PPARγ Promotes Urothelial Remodeling During Urinary Tract Obstruction.

Urinary tract obstruction (UTO) is a common cause of kidney injury that can result in chronic kidney disease and end-stage renal disease. Heterogeneity in the extent of obstructive renal damage in humans with UTO implies the existence of unknown mechanisms that protect against or accelerate kidney injury. Prior studies show that congenital and acquired UTO initiate a conserved, protective program of renal urothelium remodeling that culminates in expansion of uroplakin (UPK)+ cells to promote renal structural integrity.

Magicity versus Superfluidity around ^{28}O viewed from the Study of ^{30}F.

The neutron-rich unbound fluorine isotope ^{30}F_{21} has been observed for the first time by measuring its neutron decay at the SAMURAI spectrometer (RIBF, RIKEN) in the quasifree proton knockout reaction of ^{31}Ne nuclei at 235  MeV/nucleon. The mass and thus one-neutron-separation energy of ^{30}F has been determined to be S_{n}=-472±58(stat)±33(sys)  keV from the measurement of its invariant-mass spectrum. The absence of a sharp drop in S_{n}(^{30}F) shows that the "magic" N=20 shell gap is not restored close to ^{28}O, which is in agreement with our shell-model calculations that predict a near degeneracy between the neutron d and fp orbitals, with the 1p_{3/2} and 1p_{1/2} orbitals becoming more bound than the 0f_{7/2} one.

Keratin 5 basal cells are temporally regulated developmental and tissue repair progenitors in bladder urothelium.

Urothelium forms a distensible yet impermeable barrier, senses and transduces stimuli, and defends the urinary tract from mechanical, chemical, and bacterial injuries. Biochemical and genetic labeling studies support the existence of one or more progenitor populations with the capacity to rapidly regenerate the urothelium following injury, but slow turnover, a low mitotic index, and inconsistent methodologies obscure progenitor identity. The progenitor properties of basal keratin 5 urothelial cells (K5-UCs) have been previously investigated, but those studies focused on embryonic or adult bladder urothelium.

Vitamin C enhances co-localization of novel TET1 nuclear bodies with both Cajal and PML bodies in colorectal cancer cells.

Deregulation of ten-eleven Translocation protein 1 (TET1) is commonly reported to induce imbalances in gene expression and subsequently to colorectal cancer development (CRC). On the other hand, vitamin C (VitC) improves the prognosis of colorectal cancer by reprogramming the cancer epigenome and limiting chemotherapeutic drug resistance events. In this study, we aimed to characterize TET1-specific subcellular compartments and evaluate the effect of VitC on TET1 compartmentalization in colonic tumour cells.