526 results about "Murine model" patented technology

Vaccines and methods of inoculation for conferring immunity to Cryptococcus infection are disclosed. Strains of Cryptococcus fungi, including Cryptococcus neoformans and Cryptococcus gattii, can be administered to a human or animal subject via inhalation. Cryptococcus fungi that can be used to confer immunity can comprise one or more mutations in genes that contribute to chitosan production, such as genes encoding a chitin deacetylase (cda), a chitin synthase (chs) and/or a regulator of chitin synthase (csr). Inhalation administration of heat-killed Cryptococcus harboring deletions in cda1, cda2 and cda3 genes can confer immunity. In a murine model system, inhalation administration of Cryptococcus neoformans harboring deletions in cda1, cda2 and cda3 genes conferred immunity against subsequent exposure to wild type Cryptococcus neoformans in 100% of test animals. Inhalation administration of heat-killed Cryptococcus grown under conditions leading to reduced chitosan production can also confer immunity.

The invention discloses a single-chain antibody of human source anti-alexin C3d molecules. A light chain and a heavy chain of the antibody have a unique CDR region; excellent antigen binding activityis realized; the affinity constant reaches 1.22*10<-7> mol/L. Biological distribution experiments prove that the anti-C3d single-chain antibody provided by the invention can be highly gathered in thearthritis positions after entering a mouse model with rheumatoid arthritis; the arthritis serious degree of the three ScFv treatment groups is obviously lower than that of a PBS group; the healing degree has the obvious dose dependency relationship; the result shows that the excellent anti-adhesion/ anti-inflammatory targeted inhibition effects are achieved. In the treatment process on MRL/lpr mice with lupus erythematosus, the anti-C3d single-chain antibody provided by the invention can obviously improve the survival rate of the mice; the symptoms of proteinuria, glomerular score, interstitial inflammation, vasculitis and crescent/necrosis and the like in the treatment group are obviously relieved. The result shows that the anti C3d single-chain antibody provided by the invention has excellent application prospects in the preparation of medicine for treating autoimmune diseases.

Leptin was previously demonstrated to exert potent immune modulatory properties in several immune mediated disorders. The aim of the study was to determine leptin's anti-tumor effect in a murine model of human hepatocellular carcinoma (HCC). In vivo, Athymic T cell deficient (nude) mice transplanted with 1×10⁶ human Hep3B cells, followed by administration of two daily intraperitoneal doses of 0.5 mg/gram leptin for 6 weeks. Leptin administration induced a significant reduction in tumor size and improved survival in nude mice. Histologically, tumors of leptin-administered mice featured increased inflammatory exudate in interphase areas. Leptin-induced tumor suppression was associated with a significant increase in peripheral natural killer (NK) cell number. Splenocytes from leptin-treated mice featured decreased expression of CIS mRNA. To determine which lymphocyte subset is a prerequisite for the anti tumor effect of leptin, T&B cell deficient (Scid) mice and T,B& NK deficient (Scid-Beige) mice were subcutaneously implanted with Hep3B tumor cells, with and without the daily intraperitoneal administration of 0.5 mg/gram leptin for 6 weeks. SCID mice featured leptin-associated tumor suppression similar to those of nude mice. In contrast, NK-deficient SCID-Beige mice developed larger tumors. To further establish natural killer cell's central role in mediation of leptin's anti-tumor effect, NK cells were incubated in vitro with increasing doses of leptin, demonstrating a dose-dependent increase in cytotoxic activity. Incubation of leptin with hepatoma cell line was found to induce a dose-dependent reduction in hepatoma cell proliferation, suggesting an additive direct anti-tumor effect. Further synergism in inhibition of hepatoma cell proliferation in vitro was achieved following addition of natural killer cells. HCC cells expressed leptin receptor mRNA, while addition of leptin induced increased mRMA expression of STAT2 and SOCS1 on tumor cell lines. Leptin administration induces a significant suppression of human HCC. This effect is mediated by induction of natural killer cell proliferation and activation, and by direct inhibition of tumor growth. Decreased natural killer cell expression of inhibitory CIS protein and over expression of the anti-proliferative STAT2 and SOCS1 proteins in HCC lines may underline both anti cancerous effects of leptin.

The present invention discloses a preparation method and an application of a mussel oligopeptide, and belongs to the field of marine biotechnology application. The preparation method comprises: adopting mytilus edulis as a raw material, and adopting an alkaline cold extraction method to obtain mussel protein from mussel freeze-drying powder; and carrying out composite enzymolysis of protein to obtain mixed polypeptides, carrying out ultra-filtration to obtain the oligopeptide, adopting aging mouse models to carry out a series of anti-aging animal experiments and behavioral experiments, and carrying out a drosophila survive experiment to prove aging delay activity of the mussel oligopeptide so as to create a new approach for achievement of scientific and high-value mussel utilization. Compared with the method in the prior art, the method of the present invention has the following advantages that: the mussel protein is extracted and prepared, the optimal protease and the preferred process are adopted to carry out enzymolysis purification on the mussel protein, decomposition on the mussel protein molecule structure due to the high temperature is avoided, the grading of the mussel polypeptide at the molecular weight level is achieved, and the obtained mussel oligopeptide has the pure and good aging delay effect.

