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Biomedical subjects

M James

Publications and source records attributed to M James.

At least 91 records · Page 5Linked to original sources
PubMed1996

Utrophin-dystroglycan complex in membranes of adherent cultured cells.

In skeletal muscle, dystrophin binds to an oligomeric, transmembrane complex (DAGc; dystrophin-associated glycoprotein complex) which interacts with laminin in the extracellular matrix. We now present biochemical evidence for an association between utrophin (dystrophin-related protein, DRP) and a major DAGc component, beta-dystroglycan (43DAG) in cultured cell lines which contain little if any dystrophin. We have shown also that utrophin and beta-dystroglycan co-localise at or near the plasma membrane and that they co-sediment in large complexes on sucrose density gradients. On the lower plasma membrane, in contact with the substratum, part of the utrophin and beta-dystroglycan staining co-localised with alpha-actinin in a punctate distribution outside classical vinculin-rich focal adhesions. beta-dystroglycan, utrophin, syntrophin (59DAP), and alpha-actinin were found in all adhesion-competent cell lines studied, but levels of the last three proteins were greatly reduced in myeloma cells, which cannot readily attach to substrata. Possible roles for utrophin in cultured cells are considered in the light of recent evidence for involvement of utrophin-glycoprotein complexes in muscle in signal transduction and recruitment of acetylcholine receptors to neuromuscular junctions.

Actinin↗
PubMed1996

Accreditation at what cost?

Analyses the implications of the management of labour for an organization undertaking an accreditation exercise. Considers the King's Fund Organizational Audit (KFOA) accreditation scheme, which is concerned with process and facilities, and assesses the quality of the hospital environment in which the health care product is supplied. Concludes that, given the current enthusiasm for finding best practice in health care and the ever-increasing number of cost-effectiveness analyses of therapeutic interventions, it seems somewhat contradictory that interventions which cover the whole environment in which health care interventions are performed are not treated in the same way.

Accreditation↗
PubMed1996

Prioritising elective care: a cost utility analysis of orthopaedics in the north west of England.

STUDY OBJECTIVE: To produce a priority list for purchasers to use when purchasing elective care in the speciality of orthopaedics so that efficiency in health care purchasing (that is, maximising the benefit per unit of resource available for the resident population) can be achieved. DESIGN: The study used cost utility analysis in the elective speciality of orthopaedics. The diagnostic groups in the study were chosen on the basis of those conditions that constituted the greatest proportion of the orthopaedic waiting list, and consequently the greatest proportion of activity within the speciality. Costs were derived by two methods: the extra contractual referral tariff (ECR) and individual patient based costings. Outcome was assessed before surgery and again approximately six months afterwards. The outcome of the procedures was derived in two ways: Rosser and EuroQol indices. SETTING: The study took place at Wrightington hospital, a specialist orthopaedic hospital in north west England. PATIENTS: Prospective assessments were obtained from 99 patients for nine orthopaedics procedures. All the patients were individually interviewed on each occasion. Rosser and EuroQol assessments were completed for each patient by the patient and the patient's consultant before and after surgery. MAIN RESULTS: Priority lists presenting cost utility rankings for each of the procedures were derived from the patients' and consultants' assessments. CONCLUSIONS: It is feasible to generate priority lists in a systematic way. Purchasers may then use the results from these priority lists to help them maximise the benefits per unit of resource for their resident population.

Cost-Benefit Analysis↗
PubMed1996

Exon-scanning mutation analysis of the ATM gene in patients with ataxia-telangiectasia.

Using a polymerase chain reaction single strand conformation polymorphism (PCR-SSCP) assay, which amplifies individually all coding exons of the ATM gene deficient ataxia-telangiectasia (A-T), we have analyzed 10 patients with A-T for ATM mutations. Mutation were detected in 9 patients. We describe the first ATM mutation in the splice junction found in the 5' splice site of intron 17, leading to exon skipping. However, most mutations were small deletions or insertions resulting in premature termination of the translation product. The development of DNA-based methods for detection of unknown mutations and further characterization of ATM mutation pattern will facilitate identification of A-T carriers and assessment of their cancer risk.

Ataxia Telangiectasia↗
PubMed1995

The public and the welfare reform debate.

OBJECTIVES: To identify the core beliefs and policy preferences of the American public toward changing the welfare system and providing support for low-income families. DESIGN: Results are presented from 19 telephone and in-person surveys of adults nationwide between 1937 and February 1995. SETTING: At-home interviews with adults. PARTICIPANTS: Seventeen surveys; each survey involved 1000 to 2000 adults nationwide. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The results showed that the public supports strong welfare reform measures (eg, time limits and work requirements), but it is reluctant simply to cut off welfare benefits to people and leave them without some means of basic support. The surveys identified five underlying beliefs that shape the public's policy preferences: (1) welfare causes more harm than good because it discourages work and causes families to break up; (2) welfare should be a temporary transition to work, not a long-term subsidy for low-income families; (3) the country spends too much on welfare programs; (4) lack of economic opportunity as well as personal responsibility is the reason people need welfare; and (5) both government and people themselves have a shared responsibility for ensuring that people have a minimum standard of living. CONCLUSIONS: The outcome of the welfare reform debate will have a substantial impact on the 21% of the nation's children who now live in poverty. The jury is still out on what the public will support in the welfare reform debate. The Medicaid program is caught in the middle of the welfare reform debate, and its ultimate fate may rely on state rather than federal decision making.

