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Summer Practice Oral Presentation: September 27th, Lecture Hall

Submit your oral presentation and written report files before 5:00 PM on September 21st to Ms. Sun Xiaqin: 10811017@pku.edu.cn or call 62754880. This presentation focuses on oral presentation skills and scientific ideas.

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Summer Practice Oral Presentation: September 27th, Lecture Hall

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  1. 暑期实践口头报告会：9月27日，报告厅Oral presentation ppt fileWritten report file 请将以上2个文件在9月21日下午5：00前传至：孙夏琴：10811017@pku.edu.cn 62754880

  2. Oral Presentation Skills Scientific ideas are what you sell Modified from Samuel B. Silverstein, Dept. Physics, Stockholm University

  3. Your audience are trapped to your talk So take good care of them Interact with your audience Look at your audience Keep eye contact with your audience Watch the body language of your audience

  4. First identification of caspase inhibitory factor (CIF), the only natural inhibitor to active caspase-6, induced by 17--estradiol at physiological concentrations. Human Talking mouse First direct evidence showing caspase-6 (but not caspase-3) is the key player in human neuronal cell death and may be involved in AD development. = = Supporting evidence that both estrogen and androgens can be potential candidates for early anti-amyloid therapy for AD. Structural integrity Functional integrity Summary and Conclusions Implication of caspase-6 in human neuronal cell death Inhibition of caspase-6 in human neuronal cell death

  5. One slide, one message

  6. Caspase-6 activation is involved in intracellular A1-42 toxicity * p<0.01

  7. 100 ** p<0.01 Injection of denatured recombinant caspase-6 (100 pg csp6/neuron) 90 ** 80 45 35 60 80 25 40 ** ** % Neuronal Cell Death % Neuronal Cell Death 70 20 ** 15 0 0 4 8 16 60 5 Time (days) 50 % Neuronal Cell Death ** DMSO ** ** Z-VAD-fmk caspase-6 BOC-D-fmk Z-VEID-fmk Z-IETD-fmk Z-DEVD-fmk 40 ** ** 30 ** * ** p<0.01 * p<0.05 20 0 10 5 0 Stau 50 20 10 0.1 0.5 100 0.01 0.05 0.25 pg R-Csp-6/cell Caspase-6 induces neuronal cell death in a dose-dependent manner

  8. . 100 80 caspase-3 caspase-6 caspase-7 60 % Neuronal Cell Death caspase-8 40 20 0 0 5 10 15 20 Time (days) 100 caspase-3 80 caspase-6 cIAP1 cIAP2 NAIP caspase-7 60 % Astrocytic Cell Death caspase-8 40 116K 20 52K 0 0 5 10 15 20 actin Time (days) Different sensitivities to caspases in human neurons and astrocytes

  9. Estrogen responsive element reporter (firefly luciferase) Nucleus Thymidine Kinase (promoter) Estrogen ER Luciferase activity Lower or abolish ER+dominant negative ER constructs Transfection efficiency Luc reporter (renilla) of luciferase activity DBD PM Endogenous ER ERE (promoter) Luc reporter (firefly) X X Mutant ER ERE (promoter) Luc reporter (firefly) ER activity is measured by Luciferase reporter system Luciferase activity=(firefly/renilla)*10,000

  11. Use simple and clear background Slide transition and animation effects

  12. Caspase-6, but not caspase-3, -7 or –8, is activated during serum deprivation-induced human neuronal cell death(LeBlanc et al., 1999). Caspase-6 can cleave APP directly, which may be a pathway to increase A production(LeBlanc et al., 1999; Pellegrini et al., 1999). Active caspase-6 p10 fragments may increase in AD brains(LeBlanc et al., 1999). Caspase-6 inhibitor can block apoptotic promoting effects of APP-BP1, an APP binding protein(Chen et al., 2000). Caspase-6 specific inhibitor can block apoptosis in human neurons(LeBlanc et al., 1999). Caspase-6 may be involved in human neuronal cell death

  13. Implication and Inhibition of Caspase-6 in Human Neuronal Cell Death Yan Zhang Department of Neurology and Neurosurgery McGill University

  14. First identification of caspase inhibitory factor (CIF), the only natural inhibitor to active caspase-6, induced by 17--estradiol at physiological concentrations. Human Talking mouse First direct evidence showing caspase-6 (but not caspase-3) is the key player in human neuronal cell death and may be involved in AD development. = = Supporting evidence that both estrogen and androgens can be potential candidates for early anti-amyloid therapy for AD. Structural integrity Functional integrity Summary and Conclusions Implication of caspase-6 in human neuronal cell death Inhibition of caspase-6 in human neuronal cell death

