Incorporating plyometric exercises (PE) into soccer players' conditioning routines is vital for boosting their performance. Nevertheless, the effects of PE sessions with diverse volume loads on inflammation, oxidative stress, and muscle damage are not yet clearly understood. This study aimed to examine the effects of altering the volume-loads of PE on indicators of oxidative muscle damage and inflammation. The study involved forty young male soccer players who were randomly assigned to three different volume-loads of PE (Low volume-load [100 jumps]: LVL, n = 10; Moderate volume-load [150 jumps]: MVL, n = 10; and High volume-load [200 jumps]: HVL, n = 10) and a control group (CON = 10). The levels of various biomarkers including delayed onset muscle soreness (DOMS), serum lactate dehydrogenase (LDH), creatine kinase (CK), 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA), protein carbonyl (PC), leukocytes, neutrophils, interleukin-6 (IL-6), and C-reactive protein (CRP) were measured at different time points. These measurements were taken at rest, immediately after completion of PE, and 24-, 48-, and 72-hours post-PE. The CK, LDH, DOMS, 8-OHdG, MDA, and PC levels were significantly increased (p < 0.05) after the PE protocol, reaching their peak values between 24 to 48 hours post-PE for all the volume-loaded groups. The levels of leukocytes, neutrophils, and IL-6 also increased after the PE session but returned to resting values within 24 hours post-PE. On the other hand, CRP levels increased at 24 hours post-PE for all the treatment groups (p < 0.05). The changes observed in the indicators of muscle damage and inflammation in response to different volume-loads of PE was not significant. However, the HVL and MVL indicated significant differences compared to LVL in the 8-OHdG (at 48-hour) and MDA (at 72-hour). Athletes engaging in higher volume-loads demonstrated more pronounced responses in terms of biochemical variables (specifically, LVL < MVL < HVL); however, these changes were not statistically significant (except 8-OHdG and MDA).
To determine whether differences exist between proton and electron radiations on biological responses after total-body exposure.ICR mice (n=45) were irradiated to 2 Gray (Gy) using fully modulated 70 MeV protons (0.5 Gy/min) and 21 MeV electrons (3 Gy/min). At 36 h post-irradiation liver gene expression, white blood cell (WBC), natural killer (NK) cell and other analyses were performed.Oxidative stress-related gene expression patterns were strikingly different for irradiated groups compared to 0 Gy (P<0.05). Proton radiation up-regulated 15 genes (Ctsb, Dnm2, Gpx5, Il19, Il22, Kif9, Lpo, Nox4, Park7, Prdx4, Prdx6, Rag2, Sod3, Srxn1, Xpa) and down-regulated 2 genes (Apoe, Prdx1). After electron irradiation, 20 genes were up-regulated (Aass, Ctsb, Dnm2, Gpx1, Gpx4, Gpx5, Gpx6, Gstk1, Il22, Kif9, Lpo, Nox4, Park7, Prdx3, Prdx4, Prdx5, Rag2, Sod1, Txnrd3, Xpa) and 1 was down-regulated (Mpp4). Of the modified genes, only 11 were common to both forms of radiation. Comparison between the two irradiated groups showed that electrons significantly up-regulated three genes (Gstk1, Prdx3, Scd1). Numbers of WBC and major leukocyte types were low in the irradiated groups (P<0.001 vs. 0 Gy). Hemoglobin and platelet counts were low in the electron-irradiated group (P<0.05 vs. 0 Gy). However, spleens from electron-irradiated mice had higher WBC and lymphocyte counts, as well as enhanced NK cell cytotoxicity, compared to animals exposed to protons (P<0.05). There were no differences between the two irradiated groups in body mass, organ masses, and other assessed parameters, although some differences were noted compared to 0 Gy.Collectively, the data demonstrate that at least some biological effects induced by electrons may not be directly extrapolated to protons.
Objective To investigate the relationship between hyperuricemia and coronary heart disease (CHD) risk based on the Framingham risk score (FRS) in a middle-aged and elderly Chinese population. Methods This cross-sectional study enrolled patients undergoing routine check-ups at Xiangya Hospital between October 2013 and November 2014. Hyperuricemia was defined as uric acid ≥416 mmol/l for males and ≥360 mmol/l for females. A 10-year CHD risk was calculated from FRS. A multivariable logistic analysis model was used to evaluate associations. Results Of the 6347 patients, 3415 (53.8%) were male, 1543 (24.3%) had a CHD risk ≥10% (i.e. intermediate and high risk) and the prevalence of hyperuricemia was 18.1% ( n = 1148). After adjusting for potential confounding factors, the 10-year CHD risk was increased in patients with hyperuricemia compared with those without hyperuricemia by 0.28 times in the total population (odds ratio [OR] 1.28; 95% confidence interval [CI] 1.09, 1.48), by 0.25 times in the male population (OR 1.25; 95% CI 1.06, 1.47) and by 2.76 times in the female population (OR 3.76; 95% CI 2.08, 6.79). Conclusion Hyperuricemia was positively associated with a 10-year risk of CHD suggesting that it might be an independent CHD risk factor in middle-aged and elderly individuals.
