1645 results about "Endogeny" patented technology

Methods and apparatus for direct coronary revascularization wherein a transmyocardial passageway is formed between a chamber of the heart and a coronary blood vessel to permit blood to flow therebetween. In some embodiments, the transmyocardial passageway is formed between a chamber of the heart and a coronary vein. The invention includes unstented transmyocardial passageways, as well as transmyocardial passageways wherein protrusive stent devices extend from the transmyocardial passageway into an adjacent coronary vessel or chamber of the heart. The apparatus of the present invention include protrusive stent devices for stenting of transmyocardial passageways, intraluminal valving devices for valving of transmyocardial passageways, intracardiac valving devices for valving of transmyocardial passageways, endogenous tissue valves for valving of transmyocardial passageways, and ancillary apparatus for use in conjunction therewith.

This invention relates to a method for prevention and treatment of Atherosclerosis, Peripheral Vascular Disease, Coronary Artery Disease, and age-related disorders including Osteoporosis, Arthritis, Type II Diabetes, Dementia and Alzheimer's disease in a subject comprising administering to said subject a therapeutically effective dosage of each component or combination of statins, bisphosphonates, cholesterol lowering agents or techniques, interleukin-6 inhibitor/antibody, interleukin-6 receptor inhibitor/antibody, gp130 protein inhibitor/antibody, tyrosine kinases inhibitors/antibodies, STAT transcription factors inhibitors/antibodies, altered IL-6, partial peptides of IL-6 or IL-6 receptor, or SOCS (suppressors of cytokine signaling) protein, or a functional fragment thereof, administered separately, in sequence or simultaneously. Inhibition of the signal transduction pathway for Interleukin 6 mediated inflammation is key to the prevention and treatment of atherosclerosis, peripheral vascular disease, coronary artery disease, aging and age-related disorders including osteoporosis, type 2 diabetes, dementia and some forms of arthritis and tumors. Inhibition of Interleukin 6 mediated inflammation may be achieved indirectly through regulation of endogenous cholesterol synthesis and isoprenoid depletion or by direct inhibition of the signal transduction pathway including interleukin-6 inhibitor/antibody, interleukin-6 receptor inhibitor/antibody, gp130 protein inhibitor/antibody, tyrosine kinases inhibitors/antibodies, STAT transcription factors inhibitors/antibodies, altered IL-6, partial peptides of IL-6 or IL-6 receptor, or SOCS (suppressors of cytokine signaling) protein, or a functional fragment thereof. Said method for prevention and treatment of said disorders is based on inhibition of Interleukin-6 inflammation through regulation of cholesterol metabolism, isoprenoid depletion and inhibition of the signal transduction pathway.

The invention relates to transgenic animals lacking endogenous Ig and capable of producing transgenic antibodies, as well as methods of making the same. The invention further relates to methods for producing transgenic antibodies in such animals, and transgenic antibodies so produced.

A pharmaceutical composition for oral administration comprising PTH, wherein the in vitro release of PTH-when tested in a dissolution test of pharmacopoeia standard-is delayed with at least 2 hours and once the release starts, at least 90% w/w such as, e.g., at least 95% or at least 99% of all PTH contained in the composition is released within at the most 2 hours. The composition may also comprises a calcium containing compound and/or a vitamin, D. In particular, PTH is administered in combination with a calcium-containing compound for the treatment or prevention of bone-related diseases, so that I) an effective amount of a calcium-containing compound is administered to lower the plasma level of endogenous PTH, and II) an effective amount of PTH is administered to obtain a peak concentration of Pm once the endogeneous PTH level is lowered. This present a potential therapeutic or prophylactic regimen for bone-related disorders including osteoporosis.

PROBLEM

There are provided induced malignant stem cells capable of in vitro proliferation that are useful in cancer research and drug discovery for cancer therapy, as well as processes for production thereof, cancer cells derived from these cells, and applications of these cells.

MEANS FOR SOLVING

An induced malignant stem cell capable of in vitro proliferation are characterized by satisfying the following two requirements:

• (1) having at least one aberration selected from among (a) an aberration of methylation (high or low degree of methylation) in a tumor suppressor gene or a cancer-related genetic region in endogenous genomic DNA, (b) a somatic mutation of a tumor suppressor gene or a somatic mutation of an endogenous cancer-related gene in endogenous genomic DNA, (c) abnormal expression (increased or reduced/lost expression) of an endogenous oncogene or an endogenous tumor suppressor gene, (d) abnormal expression (increased or reduced/lost expression) of a noncoding RNA such as an endogenous cancer-related microRNA, (e) abnormal expression of an endogenous cancer-related protein, (f) an aberration of endogenous cancer-related metabolism (hypermetabolism or hypometabolism), (g) an aberration of endogenous cancer-related sugar chain, (h) an aberration of copy number variations in endogenous genomic DNA, and (i) instability of microsatellites in endogenous genomic DNA in an induced malignant stem cell; and
• (2) expressing genes including POU5F1 gene, NANOG gene, SOX2 gene, and ZFP42 gene.

