Nomogram to Predict the Prognosis of Oligodendroglioma Patients Undergoing Postoperative Adjuvant Chemoradiotherapy.

OBJECTIVE: The aim of this study was to develop a prognostic nomogram for predicting the prognosis of oligodendroglioma patients receiving combined chemoradiotherapy (CRT) after surgery. METHODS: The study used data from the Surveillance, Epidemiology, and End Results (SEER) database between 2000 and 2019. The patients were randomly divided into a development cohort (700 patients) and a validation cohort (244 patients) in a 7:3 ratio. The Cox hazards regression model was used to identify predictors, and a nomogram was constructed to visualize the prognosis. The performance of the prognostic nomogram was evaluated using the consistency index (C-index), clinical net benefit, and calibration. RESULTS: The nomogram included 5 variables: age, marital status, tumor size, site of lesions, and surgery type. The C-index of the training set and validation set were 0.77 and 0.68, respectively. The calibration plots showed that the nomogram was in good agreement with the actual observation. The clinical decision curve indicated that the nomogram had a good clinical net benefit in oligodendroglioma patients receiving CRT after surgery. CONCLUSIONS: This study established and verified a prognostic nomogram for a large cohort of oligodendroglioma patients receiving CRT after surgery based on the SEER database. The nomogram may help clinicians provide personalized treatment services and clinical decisions for patients.

Network Pharmacology-Based Approach to Investigate the Active Ingredients and Therapeutic Mechanisms of Jingu Tongxiao Pill against Osteoarthritis.

This study aimed to investigate the active ingredients and therapeutic mechanisms of Jingu Tongxiao Pill (JGTXP), a commonly used Chinese patent medicine, in treating osteoarthritis (OA) via network pharmacology analysis combined with experimental validation. First, we administered JGTXP to rat plasma and identified the candidate active compounds. Next, target prediction, protein-protein interaction, compound-target network construction, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were conducted for JGTXP. Lastly, the network-derived key targets and pathways were validated in vitro and in vivo. Finally, we identified 106 compounds in JGTXP and 24 absorbed compounds in the rat plasma. Network analysis revealed that JGTXP interferes with OA mainly via regulating the inflammatory response, collagen catabolic process, and osteoclast differentiation, and the nuclear factor kappa B (NF-κB) signaling pathway plays a pivotal role in these processes. Experimentally, JGTXP exerted potential protective effects on articular cartilage and inhibited expression of inflammatory mediators and collagen catabolism-related proteins, including interleukin 1 beta (IL-1ß), interleukin 6, tumor necrosis factor alpha (TNF-α), and matrix metalloproteinase (MMP) 3 and MMP13, in a papain-induced OA rat model. Consistently, mRNA expression levels of these factors and nitric oxide release were suppressed by JGTXP in an LPS-induced RAW 264.7 inflammation model. The reporter gene assay showed that JGTXP could reduce the transcriptional activity of NF-κB. Consecutive western blot analysis demonstrated that nuclear NF-κB p65, inducible nitric oxide synthase (iNOS), and cyclooxygenase 2 (COX-2) expression were inhibited while cytoplasmic NF-κB p65 was upregulated by JGTXP. Using a combination of chemical profiling, network pharmacology analysis, and experimental validation, we preliminarily clarified the active ingredients of JGTXP intervention for OA and demonstrated that JGTXP ameliorates OA, at least partially, by regulating the NF-κB signaling pathway.

A pan-cancer single-cell panorama of human natural killer cells.

Natural killer (NK) cells play indispensable roles in innate immune responses against tumor progression. To depict their phenotypic and functional diversities in the tumor microenvironment, we perform integrative single-cell RNA sequencing analyses on NK cells from 716 patients with cancer, covering 24 cancer types. We observed heterogeneity in NK cell composition in a tumor-type-specific manner. Notably, we have identified a group of tumor-associated NK cells that are enriched in tumors, show impaired anti-tumor functions, and are associated with unfavorable prognosis and resistance to immunotherapy. Specific myeloid cell subpopulations, in particular LAMP3+ dendritic cells, appear to mediate the regulation of NK cell anti-tumor immunity. Our study provides insights into NK-cell-based cancer immunity and highlights potential clinical utilities of NK cell subsets as therapeutic targets.

