It is a modified NTP for incorporation into messenger RNAs (mRNA) using T7 RNA Polymerase. Incorporation of N1-methylpseudouridine can reduce the immunogenicity of the resulting mRNA.
The product has passed the functionality test in transcription reaction. The solution is free of DNase and RNase contamination.
Reference Reading
1. Two barriers for sodium in vascular endothelium?
Hans Oberleithner Ann Med . 2012 Jun;44 Suppl 1(Suppl 1):S143-8. doi: 10.3109/07853890.2011.653397.
Vascular endothelium plays a key role in blood pressure regulation. Recently, it has been shown that a 5% increase of plasma sodium concentration (sodium excess) stiffens endothelial cells by about 25%, leading to cellular dysfunction. Surface measurements demonstrated that the endothelial glycocalyx (eGC), an anionic biopolymer, deteriorates when sodium is elevated. In view of these results, a two-barrier model for sodium exiting the circulation across the endothelium is suggested. The first sodium barrier is the eGC which selectively buffers sodium ions with its negatively charged proteoglycans. The second sodium barrier is the endothelial plasma membrane which contains sodium channels. Sodium excess, in the presence of aldosterone, leads to eGC break-down and, in parallel, to an up-regulation of plasma membrane sodium channels. The following hypothesis is postulated: Sodium excess increases vascular sodium permeability. Under such conditions (e.g. high-sodium diet), day-by-day ingested sodium, instead of being readily buffered by the eGC and then rapidly excreted by the kidneys, is distributed in the whole body before being finally excreted. Gradually, the sodium overload damages the organism.
2. The evils of intradialytic sodium loading
Len A Usvyat, Jochen G Raimann, Peter Kotanko, Nathan W Levin, Stephan Thijssen Contrib Nephrol . 2011;171:84-91. doi: 10.1159/000327333.
Increased salt intake is related to extracellular fluid expansion and a rise in blood pressure, and has been linked to cardiovascular disease. Several studies have also suggested that sodium can exert detrimental effects via blood pressure-independent mechanisms. Chronic kidney disease patients are particularly susceptible to the negative consequences of sodium loading. While individuals with normal kidney function are able to regulate their sodium balance, hemodialysis patients have to rely virtually entirely on the dialysis procedure for sodium elimination. Tragically, the dialysis procedure has, in many instances, turned into a de facto source of sodium loading rather than a means for sodium removal. The main sources of sodium related to the dialysis procedure are (1) diffusive influx from the dialysate, including inappropriate use of sodium profiling; (2) the use of saline solution for priming and rinsing; and (3) the treatment of intradialytic hypotension and cramps with saline solution. Creating a positive intradialytic sodium balance is effective in acutely reducing the incidence of intradialytic symptoms, but it also sustains a vicious cycle hampering the attainment of dry weight and predisposes the patient to an increased risk of intradialytic complications during the following dialysis session. Avoiding sodium loading in hemodialysis patients is a cornerstone of blood pressure and fluid status management and, therefore, deserves a conscious effort, bearing in mind not only short-term effects but also long-term goals. In the absence of routine means of quantifying sodium balance, sodium profiling should be viewed critically, as it has been shown to induce a positive sodium balance in the majority of cases. A preferred approach under these circumstances may be simple sodium alignment. In combination with the abdication of saline solution for priming, rinsing, and intradialytic infusions, these measures would go a long way to help reduce sodium overload and achieve a more physiologic sodium balance in this patient population.
3. Hypernatremia in critically ill patients
Georg-Christian Funk, Gregor Lindner J Crit Care . 2013 Apr;28(2):216.e11-20. doi: 10.1016/j.jcrc.2012.05.001.
Hypernatremia is common in intensive care units. It has detrimental effects on various physiologic functions and was shown to be an independent risk factor for increased mortality in critically ill patients. Mechanisms of hypernatremia include sodium gain and/or loss of free water and can be discriminated by clinical assessment and urine electrolyte analysis. Because many critically ill patients have impaired levels of consciousness, their water balance can no longer be regulated by thirst and water uptake but is managed by the physician. Therefore, the intensivists should be very careful to provide the adequate sodium and water balance for them. Hypernatremia is treated by the administration of free water and/or diuretics, which promote renal excretion of sodium. The rate of correction is critical and must be adjusted to the rapidity of the development of hypernatremia.
