LCP1 knockdown in monocyte-derived macrophages: mitigating ischemic brain injury and shaping immune cell signaling and metabolism.

Rationale: Ischemic stroke poses a significant health burden with limited treatment options. Lymphocyte Cytosolic Protein 1 (LCP1) facilitates cell migration and immune responses by aiding in actin polymerization, cytoskeletal rearrangements, and phagocytosis. We have demonstrated that the long non-coding RNA (lncRNA) Maclpil silencing in monocyte-derived macrophages (MoDMs) led to LCP1 inhibition, reducing ischemic brain damage. However, the role of LCP1 of MoDMs in ischemic stroke remains unknown. Methods and Results: We investigated the impact of LCP1 on ischemic brain injury and immune cell signaling and metabolism. We found that knockdown of LCP1 in MoDMs demonstrated robust protection against ischemic infarction and improved neurological behaviors in mice. Utilizing the high-dimensional CyTOF technique, we demonstrated that knocking down LCP1 in MoDMs led to a reduction in neuroinflammation and attenuation of lymphopenia, which is linked to immunodepression. It also showed altered immune cell signaling by modulating the phosphorylation levels of key kinases and transcription factors, including p-PLCg2, p-ERK1/2, p-EGFR, p-AKT, and p4E-BP1 as well as transcription factors like p-STAT1, p-STAT3, and p-STAT4. Further bioinformatic analysis indicated that Akt and EGFR are particularly involved in fatty acid metabolism and glycolysis. Indeed, single-cell sequencing analysis confirmed that enrichment of fatty acid and glycolysis metabolism in Lcp1high monocytes/macrophages. Furthermore, Lcp1high cells exhibited enhanced oxidative phosphorylation, chemotaxis, migration, and ATP biosynthesis pathways. In vitro experiments confirmed the role of LCP1 in regulating mitochondrial function and fatty acid uptake. Conclusions: These findings contribute to a deeper understanding of LCP1 in the context of ischemic stroke and provide valuable insights into potential therapeutic strategies targeting LCP1 and metabolic pathways, aiming to attenuating neuroinflammation and lymphopenia.

Bridging the Gap: Investigating the Link between Inflammasomes and Postoperative Cognitive Dysfunction.

Postoperative cognitive dysfunction (POCD) is a cluster of cognitive problems that may arise after surgery. POCD symptoms include memory loss, focus inattention, and communication difficulties. Inflammasomes, intracellular multiprotein complexes that control inflammation, may have a significant role in the development of POCD. It has been postulated that the NLRP3 inflammasome promotes cognitive impairment by triggering the inflammatory response in the brain. Nevertheless, there are many gaps in the current literature to understand the underlying pathophysiological mechanisms and develop future therapy. This review article underlines the limits of our current knowledge about the NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome and POCD. We first discuss inflammasomes and their types, structures, and functions, then summarize recent evidence of the NLRP3 inflammasome's involvement in POCD. Next, we propose a hypothesis that suggests the involvement of inflammasomes in multiple organs, including local surgical sites, blood circulation, and other peripheral organs, leading to systemic inflammation and subsequent neuronal dysfunction in the brain, resulting in POCD. Research directions are then discussed, including analyses of inflammasomes in more clinical POCD animal models and clinical trials, studies of inflammasome types that are involved in POCD, and investigations into whether inflammasomes occur at the surgical site, in circulating blood, and in peripheral organs. Finally, we discuss the potential benefits of using new technologies and approaches to study inflammasomes in POCD. A thorough investigation of inflammasomes in POCD might substantially affect clinical practice.

Overexpression of microRNA-93-5p and microRNA-374a-5p Suppresses the Osteogenic Differentiation and Mineralization of Human Aortic Valvular Interstitial Cells Through the BMP2/Smad1/5/RUNX2 Signaling Pathway.

