Temperature is generally considered as a key factor controlling algal bloom formation. Previous studies have indicated that the bloom-forming cyanobacteria Microcystis spp. overwinters near the sediment surface and does not actively grow below 158C. However, satellite images and field collections from Lake Taihu, China have shown that Microcystis spp. blooms persisted when water temperatures were below 108C during winter, although their magnitudes were smaller than during periods of higher temperature. Winter Microcystis cells maintained low activity and were able to grow again when exposed to elevated temperatures (12.58C). Hence, cyanobacterial blooms may appear year-round in eutrophic lakes. Temperature increases coupled with nutrient enrichment promoted the growth of cyanobacteria, while low temperature decreased the loss rate of Microcystis, allowing winter blooms to persist. High concentrations of overwintering vegetative cells may provide a large inoculum for blooms during warmer seasons. Controlling winter blooms may reduce their magnitude during the warmer seasons.
We have utilized a nonviral, polymeric interactive non-conoptimal doses of 24 and 48 g, respectively. While polydensing (PINC) gene delivery system to deliver IL-12 to morphonuclear cells (PMNs) were partially involved in the two different types of murine tumors, an immunogenic development of the antitumor immune response elicited by renal cell carcinoma, Renca, and a non-immunogenic IL-12/PVP treatment, CD8 + T cells were found to be the colon cell carcinoma, CT26. The delivery of IL-12/polyvinyl primary effectors. In contrast, CD4 + T cells did not appear pyrrolidone (PVP) complexes into Renca led to the to play a significant role in the development of tumor speexpression of IL-12 (146 ± 89 pg/mg) and IFN-␥ cific immunity. Finally, mice that rejected the tumors follow-(160 ± 82 pg/mg) from explanted tumors in culture supering IL-12/PVP treatment were protected against a second natants. Treated tumors showed increased infiltration of challenge with the same tumor. These data provide evi-NK, CD4+ and CD8 + T cells and up-regulation of MHC dence that a nonviral IL-12 gene delivery system is well class I molecules on leukocytes in both tumors and lymph tolerated and generates a potent immune response against nodes. Fifty per cent of tumor-bearing mice rejected Renca established tumors. or CT26 tumors following IL-12/PVP treatments given at
Brain-derived neurotrophic factor (BDNF) is a crucial regulator to support synaptic plasticity and neuronal survival, its significant decrease is a pathophysiological hallmark in Alzheimer's disease (AD) brains and accounts for poor prognosis. MicroRNAs (miRNAs) interfere with the translation of target mRNAs and control a variety of physiological and pathological processes. MiR-322 is the rodent homologue of human miR-424, it is involved in the modulation of cell differentiation, proliferation, apoptosis and metabolic activities in diverse tissues and organs. However, the roles and potential mechanisms of miR-322 remain elusive in AD pathogenesis. Here we observed miR-322 is significantly increased along with BDNF decrease in AD mouse brain. Bioinformatics prediction implicated that BDNF 3'-untranslated region (3'-UTR) possesses the putative target sequence of miR-322. Luciferase reporter assay identified that miR-322 can directly conjugate to BDNF 3'-UTR. The functional research showed that MiR-322 input deregulates BDNF expression at either mRNA or protein levels, whereas miR-322 silence restores BDNF expression in vitro. Furthermore, we found miR-322 promotes Tau phosphorylation via negatively controlling BDNF-TrkB receptor activation, otherwise MiR-322 silence restores TrkB activation and attenuates tau phosphorylation. Collectively, this study demonstrated a novel miRNA-dependent manner of BDNF degradation in AD pathogenesis, it may drive a miRNAs- or BDNF based therapeutic strategies against Alzheimer's disease.
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