Operative Therapie von Knorpelschäden

Cartilage damage is often associated with pain, reduced quality of life and decreased physical performance. In addition, even small cartilage lesions can lead to osteoarthritis. Since young active people are particularly affected, the correct treatment of cartilage damage plays an important role. Operative treatment includes bone marrow-stimulating procedures with or without a matrix, cell-based procedures and osteochondral graft transplantation. The choice of the best procedure depends on the localization, the size and the extent of the cartilage damage. In addition, especially in the treatment of cartilage damage to the lower limbs, the leg axis and loading relationships should be taken into account and possibly treated as well as additional joint instabilities. The following article gives an overview of the available surgical treatment possibilities as well as the correct indications and implementation. It also gives a brief projection of possible further treatment options associated with stem cells.     

A Mentoring Program to Help Junior Faculty Members Achieve Scholarship Success

The University of North Carolina Eshelman School of Pharmacy launched the Bill and Karen Campbell Faculty Mentoring Program (CMP) in 2006 to support scholarship-intensive junior faculty members. This report describes the origin, expectations, principles, and best practices that led to the introduction of the program, reviews the operational methods chosen for its implementation, provides information about its successes, and analyzes its strengths and limitations.     

Stochastically-modulated stimulation to slow down muscle fatigue at stimulated sites in paraplegics using functional electrical stimulation for leg extension

Abstract

This short communication is a preliminary report on a study concerning slowing down the rate of muscle fatigue when FES (Functional Electrical Stimulation) is applied for standing and walking by complete (traumatic) thoracic-level paraplegics. It is shown that randomly modulating the inter-pulse interval between FES pulses (which serve to trigger action potentials in the peripheral nerves concerned) re~lJlts in a significantly lower rate ofmuscle fatigue, as tested in a series ofleg extensions, when FES was applied at the quadriceps. Specifically, we report that the best results (longest durations of leg extension prior to onset of muscle-fatigue) were achieved with a ± 5 msec uniformly-distributed (pseudo-) white-noise modulation at a 42 msec inter-pulse interval (24 pulses per sec). These resulted in an average increase in duration of leg extension ofapproximately 37% in this pilot study, as compared with unmodulated (fixed-rate) trains ofFES pulses. This significant increase, even in a very preliminary study appears to merit careful further examination, since it may allow a possibly significant increase in standing duration and in walking range of paraplegics using FES for ambulation. [Neural Res 2000; 22: 703-704]     

Protein-energy malnutrition induces changes in insulin sensitivity

Early protein deprivation impairs glucose tolerance and insulin secretion, but the former generally recovers first. We have therefore investigated insulin sensitivity in vivo and in isolated muscle and cultured hepatocytes during protein-energy malnutrition and long-term follow-up in rats. Rats were weaned at 3 weeks onto normal rat chow (N rats) or onto 5% protein diet (LP rats). At 6 w of age LP rats were transferred to N chow. Insulin sensitivity was studied in the three systems at 3, 6, 12 and 24 w. At 6 w LP rats showed a greater and more prolonged fall in serum glucose in response to injected insulin than age--or weight--matched N, but by 12 w the difference was not significant. Similarly, soleus muscle from 6 w LP showed a higher basal rate of glucose transport and responded to a lower insulin dose than N, but there was no difference in sensitivity at 12 w. Hepatocytes from 6 w LP showed higher basal incorporation of glucose into glycogen than N, but insulin sensitivity was not different. Thymidine incorporation into hepatocyte DNA responded to lower insulin doses in 6 w LP than N. There was a decrease in insulin sensitivity with age in all experimental systems. Increased insulin sensitivity during malnutrition was seen in all tissues studied but differences between the two groups were not significant at 12 w and probably do not account for the normal glucose tolerance in the presence of low serum insulin levels previously reported.     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.