ABSTRACT: Aortic valve calcification commonly occurs in patients with chronic kidney disease (CKD). However, the regulatory functions of microRNAs (miRNAs/miRs) in the osteogenic differentiation of human aortic valvular interstitial cells (hAVICs) in patients with CKD remain largely unknown. This study aimed to explore the functional role and underlying mechanisms of miR-93-5p and miR-374a-5p in the osteogenic differentiation of hAVICs. For this purpose, hAVICs calcification was induced with high-calcium/high-phosphate medium and the expression levels of miR-93-5p and miR-374a-5p were determined using bioinformatics assay. Alizarin red staining, intracellular calcium content, and alkaline phosphatase activity were used to evaluate calcification. The expression levels of bone morphogenetic protein-2 (BMP2), runt-related transcription factor 2 (Runx2), and phosphorylated (p)-Smad1/5 were detected by luciferase reporter assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and western blot analysis. The results revealed that the expression levels of miR-93-5p and miR-374a-5p were significantly decreased in hAVICs in response to high-calcium/high-phosphate medium. The overexpression of miR-93-5p and miR-374a-5p effectively suppressed the high-calcium/high-phosphate-induced calcification and osteogenic differentiation makers. Mechanistically, the overexpression of miR-93-5p and miR-374a-5p inhibits osteogenic differentiation by regulating the BMP2/Smad1/5/Runx2 signaling pathway. Taken together, this study indicates that miR-93-5p and miR-374a-5p suppress the osteogenic differentiation of hAVICs associated with calcium-phosphate metabolic dyshomeostasis through the inhibition of the BMP2/Smad1/5/Runx2 signaling pathway.

Filtered air intervention modulates hypothalamic-pituitary-thyroid/gonadal axes by attenuating inflammatory responses in adult rats after fine particulate matter (PM2.5) exposure.

We have previously reported that filtered air (FA) intervention reduces inflammation and hypothalamus-pituitary-adrenal axis activation after fine particulate matter (PM2.5 exposure). Whether FA also modulates the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-gonadal (HPG) axes in rats after PM2.5 exposure is still unknown. Adult Sprague-Dawley rats were exposed to PM2.5 by using a "real-world" PM2.5 exposure system, and the FA intervention was conducted by renewing for 15 days. PM2.5 inhalation decreased thyrotropin-releasing hormone (TRH) and thyroxine (T4) levels in both male and female rats, and thyroid-stimulating hormone (TSH) level in male rats. FA intervention attenuated the reduction in TRH and TSH levels in male rats and reduction in T4 level in female rats. PM2.5 inhalation also reduced testosterone (T) level in male rats, and estradiol (E2) and progesterone (PROG) levels in female rats, and these changes were attenuated after FA intervention. The FA intervention attenuated the decreases in CD8 T cells and T cells induced by PM2.5 inhalation in female rats only by flow cytometry analysis. In blood, FA interventions ameliorated IL-6 and IL-1ß mRNA levels in both male and female rats after PM2.5 exposure. FA intervention restored the IL-4 and IL-10 levels in female rats after PM2.5 exposure. Moreover, FA intervention ameliorated the inflammatory responses induced by PM2.5 inhalation in the thyroid and gonads in both male and female rats. These data indicate that FA intervention exerted an effect on modulating the hormonal balance of the HPT and HPG axes, and this may be related to a reduction in the inflammatory responses in the thyroid and gonads of PM2.5-treated rats, respectively.

Ginkgo Biloba Extract EGB761 Alleviates Warfarin-induced Aortic Valve Calcification Through the BMP2/Smad1/5/Runx2 Signaling Pathway.

