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Welsh onion (Allium fistulosum L.) is one of the main and oldest vegetable crops grown in Taiwan. A severe epidemic of leaf blight in Welsh onion caused by a Stemphylium-like pathogen was found in Sanxing, Taiwan, from 2018 to 2020. However, correct species identification, biology, and control of Stemphylium leaf blight (SLB) of Welsh onion are not well-established. Therefore, the main objective of this study was to investigate the causal agent of SLB in Sanxing and evaluate the in vitro sensitivity of Stemphylium-like pathogen to commonly used fungicides. A phylogenetic analysis based on combining the internal transcribed spacer (ITS) region and glyceraldedyhe-3-phosphate dehydrogenase (gapdh) and calmodulin (cmdA) gene sequences together with morphological features identified that S. vesicarium is associated with SLB in Sanxing. When inoculated onto Welsh onion leaves, the isolates caused symptoms identical to those observed in the field; therefore, S. vesicarium was reisolated and Koch’s postulates were confirmed. We observed a higher incidence of SLB symptoms on the oldest leaves compared with younger leaves. The maximum and minimum temperatures for in vitro mycelial growth and conidial germination (%) of S. vesicarium were 20 to 30°C and 5°C, respectively. Sixteen fungicides were tested for their effectiveness to reduce the mycelial growth and conidial germination of S. vesicarium in vitro. Boscalid plus pyraclostrobin, fluopyram, fluxapyroxad, and fluxapyroxad plus pyraclostrobin were highly effective at reducing mycelial growth and conidial germination in S. vesicarium. However, strobilurin fungicides (azoxystrobin and kresoxim-methyl) commonly used in Welsh onion production in Sanxing were ineffective. This study discusses the emergence of SLB caused by S. vesicarium in the foliar disease complex affecting Welsh onion and the management of the disease using fungicides with different modes of action in Taiwan. The research will support the sustainable management of SLB in Sanxing, Taiwan; however, further field assessments of the fungicides are warranted.

Resistance to androgen deprivation therapy (ADT) represents a key step in the malignant progression of prostate cancer, and mutation to androgen receptor (AR) is one major driver to an androgen-independent phenotype. However, alternative oncogenic pathways that bypass AR signaling have emerged as an important mechanism promoting resistance to ADT. It is known that AR activation can prevent the interaction between β-catenin and T cell factor/lymphoid enhancer-binding factor (TCF/LEF) family, inhibiting the Wnt signaling pathway. The aim of this study was to determine the role of transcription factor 7 (TCF7), a transcription factor best known as a Wnt effector that forms a complex with β-catenin, in the development of advanced prostate cancer. We further investigated the molecular mechanisms by which TCF7 is induced when AR signaling is inactivated. A novel AR signaling pathway that induces microRNA-1 (miR-1) to suppress metastatic prostate cancer was recently demonstrated (AR–miR-1 signaling axis), and its regulation of Wnt signaling was explored in the current study. Clinical data sets were analyzed for potential targets of AR-miR-1 signaling in the TCF/LEF family, and tissue samples were utilized to validate the relationship. The molecular mechanism and biological functions were demonstrated in prostate cancer cell lines and a mouse xenograft model. We demonstrated a molecular mechanism of AR signaling suppressing TCF7 partly through miR-1-mediated downregulation. TCF7 exhibited oncogenic properties and compromised the tumor-suppressive effects of miR-1. Our results also showed that overexpression of TCF7 or disruption of miR-1 function promoted androgen-independent proliferation. We demonstrated that the AR–miR-1 axis negatively regulates the novel oncogenic factor, TCF7. Dysregulation of TCF7 promoted a survival advantage and resistance to androgen deprivation, suggesting its therapeutic potential for castration-resistant prostate cancer.

