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Biomedical subjects

C Turner

Publications and source records attributed to C Turner.

At least 19 recordsLinked to original sources
PubMed1992

What makes red cells dysmorphic in glomerular haematuria?

Although red cell morphology has been used to localise the site of haematuria in the urinary tract, the cause of red cell deformity is still speculative. We have conducted experiments in vitro using venous red cells which indicate that hypochromia depends mainly upon sodium concentration and occurs when this falls below 75 mmol/l. We simulated the passage of red cells through the renal tubule by sequentially treating them with fluids of composition similar to those in different tubular segments, and produced anisocytosis and hypochromia but not the typical "bizarre deformity"--the hallmark of glomerular haematuria. We conclude that dual injury is required to produce the "typical" dysmorphic red cells in glomerular haematuria. First, mechanical damage caused by passage of red blood cells through the glomerular basement membrane followed by a second, osmotic, injury sustained by red cells during passage through the hypotonic tubular segment.

Basement Membrane↗
PubMed1992

Maternal immunization with the capsular polysaccharide vaccine for Haemophilus influenzae type b.

Maternal immunization with the capsular polysaccharide (PRP) vaccine of Haemophilus influenzae type b has been shown to extend the time that protective levels of maternal antibody are detected in infants. In a randomized, blinded trial, PRP or placebo was administered uneventfully to 213 women in the third trimester of pregnancy. Infants born to PRP recipients had significantly higher levels of antibody to PRP than did infants born to placebo recipients: 2.73 micrograms/ml compared with 0.33 microgram/ml. It was estimated that infants of mothers who received the PRP vaccine would be protected for an average of 4 months compared to an average of only 2 months for those of mothers who received placebo. Infants were followed for invasive H. influenzae type b disease through the first year of life; none was detected.

Antibodies, Bacterial↗
PubMed1992

Effects of phosphate loading on metabolic and myocardial responses to maximal and endurance exercise.

Six trained male cyclists and triathletes participated in a double blind study to determine the effects of phosphate loading on maximal and endurance exercise performance. Subjects ingested either 1 gm of tribasic sodium phosphate or a glucose placebo four times daily for 3 days prior to performing either an incremental maximal cycling test or a simulated 40-km time trial on a computerized race simulator. They continued the supplementation protocol for an additional day and then performed the remaining maximal or performance exercise test. Subjects observed a 17-day washout period between testing sessions and repeated the experiment with the alternate supplement regimen in identical fashion. Metabolic data were collected at 15-sec intervals while venous blood samples and 2D-echocardiographic data were collected during each stage of exercise during the maximal exercise test and at 8-km intervals during the 40-km time trial. Results indicate that phosphate loading attenuated anaerobic threshold, increased myocardial ejection fraction and fractional shortening, increased maximal oxidative capacity, and enhanced endurance performance in competitive cyclists and triathletes.

Adult↗
PubMed1992

Role of intravenous immunoglobulin G in autoimmune hematologic disorders.

The data presented in this review established IVIG therapy as an important treatment modality in the autoantibody-mediated cytopenias and coagulation disorders of both children and adults. The immediate response to therapy is thought to be related to nonspecific Fc-receptor blockade of mononuclear phagocytes in the reticuloendothelial system (autoimmune cytopenias), or to idiotypic antibody interaction with pathologic autoantibodies (in acquired coagulation disorders). Although less frequent, long-term responses to IVIG therapy are reported. Such responses must involve an immunomodulating effect of IgG that influences T- and B-cell function, with inhibition of pathologic autoantibody formation. It is possible that idiotypic antibody interactions play a part in long-term responses. The experience with IVIG therapy in the decade following Imbach's important observations reported in 1981 has provided a sound data base regarding the use of this important therapy in patients with autoimmune hematologic disorders. The challenge of the next decade should be to further investigate mechanisms of action of this important therapy and to conduct carefully controlled studies to answer specific clinical questions. Examples of such questions include the following: (1) Can IVIG therapy, administered early in the course of illness in selected children with acute ITP, decrease the incidence of chronic ITP?; (2) Is maintenance, high-dose IVIG therapy a cost-effective method for the management of patients with chronic ITP refractory to corticosteroid therapy and splenectomy?; and (3) Can IVIG therapy administered to selected pregnant women with ITP significantly reduce the incidence of serious thrombocytopenia in their offspring? In conducting these studies, consideration should be given to the type of IVIG preparation used and to the treatment protocol implemented. It is evident that responses to unmodified IgG preparations (with the Fc-receptor part of the molecule left largely intact) are superior to preparations that have been modified during preparation. Responses are also likely to be dose-related. The data reported for IVIG therapy in patients with acquired factor VIII deficiency suggests that the idiotypic antibody content of IgG preparations is also of importance; if so, preparations selected from specific donor pools (for example, multiparous women) known to contain higher levels of circulating autoantibodies (than those from primiparous women or untransfused males) may provide a degree of benefit not seen with standard IVIG preparations. It is therefore important that clinicians and laboratory specialists work closely together in the design and conduct of future clinical trials initiated to answer those important clinical questions raised by the first decade of observations with IVIG therapy for autoimmune hematologic disorders.

