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30 results about "L929 cell" patented technology

L929/A cells can be used in the development of novel anti-cancer treatments. Resistance can be circumvented by modulating agents such as verapamil and quinine. The parent cell line L929 was derived from normal subcutaneous areolar adipose tissue.

Oligonucleotide antagonist for human tumor necrosis factor alpha (TNF-alpha)

The present invention relates to a group of new oligonucleotides sequences with human tumor necrosis factor α (TNF-α) inhibiting activity, which includes DNA sequences and RNA sequences. These oligonucleotides or aptamer can specifically be bound to TNF-α and inhibit the cytoxicity of TNF-α to L929 cells. Therefore, the aptamer of the present invention may be used to detect TNF-α and provide a therapeutic method for diseases related to the increasing level of TNF-α. Compared with other TNF antagonists such as monoclonal antibody and soluble receptor, the present invention has high specificity, high affinity, quick penetration to target tissue, rapid plasma clearance, and lower immunogenecity. Turthermore, it can be used repeatedly and keeps high concentration in target tissue and the like. It has the advantages of affinity and specificity similar to monoclonal antibodies and also has permeability and pharmacokinetics characteristics similar to small molecular polypeptide. The present invention also refers to derivative of the oligonucleotides sequence, including modified sequence. The present invention may further be manufactured as medicine for therapy and diagnosis of TNF-α related diseases.
Owner:STATION OF VIRUS PREVENTION & CONTROL CHINA DISEASES PREVENTION & CONTROL CENT

High-strength high-plasticity biodegradable Zn-Mn-Li zinc alloy and application thereof

Provided is high-strength high-plasticity biodegradable Zn-Mn-Li zinc alloy. The alloy comprises 0.01-0.8% of Mn and 0.005-0.4% of Li, wherein Mn is the main alloying element, Li is the minor alloyingelement, and the content of Mn is not lower than the content of Li in the alloy; at least one of Na, K, Ca, Sr, Ti, Mg, Fe, Cu and Ag is selected, wherein the content of Na and the content of K are both not higher than 0.1%, and the total content of Na, K and Li is not higher than 0.4%; the content of Ca, the content of Sr, the content of Ti and the content of Mg are all not higher than 0.2%, andthe total content of Ca, Sr, Ti and Mg is not higher than 0.2%; the content of Fe is not higher than 0.05%; the adding amount of Cu and the adding amount of Ag are not higher than 0.4%, and the totalcontent of Cu and Ag is not higher than 0.4%; and the total content of alloy elements added into the Zn-Mn-Li zinc alloy is not higher than 1.8%, and the balance Zn. The yield strength of the zinc alloy is 250-450 MPa, the tensile strength of the zinc alloy is 350-600 MPa, and the ductility is 20-60%; the degrading rate in simulated body fluid is not higher than 0.15 mm/year; the cytotoxicity tothe L929 cell is at the level 0 or level 1, and good cytocompatibility is presented. The zinc alloy is used for a degradable bracket or other medical implants.
Owner:北京尚宁科智医疗器械有限公司

Building method for autovaccine by aiming at human TNF(Tumor Necrosis Factor)-alpha molecule

InactiveCN102370979AMaintain immunogenicityRemove natural biological activityBacteriaAntipyreticL929 cellEscherichia coli
The invention discloses a building method for autovaccine in-vivo induced by aiming at human TNF(Tumor Necrosis Factor)-alpha molecule. With a step-by-step cloning method, a fusion gene of hTNF-TT830-844, hTNF-HEL46-61 and hTNF-PADRE is built; point mutation (T439-A,C440-G) is introduced into a natural human TNF gene to optimize a mRNA (Ribonucleic Acid) secondary structure; the fusion gene is cloned into a pET22b prokaryotic expression vector, and efficient expression is achieved in the bacterial strain of escherichia coli; three T accessory cell epitope peptides are introduced between the epitope peptide structure domains of hTNF by the computer-aided analysis and is fused with the hTNF-alpha to overcome the immunological tolerance of an organism for the autologous protein, and therefore the organism generates high-level humoral immune response; the generated high-level hTNF-alpha neutralizing polyclone antibody can neutralize killing activity of the hTNF-alpha on L929 cells in vitro; the hTNF-PADRE has the strongest immunogenicity; the high-level antibody can be induced under the condition of using no immunological adjuvant; and the vaccine has favorable protection and curing action on mouse models suffering from rheumatoid arthritis induced by the II-type collagen, cachexia and the like induced by LPS (lipopolysaccharide).
Owner:FOURTH MILITARY MEDICAL UNIVERSITY

Building method for autovaccine by aiming at human TNF(Tumor Necrosis Factor)-alpha molecule

