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Personal recovery is a complex construct frequently used as outcome measure in people with schizophrenia spectrum disorders. This study examined potential predictors of personal recovery using the two most common assessment tools for people with schizophrenia spectrum disorders living in the community: the Chinese version of the Questionnaire about the Process of Recovery and the Chinese version of the Recovery Assessment Scale.Ninety-one individuals (57 women) diagnosed with schizophrenia spectrum disorders participated in the study (mean age: 47.41 ± 9.41 years). All participants lived in the community and received community psychiatric services. The participants were evaluated via interviews, questionnaires and standardized assessments. Potential predictors included four domains: personal, disease-related, functional and social. Stepwise multiple linear regression was used to analyse the potential predictors of the recovery and recovery assessment scale.Resilience and social support were the only significant predictors of the Chinese versions of the Questionnaire about the Process of Recovery and Chinese version of the Recovery Assessment Scale. The primary predictor of the Chinese version of the Questionnaire about the Process of Recovery was social support from family and institutional staff. Conversely, resilience was the major predictor of the Chinese version of the Recovery Assessment Scale.For people with schizophrenia spectrum disorders living in the community, social support and resilience significantly predicted personal recovery. Age, educational level, disease-related and functional factors were not significant predictors of personal recovery. Therefore, it is important to develop successful personal recovery-oriented practices that enhance resilience and promote social support.

This paper presents an application of near infrared spectroscopy associated with partial least squares regression calibration, for ash content analysis of prepreg in the manufacturing progress of copper clad laminate for printed circuited boards. The performance of the model was assessed by cross validation and external validation. The correlation coefficient and the root mean squared error of calibration and validation were 0.99, 0.25% and 0.98, 0.34%, and the measurement process was accomplished in less than 2 min compared to over 60 min for traditional thermo gravimetric analyzsis. The paired t-test results revealed that there was no significant difference between the two methods.

Supplementary Figure 2 PDF file - 132K, (A) The expression levels of MnSOD evaluated by Western blotting were not changed by FoxM1-knockdown in A549 and H1355 cells. (B) The expression levels of MMP1 and MMP2 evaluated by Western blotting decreased in a dose-dependent manner; however, the change of MMP7 and MMP9 expression was not observed in MnSOD-knockdown A549 cells

Supplementary Figure 1 PDF file - 101K, The expression level of E2F1 evaluated by Western blotting was not changed by MnSOD-knockdown in H1355 cells compared with non-specific shRNA control cells

Supplementary Table 1 PDF file - 142K, Relationship of MnSOD IHC, FoxM1, MMP2 and MnSOD mRNA expression with clinical parameters in lung adenocarcinoma patients

Supplementary Table 2 PDF file - 144K, List of primer sequences (5'�|��3') and their reaction conditions used in the present study

Supplementary Data PDF file - 268K,Supplementary Figure 1. The expression level of E2F1 evaluated by Western blotting was not changed by MnSOD-knockdown in H1355 cells compared with non-specific shRNA control cells. Supplementary figure 2. (A) The expression levels of MnSOD evaluated by Western blotting were not changed by FoxM1-knockdown in A549 and H1355 cells. (B) The expression levels of MMP1 and MMP2 evaluated by Western blotting decreased in a dose-dependent manner; however, the change of MMP7 and MMP9 expression was not observed in MnSOD-knockdown A549 cells. Supplementary Table 1. Relationship of MnSOD IHC, FoxM1, MMP2 and MnSOD mRNA expression with clinical parameters in lung adenocarcinoma patients. Supplementary Table 2. List of primer sequences (5'�|��3') and their reaction conditions used in the present study