Radiotherapy combined with anti-CEACAM1 immunotherapy to induce survival advantage in glioma.

BACKGROUND: We aimed to observe the effect of radiotherapy on the expression of immune checkpoint molecule CEACAM1 in patients with glioma and the therapeutical effect of radiotherapy combined with blockade of CEACAM1 in mice with intracranial gliomas. METHODS: The expression of CEACAM1 on T-lymphocytes in the peripheral blood of patients with glioma was detected before and after radiotherapy; GL261 murine glioma cells (stably transfected with the luciferase gene) were implanted in the right caudate nucleus of C57BL/6 mice, and tumour growth was observed using the small animal in vivo imaging system. Mice were divided into 4 groups: (1) the isotype control; (2) the radiotherapy; (3) the anti-CEACAM1 treatment; and (4) the combination therapy. The survival of mice after treatment was recorded; the expression of CEACAM1 on murine glioma cells was detected by immunohistochemistry before and after radiotherapy; flow cytometry was adopted to detect CD8+ T-cells (Treg) (CD4+FoxP3+CD25+) among mouse brain-infiltrating T-cells; serum levels of IFN-γ and IL-10 were detected by ELISA; proliferation and apoptosis were observed by immunohistochemistry; Retrospective RNA-seq data analysis was conducted in a cohort of 325 patients with glioma in the Chinese Glioma Genome Atlas (CGGA) database and 702 patients in The Cancer Genome Atlas (TCGA) database. RESULTS: The expression of CEACAM1 on CD4+ and CD8+ T-cells in the peripheral blood of patients with glioma was significantly higher 1 week after radiotherapy than before radiotherapy and was further increased 1 month after radiotherapy. Combined therapy notably inhibited the growth of intracranial tumours in mice and prolonged their survival time, with some mice being capable of surviving long-term (> 90 d). Immunohistochemistry revealed that the expression of CEACAM1 in murine glioma tissues after radiotherapy was elevated in a time-dependent manner. Flow cytometry analysis showed an increase in mouse brain-infiltrating CD8+ T-lymphocytes, a decrease in Treg cells, and an increase in CD8+ T/Treg cells after treatment. ELISA demonstrated the elevated levels of IFN and decreased levels of IL-10 in the serum of mice in the combination therapy group. CONCLUSIONS: Radiotherapy combined with CEACAM1 inhibitors resulted in strong and durable anti-tumour immune responses against murine glioma and long-term survival of some mice. Hence, this study is expected to offer new effective immunotherapy strategies against glioma.

[Yiqi Yangyin Tongluo Recipe(YYTR)alleviates renal injury in diabetic nephropathy rats by inhibiting PI3K/AKT pathway and aquaporin 2 (AQP2)].

Objective To explore the effects of Yiqi Yangyin Tongluo Recipe (YYTR) on the expressions of phosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) and aquaporin 2(AQP2) in diabetic renal tissue and its mechanism. Methods Sixty Wistar rats were randomly divided into the blank group, model group, valsartan (20 mg/kg) group, YYTR (4 mg/kg or 1 mg/kg), 4 mg/kg YYTR combined with 0.5 µmol/kg 740Y-P group, with 10 rats in each group. Except the blank group, the rats in other groups were fed with high-glucose and high-fat diet and injected with streptozocin to create diabetic nephropathy (DN) rat models. The day after successful modeling, the rats were administrated intragastrically for 8 weeks. At the end of the experiment, renal function indexes were measured, and glomerular sclerosis index and renal interstitial injury index were evaluated according to the results of HE staining and Masson staining. Western blot analysis was used to detect the levels of AQP2, PI3K, AKT, p-PI3K and p-AKT. Immunohistochemical staining was used to detect the expression and distribution of AQP2 in renal tissue. Results Compared with the normal group, urine protein quantitation in 24 hours (24 h UTP), serum creatinine, urea nitrogen and ß2-microglobulin (ß2-MG) content in model group were increased. It also reported a rise of kidney index, glomerulo sclerosis index, renal interstitial injury index, AQP2 protein and PI3K, AKT, p-PI3K and p-AKT protein expressions in model group. But compared with model group, the above indexes all decreased in 4 mg/kg YYTR group. In addition, compared with 4 mg/kg YYTR group, the above indexes in YYTR combined with 740Y-P group were increased. Conclusion YYTR can protect renal function by down-regulating AQP2 protein expression and inhibiting PI3K/AKT signaling pathway activation.

