The Experts below are selected from a list of 27198 Experts worldwide ranked by ideXlab platform
William F. Crittenden - One of the best experts on this subject based on the ideXlab platform.
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a social learning theory of cross functional case education
Journal of Business Research, 2005Co-Authors: William F. CrittendenAbstract:Abstract Effective cross-functional integration is needed to solve problems and improve work processes that cross organizational lines. Cross-functional education is intended to develop managers with an organizational perspective that enhances communication, learning, and decision making. It is proposed that the social learning theory (SLT) is appropriate as a theoretical foundation to facilitate learning and teaching with cross-functional cases. The SLT explains human behavior in terms of continuous Reciprocal Interaction between cognitive, behavioral, and environmental influences. Importantly, the professor initially establishes the environment in which the class functions. The classroom stimuli first observed by the student is the basis upon which the Reciprocal determinism and learned behavior will evolve. Thus, establishing high expectations and enthusiasm about course material and student preparation and participation is paramount. It also is suggested that professors must be aware of each student's cognitive influences, must have a course and class session plan to shape the discussion environment, and be prepared to foster and/or exert consequences to shape learned behaviors that enhance cross-functional understanding.
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a social learning theory of cross functional case education
Journal of Business Research, 2005Co-Authors: William F. CrittendenAbstract:Abstract Effective cross-functional integration is needed to solve problems and improve work processes that cross organizational lines. Cross-functional education is intended to develop managers with an organizational perspective that enhances communication, learning, and decision making. It is proposed that the social learning theory (SLT) is appropriate as a theoretical foundation to facilitate learning and teaching with cross-functional cases. The SLT explains human behavior in terms of continuous Reciprocal Interaction between cognitive, behavioral, and environmental influences. Importantly, the professor initially establishes the environment in which the class functions. The classroom stimuli first observed by the student is the basis upon which the Reciprocal determinism and learned behavior will evolve. Thus, establishing high expectations and enthusiasm about course material and student preparation and participation is paramount. It also is suggested that professors must be aware of each student's cognitive influences, must have a course and class session plan to shape the discussion environment, and be prepared to foster and/or exert consequences to shape learned behaviors that enhance cross-functional understanding.
Rajvir Dahiya - One of the best experts on this subject based on the ideXlab platform.
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long noncoding rna malat1 promotes aggressive renal cell carcinoma through ezh2 and interacts with mir 205
Cancer Research, 2015Co-Authors: Hiroshi Hirata, Yuji Hinoda, Varahram Shahryari, Guoren Deng, Koichi Nakajima, Laura Z Tabatabai, Nobuhisa Ishii, Rajvir DahiyaAbstract:Recently, long noncoding RNAs (lncRNA) have emerged as new gene regulators and prognostic markers in several cancers, including renal cell carcinoma (RCC). In this study, we investigated the contributions of the lncRNA MALAT1 in RCC with a specific focus on its transcriptional regulation and its Interactions with Ezh2 and miR-205. We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas β-catenin expression was decreased through Ezh2. Reciprocal Interaction between MALAT1 and miR-205 was also observed. Lastly, MALAT1 bound Ezh2 and oncogenesis facilitated by MALAT1 was inhibited by Ezh2 depletion, thereby blocking epithelial-mesenchymal transition via E-cadherin recovery and β-catenin downregulation. Overall, our findings illuminate how overexpression of MALAT1 confers an oncogenic function in RCC that may offer a novel theranostic marker in this disease.
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long noncoding rna malat1 promotes aggressive renal cell carcinoma through ezh2 and interacts with mir 205
Cancer Research, 2015Co-Authors: Hiroshi Hirata, Yuji Hinoda, Varahram Shahryari, Guoren Deng, Koichi Nakajima, Laura Z Tabatabai, Nobuhisa Ishii, Rajvir DahiyaAbstract:Recently long non-coding RNAs (lncRNA) have emerged as new gene regulators and prognostic markers in several cancers including renal cell carcinoma (RCC). In this study, we investigated the contributions of the lncRNA MALAT1 in RCC with a specific focus on its transcriptional regulation and its Interactions with Ezh2 and miR-205. We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased while beta-catenin expression was decreased through Ezh2. Reciprocal Interaction between MALAT1 and miR-205 was also observed. Lastly, MALAT1 bound Ezh2 and oncogenesis facilitated by MALAT1 was inhibited by Ezh2 depletion, thereby blocking epithelial-mesenchyme transition via E-cadherin recovery and beta-catenin downregulation. Overall, our findings illuminate how overexpression of MALAT1 confers an oncogenic function in RCC that may offer a novel theranostic marker in this disease.
Lucio G Costa - One of the best experts on this subject based on the ideXlab platform.