Manganese superoxide dismutase (MnSOD) is an antioxidant enzyme responsible for the elimination of superoxide radical. The role of MnSOD in tumor progression in different human cancers is still controversial. In the present study, MnSOD expression in lung cancer cells was explored by knockdown or overexpression using transfection of a short hairpin RNA (shRNA) or an expression vector, respectively, to determine whether MnSOD expression mediates lung cancer cell migration, invasion, and oncogenic potential by increasing FoxM1 and MMP2 expression. Western blotting showed that FoxM1 and MMP2 expression was dependent on MnSOD expression, suggesting that FoxM1 could be upregulated by MnSOD. Three FoxM1 promoters were constructed to verify this activation of FoxM1 by MnSOD and to determine the transcription factors responsible. Luciferase reporter and chromatin immunoprecipitation assays indicated that MnSOD overexpression in lung cancer cells promoted binding of E2F1 and Sp1 to their putative FoxM1 promoter-binding sites and activated FoxM1 reporter activity. MnSOD also enhanced the potential for cell migration, invasion, and anchorage-independent colony growth on soft-agar plates, again via upregulation of FoxM1 and MMP2 expression. In patients with lung cancer, evaluation of MnSOD expression in lung tumors by immunohistochemistry indicated a positive correlation between FoxM1 and MMP2 mRNA expressions. Kaplan–Meier and Cox regression analysis revealed a poorer overall survival (OS) and relapse-free survival (RFS) in patients with MnSOD-positive tumors than with MnSOD-negative tumors. We conclude that MnSOD may promote tumor aggressiveness via upregulation of the FoxM1–MMP2 axis, and that MnSOD expression can independently predict survival and relapse in patients with resected lung adenocarcinoma. Mol Cancer Res; 11(3); 261–71. ©2012 AACR.

Overall survival and progression-free survival. Kaplan-Meier curves stratified by (A) ascitic DBP, and (B) serum DBP tested by log rank test

Grading of immunohistochemistrical intensity of vitamin D binding protein (DBP) expression

(A) Top 10 up-regulation genes expressed in ascites from ovarian cancers in our preliminary proteomic study. (B) Ascitic vitamin D binding protein (DBP) levels between groups of benign gynecologic disease, low malignant potential (LMP) ovarian tumor, and invasive ovarian cancer.

DBP expression in cancer cells and culture media from different ovarian cancer cell lines

Purpose: Malignant ascites of epithelial ovarian cancer (EOC) helps identify prognostic biomarkers or mechanisms of tumor progression. Vitamin D–binding protein (DBP) was revealed to be upregulated in EOC ascites in our previous proteomic study. Here, we examined the role of DBP in EOC.Experimental Design: We analyzed ascites, serum, and tissue samples of patients with newly diagnosed EOC to determine the prognostic effects of DBP. We verified DBP function using orthotopic animal models and DBP regulation in ovarian cancer cell lines.Results: Elevated ascitic DBP was significantly associated with poor response to chemotherapy, short progression-free interval, increased cancer progression, and death. Ascitic DBP overexpression was an independent unfavorable biomarker for progression-free survival; DBP overexpression in cancerous tissue was significantly related to chemoresistance. In vivo and in vitro investigations demonstrated an important role for DBP in ovarian cancer progression. Orthotopic model mice inoculated with DBP knockdown ovarian cancer cells displayed a significant reduction in tumor formation, malignant cell number, ascitic DBP levels, invasiveness, and metastasis, and increased survival compared with controls. In presence of vitamin D receptor (VDR), DBP promoted cell aggression (invasion and doubling time) via activation of the insulin-like growth factor-1/insulin-like growth factor–binding protein-2/Akt axis, and induced suppression of vitamin D–responsive genes. A NF-κB p65-binding site in the VDR promoter was identified as a major determinant of DBP-dependent VDR promoter activation.Conclusions: This study highlights the importance of DBP in ovarian tumor progression and the potential application of DBP as a therapeutic target for EOC. Clin Cancer Res; 24(13); 3217–28. ©2018 AACR.

