Abstract: A shell cracking device is described for applying good mechanical advantage to the shell cracking process. In one embodiment, the shell cracker also includes a base or platter providing food liquid containment, e.g., having sidewalls of sufficient height to prevent spillage, for the shell cracking process. The base may also act as a pressure base for shell cracking and provide support for the cracking assembly.

Abstract: A topographic model useful to design and synthesize memory-enhancing substances is disclosed. Administration of substances designed by this method to enhance memory in mammals, including humans, is disclosed. Such substances include peptides having the amino acid sequence Val Phe Phe.

Abstract: A method is disclosed for attenuation of nervous system damage after injury which comprises administering therapeutic amounts of PREG, PREG-S, or esters of PREG or PREG-S together with an enhancer of secretory processes in non-neural cells such as a bacterial lipopolysaccharide and a non-steroidal antiinflammatory substance such as indomethacin.

Abstract: Amnestic novel peptides are disclosed. A topographical map or surface which includes binding sites for peptides having amnestic procedures and the use of such surface to identify and synthesize such peptides is also disclosed.

Abstract: A method is disclosed for attenuation of nervous system damage after injury which comprises administering therapeutic amounts of PREG, PREG-S, or esters of PREG or PREG-S together with an enhancer of secretory processes in non-neural cells such as a bacterial lipopolysaccharide and a non-steroidal antiinflammatory substance such as indomethacin.

Abstract: Three non-amnestic and non-memory enhancing peptides, Asp Phe Phe Val Gly (SEQ ID NO: 1), Gln Phe Val Gly (SEQ ID NO: 2), and Ala Ile Phe Thr (SEQ ID NO: 3), that block the effects of .beta.-(12-28), a peptide homologous to amyloid .beta. protein (A.beta.) are disclosed. This invention relates to amelioration of amnesia and other neurotoxicitiy in Alzheimer disease (AD) caused by deposition of A.beta. and, therefore, relates to attenuation of the disease process and consequential improvement of the quality of life for individuals suffering from AD.

Abstract: A method for promoting regeneration of damaged nerve tissue, comprising administering, either alone or in combination, an effective amount of an antimitotic agent or a proton-withdrawing buffer to the damage site. Antimitotic agents reduce the rate of growth of glial cells, and buffers facilitate the growth of nerve tissue and inhibit glial cell growth. Referred antimitotic agents are cytosine arabinoside, 5-fluorouracil, and hydroxyurea. Preferred buffers are TREA and HEPES. Compositions are disclosed which include antimitotic agent, buffer, and an oxygen-supplying compound, such as hydrogen peroxide.

Abstract: Dehydroepiandrosterone and acceptable salts thereof are utilized for sexual disfunction therapy.

Abstract: A procedure for the treatment of degenerative diseases of the central nervous system, including Alzheimer's disease, multiple sclerosis and the like, by the administration of amodiaquin and related compounds is disclosed.

Abstract: Disclosed is a method for treating nervous system deterioration associated with aging and Alzheimer's disease by administering a therapeutically-effective amount of dehydroepiandrosterone or its sulfate. Also disclosed is the co-administration of dehydroepiandrosterone or its sulfate and a potassium channel antagonist. The disclosure is also directed to pharmaceutical compositions containing dehydroepiandrosterone, alone or in combination with a potassium channel antagonist. Dehydroepiandrosterone is also shown to facilitate the growth of nervous system tissue, particularly in culture.

Abstract: A procedure for the treatment of degenerative diseases of the central nervous system, including Alzeheimer's disease, multiple sclerosis and the like, by the administration of amodiaquin and related compounds is disclosed.