35 results about "CXCL1" patented technology

We disclose a new and useful biomarker for acute kidney injury (i.e., AKI), renal ischemia reperfusion injury (i.e., IRI), ischemic acute kidney injury, and / or ischemic acute tubular necrosis (i.e., ATN). The biomarker is GRO-alpha (i.e., CXCL1, chemokine C-X-C ligand 1, GRO1, GROa, MGSA, MGSA alpha, MGSA-a, NAP-3, SCYB1). We detected the biomarker using a QUANTIKINE® human GRO-alpha immunoassay (Cat. No. DGR00, R & D Systems, Minneapolis, Minn.). In addition, we disclose a method of treating lung damage.

It has been discovered that cytokines, chemokines, and growth factors in urine are biomarkers indicative of urological disorders including interstitial cystitis / painful bladder syndrome and overactive bladder syndrome. Preferred chemokine biomarkers are CCL2, CCL4 (MIP-1β), CCL11, CXCL1 (GRO-α), sCD40L, IL-12p70 / p40, IL-5, sIL-2Rα, IL-6, IL-10, IL-8, and EGF. The concentration of one or more of these chemokines in an urine sample can be used to assist in the diagnosis of urological disorders. Methods for evaluating the effectiveness of treatments for urological disorders and for assessing the severity of urological disorders are also provided.

Emphysema and COPD are diagnosed, and the efficacy of therapeutic drug candidates for the treatment of emphysema and / or COPD is evaluated, by determining biomarkers selected from the group SpB, desmosine, VEGF, IGFBP2, MMP12, TIMP1, MMP9, Crabp2, Rbp1, Cyp26a1, Tgm2, Timp3, Adam17, Serpina1, Slpi, Col1a1, Eln, TGFβ1, TGFβ-RII, Sftpa1, Csf2, Cxcl1, Cxcl2, Cxcl5, IL-8Rβ, IL-8Rα, IL-6, TNF, EGF-R, Areg, PDGFα, HpGF, FGF7, Kdr, flt1, Angpt1, Tek, HIF1α, Hyou1, PGF, and tropoelastin.

An object of the present invention is to detect a human CXCL1 protein with high sensitivity. An immunoassay method is provided for a human CXCL1 protein, by which human CXCL1 or a fragment thereof in a sample is measured using two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof, wherein:each of the two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof specifically recognizes any one of sequence regions of the amino acid sequences shown in SEQ ID NOS: 1-3, which are partial sequences of the amino acid sequence composing a human CXCL1 protein; andthe two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof specifically recognize sequence regions that differ from each other.Monoclonal antibodies or fragments thereof are provided, each of which specifically recognizes any one sequence region of the amino acid sequences shown in SEQ ID NOS: 1-3 and has a new amino acid sequence.

The invention provides methods for predicting the efficacy of anti-TNF and anti-IL17 combination therapies in the treatment of a subject suffering from inflammatory disease by determining the level CXCL1 and / or CXCL5 markers in a sample derived from the subject.

The application concerns means for determining the stage of hepatic tissue damage, in particular the hepatic fibrosis score of subjects infected with one or more hepatitis viruses. In particular, the means of the invention involve measuring the levels of expression of selected genes, said selected genes being:SPP1, andat least one gene from among A2M and VIM, andat least one gene from among IL8, CXCL10 and ENG, andoptionally, at least one gene from among the list of the following sixteen genes: IL6ST, p14ARF, MMP9, ANGPT2, CXCL11, MMP2, MMP7, S100A4, TIMP1, CHI3L1, COL1A1, CXCL1, CXCL6, IHH, IRF9 and MMP1.

The invention provides methods for predicting the efficacy of anti-TNF and anti-IL17 combination therapies in the treatment of a subject suffering from inflammatory disease by determining the level CXCL1 and / or CXCL5 markers in a sample derived from the subject.

The invention provides methods for predicting the efficacy of anti-TNF and anti-IL-17 combination therapies in the treatment of a subject suffering from inflammatory disease by determining the level LIF, CXCL1, CXCL2, CXCL4, CXCL5, CXCL8, CXCL9, CXCL10, CCL2, CCL23, IL-1β, IL-1Ra, TNF, IL-6, IL-10, IL-17A, IL-17F, IL-21, IL-22, IFNγ, CXCR1, CXCR4, CXCR5, GM-CSF, GM-CSFR, G-CSF, G-CSFR protein or nucleic acid, or a homolog, portion or derivative thereof markers in a sample derived from the subject.