Univariate and multivariate analysis of prognostic factors and pretreatment DBP expressions at diagnosis in epithelial ovarian cancers (n = 225) in NCKUH and NTUH

Ascitic and serum DBP and clinicopathological factors in epithelial ovarian cancers (n = 225) in NCKUH and NTUH

Supplementary Figures 1-4 from p53 Dysfunction by Xeroderma Pigmentosum Group C Defects Enhance Lung Adenocarcinoma Metastasis via Increased Mmp1 Expression

Supplementary Methods, Figure Legends 1-4 from p53 Dysfunction by Xeroderma Pigmentosum Group C Defects Enhance Lung Adenocarcinoma Metastasis via Increased Mmp1 Expression

Metribuzin degradation in UV/chlorine process followed pseudo-first-order kinetics.

The development of the closed-loop deep brain stimulator (DBS) for clinical trials requires verification of its safety and effectiveness in a large animal model. Due to the financial and ethical challenges of using non-human primates, it is reasonable to use an alternative large animal model. It was reported that minipigs are suitable for the establishment of the MPTP-induced parkinsonian model. However, there is currently no evidence of whether beta oscillations, the symptom-related biomarker, exist in the subthalamic nucleus (STN) of the parkinsonian minipig model. This study was to verify whether the beta oscillations could be recorded in the STN of the parkinsonian minipig model. Parkinsonism was induced by injections of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Through a protocol involving up to nine subcutaneous or intramuscular injections, delivering a cumulative dose of 8-10 mg/kg MPTP, the minipigs developed notable movement disturbance. By stereotactic surgery and microelectrode recording, beta oscillations were recorded in the STN of the MPTP-injected minipigs. Immunohistochemistry of the tyrosine hydroxylase (TH) was performed in the substantia nigra pars compacta (SNc) of each animal. Compared with the control animal injected with saline, the TH-positive cells in the SNc were significantly reduced in the MPTP-injected minipigs. This study showed that beta oscillations could be recorded in the STN of the MPTP-induced parkinsonian minipig model. This large animal model is suitable as an alternative pre-clinical model for developing closed-loop DBS in the future.

We studied Akt inhibition using SC66 in a NOD-SCID xenograft mouse model and a panel of eight ovarian cancer cell lines. Elevated phospho-Akt levels in cancerous tissue were associated with short progression-free survival and overall survival. Cell sensitivity to SC66 was inversely correlated with phospho-Akt and COL11A1 expression levels, as well as resistance to cisplatin or paclitaxel. SC66 inhibited phosphorylation of Akt and its downstream effectors 4EBP1 and p70S6 kinase. SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. SC66-sensitized chemoresistant cells to cisplatin and paclitaxel treatment, and promoted apoptosis. In addition, SC66 inhibited COL11A1 expression via decreased binding of CCAAT/enhancer-binding protein beta (c/EBPβ), reducing chemoresistance and decreasing binding of nuclear transcription factor Y (NF-YA) to COL11A1. A mouse xenograft experiment demonstrated that SC66 treatment caused a reduction in tumor formation and enhanced the therapeutic efficacy of cisplatin. This study demonstrates the role of Akt in ovarian tumor progression and chemoresistance, and supports the application of SC66 as a therapy for ovarian cancer.

In this study a reversibly fluorescence immunoassay was prepared through grafting, using hydrogen bonding, of an antibody-conjugated ZnS quantum dots (ZQD-antiHA) onto an electrospun poly (2,6-dimethyl-1,4-phenylene oxide) (PPO) fibrous mats (EPFM) with poly (n-isopropylacrylamide) (PNIPAAm) grafts. The PPO was first electrospun into a fibrous mat, then brominated and reacted with NaN3 to generate the azido-terminated EPFMs. A propargyl-terminated poly (n-isopropylacrylamide) (PNIPAAm) was synthesized and grafted onto the azido-terminated EPFMs. ZQDs were conjugated by antibodies (antiHA) to adsorb onto the PNIPAAm grafts of EPFMs with hydrogen bonding. Because of the stronger interaction between antigen (HA) and antibody (antiHA), the hydrogen bonding was blocked due to the introduction of the antigen which resulted in the desorption the ZQDs from the EPFMs. The blue fluorescence of the PNIPAAm-grafted EPFMs with antibody-conjugated ZQDs was disappeared while immersing in the solution of antigen. The 3.82 mg/m2 of ZQDs on the PNIPAAm grafts EPFMs significantly reduced to 0.22 mg/m2 after the immersion of the antigen solution which verified the transference of the ZQDs from EPFMs to the solution. The behavior of adsorption and desorption of the ZQDs was reversible up to five cycles. The revisable fluorescence immunoassay of EPFMs with PNIPAAm grafts experimentally exhibited a high potential in a simple setup for biosensing with its unique sensitivity and selectivity.

