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Nobel Conference “The Cell Cycle and Cell Death in Disease”

Date:  June 8 – 11, 2016

Location: Nobel Forum, Karolinska Institutet

Read more HERE

Nobel Laureate Revisiting Lecture

Thursday, April 7th at 4.30

Venue: Wallenbergsalen, Nobel Forum, Karolinska Institutet, Nobels väg 1

Jack Szostak, Nobel Laureate in Physiology or Medicine 2009

The Origin of Cellular Life

The amazing complexity and diversity of life is a result of billions of years of evolution.  But how did the process of evolution itself begin? I will describe how efforts to design and build very simple living cells are testing our assumptions about the nature of life, generating ideas about how life emerged from the chemistry of the early earth, and even offering clues as to how modern life evolved from its earliest ancestors.

Host: Professor Rune Toftgård

Contact: Ann-Mari Dumanski, Nobel Office, Nobel Forum
08-524 878 00,

Research Lecture at NOBEL FORUM – Mary-Claire King

Research Lecture at NOBEL FORUM
14 April, kl. 16.30
Free admission

Mary-Claire King, PhD, American Cancer Society Professor
Departments of Medicine and Genome Sciences
University of Washington, Seattle, WA


“We are extraordinarily fortunate to be living in this era of exciting discoveries and rapid scientific advancements in human genetics. There has not been a more exciting time to be involved in the genetics field since Gregor Mendel counted smooth and wrinkled peas and Charles Darwin tended finches.”
Mary-Claire King, PhD


That some families are particularly severely affected by breast cancer has been known since the time of the ancient Greek physicians and systematically documented first by the work of Paul Broca in the 19th century and then Jane Lane-Claypon in the early 20th century. The realization that this problem could be conceptualized in terms of formal human genetics and addressed by a combination of mathematical and experimental tools led to our demonstration in 1990 that breast cancer in some severely affected families was due to severe mutations in a then-still-hypothetical gene BRCA1 on human chromosome 17q. The cloning and functional characterization of BRCA1 and subsequently of BRCA2 and other sister genes has led, over the past 20 years, to widespread genetic testing for inherited predisposition to breast and ovarian cancer, to preventive interventions for women with mutations in BRCA1 or BRCA2, and to development of effective treatments based on genotypes of patients and their tumors.

Karolinska Research Lectures – Eve Marder

Research Lecture at NOBEL FORUM
17 March, kl. 16.30
Free admission

Eve Marder, PhD, Professor of Biology

Volen Center for Complex Systems, Brandeis University , Waltham, MA 02454-9110, USA

Title: “Robustness, Variability, Modulation, and Homeostasis in Neurons and Networks

All individual humans and animals are different.  How well-tuned do brains need to be to produce behavior that we consider healthy and normal?  This question has been difficult to study rigorously in animals with large brains, but small nervous systems with identified neurons and circuits have allowed us to ask this question in the past few years.  Experimental work on the crustacean stomatogastric ganglion (STG) has revealed a 2-6 fold variability in many of the parameters that are important for circuit dynamics.  These include the strength of the same synapse across animals, as well as the conductance densities of many membrane currents and the copy numbers of the mRNA that encode those currents (Goaillard et al., Nat Neuroscience. 2009).  At the same time, a body of theoretical work shows that the similar network performance can arise from diverse underlying parameter sets (Prinz et al., Nat Neuroscience 2004; Gutierrez and Marder, 2013).  Together, these lines of evidence suggest that each individual animal has found a different solution to producing “good enough” motor patterns for healthy performance in the world.  These findings raise the question of the extent to which animals with different sets of underlying circuit parameters can respond reliably and robustly to perturbations.  Consequently, we studied the effects of temperature and neuromodulation on the pyloric rhythm of crabs.  Temperature is a global perturbation that influences every membrane current differently.  Nonetheless, we find that all animals respond reliably and robustly to changes in temperature that mimic those the animals ordinarily encounter in their environment (Tang et al PLos Biol 2010), but more extreme temperature perturbations “crash” the network, resulting in a loss of rhythmic activity (Tang et al, 2012; Rinberg et al., 2013).  Each individual “crashes” in different ways, consistent with the underlying variability in parameter structure.   Moreover, neuromodulation alters the sensitivity of the networks to temperature, suggesting that one function of neuromodulation may be to enhance robustness to some kinds of perturbations.

Neurons and networks must constantly rebuild themselves in response to the continual and ongoing turnover of all of the ion channels and receptors that are necessary for neuronal signaling.   A good deal of work argues that stable neuronal and network function arises from homeostatic negative feedback mechanisms.  Nonetheless, while these mechanisms can produce a target activity or performance, they are also consistent with a good deal of recent theoretical and experimental work that shows that similar circuit outputs can be produced with highly variable circuit parameters.  I will describe new computational models (O’Leary et al., PNAS 2013; Neuron et al, 2014) for cellular homeostasis that give insight into a variety of experimental observations, including correlations in the expression of ion channel genes.  In response to perturbation these homeostatic models usually compensate for perturbations, but some perturbations elude compensation.  Moreover, situations can arise in which the homeostatic mechanisms result in aberrant behavior, such as may occur in disease.


Host:  Christian Broberger

Dept. of Neuroscience, Karolinska Institutet

Tel. 08- 524 87038;

Tatiana Goriatcheva

Nobelkansliet, Nobel Forum,

Tel. 08-524 87805,