Impact of melatonin supplementation in the rat spermatogenesis subjected to forced swimming exercise

Oxygen consumption increases many times during exercise, which can increase reactive oxygen species. It negatively affects fertility in male athletes. Melatonin is exerting a regulatory role at different levels of the hypothalamic-pituitary-gonadal axis. However, there is no evidence that the protective effects of melatonin persist after long duration exercise on the spermatogenesis. Therefore, this study was conducted to examine the impacts of melatonin on the testis following the administration of swimming exercise. Rats were separated into five different groups, including Control, sham M: received the solvent of melatonin, M: received melatonin, S: the exercise protocol, MS: received melatonin and the exercise protocol. After 8weeks, animals were scarified and antioxidant enzymes levels of testes, spermatogenic cells apoptosis and sperm quality were measured. Swimming decreased all parameters of spermatozoa. Nevertheless, melatonin could significantly improve the progressive motility of spermatozoa in MS rats. Swimming caused an increased apoptosis of S group and decreased all antioxidant enzymes. Melatonin could drastically reduce apoptosis and increased these enzymes. Therefore, melatonin seems to induce the production of antioxidant enzymes of testicular tissues and diminish the extent of apoptotic changes caused by forced exercise on the testis, which can, in turn, ameliorate the sperm parameters

Transdifferentiation of Human Dental Pulp Stem Cells Into Oligoprogenitor Cells

Introduction: The nerve fibers in central nervous system are surrounded by myelin sheet which is formed by oligodendrocytes. Cell therapy based on oligodendrocytes and their precursors transplantation can hold a promising alternative treatment for myelin sheet repair in demyelinating diseases. Methods: Human Dental Pulp Stem Cells (hDPSCs) are noninvasive, autologous and easy available source with multipotency characteristics, so they are in focus of interest in regenerative medicine. In the present study, hDPSCs were differentiated into oligoprogenitor using glial induction media, containing Retinoic Acid (RA), basic Fibroblast Growth Factor (bFGF), Platelet- Derived Growth Factor (PDGF), N2 and B27. The differentiated Oligoprogenitor Cells (OPCs) were evaluated for nestin, Olig2, NG2 and O4 using immunocytochemistry. Also, the expression of nestin, Olig2 and PDGFR-alpha gens (neuroprogenitor and oligoprogenitor markers) were investigated via RT-PCR technique. Results: The results indicate that glial differentiation medium induces the generation of oligoprogenitor cells as revealed via exhibition of specific glial markers, including Olig2, NG2 and O4. The expersion of nestin gene (neuroprogenitor marker) and Olig2 and PDGFR-alpha genes (oligoprogentor markers) were detected in treated hDPSCs at the end of the induction stage. Conclusion: hDPSCs can be induced to transdifferentiate into oligoprogenitor cells and respond to the routinely applied regents for glial differentiation of mesanchymal stem cells. These data suggest the hDPSCs as a valuable source for cell therapy in neurodegenerative diseases

Temperature - dependent life table of the predatory mite, Amblyseius swirskii (Mesostigmata: Phytoseidae) fed on stored product mite Carpoglyphus lactis (Astigmata: Carpoglyphidae)

The predatory mite, Amblyseius swirskii (Athias-Henriot) is an efficient predator of some insect pests particularly thrips and whiteflies. To evaluate the optimum temperature for  A.swirskii, a life table study, based on the age-stage, two-sex life table theory, was conducted using the stored product mite, Carpoglyphus lactis L. as the food diet. Experiments were performed at temperatures of 22, 25, 30 and 32° C, %70 ± 5 relative humidity and 16: 8 (L: D) photoperiod. Developmental time of eggs at 30° C was significantly shorter comparing to the temperatures 22 and 32° C. Developmental time of the mobile pre-adult stages, male and female, were significantly shorter at 32° C, comparing to 25° C. The highest fecundity of the predator was observed at 25° C (72.34 eggs / female). The intrinsic rate of increase (r), finite rate of population increase (λ), net reproductive rate (R0), at temperature of 22° C were 0/226 day-1, 1/25 day-1, 25/53 offspring/individual; at 25° C were 0/304 day-1, 1.35 day-1, 33/82 offspring/ individual; at 30° C were 0/097 day-1, 1/102 day-1, 2/42 offspring/ individual; at a temperature of 32° C were 0/128 day-1, 1/137 day-1, 2/67 offspring/ individual. The population parameters of A. swirskii, except mean generation times (T), at 25° C and 32° C were significantly higher than those at 30° C, and the average generation time (T), at temperature of 22° C, was found to be the highest. The total population projection demonstrated that the highest population growth of predatory mite, A. swirskii occurred at 25° C

The effect of interaguild predation on avoidance behavior of the aphidophagous midge, Aphidoletes aphidimyza (Dip.: Cecidomyiidae) on its encounter with the predatory bug Orius laevigatus (Het.: Anthocoridae)