High expression of PDZ-binding kinase is correlated with poor prognosis and immune infiltrates in hepatocellular carcinoma.

BACKGROUND: PDZ-binding kinase (PBK) encodes a serine/threonine protein kinase related to the dual specific mitogen-activated protein kinase kinase (MAPKK) family. There is evidence that overexpression of this gene is associated with tumorigenesis. However, the role of PBK in hepatocellular carcinoma (HCC) remains unclear. Therefore, we evaluated the prognostic role of PBK and its correlation with immune infiltrates in hepatocellular carcinoma. METHODS: The expression of PBK in pan-cancers was studied by Onconmine and TIMER. The expression of PBK in HCC patients and its relationship with clinicopathological characteristics were analyzed using The Gene Expression Profiling Interactive Analysis (GEPIA), The human protein atlas database (HPA), The Cancer Genome Atlas (TCGA), and Gene Expression Omnibus (GEO) databases. Receiver operating characteristic (ROC) curve was used to determine the diagnostic value of PBK in HCC patients. The relationship between PBK and prognosis of HCC was performed by GEPIA and Kaplan Meier plotter web tool. The correlations between the clinical characteristics and overall survival were analyzed by Univariate Cox regression and Multivariate Cox hazards regression to identify possible prognostic factors for HCC patients. LinkedOmics was applied to investigate co-expression associated with PBK and to analyze Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The network map of PBK and related genes is constructed by GeneMANIA. Finally, TIMER and TISIDB were used to analyze the correlations between PBK and tumor-infiltrating immune cells. RESULTS: Multiple database analysis shows that PBK was highly expressed in many types of tumors, including hepatocellular carcinoma, and was significantly related to tumor stage (P=0.0089), age (P=0.0131), and race (P=0.0024) of HCC patients. The receiver operating characteristic (ROC) curve analysis showed that PBK had high diagnostic potential to HCC in GSE76427 (AUC=0.8799), GSE121248 (AUC=0.9224), GSE62232 (AUC=0.9975), and GSE84402 (AUC=0.9541). Multivariate Cox hazards regression showed that high expression of PBK may be an independent risk factor for overall survival in HCC patients (HR = 1.566, 95% CI=1.062-2.311, P= 0.024). The Protein-protein interaction network showed that PBK significantly interacted with LRRC47, ARAF, LGALS9B, TTK, DLG1, and other essential genes. Furthermore, enrichment analysis showed that PBK and co-expressed genes participated in many biological processes, cell composition, molecular functions, and pathways in HCC. Finally, the immune infiltration analysis by TIMER and TISIDB indicated that a significant tightly correlation between PBK and macrophages, neutrophils, as well as chemokines and receptors. CONCLUSIONS: High expression of PBK is significantly correlated with poor survival and immune infiltrates in hepatocellular carcinoma. Our study suggests that PBK can be used as a biomarker of poor prognosis and potential immune therapy target in hepatocellular carcinoma.

Long-chain non-coding RNA UCA1 inhibits renal tubular epithelial cell apoptosis by targeting microRNA-206 in diabetic nephropathy.