The goal of this study was to compare the effects of acute 2 Gy irradiation with photons (0.8 Gy/min) or protons (0.9 Gy/min), both with and without pre-exposure to low-dose/low-dose-rate γ rays (0.01 Gy at 0.03 cGy/h), on 84 genes involved in stem cell differentiation or regulation in mouse lungs on days 21 and 56. Genes with a ≥1.5-fold difference in expression and P < 0.05 compared to 0 Gy controls are emphasized. Two proteins specific for lung stem cells/progenitors responsible for local tissue repair were also compared. Overall, striking differences were present between protons and photons in modulating the genes. More genes were affected by protons than by photons (22 compared to 2 and 6 compared to 2 on day 21 and day 56, respectively) compared to 0 Gy. Preirradiation with low-dose-rate γ rays enhanced the acute photon-induced gene modulation on day 21 (11 compared to 2), and all 11 genes were significantly downregulated on day 56. On day 21, seven genes (aldh2, bmp2, cdc2a, col1a1, dll1, foxa2 and notch1) were upregulated in response to most of the radiation regimens. Immunoreactivity of Clara cell secretory protein was enhanced by all radiation regimens. The number of alveolar type 2 cells positive for prosurfactant protein C in irradiated groups was higher on day 56 (12.4–14.6 cells/100) than on day 21 (8.5–11.2 cells/100) (P < 0.05). Taken together, these results showed that acute photons and protons induced different gene expression profiles in the lungs and that pre-exposure to low-dose-rate γ rays sometimes had modulatory effects. In addition, proteins associated with lung-specific stem cells/progenitors were highly sensitive to radiation.
Abstract Background Cartilage destruction is the main characteristic of osteoarthritis (OA), and osteopontin (OPN) is elevated in OA articular cartilage; however, the reason for the increased OPN level is not determined. In addition, Wnt/β-catenin signaling participates in the progression of OA. The aim of the present study was to evaluate whether canonical Wnt signaling could regulate the expression of OPN in human chondrocytes in vitro. Methods Human chondrocytes were cultured in vitro, and we first assayed the mRNA levels of OPN and β-catenin in chondrocytes. Next, we performed transient transfection of TCF 4 shRNA into chondrocytes to inhibit TCF 4 expression and explore changes in the OPN level. Then, the Wnt/β-catenin signaling inhibitor Dickkopf-1 (Dkk-1) was incubated with chondrocytes, and we assayed the changes in β-catenin and OPN. Results Our results showed that the expression of both β-catenin and OPN was increased in OA chondrocytes, but there were no correlations between β-catenin and OPN expression. TCF4 shRNA downregulated the expression of TCF 4 and OPN in chondrocytes, while after treatment with rDKK-1 at a concentration of 400 ng/ml for 24 h, the mRNA and protein expression of both β-catenin and OPN was significantly decreased in chondrocytes. Conclusions Elevated OPN expression might be regulated by the β-catenin/TCF-4 pathway, and the Wnt/β-catenin inhibitor DKK1 could inhibit the expression of β-catenin and OPN in OA chondrocytes.
AIM:To evaluate the effect of recombinant hirudin (r hirudin) in reducing neointimal proliferation after balloon angioplasty in rabbits. METHODS:Twenty four rabbits were randomized into r hirudin group ( n =12) and heparin control group ( n =12),Baloon angioplasty were performed on rabbits normal illiac arterial model. Angiograms were performed at 2 weeks and 4 weeks after procedure. Rabbits were killed 4 weeks after angioplasty. RESULTS:The mean common iliac arterial luminal diameter of r hirudin group was significant increased to compare with heparin control group at 2 weeks ( P 0.01) and 4 weeks ( P 0.01) after balloon angioplasty. At 4 weeks after angioplasty,there were the greater luminal areas ( P 0.01) and the less neointimal areas in r hirudin group ( P 0.01) than in heparin control group. CONCLUSION:r hirudin could significantly lessen neointimal proliferation and luminal stenosis of iliac arteries after balloon angioplasty in rabbits.
Abstract The aim of the study was to examine the relationship between serum calcium (Ca) levels and the prevalence of hyperuricemia (HU). The data included in this analysis were extracted from a population-based study conducted at the Xiangya Hospital Health Management Centre. Serum Ca levels were measured using the Arsenazo III method. HU was defined as the uric acid ≥416 μmol/L for male subjects, and ≥360 μmol/L for female subjects. The association between serum Ca levels and the prevalence of HU was evaluated using logistic and spline regression. The present study included a total of 6337 subjects. The overall prevalence of HU for the target population was 17.5%. Compared with the lowest quintile, the odds ratios adjusted by age, sex, body mass index, smoking, and drinking for HU were 1.51 [95% confidence interval (CI): 1.20–1.91], 1.43 (95% CI: 1.13–1.82), 2.02 (95% CI: 1.61–2.54), and 2.54 (95% CI: 2.02–3.18) for the second, third, fourth, and fifth quintiles of serum Ca levels, respectively ( P for trend <.001), and a positive dose-response relationship was observed. Similar results were observed for men and women, respectively. The findings were not materially altered by the adjustment for further potential confounders. Subjects with higher serum Ca levels are subject to a higher prevalence of HU in a dose-response relationship manner.
Objective To investigate the mechanism of the left vetricular remodeling after acute myocardial infarction,through observing the effects of 3 weeks' treatment with two angiotesin converting enzyme inhibitors, Enalapril and Captopril,on morphology in myocardial-infarcted rats. Methods The rats were divided into three groups:SO,sham-operated;MI; MI Enalapril treated and MI captopril treated. Enalapril and Captopril were given three days before infarction. Results Enalapril and Captopril had special effects on ventricular geometry in rats with infarction,which resulted in decreasing radius of left ventricular cavity by 13.2% and 12.7% respectively compared with MI rats,but the LV weight/bodyweight and the LV chamber radius had been increased 10.4% and 24.5% respectively in MI campared with SO, MI Enalapril treated and MI captopril treated.There were no differences (P0.05). Conclusion The use of Enalapril and Captopril after MI may relieve the left ventricular remodeling and improve the cardiac function,and the two angiotesin converting enzyme inhibitors have no differences.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