Acute Disease↗
PubMed1992

Covering the costs of care in neonatal intensive care units.

The continued rise of health care costs, despite private and governmental control efforts, has sustained cost containment as a central issue for health care researchers and policy makers. In keeping with these concerns, the Florida Health Care Cost Containment Board conducted a study of neonatal intensive care units (NICUs) in Florida to ascertain the costs, charges, and net revenues associated with NICU services in individual hospitals, to document cost shifting and cross-subsidization as a means of financing NICU care for indigent populations, and to assess the fiscal impact of NICUs in state-sponsored vs non-state-sponsored Regional Perinatal Intensive Care Center hospitals providing NICU care. Hospitals in the state-sponsored program reported a loss of approximately $16.5 million in contrast to the non-state-sponsored hospitals, which reported a gain of $1 million. Payment being generated by private-pay patients amounted to almost 60% of total revenues but constituted less than one third of the costs in state-sponsored hospitals, indicating a high level of cost shifting. Government support of state-sponsored NICUs, while substantial, has been insufficient; increasing constraints on this funding source would likely worsen the deficit and increase the necessity of cost shifting.

Ancillary Services, Hospital↗
PubMed1991

The relationship of antiphospholipid antibodies to thromboembolic disease in systemic lupus erythematosus: a cross-sectional study.

In order to determine whether an association exists between antiphospholipid antibodies (APLA) and thromboembolic events in patients with systemic lupus erythematosus (SLE), we performed a cross-sectional study of consecutive unselected SLE patients. The occurrence of previous thromboembolic events was determined by investigators blinded to the APLA status of the patients by critical review of objective tests that had been performed at the time of symptomatic presentation and by performing venous Doppler ultrasound of the legs to elicit venous reflux as an indication of previous venous thrombosis. The presence of APLA was determined by coagulation assays for the lupus anticoagulant (LA) using five tests with well-defined control ranges and by ELISA assay for anticardiolipin antibodies (ACLA). These tests were measured on two separate occasions. The results of the study demonstrate a statistically significant association between persistently abnormal ACLA assays and thromboembolic events and a non-significant trend between persistently abnormal LA and thromboembolic events. Transient abnormalities of LA and ACLA were less strongly associated with thromboembolic events. We conclude that in patients with SLE, there is a significant association between thromboembolism and APLA.

Autoantibodies↗
PubMed1991

Rapid anticoagulation using ancrod for heparin-induced thrombocytopenia.

In order to determine the efficacy and safety of ancrod, a rapid acting defibrinogenating drug, for patients with heparin-induced thrombocytopenia, 11 consecutive patients who required anticoagulant therapy because of venous thromboembolism and who developed acute heparin-induced thrombocytopenia or had a history of heparin-induced thrombocytopenia were treated with ancrod. Heparin therapy was discontinued (in patients receiving heparin) and ancrod started at a dose of 1 to 2 U/kg every 24 hours with subsequent daily doses adjusted to maintain fibrinogen levels between 0.5 and 1.0 g/L. Ancrod was continued until warfarin had become effective. The platelet count increased to more than 150 x 10(9)/L within 2 to 10 days in all thrombocytopenic patients. Two patients with a history of heparin-induced thrombocytopenia maintained normal platelet counts while receiving ancrod. Two patients had recurrent venous thrombosis while receiving warfarin, 10 days after ancrod was discontinued: one of these patients had metastatic pancreatic carcinoma and developed phlegmasia cerulea dolens and the other patient developed a venographically proven extension of her deep venous thrombosis. One patient suffered a bleeding episode into the thigh with a 16-g/L decrease in her hemoglobin level while receiving ancrod therapy. No other side effects were noted. Our experience indicates that ancrod therapy is a reasonable approach for patients with heparin-induced thrombocytopenia who require anticoagulant therapy.

