Abstract: The present invention demonstrates that mitochondrial DNA damage occurs prior to, or simultaneous with, atherosclerotic lesion development, that aortic mitochondrial DNA damage increases with age, and that genotype and diet both influence the level of mitochondrial DNA damage. Hence, the present invention demonstrates that mitochondrial DNA damage occurs early in atherosclerosis, and may be an initiating event in atherogenesis, and provides methods to predict coronary atherosclerotic heart disease based upon the amount of mitochondrial DNA damage.

Abstract: A method is provided for classifying or typing a prokaryote to a class or a type. The method is effected by characterizing at least one polymorphic simple sequence repeat locus in a genome of the prokaryote and, based on a characterization of the polymorphic simple sequence repeat, classifying or typing the prokaryote to a class or a type. Compounds and articles of manufacture are provided for effecting the method.

Abstract: A method for treating a mammal for inducing protective immunity against an autoimmune disease including the step of administering to the mammal a therapeutic composition including a recombinant construct including an isolated nucleic acid sequence encoding a cytokine, the nucleic acid sequence being operatively linked to one or more transcription control sequences. A method for treating a mammal for inducing protective immunity against an autoimmune disease including the steps of (a) removing cells of the mammal; (b) transducing the cells in vitro with a recombinant construct including an isolated nucleic acid sequence encoding a cytokine, the nucleic acid sequence being operatively linked to one or more transcription control sequences; and (c) reintroducing the transduced cells to the mammal.

Abstract: The subject invention provides R(+)-N-propargyl-1-aminoindan and pharmaceutically acceptable salts thereof, as well as pharmaceutical compositions containing the same. The subject invention also provides methods of treating a subject afflicted with Parkinson's disease, a memory disorder, dementia, depression, hyperactive syndrome, an affective illness, a neurodegenerative disease, a neurotoxic injury, stroke, brain ischemia, a head trauma injury, a spinal trauma injury, neurotrauma, schizophrenia, an attention deficit disorder, multiple sclerosis, or withdrawal symptoms, using R(+)-N-propargyl-1-aminoindan or the pharmaceutically acceptable salt of the subject invention. The subject invention further provides a method of preventing nerve damage in a subject.

Abstract: The present invention provides an anti-IgM antibody conjugate comprising: a monoclonal antibody which binds selectively to IgM antibody, does not bind to IgG1 or IgG2 antibody, and has a G isotype; and a cytotoxic moiety conjugated to said monoclonal antibody. The present invention also provides a method for collecting hybridoma producing IgG isotype monoclonal antibodies comprising: treating a hybrid cell population with a monoclonal antibody which has a G isotype and binds selectively to IgM antibody but does not bind to IgG1 or IgG2 antibody; subjecting said resulting immuncomplexed cells to sorting; and collecting the cells which have not complexed with said antibodies.

Abstract: The present invention provides a method of screening individuals at risk for developing diseases caused by trinucleotide repeat sequence instability. Specifically, the present invention is drawn to screening individuals at risk for developing autosomal dominant spinocerebellar ataxia type 6 by determining the length of a CAG trinucleotide repeat in the &agr;1A calcium channel gene of the individual. In addition, there is provided a method of identifying genes which are disease-causing due to trinucleotide repeat sequence instability by large scale genotyping.

Abstract: This invention is directed to compounds of the following formula wherein when a is O, b is 1 or 2; when a is 1, b is 1, m is from 0-3 X is O or S, Y is halogeno, R1 is hydrogen C1-4 alkyl, R2 is hydrogen, C1-4 alkyl, or optionally substituted propargyl and R3 and R4 are each independently hydrogen, C1-8 alkyl, C6-12 aryl, C6-12 aralkyl each optionally substituted. This invention is also directed to the use of these compounds for treating depression, Attention Deficit Disorder (ADC), Attention Deficit and Hyperactivity Disorder (ADHD), Tourette's Syndrome, Alzheimer's Disease and other dementia's such as senile dementia, dementia of the Parkinson's type, vascular dementia and Lewy body dementia. This invention is further directed to a pharmaceutical composition comprising a therapeutically effective amount of the above-defined compounds and a pharmaceutically acceptable carrier.

Abstract: A chemical composition and method of use of the composition is described. The chemical composition includes an aza-enediyne, aza-enyne allene, or an aza-diallene. These compound are preferably non-hydrolyzable, cationic compounds that bind to nucleic acids. In addition it is believed that these compounds may undergo chemical reactions in the presence of a nucleic acid to generate reactive intermediates that cleave nucleic acids.

Abstract: The present invention provides a novel composition of matter useful for the treatment of a wide variety of human cancers. The novel composition is synergistic and cytotoxic and comprised of platinum containing antineoplastic agent and tamoxifen. The present invention also provides for methods of treating cancer. That is, the present invention provides a novel method of treating non-melanoma cancers used the novel pharmacologic combination of the present invention. Other embodiments of the invention provide novel methods of reducing or overcoming resistance that develops to platinum containing antineoplastic agents, such as, cisplatin.

Abstract: The present invention provides a novel enzyme which de-O-acetylates glucuronoxylomannan of Cryptococcus neoformans and a gene encoding such enzyme. Also provided are applications of such enzyme in treating cryptococcosis.

Abstract: Pharmaceutical compositions for the treatment of a neurological disorder of neurotrauma or for improving memory in a patient comprising a therapeutically effective amount of S-(−)-N-proparygl-1-aminoindan or a pharmaceutically acceptable salt thereof as active ingredient, and a pharmaceutically active carrier. The pharmaceutical compositions are adapted, in particular for treating a neurological hypoxia or anoxia, neurodegenerative diseases. Parkinson's Disease, Alzheimer's Disease, neurotoxic injury, head trauma injury, spinal trauma injury or any other form of nerve damage.