ABSTRACT: Calcific aortic valve disease is a common heart disease that contributes to increased cardiovascular morbidity and mortality. There is a lack of effective pharmaceutical therapy because its mechanisms are not yet fully known. Ginkgo biloba extract (EGB761) is reported to alleviate vascular calcification. However, whether EGB761 protects against aortic valve calcification, a disease whose pathogenesis shares many similarities with vascular calcification, and potential molecular mechanisms remain unknown. In this study, porcine aortic valve interstitial cell (pAVIC) calcification was induced by warfarin with or without the presence of EGB761. Immunostaining was performed to establish and characterize the pAVIC phenotype. Calcium deposition and calcium content were examined by Alizarin Red S staining and an intracellular calcium content assay. Alkaline phosphatase activity was detected by the p-nitrophenyl phosphate method. The expression levels of bone morphogenetic protein-2 (BMP2), Runt-related transcription factor 2 (Runx2), homeobox protein MSX-2, and phosphorylated (p)-Smad1/5 were detected by reverse transcription-quantitative polymerase chain reaction (PCR) and Western blot analysis. Consistent with these in vitro data, we also confirmed the suppression of in vivo calcification by EGB761 in the warfarin-induced C57/Bl6 mice. The results indicated that both pAVICs and aortic valves tissue of mice stimulated with warfarin showed increased calcium deposition and expression of osteogenic markers (alkaline phosphatase, BMP2, homeobox protein MSX-2, and Runx2) and promoted p-Smad1/5 translocation from the cytoplasm to the nucleus. The addition of EGB761 significantly inhibited p-Smad1/5 translocation from the cytoplasm to the nucleus, thus suppressing calcification. In conclusion, EGB761 could ameliorate warfarin-induced aortic valve calcification through the inhibition of the BMP2-medicated Smad1/5/Runx2 signaling pathway.

Analysis of the change of clinical nursing pathway in health education among patients with ovarian carcinoma.

OBJECTIVE: To investigate the effect of health education via clinical nursing pathway (CNP) on self-care agency, quality of life, negative emotions and nursing satisfaction among patients with ovarian carcinoma. METHODS: The clinical data of 61 patients with ovarian carcinoma admitted to the Oncology Department of our hospital from January 2019 to January 2020 were analyzed retrospectively. According to the different nursing methods, the patients were divided into a control group (n=31) and an observation group (n=30). The postoperative complications, the scores of self-care agency and quality of life before and after intervention, sleep quality and negative emotions were compared and analyzed between the two groups. RESULTS: Patients in the observation group had higher mastery of health knowledge and lower incidence of postoperative complications than those in the control group. The scores of SDS, SAS and PSQI were significantly decreased in both groups after intervention compared with those before intervention (P<0.05), and the scores in the observation group were significantly lower than those in the control group (P<0.05). After intervention, both groups showed higher scores of self-care agency and quality of life than before intervention (P<0.05), and patients in the observation group showed higher scores than those in the control group (P<0.05). The overall nursing satisfaction of patient was relatively high. CONCLUSION: Health education via CNP can help patients better understand the diseases, reduce their psychological burden and improve sleep quality. Informing patients of the methods of postoperative restorative exercise through health education is able to reduce complications incidence and improve self-care agency and quality of life of patients.

Fluorescence sensing strategy based on aptamer recognition and mismatched catalytic hairpin assembly for highly sensitive detection of alpha-fetoprotein.

At present, alpha fetoprotein (AFP) is mainly used as a serum marker of primary Hepatocellular carcinoma. A simple, enzyme-free sensing strategy is introduced for highly sensitive fluorescence detection of AFP. This detection strategy is based on aptamer recognition and mismatched catalytic hairpin assembly (MCHA). At first, Trigger is locked by aptamer before the introduction of AFP in this aptamer-MCHA system. The aptamer preferentially combines with AFP via powerful attraction in the presence of AFP. This results in the release of trigger and initiation of MCHA cycle, thus forming the H1 and H2 double chain complexes (denoted as H1@H2). Finally, H1@H2 and double chain structure containing fluorophore and its quenched group- BHQ1 (denoted as F@Q) initiated displacement reaction, which caused double chain separation and fluorescence recovery. This assay produces a wide detection range, which is from 0.1 ng mL-1 to 10 µg mL-1 and the limit of detection as 0.033 ng mL-1. The whole detection process was performed at 37 °C for 60 min. In addition, this assay had high anti-interference ability and could be used to detect AFP in clinical serum. This novel AFP detection strategy is able to screen of Hepatocellular carcinoma.

