A Composite Photocatalyst Based on Hydrothermally-Synthesized Cu2ZnSnS4 Powders.

A novel composite photocatalyst based on Cu2ZnSnS4 (CZTS) powders was synthesized and investigated for use as a photocatalyst. CZTS powders were first made using a conventional hydrothermal method and were then used to grow silver nanoparticles hybridized onto the CZTS under various conditions through a microwave-assisted hydrothermal process. After the obtained samples were subsequently mixed with 1T-2H MoS2, the three synthesized component samples were characterized using X-ray diffractometry (XRD), scanning electron microscopy, transmission electron microscopy (FE-SEM, FE-TEM), UV-visible spectroscopy (UV-Vis), Brunauer-Emmet-Teller (BET), photoluminescence spectroscopy (PL), and X-ray photoelectron spectroscopy (XPS). The resulting samples were also used as photocatalysts for the degradation of methylene blue (MB) under a 300 W halogen lamp simulating sunlight with ~5% UV light. The photodegradation ability was greatly enhanced by the addition of Ag and 1T-2H MoS2. Excellent photodegradation of MB was obtained under visible light. The effects of material characteristics on the photodegradation were investigated and discussed.

Exogenous heat shock cognate protein 70 pretreatment attenuates cardiac and hepatic dysfunction with associated anti-inflammatory responses in experimental septic shock.

It has been recently demonstrated that intracellular heat shock cognate protein 70 (HSC70) can be released into extracellular space with physiologic effects. However, its extracellular function in sepsis is not clear. In this study, we hypothesize that extracellular HSC70 can protect against lipopolysaccharide (LPS)-induced myocardial and hepatic dysfunction because of its anti-inflammatory actions. In Wistar rats, septic shock developed with hypotension, tachycardia, and myocardial and hepatic dysfunction at 4 h following LPS administration (10 mg/kg, i.v.). Pretreatment with recombinant bovine HSC70 (20 µg/kg, i.v.) attenuated LPS-induced hypotension and tachycardia by 21% and 23%, respectively (P < 0.05), improved myocardial dysfunction (left ventricular systolic pressure: 33%; max dP/dt: 20%; min dP/dt: 33%, P < 0.05), and prevented hepatic dysfunction (glutamic-oxaloacetic transaminase: 81 vs. 593 IU/L; glutamic-pyruvic transaminase: 15 vs. 136 IU/L, P < 0.05) compared with LPS-treated rats at 4 h. Heat shock cognate protein 70 also prevented LPS-induced hypoglycemia (217 vs. 59 mg/dL, P < 0.05) and elevated lactate dehydrogenase (1,312 vs. 6,301 IU/L, P < 0.05). Furthermore, HSC70 decreased LPS-induced elevation of circulating tumor necrosis factor α and nitrite/nitrate, and tissue expression of inducible nitric oxide synthase, cyclooxygenase 2, and matrix metalloproteinase 9 in the heart and liver. To investigate underlying mechanisms, we found that HSC70 attenuated LPS-induced nuclear translocation of nuclear factor κB subunit p65 by blocking the phosphorylation of inhibitor of nuclear factor κB. Finally, we showed that HSC70 repressed the activation of MAPKs caused by LPS. These results demonstrate that in LPS-induced septic shock, extracellular HSC70 conveys pleiotropic protection on myocardial, hepatic, and systemic derangements, with associated inhibition of proinflammatory mediators including tumor necrosis factor α, nitric oxide, cyclooxygenase 2, and matrix metalloproteinase 9, through mitogen-activated protein kinase/nuclear factor κB signaling pathways. Therefore, extracellular HSC70 may have a promising role in the prophylactic treatment of sepsis.