BACKGROUND AND AIM It is not clear whether prophylactic clipping after endoscopic mucosal resection (EMR) of large nonpedunculated colorectal lesions (LNPCLs) prevents delayed bleeding (DB). We aimed to conduct a meta-analysis to clarify the efficacy of prophylactic clipping in prevention of DB following EMR of LNPCLs. METHODS We searched PubMed, EMBASE, Web of Science, ScienceDirect, Cochrane Library databases, and ClinicalTrials.gov for studies that compared clipping versus (vs) nonclipping in prevention of DB following EMR of LNPCLs. Pooled odds ratio (OR) was determined using a random effects model. The pooled ORs of DB, perforation, and post-polypectomy syndrome in the clipping group compared with the nonclipping group comprised the outcomes. Subgroup analyses based on study design, polyp location, and completeness of wound closure were performed. RESULTS Five studies with a total of 3112 LNPCLs were extracted. Prophylactic clipping reduced the risk of DB compared with nonclipping (3.3% vs 6.2%, OR: 0.494, P = 0.002) following EMR of LNPCLs. In subgroup analysis, prophylactic clipping reduced DB of LNPCLs at proximal location (3.8% vs 9.8%, P = 0.029), but not of them at distal location (P = 0.830). Complete wound closure showed superior efficacy to prevent DB compared with partial closure (2.0% vs 5.4%, P = 0.004). No benefit of clipping for preventing perforation or post-polypectomy syndrome was observed (P = 0.301 and 0.988, respectively). CONCLUSIONS Prophylactic clipping can reduce DB following EMR of LNPCLs at proximal location. Besides, complete wound closure showed superior efficacy to prevent DB compared with partial closure. Further cost analyses should be conducted to implement the most cost-effective strategies.

Ovarian cancer has a unique tumor microenvironment (TME) that enables cancer-associated fibroblasts (CAFs) to interact with cellular and matrix constituents and influence tumor development and migration into the peritoneal cavity. Collagen type XI alpha 1 (COL11A1) is overexpressed in CAFs; therefore this study examines its role during CAF activation in epithelial ovarian cancer (EOC). Coculturing human ovarian fibroblasts (HOFs) with high COL11A1-expressing EOC cells or exposure to the conditioned medium of these cells prompted the expression of COL11A1 and CAF phenotypes. Conversely, coculturing HOFs with low COL11A1-expressing EOC cells or COL11A1-knockdown abrogated COL11A1 overexpression and secretion, in addition to CAF activation. Increased p-SP1 expression attributed to COL11A1-mediated extracellular signal-regulated kinase activation (ERK) induced p65 translocation into the nucleus and augmented its binding to the insulin-like growth factor binding protein 2 (IGFBP2) promoter, ultimately inducing TGF-β3 activation. The CAF-cancer cell crosstalk triggered interleukin-6 release, which in turn promoted EOC cell proliferation and invasiveness. These in vitro results were confirmed by in vivo findings in a mouse model, showing that COL11A1 overexpression in EOC cells promoted tumor formation and CAF activation, which was inhibited by TGF-β3 antibody. Human tumors with high TGF-β3 levels showed elevated expression of COL11A1 and IGFBP2, which was associated with poor survival. Our findings suggest the possibility that anti-TGF-β3 treatment strategy may be effective in targeting CAFs in COL11A1-positive ovarian tumors.

