Latch mechanism for portable computer
    81.
    发明申请
    Latch mechanism for portable computer 审中-公开
    便携式电脑的锁定机构

    公开(公告)号:US20060221567A1

    公开(公告)日:2006-10-05

    申请号:US11359182

    申请日:2006-02-22

    IPC分类号: G06F1/16

    CPC分类号: G06F1/1679 G06F1/1616

    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).

    摘要翻译: 闩锁机构组件包括盖单元(30),基座单元(50),闩锁(60)和弹性构件(70)。 盖单元(30)包括一对隔开的板(312,313),并且每个板(312,313)在其中限定一个孔(315,316)。 在基座单元(50)中限定锁定槽(51)。 闩锁(60)可滑动地固定在盖单元(30)的板(312,313)之间,闩锁(60)包括钩(61),以进入闩锁槽(51)以接合基座单元 50),并且一对固定构件(65,66)从所述闩锁(60)的两端延伸以接合在所述板(312,313)的对应的孔(315,316)中。 弹性构件(70)与用于恢复闩锁(60)的闩锁(60)的一个固定构件(65)连接。

    Instant patch for dermal drug delivery
    82.
    发明申请
    Instant patch for dermal drug delivery 审中-公开
    用于皮肤药物递送的即时补丁

    公开(公告)号:US20060105029A1

    公开(公告)日:2006-05-18

    申请号:US11271114

    申请日:2005-11-10

    IPC分类号: A61F13/02 A61L15/16

    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.

    摘要翻译: 本发明涉及皮肤药物递送的系统,装置和方法。 该系统可以包含凝胶引发剂和包含药物和胶凝剂的药物组合物,其中当与凝胶引​​发剂接触时,含药组合物形成柔软的粘连固体。 还包括空腔贴片,其具有被构造为至少部分地被皮肤表面封闭的开口腔。 开放空腔可进一步构造成促进皮肤表面和凝胶之间的接触。 凝胶引发剂和含药物的组合物可以定位在系统中,使得它们彼此隔离直到使用前或使用前。

    Systems and methods for treating warts
    83.
    发明申请
    Systems and methods for treating warts 审中-公开
    用于治疗疣的系统和方法

    公开(公告)号:US20060105028A1

    公开(公告)日:2006-05-18

    申请号:US11271020

    申请日:2005-11-10

    IPC分类号: A61F13/02 A61L15/16

    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.

    摘要翻译: 本发明涉及用于治疗疣的系统和方法。 该系统可以包括疣治疗制剂,其包括用于治疗疣的物质和包括开放腔的空腔补片,该开放腔被构造成在施用时粘附到皮肤表面上成为闭合腔。 闭合的腔体可以构造成容纳疣治疗制剂。

    Adhesive peel-forming formulations for dermal delivery of drugs and methods of using the same
    84.
    发明申请
    Adhesive peel-forming formulations for dermal delivery of drugs and methods of using the same 有权
    用于皮肤递送药物的粘合剂剥离形成剂及其使用方法

    公开(公告)号:US20050276842A1

    公开(公告)日:2005-12-15

    申请号:US11146917

    申请日:2005-06-06

    IPC分类号: A61K9/70

    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.

    摘要翻译: 本发明涉及用于药物真皮递送的粘合剂剥离形成制剂。 制剂可以包括药物,溶剂载体和剥离形成剂。 溶剂载体可以包括具有一种或多种挥发性溶剂的挥发性溶剂体系和具有一种或多种非挥发性溶剂的非挥发性溶剂体系,其中所述非挥发性溶剂体系对于在窗口内的药物具有溶解性 对药物具有可操作的溶解性,使得药物可以在持续的时间段内以治疗有效率递送。 在挥发性溶剂体系蒸发之前,配方可以具有适用于皮肤表面的粘度。 当施用于皮肤时,在挥发性溶剂体系的至少一部分蒸发之后,制剂可以形成固化的可剥离层。

    Compositions and methods for bone formation and remodeling
    87.
    发明申请
    Compositions and methods for bone formation and remodeling 有权
    用于骨形成和重塑的组合物和方法

    公开(公告)号:US20050196349A1

    公开(公告)日:2005-09-08

    申请号:US10849067

    申请日:2004-05-19

    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.

