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Biomedical subjects

L Wells

Publications and source records attributed to L Wells.

At least 55 records · Page 3Linked to original sources
PubMed1992

Advancing social work practice in the health field: a collaborative research partnership.

This article describes and analyzes the development of a collaborative research model by one university faculty of social work and 10 health care settings. Established working relationships for educating students were the foundation of a research partnership formed to study questions of mutual interest. This article discusses the developmental stage of the research consortium, including needs assessment, workshop, identification of a common theme and research topic, preliminary funding, and literature review. This stage resulted in the decision to develop and test an instrument to screen for high social risk that would be capable of identifying the need for social work involvement with families to provide effective and efficient management of patients. The Delphi methodology was chosen in the first phase of the research design, and reasons for the choice of this methodology, the results from the two Delphi rounds, and a preliminary screening instrument are presented. Finally, issues in collaboration, such as institutional factors, dynamics of the working group, and leadership roles, are analyzed to identify facilitating features and problematic issues in such partnerships.

Academies and Institutes↗
PubMed1992

Neurophysiological assessment of skeletal muscle fatigue in patients with congestive heart failure.

BACKGROUND: Recent research has demonstrated that patients with congestive heart failure (CHF) exhibit significant functional impairment of skeletal muscle and that these changes may be important determinants of exercise capacity. Although muscle strength may be mildly reduced, the most significant abnormality is markedly enhanced muscle fatigue. The goal of the present study is to determine whether accelerated fatigue is caused by impaired muscle activation, as a result of inadequate central motor drive or neuromuscular transmission, or by a change in the muscle itself. METHODS AND RESULTS: The study population consisted of nine patients with New York Heart Association class I-III CHF and eight sedentary, age- and sex-matched control subjects. Maximal voluntary contraction force of the foot dorsiflexors (primarily the tibialis anterior) was quantified as a measure of muscle strength, isometric endurance was quantified by the time required for force to decline to 60% of maximal during a sustained maximal contraction, and dynamic endurance was defined as the number of maximal contractions required for force to decline to 60% of maximal under a protocol of six repetitions per minute with an incremental duty cycle. The degree of central motor drive failure was quantified by the degree of force augmentation produced by a superimposed tetanic stimulus delivered to the peroneal nerve during the initial maximal voluntary contraction and at the time when force during the sustained isometric contraction declined to 60% of maximal. Neuromuscular junction transmission was examined by quantifying the amplitude of the compound muscle action potential (M wave) in response to a single nerve stimulus during fatiguing exercise. Muscle strength was relatively preserved in the CHF patients versus the control subjects (93 +/- 41 versus 105 +/- 34 lb; p = NS), but isometric endurance (time to decline to 60%, 34 +/- 15 versus 54 +/- 19 seconds; p less than 0.02) and dynamic endurance (number of repetitions before decline to 60%, 30 +/- 6 versus 43 +/- 7 contractions; p less than 0.001) were both impaired. Tetanic nerve stimulation increased force by similar degrees in the two groups, and the amplitude of the M wave did not decline in either group during exercise. CONCLUSIONS: These findings indicate that enhanced muscle fatigue in patients with CHF is not caused by impaired central motor drive or an abnormality of neuromuscular junction transmission but rather by an abnormality in the muscle itself.

Action Potentials↗
PubMed1991

Muscle-specific accumulation of Drosophila myosin heavy chains: a splicing mutation in an alternative exon results in an isoform substitution.

We show that the molecular lesions in two homozygousviable mutants of the Drosophila muscle myosin heavy chain gene affect an alternative exon (exon 9a) which encodes a portion of the myosin head that is highly conserved among both cytoplasmic and muscle myosins of all organisms. In situ hybridization and Northern blotting analysis in wild-type organisms indicates that exon 9a is used in indirect flight muscles whereas both exons 9a and 9b are utilized in jump muscles. Alternative exons 9b and 9c are used in other larval and adult muscles. One of the mutations in exon 9a is a nonsense allele that greatly reduces myosin RNA stability. It prevents thick filament accumulation in indirect flight muscles and severely reduces the number of thick filaments in a subset of cells of the jump muscles. The second mutation affects the 5' splice site of exon 9a. This results in production of an aberrantly spliced transcript in indirect flight muscles, which prevents thick filament accumulation. Jump muscles of this mutant substitute exon 9b for exon 9a and consequently have normal levels of thick filaments in this muscle type. This isoform substitution does not obviously affect the ultrastructure or function of the jump muscle. Analysis of this mutant illustrates that indirect flight muscles and jump muscles utilize different mechanisms for alternative RNA splicing.

