Endurance training does not affect diaphragm mitochondrial respiration

We sought to determine if chronic endurance training would increase mitochondrial respiration or protein content in rat diaphragm muscle. To this end, 20 male Wistar rats were randomly assigned to control (C) or an 8-week endurance training (T) group, n = 10 per group. At the end of T, VO2 max was 13% greater in T (83.3 vs 73.8 ml X kg-1 X min-1) and peak max power output was 32% greater (2.63 vs 1.98 kg X m X min-1). Mitochondrial specific activities of pyruvate-malate and cytochrome oxidase (expressed per mg mitochondrial protein) in both plantaris and diaphragm were similar in C and T rats, as were ADP/O and respiratory control ratios. When expressed per gram wet weight, whole muscle homogenate oxygen uptake (pyruvate + malate) and cytochrome oxidase activity increased 36 and 23%, respectively (P less than 0.05) in plantaris from T rats but did not change in diaphragm. Control oxidative capacity and mitochondrial protein content in the diaphragm were ca. 2-fold those in control plantaris. Plantaris mitochondrial protein content increased ca. 50% with T while the diaphragm was unaffected. We conclude that: plantaris muscle oxidative capacity adapts to training by increasing mitochondrial protein content, since there was no evidence for functional improvement of existing mitochondria, and in the face of a substantial training effect in whole animal and plantaris, the T stimulus was not sufficient to induce mitochondrial protein changes in the diaphragm. This finding is the result of either a 'pre-adaptation' secondary to the diaphragm's high chronic activity, or a sub-threshold increase in diaphragm recruitment during the exercise conditions studied.     

Paratesticular desmoid tumor

A primary intrascrotal mass clinically mimicking a testicular tumor was found to be a desmoid tumor originating from the spermatic cord. To our knowledge, this is the first reported case of a paratesticular desmoid tumor.     

Computed tomography of acute radiation nephritis

A patient with Hodgkin’s disease received a fractionated 3, 740 rad dosage over 4 weeks to a portal that included both kidneys. Three months later a computed tomographic scan obtained 2 hours after intravenous contrast injection demonstrated sharply demarcated, dense, persistent nephrograms corresponding to the irradiated areas. These changes are ascribed to acute radiation nephritis, reflecting tubular stasis and ischemia.     

Effects of eight weeks of bicycle ergometer sprint training on human muscle buffer capacity

This investigation was undertaken to determine whether human skeletal muscle buffer capacity (BCm) is affected by training. Eight untrained males participated in 8 weeks of sprint training on bicycle ergometers. Muscle biopsy samples were taken from the vastus lateralis before and at several times following an incremental bicycle ergometer test (0 min, 5 min, 15 min). These subjects were tested before (PRE) and following (POST) the training period. Seven endurance-trained cyclists (ET) were also tested for the purpose of comparing the BCm of ET to that of PRE and POST. Biopsy samples were quick-frozen in liquid nitrogen and later analyzed for lactate concentration (HLam), homogenate pH (pHm), and creatine phosphate concentration. BCm was calculated from the change in HLam and pHm observed from rest to exhaustion and was expressed as mmol X kg-1 X pH-1 (Slykes). There was no significant difference in resting HLam or resting pHm among the groups. There was a significant difference in HLam at exhaustion between PRE (21.41 +/- 1.65 mmol X kg-1), POST (25.61 +/- 2.38 mmol X kg-1), and ET (11.16 +/- 0.31 mmol X kg-1) but no significant difference in pHm at exhaustion between PRE (6.65 +/- 0.03 pH units) and POST (6.69 +/- 0.06 pH units). pHm at exhaustion for the ET group was significantly higher than the others at 6.91 +/- 0.02 pH units. A significant difference between PRE and POST BCm was found (PRE: 44.68 +/- 3.03 S1; POST: 61.04 +/- 4.11 S1) while ET BCm (47.21 +/- 7.26 S1) was not significantly different from PRE. These data indicate that muscle buffer capacity is increased with highly intense sprint training but provide no evidence to suggest that muscle buffer capacity is affected by endurance training.     

Three-dimensional computed tomographic analysis of the normal temporomandibular joint

Ten temporomandibular joints, obtained from three asymptomatic patients and two cadavers, were examined by three-dimensional computed tomography. The osseous components of the condylar process of the mandible and the glenoid fossa of the temporal bone were well visualized. The meniscus was visualized in both the closed- and the open-mouthed positions. Advantages and disadvantages of the technique are discussed.     

P2X(7) receptors are expressed during mouse nephrogenesis and in collecting duct cysts of the cpk/cpk mouse.

BACKGROUND: Purinergic receptors are cell-surface molecules that bind extracellular nucleotides, notably ATP. The P2X family includes seven nonselective ion channels with one member, P2X(7), implicated in cytolytic pore formation and cell death. MATERIALS AND METHODS: We sought P2X(7) expression in mouse nephrogenesis and cpk/cpk renal cyst growth, conditions in which both proliferation and apoptosis are prominent. RESULTS: P2X(7) immunolocalized to condensed metanephric mesenchyme: both proliferation and apoptosis were detected in this compartment, assessed by proliferating cell nuclear antigen expression and propidium iodide-stained pyknotic nuclei respectively. Later in nephrogenesis, P2X(7) was detected in collecting ducts, a pattern persisting to maturity. A mesenchymal to epithelial shift of P2X(7) expression was also documented in ureter development. In cpk/cpk kidneys, P2X(7)-expressing collecting duct cysts dominated histology from two weeks until four weeks after birth, when animals die from uremia. In polycystic kidneys pyknotic nuclei were rarely identified in P2X(7)-expressing epithelia, but were detected between cysts, consistent with a non-apoptotic role for P2X(7) in cyst enlargement. CONCLUSION: P2X(7) is expressed during normal nephrogenesis and in a model of congenital polycystic kidney disease. Further experiments are necessary to define possible functions of P2X(7) in these settings.     

Differential Effects of Anesthetics on Mitochondrial KATP Channel Activity and Cardiomyocyte Protection

Background: Mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine.

Methods: Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoKATP channel activity, in response to the direct and highly selective mitoKATP channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoKATP channels with respect to myocyte viability.

Results: Diazoxide-induced mitoKATP channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of [alpha]-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoKATP channel activity. The significance of these modulatory effects of the anesthetics on mitoKATP channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection.