76 results about "Synovial tissue" patented technology

Systems and methods for securing a screen-type active electrode to the distal tip of an electrosurgical device used for selectively applying electrical energy to a target location within or on a patient's body. A securing electrode is disposed through the screen electrode and mechanically joined to an insulative support body while also creating an electrical connection and mechanical enagement with the screen electrode. The electrosurgical device and related methods are provided for resecting, cutting, partially ablating, aspirating or otherwise removing tissue from a target site, and ablating the tissue in situ. The present methods and systems are particularly useful for removing tissue within joints, e.g., synovial tissue, meniscus, articular cartilage and the like.

Systems and methods for securing a screen-type active electrode to the distal tip of an electrosurgical device used for selectively applying electrical energy to a target location within or on a patient's body. A securing electrode is disposed through the screen electrode and mechanically joined to an insulative support body while also creating an electrical connection and mechanical enagement with the screen electrode. The electrosurgical device and related methods are provided for resecting, cutting, partially ablating, aspirating or otherwise removing tissue from a target site, and ablating the tissue in situ. The present methods and systems are particularly useful for removing tissue within joints, e.g., synovial tissue, meniscus, articular cartilage and the like.

Compositions and methods are provided for treatment of cartilage defects in animals and humans. The compositions of the invention include synovial tissue, synovial cells and matrices containing synovial (or cambium) tissue or cells for use in filling a cartilage defect. The matrix and synovial tissue or cell preparations may also contain a proliferation agent, transforming factor or other active agents to promote healing. A controlled-release delivery system may be used to administer the transforming factor. The compositions of the invention also include a synovial covering membrane or devitalized fascial sheet for covering the cartilage defect. The methods of this invention are those in which a minimally invasive surgical intervention is performed to remove a small portion of synovial membrane from a joint. Portions of the synovial membrane, or cells expanded in vitro, are implanted alone or within a matrix, into the defect site, where they produce new cartilage tissue and repair the defect. Alternatively, partially transformed synovial-derived tissue may be formed in situ and implanted into the defect site.

Systems and methods for securing a screen-type active electrode to the distal tip of an electrosurgical device used for selectively applying electrical energy to a target location within or on a patient's body. A securing electrode is disposed through the screen electrode and mechanically joined to an insulative support body while also creating an electrical connection and mechanical engagement with the screen electrode. The electrosurgical device and related methods are provided for resecting, cutting, partially ablating, aspirating or otherwise removing tissue from a target site, and ablating the tissue in situ. The present methods and systems are particularly useful for removing tissue within joints, e.g., synovial tissue, meniscus, articular cartilage and the like.

A method for in situ repair of meniscal injuries comprising induction of meniscal repair and regeneration by introducing an adhesive collagen-polyethylene glycol (PEG) hydrogel to a site of injury alone, supplemented with a synovial tissue or in conjunction with a support matrix.

A method for in situ repair of meniscal injuries comprising induction of meniscal repair and regeneration by introducing an adhesive collagen-polyethylene glycol (PEG) hydrogel to a site of injury alone, supplemented with a synovial tissue or in conjunction with a support matrix.

The present invention relates to a mathematical and computer model of a joint. The model includes representation of the biological processes related to the synovial tissue and cartilage. In one embodiment, the model represents a human joint afflicted with rheumatoid arthritis.

The invention discloses PLAC1 (placenta-specific 1) genes which can serve as a molecular marker for early diagnosis of osteoarthritis. Expressions of the PLAC1 genes in synovial tissue of a normal person and a patient suffering from osteoarthritis prove to be different in terms of the transcriptional level and the protein level, and accordingly, the disease risk and the disease state of a subject can be judged according to the identified expression level of the PLAC1 genes. Additionally, experiments prove that interference to expression of the PLAC1 genes or inhibition on the function of PLAC protein can inhibit proliferation of synovial cells, and a new target is provided for development of medicines for treating osteoarthritis clinically.

The present invention provides methods for reducing, reversing or inhibiting neovascularization in a tissue of a mammalian subject having a pathological condition involving neovascularization by administration in vivo of nanoceria particles (cerium oxide nanoparticles) to the subject. The method of the invention is useful, for example, for reducing, treating, reversing or inhibiting neovascularization in ocular tissue such as the retina, macula or cornea; in skin; in synovial tissue; in intestinal tissue; or in bone. In addition, the method of the invention is useful for reducing or inhibiting neovascularization in a neoplasm (tumors), which can be benign or malignant and, where malignant, can be a metastatic neoplasm. As such, the invention provides compositions, which contain nanoceria particles and are useful for reducing, treating, reversing or inhibiting angiogenesis in a mammalian subject.

