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J Cochrane

Publications and source records attributed to J Cochrane.

At least 37 records · Page 2Linked to original sources
PubMed1999

Ischemic preconditioning attenuates functional, metabolic, and morphologic injury from ischemic acute renal failure in the rat.

Ischemic preconditioning has been shown to ameliorate injury due to subsequent ischemia in several organs. However, relatively little is known about preconditioning and the kidney. To address this, rats were randomized to control (C, N = 14), 2 min of ischemic preconditioning (P2 N = 10), 3 periods of 2 min of ischemia separated by 5 min periods of reflow (P2,3 N = 7), or three 5 min periods of ischemia separated by 5 min of reflow (P5,3 N = 6) prior to 45 min of bilateral renal ischemia followed by 24 hours of reperfusion. We observed a lower serum creatinine after 24 hours of reflow in P2, P2, 3 but not P5, 3 rats compared with C. Histology was examined in the C and P2, 3 groups and demonstrated less severe injury in the P2, 3 group. To gain insight into the mechanism by which preconditioning ameliorated ischemic injury, we performed near IR spectroscopy and 31P NMR spectroscopy. Based on near IR spectroscopy, the P2, 3 group had closer coupling of cytochrome aa3 redox state with that of hemoglobin during reflow. In the 31P NMR studies, the changes in ATP and pHi were similar during ischemia, but the P2, 3 group recovered ATP and pHi faster than C. These data suggest that ischemic preconditioning may ameliorate ischemic renal injury as assessed by functional, metabolic and morphological methods. The mechanism(s) by which this occurs requires additional study.

Acute Kidney Injury↗
PubMed1998

Polyploidy in myelodysplastic syndrome: a case report.

Structural chromosomal abnormalities are common in myelodysplastic syndromes (MDSs), and complex abnormalities are known to confer a poor prognosis. Polyploidy is rare. We report a patient with MDS in whom 8/15 cells were 77,XYY; 2/15 were 83,XYY, and 5/15 were diploid (46,XY). He experienced rapid evolution of disease, transforming to terminal acute leukemia.

Acute Disease↗
PubMed1998

William lees price

Explore the source record for details and available documents.

Journal Article↗
PubMed1998

Long-term trial of deferiprone in 51 transfusion-dependent iron overloaded patients.

Fifty-one transfusion-dependent iron-loaded adult patients (38 with thalassemia major) were treated with the orally active iron chelator deferiprone (1,2 dimethyl-3-hydroxypyrid-4-one, L1) at a dose of 75 mg/kg/d (range, 50 to 79). Twenty patients discontinued the drug and five died after a mean of 18.7 months (range, 4 to 35). Of the 20, 5 had arthropathy, 5 had gastrointestinal symptoms, 4 had a rising serum ferritin, 3 had agranulocytosis or neutropenia, 1 had tachycardia, 1 had renal failure, and 1 went abroad. Twenty-six patients continued deferiprone for a mean of 39.4 months (range, 12 to 49). Among these patients, there was no overall significant change in serum ferritin (initial mean, 2,937 microg/L; range, 980 to 5,970; final mean, 2,323 microg/L; range, 825 to 5,970) or in urine iron excretion (initial mean, 31.2 mg/24 h; range, 16.3 to 58. 2; final mean, 32.1 mg/24 h; range, 9.4 to 75.8), implying no overall change in iron stores. When the patients who had received deferiprone for longer than 3 years were considered separately, there was also no significant change in serum ferritin or urinary iron excretion. The initial serum ferritin levels in the 26 patients who continued deferiprone treatment were significantly lower than in those who discontinued the drug (P < .01). The liver iron content in 17 patients who had received deferiprone for 24 to 48 months ranged from 5.9 to 41.2 mg/g dry weight, 50% having levels above 15.0 mg, a level associated with a high risk of cardiac disease due to iron overload. In this study the drug caused fewer side effects and was more effective at maintaining iron status among patients previously well chelated and with lower initial serum ferritin levels.

