Eight weeks of dry dynamic breath-hold training results in larger spleen volume but does not increase haemoglobin concentration.

Purpose: It has previously been reported that repeated exposure to hypoxia increases spleen size and haemoglobin (HGB) level and recent reports on the effect apnoea has on spleen size and haematological parameters are contradictory. Therefore, this study aims to evaluate the effect apnoea training has on spleen size and haematological parameters. Methods: The breath-holding (BH) group was comprised of 12 local student-athletes with no BH exercise experience who performed BH jogging and BH jumping rope dynamic apnoea protocols, five times weekly for 8 weeks. The BH event duration was progressively increased as the apnoea tolerance of the athletes improved (20 to 35 s). The same training task was performed by the control group (n = 10) without BH. Spleen sizes were measured with an ultrasound system and a complete blood cell analysis was performed on the median cubital venous blood. Results: Spleen volume in the BH group increased from 109 ± 13 ml to 136 ± 13 ml (p < 0.001), and bulky platelets decreased from 70.50 ± 5.83 to 65.17 ± 5.87 (p = 0.034), but no changes were recorded for erythrocytes (p = 0.914), HGB (p = 0.637), PLTs (p = 0.346) and WBC (p = 0.532). No changes were recorded for the control group regarding spleen size or haematological parameters. Conclusion: Eight weeks of dry dynamic apnoea training increased spleen size and decreased the number of circulating bulky platelets in the athletes who were assessed in this study. However, the baseline RBC counts and HGB levels of the athletes were not altered by the training programme.

PFOS-induced placental cell growth inhibition is partially mediated by lncRNA H19 through interacting with miR-19a and miR-19b.

Perfluorooctane sulfonic acid (PFOS), a persistent environmental pollutant, has been associated with decreased birth weight. The dysregulation of long non-coding RNA (lncRNA) H19 has been implicated in pregnancy complications such as intra-uterine growth retardation (IUGR), preeclampsia (PE), however, the expression and function of H19 in PFOS-exerted detrimental effects in the placenta remains to be unveiled. Here, we explored the role of H19 in PFOS-induced placental toxicity. Results showed that PFOS caused decreased cell growth in human HTR-8/SVneo cells. Expression of H19 was increased, while miR-19a and miR-19b expression were decreased in mice placenta tissues and in HTR-8/SVneo cells exposed to PFOS. A significant hypomethylation was observed at the H19 promoter in the placentas of mice that were gestational exposed to high dose of PFOS. H19 was confirmed to bind with miR-19a and miR-19b, targeting SMAD4. Furthermore, H19 appeared to partially improve the cell growth of HTR-8/SVneo cells exposed to PFOS via upregulation of miR-19a and miR-19b. In summary, our findings revealed that H19/miR-19a and miR-19b/SMAD4 axis exerted important functions in PFOS-induced placenta cell toxicity.

Heliocoverpa armigera single nucleocapsid nucleopolyhedrovirus induces Hz-AM1 cell cycle arrest at the G2 phase with accumulation of cyclin B1.

The cell cycle phase distributions of Hz-AM1 cells grown in monolayer culture were G1 = 49.7 +/- 3.3%, S = 22.7 +/- 3.8% and G2/M = 27.8 +/- 4.2% without >4N DNA content. The culture doubling time was about 40 h and the duration of the G1, S and G2/M phases was estimated to be 10, 14 and 16 h, respectively. HaSNPV infection of Hz-AM1 cells resulted in both unsynchronized and synchronized G1 phase arrest at G2/M phase. HaSNPV infection also resulted in the appearance of more than 4N DNA content, which accumulated to the highest levels 72 h post-infection. We also found that the expression level of cyclin B1 increased significantly after 16 h post-infection, while cyclin A did not show any change. This observation supports the Hz-AM1-infected arrest at the G2/M phage. Cytoplasm location of cyclin B1 indicated that the Hz-AM1 cell cycle arrest was at the G2 phase.