Adult↗
PubMed1995

Small intestinal injury in a neonatal rat model of giardiasis is strain dependent.

BACKGROUND & AIMS: The factors that determine the severity of giardiasis are poorly understood. Host factors are important, but parasite virulence may also play a role. The aim of this study was to compare the apparent virulence of three genotypically different Giardia isolates (PO1, VNB3, and WB). METHODS: Infection rates, parasite loads, structural damage, disaccharidase activity, and water and electrolyte absorption were observed at 10 days after inoculation in a neonatal rat model of infection. RESULTS: DNA fingerprinting showed differences between isolates studied. The infective rate varied between 67% and 100%. There were no differences in intestinal parasite load. Infection with strains PO1 and WB, but not with VNB3, was associated with a reduction in villus height. There was precocious expression of sucrase at 10 days after inoculation in all infected groups. Water absorption of a plasma electrolyte solution was decreased in VNB3-infected animals when compared with PO1- and WB-infected animals and controls. Water absorption and lactose hydrolysis were impaired during perfusion with a lactose-containing solution in all infected groups. CONCLUSIONS: Three genotypically different Giardia isolates that infect neonatal rats with the same trophozoite load differ in their ability to cause functional mucosal damage. Infection with Giardia lamblia induced precocious expression of sucrase activity and impaired mucosal absorption.

Animals↗
PubMed1995

Type III-A hypoplastic thumb.

Thirteen type III-A hypoplastic thumbs were reviewed. The abnormalities included those found in type II hypoplasia (narrow thumb-index web space, hypoplastic thenar muscles, unstable metacarpophalangeal joint, as well as extrinsic tendon abnormalities); all had stable carpometacarpal joints. They are differentiated from type III-B hypoplastic thumbs, which have an unstable carpometacarpal joint due to a deficient base of the metacarpal. The extrinsic tendon abnormalities included absent extensor pollicis longus tendon, absent or aberrant flexor pollicis longus tendon, and a tendon interconnection between the flexor pollicis longus and extensor aponeurosis. Twelve of the thumbs had surgical reconstruction. None was treated with ablation and index pollicization.

Adolescent↗
PubMed1995

Cardiac myosin binding protein-C gene splice acceptor site mutation is associated with familial hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy (FHC) is an autosomal dominant disease characterized by a ventricular hypertrophy predominantly affecting the interventricular septum and associated with a large extent of myocardial and myofibrillar disarray. It is the most common cause of sudden death in the young. In the four disease loci found, three genes have been identified which code for beta-myosin heavy chain, cardiac troponin T and alpha-tropomyosin. Recently the human cardiac myosin binding protein-C (MyBP-C) gene was mapped to chromosome 11p11.2 (ref. 8), making this gene a good candidate for the fourth locus, CMH4 (ref. 5). Indeed, MyBP-C is a substantial component of the myofibrils that interacts with several proteins of the thick filament of the sarcomere. In two unrelated French families linked to CMH4, we found a mutation in a splice acceptor site of the MyBP-C gene, which causes the skipping of the associated exon and could produce truncated cardiac MyBP-Cs. Mutations in the cardiac MyBP-C gene likely cause chromosome 11-linked hypertrophic cardiomyopathy, further supporting the hypothesis that hypertrophic cardiomyopathy results from mutations in genes encoding contractile proteins.

Amino Acid Sequence↗
PubMed1995

Evaluation of the SA locus in human hypertension.

The SA gene is expressed at 10-fold greater levels in the kidney of the spontaneously hypertensive rat compared with the normotensive Wistar-Kyoto rat. The gene is linked to blood pressure levels in a number of crosses involving the spontaneously hypertensive rat and other strains of genetically hypertensive rats. To assess its role in human hypertension, a human SA cDNA was cloned from a liver library. The cDNA was 1513 bp in length and exhibited a high identity with the published rat SA cDNA sequence in the coding region. A microsatellite marker was developed from a yeast artificial chromosome clone containing SA and mapped by linkage to human chromosome 16p13.11-12.3. Polymerase chain reaction amplification of human genomic DNA revealed two introns located in the SA gene, one of which contains a frequent polymorphism due to a single nucleotide substitution (cytosine to thymidine at residue 79 of the intron). Association and linkage studies in a large sample of hypertensive patients, normotensive control subjects, and multiplex sibships with these markers and other microsatellites in close proximity to SA revealed no evidence favoring involvement of the gene in the disease in humans. The methodology used in this study can be applied to the evaluation of other novel candidate genes obtained from investigations of experimental models of hereditary hypertension.

Adult↗