The invention relates to a circulating tumor cell mouse model and a construction method and application thereof. The method includes the following steps of 1, subcutaneous transplantation, wherein a primary tumor tissue sample is transplanted into the body of an immunodeficient mouse to construct a primary cancer heterotransplantation model PDX; 2, collection of circulating tumor cells, wherein the circulating tumor cells in peripheral blood in the primary cancer heterotransplantation model obtained in the step 1 are collected; 3, renal sac membrane transplantation, wherein the circulating tumor cells collected in the step 2 are transplanted into the renal sac membrane of the immunodeficient mouse, and then the circulating tumor cell mouse model is successfully constructed. According to the method, the mode of transplantation with two or more times of passages is adopted, the CTCs in the primary cancer heterotransplantation model are transplanted into the body of the immunodeficient mouse through renal sac membrane, and the circulating tumor cell mouse model is obtained; the circulating tumor cell mouse model can be applied to research on the in-vivo metastasis mechanism and proliferation condition of CTCs.

The invention discloses an in vitro construction method of liver organs and applications. Mouse hepatocytes are extracted to induce to construct liver organs; the forms of the liver organs are observed under a microscope; and immunofluorescence and PCR identification are performed on dryness and epithelial cell properties. An acute hepatic failure mouse model after 70% hepatectomy is established;the liver functions on the first, fourth and seventh day after operation are evaluated after the liver organs are transplanted; liver-to-body ratio is compared; and the treatment effects of the liverorgans on acute hepatic failure are verified through HE staining and immunohistochemistry. Inflammations such as HE staining and ki-67 staining and proliferation indexes show that proliferation can beobviously enhanced after the liver organs are transplanted. The liver organs have strong dryness and proliferation functions; the liver functions of acute hepatic failure mice after 70% hepatectomy can be effectively relieved, and the liver-to-body ratio can be increased; and liver regeneration and repair of acute hepatic failure after 70% hepatectomy can be promoted by relieving inflammatory infiltration of livers.

The invention discloses an application of baicalin in preparation of a medicine for treating polycystic ovarian syndrome. As shown in an in vivo experiment, the baicalin has obvious treatment effect on a polycystic ovarian syndrome rat model and can greatly reduce the high androgen level of the rat model, promote follicle maturity and induce ovulation; as shown in an in vitro experiment, the baicalin can inhibit the expression of androgen of a polycystic ovarian syndrome cell model. More importantly, the baicalin has small side effect and incomparable security while having no liver and kidney toxicity. Therefore, the baicalin can be used for preparing the medicine for treating polycystic ovarian syndrome and has a brilliant prospect.

The invention provides a construction method of a mouse model realizing conditional site-specific double-overexpression of HPV E6/E7 genes. The construction method comprises the following steps: 1, acquiring mice: (1) respectively designing and acquiring sgRNAs; (2) respectively preparing Cas9/sgRNA mixtures; (3) constructing a targeting vector; (4) carrying out microinjection and acquiring F0-generation mice, including F0-generation mice with HPV E6 knocked in at the specific ROSA26 site and F0-generation mice with HPVE7 knocked in at the specific H11 site; (5) acquiring F1-generation mice; and (6) acquiring F2-generation positive homozygote mice; and 2, acquiring conditional site-specific HPV E6/E7 double-knock-in model mice: hybridizing the two F2-generation positive homozygote mice toobtain the conditional site-specific HPV E6/E7 double-knock-in model mice. According to the method provided by the invention, the animal model which can be stably inherited and accurately regulated and controlled can be obtained.

The invention provides a construction method and an application of an HBeAg transgenic mouse model. The method comprises the following steps: CRISPR/Cas9 technology is adopted, an HBeAg gene is inserted into a pliver-HBeAg expression cassette at the Rosa26 gene locus in a fixed-point manner through homologous recombination, and a recombinant R26-e(Alb-HBeAg)1 targeting vector is constructed with an In-Fusion cloning method and contains a 3.3kb 5' homologous arm, pliver-HBeAg and a 3.3kb 3' homologous arm; Cas9mRNA, gRNA and the recombinant R26-e(Alb-HBeAg)1 targeting vector are micro-injectedinto a zygote of a C57BL/6J mouse, then the zygote is transplanted into the uterus of a C57BL/6J female mouse, and an HBeAg transgenic mouse is obtained through propagation and purification step by step. The transgenic mouse can specifically express HBeAg in liver, thereby being capable of applying to experimental animal models for researching HBeAg infection mechanism and evaluating treatment effects of therapeutic drugs and vaccines for chronic hepatitis B.

