Abstract: An air handling unit (AHU) for a heating, ventilation, air conditioning, and refrigeration (HVACR) system includes a housing and a combustion heater disposed within the housing. The housing includes a combustion section with a first channel and a second channel. The combustion heater includes heat exchanger tubes and a tube support that supports heat exchanger tubes within the combustion section. The tube support slidably disposed in the first channel and the second channel. The combustion heater configured to be slidably removable from the AHU. An AHU for an HVACR system includes a housing with a fan section and a fan assembly disposed within the housing. The fan assembly including a pair of grooves slidably disposed on a pair of rails of the housing. The fan assembly configured to be both slidably removable from the AHU and liftably removable from the AHU.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage, enhancing the survivability of platelets during storage or transfusion and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothrombinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage. In addition, the modified annexin prevents lipid loss from platelets during storage.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage.

Abstract: Modified annexin proteins, including heterodimers and homodimer of various human annexins, are provided for treatment of cerebral thrombosis and global cerebral ischemia. Also provided are phosphatidylserine (PS) binding proteins for treatment of cerebral thrombosis and global cerebral ischemia. The modified annexins and/or PS binding proteins bind PS on cell surfaces, thereby preventing the attachment of leukocytes and platelets to endothelial cells during post-ischemic reperfusion. By maintaining endothelial cell and vascular wall integrity PS binding proteins and/or modified annexin proteins decrease cerebral hemorrhage. Modified annexins and other PS binding proteins also suppress the production of mediators of edema, the extension of cerebral damage during reperfusion and the risk of rethrombosis. Thus, modified annexin proteins and/or other PS binding proteins decrease brain damage following cerebral thrombosis and global cerebral ischemia.

Abstract: A modified annexin protein, preferably annexin V, is used to prevent thrombosis without increasing hemorrhage. Annexin binds to phosphatidylserine on the outer surface of cell membranes, thereby preventing binding of the prothrombinase complex necessary for thrombus formation. It does not, however, affect platelet aggregation necessary for hemostasis. The modified annexin molecule can be a homodimer of annexin, an annexin molecule coupled to one or more polyethylene glycol chains, or an annexin molecule coupled to another protein. By increasing the molecular weight of annexin, the modified annexin is made to remain in circulation for sufficient time to provide a sustained therapeutic effect.

Abstract: Compositions for and methods of attenuating and/or preventing ischemia-reperfusion injury (IRI) are provided. One method comprises administering to a patient in need thereof an agent that binds phosphatidylserine (PS) located on cell surfaces, i.e., PS binding agent. Another method comprises administering to an organ transplant recipient a therapeutic composition comprising a PS binding agent. A method of preventing IRI to cells is also provided. The method comprises adding a PS-binding agent to a therapeutic composition used to treat the cells. Further provided is a method of protecting an organ or a tissue susceptible to IRI. The method comprises contacting the organ or tissue with a PS-binding agent. Such an agent may, for example, attenuate IRI in patients with stroke or myocardial infarction, or following surgical operations. PS-binding agents include modified annexin proteins, antibodies against PS molecules, and other anti-PS molecules.

Abstract: A touchpad device for use with electronic apparatus is disclosed. The device has an active area that is sensitive to movement thereon and to generate electrical signals in response thereto for inputting into the electronic apparatus. The active area of the device defines a plurality of active portions, each of which is arranged to produce an electrical signal in response to at least one defined movement thereon. The device is provided with mounting means comprising a deformable portion for mounting on a substrate of variable size. It is envisaged that the substrate would be one or more fingers of a user, whereby the active portions may be activated by movement thereover of the user's thumb.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage, enhancing the survivability of platelets during storage or transfusion and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage. In addition, the modified annexin prevents lipid loss from platelets during storage.

Abstract: Modified annexin proteins, including a homodimer of human annexin V, are provided. Methods for their use, such as to prevent thrombosis without increasing hemorrhage and to attenuate ischemia-reperfusion injury (IPI), are also provided. The modified annexins bind phosphatidylserine (PS) on cell surfaces, thereby preventing the assembly of the prothromkinase complex. The modified annexin decreases the binding of leukocytes and platelets during post-ischemic reperfusion, thereby restoring microvascular blood flow and decreasing organ damage.

Abstract: Sickle-cell diseases are treated with annexin proteins that are modified to increase their half-life in the circulation.

Abstract: A modified annexin protein, preferably annexin V, is used to prevent thrombosis without increasing hemorrhage. Annexin binds to phosphatidylserine on the outer surface of cell membranes, thereby preventing binding of the prothrombinase complex necessary for thrombus formation. It does not, however, affect platelet aggregation necessary for hemostasis. The modified annexin molecule can be a homodimer of annexin, an annexin molecule coupled to one or more polyethylene glycol chains, or an annexin molecule coupled to another protein. By increasing the molecular weight of annexin, the modified annexin is made to remain in circulation for sufficient time to provide a sustained therapeutic effect.

Abstract: A modified annexin protein, preferably annexin V, is used to prevent thrombosis without increasing hemorrhage. Annexin binds to phosphatidylserine on the outer surface of cell membranes, thereby preventing binding of the prothrombinase complex necessary for thrombus formation. It does not, however, affect platelet aggregation necessary for hemostasis. The modified annexin molecule can be a homodimer of annexin, an annexin molecule coupled to one or more polyethylene glycol chains, or an annexin molecule coupled to another protein. By increasing the molecular weight of annexin, the modified annexin is made to remain in circulation for sufficient time to provide a sustained therapeutic effect.

Abstract: A modified annexin protein, preferably annexin V, is used to prevent thrombosis without increasing hemorrhage. Annexin binds to phosphatidylserine on the outer surface of cell membranes, thereby preventing binding of the prothrombinase complex necessary for thrombus formation. It does not, however, affect platelet aggregation necessary for hemostasis. The modified annexin molecule can be a homodimer of annexin, an annexin molecule coupled to one or more polyethylene glycol chains, or an annexin molecule coupled to another protein. By increasing the molecular weight of annexin, the modified annexin is made to remain in circulation for sufficient time to provide a sustained therapeutic effect.

Abstract: Sickle-cell diseases are treated with annexin proteins that are modified to increase their half-life in the circulation.

Abstract: Methods and pharmaceutical compositions containing the organic germanium polymer propagermanium are used for treating bone disorders such as myeloma bone disease, multiple myeloma, Paget's disease, secondary bone cancers, and periodontitis.

Abstract: A modified annexin protein, preferably annexin V, is used to prevent thrombosis without increasing hemorrhage. Annexin binds to phosphatidylserine on the outer surface of cell membranes, thereby preventing binding of the prothrombinase complex necessary for thrombus formation. It does not, however, affect platelet aggregation necessary for hemostasis. The modified annexin molecule can be a homodimer of annexin, an annexin molecule coupled to one or more polyethylene glycol chains, or an annexin molecule coupled to another protein. By increasing the molecular weight of annexin, the modified annexin is made to remain in circulation for sufficient time to provide a sustained therapeutic effect.

Abstract: Modified toxins including botulinum toxin or tetanus toxin coupled to polyethylene glycol, pharmaceutical compositions of modified toxins, and methods for their use are provided. The methods include treating inappropriate muscle contraction, and treatments for cosmetic purposes.