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Panax ginseng exerts good neuroprotective activity at the cell and animal level, but the specific bioactive compounds and action mechanism are needed to be investigated, verified, and confirmed. In this work, affinity ultrafiltration (AUF), UPLC-QTOF-MS, and molecular docking were integrated into one strategy to screen, identify, and evaluate the bioactive compounds in ginseng at the molecular level. Three biological macromolecules (AChE, MAO-B, and NMDA receptor) were selected as the target protein for AUF-MS screening for the first time, and 16 potential neuroactive compounds were found with suitable binding degree. Then, the bioactivity of ginseng and its components were evaluated by AChE-inhibitory test and DPPH assay, and the data indicate that ginseng extract and the screened compounds have good neuroactivity. The interaction between the three targets and the screened compounds was further analyzed by molecular docking, and the results were consistent with a few discrepancies in comparison with the AUF results. Finally, according to the corresponding relation between component-target-pathway, the action mechanism of ginseng elucidated that ginseng exerts a therapeutic effect on AD through multiple relations of components, targets, and pathways, which is in good accordance with the TCM theory.
SINGAPORE – The Only Singapore Private Hospital to Achieve Success at Asian Hospital Management Awards 2016.
UNITED STATES – Study Finds Vision Loss Due to Diabetes Is Rising Globally.
UNITED STATES – How Sleep Deprivation Harms Memory.
UNITED KINGDOM – Plasticell and CellSpring Collaborate to Validate Osteogenic Cell Therapy and 3D Cell Culture Models for High Performance Drug Screening.
JAPAN – Takeda Announces Bold, New Access to Medicines Strategy.
THAILAND – Ministry of Public Health Embarks on eHealth in Thailand with VMware Virtualization and Mobility Solutions.
AUSTRALIA – Australian-led Global Sleep Apnea Medical Device Study Shows Treatment Improves Wellbeing but Without Any Cardiovascular Benefit.
RUSSIA – R-Pharm Produces Biological Drugs in Yaroslavl with GE Healthcare's FlexFactory™ Manufacturing Platform.
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Scientists in Guangzhou engineered pig model of Huntington’s disease
Heart-on-a-chip device to aid drug screening
Nanozymes to target tumor cells
Cancer stem cell therapy breakthrough
Hong Kong researchers invent antibody drug for HIV-I prevention
SNAB technology to mark tumor cells during cancer surgeries
Draft genome of tea plant sequenced
International Earth BioGenome Project proposed to sequence DNA of all known species on Earth
Chinese pharma regulatory reforms will help to attract foreign investment
Merck receives patent for CRISPR Technology in China
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Induced pluripotent stem (iPS) cells hold great promise for regenerative medicine and drug discovery. Since the invention of iPS technology, a central goal of this field has been to derive safer and better iPS cells for human research and therapeutic applications. From the first generation of iPS cells that were only partially pluripotent, through iPS cells that were capable of germ line transmission, to current iPS cells that can produce viable mice through tetraploid complementation, the accumulating knowledge gained through mouse models is expected to extend to humans for selection and characterization of fully pluripotent human iPS cell lines. Here we review the progress and strategies toward generating fully pluripotent iPS cells, discuss the potential of patient-specific iPS cells in disease modeling and drug discovery, and discuss the potential for novel gene therapy systems combined with iPS cell-based cell replacement therapy.
Mitotic arrest deficient 2 like 1 (MAD2L1) is a component of the mitotic spindle assembly checkpoint that prevents the onset of anaphase until all chromosomes are properly aligned at the metaphase plate, a process that confirms genomic stability. As several human cancers experience abnormal expression of such components, MAD2L1 has been studied in different human cancers owing to its oncogenic behavior. Here, we employed several omics-related tools to investigate the characteristics of MAD2L1 in a pan-cancer model of analysis, with a focus on its impact on the infiltration of multiple immune components in the tumor microenvironment as a mechanism allowing for tumor progression and poor patient survival. Our analysis revealed that MAD2L1 was significantly upregulated in several human tumors, and this upregulation was further confirmed at the protein level. In addition, a significant hypomethylation status of MAD2L1 was detected in multiple cancers compared with the corresponding controls. The consequences of this upregulation on tumor progression and clinical outcome were further assessed, where tumor stage, grade and metastasis were positively correlated with MAD2L1 overexpression in a panel of tumors. Moving to the immune interaction, our analysis demonstrated that MAD2L1 significantly increased the infiltration of the myeloid-derived suppressor cells (MDSCs) and reduced the infiltration of tumor-attacking natural killer (NK) cells. Furthermore, MAD2L1 expression positively correlated with the expression of exhaustion markers and immunosuppressive chemokines. Owing to its role in tumor progression, we detected MAD2L1 as a target for anticancer therapy, where high-throughput screening (HTS) was performed to identify possible inhibitors that could act as antitumor drugs. Our screening process identified nine FDA-approved drugs with favorable binding energies (>−7 kcal/mol) among the 3180 compounds examined. Meropenem, Glipizide and Dolutegravir were particularly promising candidates, showing distinctive interactions within the active pocket of MAD2L1. Here, we describe the stages and output of our multi-omics analysis with a drug screening assessment.
The application of three-dimensional (3D) spheroids or organoids in drug testing and precision medicine has led to significant advancements in how cancer and other diseases are treated. Not only can these 3D structures mimic the architecture and structure of tumors, but organoids formed from primary patient samples are able to recapitulate the molecular and functional characteristics of the original patient tumors. These clinically and physiologically relevant organoids can therefore be used to address questions related to drug efficacy and resistance and can even be used to predict patient-specific drug responses. However, despite such evident advantages, the lack of a patient-specific tumor microenvironment (TME), or even the basic TME that includes sufficient immune cells and other cell types, limits the potential of these organoids in immunotherapy drug testing. As such, co-culture models of patient-derived organoids with immune cells have since been developed to explore cancer-immune interactions, monotherapy or combinatorial immunotherapy drug testing, and variable patient drug responses. Moreover, when coupled with artificial intelligence-driven platforms, these organoid models can be more efficiently utilized to identify better therapeutic options and improve health outcomes through precision medicine. This review aims to highlight the use of organoids and the broader implementations of such organoid models in functional precision medicine, particularly in the context of immunotherapy.