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利什曼原虫和利什曼病 - Norma Andrews P2

本视频由科普中国和生物医学大讲堂出品

Norma Andrews (U. Maryland) Part 2: Leishmania spp and Leishmaniasis

In the second part of this lecture, I will present background material on Leishmania, the intracellular protozoan parasites responsible for severe human pathology in several parts of the world. I will discuss the main disease forms, the history of identification of the causative agent and form of transmission, and recent discoveries that established important concepts in our understanding of this increasingly serious infectious disease.

Norma Andrews moved from Yale University to the University of Maryland in 2010.

2015-12-14 课时:14分钟

入侵细胞和在细胞内生存的策略 - Norma Andrews P3

本视频由科普中国和生物医学大讲堂出品

Norma Andrews (U. Maryland) Part 3: Strategies for Cell Invasion and Intracellular Survival

In the third part of this lecture, I will discuss current work from our laboratory on mechanisms used by the intracellular parasites Trypanosoma cruzi and Leishmania to interact with mammalian cells. In addition to clarifying specific molecular strategies used by these parasites to infect and survive within host cells, these studies also led, in some instances, to unexpected insights on novel pathways regulating mammalian cell function.

Norma Andrews moved from Yale University to the University of Maryland in 2010.

2015-12-14 课时:34分钟

病毒和HIV的介绍 - David Baltimore P1

本视频由科普中国和生物医学大讲堂出品

David Baltimore (Caltech) Part 1: Introduction to Viruses and HIV

Lecture Overview:
In this set of lectures, I describe the threat facing the world from the human immunodeficiency virus (HIV) and a bold proposal on how we might meet the challenge of eliminating this disease by engineering the immune system.

In part 1, I provide a broad introduction to viruses, describing their basic properties and my own history of studying the replication of RNA viruses which led to the discovery of reverse transcriptase. I also illustrate the distinguishing features of equilibrium viruses (e.g. the common cold) that have adapted to co-exist with their host and non-equilibrium viruses (e.g. HIV) that have recently jumped from another species, are not adapted to the new host, and which can lead to disastrous outcomes (e.g. loss of immune function with potential lethality in the case of HIV).

In part 2, I describe the growing health problem that is facing the world with the spread of HIV and the limitations of current drug therapies and vaccine strategies. We need new ideas for tackling this problem. Here and in the next segment, I describe bold strategies of using gene therapy to conquer HIV, The approach that I describe in this segment involves gene therapy to produce short hairpin RNAs (siRNA) that target the destruction of a critical co-receptor of HIV, which the viruses that needs to infect cells. I discuss initial proof-of-principle experiments that suggest this approach might be feasible and the next steps needed to develop this idea into a real therapy.

In this last segment, I describe another gene therapy strategy for HIV in which we propose to develop antibody-like proteins that can be expressed by a patient's B cells and will target the HIV virus for destruction. To achieve this objective, hematopoietic (blood) stem cells must to be targeted with the gene, which will ultimately develop into B cells that express the therapeutic molecule. The ultimate goal is to produce a life-long supply of anti-HIV neutralizing antibodies. In this lecture, I describe the molecular methods underlying this strategy and a development path from proof-of-principle studies in mouse to safe trials in humans. This project receives funding from the Bill and Melinda Gates Foundation. Speaker Bio: After serving as President of the California Institute of Technology for nine years, in 2006 David Baltimore was appointed President Emeritus and the Robert Andrews Millikan Professor of Biology. Born in New York City, he received his B.A. in Chemistry from Swarthmore College in 1960 and a Ph.D. in 1964 from Rockefeller University, where he returned to serve as President from 1990-91 and faculty member until 1994.

For almost 30 years, Baltimore was a faculty member at Massachusetts Institute of Technology. While his early work was on poliovirus, in 1970 he identified the enzyme reverse transcriptase in tumor virus particles, thus providing strong evidence for a process of RNA to DNA conversion, the existence of which had been hypothesized some years earlier. Baltimore and Howard Temin (with Renato Dulbecco, for related research) shared the 1975 Nobel Prize in Physiology or Medicine for their discovery, which provided the key to understanding the life-cycle of HIV. In the following years, he has contributed widely to the understanding of cancer, AIDS and the molecular basis of the immune response. His present research focuses on control of inflammatory and immune responses as well as on the use of gene therapy methods to treat HIV and cancer in a program called "Engineering Immunity".