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behavioral phenotyping for autism spectrum disorders in mice
Current protocols in immunology, 2017Co-Authors: Yuchi Chang, Toby B Cole, Lucio G CostaAbstract:Autism spectrum disorder (ASD) represents a heterogeneous group of disorders characterized by alterations in three behavioral symptom domains: Social Interactions, verbal and nonverbal communication, and repetitive behaviors. Increasing prevalence of ASD in recent years suggests that exposure to environmental toxicants may be critical in modulating etiology of this disease. As clinical diagnosis of autism still relies on behavioral evaluation, it is important to be able to assess similar behavioral traits in animal models, to provide biological plausibility of associations between environmental exposures and ASD. Rodents naturally exhibit a large number of behaviors that can be linked to similar behaviors in human. In this unit, behavioral tests are described that are relevant to the domains affected in ASD. For the repetitive domain, the T-maze spontaneous alternation test and marble burying test are described. For the communication domain, neonatal ultrasonic vocalization and olfactory habituation test toward social and non-social odor are described. Finally, for the sociability domain, the three-chambered social preference test and the Reciprocal Interaction test are presented. © 2017 by John Wiley & Sons, Inc.
Hiroshi Hirata - One of the best experts on this subject based on the ideXlab platform.
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long noncoding rna malat1 promotes aggressive renal cell carcinoma through ezh2 and interacts with mir 205
Cancer Research, 2015Co-Authors: Hiroshi Hirata, Yuji Hinoda, Varahram Shahryari, Guoren Deng, Koichi Nakajima, Laura Z Tabatabai, Nobuhisa Ishii, Rajvir DahiyaAbstract:Recently, long noncoding RNAs (lncRNA) have emerged as new gene regulators and prognostic markers in several cancers, including renal cell carcinoma (RCC). In this study, we investigated the contributions of the lncRNA MALAT1 in RCC with a specific focus on its transcriptional regulation and its Interactions with Ezh2 and miR-205. We found that MALAT1 expression was higher in human RCC tissues, where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased, whereas β-catenin expression was decreased through Ezh2. Reciprocal Interaction between MALAT1 and miR-205 was also observed. Lastly, MALAT1 bound Ezh2 and oncogenesis facilitated by MALAT1 was inhibited by Ezh2 depletion, thereby blocking epithelial-mesenchymal transition via E-cadherin recovery and β-catenin downregulation. Overall, our findings illuminate how overexpression of MALAT1 confers an oncogenic function in RCC that may offer a novel theranostic marker in this disease.
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long noncoding rna malat1 promotes aggressive renal cell carcinoma through ezh2 and interacts with mir 205
Cancer Research, 2015Co-Authors: Hiroshi Hirata, Yuji Hinoda, Varahram Shahryari, Guoren Deng, Koichi Nakajima, Laura Z Tabatabai, Nobuhisa Ishii, Rajvir DahiyaAbstract:Recently long non-coding RNAs (lncRNA) have emerged as new gene regulators and prognostic markers in several cancers including renal cell carcinoma (RCC). In this study, we investigated the contributions of the lncRNA MALAT1 in RCC with a specific focus on its transcriptional regulation and its Interactions with Ezh2 and miR-205. We found that MALAT1 expression was higher in human RCC tissues where it was associated with reduced patient survival. MALAT1 silencing decreased RCC cell proliferation and invasion and increased apoptosis. Mechanistic investigations showed that MALAT1 was transcriptionally activated by c-Fos and that it interacted with Ezh2. After MALAT1 silencing, E-cadherin expression was increased while beta-catenin expression was decreased through Ezh2. Reciprocal Interaction between MALAT1 and miR-205 was also observed. Lastly, MALAT1 bound Ezh2 and oncogenesis facilitated by MALAT1 was inhibited by Ezh2 depletion, thereby blocking epithelial-mesenchyme transition via E-cadherin recovery and beta-catenin downregulation. Overall, our findings illuminate how overexpression of MALAT1 confers an oncogenic function in RCC that may offer a novel theranostic marker in this disease.
Bong Jik Kim - One of the best experts on this subject based on the ideXlab platform.
