A Comprehensive Literature Review on Cardioprotective Effects of Bioactive Compounds Present in Fruits of Aristotelia chilensis Stuntz (Maqui).

Some fruits and vegetables, rich in bioactive compounds such as polyphenols, flavonoids, and anthocyanins, may inhibit platelet activation pathways and therefore reduce the risk of suffering from CVD when consumed regularly. Aristotelia chilensis Stuntz (Maqui) is a shrub or tree native to Chile with outstanding antioxidant activity, associated with its high content in anthocyanins, polyphenols, and flavonoids. Previous studies reveal different pharmacological properties for this berry, but its cardioprotective potential has been little studied. Despite having an abundant composition, and being rich in bioactive products with an antiplatelet role, there are few studies linking this berry with antiplatelet activity. This review summarizes and discusses relevant information on the cardioprotective potential of Maqui, based on its composition of bioactive compounds, mainly as a nutraceutical antiplatelet agent. Articles published between 2000 and 2022 in the following bibliographic databases were selected: PubMed, ScienceDirect, and Google Scholar. Our search revealed that Maqui is a promising cardiovascular target since extracts from this berry have direct effects on the reduction in cardiovascular risk factors (glucose index, obesity, diabetes, among others). Although studies on antiplatelet activity in this fruit are recent, its rich chemical composition clearly shows that the presence of chemical compounds (anthocyanins, flavonoids, phenolic acids, among others) with high antiplatelet potential can provide this berry with antiplatelet properties. These bioactive compounds have antiplatelet effects with multiple targets in the platelet, particularly, they have been related to the inhibition of thromboxane, thrombin, ADP, and GPVI receptors, or through the pathways by which these receptors stimulate platelet aggregation. Detailed studies are needed to clarify this gap in the literature, as well as to specifically evaluate the mechanism of action of Maqui extracts, due to the presence of phenolic compounds.

Lipidomic methodologies for biomarkers of chronic inflammation in nutritional research: ω-3 and ω-6 lipid mediators.

The evolutionary history of hominins has been characterized by significant dietary changes, which include the introduction of meat eating, cooking, and the changes associated with plant and animal domestication. The Western pattern diet has been linked with the onset of chronic inflammation, and serious health problems including obesity, metabolic syndrome, and cardiovascular diseases. Diets enriched with ω-3 marine PUFAs have revealed additional improvements in health status associated to a reduction of proinflammatory ω-3 and ω-6 lipid mediators. Lipid mediators are produced from enzymatic and non-enzymatic oxidation of PUFAs. Interest in better understanding the occurrence of these metabolites has increased exponentially as a result of the growing evidence of their role on inflammatory processes, control of the immune system, cell signaling, onset of metabolic diseases, or even cancer. The scope of this review has been to highlight the recent findings on: a) the formation of lipid mediators and their role in different inflammatory and metabolic conditions, b) the direct use of lipid mediators as antiinflammatory drugs or the potential of new drugs as a new therapeutic option for the synthesis of antiinflammatory or resolving lipid mediators and c) the impact of nutritional interventions to modulate lipid mediators synthesis towards antiinflammatory conditions. In a second part, we have summarized methodological approaches (Lipidomics) for the accurate analysis of lipid mediators. Although several techniques have been used, most authors preferred the combination of SPE with LC-MS. Advantages and disadvantages of each method are herein addressed, as well as the main LC-MS difficulties and challenges for the establishment of new biomarkers and standardization of experimental designs, and finally to deepen the study of mechanisms involved on the inflammatory response.

Simple New Method of Detecting Lies By Identifying Invisible Unique Physiological Reflex Response Appearing Often Less Than 10-15 Seconds on the Specific Parts of Face of Lying Person; Quick Screening of Potential Murderers & Problematic Persons.

Frequently, we cannot find any significant visible changes when somebody lies, but we found there are significant invisible changes appearing in specific areas of the face when somebody lies and their location often depends on whether the lie is serious with or without physical violence involvement. These abnormalities were detected non-invasively at areas: 1) lobules and c) a small round area of each upper lateral side of forehead; 2) the skin between the base of the 2 orifices of the nose and the upper end of upper lip and 3) Alae of both sides of nose. These invisible significant changes usually last less than 15 seconds after telling a lie. In these areas, Bi-Digital O-Ring Test (BDORT), which received a U.S. Patent in 1993, became significantly weak with an abnormal value of (-)7 and TXB2, measured non-invasively, was increased from 0.125-0.5ng to 12.5-15ng (within the first 5 seconds) and then went back down to less than 1ng (after 15 seconds). These unique changes can be documented semi-permanently by taking photographs of the face of people who tell a lie, within as short as 10 seconds after saying a lying statement. These abnormal responses appear in one or more of the above-mentioned 3 areas 1), 2) & 3). At least one abnormal pupil with BDORT of (-)8-(-)12 & marked reduction in Acetylcholine and abnormal increase in any of 3 Alzheimer's disease associated factors Apolipoprotein (Apo) E4, ß-Amyloid (1-42), Tau protein, viral and bacterial infections were detected in both pupils and forehead of murderers and people who often have problems with others. Analysis of well-known typical examples of recent mass murderers was presented as examples. Using these findings, potential murderers and people who are very likely to develop problems with others can be screened within 5-10 minutes by examining their facial photographs and signatures before school admission or employment.

