Simultaneous increases of filter-feeding fish and bivalves are key for controlling cyanobacterial blooms in a shallow eutrophic lake.

Eutrophication and cyanobacterial blooms have severely affected many freshwater ecosystems. We studied the effects of filter-feeding fish and bivalves on algal populations using a mesocosm experiment and long-term monitoring data from Lake Taihu (China). The mesocosm study, comprised of a two-way factorial design with the clam Corbicula fluminea and the fish Aristichthys nobilis at three biomass levels, resulted in lower chlorophyll a (Chl a) in high fish treatments, but no significant differences in the low and medium fish treatments. Chl a also decreased with an increase in clam biomass in the high fish treatments. Moreover, filter-feeding fish resulted in a decrease in algal sizes (e.g., the colony size of Microcystis aeruginosa was inversely related to fish biomass) which likely increased the filter-feeding efficiency of bivalves. Biomass of filter-feeding fish was found to be a key factor driving the synergistic effects of filter-feeding fish and bivalves in waters dominated by Microcystis colonies. Long-term monitoring revealed increasing trends in Chl a concentration, total fish catch per unit effort (TF-CPUE), and filter-feeding fish (FF-CPUE), and slightly decreasing trends in bivalve biomass and nitrogen to phosphorus ratios (N:P) from 2006 to 2016. Bivalve biomass and N:P were negatively correlated with Chl a, while FF-CPUE was not significantly related to Chl a. The current filter-feeding fish biomass in Lake Taihu is estimated to be too low to drive synergistic algal control effects together with bivalves. Furthermore, the lack of filter feeders in Lake Taihu may lead to top-down control by predators that cannot counteract the bottom-up effects of nutrients on phytoplankton. Collectively, these long-term monitoring and experimental data support the combined use filter-feeding fish and bivalves for managing cyanobacteria blooms in Lake Taihu.

Additive enhancement of wound healing in diabetic mice by low level light and topical CoQ10.

Diabetes, a highly prevalent disease that affects 9.3% of Americans, often leads to severe complications and slow wound healing. Preclinical studies have suggested that low level light therapy (LLLT) can accelerate wound healing in diabetic subjects, but significant improvements must be made to overcome the absence of persuasive evidence for its clinical use. We demonstrate here that LLLT can be combined with topical Coenzyme Q10 (CoQ10) to heal wounds in diabetic mice significantly faster than LLLT alone, CoQ10 alone, or controls. LLLT followed by topical CoQ10 enhanced wound healing by 68~103% in diabetic mice in the first week and more than 24% in the second week compared with untreated controls. All wounds were fully healed in two weeks following the dual treatment, in contrast to only 50% wounds or a fewer being fully healed for single or sham treatment. The accelerated healing was corroborated by at least 50% higher hydroxyproline levels, and tripling cell proliferation rates in LLLT and CoQ10 treated wounds over controls. The beneficial effects on wound healing were probably attributed to additive enhancement of ATP production by LLLT and CoQ10 treatment. The combination of LLLT and topical CoQ10 is safe and convenient, and merits further clinical study.

The cell toxicity effect of secalonic acid D on GH3 cells and the related mechanisms.

To investigate the anti-pituitary adenoma effect of secalonic acid D (SAD) extracting from marine microorganisms, we used MTT colorimetric method to evaluate the proliferation of GH3 cells treated by SAD, the time- and dose-dependent effects and the value of IC50 were recorded. Hoechst staining, Tunel and flow cytometry methods were used to analyze the apoptosis rate of GH3 cells treated by SAD. Western blotting, RT-PCR and caspase inhibitor (Z-VAD-FMK) were used to investigate the possible mechanism of SAD induced apoptosis and the expression of growth hormone (GH). The results showed that SAD has a time- and dose-dependent effect on GH3 cells and the cytotoxic effect was mainly through apoptosis. The mechanisms were partly through the activity of caspase family and also G1/S phase block. In addition, SAD also can suppress the expression levels of growth hormone in GH3 cells, however, the RT-PCR results showed that the mechanism was not through changing the expression of GH mRNA. We concluded that SAD may be a potential anti-pituitary tumor drug and further in vivo studies should be performed.