The Impact of Exercise on Improving Body Composition and PSA in High-Risk Prostate Cancer Patients on Androgen-Deprivation Therapy.

This prospective study investigated how exercise impacted chronological changes in anthropometrics, body composition, prostate-specific antigen (PSA) level and prognostic nutrition index (PNI) in high-risk prostate cancer (PCa) patients on androgen deprivation therapy (ADT). The patients were divided into either the usual care or exercise group. All patients received measurements a week before ADT initiation, six- and twelve months after treatment. The exercise group received both aerobic and resistance training. The analysis was conducted using appropriate statistical methods. There were 45 males enrolled (age 67.4 ± 8 years and BMI 25.5 ± 3.6 kg/m2). Profound changes were observed at six months follow-up. The exercise group showed a significant increase in the trunk and leg lean mass, and a lesser loss of total and arm lean mass. A significant decrease in PSA was also observed among the exercise group. PNI and PSA were significantly associated with regional lean mass. Exercise can prevent loss or even increase lean mass in high-risk PCa, especially in the early stage of ADT treatment. Moreover, a strong bond between lean mass and PNI and PSA further underscores the importance of early and continuous exercise interventions.

Neuromuscular Activity and Muscular Oxygenation Through Different Movement Cadences During In-water and On-land Knee Extension Exercise.

Chien, K-Y, Kan, N-W, Liao, Y-H, Lin, Y-L, Lin, C-L, and Chen, W-C. Neuromuscular activity and muscular oxygenation through different movement cadences during in-water and on-land knee extension exercise. J Strength Cond Res 31(3): 750-757, 2017-The purpose of this study was to determine the influence of various knee extension exercise cadences on neuromuscular activation and hemodynamic properties of the quadriceps muscle in water and on land. Seventeen young women participated in this study, and the subjects were randomly allocated to perform loaded knee extension exercises in water and on land at 4 different cadences of 30, 50, 70, and 90 b·min. Heart rate (HR), blood flow (BF), total saturation index (TSI) of oxygen, electromyography (EMG) for the extent of muscular activity, and rate of perceived exertion (RPE) were measured. Response values of HR, BF, TSI, and RPE at each cadence were obtained by subtracting the resting values from the indicator values measured at the respective cadences. We observed that BF, EMG, and RPE in water at 90 b·min were comparable with those on land. The HR and TSI changes were higher in water compared with on land (p = 0.004 and p = 0.013, respectively). In conclusion, we demonstrate that the neuromuscular activity when performing knee extension exercises at 90 b·min in water was comparable with that on land. However, exercising in water at the same cadence evoked higher TSI responses and greater cardiovascular challenges. A knee extension exercise at 90 b·min is the recommended operating speed of rehabilitation in water.

Vimentin is involved in peptidylarginine deiminase 2-induced apoptosis of activated Jurkat cells.

Peptidylarginine deiminase type 2 (PADI2) deiminates (or citrullinates) arginine residues in protein to citrulline residues in a Ca2+-dependent manner, and is found in lymphocytes and macrophages. Vimentin is an intermediate filament protein and a well-known substrate of PADI2. Citrullinated vimentin is found in ionomycin-induced macrophage apoptosis. Citrullinated vimentin is the target of anti-Sa antibodies, which are specific to rheumatoid arthritis, and play a critical role in the pathogenesis of the disease. To investigate the role of PADI2 in apoptosis, we generated a Jurkat cell line that overexpressed the PADI2 transgene from a tetracycline-inducible promoter, and used a combination of 12-O-tetradecanoylphorbol-13-acetate and ionomycin to activate Jurkat cells. We found that PADI2 overexpression reduced the cell viability of activated Jurkat cells in1a dose- and time-dependent manner. The PADI2-overexpressed and -activated Jurkat cells presented typical manifestations of apoptosis, and exhibited greater levels of citrullinated proteins, including citrullinated vimentin. Vimentin overexpression rescued a portion of the cells from apoptosis. In conclusion, PADI2 overexpression induces apoptosis in activated Jurkat cells. Vimentin is involved in PADI2-induced apoptosis. Moreover, PADI2-overexpressed Jurkat cells secreted greater levels of vimentin after activation, and expressed more vimentin on their cell surfaces when undergoing apoptosis. Through artificially highlighting PADI2 and vimentin, we demonstrated that PADI2 and vimentin participate in the apoptotic mechanisms of activated T lymphocytes. The secretion and surface expression of vimentin are possible ways of autoantigen presentation to the immune system.