Integrated Calendar

<p>In this seminar, two new models will be presented. The first new model is a first-principles description of the propagation of light in a cloud, based on a classical solution to Maxwell's equations rather than radiative transfer theory. The second new model is a fully three-dimensional, time-dependent model of the regions of possible sprite inception in the mesosphere, based on the classical method of images from electrostatics rather than finite differencing in space. The reason why each model is unique, the problems each model can solve, and the kinds of results each model can produce will be discussed</p>

<p>Cell-cell communication is essential for growth, development and function. Cells can communicate mechanically by responding to mechanical deformations generated by their neighbors in the extracellular matrix (ECM).</p><p>We use a 2D cardiac tissue model to study the role of mechanical communication between cardiac cells in the normal conduction wave. We quantify the mechanical coupling between cells in a monolayer and use this to identify a critical threshold of mechanical coupling, below which spiral waves are induced in the tissue. We demonstrate that normal conduction wave can be recovered only using mechanical stimulation. We further show that mechanical coupling reduces the sensitivity to geometrical defects in the tissue.</p><p>We show that due to the dynamic viscoelastic properties of collagen hydrogels (a major component of the cardiac ECM), the shape of the mechanical signal changes in a frequency dependent manner as it propagates through the gel, leading to a frequency dependent mechanical communication. Moreover, we show that the sensitivity of cardiac cell response to the shape of the mechanical signal results from its sensitivity to the loading rate. We also show that an optimal loading rate exists for mechanical communication, implying that there are ideal viscoelastic properties for effective mechanical communication.</p><p></p><p><strong>FOR THE LATEST UPDATES AND CONTENT ON SOFT MATTER AND BIOLOGICAL PHYSICS AT THE WEIZMANN, VISIT OUR&nbsp;WEBSITE:&nbsp;https://www.biosoftweizmann.com/</strong></p>

<p>There are two major classes of theories about the basal ganglia. The first class hypothesizes</p><p>that the basal ganglia are the site where cortical sensorimotor and dopaminergic reward</p><p>information interact to potentiate and select actions. These theories predict that content</p><p>specificity of information emerges from within the basal ganglia. The second class of</p><p>theories posits that information is manipulated within the basal ganglia through processes</p><p>such as dimensionality reduction. These theories are primarily based on the fact that there</p><p>is a large reduction in the number of neurons from the input to the output stages of the basal</p><p>ganglia. These theories posit that there are changes in the coding properties of neurons</p><p>rather than the emergence of content specificity.</p><p>In this talk, I will present a set of studies where we analyzed the eye movement system of</p><p>monkeys to compare single-neuron activity in the basal ganglia with activity in the</p><p>cerebellum and the frontal cortex. We used tasks that manipulated both eye movements</p><p>and expected rewards. We found that rather than coding specific sensorimotor or reward</p><p>parameters, the basal ganglia were unique in how they coded these parameters, both in</p><p>terms of the signal-to-noise ratio of responses and in the variety of their temporal patterns.</p><p>These results strongly suggest that the basal ganglia play a role in manipulating rather than</p><p>generating reward and sensorimotor signals.</p>

<p>As life expectancy increases, age-related diseases are becoming more prevalent. While these conditions are traditionally studied in isolation, mounting evidence points to shared, systemic mechanisms underlying these conditions. Our research highlights the vasculature as &nbsp;a key player in organ homeostasis and repair, and a system shared across all organs—making its dysfunction potential driver of age-related pathologies.</p><p>We demonstrate that manipulating <strong>VEGF signaling</strong> to counteract age-related microvascular rarefaction promotes <strong>comprehensive geroprotection</strong>, preserving organ function and delaying disease onset. Our findings also reveal a link between vascular rarefaction and altered RNA splicing. While hypoxia-driven and age-related changes in alternative RNA splicing have been studied independently, we propose a unifying mechanism that links the two. To explore this further, we also employ patient-derived organoids, which retain their biological age in culture, providing a robust in vitro platform to test anti-aging interventions.</p><p>Our findings support a <strong>vascular theory of aging</strong>, identifying vascular health as a promising target to mitigate age-related diseases and promote healthier aging.</p>

<p>Over the past few decades, immunotherapy has revolutionized cancer treatment with great success in treating cancer patients and preventing tumor recurrence after surgery. Harnessing the immune system to fight cancer largely relies on the ability of T lymphocytes to distinguish&nbsp;between “self” and “non-self” to specifically identify and eliminate malignant cells.&nbsp;This is achieved through the recognition of neoantigens, tumor-specific proteins resulting from genetic mutations.</p><p>The Samuels’ lab is exploring the immune-tumor interactions, with specific focus on the mechanisms underlying cancer-cell recognition, and developing novel strategies to increase antitumor immune responses.</p><p>In this talk, I will present results from our recent studies investigating the link between mRNA mistranslation in cancer cells and immunological tumor control.</p>

Given two distributions P, Q and an integer t, we analyze two sampling processes. In "random allocation," we first sample an index i uniformly from [t], then draw r_{i} ~ P and r_{j} ~ Q for all other j in [t]. In "Poisson sampling," we independently draw r_{i} ~ 1/t*P + (1-1/t)*Q for each i in [t]. We bound the difference between these processes' output distributions and the baseline of sampling r_{i} ~ Q for all i.

This theoretical result provides key insights for analyzing DP-SGD, a privacy-preserving variant of stochastic gradient descent. While Poisson subsampling has well-understood privacy guarantees, common implementations use element shuffling, which was recently shown to have larger privacy losses in certain regimes. Random allocation offers a middle ground, and we prove its privacy analysis reduces to comparing the distributions described above.

We show that these variants' privacy guarantees are within a constant factor of each other across all parameter regimes and converge asymptotically in t. Our proof has two key components: decomposing Poisson sampling into a mixture of random allocation processes, and showing that random allocation can be viewed as a modified Poisson process where sampling probabilities depend on previous outputs.

Joint work with Vitaly Feldman