Enhancement of bio-promoters on hexavalent chromium inhibited sulfur-driven denitrification: repairing damage, accelerating electron transfer, and reshaping microbial collaboration.

Proposing recovery strategies to recover heavy-metal-inhibited sulfur-driven denitrification, as well as disclosing recovery mechanisms, can provide technical support for the stable operation of bio-systems. This study proposed an effective bio-promoter (mediator-promoter composed of L-cysteine, biotin, cytokinin, and anthraquinone-2,6-disulfonate) to recover Cr(VI) inhibited sulfur-driven denitrification, which effectively reduced the recovery time of NO3--N reduction (18-21 cycles) and NO2--N reduction (27-42 cycles) compared with self-recovery. The mediator-promoter repaired microbial damage by promoting intracellular chromium efflux. Moreover, the mediator-promoter reduced the accumulated reactive oxygen species by stimulating the secretion of antioxidant enzymes, reaching equilibrium in the oxidative-antioxidant system. To improve electron transmission, the mediator-promoter restored S2O32- oxidation to provide adequate electron donors and increased electron transfer rate by increasing cytochrome c levels. Mediator-promoter boosted the abundance of Thiobacillus (sulfur-oxidizing bacterium) and Simplicispira (denitrifying bacterium), which were positively correlated, facilitating the rapid denitrification recovery and the long-term stable operation of recovered systems.

How halogenated aromatic compounds affect the electron supply and consumption in glucose supported denitrification?

Halogenated aromatic compounds possess bidirectional effects on denitrifying bio-electron behavior, providing electrons and potentially interfering with electron consumption. This study selected the typical 4-chlorophenol (4-CP, 0-100 mg/L) to explore its impact mechanism on glucose-supported denitrification. When COD(glucose)/COD(4-CP)=28.70-3.59, glucose metabolism remained the dominant electron supply process, although its removal efficiency decreased to 73.84-49.66 %. When COD(glucose)/COD(4-CP)=2.39-1.43, 4-CP changed microbial carbon metabolism priority by inhibiting the abundance of glucose metabolizing enzymes, gradually replacing glucose as the dominant electron donor. Moreover, 5-100 mg/L 4-CP reduced adenosine triphosphate (ATP) by 15.52-24.67 % and increased reactive oxygen species (ROS) by 31.13-63.47 %, causing severe lipid peroxidation, thus inhibiting the utilization efficiency of glucose. Activated by glucose, 4-CP dechlorination had stronger electron consumption ability than NO2--N reduction (NO3--N > 4-CP > NO2--N), combined with the decreased nirS and nirK genes abundance, resulting in NO2--N accumulation. Compared with the blank group (0 mg/L 4-CP), 5-40 mg/L and 60-100 mg/L 4-CP reduced the secretion of cytochrome c and flavin adenine dinucleotides (FAD), respectively, further decreasing the electron transfer activity of denitrification system. Micropruina, a genus that participated in denitrification based on glucose, was gradually replaced by Candidatus_Microthrix, a genus that possessed 4-CP degradation and denitrification functions after introducing 60-100 mg/L 4-CP.

Schizandrin B inhibits the cis­DDP­induced apoptosis of HK­2 cells by activating ERK/NF­κB signaling to regulate the expression of survivin.

The nephrotoxicity of cisplatin limits its clinical application. Schizandrin B (SchB) has been demonstrated to have a variety of potential cytoprotective activities. The present study explored the molecular mechanisms by which SchB inhibits the dichlorodiammine platinum (DDP)­induced apoptosis of HK­2 proximal tubule epithelial cells. In vitro assays demonstrated that SchB increased the viability of HK­2 cells, alleviated the cis­DDP­induced activation of caspase­3, reduced apoptosis and improved the nuclear morphology of HK­2 cells. Additionally, the mechanism underlying the cis­DDP­induced apoptosis was indicated to involve the activation of p53, c­Jun­N­terminal kinase (JNK) and p38 signaling. Furthermore, SchB was demonstrated to activate extracellular signal­regulated kinase (ERK) and nuclear factor κB (NF­κB) signaling, and induce the expression of survivin. The inhibition of ERK and NF­κB signaling using U0126 and pyrollidine dithiocarbamate, respectively, inhibited the expression of survivin, whereas blocking the expression of survivin using small interfering RNA inhibited the alleviating effect of SchB on cis­DDP­induced apoptosis as indicated by a reduction in cleaved caspase­3 expression. In conclusion, SchB regulates ERK/NF­κB signaling to induce the expression of survivin, thereby alleviating cis­DDP­induced renal injury.