Remote ischemic preconditioning protects against ischemic stroke in streptozotocin-induced diabetic mice via anti-inflammatory response and anti-apoptosis.

OBJECTIVE: It has been shown that remote ischemic preconditioning (RIPreC) attenuates ischemic injury after stroke in healthy rats or mice. The present study aims to examine whether RIPreC offers neuroprotection against ischemic stroke in streptozotocin-induced diabetic mice. METHODS: Streptozotocin (STZ, 120 mg/kg) was intraperitoneally injected into the mice to induce type 1 diabetic model. The immune and inflammatory changes were analyzed 2 days after reperfusion by flow cytometry and multiplex cytokine assay analysis, respectively. RESULTS: We found that RIPreC reduced infarct sizes and alleviated neurological impairment in diabetic mice. RIPreC decreased CD8 T cells infiltrated into the brain, and attenuated the decreases of CD8 T cells in the blood, CD4 T cells and CD8 T cells in the spleen. Results from multiplex cytokine assay showed that RIPreC treatment decreased IL-6, IL-1 beta and TNF alpha levels in the cortex, while it inhibited IL-6 level in the hippocampus and striatum, and TNF alpha level in the hippocampus. RIPreC treatment also downregulated IL-6 and IFN gamma level in the blood, which increased after cerebral ischemic injury. In addition, RIPreC reduced pro-apoptotic protein BAX expression in the ischemic brain. CONCLUSIONS: Our results indicate that RIPreC attenuates cerebral injuries in streptozotocin-induced diabetic mice via anti-inflammatory response and anti-apoptosis in the ischemic brain.

Micro-/Nano-Scale Biointerfaces, Mechanical Coupling and Cancer Therapy.

The interaction between cancer cells and their microenvironment is an indispensable link in cancer progression that occurs on the interfaces between them and presents typical biointerfacial behavior. Recently, the cancer cell/microenvironment interface has begun to attract more attention because of its fundamental roles in cancer growth and metastasis, which is promising for the efficacy of anti-cancer drugs and other important effects. In this review, we focused on mechanical coupling of the biointerfaces and their application in cancer early diagnosis, the pharmacology of anticancer agents and the design of the anticancer drug carriers. Newly developed strategies for cancer therapy based on mechanical coupling, such as correcting cell mechanics defects, tunable rigidity for drug delivery and topography-coupled-mechanical drug design, and drug screening, provide a proof of concept that cell mechanics offer a rich drug target space, allowing for the possible corrective modulation of tumor cell behavior. Biomechanopharmacology is therefore important to recognize the biomechanical factors and to control them not only for improvement in our knowledge of cancer but also for the development of new drugs and new uses of old drugs.

[Endogenous IFN-ß maintains M1 polarization status and inhibits proliferation and invasion of hepatocellular carcinoma cells].

