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[[alternative]]Antibodies and method for determining deletions in hbv pre-s2 region
No full text[[abstract]]本文揭露HBS特異性抗體、LHBS特異性抗體、WT LHBS特異性抗體，含有該抗體的免疫分析套組，以及使用免疫分析套組來偵測pre-S2缺失突變LHBS的方法。該方法包含孵育生物樣本與第一抗體以捕捉HBS蛋白；偵測分別結合至固定的第一抗體之LHBS和WT LHBS；以及藉由從LHBS蛋白的數量減去WT LHBS蛋白的數量以計算pre-S2缺失突變LHBS蛋白的數量。優勢地，藉由上述的方法，可輕易地計算在生物樣本內，pre-S2缺失突變LHBS的數量、在慢性HBV帶原者內HCC發生率的潛在高風險標記物、以及在肝切除手術之後HCC病患內復發率，而無WT和pre-S2突變LHBS間之相互影響並且同時降低在分析之前用於複製每個基因產物的勞力密集過程
Antibodies and method for determining deletions in HBV pre-S2 region
No full text[[abstract]]A HBS-specific antibody, a LHBS-specific antibody, a WT LHBS-specific antibody, an immunoassay kit comprising the antibodies, and a method of detecting pre-S2 deletion mutant LHBS using the immunoassay kit are disclosed herein. The method comprises incubating a biological sample with a first antibody to captured HBS proteins; detecting the LHBS and WT LHBS bound to the immobilized first antibody, respectively; and calculating the amount of the pre-S2 deletion mutant LHBS protein by subtracting the amount of the WT LHBS protein from that of the LHBS protein. Advantageously, by the method described herein, the amount of the pre-S2 deletion mutant LHBS, a potential high-risk marker for HCC incidence in chronic HBV carriers and recurrence in HCC patients after hepatectomy surgery, in a biological sample may be easily calculated without mutual influence between the WT and pre-S mutant LHBS while reducing the labor-intensive process for cloning each gene product before analysis
[[alternative]]Cell strain having increased virus production ability and production method thereof
No full text[[abstract]]本發明係關於具有增加的病毒生產能力之細胞株及其製備方法，更具體地，係關於CCCH型鋅指蛋白的過度表達而具有增加的病毒生產能力之細胞株及其製備方法。根據本發明，當經改造細胞用作產生病毒的細胞株時，可提高病毒的產量。另外，經改造細胞亦可用於研究與生產疫苗以預防病毒性感染之疾病
[[alternative]]Use of cationic biodegradable polyceramic microparticles for vaccine delivery
No full text[[abstract]]本發明係關於一種以陽離子型生物可降解性陶瓷聚合物微粒子做為遞送疫苗之載體之用途，該陽離子型生物可降解性陶瓷聚合物微粒子係以磷酸氫鈣(calcium hydrogenphosphate；CHP)修飾其表面，於本發明中，以此磷酸氫鈣修飾之陶瓷聚合物微粒子所製備之疫苗，顯現出較低的毒性，並可延長抗原之停留時間且增強免疫反應
Adenoviral vector-based vaccine against enterovirus infection
No full text[[abstract]]The present invention relates to a recombinant adenoviral vector for generating immunity against enterovirus infection. In one embodiment, the recombinant adenoviral vector of the invention comprises an expression cassette encoding a PI protein and a 3 C
[[alternative]]Scaffold for cell or tissue culture, the preparing method and use thereof in tissue engineering and regenerative medicine
No full text[[abstract]]本發明係關於一種用於細胞或組織培養並具有階梯式微結構的支架，其包含多層結構，每一層皆具有多個通孔，且每層的通孔皆與其相鄰層上所相對應的通孔連通。本發明亦提供一種培養細胞和組織再生的方法
IL-10RA governor the expression of IDO in the instruction of lymphocyte immunity
No full text[[abstract]]BackgroundIndoleamine 2,3-dioxygenase (IDO) impairs anti-pathogen and anti-tumour immunity. Mesenchymal stem cells (MSCs) modulate immunity via IDO but also suppress IFN-gamma. While MSC IDO induction by IFN-gamma is established, other drivers in this immunosuppressive setting remain unknown.MethodsHuman bone marrow mesenchymal stem cells (MSCs) with IDO or IL-10RA knockdown were co-cultured with healthy donor T cells to assess immunosuppression. PDAC organoid anticancer activity was also tested in these co-cultures.ResultsCo-culturing MSCs with T cells in an IL-10RA-enriched environment enhances IDO expression, resulting in T cell suppression. Moreover, IL-10RA-positive MSCs collected from co-cultures with IL-10 supplementation show increased IDO expression. Conversely, MSCs with IL-10RA knockdown exhibit a significant reduction in IDO RNA and protein expression, as well as STAT3 phosphorylation status, which is a known upstream signalling pathway in IDO gene regulation, in T cell co-cultures. Down-regulation of IL-10RA also inhibits IDO activity in MSCs, resulting in reduced T cell suppression, and enabling the co-cultured T cells to kill PDAC organoids.ConclusionOur research reveals IL-10RA as a pharmacological target in stromal cells for enhancing T cell-mediated PDAC eradication by downregulating IDO via blocked IL-10/IL-10RA signalling in MSCs. This advances IL-10RA interference in the tumour microenvironment (TME) to restore T cell cytotoxicity against cancers
Development of potent and selective inhibitors of methylenetetrahydrofolate dehydrogenase 2 for targeting acute myeloid leukemia: Sar, structural insights, and biological characterization
