Contribution of Protein Intake and Concurrent Exercise to Skeletal Muscle Quality with Aging.

BACKGROUND: The use of magnetic resonance imaging (MRI) derived functional cross-sectional area (FCSA) and intramuscular adipose tissue (IMAT) to define skeletal muscle quality is of fundamental importance in order to understand aging and inactivity-related loss of muscle mass. OBJECTIVES: This study examined factors associated with lower-extremity skeletal muscle quality in healthy, younger, and middle-aged adults. DESIGN: Cross-sectional study. SETTING AND PARTICIPANTS: Ninety-eight participants (53% female) were classified as younger (20-35 years, n=50) or middle-aged (50-65 years, n=48) as well as sedentary (≤1 day per week) or active (≥3 days per week) on self-reported concurrent exercise (aerobic and resistance). MEASUREMENTS: All participants wore an accelerometer for seven days, recorded a three-day food diary, and participated in magnetic resonance imaging (MRI) of the lower limbs. Muscle cross-sectional area (CSA) was determined by tracing the knee extensors (KE) and plantar flexors, while muscle quality was established through the determination of FCSA and IMAT via color thresholding. RESULTS: One-way analysis of variance and stepwise regression models were performed to predict FCSA and IMAT. KE-IMAT (cm2) was significantly higher among sedentary (3.74 ± 1.93) vs. active (1.85 ± 0.56) and middle-aged (3.14 ± 2.05) vs. younger (2.74 ± 1.25) (p < 0.05). Protein intake (g•kg•day-1) was significantly higher in active (1.63 ± 0.55) vs. sedentary (1.19 ± 0.40) (p < 0.05). Sex, age, concurrent exercise training status, and protein intake were significant predictors of KE FCSA (R2 = 0.71, p < 0.01), while concurrent exercise training status and light physical activity predicted 33% of the variance in KE IMAT (p < 0.01). CONCLUSION: Concurrent exercise training, dietary protein intake, and light physical activity are significant determinants of skeletal muscle health and require further investigation to mitigate aging and inactivity-related loss of muscle quality.

A peculiar case of Campylobacter jejuni attenuated aspartate chemosensory mutant, able to cause pathology and inflammation in avian and murine model animals.

An attenuated Campylobacter jejuni aspartate chemoreceptor ccaA mutant caused gross pathological changes despite reduced colonisation ability in animal models. In chickens, the pathological changes included connective tissue and thickening of the mesenteric fat, as well as the disintegration of the villus tips in the large intestine, whereas in mice, hepatomegaly occurred between 48-72 hours post infection and persisted for the six days of the time course. In addition, there was a significant change in the levels of IL-12p70 in mice infected with the C. jejuni ccaA mutant. CcaA isogenic mutant was hyper-invasive in cell culture and microscopic examination revealed that it had a "run" bias in its "run-and-tumble" chemotactic behaviour. The mutant cells also exhibited lower level of binding to fucosylated and higher binding to sialylated glycan structures in glycan array analysis. This study highlights the importance of investigating phenotypic changes in C. jejuni, as we have shown that specific mutants can cause pathological changes in the host, despite reduction in colonisation potential.

Metastable equilibrium solubility behavior of bone mineral.

Previous studies have shown that carbonated apatites with a range of carbonate contents and crystallinities exhibit the phenomenon of metastable equilibrium solubility (MES) distributions. The purpose of the present study was to investigate the solubility behavior of bone mineral using the concepts of MES and MES distributions and, together with crystallinity and chemical composition data, examine the similarity of bone mineral to carbonated apatite (CAP). Bone samples were harvested from 1-, 5-, and 8-month-old rats. The organic components of the bone samples were removed by hydrazine deproteination. Carbonated apatite was synthesized by the hydrolysis of dicalcium phosphate dihydrate (DCPD) in a NaHCO3-containing media at 50 degrees C. The MES distributions of bone mineral and CAP were determined by equilibrating predetermined amounts of CAP or bone mineral in a series of 0.1 M acetate buffers containing calculated levels of calcium and phosphate and maintained at essentially constant pHs of 5.0, 5.3, 5.7, and 6.5. From the compositions of the equilibrating buffer solutions, ion activity products based upon the stoichiometries of octacalcium phosphate, hydroxyapatite, and carbonated apatite were calculated in an attempt to determine the function governing the dissolution of CAP and bone mineral. The results of this study demonstrated that the MES distribution phenomenon appeared to hold for bone mineral and that the changes in crystallinity of bone mineral with age correlated well with changes in the MES values. A CAP sample was prepared that was found to be an excellent synthetic prototype closely mimicking the physicochemical behavior of bone mineral from an 8-month-old rat. Another finding of this study was that the ion activity product function based upon the hydroxyapatite stoichiometry well described the MES results obtained with both CAP and bone mineral. The interpretation that a surface complex with hydroxyapatite stoichiometry governs the solubility behavior of bone mineral is, therefore, consistent with the experimental data. Other calcium phosphate stoichiometries for the surface complex showed systematic variations in the MES profiles when the pH of the equilibrating solution was varied.

Restrospective correlation of clinical and histologic findings of 189 exchanged kidneys.

Tissues samples from 189 unsuccessful renal allografts, 47 recovered at autopsy and the others removed surgically, were examined histologically by light microscopy. Tissues samples were obtained from cadaver kidneys that had been exchanged regionally for transplantation. Each allograft tissue sample was rated as to extent of pathologic changes denoting rejection and was classified accordingly. Surgical and autopsy reports, as well as clinical data, were then obtained and these were compared with the retrospective pathologic findings of this study. Our pathologic findings agreed with the original pathologic diagnosis as to presence or absence of rejection changes in 180 cases, but disagreed with the clinical diagnosis of rejection in 28 of the 63 cases with minimal or no histologic evidence of rejection. There was less disagreement with the clinical diagnosis for the 87 cases with histologic evidence of rejection which had been judged as sufficient to cause allograft loss, 70 having been clinically diagnosed as rejected. Disagreement occurred most often where the allograft had never functioned or had been lost within 3 months. Retrospective analysis did not disclose any association between rejection histology and preformed antibodies or length of kidney perfusion time. Sufficient allografts appeared to have been lost for reasons other than rejection to cast doubt on the validity of interpreting renal allograft data only by graft survival statistics.