The present invention is directed to the inhibition of pathological angiogenesis in different tissues such as cancer, tumor, retinal or synovial tissue. It has been shown that over expression of RB2 / p130 modulates the angiogenetic balance. It has been further shown that induction of RB2 / p130 expression using a tetracycline-regulated gene expression system as well as viral-mediated gene delivery inhibits angiogenesis in vivo via pRb2 / p130-mediated down-regulation of vascular endothelial growth factor (VEGF) protein expression in vivo.

The invention relates to a surface finishing method of an artificial ligament. The surface finishing method mainly comprises the following steps: (1) a deep cleaning procedure of an artificial ligament fabric, (2) a peroxidation procedure of a fiber surface, (3) a graft polymerization procedure of the fiber surface, (4) a rewashing procedure and (5) a sectional coating procedure. The surface finishing method is characterized in that by utilizing a multi-step ultrasonic / lotion cooperative treatment manner, a relatively good surface can be obtained; by utilizing an ozone / ultraviolet combined oxidation method, the grafting efficiency is beneficially improved, and the generation of homopolymers is reduced; a grafted hydrophilic polymer layer is of a three-dimensional network-shaped gellike structure, so that a relatively good environment is provided for the development of cells; by carrying out rewashing, the surface of the ligament fabric is relatively clean, and the adhesion, growth and proliferation of the cells are promoted; by sectionally coating a biochemical reagent and a mineralization coating layer, the growth of autologous synovial tissues is easily induced by a ligament joint cavity segment, and the ligament autogeny is beneficially carried out; and the osteogenic property of a bone tunnel segment is enhanced, and the healing of the ligament and bones is relatively good.

Method of diagnosing persistent, chronic synovitis and progressive joint degradation in the joint of a mammal. The method including providing a test sample comprising synovial fluid, cell or tissue from the joint of a mammal; detecting the presence of bacterial DNA, measuring the concentration of one or more biomarkers being cathepsin K, MMP-2 and -9, cathepsin S, tartrate-resistant acid phosphatase, invariant chain, CD4+ T-lymphocytes, CD8+ T-lymphocytes, CD44+ mononuclear cells, Toll-like receptor-2, Toll-like receptor-9, or a combination thereof; and, comparing the concentration of the biomarker from the test sample to a corresponding biomarker concentration in a control sample from healthy dogs, or an internal PBMC control sample, wherein a statistically significant elevated concentration of the biomarker in the test sample indicates that the mammal's joint is diseased.

The invention relates to the field of biotechnology, and provides an aptamer specifically targeting to inflammatory synovial cells of human rheumatoid arthritis (RA), wherein the aptamer has a nucleotide sequence shown as SEQ ID NO.1. The invention further provides applications of the aptamer in preparing a biological probe for identifying the inflammatory synovial cells and applications of the aptamer in preparing medicines or medicine carriers for resisting rheumatoid arthritis in a targeting manner. The aptamer has high selectivity for the inflammatory synovial cells, and the combination with hepatic cells is eliminated or weakened. The biological probe containing the aptamer can identify in-vitro human inflammatory synovial cells, such as the inflammatory synovial cells in a synovial tissue slice of an RA patient, and thus a basis is provided for the clinical diagnosis and targeting therapy of RA.

The invention relates to a preparation method of a decellularized tendon or ligament bracket, and aims at providing a decellularized tendon or ligament collagen fiber material with good biomechanical characteristic and good biocompatibility. The preparation method comprises the following steps: acquiring animal tendon or ligament with the adventitia or synovial tissue removed, wherein during the whole decellularization process, a mixed protecting liquid containing a ligament or tendon support structure protective agent is adopted; pre-separating cells in the ligament or tendon tissue by adopting a high hydrostatic pressure technology; digesting the residual cell nuclei by adopting a compound nuclease method; removing loose broken cell sheets by adopting a detergent; and carrying out rinsing by adopting the mixed protecting liquid. Through the efficient physical means, the adoption of small amount of enzyme and the detergent removing means, the cellular constituent in the ligament or tendon can be sufficiently removed, and the protecting liquid is adopted for the whole-process protection, so that on the basis of guaranteeing the complete removal of the cell nuclei, while the immunogenicity of the tendon or ligament tissue is reduced to the maximum, the three-dimensional structure and arrangement polarity of the normal collagenous fibers of the tendon or ligament tissue are reserved.

