Effect of photoperiod on sexual activity of boar

The main objective of this study was to assess the effect of photoperiod on sexual activity of three breeds of boars: Swedish Landrace (n=34), Large White (n=38), and Duroc (n=32). Boar sexual activity was analysed based on the libido index and intensity of ejaculation. The libido index was calculated as the ratio between the duration of ejaculation and time of preparation until ejaculation. The intensity of ejaculation was the volume of ejaculate (mL) secreted in the unit of time (min). The effect of photoperiod was analysed as the effect of duration of daylight ( lt 12 h and >12 h) within photoperiod intervals (increasing and decreasing). Impact assessment was carried out by applying the General Linear Model procedure. Libido and intensity of ejaculation varied under the impact of photoperiod and the breed of boars. With the increase in age, the boar libido weakened, while the volume of ejaculate and intensity of ejaculation increased. Boars manifested better libido when the daylight lasted longer than 12 h in both photoperiod intervals. Different from libido, the volume of ejaculate and intensity of ejaculation were highest when the daylight was shorter than 12 h, but only in the decreasing photoperiod interval. Swedish Landrace boars manifested best libido, while in the production of sperm the Duroc boars were inferior compared with Swedish Landrace and Large White. The phenotypic relationship among libido, ejaculate volume, and ejaculation intensity ranges from very low to high; however, the coefficients were positive, which indicates the possibility of simultaneous improvement of these traits

Matrix Development in Self-Assembly of Articular Cartilage

Articular cartilage is a highly functional tissue which covers the ends of long bones and serves to ensure proper joint movement. A tissue engineering approach that recapitulates the developmental characteristics of articular cartilage can be used to examine the maturation and degeneration of cartilage and produce fully functional neotissue replacements for diseased tissue.This study examined the development of articular cartilage neotissue within a self-assembling process in two phases. In the first phase, articular cartilage constructs were examined at 1, 4, 7, 10, 14, 28, 42, and 56 days immunohistochemically, histologically, and through biochemical analysis for total collagen and glycosaminoglycan (GAG) content. Based on statistical changes in GAG and collagen levels, four time points from the first phase (7, 14, 28, and 56 days) were chosen to carry into the second phase, where the constructs were studied in terms of their mechanical characteristics, relative amounts of collagen types II and VI, and specific GAG types (chondroitin 4-sulfate, chondroitin 6-sulfate, dermatan sulfate, and hyaluronan). Collagen type VI was present in initial abundance and then localized to a pericellular distribution at 4 wks. N-cadherin activity also spiked at early stages of neotissue development, suggesting that self-assembly is mediated through a minimization of free energy. The percentage of collagen type II to total collagen significantly increased over time, while the proportion of collagen type VI to total collagen decreased between 1 and 2 wks. The chondroitin 6- to 4- sulfate ratio decreased steadily during construct maturation. In addition, the compressive properties reached a plateau and tensile characteristics peaked at 4 wks.The indices of cartilage formation examined in this study suggest that tissue maturation in self-assembled articular cartilage mirrors known developmental processes for native tissue. In terms of tissue engineering, it is suggested that exogenous stimulation may be necessary after 4 wks to further augment the functionality of developing constructs

3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings

RATIONALE: 3,4-Methylenedioxymethamphetamine (MDMA) is a widely abused illicit drug. In animals, high-dose administration of MDMA produces deficits in serotonin (5-HT) neurons (e.g., depletion of forebrain 5-HT) that have been interpreted as neurotoxicity. Whether such 5-HT deficits reflect neuronal damage is a matter of ongoing debate. OBJECTIVE: The present paper reviews four specific issues related to the hypothesis of MDMA neurotoxicity in rats: (1) the effects of MDMA on monoamine neurons, (2) the use of “interspecies scaling” to adjust MDMA doses across species, (3) the effects of MDMA on established markers of neuronal damage, and (4) functional impairments associated with MDMA-induced 5-HT depletions. RESULTS: MDMA is a substrate for monoamine transporters, and stimulated release of 5-HT, NE, and DA mediates effects of the drug. MDMA produces neurochemical, endocrine, and behavioral actions in rats and humans at equivalent doses (e.g., 1–2 mg/kg), suggesting that there is no reason to adjust doses between these species. Typical doses of MDMA causing long-term 5-HT depletions in rats (e.g., 10–20 mg/kg) do not reliably increase markers of neurotoxic damage such as cell death, silver staining, or reactive gliosis. MDMA-induced 5-HT depletions are accompanied by a number of functional consequences including reductions in evoked 5-HT release and changes in hormone secretion. Perhaps more importantly, administration of MDMA to rats induces persistent anxiety-like behaviors in the absence of measurable 5-HT deficits. CONCLUSIONS: MDMA-induced 5-HT depletions are not necessarily synonymous with neurotoxic damage. However, doses of MDMA which do not cause long-term 5-HT depletions can have protracted effects on behavior, suggesting even moderate doses of the drug may pose risks

Expression and functional involvement of N-cadherin in embryonic limb chondrogenesis.