The present invention discloses a fodder formulation for constructing nutritive obesity animal model, and especially fodder formulation for constructing nutritive obesity rat model. Obesity is dystrophic disease caused by the mutual action of genetic factors and environment factors and is inducement of several chronic diseases. The present inventor prepares fodder with the pre-mixed material of corn, lard, casein, flour, dried pork floss, grass powder, fish meal, bran and mineral salt, and the pre-mixed material of cholesterol and vitamins. The fodder is used in raising rat to obtain obesity model with obvious difference to the contrast in weight index and biochemical blood indexes. The animal model may be used as the platform for obesity research, medicine screening, and functional food development and identification.

The invention provides an inactivated or attenuated gene functionally linked to a hotspot for somatic hypermutation. Inventive nucleic acids include inactivated genes operatively linked to immunoglobulin gene control elements. Embodiments of the invention include murine models of plasma cell disease and germinal center cell lymphoma.

The invention discloses application of recombinant human cytoglobin (rhCYGB) in preparation of drugs treating hyperlipidemia and atherosclerosis. A hyperlipidemia rat model and an atherosclerosis rat model are respectively established by the inventor, and subcutaneous injection of rhCYGB is carried out for treatment. Experimental results show that the rhCYGB drug is non-toxic, compared with a model control group, the rhCYGB treatment group has significant improvement, the four items of blood lipid test are significantly decreased than those of a model group, and the four items of blood lipid test of a polysaccharide sulfate treatment group are significantly higher than normal, thus rhCYGB has better efficacy than polysaccharide sulfate in treatment of hyperlipidemia caused by high fat diet. In the atherosclerosis rat model, compared with the model group, the four items of blood lipid test of the treatment group are also significantly reduced, and atherosclerotic plaques also obviously decreased. Therefore, treatment of hyperlipidemia and atherosclerosis by the recombinant human cytoglobin has the advantages of low toxicity, safety and effectiveness.

The invention discloses application of N6022 in treatment of aortic dissection and aortic aneurysm, and relates to the field of cardiovascular diseases. In mouse models of aortic dissection and aorticaneurysm, dilation of aorta can be inhibited after intravenous injection of the N6022 into tail veins, thereby reducing incidence and mortality of aortic dissection and aortic aneurysm; and moreover,the N6022 is capable of reducing rupture of aortic aneurysm, inhibiting occurrence of hematoma in inner walls of lumen and excessive collagen deposition on vascular walls, maintaining integrity of elastic fibers in the vascular walls, and treating the aortic dissection and the aortic aneurysm. The application of the N6022 in the treatment of the aortic dissection and the aortic aneurysm opens upa new application field of the N6022, and provides a meaningful reference for the prevention and the treatment of the aortic dissection and the aortic aneurysm diseases as well as improvement of vascular lesions.

Described herein are methods and apparatus for increasing sensitivity of ultrasound imaging of fluid flow in an object of interest. Ultrasound imaging of blood perfusion can be performed without contrast enhancement. Embodiments include transforming a spatiotemporal echo data array into a three-dimensional perfusion data array having a spatial dimension, a slow-time dimension, and a frame-time dimension, and filtering the perfusion data array with an eigen passband clutter filter. The clutter filter can increase sensitivity and utility of ultrasound imaging of fluid flow. In some aspects, the method can yield blood flow signal power and perfusion values well separated from tissue clutter. In an example, enhancements to ischemic tissue perfusion maps in a murine model are shown.

The invention discloses application of long non coding RNA (lncRNA) and interfering RNA thereof to treatment on atherosclerosis. Through high-throughput sequencing on an aortic tissue of an atherosclerosis mouse model, the invention discovers that the expression of lncRNA molecules in normal and late atherosclerosis mice is obviously different; and meanwhile, the lncRNA molecules are highly expressed in the atherosclerosis tissue and the lncRNA molecules are named as lncRNA-AFIAR. The experiment proves that the lncRNA-AFIAR has the functions of enhancing proliferation of macrophages, inhibiting macrophage apoptosis and the like and participates in the process of promoting the progress of the atherosclerosis. The aims of inhibiting the proliferation of the macrophages and reducing plaque formation can be fulfilled by inhibiting the lncRNA-AFIAR, so that the aim of inhibiting the progress of the AS. Therefore, the invention provides new molecular markers and intervention targets for diagnosing and treating the atherosclerosis and also provides new technical means for treating the atherosclerosis.