Objective To investigate the effect of endogenous interferon ß (IFN-ß) on the polarization of M1 macrophages as well as the proliferation and invasion activities of hepatocellular carcinoma cells (HCCs) mediated by M1 macrophages. Methods U937-M1 macrophages derived from human monocytic tumor cells U937 was established and the cell phenotypes were identified by real-time quantitative PCR, ELISA and flow cytometry. After IFN-ß gene was knocked down with siRNA or IFN-ß was neutralized with IFN-ß monoantibody in U937-M1 macrophages, the change of M1/M2 phenotype was again analyzed by the above methods. The expressions of interferon regulatory factor 1 (IRF1) and IRF5 were detected by real-time quantitative PCR and Western blotting. The proliferation and invasion activities of HCCs, which were cultured with conditioned medium (CM) collected from different macrophage groups, were analyzed by CCK-8 assay and Transwell(TM) experiments, respectively. Results U937-M1 macrophages showed higher expressions of interleukin 12p35 (IL-12p35), interleukin 12p40 (IL-12p40), interleukin 12p70 (IL-12p70), interleukin 23p19 (IL-23p19), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and CD86 than U937-M0 did. But both U937-M0 macrophages and U937-M1 macrophages showed low expression of CD206. However, compared with the U937-M1 macrophages, the IFN-ß-blocked U937-M1 macrophages presented decreased expressions of the above M1 macrophages-associated markers, but increased expressions of M2 macrophages-associated markers IL-10 and CD206, as well as lower expressions of IRF1 and IRF5. The inhibited proliferation/invasion activities of HCCs mediated by U937-M1 macrophages were reversed by IFN-ß-blocked U937-M1 macrophages. Conclusion Blocking endogenous IFN-ß could inhibit the U937-M1 polarization status and U937-M1 macrophages-mediated anti-tumor activity of HCCs. IFN-ß might be involved in modulating the expressions of IRF1 and IRF5 as well as maintaining the M1 polarization status and its function.

[IL-12 induces autophagy via AKT/mTOR/STAT3 signaling pathway in human hepatoma cells].

Objective To investigate the effect of IL-12 on autophagy and the relative possible mechanism in HepG2 and SMMC-7721 human hepatoma cells. Methods The hepatoma cells were treated with IL-12 (10 ng/mL) for 6 hours. Western blotting was applied to detect the expressions of microtubule-associated protein 1 light chain 3 (LC-3), Beclin 1 and the phosphorylated levels of protein kinase B (AKT), mammalian target of rapamycin (mTOR), signal transducer and activator of transcription 3 (STAT3); immunofluorescence assay (IFA) and transmission electron microscopy (TEM) were used to observe the formation of autophagosome. After STAT3 was inhibited by STATTIC or siSTAT3 and AKT was activated by insulin-like growth factor (IGF-1), Western blotting and IFA were performed again to analyze the change of IL-12-induced autophagy. After the cells were treated with IL-12 (10 ng/mL) for 1, 2, 3, 4, 5 days, CCK-8 assay was used to determine the growth ability. After the hepatoma cells were treated with IL-12 (10 ng/mL) for 48 hours, trypan blue staining was used to detect the death rate of the cells. After cell autophagy was inhibit by siBeclin 1, CCK-8 assay and trypan blue staining were performed again to study the effect of IL-12 on the proliferation and death of human hepatoma cells. Results IL-12 induced autophagy and inhibited cell growth in the hepatoma cells. Silencing Beclin 1 gene enhanced IL-12-mediated growth inhibition and cell death. Furthermore, IL-12 treatment also decreased the expressions of p-AKT, p-mTOR and p-STAT3. The pretreatment of siSTAT3 or STATTIC inhibited STAT3-enhanced IL-12-induced autophagy. Accordingly, activation of AKT with IGF-1 decreased IL-12-induced autophagy. Conclusion IL-12 could induce autophagy through AKT/mTOR/STAT3 signaling pathways and the induction of autophagy attenuates the growth-inhibitory effect of IL-12 on hepatoma cells.

Porous Matrix Stiffness Modulates Response to Targeted Therapy in Breast Carcinoma.

Porous matrix stiffness modulates response to targeted therapy. Poroelastic behavior within porous matrix may modulate the molecule events in cell-matrix and cell-cell interaction like the complex formation of human epidermal growth factor receptor-2 (HER2)-Src-α6ß4 integrin, influencing the targeted therapy with lapatinib.

Effects of IRF1 and IFN-ß interaction on the M1 polarization of macrophages and its antitumor function.