The predatory bug, Orius laevigatus (Fibber), and the predatory midge, Aphidoletes aphidimyza Rondani, belong to an aphidophagous guild, feeding on the cotton aphid Aphis gossypii Glover. In this study some avoidance behavior of the predatory midge such as dropping from the plant and choosing an oviposition site in the face of interaguild (IG) predator O. laevigatus are investigated. The results indicate that A. aphidimyza females prefer not to lay eggs when they discover that their offspring would be at risk of being attacked by the IG predator. The experiment also shows that the dropping behavior of predatory midge larva, upon being spotted by the predatory bug (44.5%), is significantly higher than the control (6.5%). Both the dropping behavior and mortality of IG prey are found to be influenced by all developmental stages of the cotton aphid. The percentage of mortality and dropping rates of A. aphidimyza larvae in the presence of 2nd instar nymphs of aphids were 10% and 12.5% and for 4th instar nymphs were 31% and 44.5%, respectively. These findings confirm the correlation between habitat choice of A. aphidimyza, in relation to predation risk for its offspring, and also underscore the population structure of prey for avoidance behavior strategy of the aphidophagous midge in an interaguild predation system

Fitness costs of cornicle secretions as a defense mechanism for cotton aphid, Aphis gossypii (Hem.: Aphididae)

The cornicle secretion is a defensive mechanism in many aphid species to warn the related individuals of predation by natural enemies. Many researches have been conducted on the benefits of cornicle droplet and alarm pheromone but the cost of this phenomenon is poorly investigated. This study is intended to evaluate the direct fitness cost of cornicle secretion of immature as well as mature cotton aphids, Aphis gossypii Glover. Aphids were artificially forced to produce cornicle droplets at different stages of their development (second, third and fourth instars as well as adults). They were lightly stroked on the anterior portion of the thorax with a fine brush, resulting in the secretion of visible cornicle droplets. After this manipulation, life-history parameters of aphids were recorded until the death of the last adult individual. Experiments were conducted in a growth chamber at 25 ± 1°C, 50 ± 5% RH and a photoperiod of 16 L: 8 D hours. The results showed that the secretion of cornicle droplets by second and third instar nymphs of cotton aphid did not affect their survivorship and the number of offspring produced by their adult stage. In contrast, fourth instar nymphs as well as adults that emitted cornicle droplets had significantly lower survivorship and offspring production than non-secretors. The cornicle secretion has also fitness costs on the late instar and adult cotton aphids

Anthrax Lethal Factor Cleavage of Nlrp1 Is Required for Activation of the Inflammasome

NOD-like receptor (NLR) proteins (Nlrps) are cytosolic sensors responsible for detection of pathogen and danger-associated molecular patterns through unknown mechanisms. Their activation in response to a wide range of intracellular danger signals leads to formation of the inflammasome, caspase-1 activation, rapid programmed cell death (pyroptosis) and maturation of IL-1β and IL-18. Anthrax lethal toxin (LT) induces the caspase-1-dependent pyroptosis of mouse and rat macrophages isolated from certain inbred rodent strains through activation of the NOD-like receptor (NLR) Nlrp1 inflammasome. Here we show that LT cleaves rat Nlrp1 and this cleavage is required for toxin-induced inflammasome activation, IL-1 β release, and macrophage pyroptosis. These results identify both a previously unrecognized mechanism of activation of an NLR and a new, physiologically relevant protein substrate of LT

Inflammasome Sensor Nlrp1b-Dependent Resistance to Anthrax Is Mediated by Caspase-1, IL-1 Signaling and Neutrophil Recruitment

Bacillus anthracis infects hosts as a spore, germinates, and disseminates in its vegetative form. Production of anthrax lethal and edema toxins following bacterial outgrowth results in host death. Macrophages of inbred mouse strains are either sensitive or resistant to lethal toxin depending on whether they express the lethal toxin responsive or non-responsive alleles of the inflammasome sensor Nlrp1b (Nlrp1bS/S or Nlrp1bR/R, respectively). In this study, Nlrp1b was shown to affect mouse susceptibility to infection. Inbred and congenic mice harboring macrophage-sensitizing Nlrp1bS/S alleles (which allow activation of caspase-1 and IL-1β release in response to anthrax lethal toxin challenge) effectively controlled bacterial growth and dissemination when compared to mice having Nlrp1bR/R alleles (which cannot activate caspase-1 in response to toxin). Nlrp1bS-mediated resistance to infection was not dependent on the route of infection and was observed when bacteria were introduced by either subcutaneous or intravenous routes. Resistance did not occur through alterations in spore germination, as vegetative bacteria were also killed in Nlrp1bS/S mice. Resistance to infection required the actions of both caspase-1 and IL-1β as Nlrp1bS/S mice deleted of caspase-1 or the IL-1 receptor, or treated with the Il-1 receptor antagonist anakinra, were sensitized to infection. Comparison of circulating neutrophil levels and IL-1β responses in Nlrp1bS/S,Nlrp1bR/R and IL-1 receptor knockout mice implicated Nlrp1b and IL-1 signaling in control of neutrophil responses to anthrax infection. Neutrophil depletion experiments verified the importance of this cell type in resistance to B. anthracis infection. These data confirm an inverse relationship between murine macrophage sensitivity to lethal toxin and mouse susceptibility to spore infection, and establish roles for Nlrp1bS, caspase-1, and IL-1β in countering anthrax infection

