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公开(公告)号:US20230391810A1
公开(公告)日:2023-12-07
申请号:US17805747
申请日:2022-06-07
发明人: Chung Hang LEUNG , Dik Lung MA , Ligen LIN , Guodong LI , Chung Nga KO , Dan LI , Chao YANG
CPC分类号: C07F15/0033 , C07F15/0073 , A61P17/02
摘要: Method of inhibiting a protein-protein interaction between Von Hippel-Lindau tumor-suppressor protein and hypoxia-inducible factor 1-alpha useful in the treatment of angiogenesis-related diseases and promoting wound healing.
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公开(公告)号:US20220392199A1
公开(公告)日:2022-12-08
申请号:US17819777
申请日:2022-08-15
申请人: BEIJING BAIDU NETCOM SCIENCE TECHNOLOGY CO., LTD. , State Key Laboratory of Internet of Things for Smart City (University of Macau)
发明人: Kafeng WANG , Chengzhong XU , Haoyi XIONG , Xingjian LI , Dejing DOU
IPC分类号: G06V10/774 , G06V10/764 , G06V10/82 , G06V10/778
摘要: A method and an apparatus for training a classification model and data classification includes: obtaining a sample set and a pre-trained classification model, wherein the classification model includes at least two convolutional layers, each convolutional layer is connected to a classification layer through a fully connected layer; inputting the sample set into the classification model, and obtaining a prediction result output by each classification layer, wherein the prediction result includes a prediction probability of a class to which each sample belongs; calculating a probability threshold of each classification layer based on the prediction result output by each classification layer; setting a prediction stopping condition for the classification mode according to the probability threshold of each classification layer.
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公开(公告)号:US11517904B2
公开(公告)日:2022-12-06
申请号:US16416337
申请日:2019-05-20
申请人: University of Macau
发明人: Yanwei Jia , Liang Wan , Cheng Dong , Haoran Li , Tianlan Chen , Pui-In Mak , Rui Paulo da Silva Martins
IPC分类号: C12Q1/68 , B01L7/00 , C12Q1/686 , B01L3/00 , G01N27/447
摘要: Provided is a digital microfluidic device for quick polymerase chain reaction. The digital microfluidic device includes an enclosed chamber for holding droplets comprising PCR mixtures. The chamber has an upper layer and a lower layer, which provide a top heater and a bottom heater contained in a thermal electrode respectively to form dual heaters. The lower layer further has an array of electrodes and a dielectric layer, e.g. Norland Optical adhesive 61, coating thereon. Such arrangement of the digital microfluidic device allows quick and homogeneous heating of droplets to lower the heating voltage, shorten the reaction time, and prevent the dielectric layer from breakdown during the thermal cycle.
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4.
公开(公告)号:US20220184133A1
公开(公告)日:2022-06-16
申请号:US17258726
申请日:2020-07-17
申请人: UNIVERSITY OF MACAU
发明人: Renhe XU , Roma Pradeep BORKAR , Dejin ZHENG , Enqin LI
IPC分类号: A61K35/28 , C12N5/0775 , A61P17/02
摘要: The present disclosure discloses use of mesenchymal stem cells in preparation of a formulation for promoting fat transplantation, relating to the field of biotechnologies. The inventors found through research that compared with MSCs derived from somatic cells, MSCs derived from human pluripotent stem cells have more stable quality, are not affected by donor's physical quality, disease and treatment process, and can promote fat transplantation by enhancing tissue remodeling, angiogenesis and adipose cell survival and decreasing tissue fibrosis.
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公开(公告)号:US11098281B2
公开(公告)日:2021-08-24
申请号:US16041518
申请日:2018-07-20
申请人: University of Macau
IPC分类号: C12N5/00 , C12N5/0775 , A61K9/00 , A61K35/28
摘要: A method of differentiating pluripotent stem cells into mesenchymal stem cells, a culture medium used in the method of differentiating pluripotent stem cells into mesenchymal stem cells and a method of performing tissue and organ regeneration by using the mesenchymal stem cells obtained by differentiation using the method of differentiating pluripotent stem cells into mesenchymal stem cells are provided. The method of differentiating pluripotent stem cells into mesenchymal stem cells comprises differentiating, completely under 3D suspension conditions, pluripotent stem cells into trophoblast-like cells using BMP4 and A8301, and then differentiating the trophoblast-like cells into mesenchymal stem cells. Neither of two differentiation processes needs passaging or replacement of a culture container.
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公开(公告)号:US10858441B2
公开(公告)日:2020-12-08
申请号:US16033654
申请日:2018-07-12
申请人: UNIVERSITY OF MACAU
发明人: Hang Fai Kwok , Ruiyu Xie
IPC分类号: C07K16/28 , A61K31/7068 , A61K31/519 , A61K31/517 , A61K39/395 , A61K31/437 , A61P35/00 , A61K31/513 , A61K39/00 , A61K31/282
摘要: Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of tumor amongst all human cancers due to late diagnosis and resistant to treatment with chemotherapy and radiation. Preclinical and clinical studies have revealed that ErbB family for example epidermal growth factor receptor (EGFR) is a validated molecular target for pancreatic cancer prevention and therapy. The ErbB signaling cascade is regulated by a member of the ADAM (a disintegrin and metalloprotease) family, namely ADAM17, by enzymatic cleavage of precursor ligands into soluble cytokines and growth factors. Mouse genetic studies have demonstrated that ADAM17 is required for PDAC development. In this study, we evaluated the anti-tumor effects of A9(B8) IgG—the first specific ‘human and mouse cross-reactive’ ADAM17 inhibitory antibody on pancreatic malignant transformation. We found that inhibition of ADAM17 with A9(B8) IgG efficiently suppressed the shedding of ADAM17 substrates both in vivo and in vitro. Furthermore, we demonstrated that administration of A9(B8) IgG significantly suppressed motility in human pancreatic cancer cells and also significantly delayed tumorigenesis in the Pdx1Cre;KrasG12D;Trp53fl/+ PDAC mouse model. Inhibition of ADAM17 with A9(B8) IgG particularly affected the progression of pre-invasive pancreatic lesions to advanced PDAC in mice. Taken together, the preclinical data presented here will provide a starting point for clinical applications of ADAM17 targeted therapy.