Baltimore played an important role in creating a consensus on national science policy regarding recombinant DNA research. He served as founding director of the Whitehead Institute for Biomedical Research at MIT from 1982 until 1990. He co-chaired the 1986 National Academy of Sciences committee on a National Strategy for AIDS and was appointed in 1996 to head the National Institutes of Health AIDS Vaccine Research Committee.

In addition to receiving the Nobel Prize, Baltimore's numerous honors include the 1999 National Medal of Science, election to the National Academy of Sciences in 1974, the Royal Society of London, and the French Academy of Sciences. For 2007/8, he is President of the AAAS. He has published more than 600 peer-reviewed articles.

2015-12-14 课时:35分钟

为什么基因治疗能成为消灭HIV的合理工具 - David Baltimore P2

本视频由科普中国和生物医学大讲堂出品

David Baltimore (Caltech) Part 2: Why Gene Therapy Might be a Reasonable Tool for Attacking HIV

Lecture Overview:
In this set of lectures, I describe the threat facing the world from the human immunodeficiency virus (HIV) and a bold proposal on how we might meet the challenge of eliminating this disease by engineering the immune system.

In part 1, I provide a broad introduction to viruses, describing their basic properties and my own history of studying the replication of RNA viruses which led to the discovery of reverse transcriptase. I also illustrate the distinguishing features of equilibrium viruses (e.g. the common cold) that have adapted to co-exist with their host and non-equilibrium viruses (e.g. HIV) that have recently jumped from another species, are not adapted to the new host, and which can lead to disastrous outcomes (e.g. loss of immune function with potential lethality in the case of HIV).

In part 2, I describe the growing health problem that is facing the world with the spread of HIV and the limitations of current drug therapies and vaccine strategies. We need new ideas for tackling this problem. Here and in the next segment, I describe bold strategies of using gene therapy to conquer HIV, The approach that I describe in this segment involves gene therapy to produce short hairpin RNAs (siRNA) that target the destruction of a critical co-receptor of HIV, which the viruses that needs to infect cells. I discuss initial proof-of-principle experiments that suggest this approach might be feasible and the next steps needed to develop this idea into a real therapy.

In this last segment, I describe another gene therapy strategy for HIV in which we propose to develop antibody-like proteins that can be expressed by a patient's B cells and will target the HIV virus for destruction. To achieve this objective, hematopoietic (blood) stem cells must to be targeted with the gene, which will ultimately develop into B cells that express the therapeutic molecule. The ultimate goal is to produce a life-long supply of anti-HIV neutralizing antibodies. In this lecture, I describe the molecular methods underlying this strategy and a development path from proof-of-principle studies in mouse to safe trials in humans. This project receives funding from the Bill and Melinda Gates Foundation.

Speaker Bio: After serving as President of the California Institute of Technology for nine years, in 2006 David Baltimore was appointed President Emeritus and the Robert Andrews Millikan Professor of Biology. Born in New York City, he received his B.A. in Chemistry from Swarthmore College in 1960 and a Ph.D. in 1964 from Rockefeller University, where he returned to serve as President from 1990-91 and faculty member until 1994.

For almost 30 years, Baltimore was a faculty member at Massachusetts Institute of Technology. While his early work was on poliovirus, in 1970 he identified the enzyme reverse transcriptase in tumor virus particles, thus providing strong evidence for a process of RNA to DNA conversion, the existence of which had been hypothesized some years earlier. Baltimore and Howard Temin (with Renato Dulbecco, for related research) shared the 1975 Nobel Prize in Physiology or Medicine for their discovery, which provided the key to understanding the life-cycle of HIV. In the following years, he has contributed widely to the understanding of cancer, AIDS and the molecular basis of the immune response. His present research focuses on control of inflammatory and immune responses as well as on the use of gene therapy methods to treat HIV and cancer in a program called "Engineering Immunity".

