Control Effects of Short-Term Heatwaves on a Holocyclic Aphid.

The soybean aphid, A. glycines, is an important soybean pest. Harbin, in the Heilongjiang Province, is an area with increasing temperatures in China that faces frequent short-term heatwaves. In this study, the development, reproduction, and morph differentiation of A. glycines have been studied when they were exposed to diurnal at 35 °C for seven days, beginning at different developmental stages. The nymph stage duration of A. glycines was longer, the adult lifespans and total lifespans were shorter, and their bodies were smaller when exposed to a diurnal of 35 °C beginning at the 1st to 4th stadium. The adult reproduction period was shorter, and the adult fecundity and intrinsic rate of increase were smaller than those of aphids reared at a diurnal of 25 °C. A higher and lower proportion of gynoparae and males were deposited as offspring on day 13 by adults when exposed to diurnal at 35 °C, beginning at the 1st to 4th stadium, respectively, than those of aphids reared at a constant of 20 °C. These results are important for predicting the dynamics of A. glycines in Harbin soybeans. This provides evidence that short-term heatwaves are probably useful for controlling A. glycines, by inhibiting development and male morphogenesis.

Delivery of bone morphogenetic protein-2 by crosslinking heparin to nile tilapia skin collagen for promotion of rat calvaria bone defect repair.

Collagen has been widely used as a biomaterial for tissue regeneration. At the present, aqua-collagen derived from fish is poorly explored for biomedical material applications due to its insufficient thermal stability. To improve the bone repair ability and thermal stability of fish collagen, the tilapia skin collagen was crosslinked by EDC/NHS with heparin to bind specifically to BMP-2. The thermal stability of tilapia skin collagen crosslinked with heparin (HC-COL) was detected by differential scanning calorimetry (DSC). Cytotoxicity of HC-COL was assessed by detecting MC3T3-E1 cell proliferation using CCK-8 assay. The specific binding of BMP-2 to HC-COL was tested and the bioactivity of BMP-2-loaded HC-COL (HC-COL-BMP-2) was evaluated in vitro by inducing MC3T3-E1 cell differentiation. In vivo, the bone repair ability of HC-COL-2 was evaluated using micro-CT and histological observation. After crosslinking by EDC/NHS, the heparin-linked and the thermostability of the collagen of Nile Tilapia were improved simultaneously. HC-COL has no cytotoxicity. In addition, the binding of BMP-2 to HC-COL was significantly increased. Furthermore, the in vitro study revealed the effective bioactivity of BMP-2 binding on HC-COL by inducing MC3T3-E1 cells with higher ALP activity and the formation of mineralized nodules. In vivo studies showed that more mineralized and mature bone formation was achieved in HC-COL-BMP-2 group. The prepared HC-COL was an effective BMP-2 binding carrier with enough thermal stability and could be a useful biomaterial for bone repair.

Apelin alleviated neuroinflammation and promoted endogenous neural stem cell proliferation and differentiation after spinal cord injury in rats.

BACKGROUND: Spinal cord injury (SCI) causes devastating neurological damage, including secondary injuries dominated by neuroinflammation. The role of Apelin, an endogenous ligand that binds the G protein-coupled receptor angiotensin-like receptor 1, in SCI remains unclear. Thus, our aim was to investigate the effects of Apelin in inflammatory responses and activation of endogenous neural stem cells (NSCs) after SCI. METHODS: Apelin expression was detected in normal and injured rats, and roles of Apelin in primary NSCs were examined. In addition, we used induced pluripotent stem cells (iPSCs) as a carrier to prolong the effective duration of Apelin and evaluate its effects in a rat model of SCI. RESULTS: Co-immunofluorescence staining suggested that Apelin was expressed in both astrocytes, neurons and microglia. Following SCI, Apelin expression decreased from 1 to 14 d and re-upregulated at 28 d. In vitro, Apelin promoted NSCs proliferation and differentiation into neurons. In vivo, lentiviral-transfected iPSCs were used as a carrier to prolong the effective duration of Apelin. Transplantation of transfected iPSCs in situ immediately after SCI reduced polarization of M1 microglia and A1 astrocytes, facilitated recovery of motor function, and promoted the proliferation and differentiation of endogenous NSCs in rats. CONCLUSION: Apelin alleviated neuroinflammation and promoted the proliferation and differentiation of endogenous NSCs after SCI, suggesting that it might be a promising target for treatment of SCI.