Establishment of a novel therapeutic vector targeting the trigeminal ganglion in rats.

BACKGROUND: In the pathogenesis of herpes simplex keratitis, herpes simplex virus type 1 (HSV-1) infection begins in corneal epithelium cells and then progresses through the sensory nerve endings and finally travels up forward to the trigeminal ganglion (TG), where it remains as latent virus. The available anti-HSV therapies do not completely suppress the recurrence of active HSV-1 infection. The aim of this study was to establish a novel replication-defective (rd) HSV-1 (rdHSV) vector (rdHSV-interferon gamma [IFNγ]) that could effectively target the TG. METHODS: Recombinant HSV-1 virus was inserted into a shuttle plasmid carrying IFNγ to establish the rdHSV-IFNγ vector. Safety was evaluated in vitro by 50% cellular cytotoxicity in transfected SH-SY5Y neuroblastoma cells and in vivo by Kaplan-Meier survival estimate and infection rate. Wistar rats were immunized with rdHSV-IFNγ to evaluate the TG targeting efficiency. Real-time polymerase chain reaction and Western blot assays were used to evaluate IFNγ mRNA and protein expression and rdHSV-IFNγ localization. RESULTS: The rdHSV-IFNγ vector was successfully constructed and showed high in vitro safety and overall survival and a corneal infection rate similar to that of control rats immunized with saline (control group; P>0.05). Real-time polymerase chain reaction and immunohistochemistry assays confirmed IFNγ expression and effective TG targeting on days 14 and 21, which increased with postimmunization time. Moreover, IFNγ was expressed sufficiently in the TG tissues. CONCLUSION: The rdHSV-IFNγ can act as an effective gene transporting vector that carries the therapeutic genes to the TG and triggers its expression.

Association between the apolipoprotein E4 and postoperative cognitive dysfunction in elderly patients undergoing intravenous anesthesia and inhalation anesthesia.

BACKGROUND: Intravenous and inhalation anesthesia are commonly used in the clinical setting. Recovery of cognitive function in elderly patients after surgery has received increased attention. In this study, the authors compared recovery of cognitive function in patients after different anesthesia techniques, and investigated which technique is safer. The authors also explored association between apolipoprotein E4 and postoperative cognitive dysfunction in patients undergoing general anesthesia. METHODS: A total of 2,000 patients were equally and randomly divided into intravenous and inhalation anesthesia groups. Total intravenous and inhalation anesthesia were used. Within 10 days after surgery, cognitive function was assessed daily using the Mini-Mental State Examination (MMSE). Restriction fragment length polymorphism of apolipoprotein E gene was analyzed. The primary outcome was MMSE score, frequency distribution of apolipoprotein E alleles and genotypes. P < 0.01 was used as statistically significant. RESULTS: MMSE score in inhalation preoperative baseline group significantly decreased at day 3 after surgery compared with the preoperational and intravenous anesthesia group. The proportion of patients scoring less than 25 points was significantly greater in the inhalation anesthesia group than in the intravenous anesthesia group at 3 days after surgery. In the inhalation anesthesia group, the decrease in MMSE score was closely related with apolipoprotein E ε4 allele. In the intravenous anesthesia group, the decrease in MMSE score was not correlated with apolipoprotein E ε4 allele. CONCLUSIONS: There was a strong association between the apolipoprotein E ε4 and postoperative cognitive dysfunction in elderly patients undergoing inhalation anesthetics.