Background: People with dementia survive an average 8 more years postdiagnosis, and more than 70% caregivers are relatives who provide care at home [ref:1]. Those with mild and moderate dementia and who are cared by relatives dwell in the community, and there may be a relationship between[for full text, please go to the a.m. URL], 15th Congress of the European Forum for Research in Rehabilitation (EFRR)

Background: Exercise intervention is effective to prevent or delay disability in people with dementia [ref:1], however the effects of a community based exercise intervention for a city in Taiwan still needs to be investigated. Aim: To investigate the effects of community based exercise [for full text, please go to the a.m. URL], 15th Congress of the European Forum for Research in Rehabilitation (EFRR)

Transforming growth factor-β (TGFβ) is enriched in the bone matrix and serves as a key factor in promoting bone metastasis in cancer. In addition, TGFβ signaling activates mammalian target of rapamycin (mTOR) functions, which is important for the malignant progression. Here, we demonstrate that TGFβ regulates the level of microRNA-96 (miR-96) through Smad-dependent transcription and that miR-96 promotes the bone metastasis in prostate cancer. The enhanced effects in cellular growth and invasiveness suggest that miR-96 functions as an oncomir/and metastamir. Supporting this idea, we identified a downstream target of the TGFβ-miR-96 signaling pathway to be AKT1S1 mRNA, whose translated protein is a negative regulator of mTOR kinase. Our findings provide a novel mechanism accounting for the TGFβ signaling and bone metastasis.

Current therapeutic regimens for prostate cancer focus on targeting androgen receptor (AR) signaling. However, the AR is a key factor in luminal epithelium differentiation and was shown to have a role as a tumor suppressor. Thus, its inhibition may activate oncogenic pathways that contribute to metastatic castration-resistant prostate cancer (CRPC). Herein, we report a novel tumor promoter, ZBTB46, which is negatively regulated by AR signaling via microRNA (miR)-1-mediated downregulation. ZBTB46 is associated with malignant prostate cancer and is essential for metastasis. Its overexpression can overcome the antitumor effects of miR-1 and promote androgen-independent proliferation. We demonstrated that ZBTB46 can transcriptionally regulate SNAI1, a key epithelial-to-mesenchymal transition (EMT) driver, which could contribute to induction of the EMT after androgen-deprivation therapy and metastasis. Our findings are supportive of the model that disruption of AR's function may predispose prostate cancer to progress to metastatic CRPC.

© 2017, Springer International Publishing AG. Cloud services registry is a cloud services datadase which contains thousands of records of cloud consumers’ reviews and cloud services, such as Platform as a Service (PaaS) and Infrastructure as a Service (IaaS). The data set is harvested from a web portal called www.serchen.com. Each record holds detail information about the service such as service name, service description, categories, key features, service provider link and review list. Each review contains reviewer name, review date and review content. This work is an extension of our previous work Blue Pages data set [6]. The data set is valuable for future research in cloud service identification, discovery, comparison and selection.

Xenobiotic phthalate esters (PAEs) are considered endocrine disrupting chemicals and are known to cause immunotoxicity, having been linked with the susceptibility of shrimp to pathogens; however, the effect on other physiological functions has not been explored. This study sought to understand the genetic responses of Neocaridina denticulate, a common freshwater shrimp, to three different PAEs, i.e., diethyl phthalate (DEP), dipropyl phthalate (DPrP), and diphenyl phthalate (DPP). The differential expression of 10 functional known expressed sequence tags derived from N. denticulate were analyzed by semi-quantitative RT-PCR after 24 h of exposure to non-lethal concentrations (0, 0.1, 1.0, and 10 mg/L) of PAEs in pond water. Compared with the control group, nine genes were differentially expressed in the DEP-treated groups, seven genes were differentially expressed in the DPrPtreated groups, and five genes were differentially expressed in the in DPP-treated groups. These PAE-affected genes primarily belonged to three functional classes: defense-related genes (qm: QM protein hc: hemocyanin), metabolism-related genes (cathepsin-L like catl: cysteine protease; gdh: glutamate dehydrogenase and impdh-1: inosine monophosphate dehydrogenase 1 ) and stress-related genes (hsp70: 70 kDa-heat shock protein; gst: glutathione S-transferase, and tps: trehalose-6-phosphate synthase). Among these, the stress-related genes were significantly up-regulated by DEP, DPrP, and DPP. These effects of PAEs on the expression of genes required for multiple physiological functions suggest that even with non-lethal concentrations of PAEs, a polluted aquatic environment may still present a potential risk to N. denticulate.

