Pain-related beliefs are associated with arm function in persons with frozen shoulder.

BACKGROUND: Frozen shoulder is a painful glenohumeral joint condition. Pain-related beliefs are recognized drivers of function in musculoskeletal conditions. This cross-sectional study investigates associations between pain-related beliefs and arm function in frozen shoulder. METHODS: Pain intensity, arm function (Disabilities of the Arm, Shoulder and Hand Questionnaire (DASH)), pain catastrophizing (Pain Catastrophizing Scale (PCS)), pain-related fear (Tampa Scale for Kinesiophobia (TSK-11)) and pain self-efficacy (Pain Self-Efficacy Questionnaire (PSEQ)) were administered in 85 persons with frozen shoulder. Correlation analyses assessed associations between pain-related beliefs and arm function. Regression analysis calculated the explained variance in arm function by pain-related beliefs. RESULTS: Pain-related fear, pain catastrophizing and pain self-efficacy were significantly associated with arm function (r = 0.51; r = 0.45 and r = -0.69, all p < .0001, respectively). Thirty-one percent of variance in arm function was explained by control variables, with pain intensity being the only significant one. After adding TSK-11, PCS and PSEQ scores to the model, 26% extra variance in arm function was explained, with significant contributions of pain intensity, pain-related fear and pain self-efficacy (R2 = 0.57). CONCLUSIONS: Attention should be paid towards the negative effect of pain-related fear on outcomes in frozen shoulder and towards building one's pain self-efficacy given its protective value in pain management.

Ketogenic effects of carnitine in patients with muscular dystrophy and cytochrome oxidase deficiency.

The effects of a single oral dose of carnitine on fasting-induced ketosis was investigated in four normal individuals, five patients with muscular dystrophy, and one patient with a generalized cytochrome c oxidase deficiency. Plasma carnitine, free fatty acids, glucose, insulin, and glucagon were also measured. Normal individuals showed an average 0.09 mM increase in blood beta-hydroxybutyrate concentration during a 12- to 18-hr period of fasting and carnitine administration did not affect this response (average: 0.12 mM). Muscular dystrophy patients showed a greater fasting-induced elevation in beta-hydroxybutyrate (average 0.29 mM) and carnitine administration greatly enhanced this ketogenic response (average 0.84 mM). The cytochrome c oxidase deficient patient showed an even larger increase in beta-hydroxybutyrate with fasting (1.67 mM) and carnitine further augmented this ketotic effect (3.78 mM). Plasma free fatty acids were also elevated in patients that showed enhanced ketosis. Plasma glucagon concentration did not change, but insulin levels decreased during the 12- to 18-hr period of fasting; no major differences were found between controls and patients. These results indicate that some patients with muscular dystrophy and cytochrome c oxidase deficiency are more prone to develop ketosis than normal individuals and that carnitine administration enhances this response. Since both muscular dystrophy patients and the patient with cytochrome c oxidase deficiency had similar ketogenic responses, the data suggest that ketone body utilization may be impaired in these patients. The ability of L-carnitine to be ketogenic should be considered in the treatment of these patients.

Protection of the ischaemic myocardium by L-propionylcarnitine: effects on the recovery of cardiac output after ischaemia and reperfusion, carnitine transport, and fatty acid oxidation.

The effects of L-propionylcarnitine on the recovery of cardiac contractile performance after global ischaemia and reperfusion were studied in isolated perfused rat hearts. The addition of either 5.5 or 11 mmol X litre-1 L-propionylcarnitine significantly improved the recovery of cardiac output, left ventricular pressure, and dP/dt after 90 min of ischaemia and 15 min of reperfusion. Myocardial adenosine triphosphate and creatine phosphate concentrations were significantly higher in the L-propionylcarnitine treated hearts than in controls, but the concentrations of long chain acyl carnitine and coenzyme A were unaffected. The protecting effects of L-propionylcarnitine were compared with those of L-carnitine and L-acetylcarnitine. A 11 mmol X litre-1 dose of L-propionylcarnitine and L-acetylcarnitine significantly improved the recovery of cardiac output after 90 min of ischaemia and 15 min of reperfusion, but L-carnitine did not. L-Propionylcarnitine was the most protective agent. The effects of these derivatives on L-3H-carnitine transport and 14C-palmitate oxidation were also measured. All of these derivatives competitively inhibited L-3H-carnitine transport in isolated cardiac myocytes, but L-propionylcarnitine was the most potent. Carnitine and L-propionylcarnitine stimulated palmitate oxidation in the homogenate, whereas L-acetylcarnitine inhibited it. In myocytes only L-propionylcarnitine affected palmitate oxidation. These data show that L-propionylcarnitine protects the ischaemic myocardium. Its protection is greater than that for L-carnitine or L-acetylcarnitine, and the difference in effectiveness may relate to the rate of transport into the cells and the effects on fatty acid utilisation.

Improvement of myocardial function in diabetic rats after treatment with L-carnitine.

The effects of L-carnitine administration on the severity of diabetes were investigated. Serum glucose, free fatty acids (FFA), triglycerides, and ketones from diabetic and normal rats injected for 2 weeks with 3 g/kg/d of either L-carnitine or saline were assayed. Hearts were analyzed for carnitine and long-chain acyl coenzyme A. L-carnitine treatment to diabetic rats significantly reduced serum glucose, FFA, triglycerides, and ketones. In nondiabetic rats, carnitine increased serum ketones while FFA and triglycerides were decreased. L-carnitine treatment to diabetic rats prevented a decrease in myocardial total carnitine content. Long-chain acyl carnitine increased while long-chain acyl coenzyme A decreased. In another experiment, L-carnitine administration (750 mg/kg/d for 14 days) significantly improved the recovery of cardiac output after 60, 90, and 120 minutes of ischemia in diabetic perfused hearts. These results suggest that L-carnitine therapy may reduce the severity of diabetes mellitus and improve myocardial performance.

Antimalarial amino alcohols II: anthraceneaminoethanols and anthraceneaminopropanols (1- and 9-substituted).

The syntheses of seven anthracene amino alcohols with one, two, or three additional substituents are described. These compounds include three 1-aminoethanols, two 9-aminoethanols, and two 9-aminopropanols, prepared from substituted anthraquinones or from 10-chloro-9-anthraldehydes. The antimalarial activity of these compounds, as well as tentative structure-activity relationships, is discussed in the light of previously published work.