In this study, the inhibitory effect of long-chain non-coding RNA urothelial carcinoma associated 1 (UCA1) on renal tubular epithelial cell apoptosis by targeting microRNA (miRNA)-206 in diabetic nephropathy (DN) was investigated through DN rat model. The results showed that UCA1 expression was significantly reduced in diabetic renal tubular epithelial tissues and HG-induced HK-2 cells. UCA1 significantly inhibited HG-induced apoptosis and inflammation of renal tubular epithelial cells in HK-2 cells. In addition, UCA1 can directly act as an anti-pro-cytokine by inhibiting the expression of miR-206, and finally inhibit the apoptosis and inflammation of renal tubular epithelial cells. We conclude that UCA1 inhibits renal tubular epithelial cell apoptosis by targeting miRNA-206 in DN and can be used as a potential therapeutic target for DN.

Clinical association between pre-treatment levels of plasma fibrinogen and bone metastatic burden in newly diagnosed prostate cancer patients.

BACKGROUND: Due to the different treatments for low-volume metastatic prostate cancer (PCa) as well as high-volume ones, evaluation of bone metastatic status is clinically significant. In this study, we evaluated the correlation between pre-treatment plasma fibrinogen and the burden of bone metastasis in newly diagnosed PCa patients. METHODS: A single-center retrospective analysis, focusing on prostate biopsies of newly diagnosed PCa patients, was performed. A total of 261 patients were enrolled in this study in a 4-year period. All subjects were submitted to single-photon emission computerized tomography-computed tomography to confirm the status of bone metastasis and, if present, the number of metastatic lesions would then be calculated. Clinical information such as age, prostate-specific antigen (PSA), fibrinogen, clinical T stage, and Gleason score were collected. Patients were divided into three groups: (i) a non-metastatic group, (ii) a high volume disease (HVD) group (>3 metastases with at least one lesion outside the spine), and (iii) a low volume disease (LVD) group (metastatic patients excluding HVD ones). The main statistical methods included non-parametric Mann-Whitney test, Spearman correlation, receiver operating characteristic (ROC) curves, and logistic regression. RESULTS: Fibrinogen positively correlated with Gleason score (r = 0.180, P = 0.003), PSA levels (r = 0.216, P < 0.001), and number of metastatic lesions (r = 0.296, P < 0.001). Compared with the non-metastatic and LVD groups, the HVD group showed the highest PSA (104.98 ng/mL, median) and fibrinogen levels (3.39 g/L, median), as well as the largest proportion of Gleason score >7 (86.8%). Both univariate (odds ratio [OR] = 2.16, 95% confidential interval [CI]: 1.536-3.038, P < 0.001) and multivariate (OR = 1.726, 95% CI: 1.206-2.472, P = 0.003) logistic regressions showed that fibrinogen was independently associated with HVD. The ROC curve suggested that fibrinogen acts as a predictor of HVD patients, yielding a cut-off of 3.08 g/L, with a sensitivity of 0.684 and a specificity of 0.760 (area under the curve = 0.739, 95% CI: 0.644-0.833, P < 0.001). CONCLUSIONS: Pre-treatment plasma fibrinogen is positively associated with bone metastatic burden in PCa patients. Our results indicate that fibrinogen might be a potential predictor of HVD.

How do surgeons' trade-off between patient outcomes and risk of complications in total knee arthroplasty? a discrete choice experiment in Australia.

OBJECTIVE: To measure the trade-off between risk of complications versus patient improvement in pain and function in orthopaedic surgeons' decisions about whether to undertake total knee arthroplasty (TKA). METHODS: A discrete choice experiment asking surgeons to make choices between experimentally-designed scenarios describing different levels of operative risk and dimensions of pain and physical function. Variation in preferences and trade-offs according to surgeon-specific characteristics were also examined. RESULTS: The experiment was completed by a representative sample of 333 orthopaedic surgeons (n=333): median age 52 years, 94% male, 91% fully qualified. Orthopaedic surgeons were willing to accept substantial increases in absolute risk associated with TKA surgery for greater improvements in a patient's pain and function. The maximum risk surgeons were willing to accept was 40% for reoperation and 102% for the need to seek further treatment from a general practitioner or specialist in return for a change from postoperative severe night-time pain at baseline to no night-time pain at 12 months. With a few exceptions, surgeon-specific characteristics were not associated with how much risk a surgeon is willing to accept in a patient undergoing TKA. CONCLUSION: This is the first study to quantify risk-benefit trade-offs among orthopaedic surgeons performing TKA, using a discrete choice experiment. This study provides insight into the risk tolerance of surgeons.