Adenoviral expression of a bispecific VHH-based neutralizing agent that targets protective antigen provides prophylactic protection from anthrax in mice

Bacillus anthracis, the causative agent of anthrax, secretes three polypeptides, which form the bipartite lethal and edema toxins (LT and ET, respectively). The common component in these toxins, protective antigen (PA), is responsible for binding to cellular receptors and translocating the lethal factor (LF) and edema factor (EF) enzymatic moieties to the cytosol. Antibodies against PA protect against anthrax. We previously isolated toxin-neutralizing variable domains of camelid heavy-chain-only antibodies (VHHs) and demonstrated their in vivo efficacy. In this work, gene therapy with an adenoviral (Ad) vector (Ad/VNA2-PA) (VNA, VHH-based neutralizing agents) promoting the expression of a bispecific VHH-based neutralizing agent (VNA2-PA), consisting of two linked VHHs targeting different PA-neutralizing epitopes, was tested in two inbred mouse strains, BALB/cJ and C57BL/6J, and found to protect mice against anthrax toxin challenge and anthrax spore infection. Two weeks after a single treatment with Ad/VNA2-PA, serum VNA2-PA levels remained above 1 μg/ml, with some as high as 10 mg/ml. The levels were 10- to 100-fold higher and persisted longer in C57BL/6J than in BALB/cJ mice. Mice were challenged with a lethal dose of LT or spores at various times after Ad/VNA2-PA administration. The majority of BALB/cJ mice having serum VNA2-PA levels of >0.1 μg/ml survived LT challenge, and 9 of 10 C57BL/6J mice with serum levels of >1 μg/ml survived spore challenge. Our findings demonstrate the potential for genetic delivery of VNAs as an effective method for providing prophylactic protection from anthrax. We also extend prior findings of mouse strain-based differences in transgene expression and persistence by adenoviral vectors

Proteolytic Processing of Nlrp1b Is Required for Inflammasome Activity

Nlrp1b is a NOD-like receptor that detects the catalytic activity of anthrax lethal toxin and subsequently co-oligomerizes into a pro-caspase-1 activation platform known as an inflammasome. Nlrp1b has two domains that promote oligomerization: a NACHT domain, which is a member of the AAA+ ATPase family, and a poorly characterized Function to Find Domain (FIIND). Here we demonstrate that proteolytic processing within the FIIND generates N-terminal and C-terminal cleavage products of Nlrp1b that remain associated in both the auto-inhibited state and in the activated state after cells have been treated with lethal toxin. Functional significance of cleavage was suggested by the finding that mutations that block processing of Nlrp1b also prevent the ability of Nlrp1b to activate pro-caspase-1. By using an uncleaved mutant of Nlrp1b, we established the importance of cleavage by inserting a heterologous TEV protease site into the FIIND and demonstrating that TEV protease processed this site and induced inflammasome activity. Proteolysis of Nlrp1b was shown to be required for the assembly of a functional inflammasome: a mutation within the FIIND that abolished cleavage had no effect on self-association of a FIIND-CARD fragment, but did reduce the recruitment of pro-caspase-1. Our work indicates that a post-translational modification enables Nlrp1b to function

Quantum Gravitational Corrections to the Real Klein-Gordon Field in the Presence of a Minimal Length

The (D+1)-dimensional $(\beta,\beta')$-two-parameter Lorentz-covariant deformed algebra introduced by Quesne and Tkachuk [C. Quesne and V. M. Tkachuk, J. Phys. A: Math. Gen. \textbf {39}, 10909 (2006).], leads to a nonzero minimal uncertainty in position (minimal length). The Klein-Gordon equation in a (3+1)-dimensional space-time described by Quesne-Tkachuk Lorentz-covariant deformed algebra is studied in the case where $\beta'=2\beta$ up to first order over deformation parameter $\beta$. It is shown that the modified Klein-Gordon equation which contains fourth-order derivative of the wave function describes two massive particles with different masses. We have shown that physically acceptable mass states can only exist for $\beta<\frac{1}{8m^{2}c^{2}}$ which leads to an isotropic minimal length in the interval $10^{-17}m<(\bigtriangleup X^{i})_{0}<10^{-15}m$. Finally, we have shown that the above estimation of minimal length is in good agreement with the results obtained in previous investigations.Comment: 10 pages, no figur