A Quadratic Deformation of the Heisenberg-Weyl and Quantum Oscillator Enveloping Algebras

A new 2-parameter quadratic deformation of the quantum oscillator algebra and its 1-parameter deformed Heisenberg subalgebra are considered. An infinite dimensional Fock module representation is presented which at roots of unity contains null vectors and so is reducible to a finite dimensional representation. The cyclic, nilpotent and unitary representations are discussed. Witten's deformation of $sl_2$ and some deformed infinite dimensional algebras are constructed from the $1d$ Heisenberg algebra generators. The deformation of the centreless Virasoro algebra at roots of unity is mentioned. Finally the $SL_q(2)$ symmetry of the deformed Heisenberg algebra is explicitly constructed.Comment: 23 pages of plain TeX (with phyzzx.tex macros). I've made a few minor corrections and added 2 reference

3D models of lamprey corticoid receptor complexed with 11-deoxycortisol and deoxycorticosterone

The serum of Atlantic sea lamprey, a basal vertebrate, contains two corticosteroids, 11-deoxycortisol and deoxycorticosterone. Only 11-deoxycortisol has high affinity [Kd~3 nM] for the corticoid receptor [CR] in lamprey gill cytosol. To investigate the binding of 11-deoxycortisol to the CR, we constructed 3D models of lamprey CR complexed with 11-deoxycortisol and deoxycorticosterone. These 3D models reveal that Leu-220 and Met-299 in lamprey CR have contacts with the 17[alpha]-hydroxyl on 11-deoxycortisol. Lamprey CR is the ancestor of the mineralocorticoid receptor [MR] and glucocorticoid receptor [GR]. Unlike human MR and human GR, the 3D model of lamprey CR finds a van der Waals contact between Cys-227 in helix 3 and Met-264 in helix 5. Mutant human MR and GR containing a van der Waals contact between helix 3 and helix 5 display enhanced responses to progesterone and glucocorticoids, respectively. We propose that this interaction was present in the CR and lost during the evolution of the MR and GR, leading to changes in their response to progesterone and corticosteroids, respectively

Notch Signaling Determines Lymphatic Cell Fate and Regulates Sprouting Lymphangiogenesis

The lymphatic vascular system is necessary for physiological regulation of tissue fluid homeostasis and absorption of dietary fat. Lymphatics also function in the inflammatory response and are involved in pathological conditions such as wound healing and cancer. We show that the Notch signaling pathway is a regulator of both developmental and pathological lymphangiogenesis. Notch1 and Notch4 are expressed by the lymphatic endothelium, and Delta-like ligand 4 (Dll4) is the predominantly expressed Notch ligand in the developing lymphatic vessels of the embryonic dermis and pathological lymphatic vessels of the wounded cornea. Dll4 was able to induce Notch activation in human dermal lymphatic endothelial cells (HDLECs), whereas Jagged1 (Jag1) was not. In HDLECs, Notch signaling is activated in response to Vascular Endothelial Growth Factor (VEGF) or Vascular Endothelial Growth Factor-C (VEGF-C) stimulation. In vitro assays demonstrated that Notch activation inhibits HDLEC proliferation, migration, and capillary network formation; these effects were coincident with increased levels of HEY1 and HEY2, biphasic regulation of VEGFR-3, and decreased levels of VEGFR-2. Using genetic intervention of Notch signaling, we demonstrated that Notch regulates developmental sprouting lymphangiogenesis by restricting growth and sprouting of lymphatics in the murine embryonic dermis. Using pharmacological intervention of Notch signaling, we found that Notch restricted pathological sprouting lymphangiogenesis in the corneal suture assay, which models inflammation-induced lymphangiogenesis. However, pharmacological intervention of Notch signaling did not measurably affect pathological sprouting lymphangiogenesis in an orthotopic tumor model of human breast cancer. Our data from analysis of HDLECs, dermis, and sutured cornea support a role for Dll4-driven Notch signaling in restricting sprouting lymphangiogenesis. Lymphatic specification/separation requires a venous endothelial cell to become a lymphatic endothelial cell, and lymphatic valve formation requires a duct endothelial cell to become a valve endothelial cell. Through analysis of genes regulated by Notch in HDLECs, we demonstrated that Notch determines lymphatic endothelial cell fates. Notch inhibits genes critical for lymphatic specification and separation (PROX1, PDPN), and induces genes important for lymphatic valve formation (FNEIIIA, ITGA9, CX37). We conclude that Notch is a context-dependent regulator of lymphangiogenesis. Notch functions in the tip/stalk, venous to lymphatic, and duct endothelial to valve endothelial cell fate decisions in lymphatic vasculature. Given the critical functions of the lymphatic vasculature in multiple physiological and pathological settings, understanding Notch functions in the lymphatic vasculature is critical to design treatments for conditions caused by lymphatic malfunction

Scrambled Scandals of 1935

Playbill from University of Hawaii theatrical or dance productions

The Lady's Not for Burning (Fry)

Playbill from University of Hawaii theatrical or dance productions

Missouri Legend

Playbill from University of Hawaii theatrical or dance productions

A Phoenix Too Frequent (Fry)

Playbill from University of Hawaii theatrical or dance productions