All or a portion of a surface of an implantable sensor is covered with a biocompatible coating formed at least partially of a biomaterial matrix having properties that promote a substantially even growth of tissue cells over the surface of the coating. Additional materials, such as growth factors, agents that recruit endogenous stem cells, and cell adhesion motif arginine, glycine, aspartic acid may be included in the coating. Autologous cells may be added to the coating prior to implantation. The sensor surface may also be textured, by etching or abrading, in order to promote even tissue growth. Alternatively, the sensor surface may be covered with a coating having properties that inhibit the growth of tissue. These coatings may include a biomaterial, a biomaterial matrix having a drug, such as a sirolimus or a steroid, an active component, or a self assembled monolayer.

An apparatus and method according to the present invention can be provided, e.g., for a cell specific laser therapy of atherosclerotic plaques, particularly to systems and methods for targeting endogenous light absorbers present within plaque macrophages and exogenous nanoparticle targeting. In one exemplary embodiment, an electro-magnetic radiation can be forwarded to an anatomical structure. The electromagnetic radiation may have at least one property configured to (a) modify at least one characteristic of at least one first cell, and (b) minimize any modification of and/or modify at least one characteristic of at least second cell. The first and second cells may be different from one another, the characteristics of the first and second cells can be different from one another, and the first cell and/or the second cell may have at least one macrophage feature, and the characteristic of the at least one first cell and/or the at least one second cell can be temperature. According to still another exemplary embodiment, a location associated with the first cell and the second cell can be determined. For example, the electromagnetic radiation can be forwarded in a vicinity of the location.

Disclosed herein are antibodies that bind with high specificity to soluble oligomers of amyloid β (Abeta) and methods of employing those antibodies. The antibodies are able to distinguish between Alzheimer's Disease (AD) and control human brain extracts. The antibodies identify endogenous Abeta oligomers in AD brain slices and also bind to Abeta oligomers on cultured hippocampal cells. The antibodies neutralize endogenous Abeta oligomers and Abeta oligomers produced in solution.

The present invention relates to methods and compositions for reducing Distress Dysfunction by restoring and maintaining homeostatic balance in the neurotransmitter systems underlying the Stress Response and the experience of distress and hedonic tone. Distress Dysfunction refers to the experience of dysfunctional emotional and physical distress that interferes with the individual's quality of life and functioning. A novel understanding of the bimodal opioid modulation of pain, and its impact, through serotonergic, dopaminergic, epinephrinergic, and norepinephrinergic processes, on hedonic tone, leads directly to new generation pharmaceutical formulations that are remarkably safe and effective for the treatment of a wide variety of Distress Dysfunctions, including anxiety, depression, anger, insomnia, mood disorders, eating disorders, sexual problems, pain, substance and behavioral addictions, gastrointestinal disorders, autistic spectrum disorders, attention-deficit and hyperactivity disorders, and other emotional and physical distress disorders. The foundation of this discovery is the power of Receptor Switchers, such as ultra-low-dose and very-low-dose opioid antagonists and GM1 ganglioside attenuators, in blocking acute and protracted excitatory opioid receptor signaling. Co-administration of Receptor Switchers with Endorphin Enhancers, such as specific cAMP PDE inhibitors and excitatory amino acids, is an excellent formulation for restoring healthy homeostatic balance to the endogenous opioid system, using the body's endorphins to reduce emotional and physical distress, and through synergistic and homeostatic processes, restoring positive hedonic tone. The addition of Synergistic Enhancers, such as amino acids, SSRI and SNRI agents, and non-opioid analgesics, as well as Exogenous Opioids, enhances and prolongs these therapeutic benefits. The novel principles discovered by this invention also teach a new generation of safe and effective formulations for the treatment of respiratory conditions, neuropathy, and nociceptive pain.

The invention provides DNA molecules encoding a chimeric polypeptide comprising (a) a component of a MHC molecule capable of association on a cell surface with an endogenous MHC molecule component of the same class, and (b) an intracellular region of a signal transduction element capable of activating T cells. Component (a) may be a monomorphic component and is preferably beta 2-microglobulin, or a polymorphic class I or class II component. The signal transduction element (b) capable of activating T cells may be a component of T-cell receptor CD3, preferably the CD3 zeta (zeta) polypeptide, a B cell receptor polypeptide or an Fc receptor polypeptide. Immune cells such as a CTLs expressing said chimeric MHC molecules specifically eliminate or inactivate harmful T cells and are useful for treating graft rejection and autoimmune diseases.

PCT No. PCT/SE97/00610 Sec. 371 Date Dec. 8, 1998 Sec. 102(e) Date Dec. 8, 1998 PCT Filed Apr. 11, 1997 PCT Pub. No. WO97/37587 PCT Pub. Date Oct. 16, 1997Device and method for collecting endogenous gaseous nitric oxide (NO), in the urogenital tract, for example in the urinary tract and in the uterus and oviducts. According to one embodiment, a NO permeable, liquid impermeable inflatable body (16) is positioned in the urethra (5) surrounded by the prostate gland (17), whereby an additional inflatable body (4) positioned in the bladder (2) serves to seal off the bladder from the urethra and helps in the positioning of the device. The present invention further relates to a method and a system for use in the diagnosis of inflammatory states in said organs.