Abstract: A Distributed Shared Memory (DSM) system that provides a single address space shared by a number of processes The DSM is capable of accomplishing lowered granularity of distributed shared memory. The DSM system includes the address space constituting a virtual address space that includes virtual pages. Two or more virtual pages in the virtual address space are mapped to the same memory page that includes one page. The page includes two or more minipages. There is further provided an assignor assigning independently, through the virtual pages, access permission to minipages that reside in the same page of the memory object. There is further provided processor processing independently in different processes minipages that reside in the same page.

Abstract: This invention is directed to compounds of the following formula: wherein m is from 0-4; X is O or S; Y is halogeno; R1 is hydrogen or C1-4 alkyl; R2 is hydrogen, C1-4 alkyl or optionally substituted propargyl; and R3 and R4 are each independently hydrogen, C1-8 alkyl, C6-12 aryl, C6-12 cycloalkyl or C6-12 aralkyl, R5 is hydrogen or C1-4 alkyl; and pharmaceutically acceptable salts thereof, provided that when X is O, R2 is optionally substituted propargyl. This invention is also directed to the use of these compounds for treating depression, Attention Deficit Disorder (ADD), Attention Deficit and Hyperactivity Disorder (ADHD), Tourette's Syndrome, Alzheimer's Disease and other dementia's such as senile dementia, dementia of the Parkinson's type, vascular dementia and Lewy body dementia. This invention is further directed to a pharmaceutical composition comprising a therapeutically effective amount of the above-defined compounds and a pharmaceutically acceptable carrier.

Abstract: Methods for determining a potential of a hyperglycemic patient to develop vascular complications in response to oxidative stress and for determining the importance of reducing oxidative stress in a specific hyperglycemic patient are disclosed. Each method includes the step of determining a haptoglobin phenotype of the patient. A variety of means of making this determination are further disclosed.

Abstract: The present invention provides a non-viral vector, comprising a cell binding component having a biotin-binding element conjugated to a biotinylated moiety. Also, provided is a method of introducing genetic material inside a specific cell comprising the administration of the non-viral vector to a human, wherein said non-viral vector comprises a cell binding component having a biotin-binding element conjugated to a biotinylated moiety. In addition, there is provided a method of delivering a cytotoxic moiety to a cell comprising the administration of the non-viral vector to a human.

Abstract: The present invention provides DNA encoding a m-rigui2 protein selected from the group consisting of: (a) isolated DNA which encodes a m-rigui2 protein; (b) isolated DNA which hybridizes to isolated DNA of (a) above and which encodes a m-rigui2 protein; and (c) isolated DNA differing from the isolated DNAs of (a) and (b) above in codon sequence due to the degeneracy of the genetic code, and which encodes a m-rigui2 protein. Also provided is a vector capable of expressing the DNA adapted for expression in a recombinant cell and regulatory elements necessary for expression of the DNA in the cell. Further, a host cell transfected with the vector disclosed herein the vector expressing a m-rigui2 protein.

Abstract: An electric storage cell (10) comprises a zinc anode (12) and a sulfur cathode (14), wherein the zinc and the sulfur are in contact with an aqueous solution (22) containing sulfur during the process of battery discharge. In this invention, specific conditions for the aqueous sulfur electrolyte are chosen to overcome the normal ineffectiveness of zinc oxidation in the presence of aqueous zero valent sulfur. Normally, a zinc anode (12) cannot be oxidized in an aqueous solution containing sulfur, because the product of the discharge would be zinc sulfide. This zinc sulfide is a highly insoluble salt and creates a layer which passivates the zinc and renders it completely ineffective to battery discharge. The performance of the battery is made possible by high OH- and HS-ion concentrations formed by the addition of salts to the aqueous zero valent sulfur solution, and permits effective and efficient battery discharge.

Abstract: A tool kit for use in the inducement of the reconstitution and healing of the sternum after an operation on a patient in the chest region in which during the operation the sternum is cut into two hemisterna. The kit serves for the post-operational approximation and fixation of the hemisterna in a position which enables their spontaneous growing together. The kit includes an approximation tool for the application of a selected force to the hemisterna to brig them into reconstituted configuration, and a set of clamping apparatus for firmly locking the hemisterna in the reconstituted configuration. The clamping apparatus is made of a non-immunogenic polymeric material that is readily degraded in the patient's body to yield degradation products readily absorbed by the patient's body.

Abstract: The present invention provides mutants of the Rb gene and methods utilizing these mutants. Along with mutated Rb genes, the present invention provides plasmids containing a mutated Rb gene. In addition, the present invention provides cells transfected with the plasmids of the present invention. Moreover, the present invention provides for methods of inhibiting pathophysiological cell proliferation.

Abstract: The present invention provides DNA encoding a RIGUI protein selected from the group consisting of: (a) isolated DNA which encodes a RIGUI protein; (b) isolated DNA which hybridizes to isolated DNA of (a) above and which encodes a RIGUI protein; and (c) isolated DNA differing from the isolated DNAs of (a) and (b) above in codon sequence due to the degeneracy of the genetic code, and which encodes a RIGUI protein. Also provided is a vector capable of expressing the DNA adapted for expression in a recombinant cell and regulatory elements necessary for expression of the DNA in the cell. Further, a host cell transfected with the vector disclosed herein the vector expressing a RIGUI protein.