The invention discloses a method for screening a therapeutic target of acute radiation-induced gastrointestinal syndrome and use of TIGAR target in the preparation of a medicine for treating radiation-induced gastrointestinal syndrome. The CreERT-loxP transgenic mouse model is used, in which quiescent intestinal crypt stem cells are effectively promoted to proliferate after exposure to high-dose ionizing radiation, to screen a therapeutic target that still has a therapeutic effect for radiation-induced gastrointestinal syndrome 18-24 h after ionizing radiation. Gene splicing occurs in particular cells in the CreERT-loxP transgenic mice only after the injection of tamoxifen, thereby regulating gene expression. The actual situation of initial exposure and then treatment after a nuclear accident is well simulated, so the invention is of great practical significance. The screened therapeutic target is developed into a medicine for treatment after nuclear accidents, to save precious time for the treatment after nuclear accidents.

The present invention relates to the fields of life sciences and cell and tissue cultures, especially 3D cultures. Specifically, the invention relates to a method of maintaining the presence or activity of a human or mouse estrogen receptor (ER) in a cell of an ex vivo mammary cell or tissue culture or in a cell of other hormone responsive cell or tissue culture. Also, the present invention relates to a method of maintaining a luminal epithelial phenotype and/or cell identity of a mammalian cell in an ex vivo cell or tissue culture. Still, the present invention relates to a 3D matrix or 3D medium comprising the matrix for ex vivo culture, wherein said 3D matrix or 3D medium comprises one or more mammalian cells or tissues embedded in said 3D matrix or 3D medium, and to a system for ex vivo culture, wherein the system comprises mammalian cells or tissues embedded in a 3D matrix or 3D medium comprising said matrix. Still furthermore, the present invention relates to use of the 3D matrix, 3D medium or system of the present invention e.g. for ex vivo culture of a mammalian cell, drug discovery methods, biomarker studies and/or estrogen receptor (ER) signaling studies.

The present invention relates to Rucaparib and/or Talazoparib and/or Veliparib and/or Olaparib, and/or AZD 2461, or a pharmaceutically acceptable salt thereof, for use in the treatment of impaired skin wound healing in a subject, an in vitro method for identifying a subject suffering from impaired skin wound healing to be responsive to the treatment with Rucaparib and/or Talazoparib and/or Veliparib and/or Olaparib and/or AZD 2461, and kits and kits-of-part related thereto.

A pharmaceutical composition containing human ribonuclease 1 is disclosed. The molecule according to the invention (or the analogous variants) is suitable for use as a medicament for therapy of renal diseases of various aetiologies. The drug according to the invention causes regeneration of glomerular podocytes. The molecule according to the invention can be further used by analytical determination of blood concentration as a marker of disease progression of renal syndromes and for prognosis and prevention of renal insufficiency as a valuable factor of laboratory medicine.

Provided herein are methods of identifying a marker for a biological interaction, the method comprising: quantifying genome-wide RNA expression in cells; exposing the cells to a perturbagen for a period of time sufficient to induce the biological interaction in the cells, wherein the induced biological interaction comprises inducing changes in RNA expression in the cells that are exposed to the perturbagen; quantifying genome-wide nascent RNA expression in the cells that were exposed to the perturbagen; calculating a difference in the genome-wide nascent RNA expression between (i) the genome-wide RNA expression in the cells absent the perturbagen and (ii) the genome-wide nascent RNA expression in the cells that were exposed to the perturbagen; and identifying the marker using the calculated difference in the genome-wide nascent RNA expression.

Described herein are materials and methods for the treatment of prostate cancer.

The present invention is directed to a method for treating an IFN-γ associated disease or disorder in a subject in need thereof, including administering to the subject a pharmaceutical composition including a therapeutically effective amount of a compound capable of manipulating or modulating PD-L1 signaling or pathway.

Combinations of the antibody-drug conjugate trastuzumab-MCC-DM1 and chemotherapeutic agents, including stereoisomers, geometric isomers, tautomers, solvates, metabolites and pharmaceutically acceptable salts thereof, are useful for inhibiting tumor cell growth, and for treating disorders such as cancer mediated by HER2 and KDR (VEGFR receptor 1). Methods of using such combinations for in vitro, in situ, and in vivo diagnosis, prevention or treatment of such disorders in mammalian cells, or associated pathological conditions, are disclosed.

The invention provides a method of treatment comprising reducing therapy-induced adverse effects (TIAE), including chemotherapy-induced adverse effects (CIAE), such as chemotherapy-induced peripheral neuropathy (CIPN) and/or chemotherapy-induced cardiovascular adverse effects (CICAE) in a subject being treated with a CIAE-inducing anti-cancer active ingredient by co-administering to the subject a pharmaceutically effective amount of a NCS-1-protective composition. Related pharmaceutical compositions, diagnostics and screening techniques are also provided.

Disclosed are bioprinted, three-dimensional, biological skin tissues comprising: a dermal layer comprising dermal fibroblasts; and an epidermal layer comprising keratinocytes, the epidermal layer in contact with the dermal layer to form the three-dimensional, engineered, biological skin tissue. Also disclosed are arrays of engineered skin tissues and methods of making engineered skin tissues.