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公开(公告)号:US10756643B2
公开(公告)日:2020-08-25
申请号:US15821862
申请日:2017-11-24
申请人: University of Macau
摘要: A flipping-capacitor rectifier circuit that enhances an output power of a piezoelectric energy harvester (PEH). The flipping-capacitor rectifier circuit includes a flipping capacitor, a plurality of switches, and an active rectifier. The flipping capacitor is connected in parallel with the PEH and forms at least three reconfiguration phases by turning on one or more of the switches. The active rectifier connects with the flipping capacitor in parallel and rectifies an AC voltage of the PEH. The flipping capacitor flips a voltage across a capacitor of the PEH to enhance the output power of the PEH by extracting power from the capacitor of the PEH.
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8.
公开(公告)号:US20190015505A1
公开(公告)日:2019-01-17
申请号:US16032482
申请日:2018-07-11
申请人: UNIVERSITY OF MACAU
发明人: Hang Fai KWOK
IPC分类号: A61K39/395 , C07K16/40 , A61P9/12 , A61K45/06
摘要: Angiotensin II (AngII) has been strongly implicated in hypertension and its complications. Evidence suggests the mechanisms by which angiotensin II (AngII) elevates blood pressure and enhances cardiovascular remodeling and damage may be distinct. However, the signal transduction cascade by which AngII specifically initiates cardiovascular remodeling such as hypertrophy and fibrosis remains insufficiently understood. In vascular smooth muscle cells, a metalloproteinase ADAM17 mediates epidermal growth factor receptor (EGFR) transactivation, which may be responsible for cardiovascular remodeling but not hypertension induced by AngII. Thus, the objective of this study was to test the hypothesis that activation of vascular ADAM1.7 is indispensable for vascular remodeling but not for hypertension induced by AngII. Vascular ADAM17 deficient mice and control mice were infused with AngII for 2 weeks. Control mice infused with Angti showed cardiac hypertrophy, vascular medial hypertrophy and perivascular fibrosis. These phenotypes were prevented in vascular ADAM17 deficient mice independent of blood pressure alteration. AngII infusion enhanced ADAM17 expression, EGFR activation and ER stress in the vasculature, which were diminished in ADAM17 deficient mice. Treatment with a human cross-reactive ADAM17 inhibitory antibody also prevented cardiovascular remodeling and ER stress but not hypertension in C57B1/6 mice infused with AngII. In vitro data further supported these findings. In conclusion, vascular ADAM17 mediates AngThinduced cardiovascular remodeling via EGFR activation independent of blood pressure regulation. ADAM17 seems to be a unique therapeutic target for the prevention of hypertensive complications.
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公开(公告)号:US10016759B2
公开(公告)日:2018-07-10
申请号:US14683316
申请日:2015-04-10
申请人: University of Macau
发明人: Cheng Dong , Tianlan Chen , Jie Gao , Yanwei Jia , Pui-In Mak , Mang-I Vai , Rui Paulo da Silva Martins
IPC分类号: B01L3/00 , G01N27/447
CPC分类号: B01L3/502784 , B01L2200/143 , B01L2300/025 , B01L2300/0887 , B01L2400/0427
摘要: According to one aspect of the present disclosure, a control-engaged electrode-driving method for droplet actuation is provided. The method includes, a first pulse is provided to a first electrode for kicking off a droplet till a centroid of the droplet reaching a centroid of the first electrode. A second pulse is provided to a second electrode when a leading edge of the droplet reaching the second electrode.
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公开(公告)号:US09673781B2
公开(公告)日:2017-06-06
申请号:US14884860
申请日:2015-10-16
申请人: University of Macau
IPC分类号: H04B1/00 , H04J11/00 , H03H11/04 , H03H19/00 , H03H11/12 , H03F1/02 , H03F3/19 , H03F3/45 , H04B1/16 , H03B5/12
CPC分类号: H03H11/0472 , H03B5/1237 , H03B5/1246 , H03B2202/06 , H03F1/0205 , H03F3/19 , H03F3/45076 , H03F2200/294 , H03F2200/451 , H03H11/1291 , H03H19/002 , H03H19/004 , H03H2011/0483 , H03H2210/025 , H04B1/16 , H04B1/1638
摘要: According to another aspect of the present disclosure, a radio-frequency-to-baseband-function-reuse receiver with shared amplifiers for common-mode and differential-mode amplification is provided. The receiver includes two set networks connected in parallel. The set networks includes a first and a second input capacitors, a first and a second output capacitors, a first transconductance amplifier having an input terminal, a second transconductance amplifier having an input terminal, a first switch, and a second switch. The first and the second input capacitors connect to a first node. The first and the second output capacitors connect to a second node. The first transconductance amplifier connects between the first input capacitor and the first output capacitor. The second transconductance amplifier connects between the second input capacitor and the second output capacitor. The first switch connects between the input terminal of the first transconductance amplifier and the second node. The second switch connects between the input terminal of the second transconductance amplifier and the second node.
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