Baltimore played an important role in creating a consensus on national science policy regarding recombinant DNA research. He served as founding director of the Whitehead Institute for Biomedical Research at MIT from 1982 until 1990. He co-chaired the 1986 National Academy of Sciences committee on a National Strategy for AIDS and was appointed in 1996 to head the National Institutes of Health AIDS Vaccine Research Committee.

In addition to receiving the Nobel Prize, Baltimore's numerous honors include the 1999 National Medal of Science, election to the National Academy of Sciences in 1974, the Royal Society of London, and the French Academy of Sciences. For 2007/8, he is President of the AAAS. He has published more than 600 peer-reviewed articles.

2015-12-14 课时:31分钟

HIV:免疫工程的大挑战 - David Baltimore P3

本视频由科普中国和生物医学大讲堂出品

David Baltimore (Caltech) Part 3: HIV: The Grand Challenge - Engineering Immunity

Lecture Overview:
In this set of lectures, I describe the threat facing the world from the human immunodeficiency virus (HIV) and a bold proposal on how we might meet the challenge of eliminating this disease by engineering the immune system.

In part 1, I provide a broad introduction to viruses, describing their basic properties and my own history of studying the replication of RNA viruses which led to the discovery of reverse transcriptase. I also illustrate the distinguishing features of equilibrium viruses (e.g. the common cold) that have adapted to co-exist with their host and non-equilibrium viruses (e.g. HIV) that have recently jumped from another species, are not adapted to the new host, and which can lead to disastrous outcomes (e.g. loss of immune function with potential lethality in the case of HIV).

In part 2, I describe the growing health problem that is facing the world with the spread of HIV and the limitations of current drug therapies and vaccine strategies. We need new ideas for tackling this problem. Here and in the next segment, I describe bold strategies of using gene therapy to conquer HIV, The approach that I describe in this segment involves gene therapy to produce short hairpin RNAs (siRNA) that target the destruction of a critical co-receptor of HIV, which the viruses that needs to infect cells. I discuss initial proof-of-principle experiments that suggest this approach might be feasible and the next steps needed to develop this idea into a real therapy.

In this last segment, I describe another gene therapy strategy for HIV in which we propose to develop antibody-like proteins that can be expressed by a patient's B cells and will target the HIV virus for destruction. To achieve this objective, hematopoietic (blood) stem cells must to be targeted with the gene, which will ultimately develop into B cells that express the therapeutic molecule. The ultimate goal is to produce a life-long supply of anti-HIV neutralizing antibodies. In this lecture, I describe the molecular methods underlying this strategy and a development path from proof-of-principle studies in mouse to safe trials in humans. This project receives funding from the Bill and Melinda Gates Foundation.

Speaker Bio: After serving as President of the California Institute of Technology for nine years, in 2006 David Baltimore was appointed President Emeritus and the Robert Andrews Millikan Professor of Biology. Born in New York City, he received his B.A. in Chemistry from Swarthmore College in 1960 and a Ph.D. in 1964 from Rockefeller University, where he returned to serve as President from 1990-91 and faculty member until 1994.

For almost 30 years, Baltimore was a faculty member at Massachusetts Institute of Technology. While his early work was on poliovirus, in 1970 he identified the enzyme reverse transcriptase in tumor virus particles, thus providing strong evidence for a process of RNA to DNA conversion, the existence of which had been hypothesized some years earlier. Baltimore and Howard Temin (with Renato Dulbecco, for related research) shared the 1975 Nobel Prize in Physiology or Medicine for their discovery, which provided the key to understanding the life-cycle of HIV. In the following years, he has contributed widely to the understanding of cancer, AIDS and the molecular basis of the immune response. His present research focuses on control of inflammatory and immune responses as well as on the use of gene therapy methods to treat HIV and cancer in a program called "Engineering Immunity".

Baltimore played an important role in creating a consensus on national science policy regarding recombinant DNA research. He served as founding director of the Whitehead Institute for Biomedical Research at MIT from 1982 until 1990. He co-chaired the 1986 National Academy of Sciences committee on a National Strategy for AIDS and was appointed in 1996 to head the National Institutes of Health AIDS Vaccine Research Committee.