The invention discloses a two-step enzyme measuring method and measuring reagents for creatinine in blood serum. The hydrogen peroxide generated by endogenous creatine is eliminated by utilizing catalase in a reagent 1 of the creatinine measuring reagents, and the catalase in the reagent 1 is suppressed by utilizing the catalase in a reagent 2 of the creatinine measuring reagents, so that the creatinine content in a sample is measured. The invention has the advantages that the phenomenon that the cost is increased because of oxidizing hydrogen peroxide by the catalase, so that the detection result is low in accuracy and precision is avoided.

The invention provides a nucleic acid construct for endogenously expressing RNA polymerase in cells, and particularly discovers a novel nucleic acid construct capable of greatly enhancing protein translation efficiency. The nucleic acid construct consists of a promoter with specific promotion intensity (such as RNR2, ADH1, GAPDH, TEF1, PGK1 and SED1) and coding sequences of proteins of RNAP (suchas T7RNAP, T3RNAP, T4RNAP and T5RNAP), if the nucleic acid construct of the invention is applied into a yeast extracorporeal protein synthesis system, the activity of synthesized luciferase is quite high relative to light unit value (RLU), and the effect can be the same as the effect of T7RNAP added exogenously. The effect can reach up to 6.6* 107.

Methods, cells and compositions of matter are provided for treatment of erectile dysfunction using stem cell therapy. In particular, various stem cells are modified or administered freshly isolated in order to induce smooth muscle regeneration, neural regeneration, and restoration of endothelial function. In some embodiments endogenous stem cells are mobilized or activated to achieve therapeutic benefit. In other embodiments compositions derived from stem cells are utilized for treatment of erectile dysfunction.

The invention relates to a fluorescence probe for detecting intracellular hydrogen sulfide and a preparation method and application of the fluorescence probe. Cy7 fluorochrome and sodium acetate are dissolved in anhydrous dimethylformamide (DMF), heating reflux is carried out for 2-4 hours under protection of Ar gas, cooling and suction filtration are carried out on an obtained mixture, mother liquor is crystallized under the low temperature of minus 4-20 DEG C, and keto form cyanine reddish brown crystals are obtained after the suction filtration; toluoyl benzoic acid and oxalyl chloride are dissolved in anhydrous CH2Cl2, then a bit of DMF is added, mixing is carried out for 2-6 hours under the temperature of 0 DEG C, and toluoyl benzoyl chloride is obtained; and keto form cyanine and triethylamine are dissolved in the anhydrous CH2Cl2 and are cooled to be 0 DEG C, the toluoyl benzoyl chloride is added dropwise, mixing is carried out for 10-30 minutes under the temperature of 0 DEG C, the mixture is heated to be in the room temperature, mixing is carried out overnight, suction filtration and spinning drying are carried out, separation is carried out through a chromatographic column, green solids are obtained after the spinning drying, and the structural formula is as follows. The fluorescence probe is simple in composition, high in detection speed, free of long-term incubation in a detection process, high in sensitivity, and capable of detecting intracellular endogenic hydrogen sulfide.

The present disclosure provides a method for enhancing the anti-tumor efficacy of an Fc fusion protein which binds specifically to a target, e.g., a co-inhibitory or co-stimulatory receptor of ligand, on a T cell in a subject afflicted with a cancer or a disease caused by an infectious agent and alters the activity of the immunomodulatory target, thereby potentiating an endogenous immune response against cells of the cancer or the infectious agent, wherein the method comprises selecting, designing or modifying the Fc region of the Fc fusion protein so as to enhance the binding of said Fc region to an activating Fc receptor (FcR). The disclosure also provides an Fc fusion protein produced by said method which has an enhanced ability to potentiate an endogenous immune response against cells of a cancer or an infectious agent in a subject. The disclosure further provides a method for treating a subject which comprises administering to the subject a therapeutically effective amount of an Fc fusion protein, wherein the Fc region of the Fc fusion protein has been selected, designed or modified so as to increase the binding of said Fc region to an activating FcR.

The invention discloses a determination method of a urine metabolic marker for early diagnosis of diabetic nephropathy. The method mainly utilizes analysis technique and method such as gas mass spectrometry and mass liquid spectrometry for quantitative determination of endogenous small molecule compounds in urine of patients with diabetes and diabetic nephropathy; and relative concentration difference between endogenous small molecule compounds in a pathological group and a normal group is calculated and compared, so as to be applied to clinical early diagnosis of diabetic nephropathy. Compared with other existing clinical diagnosis indexes, the method has advantages of wide adaptation range, sensitivity, simple sampling and operation, and no harm on the body. The method is more suitable for screening of diabetic nephropathy in early stage with some uncertain physiological and biochemical indexes, so as to avoid missing of the best treatment time due to delayed diagnosis.