Macrophages that differentiate from precursor monocytes can be polarized into a classically activated (M1) or alternatively activated (M2) status depending on different stimuli. Generally, interferon (IFN)-γ and lipopolysaccharide (LPS) are considered the classical stimuli with which to establish M1 polarization. IFN regulatory factor (IRF)1 and IFN-ß are two crucial molecules involved in IFN-γ- and LPS-initialed signaling. However, the association between IRF1 and IFN-ß in the context of the M1 polarization of macrophages is not yet fully understood. In this study, we demonstrate that U937-derived macrophages, in response to IFN-γ and LPS stimulation, readily acquire an M1 status, indicated by the increased expression of interleukin (IL)-12, IL-6, IL-23, tumor necrosis factor (TNF)-α and the M1-specific cell surface antigen, CD86, and the decreased expression of the M2-specific mannose receptor, CD206. However, the knockdown of IRF1 in U937-derived macrophages led to an impaired M1 status, as indicated by the decreased expression of the above-mentioned M1 markers, and the increased expression of the M2 markers, CD206 and IL-10. A similar phenomenon was observed in the M1 macrophages in which IFN-ß was inhibited. Furthermore, we demonstrated that IRF1 and IFN-ß may interact with each other in the IFN-γ- and LPS-initiated signaling pathway, and contribute to the IRF5 regulation of M1 macrophages. In addition, the conditioned medium collected from the M1 macrophages in which IRF1 or IFN-ß were inhibited, exerted pro-tumor effects on the HepG2 and SMMC-7721 cells, as indicated by an increase in proliferation, the inhibition of apoptosis and an enhanced invasion capability. The findings of our study suggest that the interactions of IRF1, IFN-ß and IRF5 are involved in the M1 polarization of macrophages and have antitumor functions. These data may provide a novel antitumor strategy for targeted cancer therapy.

Interleukin-12 inhibits the hepatocellular carcinoma growth by inducing macrophage polarization to the M1-like phenotype through downregulation of Stat-3.

Hepatocellular carcinoma is the third most common cause of cancer death worldwide. Novel early detection biomarkers and efficacious therapy strategies are needed. Macrophages recruited from circulation monocytes are the major component of solid cancer and play an important role in the carcinogenesis. Whether overexpression of L-12 in monocytes could induce the phenotype directional differentiation into tumoricidal M1 macrophages and inhibit HCC growth in tumor microenvironment was investigated in this study. For the establishment of the monocyte/IL-12 and polarization of M1-like macrophage, the IL-12 overexpressing recombinant monocyte/IL-12 cells were established by infecting with pAd5F35-CMV/IL-12 adenovirus and co-cultured with HCC SMMC-7721 and Hep3B cells. It was found that the phenotype of monocyte/IL-12 polarized to M1-like macrophages with CD197high IL-12high CD206low IL-10low, and decreased expression of TGF-ß, VEGF-A, and MMP-9. In order to explore the mechanism underlying the macrophages polarization, we detected the Stat-3 pathway and its downstream transcription factor c-myc, and found that the p-Stat-3 and c-myc were down-regulated. To evaluate the effects of monocyte/IL-12 on inhibiting HCC growth, various assays including CCK8, flow cytometry, colony-forming and Transwell assays in vitro, and xenograft mouse models and immunohistochemical analyses in vivo were used to detect the HCC growth and relative markers. Treated with IL-12 overexpressing monocytes, the xenograft tumor growth was significantly inhibited in vivo. These results have proven that IL-12-overexpressed monocytes could directionally differentiate to M1-like macrophages through downregulation of Stat-3 and result in the inhibition of HCC growth.

Substrate stiffness modulates mRNA expression profiling in breast cancer cells.