Amino Acid Sequence↗
PubMed1991

Asymmetric growth of the lateral cerebral ventricle in infants with posthemorrhagic ventricular dilation.

Lateral cerebral ventricular volume in 36 preterm infants with or without an intraventricular hemorrhage, and with or without posthemorrhagic hydrocephalus, was measured longitudinally and compared with the ventricular index measurements of the same ventricles. A poor correlation was found (r2 = 0.67). To determine a reason for this poor relationship, we analyzed the volumes of the regions of the ventricles by a segmental volume analysis. The occipital region of the lateral cerebral ventricle enlarged at a much faster rate (1.904 +/- 0.477 ml/day) than either the anterior region (0.546 +/- 0.253 ml/day; p less than 0.01) or the middle region (-0.209 +/- 0.334 ml/day; p less than 0.01) in infants with posthemorrhagic hydrocephalus. The rate of growth of the middle region of the lateral cerebral ventricles was the same for all infants. Linear indexes, such as the ventricular index and the lateral ventricular ratio, do not allow for accurate serial estimates of ventricular size in posthemorrhagic hydrocephalus because of asymmetric growth of the lateral cerebral ventricle. We conclude that sequential volume measurements are more useful than ventricular index measurements to follow ventricular size sequentially in infants with posthemorrhagic hydrocephalus.

Cerebral Hemorrhage↗
PubMed1991

Impaired skeletal muscle function in patients with congestive heart failure. Relationship to systemic exercise performance.

In patients with congestive heart failure (CHF), the poor relationship between systemic exercise performance and cardiac function, together with morphologic and metabolic abnormalities in skeletal muscle, raises the possibility that skeletal muscle function may be impaired and limit systemic exercise performance. We assessed strength and endurance of the knee extensors during static and dynamic exercise in 16 patients with Class I-IV CHF and eight age-matched sedentary controls and related these measurements to systemic exercise performance. To assess skeletal muscle function independent of peripheral blood flow, endurance was repeated under ischemic conditions. Strength was not significantly different in the two groups. Dynamic endurance, quantified as the decline in peak torque during 15 successive isokinetic knee extensions, was significantly reduced in the patients compared to controls during aerobic (peak torque 65 vs. 86% of initial for exercise at 90 deg/s and 60 vs. 85% for exercise at 180 deg/s; P less than 0.002 for both), and during ischemic exercise (56 vs. 76% of initial torque; P less than 0.01). Static endurance, defined as the time required for force during a sustained maximal voluntary contraction to decline to 60% of maximal, was reduced in the patients compared to controls (40 +/- 14 vs. 77 +/- 29 s; P less than 0.02). There were highly significant relationships between systemic exercise performance and skeletal muscle endurance at 90 and 180 deg/s in the patients with CHF (r = 0.90 and 0.66, respectively). These findings indicate that skeletal muscle endurance is impaired in patients with CHF, that this abnormality is in part independent of limb blood flow, and that these changes may be important determinants of systemic exercise performance.

Adult↗
PubMed1991

1,25-Dihydroxyvitamin D3 and muscle strength in the elderly: a randomized controlled trial.

An unexplained loss of muscle strength occurs with aging. Vitamin D deficiency can cause myopathy and administration of 1,25-dihydroxyvitamin D3 [1,25-(OH2)D3] to persons with low serum concentrations can improve strength. To test the hypothesis that the weakness associated with aging is in part due to inadequate serum concentrations of [1,25-(OH2)D3], we conducted a randomized, controlled, double blinded trial in 98 men and women volunteers over 69 yr old. Treatment consisted of 0.25 micrograms 1,25-(OH)2D3, orally, twice per day or identical placebo for 6 months. Leg muscle strength of the quadriceps was measured with an isokinetic dynamometer. There was no difference between the two groups at 1 week, 1 month, or 6 months of treatment in any of the measures of muscle strength. We conclude that oral administration of 0.5 micrograms 1,25-(OH)2D3/day does not improve muscle strength in older persons. Further research is needed to determine the etiology of the decline in muscle strength associated with aging.

Aged↗
PubMed1990

Measurement of progressive cerebral ventriculomegaly in infants after grades III and IV intraventricular hemorrhages.