Aged↗
PubMed1991

Inherited bleeding disorders.

Congenital bleeding disorders comprise a heterogeneous group of diseases that reflect abnormalities of blood vessels, coagulation proteins and platelets. Studies of these diseases, many of which are rare and several of which result in a mild bleeding diathesis only, have significantly increased our understanding of normal haemostasis. Two lessons have been learned. First, quantitative abnormalities of coagulation proteins and platelets are an important, but not the only, cause of significant haemorrhage; some cases of inherited bleeding disorders reflect synthesis of a dysfunctional coagulation protein or production of abnormal platelets. Diagnostic tests that reflect qualitative abnormalities are therefore important in the evaluation of selected patients with inherited bleeding disorders. Second, in occasional patients the inherited disorder is complex and reflects combined abnormalities of coagulation proteins alone or in association with platelet disorders. In clinical practice it is useful to distinguish disorders that cause significant clinical bleeding from those that cause few or no symptoms. Examples of the former include severe deficiencies of factors VIII and IX, and the homozygous forms of factor II, V, VII, X, XI, XIII, fibrinogen and von Willebrand factor. Comparable platelet disorders include the inherited thrombocytopenias with platelet counts less than 20 x 10(9) litre-1 and the homozygous forms of Bernard-Soulier syndrome and Glanzmann's thrombasthenia. The most frequently encountered mild haemostatic abnormalities include type I von Willebrand's disease, the platelet storage pool deficiency syndromes and the mild and moderate forms of haemophilia A and B; occasionally heterozygous or homozygous forms of the rarer coagulation disorders, e.g. factor XI deficiency, may present with a mild bleeding diathesis. Finally, some disorders are entirely asymptomatic, e.g. factor XII deficiency and deficiencies of other contact coagulation factors. Management of patients with inherited bleeding disorders should reflect knowledge of the specific disorder to be treated plus careful consideration of the clinical circumstance for which therapy is proposed. In all cases, once a decision to treat has been made, the safest efficacious therapy should be given (for example DDAVP in the treatment of patients with mild haemophilia A or type I von Willebrand's disease). Although blood products are now much safer and the risk of blood transmitted viral infections is low, there still remains a risk that transfusion of any blood product may be associated with serious side-effects. As a result, therapy should be given only after careful consideration of the risk: benefit ratio and not merely to treat an abnormal laboratory result.(ABSTRACT TRUNCATED AT 400 WORDS)

Afibrinogenemia↗
PubMed1991

Sedation and histamine H1-receptor antagonism: studies in man with the enantiomers of chlorpheniramine and dimethindene.

1. The effects of 10 mg (+)- and (-)-chlorpheniramine and 5 mg (+)- and (-)-dimethindene on daytime sleep latencies, digit symbol substitution and subjective assessments of mood and well-being were studied in 6 healthy young adult humans. Each subject also took 5 mg triprolidine hydrochloride as an active control and two placebos. 2. Daytime sleep latencies were reduced with triprolidine, (+)-chlorpheniramine and (-)-dimethindene, and subjects also reported that they felt more sleepy after (+)-chlorpheniramine and (-)-dimethindene. Performance on digit symbol substitution was impaired with (+)-chlorpheniramine. 3. Changes in measures with (-)-chlorpheniramine and (+)-dimethindene were not different from changes with placebo. 4. In the present study, changes in measures of drowsiness and performance were limited to the enantiomers with high affinity for the histamine H1-receptor. These findings strongly suggest that sedation can arise from H1-receptor antagonism alone, and provide further support for the belief that the histaminergic system is concerned with the regulation of alertness in man.

Adult↗
PubMed1990

Measurement of beta 2-microglobulin, retinol-binding protein, alpha 1-microglobulin and urine protein 1 in healthy children using enzyme-linked immunosorbent assay.