Adult↗
PubMed1995

Fragile X mental retardation syndrome: DNA diagnosis and carrier detection in New Zealand families.

AIMS: To establish a DNA-based test for the diagnosis and carrier detection of fragile X syndrome, and to investigate the nature of the mutation and patterns of inheritance in New Zealand families. METHODS: A probe for the FRAXA region was generated by polymerase chain reaction, cloned in a plasmid vector, and its structure was confirmed by DNA sequencing. This probe was used in a Southern blot assay to detect full mutations or premutations associated with fragile X syndrome in DNA from peripheral blood samples submitted to our laboratory for routine testing. RESULTS: We tested 379 individuals from throughout New Zealand. Full mutations were found in 29 males, leading to a fragile X diagnosis, or confirmation of an earlier cytogenetic diagnosis. Premutations were detected in 45 females and 11 males, all of whom are asymptomatic carriers of the disease. CONCLUSIONS: The DNA test is rapid and accurate, in contrast to the cytogenetic test. It allows unequivocal detection of carriers, enabling effective counselling, prenatal testing, and more generalised screening of at-risk populations. Our discovery of one large pedigree with many carriers and no prior history of X-linked mental retardation demonstrates that the DNA test is appropriate even in apparently sporadic cases of mental retardation.

Blotting, Southern↗
PubMed1995

1,3-Butadiene working group report.

During the Workshop in North Carolina, the in vivo metabolism, adduct formation and genotoxicity data available from rodent and human exposure to 1,3-butadiente (BD) were reviewed and they are summarized in the present report. BD is metabolized by cytochrome P-450-dependent monoxygenases to the primary metabolite 1,2-epoxybutene-3 (epoxybutene, EB). EB is subjected to further metabolism: oxidation to 1,2:3,4-diepoxybutane (DEB), hydrolysis to 3-butene-1,2-diol and conjugation to glutathione. The first pathway seems to prevail in mice while the latter is characteristic for rats and possibly for humans. Species differences exist in adduct formation of the monoepoxide to hemoglobin, for which the following pattern has been found: mice > rats > humans. Genotoxity of BD was found in mice with all applied tests; however, negative results were obtained in rats. In exposed humans, the cytogenetic studies in peripheral blood lymphocytes did not show genotoxic effects, although one report described elevated hprt variant levels in peripheral blood lymphocytes of exposed workers. It was concluded that the presently available data are insufficient for the application of the parallelogram model to estimate genetic risk for humans. As an alternative approach, a tentative estimate of the doubling dose for induction of hprt mutations in somatic cells of mice and men was performed and the calculated values were surprisingly similar, i.e. 9000 ppmh. However, this estimate is burdened with a number of caveats which were discussed in detail. The working group identified a series of urgent research needs to provide the appropriate data for the application of the parallelogram model, such as identification of metabolic pathways in different rodent species and humans, metabolic studies in mice, rats and humans considering metabolic polymorphisms, studies of adducts to DNA and hemoglobin especially of DEB and other butadiene metabolites in rodents and humans, studies of mutational spectra (mutational fingerprinting) in somatic and germinal cells, confirmation of the human hprt mutation data, conformation of the rodent malformation data, dose-response studies in rodent germ cell tests and studies on repair kinetics of mono-adducts induced by EB as opposed to repair of cross-links produced by DEB. Finally, it was suggested that the original parallelogram consisting of data from somatic cell studies in rodents and humans plus studies of heritable effects in rodents to extrapolate to germ cell risk for humans should be supplemented with studies in sperm of experimental animals and exposed men.

Animals↗
PubMed1995

Patient education: lessons from epilepsy.

