Abstract: An anchor device is provided for securing a watercraft via an improved anchor. The anchor device may include a spine component, rotation members rotatable about the spine component, slats, and additional features. During operation, the anchor device advantageously provides increased contacting edges to grip an uneven anchoring surface, such as a rocky lakebed or river bottom. A method for securing a watercraft via an improved anchor using the anchor device is also provided.

Abstract: Methods and compositions for the treatment of hypoxia associated disorders by directional angiogenesis/arteriogenesis. Conditionally silenced vectors expressing a therapeutic molecule under hypoxic conditions avoid chaotic vascularization and allow for the orderly growth of new vessels into damaged tissue.

Abstract: Methods and compositions for the treatment of hypoxia associated disorders by directional angiogenesis/arteriogenesis. Conditionally silenced vectors expressing a therapeutic molecule under hypoxic conditions avoid chaotic vascularization and allow for the orderly growth of new vessels into damaged tissue.

Abstract: The methods, compositions, cells and kits described herein are based on the discovery that stem cells, when injected into ischemic tissue of mammals, can be protected by preconditioning of the ischemic tissue with hypoxia-regulated human VEGF and human IGF-1. Methods, compositions, cells and kits for treating tissue injured by ischemia or at risk of ischemic injury in a subject are thus described herein.

Abstract: Described herein are compositions, kits and methods for treating and preventing obesity and overweight, as well as treating and preventing hyperglycemia, in a subject (e.g., a human), based on the discoveries that reduced expression of miR-205 may be a cause of obesity, and that miR-411 regulates gluconeogenic genes by targeting transcription factors, respectively. The compositions, kits and methods for treating and preventing obesity and overweight involve increasing expression of one or more microRNAs (e.g., miR-205) involved in adipogenesis, and provide a new therapy for treating patients that have eating disorders and/or are predisposed to obesity, and that are obese or overweight. The compositions, kits and methods described herein for treating and preventing hyperglycemia involve increasing expression of miR-411 and provide a new therapy for treating hyperglycemia associated with, for example, type 2 diabetes.

Abstract: Described herein are compositions, kits and methods for stimulating angiogenic functions of stem cells and/or progenitor cells having pro-angiogenic potential (e.g., endothelial progenitor cells (EPCs), mesenchymal stem cells (MSCs)) before transplantation (e.g., ex vivo cell therapy) based on the discovery that functional recovery of CD34+ cells from coronary artery disease (CAD) patients is improved by transfection of antagomirs against one or more miRs of a plurality of miRs identified to be over-expressed in cells from CAD patients. Described herein are methods to recover the functions of EPCs isolated from patients with cardiovascular disease (e.g., CAD or peripheral artery disease (PAD)) by bioengineering the cells with antagomirs and/or premirs to specific micro-RNAs. The bioengineered cells can then be used to treat patients with ischemic or ischemic-related disease (e.g., CAD or PAD) by autologous stem cell therapy.

Abstract: The methods, compositions, cells and kits described herein are based on the discovery that stem cells, when injected into ischemic tissue of mammals, can be protected by preconditioning of the ischemic tissue with hypoxia-regulated human VEGF and human IGF-1. Methods, compositions, cells and kits for treating tissue injured by ischemia or at risk of ischemic injury in a subject are thus described herein.

Abstract: Methods and compositions for the treatment of hypoxia associated disorders by directional angiogenesis/arteriogenesis. Conditionally silenced vectors expressing a therapeutic molecule under hypoxic conditions avoid chaotic vascularization and allow for the orderly growth of new vessels into damaged tissue.

Abstract: Expression vectors are disclosed that are comprised of (a) one or more silencer elements and conditionally inducible elements to form silencer-inducible regions and (b) promoters in operative linkage upstream of at least one expressed region. The expression vector thereby regulates expression of at least one downstream region by conditional silencing in which an expressed DNA region of a gene is transcribed to produce RNA transcripts, which may or may not be translated to produce polypeptides. Genetically engineered mammalian cells and non-human mammals can be made using such expression vectors through transfection and transgenic techniques. Moreover, processes of making and using the aforementioned products are disclosed (e.g., the expression vector may be used diagnostically, therapeutically, or prophylactically).

Abstract: Expression vectors are disclosed that are comprised of (a) one or more silencer elements and conditionally inducible elements to form silencer-inducible regions and (b) promoters in operative linkage upstream of at least one expressed region. The expression vector thereby regulates expression of at least one downstream region by conditional silencing in which an expressed DNA region of a gene is transcribed to produce RNA transcripts, which may or may not be translated to produce polypeptides. Genetically engineered mammalian cells and non-human mammals can be made using such expression vectors through transfection and transgenesis techniques. Moreover, processes of making and using the aforementioned products are disclosed (e.g., the expression vector may be used diagnostically, therapeutically, or prophylactically).

Abstract: Hypoxia-acidosis-associated cell death is mediated by BNIP3, a member of the Bcl-2 family of apoptosis-regulating proteins. Chronic hypoxia induced the expression and accumulation of BNIP3 mRNA and protein in cardiac myocytes but acidosis was required to activate the death pathway. Acidosis stabilized BNIP3 protein and increased the association with mitochondria. Cell death by hypoxia-acidosis was blocked by pretreatment with antisense BNIP3 oligonucleotides. The pathway included extensive DNA fragmentation and opening of the mitochondrial permeability transition pore but no apparent caspase activation. Overexpression of wild type BNIP3, but not a translocation-defective mutant activated cardiac myocyte death when the myocytes were acidotic or hypoxic.

Abstract: Methods and compositions relating to chimeric genes containing (i) a tissue-specific promoter and (ii) a hypoxia response enhancer element, both of which are operably linked to a selected gene, such as a reporter gene, therapeutic gene (e.g., bcl-2, NOS, catalase and SOD), or deleterious gene are disclosed. Expression of the selected gene is enhanced in the target tissue under hypoxia conditions, such as conditions encountered during episodes of ischemia and reperfusion. The methods and compositions may be used as therapeutics and/or diagnostics.

Abstract: Methods and compositions relating to chimeric genes containing (i) a tissue-specific promoter and (ii) a hypoxia response enhancer element, both of which are operably linked to a selected gene, such as a reporter gene, therapeutic gene (e.g., bcl-2, NOS, catalase and SOD), or deleterious gene are disclosed. Expression of the selected gene is enhanced in the target tissue under hypoxic conditions, such as conditions encountered during episodes of ischemia and reperfusion. The methods and compositions may be used as therapeutics and/or diagnostics.

Abstract: The present invention relates to a device for latching a terminal to a battery post. More specifically, a finger on the free end of the terminal's hoop has several sets of teeth and the channel of the terminal has an opening through which the finger is inserted. Further, the finger has support means so that a pair of pliers may be used to tighten the hoop about the battery post by passing the finger into the opening and latching a set of teeth on the channel member wall.