Compositions and methods are provided for treatment of cartilage defects in animals and humans. The compositions of the invention include synovial tissue, synovial cells and matrices containing synovial (or cambium) tissue or cells for use in filling a cartilage defect. The matrix and synovial tissue or cell preparations may also contain a proliferation agent, transforming factor or other active agents to promote healing. A controlled-release delivery system may be used to administer the transforming factor. The compositions of the invention also include a synovial covering membrane or devitalized fascial sheet for covering the cartilage defect. The methods of this invention are those in which a minimally invasive surgical intervention is performed to remove a small portion of synovial membrane from a joint. Portions of the synovial membrane, or cells expanded in vitro, are implanted alone or within a matrix, into the defect site, where they produce new cartilage tissue and repair the defect. Alternatively, partially transformed synovial-derived tissue may be formed in situ and implanted into the defect site.

Use of a non-human mammalian disease model, wherein the non-human mammal has been implanted with human synovial tissue or other human inflamed tissue containing anti-CCP (cyclic citrullinated peptide) antibody producing cells for (i) analyzing cellular processes in a disease associated with anti-CCP antibodies in such human synovial tissue or other human inflamed tissue, (ii) studying the role of anti-CCP antibodies in the induction and progression of a disease associated with anti-CCP antibodies, (iii) testing the efficacy of a therapeutic agent for the prevention or treatment of a disease associated with anti-CCP antibodies, and (iv) identifying a therapeutic agent useful for the prevention or treatment of a disease associated with anti-CCP antibodies. In one embodiment the non-human mammalian disease model is a mouse, such as a SCID mouse, and the disease associated with anti-CCP antibodies is arthritis, such as RA (rheumatoid arthritis).

Four unique transcripts have been isolated from the beta chain of the T cell receptor in T cells in the synovial tissue of a patient with rheumatoid arthritis. Two of these transcripts were isolated from fresh synovial tissue and two were isolated from a T cell line derived from the synovial tissue. The sequences of the four transcripts are highly homologous, with a conserved amino acid sequence of IGQ-N in the highly diverse V-D junction. The alpha chain and the antigenic specificity of the T cell line derived transcripts has also been characterized.

The present invention provides methods for reducing, reversing or inhibiting neovascularization in a tissue of a mammalian subject having a pathological condition involving neovascularization by administration in vivo of nanoceria particles (cerium oxide nanoparticles) to the subject. The method of the invention is useful, for example, for reducing, treating, reversing or inhibiting neovascularization in ocular tissue such as the retina, macula or cornea; in skin; in synovial tissue; in intestinal tissue; or in bone. In addition, the method of the invention is useful for reducing or inhibiting neovascularization in a neoplasm (tumors), which can be benign or malignant and, where malignant, can be a metastatic neoplasm. As such, the invention provides compositions, which contain nanoceria particles and are useful for reducing, treating, reversing or inhibiting angiogenesis in a mammalian subject.

The present invention discloses a novel protein called Synoviolin and a gene that encodes it. This protein is expressed specifically by synovial tissue and also accompanies the presence of an auto-antibody that recognizes this protein in rheumatoid arthritis (RA) patients. The protein according to the present invention and its antibody can be expected to be used as specific diagnostic markers for RA. In addition, the gene or protein according to the present invention may be used to permit the screening of drugs to treat RA. Moreover, the present invention provides synoviolin gene transgenic animals. The transgenic animals according to the present invention can be used as RA model animals in the development of pharmaceuticals to treat RA.

Disclosed is a composition for treating a joint disease, which is characterized by comprising, as an active ingredient, a univalent metal salt of alginic acid which has an endotoxin level reduced to such an extent that an inflammation or attach of fever is not substantially induced. It becomes possible to provide a composition for treating a joint disease, which has an effect of protecting a cartilage from a mechanical stimulus, an effect of preventing the degeneration / deformation of a cartilage caused by friction or an inflammation, an effect of repairing a damaged part in an cartilage, an effect of preventing an inflammation or a pain in ajoint tissue, an effect of preventing the degeneration of a synovial tissue, and an effect of preventing the destruction of a bone or cartilage.

Four unique transcripts have been isolated from the beta chain of the T cell receptor in T cells in the synovial tissue of a patient with rheumatoid arthritis. Two of these transcripts were isolated from fresh synovial tissue and two were isolated from a T cell line derived from the synovial tissue. The sequences of the four transcripts are highly homologous, with a conserved amino acid sequence of IGQ_N in the highly diverse V-D junction. The alpha chain and the antigenic specificity of the T cell line derived transcripts has also been characterized.