In addition to receiving the Nobel Prize, Baltimore's numerous honors include the 1999 National Medal of Science, election to the National Academy of Sciences in 1974, the Royal Society of London, and the French Academy of Sciences. For 2007/8, he is President of the AAAS. He has published more than 600 peer-reviewed articles.

2015-12-14 课时:19分钟

细菌交流通过群感效应 - Bonnie Bassler P1

本视频由科普中国和生物医学大讲堂出品

Bonnie Bassler (Princeton) Part 1: Bacterial Communication via Quorum Sensing

Bacteria, primitive single-celled organisms, communicate with chemical languages that allow them to synchronize their behavior and thereby act as enormous multi-cellular organisms. This process is called quorum sensing and it enables bacteria to successfully infect and cause disease in plants, animals, and humans. Investigations of the molecular mechanisms underlying quorum sensing are leading to the development of novel strategies to interfere with quorum sensing. These strategies form the basis of new therapies to be used as antibiotics. See more at http://www.ibioseminars.org

2015-12-14 课时:54分钟

霍乱弧菌群体感应和新型抗生素 - Bonnie Bassler P2

本视频由科普中国和生物医学大讲堂出品

Bonnie Bassler (Princeton) Part 2: Vibrio Cholerae Quorum Sensing and Novel Antibiotics

Bacteria, primitive single-celled organisms, communicate with chemical languages that allow them to synchronize their behavior and thereby act as enormous multi-cellular organisms. This process is called quorum sensing and it enables bacteria to successfully infect and cause disease in plants, animals, and humans. Investigations of the molecular mechanisms underlying quorum sensing are leading to the development of novel strategies to interfere with quorum sensing. These strategies form the basis of new therapies to be used as antibiotics. See more at http://www.ibioseminars.org

2015-12-14 课时:20分钟

细胞粘附、信号和癌症 - Mary Beckerle P1

本视频由科普中国和生物医学大讲堂出品

Mary Beckerle (University of Utah) Part 1: Adhesion, Signaling and Cancer

Cell-substratum adhesion is mediated by integrins, a family of transmembrane, heterodimeric, extracellular matrix receptors that are concentrated at focal adhesions. Integin engagement influences a variety of signaling pathways and regulates cell behaviors including motility, proliferation, and survival. Disturbance of normal integrin function is associated with a variety of pathologic conditions including cancer. In the first segment of my seminar, I provide a broad overview of the cancer problem for a lay audience. Advances in our understanding of cancer as a genetic disease are discussed. The influence of cell adhesion on control of cell growth is reviewed. See more at http://www.ibiology.org

2015-12-14 课时:37分钟

粘着蛋白的发现和表征 - Mary Beckerle P2

本视频由科普中国和生物医学大讲堂出品

Mary Beckerle (University of Utah) Part 2: Discovery and Characterization

In the second segment, I describe the identification of the focal adhesion protein, zyxin, by my lab. Recent work revealed that zyxin is down-regulated upon expression of the Ewing sarcoma oncoprotein, EWS-FLI. Loss of zyxin expression results in enhanced cell motility and is also associated with failed apoptotic signaling. Evidence that zyxin shuttles between focal adhesions and the nucleus is presented. The impact of reduced zyxin expression on tumor progression is discussed. See more at http://www.ibiology.org

2015-12-14 课时:51分钟

焦点粘连作为压力传感器 - Mary Beckerle P3

本视频由科普中国和生物医学大讲堂出品

Mary Beckerle (University of Utah) Part 3: Focal Adhesions as Stress Sensors

In the third segment of my seminar, I address a new frontier in cell biology, that is how cells respond to mechanical information. Cells and tissues are exposed to physical forces in vivo and excessive mechanical stress leads to a variety of pathological consequences. I describe a system for exposing cells to controlled mechanical stress and discuss the stretch response. We have discovered that the focal adhesion protein, zyxin, is exquisitely sensitive to mechanical stimulation and is required for the ability of cells to reinforce the actin cytoskeleton when challenged by exposure to cyclic stretch. See more at http://www.ibiology.org

2015-12-14 课时:31分钟