The treatment of some inborn metabolism errors requires cholesterol substitution therapy. Cholesterol plays a vital role in the human body. Therefore, the majority of cholesterol determination techniques are targeted to blood and blood serum. Nevertheless, cholesterol determination in food is important as well. In this paper, cholesterol determination using differential pulse voltammetry (DPV) in dairy products (e.g., milk, clotted cream, yogurt, butter, etc.) is reported with a novel nonenzymatic sensor based on diphosphonic acid of 1,4-diacetylglycoluril (DPADGU) as an electrode surface modifier. Stable anodic response was obtained from cholesterol on the modified carbon-based electrode. The sensor has high stability, sensitivity (20 μA mol L-1 cm-2), and a wide linear range from 1 up to 200 μM. The LOD and LOQ values are 1.5 and 5.1 μM, respectively. The developed methods were successfully applied to the above mentioned dairy products. Graphical abstract ᅟ.

The study aimed to explore the prevalence of human adenovirus-36 (HAdV-36) infection and the association of HAdV-36 with obesity in Chinese Han population. A qualitative determination using enzyme-linked immunosorbent assay was performed to determine by duplication the antibodies to HAdV-36 in the serum samples. Logistic regression analysis was used to analyze the association between HAdV-36 seropositivity and obesity. The overall HAdV-36 seroprevalence was 49.8% among 824 participants. The prevalence of HAdV-36 seropositive was 42.9% and 51.4% in the obese and non-obese participants, respectively, which was not statistically significant ( P =0.05). There were significant differences in anthropometric and biochemical parameters observed between the two groups except for height ( P =0.067) and total cholesterol ( P <0.29). After the adjustment for age and gender, HAdV-36 seropositivity was a protective factor for obesity (OR=0.69, 95% CI 0.48-0.97, P =0.03). In the male population, the adjusted OR for AD-36 antibody-positive status was statistically decreased for obese adults (OR=0.59; 95% CI, 0.39-0.91; P =0.02). However, the similar result was not obtained in the female population (OR=0.90; 95% CI, 0.48-1.67; P =0.73). We found a high prevalence of HAdV-36 infection in China and significant association between HAdV-36 infection and obesity or weight gain after the adjustment for age and gender. The HAdV-36 infection may be related to the weight loss in Chinese Han population, especially in the male group, which needs to be further confirmed.

Atherosclerosis is a slowly progressing, chronic multifactorial disease characterized by the accumulation of lipids, inflammatory cells, and fibrous tissue that drives to the formation of asymmetric focal thickenings in the tunica intima of large and mid-sized arteries. Despite the high therapeutic potential of ApoA-1 proteins, the purification and delivery into the disordered organisms of these drugs is still limited by low efficiency in these processes.

There is accumulating evidence that vascular inflammation plays critical roles in pathophysiology of atherosclerosis. It is widely accepted that both innate and adaptive immune responses are important for initiation and progression of atherosclerosis, which mainly consist of monocytes, macrophages, neutrophils, T lymphocytes, and B lymphocytes. Moreover, inflammatory biomarkers such as high-sensitivity C-reactive protein and interleukin-6 are known to predict future cardiovascular events, as well as conventional low-density or high-density lipoprotein cholesterol. Thus, current understanding of the inflammatory mechanisms of atherosclerosis have led us to explore novel therapeutic approaches that reducing vascular inflammation itself could lower the rates of critical cardiovascular events. To address the inflammatory hypothesis of atherosclerosis, results of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) trial have been recently reported that anti-inflammatory therapy using canakinumab, a monoclonal antibody targeting interleukin-1β, significantly reduced recurrent cardiovascular events for secondary prevention of myocardial infarction at high inflammatory risk. In this review, we will first outline the mechanisms of atherosclerosis, especially focusing on their inflammatory aspects. Then we will introduce several critical inflammatory biomarkers that contribute to risk stratification of clinical cardiovascular events. Lastly, we will discuss potentiality and future perspectives of reducing inflammation as a novel therapeutic target for atherosclerotic cardiovascular diseases.