Modeling Sporadic Progressive Supranuclear Palsy in 3D Midbrain Organoids: Recapitulating Disease Features for In Vitro Diagnosis and Drug Discovery.

Objective: Progressive Supranuclear Palsy (PSP) is a severe neurodegenerative disease characterized by tangles of hyperphosphorylated tau protein and tufted astrocytes. Developing treatments for PSP is challenging due to the lack of disease models reproducing its key pathological features. This study aimed to model sporadic PSP-Richardson's syndrome (PSP-RS) using multi-donor midbrain organoids (MOs).

Generation of hiPSCs lines from three sporadic Parkinson's disease patients.

Here, we described the generation of human induced pluripotent stem cell lines (hiPSCs) from three sporadic Parkinson's disease (sPD) patients by reprogramming of their peripheral blood mononuclear cells (PBMC).

Treatment of facial lipodystrophy induced by a biologic agent (IPD-1): a literature review.

Agents that inhibit programmed cell death (IPD-1) in T lymphocytes are indicated for patients with advanced cancer. However, some individuals may develop endocrinological conditions, such as diabetes, thyroid dysfunction, and lipodystrophy, after treatment. This systematic review and case report of IPD-1 lipodystrophies describes a patient who received nivolumab treatment for advanced clear cell renal carcinoma and subsequently developed diabetes as well as facial and body lipodystrophy.

Infrared Fingerprint and Unimolecular Decay Dynamics of the Hydroperoxyalkyl Intermediate (•QOOH) in Cyclopentane Oxidation.

A transient carbon-centered hydroperoxyalkyl intermediate (•QOOH) in the oxidation of cyclopentane is identified by IR action spectroscopy with time-resolved unimolecular decay to hydroxyl (OH) radical products that are detected by UV laser-induced fluorescence. Two nearly degenerate •QOOH isomers, β- and γ-QOOH, are generated by H atom abstraction of the cyclopentyl hydroperoxide precursor. Fundamental and first overtone OH stretch transitions and combination bands of •QOOH are observed and compared with anharmonic frequencies computed by second-order vibrational perturbation theory.

Inactivation of HIPK2 attenuates KRAS activity and prevents pancreatic tumorigenesis.

Background: Pancreatic ductal adenocarcinoma (PDAC) features KRAS mutations in approximately 90% of human cases and excessive stromal response, termed desmoplastic reaction. Oncogenic KRAS drives pancreatic carcinogenesis by acting on both epithelial cells and tumor microenvironment (TME). We have previously shown that Homeodomain-Interacting Protein Kinase 2 (HIPK2) cooperates with KRAS in sustaining ERK1/2 phosphorylation in human colorectal cancers.