Ácidos grasos omega-3 en las lesiones deportivas ¿una posible ayuda terapéutica? (i) / Omega-3 fatty acid: a possible therapeutic aid? (i)

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Lipid, lipoprotein, and hemostatic effects of fish vs fish-oil n-3 fatty acids in mildly hyperlipidemic males.

The effects of fish and fish oil on lipids, hemostasis, and blood pressure were compared in 25 mildly hyperlipidemic men who received 4.5 g eicosapentaenoic acid (EPA) plus docosahexaenoic acid (DHA) daily for 5 wk. Six additional subjects served as controls. Fish and fish oil lowered plasma triglycerides 20% and 28% and very-low-density-lipoprotein (VLDL) triglycerides 42% and 52%, respectively (all P less than 0.05 compared with control). High-density-lipoprotein (HDL) cholesterol increased by 10% and 9%, with 34% and 32% increases in the proportion of HDL2 particles for fish and fish oil, respectively. Changes in total cholesterol, LDL cholesterol, apolipoprotein B, and blood pressure with fish and fish oil were not significantly different from changes for the control diet. The fish lowered fibrinogen (15.7%) and thromboxane (10.5%) and increased bleeding time (10.8%) (P less than 0.05 compared with control). Eating fatty fish and fish oil produced comparable lipid and lipoprotein changes, but only the fish improved hemostatic factors.

Dietary fish oil modulates macrophage fatty acids and decreases arthritis susceptibility in mice.

B10.RIII and B10.G mice were transferred from a diet of laboratory rodent chow to a standard diet in which all the fat (5% by weight) was supplied as either fish oil (17% eicosapentaenoic acid [EPA], 12% docosahexaenoic acid [DHA], 0% arachidonic acid [AA], and 2% linoleic acid) or corn oil (0% EPA, 0% DHA, 0% AA, and 65% linoleic acid). The fatty acid composition of the macrophage phospholipids from mice on the chow diet was similar to that of mice on a corn oil diet. Mice fed the fish oil diet for only 1 wk showed substantial increases in macrophage phospholipid levels of the omega-3 fatty acids (of total fatty acid 4% was EPA, 10% docosapentaenoic acid [DPA], and 10% DHA), and decreases in omega-6 fatty acids (12% was AA, 2% docosatetraenoic acid [DTA], and 4% linoleic acid) compared to corn oil-fed mice (0% EPA, 0% DPA, 6% DHA, 20% AA, 9% DTA, and 8% linoleic acid). After 5 wk this difference between the fish oil-fed and corn oil-fed mice was even more pronounced. Further small changes occurred at 5-9 wk. We studied the prostaglandin (PG) and thromboxane (TX) profile of macrophages prepared from mice fed the two diets just before being immunized with collagen. Irrespective of diet, macrophages prepared from female mice and incubated for 24 h had significantly more PG and TX in the medium than similarly prepared macrophages from male mice. The increased percentage of EPA and decreased percentage of AA in the phospholipids of the macrophages prepared from the fish oil-fed mice was reflected in a reduction in the amount of PGE2 and PGI2 in the medium relative to identically incubated macrophages prepared from corn oil-fed mice. When this same fish oil diet was fed to B10.RIII mice for 26 d before immunization with type II collagen, the time of onset of arthritis was increased, and the incidence and severity of arthritis was reduced compared to arthritis induced in corn oil-fed mice. The females, especially those on the fish oil diet, tended to have less arthritis than the males. These alterations in the fatty acid pool available for PG and leukotriene synthesis suggest a pivotal role for the macrophage and PG in the immune and/or inflammatory response to type II collagen.

Concentrations of prostaglandins D2, E2, F2 alpha, 6-keto-F1 alpha and thromboxane B2 in synovial fluid from patients with inflammatory joint disorders and osteoarthritis.

The concentrations of PGD2, PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2 in synovial fluid from patients with rheumatoid arthritis (RA), Reiter's disease (RD), acute gouty arthritis (GA) and osteoarthritis (OA) were measured by radioimmunoassay. PGE2 was found to be the most predominant prostanoid (pg/ml; Mean +/- S.E.M.): RA 887 +/- 85, RD 870 +/- 71, GA 1064 +/- 155 and OA 665 +/- 71. In patients with OA lower mean levels of all the prostanoids were found than compared to the other groups of patients. Only in patients with RA a slight correlation between PGD2/PGF2 alpha, PGE2/PGF2 alpha and PGE2/6-keto-PGF1 alpha could be demonstrated. No significant correlations between the leucocyte cell counts in the synovial fluid and the prostanoid concentrations were found. In patients with RA developing recurrent knee joint effusions within four weeks after the first sampling significantly lower levels of PGE2 and TXB2 were found in the recurrent samples (PGE2 792 +/- 183; TXB2 179 +/- 33) than compared with the original samples (PGE2 984 +/- 146; TXB2 239 +/- 32).