Abstract: This disclosure provides non-human animal models for age-related disorders and age-sensitive traits, particularly those caused by senescence-inducing stimuli, wherein the models comprise transgenes selectively expressed by senescent cells. The disclosure further provides methods for identifying therapeutic agents effective for treating or preventing age-related disorders and age-sensitive traits using the animal models, therapeutic agents identified using such methods, pharmaceutical compositions comprising the identified therapeutic agents, and methods of treating or preventing age-related disorders and age-sensitive traits.

Abstract: This disclosure provides non-human animal models for age-related disorders and age-sensitive traits, particularly those caused by senescence-inducing stimuli, wherein the models comprise transgenes selectively expressed by senescent cells. The disclosure further provides methods for identifying therapeutic agents effective for treating or preventing age-related disorders and age-sensitive traits using the animal models, therapeutic agents identified using such methods, pharmaceutical compositions comprising the identified therapeutic agents, and methods of treating or preventing age-related disorders and age-sensitive traits.

Abstract: This invention provides a transgenic mouse with a p16INK4a promoter sequence that controls expression of a protein such that it is expressed preferentially in senescent cells. The protein either directly induces apoptosis, or converts a prodrug to a cytotoxic compound. In addition, the mouse is injected with syngeneic tumor cells, or has second transgene that causes tumors to form. Removing senescent cells from the mouse may result in the formation of fewer tumors.

Abstract: This invention provides a transgenic mouse for studying the role of senescent cells on an age-related disorder or an age-sensitive trait. The transgene contains a p16 promoter sequence that controls expression of an enzyme so as to cause the enzyme to be expressed in senescent cells in the mouse. The enzyme converts a prodrug to a cytotoxic agent, so that treating the mouse with the prodrug results in the prodrug selectively killing the senescent cells. As a result, progression of an age-related disorder or an age-sensitive trait is delayed. Included is the 3MR mouse model, which also expresses bioluminescent and fluorescent markers under control of the p16 promoter so that senescent cells in the mice can be visualized.

Abstract: Methods are provided herein for enhancing the effectiveness of medical therapies by administering agents that suppress a biological damage response that is inducible by the medical therapy administered to a subject. In certain embodiments, a method is provided for administering an anti-senescent cell agent that suppresses a biological response comprising cellular senescence that is induced by the medical therapy.

Abstract: The present invention relates generally to an improved ladder boat for supporting semiconductor wafers during thermal treatments which comprises top and bottom plates vertically opposing each other and support rods secured to said plates. Said support rods are provided with dividers for supporting a plurality of wafers one above another in a parallel arrangement. The dividers have a special profile to include a ramp portion so that the wafer is seated at a sharp corner thereof. Therefore, the contact surface between the wafer backside at its periphery and the dividers is segmental or punctual. This contact is preferably performed outside the contact area between the wafer backside and the wafer support zones of the electrostatic chuck of the photolithography tool to be subsequently used in the course of the wafer manufacturing.

Abstract: There is disclosed a method of forming a buried strap (BS) and its quantum conducting barrier (QCB) in a structure wherein a doped polycrystalline silicon region is exposed at the bottom of a recess and separated from a monocrystalline region of a silicon substrate by a region of an insulating material. First, a thin continuous layer of undoped amorphous silicon is deposited by LPCVD to coat said regions. The surface of this layer is nitridized to produce a Si3N4 QCB film. Now, at least one dual layer comprised of an undoped amorphous silicon layer and a dopant monolayer is deposited onto the structure by LPCVD. The recess is filled with undoped amorphous silicon to terminate the buried strap and its QCB. Finally, the structure is heated to activate the dopants in the buried strap to allow an electrical continuity between said polycrystalline and monocrystalline regions through the QCB by a quantum mechanical effect. All these steps are performed in situ in the same LPCVD tool.

Abstract: A multilayered quantum conducting barrier (MQCB) structure formed on two semiconductor regions having a different crystalline nature and a thin layer of an insulating material sandwiched between said semiconductor regions. An undoped amorphous silicon layer continuously coats these two semiconductor regions and insulating layer. The surface of the undoped amorphous silicon layer is nitridized to produce a superficial film of a nitride based material to form the desired quantum conducting barrier (QCB). A stack consisting of at least one dual layer comprised of a bottom undoped amorphous silicon layer and a top dopant monolayer is formed on said undoped amorphous silicon layer. After thermal processing, the MQCB structure operates as a strap allowing an electrical continuity between these semiconductor regions through the QCB by a quantum mechanical effect.

Abstract: Improved reliability structures containing quantum conductive barrier layer structures are obtained by employing quantum conductive layers in combination with thin regions of amorphous or microcrystalline semiconductor material. The quantum conductive structures are especially useful when incorporated into trench capacitors to reduce or eliminate the occurrence of low temperature fails and single cell fails in DRAM circuits.