MicroRNA-195 reverses the resistance to temozolomide through targeting cyclin E1 in glioma cells.

Glioma is the most common malignant tumor of the central nervous system with poor survival. Temozolomide (TMZ) is the first-line chemotherapy drug for initial and recurrent glioma treatment with a relatively good efficacy, which exerts its antitumor effects mainly through cell death induced by DNA double-strand breaks in the G1 and S phases. However, endogenous or acquired resistance to TMZ limits glioma patients' clinical outcome and is also an important cause of glioma replase. MicroRNA-195 (miR-195) plays an important role in the regulation of G1-phase/S-phase transition, DNA damage repair, and apoptosis of tumor cells. We found that miR-195 expression was significantly decreased in TMZ-resistant glioma cells induced with TMZ and correlated to the resistance index negatively. Also, the exogenous expression of miR-195 reversed TMZ resistance and induced the apoptosis of TMZ-resistant glioblastoma cells. Further bioinformatics analysis showed cyclin E1 (CCNE1) was a potential target gene of miR-195. Knockdown of CCNE1 partially reversed the effect of decreased miR-195 on TMZ resistance. The data from The Cancer Genome Atlas - Cancer Genome further suggested that hsa-miR-195 could negatively regulate the expression of CCNE1 in glioma. In conclusion, miR-195 reverses the resistance to TMZ by targeting CCNE1 in glioma cells and it could act as a potential target for treatment in glioma with TMZ resistance.

Accuracy of patient recall for self-reported doctor visits: Is shorter recall better?

In health economics, the use of patient recall of health care utilisation information is common, including in national health surveys. However, the types and magnitude of measurement error that relate to different recall periods are not well understood. This study assessed the accuracy of recalled doctor visits over 2-week, 3-month, and 12-month periods by comparing self-report with routine administrative Australian Medicare data. Approximately 5,000 patients enrolled in an Australian study were pseudo-randomised using birth dates to report visits to a doctor over three separate recall periods. When comparing patient recall with visits recorded in administrative information from Medicare Australia, both bias and variance were minimised for the 12-month recall period. This may reflect telescoping that occurs with shorter recall periods (participants pulling in important events that fall outside the period). Using shorter recall periods scaled to represent longer periods is likely to bias results. There were associations between recall error and patient characteristics. The impact of recall error is demonstrated with a cost-effectiveness analysis using costs of doctor visits and a regression example predicting number of doctor visits. The findings have important implications for surveying health service utilisation for use in economic evaluation, econometric analyses, and routine national health surveys.

Abnormal expression of circulating and tumor-infiltrating carcinoembryonic antigen-related cell adhesion molecule 1 in patients with glioma.

Glioma, the most prevalent primary tumor of the central nervous system, is known to evade immune surveillance and escape immune attacks by inducing immunosuppression. The homophilic interactions of the carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) serve a critical function in immunoregulation. In the present study, the expression levels of CEACAM1 in peripheral blood mononuclear cells and tumor-infiltrating lymphocytes (TILs) from patients with gliomas were assessed. Furthermore, associations between CEACAM1 expression and multiple clinicopathological characteristics in patients with gliomas were analyzed. The results of the present study suggested that the expression of CEACAM1 in circulating T cells was markedly increased in patients with gliomas compared with control subjects, and was further increased in TILs. Patients with high-grade gliomas [World Health Organization (WHO) grade III-IV] demonstrated a significantly increased expression of CEACAM1 on T cells compared with those with low-grade gliomas (WHO grade I-II). Furthermore, the expression of CEACAM1 on T cells was negatively correlated with the Karnofsky score and the plasma level of interferon-γ in patients with gliomas. Immunohistochemical analysis revealed that the expression levels of CEACAM1 in high-grade glioma tissues (WHO grade III-IV) were increased compared with the expression levels in the controls, and were associated with the expression of CEACAM1 in TILs. In summary, the results of the present study indicate that homophilic interactions of CEACAM1 may participate in the progression and development of gliomas through their negative regulatory effects on T cells. Thus, CEACAM1 may be a promising candidate for targeted glioma immunotherapy.