The invention discloses a system for multi-index combined diagnosis of ovarian cancer and / or non-ovarian malignant tumors. The system for auxiliary diagnosis of the ovarian cancer and / or non-ovarian derived malignant tumors includes a system for detection of the content of six proteins in serum, wherein the six proteins comprise CCL18, CXCL1, a C1D IgG type self antibody, a TM4SF1 IgG type self antibody, an FXR1 IgG type self antibody and a TIZ IgG type self antibody; the non-ovarian malignant tumors comprise breast cancer, liver cancer or lung cancer. The system has relatively high diagnostic efficiency for ovarian cancer, breast cancer, liver cancer and lung cancer.

This invention relates to a method for detecting in vitro a urothelial cancer, comprising measuring CXCL1 protein, or expression of a gene encoding the protein, in a biological sample from a subject, and to a kit for diagnosing a urothelial cancer comprising an antibody or nucleic acid probe, which is capable of binding specifically to the CXCL1 protein or a gene encoding the protein, respectively.

The invention belongs to the fields of biotechnology and medicine, and relates to an inhibitor capable of inhibiting the excessive proliferation of keratinocytes, an inhibitor composition, and applications of the inhibitor. The inhibitor taking triptolide, triptonide or tripterine as the representative can inhibit the excessive proliferation of the keratinocytes, specifically, the expression levels of STAT1 and p-STAT1 can be inhibited, then the expression level of miR-17-92mRNA is down-regulated, then, miR-17-92 target gene CDKN2B is regulated, the secretion levels of inflammatory factors CXCL1, CXCL10, CXCL16 and IL-6 in cells are inhibited, and finally, the cell cycle progression and immune function abnormity are inhibited; triptolide, tripterine and triptonide can effectively inhibit the proliferation of the keratinocytes, and the effective doses respectively achieve 60nM, 100nM and 80nM.

The invention refers to a method for identifying senescent mesenchymal stem cells growing in in vitro culture, comprising: measuring the length of chromosome telomeres, determining the level of ploidy in the cell, detecting the presence of multipolar mitosis and determining the level of expression of the genes SCIN, AKAP9, EDN-1, CXCL1, CXCL12 and / or CD70. This method can be used for performing genetic stability studies in mesenchymal stem cell cultures, enabling identification and selection of the most stable and appropriate cells for use in cell therapy.

We disclose a new and useful biomarker for acute kidney injury (i.e., AKI), renal ischemia reperfusion injury (i.e., IRI), ischemic acute kidney injury, and / or ischemic acute tubular necrosis (i.e., ATN). The biomarker is GRO-alpha (i.e., CXCL1, chemokine C-X-C ligand 1, GRO1, GROa, MGSA, MGSA alpha, MGSA-a, NAP-3, SCYB1). We detected the biomarker using a QUANTIKINE® human GRO-alpha immunoassay (Cat. No. DGR00, R & D Systems, Minneapolis, Minn.). In addition, we disclose a method of treating lung damage.

The present invention provides a method for screening anti-breast cancer metastasis compounds by using a tumor metastasis gene map. The method comprises: randomly selecting at least one gene from 18 genes such as MMP1, FSCN1, PTGS2, EREG, ANGPTL4, VCAM1, CXCR4, CXCL1, RARRES3, ID1, TNC, LY6E, LTBP1, C10orf116, KRTHB1, KYNU, MAN1A1 and NEDD9; and designing probes, and selecting compounds for converting the expression levels of the genes in breast cancer cells after metastasis to the expression levels of the genes in in-situ carcinoma cells or normal cells. According to the present invention, the 20 compounds are selected through the method, and the cytological level and animal level experiment results demonstrate that the compounds or the combinations thereof exhibit the anti-breast cancermetastasis activity to different degrees.

An object of the present invention is to detect a human CXCL1 protein with high sensitivity. An immunoassay method is provided for a human CXCL1 protein, by which human CXCL1 or a fragment thereof in a sample is measured using two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof, wherein:each of the two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof specifically recognizes any one of sequence regions of the amino acid sequences shown in SEQ ID NOS: 1-3, which are partial sequences of the amino acid sequence composing a human CXCL1 protein; andthe two or more types of anti-human CXCL1 monoclonal antibodies or fragments thereof specifically recognize sequence regions that differ from each other.Monoclonal antibodies or fragments thereof are provided, each of which specifically recognizes any one sequence region of the amino acid sequences shown in SEQ ID NOS: 1-3 and has a new amino acid sequence.

The invention provides a detecting reagent knit used for detecting an early oophoroma diagnosis, which is composed of a ninety-six-hole polystyrene ELISA plate, a peroxydase labeled object, a mouse anti-human CCL18 single clone antibody, a mouse anti-human CXCL1 single clone antibody, a rabbit anti-human CCL18 polyclonal antibody, a rabbit anti-human CXCL1 polyclonal antibody, a development liquid, a stopping liquid, a titer and a cover board film. The reagent knit uses an oophoroma serum marker CCL18 and an oophoroma serum marker CXCL2. The reagent knit can be used for detecting benign and malign ovarian tumors, especially detecting early oophoroma.

