As the business environment rapidly changes, closer connected activities have been involved in the buyer–supplier relationship. Among the four aspects of supply chain integration (cash flow, material flow, product flow and information flow), the integration of information flow is the most critical element in enabling coordinating activities and supply chain alliances. Yet, there are unanswered questions regarding the extent to which information exchanged is effective in the supply chain alliance. In this study, we adopted the ‘contingency theory’ as the theoretical foundation, and interviewed eight selected firms to investigate the impact of supply chain partners among organizations on information sharing quality, and the impact of inter-organizational information sharing quality on the supply chain integrated-performance. The results show that (1) supply chain partners within and between groups have a positive impact on inter-organizational information sharing quality, (2) inter-organizational information sharing quality has a positive impact on the supply chain integrated performance, and (3) information sharing quality should be multi-dimensional. We believe that the successful implementation of SCM systems among firms will produce significant synergy and be associated with the competitive advantages. Implications for theory and practice are discussed.

Four new oxygenated dibenzocyclooctadiene lignans, arisanschinins A-D ( 1- 4), and a new 1,4-bis(phenyl)-2,3-dimethylbutane lignan, arisanschinin E ( 5), together with 15 known compounds, were isolated from the EtOAc-soluble fraction of the aerial parts of SCHISANDRA ARISANENSIS Hay. The structures of 1- 5 were elucidated on the basis of extensive spectroscopic analyses, including 2D NMR (HMQC, HMBC, and NOESY) experiments. The configurations of the biphenyl and octadiene moieties were deduced from circular dichroism (CD) and NOESY spectra, respectively. Compound 1 showed significant inhibition of α-glucosidase IN VITRO. The radical-scavenging activities of these compounds were evaluated using DPPH.

No abstract

<div>Abstract<p>E1B-55kD-deleted adenoviruses have been used as conditionally replicative adenoviruses (CRAds) for therapeutic purposes in tumors with loss-of-function p53 mutation. To target cancer cells that harbor activating mutant KRAS (KRAS^aMut) but spare p53^wild normal cells, we constructed and examined by reporter assays a KRAS^aMut but not p53-responsive promoter, the Δ<i>p53RE</i>P2 promoter. The Δ<i>p53RE</i>P2 promoter, derived from human double minute 2 (<i>hdm2</i>) P2 promoter with its p53 response elements being deleted, was used to regulate the expression of the <i>hdm2 </i>transgene in a novel E1B-55kD-deleted CRAd, the Ad-KRhdm2. The Ad-KRhdm2 selectively replicated in and exerted cytopathic effects on KRAS^aMut colorectal cancer cell lines (HCT116, LoVo, LS174T, LS123, and SW620), regardless of their <i>p53</i> gene statuses, by forming plaques and exhibiting cytopathic effect in cultured cells. Ad-KRhdm2, like other E1B-55kD-deleted adenoviruses, also exerted selective cytopathic effects on tumor cells with loss-of-function p53 mutant. The multiplicities of infection of Ad-KRhdm2 required to decrease 50% viability of KRAS^aMut tumor cells cultured for 7 days were 440 to 3,400 times less than those of MRC5 normal fibroblasts and KRAS^wild/p53^wild RKO tumor cells. Intratumoral injection of Ad-KRhdm2 vectors exhibited specific lytic activities in nude mouse xenografts of KRAS^aMut cell lines (LoVo, SW620, and LS174T) but not in xenografts of RKO cells. Transduction of KRAS^aMut/p53^wild HCT116, LoVo, and LS174T cells by Ad-KRhdm2 significantly increased Hdm2 expression, decreased p53 level, and abolished the p53-transactivating <i>p21^Cip1</i> promoter activity. Ad-KRhdm2 has shown its therapeutic potential in KRAS^aMut cancer cells and warrants further clinical trials. Mol Cancer Ther; 9(2); 450–60</p></div>

<div>Abstract<p>E1B-55kD-deleted adenoviruses have been used as conditionally replicative adenoviruses (CRAds) for therapeutic purposes in tumors with loss-of-function p53 mutation. To target cancer cells that harbor activating mutant KRAS (KRAS^aMut) but spare p53^wild normal cells, we constructed and examined by reporter assays a KRAS^aMut but not p53-responsive promoter, the Δ<i>p53RE</i>P2 promoter. The Δ<i>p53RE</i>P2 promoter, derived from human double minute 2 (<i>hdm2</i>) P2 promoter with its p53 response elements being deleted, was used to regulate the expression of the <i>hdm2 </i>transgene in a novel E1B-55kD-deleted CRAd, the Ad-KRhdm2. The Ad-KRhdm2 selectively replicated in and exerted cytopathic effects on KRAS^aMut colorectal cancer cell lines (HCT116, LoVo, LS174T, LS123, and SW620), regardless of their <i>p53</i> gene statuses, by forming plaques and exhibiting cytopathic effect in cultured cells. Ad-KRhdm2, like other E1B-55kD-deleted adenoviruses, also exerted selective cytopathic effects on tumor cells with loss-of-function p53 mutant. The multiplicities of infection of Ad-KRhdm2 required to decrease 50% viability of KRAS^aMut tumor cells cultured for 7 days were 440 to 3,400 times less than those of MRC5 normal fibroblasts and KRAS^wild/p53^wild RKO tumor cells. Intratumoral injection of Ad-KRhdm2 vectors exhibited specific lytic activities in nude mouse xenografts of KRAS^aMut cell lines (LoVo, SW620, and LS174T) but not in xenografts of RKO cells. Transduction of KRAS^aMut/p53^wild HCT116, LoVo, and LS174T cells by Ad-KRhdm2 significantly increased Hdm2 expression, decreased p53 level, and abolished the p53-transactivating <i>p21^Cip1</i> promoter activity. Ad-KRhdm2 has shown its therapeutic potential in KRAS^aMut cancer cells and warrants further clinical trials. Mol Cancer Ther; 9(2); 450–60</p></div>