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Background
Parathyroid hormone has 84 amino acids. It balances the serum calcium – directly in the kidneys and bones, indirectly in the intestines. PTH suppresses phosphate re-absorption in the proximal tubule to promote phosphate release in the urine. Meanwhile, it helps calcium re-absorb at the distal tubule to reduce calcium excretion. The second is that PTH induces the enzyme 1-alpha-hydroxylase in the kidneys to generate more active 1,25-(OH)2D3, indirectly modulating gut calcium and blood calcium. PTH is on 11p15, and regulated by blood calcium, 1,25-(OH)2D3, phosphate, oestrogen and progesterone. The biological function of PTH is most closely regulated by its N-terminal amino acid sequence (from 1-34). There are two -helical regions (positions 10-15 and 24-34) which allow PTH to bind to its receptor and set the ratio of PTH/PTHrP to the receptor.
Figure 1. Action of calcium, 1,25(OH)₂D and FGF23 on PTH production in the parathyroid cell (Source: Goltzman D. 2018)
The metabolism of PTH is closely associated with blood calcium levels. When blood calcium concentrations are high, PTH is rapidly proteolyzed after synthesis. About 60%-70% of the hormone is carried through the bloodstream into the liver where it's metabolised and cleared by Kupffer cells. Another 20-30% is filtered away by the kidneys, and only a small fraction is taken up by bone cells. Additionally, PTH in the bloodstream is quickly cleaved by endoproteases, generating a series of carboxy-terminal fragments. These carboxy-terminal fragments account for 50%-90% of the immunoreactivity of PTH in circulation.
Primary hyperparathyroidism is an endocrine disorder in which PTH is secreted by internal parathyroid gland defects (hyperplasia or tumors), leading to hypercalcemia and hypophosphatemia, and can be refractory to many organ systems. The vascular smooth muscle cell, the endothelial cell, and the cardiomyocyte express PTH receptor 1 (PTHR1). PTH can directly target cardiomyocytes by binding to protein kinase C (PKC) and producing cardiac hypertrophy. Increases calcium input, too, by triggering excitatory G protein-activated adenylyl cyclase and its successor myocardial L-type calcium channels. SHPT is an acute, severe complication of chronic renal failure (CRF) and it leads to systemic CRF patients' skin, bone and cardiovascular problems that impair quality of life. During CKD patients, impaired kidney function increases gradually the PTH and hyperplasia and swelling of the parathyroid gland. That is caused by hypocalcemia and an imbalance in 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3), which occur as kidney disease progresses.
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References
Post-Traumatic Headache in Children and Adolescents: a Narrative Review with a Focus on Management
CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS
Authors: Monsour, Danny Adel; Lay, Christine; Ansari, Tasjeel; Lagman-Bartolome, Ana Marissa
Purpose of Review Although common, post-traumatic headache (PTH) in the pediatric population is a niche group with a paucity of published evidence on the diagnosis, most appropriate acute and preventative management, and prognosis. This article aims to review pediatric PTH, its epidemiology and pathophysiology with a focus on management and future directions. Recent Findings Using MEDLINE, EMBASE, 52 articles on PTH in children and adolescents from 2016 to 2020 were identified. Over the last 4 years, our understanding of traumatic brain injury pathophysiology has grown, expanding the potential for more therapeutic targets. Despite this achievement, and recently published consensus guidelines, the review demonstrated a lack of published controlled trials to help guide management of pediatric PTH. The last 4 years have provided new insights into the potential pathophysiological mechanisms through laboratory research and advanced MR imaging; however, there continues to be a translational gap to clinical practice.
Electrochemical synthesis and characterization of poly(thionine)-deep eutectic solvent/carbon nanotube-modified electrodes and application to electrochemical sensing
MICROCHIMICA ACTA
Authors: Dalkiran, Berna; Fernandes, Isabel P. G.; David, Melinda; Brett, Christopher M. A.
Electropolymerization of thionine (TH) on multiwalled carbon nanotube (MWCNT)-modified glassy carbon electrodes (GCE) in ethaline deep eutectic solvent (DES) was carried out for the first time, to prepare poly(thionine) (PTH) films with different nanostructured morphologies. PTH films were formed on MWCNT/GCE by potential cycling electropolymerization in ethaline with the addition of different acid dopants CH3COOH, HClO4, HNO3, H(2)SO(4)and HCl, acetic acid being the best. The electropolymerization process was monitored with an electrochemical quartz crystal microbalance. The polymerization scan rate was a key factor affecting the electrochemical and morphological properties of the PTHEthaline-CH3COOH/MWCNT/GCE; electrodeposition at 200 mV s(-1)showing the best performance. The PTH/MWCNT/GCE platform was characterized using cyclic and differential pulse voltammetry, electrochemical impedance spectroscopy and scanning electron microscopy. The analytical characteristics of the PTH films were evaluated for sensing of ascorbic acid and biosensing of uric acid. The developed sensor exhibited a low detection limit (1.1 mu M), wide linear range (2.8-3010 mu M) and high sensitivity (1134 mu A cm(-2) mM(-1)) for ascorbic acid. After immobilization of uricase, UOx, on PTH/MWCNT/GCE, the biosensor was successfully applied to the determination of uric acid, with fast response (< 7 s), good sensitivity (450 mu A cm(-2) mM(-1), wide linear range (0.48-279 mu M) and low detection limit (58.9 nM), better than in the literature and than with PTH prepared in aqueous solution. The determination of uric acid in synthetic urine samples was successfully tested and the mean analytical recovery was 100.8 +/- 1.4%. This is a promising approach for the determination of uric acid in real samples.
COA
Publication 
Figure 1. Action of calcium, 1,25(OH)₂D and FGF23 on PTH production in the parathyroid cell
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