Here we assessed population dynamics, natural enemy fauna (with emphasis on egg parasitoid), and population genetic structure (based on mitochondrial DNA) of the invasive litchi stink bug (LSB), Tessaratoma papillosa in Taiwan. Our major findings include: (1) fluctuations of LSB in numbers of adults, mating pairs, and egg masses over a 2-year period in Taiwan generally resemble those in the native populations; (2) Anastatus dexingensis and A. fulloi are among the most dominant LSB egg parasitoids, with the former consistently outnumbering the latter throughout Taiwan; (3) the presence of two genetically distinct clades suggests LSB in Taiwan most likely derived from multiple invasions. All these data practically improve our understanding of this invasive insect pest, particularly its ecological and genetic characteristics in the introduced area, which represents critical baseline information for the design of future integrated pest management strategies.

A miniaturized intracerebral potential recorder for long-term local field potential (LFP) of deep brain signals is proposed. LFP can be recorded by deep brain electrodes. The abnormal beta-band oscillation of LFP in subthalamic nucleus and internal globus pallidus in patients with Parkinson's disease (PD) are associated with the severity of the symptoms. The LFP signal from patients who have been implanted with deep brain electrode can be monitored by our system for at least 24 hours in real time. Graphical user interface has also been developed for use by medical personnel. Imitation experiments and in vivo experiments were performed to successfully verify that our system can measure LFP signals. With 24-hour intracerebral signals, researchers can analyze what is happened in the brain in daily life. In the future, more effective PD treatment can be developed, such as intelligent closed-loop deep brain stimulation.

In Taiwan, the agricultural policy, ‘Reduce the consumption of pesticide to half in the next 10 years’, was launched in 2017. Pesticide application, which results in contamination of food by chemic...

ObjectiveSeveral studies suggested a potential role of viral infection in the pathophysiology of Parkinson’s disease (PD). However, the association between herpes zoster and PD was not investigated well till now.MethodsUsing the Taiwan National Health Insurance Research Database, 13 083 patients aged ≥45 years with herpes zoster and 52 332 (1:4) age-/sex-matched controls were enrolled between 1998 and 2008 and followed to the end of 2011. Those who developed PD during the follow-up period were identified.ResultsThe Cox regression analysis with adjustment of demographic characteristics, health system utilization, and comorbidities demonstrated that patients with herpes zoster had an increased risk (hazard ratio [HR]: 1.80, 95% confidence interval [CI]: 1.43-2.28) of developing PD in later life compared to the control group. Sensitivity tests after excluding the first year (HR: 1.50, 95% CI: 1.16-1.93) and first 2-year (HR: 1.44, 95% CI: 1.10-1.88) observation periods showed consistent results.ConclusionsPatients with herpes zoster were more likely to develop PD in later life compared to the controls. Additional studies are necessary for validating our results and to clarify the underlying pathophysiology between herpes zoster and PD.

Purpose: Malignant ascites of epithelial ovarian cancer (EOC) helps identify prognostic biomarkers or mechanisms of tumor progression. Vitamin D–binding protein (DBP) was revealed to be upregulated in EOC ascites in our previous proteomic study. Here, we examined the role of DBP in EOC. Experimental Design: We analyzed ascites, serum, and tissue samples of patients with newly diagnosed EOC to determine the prognostic effects of DBP. We verified DBP function using orthotopic animal models and DBP regulation in ovarian cancer cell lines. Results: Elevated ascitic DBP was significantly associated with poor response to chemotherapy, short progression-free interval, increased cancer progression, and death. Ascitic DBP overexpression was an independent unfavorable biomarker for progression-free survival; DBP overexpression in cancerous tissue was significantly related to chemoresistance. In vivo and in vitro investigations demonstrated an important role for DBP in ovarian cancer progression. Orthotopic model mice inoculated with DBP knockdown ovarian cancer cells displayed a significant reduction in tumor formation, malignant cell number, ascitic DBP levels, invasiveness, and metastasis, and increased survival compared with controls. In presence of vitamin D receptor (VDR), DBP promoted cell aggression (invasion and doubling time) via activation of the insulin-like growth factor-1/insulin-like growth factor–binding protein-2/Akt axis, and induced suppression of vitamin D–responsive genes. A NF-κB p65-binding site in the VDR promoter was identified as a major determinant of DBP-dependent VDR promoter activation. Conclusions: This study highlights the importance of DBP in ovarian tumor progression and the potential application of DBP as a therapeutic target for EOC. Clin Cancer Res; 24(13); 3217–28. ©2018 AACR.

