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The Role of Light and Electromagnetic Fields in Maintaining Vascular Health
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
The NaS1 sulfate transporter is an important regulator of sulfate levels in the body, as it actively transports sulfate across the gut border and returns sulfate back into circulation in the renal tubules. There is a high incidence of genetic variants in NaS1 among autistic children, associated with renal sulfate wasting [20]. Mice engineered to be NaS1−/− exhibited a 12-fold increased rate of tumor growth along with more than double the density of a tumor vascular supply compared to NaS1+/+ mice [21]. Their tumors were also severely impoverished in collagen.
Fetal Skeletal Dysplasias: Radiologic-Pathologic Classification of 72 Cases
Published in Fetal and Pediatric Pathology, 2022
Sulfation disorders are associated with DTDST/SLC26A2 deficiency, a transmembrane protein that transports sulfate into chondrocytes to maintain adequate sulfoconjugation of proteoglycans and normal cartilage development. This sulfate transporter is a key limiting factor in the bone growth because of the low capacity of sulfate endogenous synthesis. The lethal form, achondrogenesis type 1B, is associated with lesser capacity of the chondrocyte to incorporate the sulfate, resulting in lack of the ground glass appearance and rarefaction of the cartilage matrix which tends to form dense collagenous rings around chondrocytes, and in severe defects in the intramembranous and endochondral ossifications [24]. These severe histologic alterations are correlated with the significant phenotypic and radiologic anomalies that associate extreme micromelia, short trunk with narrow chest, and diffuse severe ossification defects encompassing lucent skull, thin and short ribs with flared and cupped ends, extremely short long bones with flared, irregular and cupped metaphyses, delayed ossification of the vertebral bodies and sacrum and small square-shaped iliac wings. The cartilage matrix displays in the moderate form, diastrophic dysplasia, variable amount of matrix with pale areas, related to undersulfation of proteoglycans, interspersed with normal areas, along with disruption of the proliferative and hypertrophic zones due to irregular invasion of the metaphyseal capillaries and fibrosis [25]. Consistent with these moderate alterations, micromelia is less severe and the long bones have a normal tubular shape with enlarged metaphyses.
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
Oxalate is freely filtered by the glomerulus and also secreted into the proximal tubule through the apical oxalate/chloride transporter SLC26A6 and basolateral oxalate/sulfate transporter SLC26A1. Oxalate secretion, calculated from urine and plasma oxalate concentrations, does not appear to be significant in normal individuals and common stone formers but is persistently >1 in PH patients [25]. In the renal tubule, oxalate combines with calcium and can reach a supersaturated state as water is removed from the tubular fluid, notably in the S3 section of the proximal tubule. Crystals, an indicator of supersaturation, have indeed been shown in this region in renal biopsies from PH patients with recent onset end-stage renal disease while after prolonged dialysis, calcium oxalate deposits are widely scattered throughout the entire renal cortex [26]. Biopsies from PH patients with normal renal function also identified calcium oxalate crystal deposition but to a lesser extent than in those with chronic kidney disease.