteroids, and the leukemia to chemotherapy.

Cellulitis↗