Identifying effective targets induced by ECM stiffness is of critical importance for treating metastatic cancer diseases, which are followed by changes in the mechanical microenvironment in cancer cells. In this study, polyacrylamide hydrogel substrates with different stiffnesses were prepared and mRNA microarrays were performed to analyze the mRNA expression profiles in breast cancer cell line SK-BR-3 grown on different stiffness substrates. The results indicated that the expressions of 1831 genes were changed significantly in the SK-BR-3 cells on the different stiffness substrates. GO and KEGG pathway analyses of the differently expressed genes in five significant profiles annotated that the most significant pathways were cell cycle, ubiquitin mediated proteolysis RNA transport and pathways in cancer. Finally, the network of genes and gene interaction based on these differently expressed genes was established, and the phosphorylation of AKT and ERK, respectively the downstreams of the PI3K and Ras signal pathways, was further validated. The genes identified in this study may represent good therapeutic targets, and further study of these targets may help to increase our understanding of the mechanisms underlying the pathological processes and therapy for metastatic breast cancer disease.

Electron Donor Substances and Iron Oxides Stimulate Anaerobic Dechlorination of DDT in a Slurry System with Hydragric Acrisols.

The interactive effects between electron donor substances and iron (Fe) oxides have significant influence on electron transfer and the growth of Fe-reducing bacteria, which may affect the reductive dechlorination of 1,1,1-trichoro-2,2-bis(p-chlorophenyl)ethane (DDT) in soils. To evaluate the roles of volatile fatty acids and Fe(III) oxide in accelerating the reductive dechlorination of DDT in Hydragric Acrisols, a batch anaerobic incubation experiment was conducted in a slurry system with the following seven treatments: sterile soil, control (DDT-contaminated soil), lactic acid, propionic acid, goethite, lactic acid + goethite, and propionic acid + goethite. Results showed that after 20 d of incubation, DDT residues for these treatments decreased by 34, 65, 77, 81, 77, 90, and 92% of the initial quantities, respectively, with 1,1-dichloro-2,2-bis(4-chlorophenyl)-ethane as the dominant metabolite. The application of lactic acid had no significant effect on DDT dechlorination in the first 8 d while the methanogenesis rate increased quickly but accelerated DDT dechlorination after Day 8 while the methanogenesis rate decreased and Fe(II) contents increased. The application of propionic acid enhanced DDT dechlorination rates throughout the incubation. The amendment by goethite stimulated microbial reduction of Fe(III) oxides to generate Fe(II), which was an efficient electron donor, thus accelerating DDT dechlorination significantly in the early incubation period. A synergetic interaction that accelerated DDT dechlorination, either between lactic acid and goethite or between propionic acid and goethite, was obtained. The results will be of great significance to develop efficient in situ remediation technology of DDT-contaminated soil.

Involvement of an antioxidant defense system in the adaptive response to cadmium in maize seedlings (Zea mays L.).

Chemical and biological analyses were used to investigate the growth response and antioxidant defense mechanism of maize seedlings (Zea mays L.) grown in soils with 0-100 mg kg(-1) Cd. Results showed that maize seedlings have strong abilities to accumulate and tolerate high concentrations of Cd. For soil with 50 mg kg(-1) Cd, the Cd contents in roots and shoots of maize seedlings are as large as 295.6 and 153.0 mg kg(-1) DW, respectively, without visible symptoms of toxicity. Lower soil Cd concentrations lead to a decrease in reduced glutathione (GSH) content in leaves of maize seedlings, whereas higher soil Cd concentrations resulted in an increase in the activities of superoxide dismutase, guaiacol peroxidase, catalase, and ascorbate peroxidase. Maize seedlings have strong capacities to adapt to low concentrations of Cd by consuming GSH and to develop an antioxidative enzyme system to defend against high-Cd stress.

[Combined stress of enhanced UV-B radiation and 1,2,4-trichlorobenzene contamination on the growth of green vegetable].