Metastatic progression in patients with prostate cancer is common despite pharmacologic inhibition of androgen receptor signaling. This drug resistance is associated with increased signaling through the transforming growth factor-β (TGF-β) signaling pathway. We found the type I/II/IV collagen-binding protein transforming growth factor-β (TGF-β)-induced (TGFBI) is an important factor in the epithelial-to-mesenchymal transition (EMT) and malignant progression of prostate cancer. We identified that an androgen-responsive gene, SPDEF, navigates between AR and TGFβ signaling during prostate cancer progression to metastasis though a physical interaction with the promoter region of the TGFBI gene. We show that loss of AR-regulated SPDEF induces TGFBI expression in prostate cancer cells, leading to drastic and aggressive physiologic changes. Furthermore, we confirmed the negative correlation between SPDEF and TGFβ singling in prostate cancer patients and demonstrated that ADT can reduce SPDEF and increase TGFβ signaling. Our results support an inhibitory role of the AR on TGFβ signaling through SPDEF-mediated suppression of TGFBI, and that disruption of this pathway promotes metastatic progression in prostate cancer. Citation Format: Yen-Nien Liu, Wei-Yu Chen, Yuan-Chin Tsai, Hsiu-Lien Yeh, Florent Suau, Jiaoti Huang. Androgen deprivation therapy-induced TGFBI signaling promotes EMT and bone metastasis of prostate cancer [abstract]. In: Proceedings of the AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; 2017 Dec 2-5; Orlando, Florida. Philadelphia (PA): AACR; Cancer Res 2018;78(16 Suppl):Abstract nr A031.

To examine whether scheduled forced wheel activity counteracts the increased body weight gain in rats undergoing chronic circadian desynchronization induced by repeated 12-h shifts in the light–dark cycle. Four age- and body weight-matched groups of adult male F344 rats were subjected to 12-h intermittent forced wheel activity daily (2.2 km/day). Each group had the following schedule for 13 weeks: a fixed schedule of a daily 12:12-h light–dark cycle and activity training (WF); a fixed light–dark cycle and 12-h shifts twice a week in activity training (WS); 12-h shifts twice a week in the light–dark cycle and a fixed schedule of activity training (LSWF); and 12-h shifts twice a week in both the light–dark cycle and activity training (LSWS). Two additional age- and body weight-matched sedentary rat groups were selected from our database: one was maintained on a fixed light–dark cycle (LC) and the other was subjected to 12-h shifts twice a week in the light–dark cycle (LS). The four rat groups that were exercised showed different response patterns of the daily body temperature rhythm to different combinations of forced activity and lighting schedules. Their food intake was more than that of the two sedentary rat groups, but their body weight was comparable with that of the LC rats and less than that of the LS rats during the forced activity period. The LSWS rats were heavier than the WF and WS rats in the first and second months of the experimental treatment, but their body weight was comparable with that of the WS and WF rats in the third month. Forced activity was effective in reducing the body weight gain in chronic circadian desynchronization that was induced by repeated shifts in the light–dark cycle, although such an effect might become significant only after some time.

To report a large multi-institutional series of laparoendoscopic single-site (LESS) nephroureterectomy (NU).Data on all cases of LESS-NU performed between 2008 and 2012 at 15 institutions were retrospectively gathered. The main demographic data and perioperative outcomes were analysed.The study included 101 patients whose mean (SD) age was 66.4 (9.9) years and mean (SD) body mass index was 24.8 (4) kg/m², and of whom 29.7% had undergone previous abdominal/pelvic surgery. The mean (SD) operating time was 221.4 (73.7) min, estimated blood loss 231.7 (348.0) mL. A robot-assisted LESS technique was applied in 25.7% of cases. An extra trocar was inserted in 28.7% of cases to complete the procedure. Conversion to open surgery was necessary in three cases (3.0%). There was no bladder cuff excision in 20.8% of cases, and excision was carried out using a variety of techniques in the remaining cases. Six intra-operative complications occurred (5.9%). The mean (SD) length of hospital stay was 6.3 (3.5) days. The overall postoperative complication rate was 10.0%, and most of the complications were low grade (Clavien grades 1 and 2). The mean tumour size was 3.1 (1.9) cm. Pathological staging was pTis in two patients, pTa in 12 patients, pT1 in 42 patients, pT2 in 20 patients, pT3 in 23 patients and pT4 in two patients. Pathological grade was high in 71 and low in 30 patients. At a mean follow-up of 14 months, six patients (5.9%) had died. Disease recurrence (including distant and bladder recurrence) was detected in 22.8% of patients, with a mean time to recurrence of 11.5 months.This study reports the largest multi-institutional experience of LESS-NU to date. Peri-operative outcomes mirror those of published standard laparoscopy series. Despite encouraging early findings, longer follow-up is needed to determine the oncological efficacy of the procedure.

