Engineered bacterium-binding protein promotes root recruitment of functional bacteria for enhanced cadmium removal from wastewater by phytoremediation.

Functional bacteria promote the efficiency of phytoremediation by enhancing plant growth and participating in decontamination. However, their activity is frequently compromised by the weakness of their interaction with plant roots. In this study, we designed the artificial protein LcGC composed of a bacterium-binding domain, a GFP fluorescence reporter, and a carbohydrate-binding domain to function as a physical contact between functional bacteria and plant roots. This protein was then expressed in an engineered yeast cell factory and extracted to assess its effect on rhizosphere microbiome composition, plant growth, and cadmium removal in a simulated phytoremediation system containing the remediation plant Lemna minor and the functional heavy metal-capturing bacteria Cupriavidus taiwanensis and Pseudomonas putida. LcGC efficiently bound bacterial cell wall components and glucan, endowing it high efficiency to bind both functional bacteria and plant roots. Scanning microscopy and microbiome analysis revealed that LcGC enhanced root recruitment and colonization of functional bacteria on the root surfaces. Furthermore, LcGC with the aid of single C. taiwanensis or of C. taiwanensis and P. putida in combination promoted plant growth, enhanced tolerance to cadmium-induced oxidative stress, and consequently improved cadmium-removing capacity of the plants, with the percent of cadmium removal reaching up to 91% for LcGC plus C. taiwanensis, and to 96% for LcGC plus C. taiwanensis and P. putida on day 7. This study provided a physical contact-based strategy to enhance the interaction between functional microbes and plant roots for efficient phytoremediation.

Recent strategies for improving hemocompatibility and endothelialization of cardiovascular devices and inhibition of intimal hyperplasia.

Cardiovascular diseases have become one of the leading causes of mortality worldwide. Stents and artificial grafts have been used to treat cardiovascular diseases. Thrombosis and restenosis seriously impact the clinical outcome of stents and artificial vascular grafts. For the purpose of antithrombosis and anti-restenosis, numerous strategies have been developed to construct highly hemocompatible surfaces, enhance endothelialization, and inhibit intimal hyperplasia. Rapid endothelialization and inhibited intimal hyperplasia play an important role in artery repair after stent implantation and coronary artery bypass graft surgery. This review focuses on the recently developed strategies for improving the hemocompatibility and endothelialization of cardiovascular devices. We also introduce drug, gene and RNA delivery technologies for inhibiting intimal hyperplasia. The challenges and future perspectives about promoting endothelialization are also briefly discussed with the hope to help inspire further innovations.

Effects of sodium sulfonate daidzein on stress-induced gastric ulcer and its possible mechanism / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of sodium sulfonate daidzein (SSD) on stress-induced gastric ulcer and explore its possible mechanism.</p><p><b>METHODS</b>Using exhausted swimming and counting the number of gastric ulcer to establish the model of stress-induced gastric ulcer. Mouse experience intraperitoneal injection of different doses of SSD and L-NAME, and NDP histochemical method was used to detect the changes of nitric oxide synthase (NOS) positive neurons in stomach.</p><p><b>RESULTS</b>SSD had dose-dependent protective effect on gastric mucosa. L-NAME could prevent stress induced gastric lesion. After combined injection of L-NAME and effective dose of SSD, the protective effect of SSD on gastric mucosa was reinforced. The number of NOS ganglion was constant, and effective dose of SSD had slight effect on NOS-positive neurons in normal mouse while it decreased NOS positive neurons in per area and in per ganglia after stress.</p><p><b>CONCLUSION</b>The increased nitric oxide (NO) leads to gastric ulcer during stress, SSD has protective effect on gastric mucosa and this effect may be mediated by inhibiting NOS and restricting the overproduction of NO during stress.</p>