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In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Paricalcitol is the third generation of vitamin D analog, and is a selective activator of VDR used for the treatment of secondary hyperparathyroidism. The vascular calcification process in chronic kidney disease is also directly influenced by paricalcitol. [1]Vitamin D has important roles in physiological processes, and is primarily involved in calcium and phosphorus homeostasis and bone metabolism. Vitamin D can prevent or ameliorate inflammatory disease in animal autoimmune disease models and in patients. The mechanism by which vitamin D regulates inflammatory response appears to be dependent on the activation of regulatory CD4+T cells. [2]The intraperitoneal administration of paricalcitol modulates peritoneal dialysis fluid (PDF)-induced peritoneal fibrosis. The treatment reduced peritoneal IL-17 levels. In vitro studies demonstrate that both CD4+ and CD8+ regulatory T cells appear to impact the regulation of IL-17. Paricalcitol treatment resulted in a significantly increased frequency of CD8+ T cells showing a regulatory phenotype. The frequency of CD4+ Tregs tends to be increased. However, paricalcitol treatment increased the number of CD4+ and CD8+ Treg cells in vivo. In conclusion, the activation of immunological regulatory mechanisms by VDR signaling could prevent or reduce fibrosis, as shown in peritoneal fibrosis induced by PDF exposure in mice. In a rat model of gentamicin-induced renal injury, paricalcitol preventes upregulated inflammatory cytokines, nuclear factor-kappaB and phosphorylated ERK1/2 expression, and adhesion molecules (monocyte chemoat¬tractant protein-1, ICAM-1, VCAM-1), and they reversed the transforming growth factor (TGF)-beta1-induced epithelial-to-mesenchymal transition process and extracel¬lular matrix accumulation. [2]Paricalcitol has a good effect on proteinuria in non-dialysis CKD patients with secondary hyperparathyroidism treated according to Kidney Disease. After treatment with paricalcitol, statistically significant reduction (paired t-test) in 24hUA (P < 0.011) and 24hUQP (P < 0.0001) are found. The reduction of UACR was not significant (P = 0.074). In the observational period no statistically significant reduction in 24hABP was found. Treatment with 1 mg paricalcitol daily according to clinical practice in non-dialysisCKDpatients with secondary hyperparathyroidism and proteinuria significantly reduces 24hUA and 24hUQP without significant change in 24hABP. [3]References:[1]Darko Duplancic, Marijan Cesarik, Nikola Kolja Poljak et al. The influence of selective vitamin D receptor activator paricalcitol on cardiovascular system and cardiorenal protection. Clinical Interventions in Aging 2013:8 149–156[2]Guadalupe T. Gonza´lez-Mateo et al. Paricalcitol Reduces Peritoneal Fibrosis in Mice through the Activation of Regulatory T Cells and Reduction in IL-17 Production. PLOS ONE October 2014 | Volume 9 | Issue 10 | e108477[3]Nina Hojs, Sebastjan Bevc et al. Paricalcitol Reduces Proteinuria in Non-Dialysis Chronic Kidney Disease Patients Therapeutic Apheresis and Dialysis 2013; 17(4):368–372