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mutational and phenotypic spectrum of otof related auditory neuropathy in koreans eliciting Reciprocal Interaction between bench and clinics
Journal of Translational Medicine, 2018Co-Authors: Ah Reum Kim, Chung Lee, Bong Jik Kim, Jeong Hun Jang, Jin Hee Han, Hye-rim Park, Seungmin Lee, Min Young Kim, Nayoung KimAbstract:While auditory neuropathy spectrum disorder (ANSD) is a heterogeneous disorder and its management quite varies depending upon the etiology, even including self-resolution, OTOF is an important molecular etiology of prelingual ANSD and has emerged as an attractive target for implementation of precision medicine in terms of timing and prognosis prediction of auditory rehabilitation. However, to date, the literature is lacking in the genotype–phenotype relationship of this gene as well as efficient molecular testing strategy in the clinic in many populations and to make things more complicated in Koreans, the most prevalent variant p.Arg1939Gln among Korean ANSD children frequently evaded detection by next generation sequencing (NGS), resulting in delayed genetic diagnosis and late cochlear implantation (CI). The aims of this study are to document the mutational and phenotypic spectrum of OTOF-related ANSD (DFNB9) in the Korean population, further establishing genotype–phenotype correlation and proposing a set of the most commonly found OTOF variants to be screened first. Genetic diagnosis through the NGS-based sequencing was made on patients with ANSD in two tertiary hospitals. Genotype and phenotypes of eleven DFNB9 patients were reviewed. For data analysis, Mann–Whitney test and Fisher’s exact test were applied. This study disclosed four prevalent variants in Koreans: p.Arg1939Gln with an allele frequency of 40.9%, p.Glu841Lys (13.6%), p.Leu1011Pro and p.Arg1856Trp (9.1%). Three novel variants (c.4227 + 5G > C, p.Gly1845Glu, and p.Pro1931Thr) were identified. Interestingly, a significant association of p.Arg1939Gln with worse ASSR thresholds was observed despite consistently no ABR response. Ten of 11 DFNB9 patients received CI for auditory rehabilitation, showing favorable outcomes with more rapid improvement on early-CI group (age at CI ≤ 18 mo.) than late-CI group. This study included the largest Korean DFNB9 cohort to date and proposed a set of the most frequent four OTOF variants, allowing the potential prioritization of exons during Sanger sequencing. Further, a significant association of p.Arg1939Gln homozygotes with poor residual hearing was observed. We may have to suspect p.Arg1939Gln homozygosity in cases of poor auditory thresholds in ANSD children with putative negative OTOF variants solely screened by NGS. Reciprocal feedback between bench and clinics regarding DFNB9 would complement each other.
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Mutational and phenotypic spectrum of OTOF-related auditory neuropathy in Koreans: eliciting Reciprocal Interaction between bench and clinics
BMC, 2018Co-Authors: Bong Jik Kim, Ah Reum Kim, Chung Lee, Jeong Hun Jang, Jin Hee Han, Hye-rim Park, Seungmin Lee, Min Young Kim, Nayoung K D KimAbstract:Abstract Background While auditory neuropathy spectrum disorder (ANSD) is a heterogeneous disorder and its management quite varies depending upon the etiology, even including self-resolution, OTOF is an important molecular etiology of prelingual ANSD and has emerged as an attractive target for implementation of precision medicine in terms of timing and prognosis prediction of auditory rehabilitation. However, to date, the literature is lacking in the genotype–phenotype relationship of this gene as well as efficient molecular testing strategy in the clinic in many populations and to make things more complicated in Koreans, the most prevalent variant p.Arg1939Gln among Korean ANSD children frequently evaded detection by next generation sequencing (NGS), resulting in delayed genetic diagnosis and late cochlear implantation (CI). The aims of this study are to document the mutational and phenotypic spectrum of OTOF-related ANSD (DFNB9) in the Korean population, further establishing genotype–phenotype correlation and proposing a set of the most commonly found OTOF variants to be screened first. Methods Genetic diagnosis through the NGS-based sequencing was made on patients with ANSD in two tertiary hospitals. Genotype and phenotypes of eleven DFNB9 patients were reviewed. For data analysis, Mann–Whitney test and Fisher’s exact test were applied. Results This study disclosed four prevalent variants in Koreans: p.Arg1939Gln with an allele frequency of 40.9%, p.Glu841Lys (13.6%), p.Leu1011Pro and p.Arg1856Trp (9.1%). Three novel variants (c.4227 + 5G > C, p.Gly1845Glu, and p.Pro1931Thr) were identified. Interestingly, a significant association of p.Arg1939Gln with worse ASSR thresholds was observed despite consistently no ABR response. Ten of 11 DFNB9 patients received CI for auditory rehabilitation, showing favorable outcomes with more rapid improvement on early-CI group (age at CI ≤ 18 mo.) than late-CI group. Conclusions This study included the largest Korean DFNB9 cohort to date and proposed a set of the most frequent four OTOF variants, allowing the potential prioritization of exons during Sanger sequencing. Further, a significant association of p.Arg1939Gln homozygotes with poor residual hearing was observed. We may have to suspect p.Arg1939Gln homozygosity in cases of poor auditory thresholds in ANSD children with putative negative OTOF variants solely screened by NGS. Reciprocal feedback between bench and clinics regarding DFNB9 would complement each other