To develop guidelines that might help predict prospectively which infants with severe intraventricular hemorrhage (IVH) would require intervention, we obtained serial cranial sonograms to measure the rate of growth of cerebral ventricular volumes in 48 preterm infants with and without IVH. The infants were divided into three groups: (1) those with no IVH (22 infants), (2) those with IVH with acute ventricular dilation (13 infants), and (3) those with IVH with progressive ventricular dilation requiring intervention (13 infants). The decision to intervene because of progressive ventricular dilation was based on clinical criteria and the subjective assessment of increasing ventricular size on weekly cranial sonograms. The rate of cerebral ventricular volume growth in infants with IVH who needed intervention was greater (4.2 +/- 3.3 ml/day) than that in infants without IVH (0.0 +/- 0.1 ml/day; p less than 0.001) and in infants with IVH and acute ventricular dilation (0.0 +/- 0.2 ml/day; p less than 0.001). Using these data, we generated guidelines for predicting prospectively which infants with IVH and ventricular dilation will need intervention for posthemorrhagic hydrocephalus. The guidelines were then confirmed prospectively in 10 infants.

Cerebral Hemorrhage↗
PubMed1987

Preliminary results of a double-blind, randomized, placebo-controlled trial of cyclosporine in myasthenia gravis.

We randomly assigned 20 patients with progressively worsening generalized myasthenia gravis of recent onset whose illness was not controlled by anticholinesterase therapy to treatment with either cyclosporine (6 mg per kilogram of body weight per day) or placebo. Patients who had been treated with thymectomy, steroids, or other immunosuppressive agents were excluded. The duration of treatment was 12 months. Disease activity was assessed by quantified strength testing and by measurements of antihuman acetylcholine-receptor antibody. Patients were assessed at 6 months and 12 months, or at the following early end points: drug failure (doubling of creatinine), treatment failure (respiratory or swallowing difficulty), or protocol violation (stopping medication for more than five days). At six months, patients in the cyclosporine group had had significantly more objective improvement in strength; one early end point had been reached (drug failure; no treatment failures). In the placebo group, three early end points had been reached (all treatment failures). The decline in titers of acetylcholine-receptor antibody was larger in the treated group, although the difference was not statistically significant. At the end of the study (after 12 months of treatment or arrival at an earlier end point), improvement in strength and reduction in titers of anti-receptor antibody continued to be greater in the cyclosporine group. Nephrotoxicity occurred in three patients receiving cyclosporine but was nonprogressive with a reduction in dosage and reversible with discontinuation of the drug. These results are preliminary and need confirmation, but we conclude that cyclosporine is probably an effective therapy in some patients with myasthenia gravis.

Adult↗
PubMed1987

HLA and C4 polymorphism in diabetic microangiopathy.

We have reported an increased frequency of the rare B3 allotype of the fourth component of complement (C4B3) in insulin-dependent diabetics, especially in those with microangiopathy. This study has now been expanded--20 of 106 subjects with microangiopathy and 9 of 116 without possessed the C4B3 allotype (p less than 0.02). C4B3 is said to be in linkage disequilibrium with HLA-DR4. HLA typing was performed on 94 of these patients, 52 with and 42 without microangiopathy. There was no significant difference in the frequency of DR4 (62 vs 50%), DR3 (65 vs 52%), B8 (40 vs 40%) or B15 (32 vs 19%) respectively between these 2 groups. These results confirm an HLA-linked predisposition to microangiopathy, but do not determine whether the primary association is with C4B3, DR4 or another gene with which they are in linkage disequilibrium.

Complement C4↗
PubMed1986

X-linked mesangiocapillary glomerulonephritis.

Two related male patients with mesangiocapillary glomerulonephritis (MCGN) are described demonstrated by renal biopsy, inherited as an X-linked disorder. Family investigations failed to reveal any underlying immunological defects or a marker for the female carrier state. The age at diagnosis, the result of discovery of proteinuria on routine urine testing during infancy, is earlier than in any other reported cases of MCGN. This raises the possibility that this variety of MCGN may develop in utero and be detectable by alpha-fetoprotein maternal screening.

Genes, Recessive↗
PubMed1985

Genetically determined low C4: a predisposing factor to autoimmune chronic active hepatitis.

Of 26 patients with autoimmune chronic active hepatitis (CAH) starting in childhood 18 (69%) had low C4 and 5 (19%) had low C3 serum levels. Impaired hepatic synthesis and immune-consumption were unlikely since transferrin levels were normal in all patients, albumin levels were persistently low in only 3, and only 3 had raised levels of activation fragment C3d. C4d was normal in all patients studied. In the families of 12 probands with low C4, 7 parents had low C4 and 2 had levels which were at the lower limit of normal. 5 of 10 siblings from 5 families had low C4. These results suggest that low C4 levels in CAH are genetically determined. C4 phenotyping in 20 patients and in 26 parents showed that 90% and 81%, respectively, had null allotypes at either the C4A or C4B locus compared with 59% in controls, indicating that defective expression of structural genes may contribute to the observed C4 deficiency.

Adolescent↗