ETV6 is an ETS transcription factor and a putative tumor suppressor in prostate cancer according to several genomic analyses. However, its cellular functions and upstream regulating signaling remain unclear. We demonstrated that ETV6 suppresses the prostate cancer progression and that ETV6 levels are negatively associated with advanced prostate cancer, supporting the idea that ETV6 acts as a tumor suppressor. Furthermore, ETV6 can be regulated by epidermal growth factor receptor (EGFR) signaling through microRNA (miR)-mediated downregulation. One of the miRs, miR-96, can be transcriptionally-regulated by nuclear EGFR. The association patterns connecting miR-96, EGFR activation, and ETV6 were further validated in the clinical tissue samples. We proposed an EGFR-miR-96-ETV6 signaling pathway in promoting prostate cancer. Note: This abstract was not presented at the meeting. Citation Format: Yen-Nien Liu, Yuan-Chin Tsai, Wei-Yu Chen, Man Kit Siu, Hsiu-Lien Yeh. ETV6 is a tumor suppressor regulated by EGFR-miR-96 pathway in prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4467. doi:10.1158/1538-7445.AM2017-4467

In prostate cancer, Krüppel-like factor 4 (KLF4) depletion occurs frequently, suggesting a role as suppressor tumor. KLF4 is a transcription factor associated with androgen receptor (AR) expression; however, its cellular functions and signaling regulation mechanism remain largely unknown. In this study, we demonstrated that activated AR binds to the KLF4 promoter and enhances KLF4 expression, which reciprocally targets the AR promoter, thus sustaining KLF4 activity. Ectopic KLF4 expression in androgen-independent prostate cancer cells induced AR expression and decreased cell proliferation, invasion and bone metastasis. We previously showed that increased microRNA (miR)-1 expression is associated with reduced bone metastasis of prostate cancer cells. Here we observed that KLF4 targets the primary miR-1-2 stem-loop promoter and stimulates miR-1 expression. In clinical prostate cancer specimens, KLF4 levels were positively correlated with miR-1 and AR levels. These data suggest that the loss of KLF4 expression is one mechanistic link between aggressive prostate cancer progression and low canonical AR output through miR-1 inactivation.

Among eight human bladder cancer cell lines we examined, only T24 cells were resistant to the growth inhibition effect of genistein, an isoflavone and potent anticancer drug. Since the T24 cell line was the only cell line known to overexpress oncogenic H-Ras(val 12), we investigated the role of H-Ras(val 12) in mediating drug resistance. Herein, we demonstrate that the phenotype of T24 cells could be dramatically reversed and became relatively susceptible to growth inhibition by genistein if the synthesis of H-Ras(val 12) or its downstream effector c-Fos had been suppressed. The inhibition of Ras-mediated signalling with protein kinase inhibitors, such as PD58059 and U0126 which inhibited MEK and ERK, in T24 cells also rendered the identical phenotypic reversion. However, this reversion was not observed when an inhibitor was used to suppress the protein phosphorylation function of PI3 K or PKC. These results suggest that the signal mediated by H-Ras(val 12) is predominantly responsible for the resistance of the cells to the anticancer drug genistein.

A case is presented of replantation of 10 digits at the proximal phalangeal level. Seven digits survived. Osteotomies and flexor tenolysis were done on the right thumb, long, and ring fingers and left index and long fingers 11 months later. A toe-to-hand transfer was done to reconstruct the failed left thumb replantation. Functional and sensory recovery is satisfactory.

Severe hand trauma caused by an industrial accident resulted in composite tissue loss in the basal joint area of the right hand. The crushed metacarpal bone was replaced, and ligamentous and capsular reconstruction was performed with flexor carpi radialis tendon and additional tendon graft. We present our experience, with a follow-up of one year and eight months.