  15. Acknowledgements Dr. Andréa C. LeBlanc Alzheimer Society Canada for “Doctoral Training Award” Dr. Stefano Stifani Dr. Bernard Turcotte Dr. Heather Durham Dr. Judes Poirier Dr. Antonis Koromilas Dr. Mark Trifiro Dr. Lenore Beitel Dr. Sylvie Mader Dr. Cynthia Goodyer Dr. Nathalie Champagne Dr. Lina Musallam Dr. Xavier Roucou Dr. Omar Tounekti Dr. Malcolm Gains Jennifer Hammond Megan Blacker Tracy Petzke Qi Guo Huishan Guo Nicole Quenneville Beverly Akerman Guy Klaiman Younes Bounhar

  16. Intracellular A1-42 Androgen (testosterone and methyl-testosterone) p53 phosphorylation AR Genomic pathway Upregulate Bax Transcriptional regulation of responsive genes Activate caspase-6 CIF? Cell death Other survival pathways Signal transduction pathway Cellular ER Estrogen (17--estradiol)

  17.  

  18. a. 对突触AMPA受体的特性、亚基组成和运输的改变 （1）AMPA受体的亚基组成的调节作用 1. 在成熟的海马组织中，AMPA受体主要由GluR1/GluR2组成，其次是GluR3/GluR2。 2. GluR2对AMPA受体有着多种调节作用：GluR2-lacking AMPAR有着高度的Ca的通透性，高的通道电导，高的开放几率，和整流能力（rectification,内源的细胞内多胺与其相互作用）。所以受体组成对突触传导有重要的调节作用。 （2）AMPA受体亚基磷酸化的调节作用：直接改变受体特性，或者作为一个readout，与突触可塑性和学习有关的信号通路联系起来。 1. 缺少GluR1的831位和845位氨基酸（两个重要的磷酸化位点）的小鼠不能建立ＬＴＤ和ＬＴＰ，并且有空间学习能力的障碍。 2. CaMKII磷酸化GluR1的831位丝氨酸，能极大提高同聚GluR1型AMPAR的单通道电导。在海马CA1区表达CaMKII的组成激活型，可以提高AMPAR的单通道电导。而AMPAR单通道电导的提高在ＬＴＰ时发生。所以被认为是早期ＬＴＰ的机制。 3. PKA对GluR1的845位丝氨酸磷酸化，能提高同聚GluR1型AMPAR的开放频率。 （3）AMPA受体运输的调节作用: AMPAR在突触膜上的密度受到动态的插膜和内化的调节。静息时，GluR2/GluR3型AMPAR有组成性循环。Ca通过NMDAR的内流是受体循环的重要调节信号。GluR1似乎对ＬＴＰ期AMPAR的插膜调节有关；GluR2似乎对LＴＤ期AMPAR的内化有关。

  19. AMPA受体运输（AMPA receptor trafficking）是一个有趣的研究领域。1998年Neuron上首次报道AMPA受体总是处于迅速的插膜和内化的循环中。突触后膜的AMPA受体数量的调控很可能是产生LTP和synaptic plasticity的主要机制。 Regulation of trafficking 4 Biosynthesis of AMPA receptors 1 Transport along dendrites 2 Local insertion and removal from synapses 3

  20. 但是现实中GluR1和GluR2异源聚合成的AMPAR的电导比同聚GluR1型的低很多，虽然CaMKII仍然磷酸化GluR1的831位丝氨酸，其对通道电导没有影响（GluR2似乎存在对GluR1的上位作用）。PKA对GluR1的845位丝氨酸磷酸化，能提高同聚GluR1型AMPAR的开放频率，其作用是否在现实的GluR1/GluR2异聚体也会被GluR2掩盖，有待研究。但是现实中GluR1和GluR2异源聚合成的AMPAR的电导比同聚GluR1型的低很多，虽然CaMKII仍然磷酸化GluR1的831位丝氨酸，其对通道电导没有影响（GluR2似乎存在对GluR1的上位作用）。PKA对GluR1的845位丝氨酸磷酸化，能提高同聚GluR1型AMPAR的开放频率，其作用是否在现实的GluR1/GluR2异聚体也会被GluR2掩盖，有待研究。

  21. Typos Explain the x and y axis Going back and forth Pointer When mistake happens… Bad data A slide disappears Confuse your audience

  22. Arrive early Check: any technical problems? your audience Back up your talk Question period Never cut off questions When you don’t know… Repeat or rephrase the questions Fill up the time Know the literature

  23. Fears of talking in front of people Know your audience Who are they? How many of them? Send one (and only one) message per talk Practice, practice, practice Attitude is everything Be enthusiastic

  24. 《英雄本色》 有信心不一定会成功，没信心一定不会成功。

  25. 暑期实践口头报告会：9月27日，报告厅Oral presentation ppt fileWritten report file 请将以上2个文件在9月21日下午5：00前传至：孙夏琴：10811017@pku.edu.cn 62754880

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