    摘要翻译: 研究了Wnt共同受体LRP5的高骨量(HBM)突变(G171V)调节规范Wnt信号传导的机制。 以前显示突变可以降低Dkk蛋白-1介导的拮抗作用,这表明G171位于第一个YWTD重复结构域可能是Dkk蛋白介导的拮抗作用的原因。 然而,我们发现第三个YWTD重复,但不是第一个重复结构域,是DKK1介导的拮抗作用所必需的。 相反,我们发现G171V突变破坏了LRP5与Mesd的相互作用,Mesd是共受体转运到细胞表面所需的LRP5 / 6的伴侣蛋白,导致细胞表面上较少的LRP5分子。 尽管细胞表面LRP5分子水平的降低导致旁分泌范例中Wnt信号传导的降低,但突变似乎不影响共表达Wnt在自分泌范式中的活性。 连同观察到成骨细胞产生自分泌的正常Wnt,Wnt7b,并且该骨细胞产生旁分泌的Dkk1,我们认为G171V突变可能通过减少旁分泌Dkk1靶向拮抗的数目而引起成骨细胞中Wnt活性的增加,而不影响 自分泌Wnt的活性。

    NF-kappaB oligonucleotide decoy molecules
    88.
    发明申请
    NF-kappaB oligonucleotide decoy molecules 失效
    NF-κB寡核苷酸诱饵分子

    公开(公告)号:US20050182012A1

    公开(公告)日:2005-08-18

    申请号:US11004512

    申请日:2004-12-02

    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.

    摘要翻译: 本发明涉及含有能够与NF-κB转录因子特异性结合的核心序列的双链NF-κB诱饵寡脱氧核苷酸(NF-kappaB dsODN)分子。 在一个特定方面,本发明涉及在p50 / p50同源二聚体上优先结合p50 / p65和/或cRel / p50异二聚体的NF-kappaB诱饵分子。 另一方面,本发明涉及对p65具有改善的结合亲和力的NF-κB诱饵分子。

    PARP inhibitors, pharmaceutical compositions comprising same, and methods of using same
    90.
    发明授权
    PARP inhibitors, pharmaceutical compositions comprising same, and methods of using same 失效
    PARP抑制剂,包含其的药物组合物及其使用方法

    公开(公告)号:US06635642B1

    公开(公告)日:2003-10-21

    申请号:US09145176

    申请日:1998-09-01

    IPC分类号: A61K3150

    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.

    摘要翻译: 本发明涉及PARP抑制剂,包含其的药物组合物及其用途,用于治疗由于坏死或凋亡引起的细胞损伤或死亡引起的组织损伤,影响不被NMDA毒性介导的神经元活性; 治疗由缺血和再灌注损伤,神经系统疾病和神经退行性疾病引起的神经组织损伤; 预防或治疗血管中风; 治疗或预防心血管疾病; 治疗年龄相关性黄斑变性,艾滋病和其他免疫衰老疾病,关节炎,动脉粥样硬化,恶病质,癌症,涉及复制衰老的骨骼肌退行性疾病,糖尿病,头部创伤,免疫衰老,炎性肠等其他病症和/或病症 疾病(如结肠炎和克罗恩病),肌营养不良症,骨关节炎,骨质疏松症,慢性和/或急性疼痛(如神经性疼痛),肾衰竭,视网膜缺血,败血性休克(如内毒素性休克),移植器官损伤 ,皮肤老化; 延长细胞的寿命和增殖能力; 改变衰老细胞的基因表达; 或放射性敏感的缺氧性肿瘤细胞。