The present invention provides a method for predicting the treatment response to anti-cancer immunotherapy of a mammalian cancer patient, the method comprising: a) measuring the gene expression of at least 2 the following cancer promoting genes: PTGS2, VEGFA, CCL2, IL8, CXCL2, CXCL1, CSF3, IL6, IL1B and IL A in a sample obtained from the tumour of the patient; b) measuring the gene expression of at least 2 of the following cancer inhibitory genes: CXCL11, CXCL10, CXCL9, CCL5, TBX21, EOMES, CD8B, CD8A, PRF1, GZMB, GZMA, STAT1, IFNG, IL12B and IL12A in a sample obtained from the tumour of the patient; c) computing a ratio of the gene expression of said at least 2 cancer promoting genes and the gene expression of said at least 2 cancer inhibitory genes; and d) making a prediction of the treatment response and / or prognosis of the patient based on the gene expression ratio computed in step c). Also provided are related methods for stratifying patients and for treating patients, including with immune checkpoint blockade therapy.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and / or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

The invention discloses a screening method and application of a gene marker for predicting the treatment response of Crohn's disease. According to the technical scheme, the gene markers (TLR2, TREM1, CXCL1, FPR1 and FPR2) which can be used for predicting primary drug resistance of anti-TNF alpha drug treatment of patients with the Crohn disease are screened through the scheme of the invention, and a more powerful weapon can be provided for precise medication and clinical management of the patients with the Crohn disease and even patients with the inflammatory bowel disease.

The present invention provides a method for predicting the treatment response to anti-cancer immunotherapy of a mammalian cancer patient, the method comprising: a) measuring the gene expression of atleast 2 the following cancer promoting genes: PTGS2, VEGFA, CCL2, IL8, CXCL2, CXCL1, CSF3, IL6, IL1B and IL1A in a sample obtained from the tumour of the patient; b)measuring the gene expression of atleast 2 of the following cancer inhibitory genes: CXCL11, CXCL10, CXCL9, CCL5, TBX21, EOMES, CD8B, CD8A, PRF1, GZMB, GZMA, STAT1, IFNG, IL12B and IL12A in a sample obtained fromthetumour of the patient; c) computing a ratio of the gene expression of said at least 2 cancer promoting genes and the gene expression of said at least 2 cancer inhibitory genes; and d) making a prediction of the treatment response and / or prognosis of the patient based on the gene expression ratio computed in step c). Also provided are related methods for stratifying patients and for treating patients, including withimmune checkpoint blockade therapy.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and / or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and / or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and / or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

Provided are a method for screening agents for the prevention or treatment of diseases caused by interleukin 6, interleukin 13, TNF, G-CSF, CXCL1, CXCL2, or CXCL5 and an agent for the prevention or treatment of diseases caused by interleukin 6, interleukin 13, TNF, G-CSF, CXCL1, CXCL2, or CXCL5. A method for screening agents for the prevention or treatment of diseases caused by interleukin 6, interleukin 13, TNF, G-CSF, CXCL1, CXCL2, or CXCL5 having as the index at least one selected from the group consisting of changes in the expression of the MEX3B gene or MEX3B protein and changes in the function of the MEX3B protein.

This invention relates to a method for detecting in vitro a urothelial cancer, comprising measuring CXCL1 protein, or expression of a gene encoding the protein, in a biological sample from a subject, and to a kit for diagnosing a urothelial cancer comprising an antibody or nucleic acid probe, which is capable of binding specifically to the CXCL1 protein or a gene encoding the protein, respectively.

The invention discloses applications of sodium ferulate and expression of CXCL1 genes controlled by sodium ferulate in a mechanism for preventing and controlling atherosclerosis, and relates to a protective effect of sodium ferulate on a human umbilical vein endothelial cell (HUVEC) strain damaged by oxidized low-density lipoprotein (Ox-LDL), and discusses an action mechanism. Human umbilical vein endothelial cells are used to carry out experiments, influences of sodium ferulate on proliferation, migration and apoptosis of HUVEC treated by the oxidized low-density lipoprotein are determined by MTT, scratch test, flow cytometry and confocal microscopy; total RNA of the cells are extracted; marked hybrid experiments are carried out by using a CapitalBio whole-genome chip; differential genes are screened out by analyzing differential expression genes through clustering analysis, GO function and enrichment degree and pathway association degree, so that a gene expression spectrum can be obtained; and transcription and translation of the expressed differential genes in the HUVEC are detected by adopting a real-time quantitative PCR method. The results demonstrate that sodium ferulate can regulate CXCL1 gene expression downwards and has an obvious protective effect on the HUVEC damaged by Ox-LDL.