Concert recording 2018-11-13

[Track 1]. Douzes etudes pour Caisse Claire. No. 1 / Jacques Delecluse -- [Track 2]. Ghost garden / Adam Hopper -- [Track 3]. Rotation no. 4 / Eric Sammut -- [Track 4]. Nine French-American rudimental solos. No. 6 / Unknown -- [Track 5]. Advanced studies for snare drum. No. 3 / Mitchell Peters -- [Track 6]. Tempest / Todd Ukena -- [Track 7]. Excerpt from Northern lights / Eric Ewazen -- [Track 8]. Caleidoscópio / Gene Koschinksi -- [Track 9]. Advanced studies for snare drum. No. 1 / Peters -- [Track 10]. Sweet dreams from Album for the young / Tchaikovsky arranged by L.H. Stevens -- [Track 11]. Furioso and valse in D minor / Earl Hatch -- [Track 12]. Pratt\u27s taps / William Schinstine -- [Track 13]. Max / J.C. Combs -- [Track 14]. Raga no. 1 / William Cahn -- [Track 15]. Sechs Miniaturen. No. 3 / Matthias Schmitt -- [Track 16]. Eden / Adam Miller -- [Track 17]. Four pieces for timpani. Mvts. 3 & 4 / John Bergamo -- [Track 18]. Swerve / Gene Kaschinski -- [Track 19]. White knuckle stroll / Casey Cangelosi -- [Track 20]. Evergreen / Benjamin Finley -- [Track 21]. Time remembered / Branden Steinmetz

Concert recording 2019-04-16

[Track 1]. Rotation #2 / Eric Sammut -- [Track 2]. Pines of Rome mvt 1 / Ottorino Respighi -- [Track 3]. Chart #2 / Fernando Valencia -- [Track 4]. Chopstakovich / Jesse Sieff -- [Track 5]. Drei Skizzen mvt. III / Matthias Schmitt -- [Track 6]. Sonata no. 1 for G in violoncello. Prelude [Track 7]. Sarabande [Track 8]. Courante / J.S. Bach -- [Track 9]. #1 from Douze Etudes / Jacques Delecluse -- [Track 10]. The offering / Michael Burritt -- [Track 11]. Prelude and blues / Ney Rosauro -- [Track 12]. Danny boy / traditional arranged by Brian Mueller -- [Track 13]. Ransom / Mark Ford -- [Track 14]. Sonata for timpani mvt III / John Beck -- [Track 15]. Dr. Gradus ad Parnassum / Claude Debussy arranged by Paul Bissell -- [Track 16]. Etude #1 / Vic Firth -- [Track 17]. Highlights from Northern lights / Eric Ewazen -- [Track 18]. Jesus loves me / Chad Floyd -- [Track 19]. Faded lines / Andrea Venet - [Track 20]. Triplets / George Hamilton Green arranged by Bob Becker -- [Track 21]. Girlfriends medley / Bob Becker -- [Track 22]. Selections from Oru Secu. Guaguancó [Track 23]. Guarapachangueo / Traditional trans. Valencia

Identifying New Treatments For Memory Disorders: From Mice To Men

The population of older Americans will expand greatly in the next 20 years and, as a consequence, disorders of aging, such as Alzheimer’s disease, will become more prevalent. Drug treatments for Alzheimer’s disease currently exist, however they are either ineffective for some people or cause significant side effects. These drugs were developed to correct imbalances in brain chemistry, which may or may not exist early in the disease. However, a brain abnormality that clearly appears early in the course of Alzheimer’s disease is neuronal injury and/or loss in the hippocampus and related medial temporal lobe structures of the brain. The purpose of our research has been to experimentally produce a similar condition of neuronal loss in laboratory animals and to use these animals to test the efficacy of potential new treatments for Alzheimer’s disease. Animals (rats and mice) with neuronal loss in the hippocampus exhibit changes in activity that may be relevant to the agitation observed in Alzheimer’s disease. Moreover, such animals demonstrate profound memory deficits, especially in the area of spatial memory. Our research to date has shown that drugs that are currently used in the treatment of Alzheimer’s disease are ineffective in improving memory in animals with hippocampal neuronal loss. However, some antipsychotic drugs that are prescribed for agitation in Alzheimer’s disease also seem to slightly improve memory in animals with hippocampal neuronal loss. This research should enhance our understanding of the biological basic of memory and offer new insights into improving treatment for memory disorders

Genetic Association and Risk Scores in a Chronic Obstructive Pulmonary Disease Meta-analysis of 16,707 Subjects.

The heritability of chronic obstructive pulmonary disease (COPD) cannot be fully explained by recognized genetic risk factors identified as achieving genome-wide significance. In addition, the combined contribution of genetic variation to COPD risk has not been fully explored. We sought to determine: (1) whether studies of variants from previous studies of COPD or lung function in a larger sample could identify additional associated variants, particularly for severe COPD; and (2) the impact of genetic risk scores on COPD. We genotyped 3,346 single-nucleotide polymorphisms (SNPs) in 2,588 cases (1,803 severe COPD) and 1,782 control subjects from four cohorts, and performed association testing with COPD, combining these results with existing genotyping data from 6,633 cases (3,497 severe COPD) and 5,704 control subjects. In addition, we developed genetic risk scores from SNPs associated with lung function and COPD and tested their discriminatory power for COPD-related measures. We identified significant associations between SNPs near PPIC (P = 1.28 × 10-8) and PPP4R4/SERPINA1 (P = 1.01 × 10-8) and severe COPD; the latter association may be driven by recognized variants in SERPINA1. Genetic risk scores based on SNPs previously associated with COPD and lung function had a modest ability to discriminate COPD (area under the curve, ∼0.6), and accounted for a mean 0.9-1.9% lower forced expiratory volume in 1 second percent predicted for each additional risk allele. In a large genetic association analysis, we identified associations with severe COPD near PPIC and SERPINA1. A risk score based on combining genetic variants had modest, but significant, effects on risk of COPD and lung function