Throughout the world some 40 lay associations are in the business of enabling patients with epilepsy to come to an understanding of their condition. This article aims to present the bones of this collective experience by detailing the positive outcomes that can be achieved for patients, for health professionals and for society in general, if patient education is delivered in a way that promotes confidence building, ensures that the educational locus is centred on the patient and enables the patient to be a partner in any decision-making process. This article will also suggest general guidelines that should underpin any patient education programme, as well as specific content. The questions of who should be responsible for delivering the programme and how patient education programmes can in reality become an integral part of health care plans are also addressed.

Curriculum↗
PubMed1995

Growth characteristics in vitro of myeloid leukaemic cells with t(6;9).

We report an analysis of in vitro growth characteristics of leukaemic cells from five patients with t(6;9)(p23;q34). Consistent with other reports of this abnormality, our patients were comparatively young (median age at diagnosis, 29 years), and responded poorly to conventional treatment (median survival from diagnosis, 10 months). During active disease the CFU-GM growth patterns were characterized by an abundance of granulocytic aggregates (mostly 20-100 cells in size) whose leukaemic origin was confirmed by cytogenetic analysis. During remission induction, colonies derived from regenerating normal progenitor cell colonies could be distinguished from those derived from persisting leukaemic cells on the basis of differences in size, morphology, in situ staining characteristics, and karyotype. Remission growth patterns were those of a normal bone marrow. Our findings add to a growing recognition that the t(6;9) identifies a subset of leukaemic patients with distinctive clinical, haematologic, molecular, and in vitro growth characteristics for whom conventional treatment offers little hope of cure or long survival.

Adolescent↗
PubMed1994

The Larimer County Children's Clinic. A public-private partnership to provide medical care to indigent children.

OBJECTIVE: To describe a unique collaboration between private and public entities to provide comprehensive health care to medically indigent children in rural Larimer County, Colo. SETTING: The Children's Clinic, Fort Collins, Colo. STUDY PARTICIPANTS: Uninsured children and those eligible for Medicaid, living in families with incomes below 150% of the federal poverty level. SELECTION PROCEDURES: Eligible patients have been enrolled in the Children's Clinic on a first-come, first-served basis. INTERVENTIONS: A community collaboration involving an interactive system with the Children's Clinic staff, the Larimer County Department of Health and Environment, private primary care and subspecialty physicians, ancillary health providers, and the family practice residency program at Poudre Valley Hospital, Fort Collins. Funding for this endeavor has been composed of city and county funds, public and private grants, community business support, and local fund-raising efforts, as well as Medicaid reimbursements. MEASUREMENTS/MAIN RESULTS: Since 1989, comprehensive pediatric care has been provided to a growing number of eligible children. At present, 3619 children, aged birth to 18 years, from 2230 families are being served. From this population, there were 8945 office visits to the Children's Clinic, 1392 patient contacts by the clinic social workers, 1287 visits to the Larimer County Department of Health and Environment for well-child care, 543 referrals to subspecialists and other community health care providers, and 615 after-hours visits to the Poudre Valley Hospital emergency department between July 1, 1992, and June 30, 1993. The clinic's professional staff consists of 2 1/4 full-time pediatric care providers, one nurse, one medical social worker, one receptionist, and one administrator, with an expenditure of $356,471. CONCLUSIONS: The Children's Clinic collaboration has provided comprehensive pediatric health care to a population that previously received only fragmented care. The next step is to assess the impact of this program on the frequency of emergency department visits for these patients.

Adolescent↗
PubMed1990

Molecular analysis of hprt mutants induced by 2-cyanoethylene oxide in human lymphoblastoid cells.