A pot experiment was conducted to study the effects of UV-B radiation enhancement alone, 1,2,4-trichlorobenzene (TCB) contamination soil alone, and the combined stress on the growing process, stomatal resistance and leaf structure of green vegetable. The results showed that 1,2,4-TCB contamination alone had more significant inhibitory effect on the growth of green vegetable than the combined stress. Both UV-B radiation enhancement and 1,2,4-TCB contamination reduced the stomatal resistance of front and reverse leaves. Enhanced UV-B radiation resulted in the albino of leaves. 1,2,4-TCB contamination resulted in the fading of leaf color and the appearing of black spots on leaf surfaces, and the enhanced UV-B radiation strengthened the black-spot symptom. In conclusion, the effects of UV-B radiation enhancement alone, 1,2,4-trichlorobenzene (TCB) contamination soil alone and the combined stress on the growth indicators of green vegetable were different.

[Influence of the interaction between iron oxide and electron donor substances on 1,1,1-trichloro- 2, 2-bis (p-chlorophenyl) ethane ( DDT) reductive dechlorination in hydragric acrisols].

The interaction between iron oxide and electron donor substance have significant influences on electron transfer and the growth of iron-reducing bacteria, which may affect the reductive dechlorination of polychlorinated organic compounds in soil. Anaerobic soil incubation experiment was conducted to study the effect and its mechanism of iron oxide (goethite), electron donor substances (butyrate and ethanol), and their interaction on DDT reductive dechlorination in Hydragric Acrisols. Results showed that after 6 weeks of anaerobic incubation, the extractable residues of DDT were between 1.29% and 2.01% of initial DDT amounts in soils, which was attributed to the dechlorinated degradation of DDT and formation of bound residues of DDT and its dechlorinated products. The main product of DDT anaerobic dechlorination was 1,1-dichloro-2,2-bis (p-chloro-phenyl) ethane (DDD). During the prophase of incubation, the application of butyrate or ethanol led to the decreased pH and increased Eh for reaction system, thus inhibited DDT dechlorination. The applications of only goethite or goethite and electron donor substances resulted in the increased soil pH, decreased soil Eh and increased Fe( II ) contents, thus accelerated DDT dechlorination. There was no significant interaction between butyrate and iron oxide on DDT dechlorination, whereas there was antagonistic action between ethanol and iron oxide on DDT dechlorination. The results will be of great significance for developing efficient and in-situ remediation technology of DDT contaminated soil.

The expression of Tim-3 in peripheral blood of ovarian cancer.

Ovarian cancer remains a challenging disease for which improved treatments are urgently needed. Tim-3 acts as a negative regulatory molecule and plays a critical role in immune tolerance. In the current study, we investigated the expression of Tim-3 on peripheral CD4+ T and CD8+ T cells in ovarian cancer. A total of 52 ovarian cancer patients and 56 healthy controls were recruited and leukocytes from peripheral blood mononuclear cells were analyzed for Tim-3 surface expression by flow cytometry. Data showed that expression of Tim-3 was significantly increased in both CD4+ and CD8+ T cells in ovarian cancer cases than in controls (p<0.0001 and p<0.0001, respectively). Patients who had recurrent ovarian cancer had a higher proportion of Tim-3+CD4+ T cells than when they were newly diagnosed (p=0.013). When analyzing Tim-3 expression with cancer progression, results revealed elevated Tim-3 expression in both CD4+ and CD8+ T cells in cases with advanced International Federation of Gynecology and Obstetrics (FIGO) staging (III/IV) than those with stage I and II (p=0.009 and p=0.037, respectively). We also tested Tim-3 with tumor grade, and observed that patients with a higher tumor grade (G3) demonstrated further augmented Tim-3 expression in CD4+ and CD8+ T cells compared to those with lower tumor grades (p=0.010 and p=0.042, respectively). Our study suggested that Tim-3 may participate in the development and progression of ovarian cancer by its negative regulation on various T-cell subsets, and Tim-3 expression in CD4+ T cells could serve as a predictive marker for anticancer therapies.