摘要:
A latch mechanism assembly includes a cover unit (30), a base unit (50), a latch (60) and an elastic member (70). The cover unit (30) includes a pair of spaced plates (312, 313), and each of the plates (312, 313) defines a hole (315, 316) therein. A latching slot (51) is defined in the base unit (50). The latch (60) is slideably fixed between the plates (312, 313) of the cover unit (30), the latch (60) includes a hook (61) to enter the latching slot (51) to engage in the base unit (50), and a pair of fixing members (65, 66) extends from two ends of the latch (60) to engage in corresponding holes (315, 316) of the plates (312, 313). The elastic member (70) is connected with one fixing member (65) of the latch (60) for restoring the latch (60).
摘要:
The present invention is drawn toward systems, devices, and methods of dermal drug delivery. The system can comprise a gel-triggering agent and a drug-containing composition including a drug and a gelling agent, wherein the drug-containing composition forms a soft, coherent solid when contacted with the gel-triggering agent. A cavity patch is also included having an open cavity configured to be closed at least in part by a skin surface. The open cavity can be further configured to facilitate contact between the skin surface and the gel. The gel-triggering agent and the drug-containing composition can be positioned in the system such that they are kept isolated from one another until immediately before or during use.
摘要:
The present invention is drawn to systems and methods for treating warts. The system can comprise a wart treatment formulation comprising a substance for treating warts and a cavity patch comprising an open cavity being configured to become a closed cavity upon application and adherence to a skin surface. The closed cavity can be configured to contain the wart treatment formulation.
摘要:
The present invention is drawn to adhesive peel-forming formulations for dermal delivery of a drug. The formulation can include a drug, a solvent vehicle, and a peel-forming agent. The solvent vehicle can include a volatile solvent system having one or more volatile solvent, and a non-volatile solvent system having one or more non-volatile solvent, wherein the non-volatile solvent system has a solubility for the drug that is within a window of operable solubility for the drug such that the drug can be delivered at therapeutically effective rates over a sustained period of time. The formulation can have a viscosity suitable for application to a skin surface prior to evaporation of the volatile solvents system. When applied to the skin, the formulation can form a solidified peelable layer after at least a portion of the volatile solvent system is evaporated.
摘要:
The present invention is directed toward an apparatus to rapidly deliver a drug to a patient The invention comprises a drug beneath a patient's skin in a drug depot site. A heating component is placed near the drug depot site and generates heat in and near the drug depot site. A control component connected to the heating component is used to control the magnitude and duration of heat generated by the heating component.
摘要:
The mechanism by which the high bone mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates the canonical Wnt signaling was investigated. The mutation was previously shown to reduce Dkk protein-1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for Dkk protein-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperon protein for LRP5/6 that is required for the coreceptors' transport to cell surfaces, resulting in less LRP5 molecules on the cell surface. Although the reduction in the level of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine Dkk1, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblasts by reducing the number of targets for paracrine Dkk1 to antagonize without affecting the activity of autocrine Wnt.
摘要:
The present invention concerns double-stranded NF-κB decoy oligodeoxynucleotide (NF-κB dsODN) molecules that contain a core sequence capable of specific binding to an NF-κB transcription factor. In a particular aspect, the invention concerns NF-κB decoy molecules that preferentially bind p50/p65 and/or cRel/p50 heterodimers over p50/p50 homodimers. In another aspect, the invention concerns NF-κB decoy molecules with improved binding affinity to p65.
摘要:
The present invention relates to PARP inhibitors, pharmaceutical compositions comprising the same, and methods of using the same to treat tissue damage resulting from cell damage or death due to necrosis or apoptosis, effect neuronal activities not mediated by NMDA toxicity; to treat neural tissue damage resulting from ischemia and reperfusion injury, neurological disorders and neurodegenerative diseases; to prevent or treat vascular stroke; to treat or prevent cardiovascular disorders; to treat other conditions and/or disorders such as age-related macular degeneration, AIDS and other immune senescence diseases, arthritis, atherosclerosis, cachexia, cancer, degenerative diseases of skeletal muscle involving replicative senescence, diabetes, head trauma, immune senescence, inflammatory bowel disorders (such as colitis and Crohn's disease), muscular dystrophy, osteoarthritis, osteoporosis, chronic and/or acute pain (such as neuropathic pain), renal failure, retinal ischemia, septic shock (such as endotoxic shock), organ damage due to transplantation, and skin aging; to extend the lifespan and proliferative capacity of cells; to alter gene expression of senescent cells; or to radiosensitize hypoxic tumor cells.