The invention provides a primary culture method of rheumatoid arthritis synovial fibroblasts. The method comprises the steps of sufficiently crushing pretreated synovial tissue; adding type-III collagenase and type-II collagenase into the synovial tissue and conducting blowing and beating; after culture digestion, scattering the synovial tissue into single cells; after filtering, centrifuging a filtrate, taking a substratum precipitate, and inoculating the substratum precipitate into a DMEM high-glucose culture medium for adherent culture; adopting a natural purification method and a repeatedadherent method for purifying the cells to obtain the rheumatoid arthritis synovial fibroblasts. By means of the culture method, about 1,010 RASFs can be obtained within 30 days, the cell yield is greatly increased, multiple experiment demands can be met, and therefore, the primary culture method is a quick and effective primary RASFS isolation culture method. In the meanwhile, compared with synovial cell lines of in-vitro construction lines, the RASFs obtained through primary culture have higher study value, and have a good practical application prospect.

The present invention provides compositions and methods for treating a joint disease containing as an active ingredient thereof a monovalent metal salt of alginic acid for which the endotoxin level thereof has been lowered to an extent that does not substantially induce inflammation or fever. As a result, it is possible to provide a composition for treating a joint disease which has the effects of protecting cartilage from mechanical irritation, inhibiting degenerative changes in cartilage caused by wear and inflammation, repairing cartilage injuries, suppressing inflammation and pain of joint tissue, inhibiting degeneration of synovial tissue, and inhibiting osteochondral destruction.

The present invention provides prognostic, predictive, and therapeutic methods for the treatment of rheumatoid arthritis (RA). The invention is based, at least in part, on the discovery that the expression level of one or more biomarkers described herein in a sample (e.g., a synovial tissue sample, a synovial fluid sample, or a combination thereof) from an individual having RA can be used in methods of determining whether an individual having RA is likely to exhibit disease progression, identifying an individual having RA who is likely to respond to a treatment including a disease modifying anti-rheumatic drug (DMARD), predicting responsiveness of an individual having RA to a treatment including a DMARD, selecting a therapy for an individual having RA, and treating an individual having RA,as well as related kits.

The invention provides a preparation method and application of an angiogenesis model. The method includes the following steps that firstly, vascular endothelial cells are inoculated to matrigel to primarily form vasoganglion; secondly, type I collagen is added to stimulate secondary angiogenesis. The preparation method is suitable for simulating the pathogenesis process of angiogenesis in joint synovial tissue and particularly suitable for simulating and building angiogenesis conditions in temporo-mandibular joint synovial tissue of a human body, and provides a new platform for research of action modes of new cytokines in the aspect of angiogenesis promotion or inhibition. The model is simple in manufacturing material and short in consumed time and has good development, expansion and tissue engineering application prospects.

The onset ratios and pathological conditions of collagen-induced arthritis and adjuvant arthritis in model mice and rats, respectively, were successfully ameliorated by topically expressing the cyclin-dependent kinase inhibitors p16INK4a and p21Cip1 p in articular tissues using adenoviral vectors. In the synovial cells of CDKI-transduced mice, expression of inflammatory cytokines was inhibited. Described are the use of the p21Cip1 protein for inhibiting abnormal proliferation of synovial tissues, inflammation in synovial tissues and / or expression of inflammatory cytokines in synovial tissues; the p21Cip1 gene; compounds promoting the activity or expression of the p21Cip1 protein; and pharmaceutical compositions containing these molecules. Also provided are method of screening for compounds participating in the abnormal proliferation of synovial tissues, inflammation in synovial tissues and / or the expression of inflammatory cytokines in synovial tissues targeting the p21Cip1 protein. Rheumatoid arthritis and other disorders associated with inflammation of the synovial tissue can be prevented or treated by promoting expression or function of p21Cip1 protein.

The invention discloses that a KHDC1L gene and KHDC1L protein can be served as molecular markers of osteoarthritis diagnosis. The invention uses tests to prove that: compared with a normal person, the expression quantity of the KHDC1L gene and the KHDC1L protein in the synovial tissues of a patient with osteoarthritis is high, and the difference has statistical significance. The invention also discloses that the KHDC1L gene and the KHDC1L protein can be used for preparing the medicine for curing osteoarthritis, and a cell proliferation test proves that by disturbing the KHDC1L gene or inhibiting the activity of the KHDC1L protein, synoviocyte proliferation can be inhibited. The research result of the invention provides a new bone and arthrosis clinical diagnosis method, and simultaneously provides a medicine new target for curing bone and arthrosis.