Study on transepithelial movement of 3H-androgen in the rat seminiferous and epididymal tubules

微小穿刺法と微小灌流法を用いた。精細管の管内アンドロゲン濃度は間質液中のその濃度が10-2, 000nMに増大するに従い直線的に増大したが, 精巣上体頭部における管内アンドロゲン濃度は間質液中の濃度が増大するに従い双曲線的に増大し, 精細管におけるそれよりもはるかに高い値を示した。灌流液中に0.1nMのジニトロフェノール, 0.1mMのKCN, 100μg/mlのサイクロヘキサミドを加えたとき, 管内アンドロゲンの移行は組織ATP濃度とともに有意に減少した。アンドロゲン結合蛋白を含まない人工的精上体頭部の管内液で管内を灌流したとき濃度勾配に抗したアンドロゲン移行は完全に抑制されたThe mechanisms involved in the maintenance of the endocrinological microenvironment of the seminiferous and epididymal tubules were examined in a series of experiments utilizing in vivo microperifusion, microperfusion, and micropuncture technique. The intraluminal 3H-androgen concentration in the seminiferous tubules increased linearly as the interstitial 3H-androgen concentrations increased from 10 nM to 2, 000 nM, but in the caput epididymidal tubules, the intraluminal 3H-androgen concentration increased hyperbolically across the same range of peritubular 3H-androgen concentration. Intraluminal 3H-androgen concentrations in the caput epididymidis did not rise above approximately 340 nM even when the peritubular 3H-androgen concentration exceeded 2, 000 nM. Perifusion of caput tubules with 0.1 mM dinitrophenol or potassium cyanide or 100 micrograms/ml cyclohexamide significantly reduced the proluminal 3H-androgen movement, but tubules perifused with control medium did not support antigrade 3H-androgen movement in the absence of native lumen fluids which contain androgen-binding protein. Energy-requiring protein synthesis is necessary for antigrade 3H-androgen movement in the caput epididymidis, but the mechanism for the interaction of intracellular protein(s) and 3H-androgen movement remains undetermined

Additional file 2: of Genome-wide methylomic analysis in individuals with HNF1B intragenic mutation and 17q12 microdeletion

Figure S1. This figure illustrates the extent of the 17q12 deletion in each patient as estimated by the CNV calling algorithm within the CHAMP package. (PDF 15 kb

Additional file 1: of Genome-wide methylomic analysis in individuals with HNF1B intragenic mutation and 17q12 microdeletion

Table S1. SLC1A3 bisulfite pyrosequencing assay conditions. (XLSX 11 kb

Additional file 5: of Genome-wide methylomic analysis in individuals with HNF1B intragenic mutation and 17q12 microdeletion

Figure S2. This Figure shows four significant differentially methylated regions (DMRs) identified between controls and 17q12 deletion carriers. A) SYNRG (corrected P = 1.32E-17), B) AATF (corrected P = 1.64E-11). C) LHX1 (corrected P = 3.37E-18), D) SMIM24 (corrected P = 1.01E-07). (PDF 223 kb

Effects of rare kidney diseases on kidney failure: a longitudinal analysis of the UK National Registry of Rare Kidney Diseases (RaDaR) cohort

Individuals with rare kidney diseases account for 5-10% of people with chronic kidney disease, but constitute more than 25% of patients receiving kidney replacement therapy. The National Registry of Rare Kidney Diseases (RaDaR) gathers longitudinal data from patients with these conditions, which we used to study disease progression and outcomes of death and kidney failure.People aged 0-96 years living with 28 types of rare kidney diseases were recruited from 108 UK renal care facilities. The primary outcomes were cumulative incidence of mortality and kidney failure in individuals with rare kidney diseases, which were calculated and compared with that of unselected patients with chronic kidney disease. Cumulative incidence and Kaplan-Meier survival estimates were calculated for the following outcomes: median age at kidney failure; median age at death; time from start of dialysis to death; and time from diagnosis to estimated glomerular filtration rate (eGFR) thresholds, allowing calculation of time from last eGFR of 75 mL/min per 1·73 m2 or more to first eGFR of less than 30 mL/min per 1·73 m2 (the therapeutic trial window).Between Jan 18, 2010, and July 25, 2022, 27 285 participants were recruited to RaDaR. Median follow-up time from diagnosis was 9·6 years (IQR 5·9-16·7). RaDaR participants had significantly higher 5-year cumulative incidence of kidney failure than 2·81 million UK patients with all-cause chronic kidney disease (28% vs 1%; p Background Methods Findings Interpretation Funding</p