In this study a thermo-sensitive switching membrane was prepared through grafting, using a click reaction, of an N -isopropylacrylamide (NIPAAm) derivative onto an electrospun poly(2,6-dimethyl-1,4-phenylene oxide) (PPO) fibrous membrane (EPFM). The PPO was first electrospun into a fibrous membrane, then brominated and reacted with NaN 3 to generate the azido-terminated EPFMs. A propargyl-terminated poly( N -isopropylacrylamide) (PNIPAAm) was synthesized and grafted onto the azido-terminated EPFMs. The surface roughness of PPO fibers was increased due to the presence of PNIPAAm grafts, such that the thermoresponse of the static water contact angle (SWCA) of PNIPAAm-grafted EPFMs between 25 and 45 °C was significantly greater than that of the same PNIPAAm grafted on a flat surface. Thermo-sensitive affinity of the membrane with water resulted the average pore dimension responded to temperature changes. Taking advantage of this temperature-responsive affinity, we applied the membranes as protein valves that blocked and released an antibody. At 25 °C, the collection efficiency was 90% for antibody concentrations of up to 5 ng/mL. Increasing the temperature to 45 °C caused the collection efficiency to decrease abruptly, to 7.5%, when the antibody concentration was greater than 1.5 ng/mL. Accordingly, this system of PNIPAAm-grafted PPO fibers functioned as a protein valve, allowing the blocking and release of proteins.

Simple Summary High collagen type XI alpha 1 (COL11A1) levels are associated with tumor progression, chemoresistance, and poor patient survival in several cancer types. We examined the role of miRNAs in regulating COL11A1 expression. This study highlighted the importance of miR-335 in downregulating COL11A1-mediated ovarian tumor progression, chemoresistance, and poor survival and suggested its potential application as a therapeutic target. Abstract High collagen type XI alpha 1 (COL11A1) levels are associated with tumor progression, chemoresistance, and poor patient survival in several cancer types. MicroRNAs (miRNAs) are dysregulated in multiple cancers, including epithelial ovarian carcinoma (EOC); however, the regulation of COL11A1 by miRNAs in EOC remains unclear. We examined the role of miRNAs in regulating COL11A1 expression. We identified miR-509 and miR-335 as the candidate miRNAs through an online database search. EOC cell treatment with miR-335 mimics abrogated COL11A1 expression and suppressed cell proliferation and invasion, besides increasing the sensitivity of EOC cells to cisplatin. Conversely, treatment with miR-335 inhibitors prompted cell growth/invasiveness and chemoresistance of EOC cells. miR-335 inhibited COL11A1 transcription, thus reducing the invasiveness and chemoresistance of EOC cells via the Ets-1/MMP3 and Akt/c/EBPβ/PDK1 axes, respectively. Furthermore, it did not directly regulate PDK1 but increased PDK1 ubiquitination and degradation through COL11A1 inhibition. In vivo findings highlighted significantly decreased miR-335 mRNA expressions in EOC samples. Furthermore, patients with low miR335 levels were susceptible to advanced-stage cancer, poor response to chemotherapy, and early relapse. This study highlighted the importance of miR-335 in downregulating COL11A1-mediated ovarian tumor progression, chemoresistance, and poor survival and suggested its potential application as a therapeutic target.