BackgroundTPN infusions are usually administered during a treatment period of 10–24 hours per day due to the metabolic capacity of the liver. During this time interval physicochemically stable TPN solution (emulsion) is needed for the treatment. The purpose of the present study was to examine how the kinetic stability features of ready-made total parenteral nutrition admixtures containing olive oil and soybean oil will change under the usage-modeling 24-hour application with and without overdose Ca2+.MethodsParticle size analysis and zeta potential measurements were carried out to evaluate the possible changes in the kinetic stability of the emulsions.ResultsOur results indicate that in two of the four mixtures bimodal droplet-size distribution figures were detected and appearance of fat particles over 5 μm can not be disclosed. The tendency for separation of large diameter droplets in the two types of oil-based emulsion systems was different. In case of soybean containing emulsion second peak of droplets appeared in the bottom of the container in contrast to the olive oil containing emulsions where the second peak appeared in the surface layer. Interestingly this phenomenon is independent of calcium-content.ConclusionsFrom therapeutic point the emulsions of the bigger droplets containing upper layer are safer because the potentially dangerous big droplets could remain in the infusion bag after the administration.
The renin–angiotensin system (RAS) plays a pivotal role in blood pressure regulation. In some cases, this steering mechanism is affected by various deleterious factors (mainly via the overactivation of the RAS) causing cardiovascular damage, including coronary heart disease (CHD) that can ultimately lead to chronic heart failure (CHF). This not only causes cardiovascular disability and absenteeism from work but also imposes significant healthcare costs globally. The incidence of cardiovascular diseases has escalated exponentially over the years with the major outcome in the form of CHD, stroke, and CHF. The involvement of the RAS in various diseases has been extensively researched with significant limelight on CHD. The RAS may trigger a cascade of events that lead to atherosclerotic mayhem, which causes CHD and related aggravation by damaging the endothelial lining of blood vessels via various inflammatory and oxidative stress pathways. Although there are various diagnostic tests and treatments available in the market, there is a constant need for the development of procedures and therapeutic strategies that increase patient compliance and reduce the associated side effects. This review highlights the advances in the diagnostic and treatment domains for CHD, which would help in subjugating the side effects caused by conventional therapy.
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