Combined Blockade of T Cell Immunoglobulin and Mucin Domain 3 and Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Results in Durable Therapeutic Efficacy in Mice with Intracranial Gliomas.

BACKGROUND Glioblastoma multiforme (GBM) evades immune surveillance by inducing immunosuppression via receptor-ligand interactions between immune checkpoint molecules. T cell immunoglobulin and mucin domain 3 (Tim-3) is a key checkpoint receptor responsible for exhaustion and dysfunction of T cells and plays a critical role in immunosuppression. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) has been recently identified as a heterophilic ligand for Tim-3. MATERIAL AND METHODS We established an intracranial GBM model using C57BL/6 mice and GL261 cells, and treated the mice with single or combined monoclonal antibodies (mAbs) against Tim-3/CEACAM1. The CD4+, CD8+, and regulatory T cells in brain-infiltrating lymphocytes were analyzed using flow cytometry, and the effector function of T cells was assessed using ELISA. We performed a rechallenge by subcutaneous injection of GL261 cells in the "cured" (>90 days post-orthotopic tumor implantation) and naïve mice. RESULTS The mean survival time in the control, anti-Tim-3, anti-CEACAM1, and combined treatment groups was 29.8, 43.4, 42.3, and 86.0 days, respectively, with 80% of the mice in the combined group becoming long-term survivors showing immune memory against glioma cells. Infiltrating CD4+ and CD8+ T cells increased and immunosuppressive Tregs decreased with the combined therapy, which resulted in a markedly elevated ratio of CD4+ and CD8+ cells to Tregs. Additionally, plasma IFN-γ and TGF-ß levels were upregulated and downregulated, respectively. CONCLUSIONS Our data indicate that combined blockade of Tim-3 and CEACAM1 generates robust therapeutic efficacy in mice with intracranial tumors, and provides a promising option for GBM immunotherapy.

Using discrete choice experiments as a decision aid in total knee arthroplasty: study protocol for a randomised controlled trial.

BACKGROUND: Osteoarthritis (OA) is a leading cause of disability in developed nations. Total knee arthroplasty (TKA) is a clinically effective treatment for people with end-stage knee OA, and represents one of the highest volume medical interventions globally. However, up to one in three patients remain dissatisfied following TKA. Research indicates that the strongest predictor of patient dissatisfaction following TKA is unmet expectations. This study will use a discrete choice experiment (DCE) provided to patients to improve knowledge of the expected outcomes of TKA. This increased knowledge is based on actual outcome data and is hypothesised to optimise patient expectations of TKA outcomes, thereby increasing their satisfaction and self-reported health outcomes. METHODS/DESIGN: One hundred and thirty-two people with end-stage OA on the waiting list for TKA will be recruited and randomly allocated to one of two groups using computer-generated block randomisation. A randomised controlled trial (RCT) adhering to SPIRIT and CONSORT guidelines will evaluate the effect of administering a DCE prior to surgery on patient-reported pain and function and satisfaction following TKA. Patients in the intervention arm will complete a survey containing the DCE, compared to the control group who will complete a modified survey that does not contain the DCE activity. The DCE contains information on actual risks of postoperative complications, as well as health status after TKA. The DCE encourages patients to actively make trade-offs between risks and health outcomes to elicit their preferences. Participants in both groups will be required to complete the survey after consenting to have the procedure, but prior to surgery during their routine preadmission appointment at St. Vincent's Hospital, Melbourne, Australia (SVHM). Patients in both the intervention and control groups will also be required to complete a brief patient expectation survey 1 week prior to scheduled TKA. In addition, orthopaedic surgeons will complete a brief expectations survey for each patient consented for TKA to compare matched surgeon and patient expectations for recovery following TKA. Primary outcomes will be evaluated by a blinded examiner at 12 months post surgery using a validated self-reported pain and physical function scale, and a validated patient satisfaction scale. Secondary outcomes will include a range of validated measures of health and psychological wellbeing. All analyses will be conducted on an intention-to-treat basis using linear regression models. DISCUSSION: This study is the first of its kind to use a DCE to provide information to patients to optimise their expectations of the outcomes of surgery. Reducing the rate of patient dissatisfaction commonly seen in patients following TKA will help to reduce the burden associated with poor outcomes on the health system. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ( ACTRN12615001226594p ). Version 1; registered on 9 November 2015.

