niantly affect motor function in either male or female mice, nor in both sexes combined, although a longitudinal analysis method showed that the in- teraction of the three doses with the time when rotarod measurements were performed (before vs. after treatment) tended toward a protective effect of 17-AAG  Conclusions: Motor function Bleomycin tended to decline less in mice receiving7-AAG, while there was a strong dichotomy by sex in the ef- fect of7-AAG on NFT. A larger study with a less toxic method of adminis- tration is warranted. vestigate the effects of a novel compound (Val8) GLP-1, a GLP-1 recep- P3-364 ACCUMULATION OF P27 KIP1 IS ASSOCIATED tor agonist and the GLP-1 antagonist Exendin(9-36). We investigate the effects of these compounds have on learning and memory. Further we in- vestigated if these compounds cross the BBB. Methods: 36 C57B16 mice where injected for 21 days with (Val8)GLP-1 (25nMol/kg), Exendin (9-36) (25nMol/kg), or saline for 21 days. Learning and memory was as- sessed using the Morris Watermaze(MWM) and the Novel

Object Recog- nition Task (NOR). Electrophysiology was used to assess the effects on synaptic plasticity and Long Term Potentiation. BrdU immunohistochem- istry was used to assess proliferation of progenitor cells in the hippocam- pus. The RIA was used to buy Bleomycin investigate if (Val8)GLP-1 & GLP-1 crosses the BBB. Subjects were injected with either 25nMol/kg or 250nMol/kg (Val8)GLP-1 or GLP-1. Glucose and insulin levels where also measured. Results: We found that GLP-1 crosses the BBB. Both doses showed a signiant increase of concentrations in the brain (p < 0.05 & p < 0.01). Administration of (Val8) GLP-1 at 25nmol and 250nmol also showed signiantly higher levels of GLP-1 when compared to controls (P < 0.05 & P < .01).(Val8) GLP-1 did promote progenitor cells in the hippocampus when compared to controls. We found that (Val8) GLP-1 signiantly improved learning and memory in the Novel Object WITH RETINOIC ACID-INDUCED GROWTH ARREST AND NEURONAL DIFFERENTIATION OF IMMORTALIZED HUMAN NEURAL PROGENITOR CELLS Yongmei Zhao , Haiyan Zhang 2 , Qiuyan Xu , Qunyuan Xu 3 , Xuanwu Hospital, Capital Medical University, Beijing, China; 2

Department of Cell Biology, Capital Medical University, Beijing, China; 3 Beijing Institute for Neuroscience, Capital Medical University, Beijing, China. Contact e-mail: Background: Neural progenitor cells from human brain are crucial for suc- cessful  purchase Bleomycin development of approaches to cell therapy for neurodegenerative dis- eases including Alzheimer s disease. The objectives of this study are to investigate whether immortalized human neural progenitor cells (hSN12W- TERT cells) can be induced to differentiate toward a neuronal phenotype by all-trans retinoic acid (RA), and to investigate whether there is any func- tional link between p27 Kip1 function and RA in the control of growth arrest and neuronal differentiation in hSN12W-TERT cells. Methods: Human neu- ral progenitor cells derived from the striatums of human embryos at2 weeks? School of Pharmacy, The Chinese University of Hong Kong, Shatin, Hong 2 JOURNAL OF SURGICAL RESEARCH: VOL. – , NO. – , – 2011 degradation of vital cellular proteins in the proteasome leads to cell death [3, 4] . Preclinical experiments led to the surprising observation that cancer cells, because of their so-called inase addiction,?are signiantly more sensitive to HSP90 inhibition

than nontrans- formed cells are [5, 6] . This ding raised the possibility that HSP90 inhibitors could be used in cancer patients as new chemotherapeutic agents. A  base level geldanamycin derivative with a more favorable toxicity proe,7-allylamino-17-demethoxy-geldanamycin (17-AAG), has entered clinical phase I/II trials for breast cancer, myeloma, and metastatic melanoma after being tested in xenograft and transgenic mouse models [7?] . The membrane transporter P-glycoprotein (also called ABCB1 or MDR1) functions as a drug efx pump that actively transports drugs from the inside to the