Enzyme-linked immunosorbent assays (ELISA) have been developed for the measurement of beta 2-microglobulin (B2M), retinol-binding protein (RBP), alpha 1-microglobulin (A1M) and urine protein 1 (UP1) in children. Results from random urine samples in 43 children (31 for B2M) are, when corrected for urine creatinine (geometric mean (range)): B2M 9.8 (6.0-40.7) micrograms/mmol, RBP 8.1 (less than 1-24.5) micrograms/mmol, A1M 0.4 (0.1-2.2) mg/mmol and UP1 17.8 (less than 2-309.4) micrograms/mmol. Fractional excretions (FE) in 23 children (14 for B2M) are (geometric mean (range)): FEB2M 0.04% (0.02-0.10%) and FEUP1 0.10% (0.01-1.21%). Results in overnight urine collections are also presented. Our results extend existing data for normal ranges in adults to include children and provide data on UP1 concentrations.

Adolescent↗
PubMed1979

A simple micromethod for 25-hydroxyvitamin D estimation.

A quick and simple method for estimating 25-hydroxyvitamin D is described, It involves dichloromethane extraction followed by competitive protein-binding assay without chromatography. This assay can be performed on 100 microliter of serum and enables 50 samples to be estimated in one working day. The simplicity, speed, and sample size of this method make it very suitable for use in a routine clinical biochemistry laboratory. It is particularly useful when calcium disorders secondary to abnormalities in vitamin D intake and metabolism are suspected.

Animals↗
PubMed1977

Relationship between amplitude of pattern displacement and visual evoked potentials.

Thirteen subjects looked at a 7 mm2 black and white checkerboard which was displaced through 0.25, 0.50, 0.75 and full pattern displacement. One hundred and twenty eight averages were taken for each displacement and the peak to peak amplitude of the visual evoked potential was measured. This showed a linear relationship between pattern displacement and size of the evoked potential. Latency was unaffected for 0.25, 0.50 and 0.75 displacement but was significantly longer for the full pattern stimulation.

Adolescent↗
PubMed1977

The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

We have shown that when one of the spinal nerves supplying the salamander hind limb is cut or treated with colchicine, the fields of the remaining nerves enlarge in area; whereas nerve section produces Wallerian degeneration, the colchicine-treated nerves conducted action potentials normally and their peripheral fields remained unchanged in area (Aguilar, Bisby, Cooper & Diamond, 1973). Since colchicine-treatment reduced neuronal transport, and nerve-section eliminated it, we proposed that nerve sprouting is regulated by factors normally conveyed to the endings by axoplasmic transport. 1. We have now investigated the effects of colchicine on the thresholds and distribution of individual mechanosensory endings in the skin. If reduction of neuronal transport were enough to cause the threshold to be increased to the point of total unresponsiveness, then this could be a sign of an early stage of degernation in those terminals. It could then be hypothesized that products of degeneration were providing a stimulus for adjacent nerves to sprout. 2. Quantitative physiological studies of the effects of colchicine doses known to interfere with fast axoplasmic transport, indicate that in some experiments the terminal field of the treated nerve was invaded by sprouting fibres from neighbouring axons, when its own endings were unchanged in number, distribution and sensory thresholds. In other experiments the colchicine-treated nerve endings showed an increase in threshold but their function was otherwise unchanged; a similar adjacent nerve sprouting occurred. In a final group, colchicine caused total unresponsiveness of some endings of the treated nerve. 3. When a region of skin was partially denervated by nerve section, the physiological analysis indicated that the number of new mechanosensory endings which sprouted from the remaining axons exactly matched the number lost by nerve degeneration: furthermore the distribution of the endings was normal. It therefore appears that sprouting ceased when the original density of mechanosensory endings in the skin was restored. 4. The possibility that the drug induced sprouting as a consequense of a direct action on the skin is unlikely. With [3H]colchicine, we found that the accumulation of label in the skin of the untreated limb, in which sprouting did not occur, equalled that of the opposite limb. 5. The present results lend support to the original hypothesis of Aguilar et al. (1973), which proposed that collateral sprouting of intact nerves occurs when the supply of neuronally transported factors becomes inadequate to balance out the effects of a postulated target-tissue stimulus. In the Discussion other examples of collateral nerve sprouting, such as that following adjacent denervation, are shown to be explainable by this hypothesis.

Action Potentials↗