No full text[[abstract]]Methylenetetrahydrofolate dehydrogenase/cyclohydrolase 2 (MTHFD2), a pivotal mitochondrial enzyme in one-carbon metabolism, is significantly upregulated in various cancers but minimally expressed in normal proliferating cells. In contrast, MTHFD1, which performs similar functions, is predominantly expressed in normal cells. Therefore, targeting MTHFD2 with selective inhibitors holds promise for a broader therapeutic window with reduced toxicity and fewer side effects. This study identified selective 2,4-diamino-6-oxo-1,6-dihydropyrimidin-5-yl ureido-based derivatives through systematic chemical modifications and SAR studies. Structural biology investigations revealed substitutions in the phenyl ring and tail region modulate potency and selectivity toward MTHFD2. Additionally, a comprehensive cell screening platform revealed acute myeloid leukemia cells with FLT3 internal tandem duplication mutations are particularly sensitive to these inhibitors. Furthermore, synergistic effects were observed when combining potential compounds with Alimta. Compound 16e emerged as a leading candidate, demonstrating superior inhibition and selectivity for MTHFD2, favorable pharmacokinetics, and potent antitumor efficacy in MOLM-14 xenograft models
The potential immunotherapy effect of Ginkgolide B thwarts oral squamous cell carcinoma progression by targeting the SREBP1/KLK8/CCL22 axis
No full text[[abstract]]Background: Oral cancer is a malignant tumor of the oral cavity, with regulatory T cell (Treg) infiltration associated with poor prognosis. Ginkgolide B (GB) has demonstrated effects on lipid metabolism; however, its potential immunotherapeutic effects on oral cancer have not been elaborated. Purpose: This study aimed to explore the immunotherapeutic effects of Ginkgolide B (GB) in oral cancer. Study design: We investigated the interactive mechanisms between Tregs and oral cancer cells in regulating sterol regulatory element-binding protein 1 (SREBP1)/ kallikrein-related peptidase 8 (KLK8)/ CC motif chemokine ligand 22 (CCL22) axis by GB treatment. Methods: Tissue array staining and the gene expression omnibus (GEO) database were used to identify the correlation between SREBP1/ KLK8/ CCL22 in oral cancer prognosis. The molecular effects of GB on SAS, KYSE-510, and TE-1 cells were examined by RNA sequencing. Electrophoretic mobility shift assay was used to analyse SREBF1/KLK8 transcription promoter activity. SREBP1 and KLK8 genetic engineering or recombinant proteins were used to evaluate CCL22 expression and Treg chemotactic response. An MOC-2-implanted mouse model was used to evaluate the therapeutic effects of GB and genetic engineering conditions. Results: Web-based visualization platform and tissue array data showed that SREBP1 expression was negatively correlated with oral cancer prognosis and SREBP1 and KLK8 positively correlated (R = 0.4648, p < 0.001). In addition, in vivo, ex vivo and in vitro experiments demonstrated that GB treatment or SREBP1 knockdown inhibited cancer cells proliferation, migration and Tregs chemotaxis. Mechanistically, GB treatment or SREBP1 knockdown attenuated SREBP1-regulated transcription of KLK8, reducing CCL22 secretion. Conversely, treatment with U18666a or SREBP1 transfection reversed these effects. Conclusions: GB is a novel SREBP1 inhibitor that effectively prevents immune escape by oral cancer cells through modulation of the SREBP1/KLK8/CCL22 axis, presenting a promising new approach for oral cancer immunotherapy
Dyslipidemia progression and increased lung cancer risk: A prospective cohort study
No full text[[abstract]]ObjectivesTo investigate the associations of changes in lipidemic profile with the risk of lung cancer incidence, and to elucidate how modifiable risk factors contribute to the associations.Design and participantsThe prospective study enrolled a cohort of 137,075 individuals with lipidemic profiles spanning from January 1, 1996 to December 31, 2006 in the Taiwan MJ Cohort. Follow-up was extended from the second clinical visit until December 31, 2007, with an average duration of 6.3 years. Participants was divided into four groups based on alterations in their lipidemic profile within a 1-3 year interval subsequent to initial enrollment. The associations of changes in lipidemic profiles with the incidence of lung cancer were assessed with Cox proportional hazard models. Associations between modifiable risk factors and lipidemic profile changes were evaluated using multivariable logistic regression models.ResultsOf 137,075 participants with lipidemic profile, progression to dyslipidemia within a 3-year period was associated with elevated risks of lung cancer incidence (hazard ratio [HR] = 1.46; 95% CI: 1.01, 2.10) in comparison to persistent normolipidemic. However, reversion to normolipidemic did not contribute to a decreased lung cancer incidence risk (HR = 1.10; 95% CI: 0.74, 1.63), in comparison to persistent dyslipidemia. Body mass index and smoking as risk factors, along with physical activity as a protective factor, were associated with changes in lipidemic profile.ConclusionsWithin this large-scale cohort, progression to dyslipidemia emerged as a risk factor for lung cancer incidence, highlighting the significance of lipid control. The modifiable risk factors associated with dyslipidemia progression encompassed body mass index, physical activity, and smoking status, suggesting potential interventions targets