Integrated Calendar

The tumor suppressor p53 is an important regulator that controls various cellular networks, including cell differentiation. Interestingly, some studies suggest that p53 facilitates cell differentiation, whereas others claim that it suppresses differentiation. Therefore, it is critical to evaluate whether this inconsistency represents an authentic differential p53 activity manifested in the various differentiation programs. To clarify this important issue, we conducted a comparative study of several mesenchymal differentiation programs. The effects of p53 knockdown or enhanced activity were analyzed in mouse and human mesenchymal cells, representing various stages of several differentiation programs. We found that p53 down-regulated the expression of master differentiation-inducing transcription factors, thereby inhibiting osteogenic, adipogenic and smooth muscle differentiation of multiple mesenchymal cell types. In contrast, p53 is essential for skeletal muscle differentiation and osteogenic re-programming of skeletal muscle committed cells. These comparative studies suggest that, depending on the specific cell type and the specific differentiation program, p53 may exert a positive or a negative effect, and thus can be referred as a "guardian of differentiation" at large

In the 104 years since Alois Alzheimer first described the neuropathological features underlying dementia in the disease that now bears his name, the changes in neuronal activity underlying the symptoms of the disease are still not understood. Using transgenic mouse models, it is now possible to directly measure changes in neuronal structure and function resulting from the accumulation of AD neuropathology.
We measured the changes in evoked responses to electrical and sensory stimulation of neocortical neurons in mice transgenic for human APP, in which soluble amyloid-β accumulates and insoluble plaques aggregate in an age-dependent manner. Our results reveal a specific synaptic deficit present in neocortical neurons in brains with a significant amount of plaque aggregation. We show that this deficit is related to the distortion of neuronal process geometry by plaques, and the degree of response distortion is directly related to the amount of plaque-burdened tissue traversed by the afferent neuronal processes, indicating that the precise connectivity of the neocortex is essential for normal information processing. Furthermore, we show that the physical distortion of neuronal processes by plaques is reversible by immunotherapy, revealing a larger degree of structural plasticity in neocortical neurons of aged animals. Taken together, these results indicate that it may be possible to slow or reverse the symptoms of AD.

The master equation approach is applied to quantify structural features of
growing, preferential-attachment networks. The degree distribution is solved
for the generic situation where the attachment rate to an existing node of
degree k grows as a power law in k. The specific case of linear preferential
attachment gives a non-robust degree distribution whose exponent depends on
microscopic details of the network growth. This sensitivity stems from an
underlying multiplicative nature of the network growth. It will also be
shown that redirection, where a new nodes attaches to a random-selected node
or to its ancestor, also generates linear preferential attachment. Finally,
the master equation will be used to understand the genealogy of growing
networks and to also answer the basic question of whether the rich really do
get richer.

Conventional lasers are usually made of regular cavities or ordered
structures. We have studied lasing in open systems with complex and chaotic ray dynamics,
e.g. random structures, chaotic microcavities, and deterministic aperiodic
arrays. The lasing properties are distinct from the conventional ones, leading
to novel functionalities and new applications.

We show that the combination of spin-orbit coupling with a Zeeman field or strong interactions may lead to the formation of a helical liquid in single-channel quantum wires. In a helical liquid, electrons with opposite velocities have opposite spin precession. We argue that zero-energy Majorana bound states are formed in various situations when the wire is situated in proximity to a conventional s-wave superconductor. This occurs when the external magnetic field, the superconducting gap, or, in particular, the chemical potential vary along the wire. We discuss experimental consequences of the formation of the helical liquid and the Majorana bound states.