Studies on the Low-Temp Oxidation of Coal Containing Organic Sulfur and the Corresponding Model Compounds.

This paper selects two typical compounds containing organic sulfur as model compounds. Then, by analyzing the chromatograms of gaseous low-temp oxidation products and GC/MS of the extractable matter of the oxidation residue, we summarizing the mechanism of low-temp sulfur model compound oxidation. The results show that between 30°C to 80°C, the interaction between diphenyl sulfide and oxygen is mainly one of physical adsorption. After 80°C, chemical adsorption and chemical reactions begin. The main reaction mechanism in the low-temp oxidation of the model compound diphenyl sulfide is diphenyl sulfide generates diphenyl sulfoxide, and then this sulfoxide is further oxidized to diphenyl sulphone. A small amount of free radicals is generated in the process. The model compound cysteine behaves differently from diphenyl sulfide. The main reaction low-temp oxidation mechanism involves the thiol being oxidized into a disulphide and finally evolving to sulfonic acid, along with SO2 being released at 130°C and also a small amount of free radicals. We also conducted an experiment on coal from Xingcheng using X-ray photoelectron spectroscopy (XPS). The results show that the major forms of organic sulfur in the original coal sample are thiophene and sulfone. Therefore, it can be inferred that there is none or little mercaptan and thiophenol in the original coal. After low-temp oxidation, the form of organic sulfur changes. The sulfide sulfur is oxidized to the sulfoxide, and then the sulfoxide is further oxidized to a sulfone, and these steps can be easily carried out under experimental conditions. What's more, the results illustrate that oxidation promotes sulfur element enrichment on the surface of coal.

Does more education lead to better health habits? Evidence from the school reforms in Australia.

The current study provides new empirical evidence on the causal effect of education on health-related behaviors by exploiting historical changes in the compulsory schooling laws in Australia. Since World War II, Australian states increased the minimum school leaving age from 14 to 15 in different years. Using differences in the laws regarding minimum school leaving age across different cohorts and across different states as a source of exogenous variation in education, we show that more education improves people's diets and their tendency to engage in more regular exercise and drinking moderately, but not necessarily their tendency to avoid smoking and to engage in more preventive health checks. The improvements in health behaviors are also reflected in the estimated positive effect of education on some health outcomes. Our results are robust to alternative measures of education and different estimation methods.

Amphiphilic cylindrical copolypeptide brushes as potential nanocarriers for the simultaneous encapsulation of hydrophobic and cationic drugs.

Cylindrical copolypeptide brushes PLLF-g-(PLF-b-PLG) with poly(L-lysine-co-L-phenylalanine) (PLLF) as the backbone and poly(L-phenylalanine)-b-poly(L-glutamic acid) (PLF-b-PLG) as the side chains have been synthesized and evaluated as drug delivery carriers. The synthesized copolypeptide brushes were characterized by (1)H NMR, gel permeation chromatography (GPC), and transmission electron microscopy (TEM). In aqueous solution, the copolypeptide brushes adopt cylindrical morphologies and resemble unimolecular polymeric micelles with a hydrophobic poly(L-phenylalanine) core and a hydrophilic poly(L-glutamate) shell. An encapsulation study demonstrated that these water soluble, biodegradable copolypeptide brushes encapsulate hydrophobic compounds and cationic hydrophilic guest molecules simultaneously. Furthermore, the encapsulated cationic model compounds exhibit a pH-responsive releasing property.