InactiveCN102370979BMaintain immunogenicityRemove natural biological activityBacteriaAntipyreticEscherichia coliL929 cell
The invention discloses a building method for autovaccine in-vivo induced by aiming at human TNF(Tumor Necrosis Factor)-alpha molecule. With a step-by-step cloning method, a fusion gene of hTNF-TT830-844, hTNF-HEL46-61 and hTNF-PADRE is built; point mutation (T439-A,C440-G) is introduced into a natural human TNF gene to optimize a mRNA (Ribonucleic Acid) secondary structure; the fusion gene is cloned into a pET22b prokaryotic expression vector, and efficient expression is achieved in the bacterial strain of escherichia coli; three T accessory cell epitope peptides are introduced between the epitope peptide structure domains of hTNF by the computer-aided analysis and is fused with the hTNF-alpha to overcome the immunological tolerance of an organism for the autologous protein, and therefore the organism generates high-level humoral immune response; the generated high-level hTNF-alpha neutralizing polyclone antibody can neutralize killing activity of the hTNF-alpha on L929 cells in vitro; the hTNF-PADRE has the strongest immunogenicity; the high-level antibody can be induced under the condition of using no immunological adjuvant; and the vaccine has favorable protection and curing action on mouse models suffering from rheumatoid arthritis induced by the II-type collagen, cachexia and the like induced by LPS (lipopolysaccharide).
Owner:FOURTH MILITARY MEDICAL UNIVERSITY

A kind of high-strength and high-plastic biodegradable zn-mn-li series zinc alloy and its application

Provided is high-strength high-plasticity biodegradable Zn-Mn-Li zinc alloy. The alloy comprises 0.01-0.8% of Mn and 0.005-0.4% of Li, wherein Mn is the main alloying element, Li is the minor alloyingelement, and the content of Mn is not lower than the content of Li in the alloy; at least one of Na, K, Ca, Sr, Ti, Mg, Fe, Cu and Ag is selected, wherein the content of Na and the content of K are both not higher than 0.1%, and the total content of Na, K and Li is not higher than 0.4%; the content of Ca, the content of Sr, the content of Ti and the content of Mg are all not higher than 0.2%, andthe total content of Ca, Sr, Ti and Mg is not higher than 0.2%; the content of Fe is not higher than 0.05%; the adding amount of Cu and the adding amount of Ag are not higher than 0.4%, and the totalcontent of Cu and Ag is not higher than 0.4%; and the total content of alloy elements added into the Zn-Mn-Li zinc alloy is not higher than 1.8%, and the balance Zn. The yield strength of the zinc alloy is 250-450 MPa, the tensile strength of the zinc alloy is 350-600 MPa, and the ductility is 20-60%; the degrading rate in simulated body fluid is not higher than 0.15 mm / year; the cytotoxicity tothe L929 cell is at the level 0 or level 1, and good cytocompatibility is presented. The zinc alloy is used for a degradable bracket or other medical implants.
Owner:北京尚宁科智医疗器械有限公司

(S,R)-3-phenyl-4,5 dihydro-5-isoxazole acetic acid-nitric oxide and use thereof as anti-cancer and antiviral agent

The present invention relates to an isoxazole derivative, the compound of formula (I)herein after referred to as GIT27-NO, which is the NO-donating structurally modified form of (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid, herein after referred to as VGX-1027. Treatment of three tumor cell lines, rat astrocytoma C6, mouse fibrosarcoma L929, and mouse melanoma B16 cells with GIT27-NO resulted in a significant reduction of cell respiration and of number of viable cells, while VGX-1027 was completely ineffective. Hemoglobin, which act as NO-scavenger, restored cell viability, thus indicating the NO-mediated tumoricidal effect of compound (I). GIT27-NO triggered apoptotic cell death in L929 cell cultures, while autophagic cell death is mainly responsible for the diminished viability of C6 and B16 cells. Moreover, GIT27-NO induced the production of reactive oxygen species which can be neutralized by antioxidant N-acetyl cysteine (NAC), indicating that reactive oxygen species (ROS) are at least partly involved in the reduction of cell viability. The anti-tumor activity of GIT27-NO is mediated through activation of MAP kinases (ERK1 / 2, p38 and JNK) in cell-specific manner. The role of MAP kinases was further confirmed by specific inhibitors of these molecules, PD98059, SB202190, and SP600125. Finally, in vivo treatment with GIT27-NO significantly reduced tumor growth in syngeneic C57BL / 6 mice implanted with B16 melanoma.
Owner:ONCONOX

(s,r.)-3-phenyl-4,5 dihydro-5-isoxazole acetic acid-nitric oxide and use thereof as Anti-cancer and antiviral agent

The present invention relates to an isoxazole derivative, the compound of formula (I)
herein after referred to as GIT27-NO, which is the NO-donating structurally modified form of (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid, herein after referred to as VGX-1027.
Treatment of three tumor cell lines, rat astrocytoma C6, mouse fibrosarcoma L929, and mouse melanoma B16 cells with GIT27-NO resulted in a significant reduction of cell respiration and of number of viable cells, while VGX-1027 was completely ineffective. Hemoglobin, which act as NO-scavenger, restored cell viability, thus indicating the NO-mediated tumoricidal effect of compound (I). GIT27-NO triggered apoptotic cell death in L929 cell cultures, while autophagic cell death is mainly responsible for the diminished viability of C6 and B16 cells. Moreover, GIT27-NO induced the production of reactive oxygen species which can be neutralized by antioxidant N-acetyl cysteine (NAC), indicating that reactive oxygen species (ROS) are at least partly involved in the reduction of cell viability. The anti-tumor activity of GIT27-NO is mediated through activation of MAP kinases (ERK1/2, p38 and JNK) in cell-specific manner. The role of MAP kinases was further confirmed by specific inhibitors of these molecules, PD98059, SB202190, and SP600125. Finally, in vivo treatment with GIT27-NO significantly reduced tumor growth in syngeneic C57BL/6 mice implanted with B16 melanoma.
Owner:ONCONOX
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