X Particles 2.59 Serial 13: A Review of Features and Performance

The test line signal intensity was measured against a serial two-fold dilution series of DENV-1 NS1 (A), DENV-2 NS1 (B), DENV-3 NS1 (C) and DENV-4 NS1 (D) from 512 ng/mL to 0.5 ng/mL. The analytical limit of detection was determined as the lowest concentration required to produce a positive result of 8.5 mABS (absorbance) units using interpolation from a non-linear regression. An absorbance value of 8.5 mABS was determined to be the cut-off value for visualisation of the test line.

x particles 2.59 serial 13

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MI and cerebrovascular incidents are most commonly triggered by the rupture of an unstable/vulnerable atherosclerotic plaque [11]. Atherosclerosis is a lipid-driven inflammatory disorder of the arterial wall caused by cholesterol deposition in the intima-media of vessels supplying cardiac or brain tissue [12]. Elevated concentrations of atherogenic lipid particles that carry cholesterol in the blood represent the fundamental risk factor for ASCVD [3, 13, 14]. This is especially true in the diabetes population, which is enriched with dyslipidemia of insulin resistance [15, 16]. The cholesterol contained within apolipoprotein B (apo B) particles, also referred to as non-high-density lipoprotein cholesterol (non-HDL-C), is strongly associated with the pathogenesis of atherosclerosis [3]. Non-HDL-C is calculated as total cholesterol minus HDL-C, and includes very-low-density lipoprotein (VLDL), VLDL remnants, intermediate-density lipoprotein, chylomicrons, chylomicron remnants, lipoprotein(a), and the predominant cholesterol-carrying lipoprotein, low-density lipoprotein cholesterol (LDL-C). Elevated levels of atherogenic lipoprotein particles containing both cholesterol and triglycerides (TGs) can be attributed to a number of genetic disorders, common diseases, and altered metabolic states (e.g. hypothyroidism, pregnancy, menopause, diabetes, chronic kidney disease [CKD], nephrotic syndrome, and human immunodeficiency virus [HIV] infection). Furthermore, risks such as hyperglycemia, hypertension, and obesity, as well as lifestyle factors (e.g. tobacco use, unhealthy diet, physical inactivity, and excessive use of alcohol) can accelerate the lipid-driven atherosclerosis process [1, 3].

The implications of changes in lipid levels might become a particularly important issue in patients with T2DM if one assumes stability of lipids on current therapies. The risk of cardiovascular disease (CVD) has been shown to increase with the duration and an earlier onset of T2DM [21]. Additionally, many patients with T2DM will not only experience atherogenic dyslipidemia [4, 16, 22], but usually will also experience one or a combination of additional accelerating risk factors associated with ASCVD, including hypertension, CKD, obesity, and insulin resistance/hyperinsulinemia [23, 24]. Insulin resistance, prediabetes, DM, and CKD are frequently associated with varying degrees of dyslipidemia (i.e. elevated TG levels, decreased HDL-C levels, and low or below-normal LDL-C levels). These common, often subtle, lipid profile findings are highly atherogenic because of the presence of elevated apo B particles of small, dense LDL particles (LDL-P) and TG-rich VLDL and their remnants, even when LDL-C or non-HDL-C are at relatively lower or even normal levels; this combination is often referred to as unfavorable discordance. Unlike the general population, in this setting, where the population (i.e. insulin resistance, obesity, prediabetes, metabolic syndrome, high TG levels, low HDL-C levels, T2DM) is enriched with unfavorable discordance, apo B or LDL-P concentrations are much more predictive as biomarkers of ASCVD risk [4, 13, 14, 16, 24, 25]. Dyslipidemia associated with insulin resistance is often exacerbated if glucose levels are not well controlled [25].

To clarify, no studies have clearly demonstrated that raising the cholesterol content of HDL-C particles or lowering TG levels translate to a reduction in ASCVD risk. Furthermore, to demonstrate a statistically significant reduction in ASCVD risk, clinical trials investigating the effects of lowering LDL-C levels have shown that a threshold between-group difference in LDL-C levels, usually exceeding 25 mg/dL [0.65 mmol/L], is required in the typical 3- to 5-year studies. Therefore, it should be remembered that, despite significant clinical effects of some medications on the lipid profile, little is known about the clinical relevance of these changes. However, effects on the lipid profile, whether significant or nominal for any single agent, should not be considered in isolation, since most patients will be taking multiple medications from various classes to treat multiple comorbidities. For this reason, it is important to observe the overall changes governing the ultimate management of dyslipidemia to reduce the ASCVD risk.

Adverse effects associated with early β-blockers, such as negative effects on glycemic control, dyslipidemia, and masking of hypoglycemia, have long contributed to controversy around their use [93]. However, as β-blockers have evolved, some of these effects have changed. The first-generation β1- and β2-nonselective adrenergic receptor blockers, such as propranolol and nadolol, have negligible effects on LDL-C levels, but increase TG levels and decrease HDL-C levels [17, 106]; their use results in a shift to more atherogenic, smaller, denser LDL-P [41]. In the case of propranolol, none of the associated lipid changes were considered to be strongly predictive of coronary events or mortality [106]. Use of second-generation β1-selective agents, such as atenolol and metoprolol, has been found to be associated with the development of fewer atherogenic particles [93].

This page lists LAMMPS performance on several benchmark problems, runon various machines, both in serial and parallel and on GPUs. Notethat input and sample output files for many of these benchmark testsare provided in the bench directory of the LAMMPS distribution. Seethe bench/README file for details. 2ff7e9595c