Cell adhesion molecules have been shown to be important mediators of morphogenesis and pattern formation. In this study, we have shown that N-cadherin is expressed in a specific spatiotemporal manner in the developing limb bud during chondrogenesis in vivo and in cultured limb mesenchyme in vitro. The time period of maximal expression of N-cadherin corresponds to the period of active cellular condensation, an event believed to be a necessary prerequisite for chondrogenic differentiation. To directly assess the functional involvement of N-cadherin in cellular condensation, we have examined the effects of perturbing N-cadherin activity on both cell aggregation and chondrogenesis using NCD-2, a rat monoclonal antibody directed against the binding region of N-cadherin. Non-immune rat IgG was used as a control. Our results show that functional N-cadherin is necessary for chondrogenesis to proceed both in vivo and in vitro. Limb mesenchymal cells exhibited characteristic Ca(2+)-dependent cell aggregation in suspension, which was inhibited in the presence of exogenous NCD-2. In micromass cultures of limb mesenchymal cells, NCD-2 inhibited overt chondrogenesis in a dose-dependent manner. Furthermore, NCD-2 inhibition of chondrogenesis in micromass cultures was time-dependent, suggesting that N-cadherin is crucially involved during the latter half of the first 24 hours of culture, a time period most likely corresponding to active cellular condensation. NCD-2 also significantly influenced limb development when injected into embryonic limb buds in vivo. In addition to significant inhibition of chondrogenesis and developmental delays, gross developmental deformities and perturbation of overall pattern formation were also observed. Taken together, these results demonstrate that N-cadherin is functionally required in mediating the cell-cell interactions among mesenchymal cells important for chondrogenesis in micromass culture in vitro and in the intact limb bud in vivo

Spatiotemporal profile of N-cadherin expression in the developing limb mesenchyme.

During embryonic limb development, chondrogenesis of the mesenchyme is preceded by a crucial cellular condensation phase. Because condensation is likely to result from specific cell-cell interactions, we have examined the possible involvement of N-cadherin, a Ca(2+)-dependent cell adhesion molecule, in this condensation event. Previously, we have reported that N-cadherin is expressed in chick embryonic limb bud, and that perturbation of N-cadherin-mediated cell adhesion significantly inhibits limb mesenchymal cellular aggregation and chondrogenesis both in vivo and in vitro. To further examine the relationship between N-cadherin expression and chondrogenesis, we have quantified and characterized the spatiotemporal expression of N-cadherin mRNA and protein in the developing chick embryonic limb, and analyzed the mechanism whereby exogenous Ca2+ stimulates chondrogenesis in vitro. Immunohistochemistry revealed that N-cadherin is expressed on mesenchymal cell surface in a developmentally specific manner during limb bud maturation. N-Cadherin was detected in the mesenchyme of the central core of the early limb bud, and was maximally expressed between stages 24 to 26, corresponding to the period of cellular condensation in vivo. Mature cartilage did not express N-cadherin. In chick limb mesenchyme micromass cultures in vitro, N-cadherin protein expression was seen associated with distinct cellular aggregates of condensing mesenchyme, but not in mature cartilaginous nodules or the mesenchyme situated between the condensing aggregates. In situ hybridization localized N-cadherin mRNA expression in condensing regions of limb mesenchyme in a stage 25/26 limb bud; at later stages, N-cadherin mRNA expression was seen in the perichondrium and the dense mesenchyme, but not in mature cartilage. The agreement between the mRNA and protein data thus suggests that N-cadherin expression in the developing limb bud is regulated at the transcriptional level. Western immunoblot analysis further confirmed that, from stages 19 to 36, the level of N-cadherin in the limb bud increased 5-fold through stage 25/26, then decreased during the progression of chondrogenesis and osteogenesis. A parallel profile was also seen in micromass limb mesenchyme cultures in vitro. The importance of N-cadherin for Ca2+ mediated mesenchymal cell aggregation and chondrogenesis was examined by selective, proteolytic dissociation of the mesenchymal cells with retention or removal of N-cadherin. Cells with N-cadherin were shown to exhibit Ca(2+)-dependent aggregation and were consistently more chondrogenic than those without N-cadherin. These results provide strong support for the functional role of N-cadherin in chondrogenesis