Chronic stretching and running economy.

Research demonstrates an inverse relationship between the range of motion of selected joint movements (flexibility) and running economy. Since stretching exercises have been shown to increase joint range of motion, stretching exercises may be contraindicated for endurance running performance. Hence, this study investigated the influence of a 10-week program of stretching exercises on the oxygen costs of a 10 min sub-maximal (approx. 70% peak VO(2)) treadmill run. Thirty-two (16 female, 16 male) physically active, treadmill accommodated, college students participated in the study. All participants maintained their current activity level, with half the participants (8 female, 8 male) adding a 40 min, 3 days per week session of thigh and calf muscle stretching exercises. After 10 weeks, the stretching group (STR) exhibited a significant (P<0.05) increase (3.1+/-2.2 cm) in the sit-and-reach, while the non-stretching group (CON) experienced no significant (P>0.05) change (0.0+/-0.4 cm). However, neither the STR nor the CON exhibited a significant (P>0.05) change in the O(2) cost for the submaximal run. It is concluded, therefore, that a chronic stretching program does not necessarily negatively influence running economy.

Analysis of T cells and major histocompatibility complex class I and class II mRNA and protein content and distribution in antiglomerular basement membrane disease in the rabbit.

The major interacting components of the immune system, major histocompatibility complex (MHC) class I and class II proteins and T cells were analyzed in a model of anti-GBM (glomerular basement membrane) disease in the rabbit that progresses to develop cellular crescents and glomerular and interstitial fibrosis. Class I and II mRNA and protein were measured in isolated glomeruli and whole renal cortex using cDNA probes and monoclonal antibodies. The distribution of T cells and class I and II proteins was assessed by immunofluorescence. Normal glomeruli contained no T cells and were class II negative. By day 4, glomeruli contained MHC class I and II mRNA and protein and class II positive T cells. Although some animals had T cells in the periglomerular area, these cells were class II negative. By day 7 periglomerular T cells were largely class II positive (activated) and there was increased MHC class I and II mRNA and protein in whole renal cortex. Later T cells accumulated in the tubulo-interstitial compartment, which became diffusely positive for MHC classes I and II, but to a variable extent in different animals. Those with high class II mRNA expression also had detectable T cell antigen receptor mRNA by Northern analysis. The authors conclude 1) in this model there was a close association between mRNA abundance and protein expression for both MHC classes I and II in glomeruli and renal cortex as a whole; 2) in this model of glomerular injury there are three phases of activation. The first phase takes place in the glomerulus and is associated with accumulation of activated T cells and MHC class I and II protein in the glomerulus. Phase 2 is associated with the accumulation of periglomerular T cells and their becoming class II positive. There is subsequent dissemination (phase 3) of activated T cells and accumulation of class I and II mRNA and protein throughout the interstitial compartment. This spacial progression of glomerulocentric inflammation is likely associated with degree of injury and permanent loss of renal function.

Ibuprofen-associated renal dysfunction. Pathophysiologic mechanisms of acute renal failure, hyperkalemia, tubular necrosis, and proteinuria.

Ibuprofen-associated, acute, reversible renal failure with hyperkalemia, tubular necrosis, and proteinuria developed in a patient who had no predisposing underlying disease. A renal biopsy specimen revealed mesangial hypercellularity without glomerular crescent formation. A profound interstitial nephritis with focal inflammatory cell infiltrates of predominantly mononuclear cells and neutrophils as well as focal tubular destruction was seen. Vasculitis was not observed. Ultrastructural studies confirmed the light microscopic diagnosis of a tubulointerstitial nephritis and, in addition, indicated the presence of electron-dense mesangial and subepithelial deposits. Direct immunofluorescence examination showed diffuse mesangial IgM and C3 deposition as well as vascular C3 deposition. Renal failure rapidly resolved after discontinuation of ibuprofen therapy and initiation of steroid therapy, with return to normal levels of serum creatinine, urea nitrogen, potassium, and sodium. Proteinuria also resolved.