The mutagenic epoxide metabolite of acrylonitrile, 2-cyanoethylene oxide (ANO), was used to treat human TK6 lymphoblasts (150 microM x 2 h ANO). A collection of hypoxanthine-phosphoribosyltransferase (hprt) mutants was isolated and characterized by dideoxy sequencing of cloned hprt cDNA. Base-pair substitution mutations in the hprt coding region were observed in 19/39 of hprt mutants: 11 occurred at AT base pairs and 8 at GC base pairs. Two -1 frameshift mutations involving GC bases were also observed. Approximately half (17/39) of the hprt mutants displayed the complete loss of single and multiple exons from hprt cDNA, as well as small deletions, some extending from exon/exon junctions. Southern blot analysis of 5 mutants with single exon losses revealed no visible alterations. Analysis of 1 mutant missing exons 3-6 in its hprt mRNA revealed a visible deletion in the corresponding region in its genomic DNA. The missing exon regions of 4 mutants (one each with exons 6, 7 and 8 loss and one mutant with a 17-base deletion of the 5' region of exon 9) were PCR amplified from genomic DNA and analyzed by Southern blot using exon-specific probes. The exons missing from the hprt mRNA were present in the genomic hprt sequence. DNA sequencing of the appropriate intron/exon regions of hprt genomic DNA from a mutant with exon 8 loss and a mutant exhibiting aberrant splicing in exon 9 revealed point mutations in the splice acceptor site of exon 8 (T----A) and exon 9 (A----G), respectively.

Base Composition↗
PubMed1990

DNA sequence analysis of in vivo hprt mutation in human T lymphocytes.

We have determined the molecular basis of hypoxanthine-guanine phosphoribosyltransferase (hprt) mutations that arose in vivo in the T lymphocytes of a normal male subject. In previous studies approximately 16% (23/141) of the mutants from this individual analyzed by Southern blot displayed large structural alterations in hprt. Thirty-two mutants without these large hprt structural alterations produced sufficient hprt cDNA for polymerase chain reaction amplification and DNA sequence analysis. Base substitutions in hprt cDNA resulting in missense mutations and one mRNA splicing aberration (inclusion of intron sequences) were observed in 18/32 of these these mutants; substitutions occurred at both AT and GC base pairs. Small deletions (3/32), a tandem change and a single base insertion were also observed among the hprt cDNAs. Exon skipping and inclusion of hprt intron sequences in the hprt cDNA were observed in an additional 9/32 of the mutants. Analysis of T cell receptor (TCR) gene rearrangements revealed that six of eight mutants with an identical hprt T----A transversion displayed the same TCR rearrangement pattern, indicating that they were clonally related and arose from a single in vivo mutational event.

Base Sequence↗
PubMed1986

The use of surveys as a critical tool in consultation: the coronary primary prevention trial.

Selected findings from each of three surveys administered to the staff of the Canadian site of the Coronary Primary Prevention Trial during a consulting assignment are provided to illustrate the benefits of using surveys in Mental Health consultation. As demonstrated, survey results can assist the consultant to identify and prioritize staff concerns, convince management of the need for action and direct and monitor consulting activities over time.

Anticholesteremic Agents↗
PubMed1984

Life event stress: implications for the workplace.

In the light of recent research findings and clinical experience, the authors review the concept of "life event stress" and discuss the potential impact of major life events and crises on performance, work relationships and quality of life in the workplace. Because employees' responses to major life events and crises are affected by a number of factors, including personal resources and access to social support networks, it is in the interest of the employer to provide appropriate education, counselling and referral resources, reasonable accommodation regarding leave and responsibilities, and other forms of assistance and support in the wake of a major life event or crisis. Co-workers can also lend support.

Humans↗
PubMed1981

A psychosocial analysis of risk of psychological impairment following bereavement.

A multiple regression analysis was used to investigate the explanatory potential of a multidimensional approach to risk of psychological impairment. Information from a study of bereavement in Canadian women included meaning of the event to the individual, personality attributes, social supports available following bereavement and sociodemographic data. Risk of psychological impairment was estimated by score on the General Health Questionnaire (GHQ). Sixty-four per cent of the variance in GHQ scores at one month postbereavement was accounted for. The authors hypothesize that the addition of a measure of coping styles and more comprehensive measures of the other dimensions studied would increase the power of the technique. It seems critical to take into account the possible large effects of sociodemographic factors.

Age Factors↗