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Biomedical subjects

U A Walker

Publications and source records attributed to U A Walker.

29 records · Page 2Linked to original sources
PubMed2000

Patients with fibromyalgia benefit from aerobic endurance exercise.

Fibromyalgia (FM) is a disorder characterised by diffuse widespread musculoskeletal aching and stiffness and multiple tender points [1]. Its pathophysiology is poorly understood. The influence of aerobic endurance exercise on pain in patients with FM was investigated. Twenty-seven patients (25 female, 2 male) participated in a controlled clinical study and performed 12 weeks of jogging, walking, cycling or swimming following a given schedule. Twelve sedentary FM patients (11 female, 1 male) served as controls. Before and after training both the study and the control groups were evaluated spiroergometrically. Tender point pain was quantified by dolorimetry. The painful body surface was estimated by a pain body diagram, and its intensity by a visual analogue scale and a ranking scale. Patients trained for an average of 25 min two to three times a week, with an average intensity of 50% of maximal oxygen uptake (VO2max). Unlike the control group, the training group exhibited a decrease in heart rate and VO2 and an increase in respiratory quotient during submaximal workload. Maximal performance capacity and VO2max remained unchanged, whereas the wattpulse (watt/heart rate) improved at maximal workload. Pain parameters remained unchanged in the control group, but in the training group the mean number of positive tender points (15.4/12.7), the mean pain threshold of the gluteal tender point (2.89 kp/3.50 kp) and the painful body surface (18%/15% body surface) decreased significantly. Subjective general pain condition deteriorated in two patients but improved in 17. Our results suggest a positive effect of aerobic endurance exercise on fitness and well-being in patients with FM.

Adult↗
PubMed1998

Neurotrophin-4 is up-regulated in ragged-red fibers associated with pathogenic mitochondrial DNA mutations.

Ragged-red fibers (RRFs) are found more frequently in highly oxidative type I fibers than in glycolytic type II fibers in the muscle of many patients with mitochondrial myopathies. Neurotrophin-4 (NT-4), a neuronal signaling molecule, is also expressed in skeletal muscle, predominantly in type I fibers. We found that NT-4 protein and mRNA were present in both type I and type II fibers but were up-regulated in RRFs of patients with mitochondrial encephalomyopathies; it is noteworthy that NT-4 was not up-regulated in muscle fibers from healthy aerobically trained athletes. Thus, NT-4 might represent a member of a new class of candidate molecules involved in the compensatory adjustments of muscle fibers to oxidative dysfunction, and may even play a role as a signaling molecule for mitochondrial proliferation.

Biopsy↗
PubMed1997

Mitochondrial mobility in differentiating muscle heterokaryons.

Ragged-red fibers, a morphological hallmark of many patients with mitochondrial encephalomyopathies who harbor mitochondrial DNA (mtDNA) mutations, usually contain varying ratios of mutated and wild-type mtDNAs. Deficient respiratory function in muscle is almost invariably segmental. To investigate whether this observation may be explained by restricted lateral movement of mitochondria within myofibers, we studied the spatial and temporal behavior of two different mitochondrial populations within multinucleate myotubes. We co-cultured normal human and mouse myoblasts, allowed them to fuse into muscle heterokaryons and investigated whether the mitochondria remained segregated, or migrated and intermixed. Human and mouse nuclei were identified by their differential staining pattern with the dye Hoechst 33 258 and mitochondria were distinguished immunologically and by in situ hybridization. Although we observed some territoriality at very early time points after myoblast fusion, there was rapid intermixing of the mitochondrial populations, as early as 48 h after myoblast fusion. We conclude that mitochondria, unlike many other muscle components, lack territorial organization in cultured, differentiating heterokaryons.

Animals↗
PubMed1996

Respiratory chain encephalomyopathies: a diagnostic classification.

Mitochondrial encephalomyopathies are a heterogenous group of disorders with various biochemical defects of the respiratory chain (RC). Due to the considerable phenotypic diversity of the RC encephalomyopathies, they are included in the differential diagnosis of many cases of multisystem disease. Aside from clinical evaluation and family history, diagnosis can be supported by many other sources. The complexity of diagnostic information can make it difficult for the clinician to establish the level of certainty at which a RC cytopathy is diagnosed in atypical cases. We review the parameters (clinical, pathological, biochemical and molecular) which are used to aid diagnosis of RC encephalomyopathy and identify levels of abnormality in each that strongly or less strongly support the diagnosis. A system is developed that allows classification of the diagnosis in possible, probable and definite categories of certainty, which will be of value to the clinician.

Biomarkers↗
PubMed1995

The therapy of respiratory chain encephalomyopathy: a critical review of the past and current perspective.

The mitochondrial respiratory chain encephalomyopathies represent an important group of multisystem disorders. No curative treatment is currently available. A number of measures have been reported to have a theoretical potential to improve respiratory function. These treatment strategies have variable scientific support, many reports being anecdotal. We critically review the various therapeutic measures employed and suggest future treatment directions.

Benzoquinones↗
PubMed1994

Intravascular lymphoma simulating vasculitis.

The case history of a patient with intravascular lymphoma (IL) is reported. Signs of a systemic illness including fever, muscular weakness, telangiectasias, nephrotic syndrome, and neurologic manifestation suggested vasculitis. Cyclophosphamide treatment produced almost complete remission, but the patient died of respiratory failure 13 months after presentation due to lung involvement. The diagnosis was not revealed until postmortem examination. The differential diagnosis of IL is provided.

Diagnosis, Differential↗
PubMed1993

[Reduced "oxidative burst" in a granulocyte subpopulation in a case of Sweet syndrome].

Oxidative burst was defective in 50% of peripheral blood neutrophils in a case of Sweet syndrome with leukemoid granulocytosis. Phagocytosis was normal. We suggest that the decreased ability to produce oxygen radicals observed in this patient might lead to a compensatory recruitment of hematopoietic growth factors. Consecutive activation, increased chemotaxis and adhesion of polymorphonuclear granulocytes might be the cause of the neutrophilic dermal infiltrate of Sweet syndrome.

Adult↗