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Berries are a rich source of anthocyanins, and clinical data suggest that a polyphenol-rich diet may exert health-promoting effects by reducing oxidative stress. The aim of this study was to elucidate the effects of dietary supplementation with Delphinol (trademark owned by MNL Chile) standardized maqui berry (Aristotelia chilensis) extract on products of lipid peroxidation in healthy, overweight, and smoker subjects.

In a double-blind, placebo-controlled design, 42 participants (age 45-65years) consumed in random order either a standardized extract of maqui berry (162mg anthocyanins) or a matched placebo, given 3times daily for 4weeks. The samples were collected at baseline, after the end of the supplementation, and 40days after the end of the study. Primary outcome was the measure of oxidized low-density lipoprotein (Ox-LDL) and F2-isoprostanes in plasma and urine, respectively. Secondary outcomes included anthropometric measures, blood pressure, and lipid profile.

Delphinol supplementation was associated with reduced levels of Ox-LDL in the anthocyanin group compared to baseline (p < 0.05). There was also a decrease in urinary F2-isoprostanes (8-iso-prostaglandin F2α) at 4weeks versus baseline in the Delphinol-supplemented group (p < 0.05). However, no differences in primary outcomes were evident at 40days of follow-up. AZD7648 In the fourth week of the intervention, no significant differences were noted for anthropometric characteristics, ambulatory blood pressure, and lipid profile.

Our observations suggest that dietary interventions with maqui berry extract may improve oxidative status (Ox-LDL and F2-isoprostanes) in healthy adults, overweight adults, and adult smokers.

Our observations suggest that dietary interventions with maqui berry extract may improve oxidative status (Ox-LDL and F2-isoprostanes) in healthy adults, overweight adults, and adult smokers.Cardiovascular diseases (CVDs) are the leading cause of mortality in the Western world. Multiple factors are involved in CVD, including genetic factors and modifiable factors such as diet, physical activity, and smoking. CVD incidence and prevalence increase progressively with age, and it is estimated that over 80% of men and women older than 75 years have clinically manifest CVD. To reduce the gap between life expectancy (LE) and healthy life expectancy is one of the main challenges of the 21st century. Lifestyle improvement appears to be the only sustainable approach to face the dramatic chronic-degenerative disease burden of an aging population. A healthy lifestyle, represented by avoiding smoking, following a healthy diet, and practicing physical activity, protects from chronic-degenerative disease onset and progression. A healthy dietetic approach specifically formulated for elderly people, with a defined pattern of nutraceutical bioactive compounds, may represent a key strategy to improve the aging process and increase the life span. This short review summarizes the biochemical mechanisms underpinning the cardiovascular protective effects of some nutraceutical compounds such as quercetin and sulforaphane.Chronic disease is driven by inflammation. This article will provide an overview on how the balance of macronutrients and omega-6 and omega-3 fatty acids in the diet can alter the expression of inflammatory genes. In particular, how the balance of the protein to glycemic load of a meal can alter the generation of insulin and glucagon and the how the balance of omega-6 and omega-3 fatty acids can effect eicosanoid formation. Clinical results on the reduction of inflammation following anti-inflammatory diets are discussed as well as the molecular targets of anti-inflammatory nutrition. To overcome silent inflammation requires an anti-inflammatory diet (with omega-3s and polyphenols, in particular those of Maqui). The most important aspect of such an anti-inflammatory diet is the stabilization of insulin and reduced intake of omega-6 fatty acids. The ultimate treatment lies in reestablishing hormonal and genetic balance to generate satiety instead of constant hunger. Anti-inflammatory nutrition, balanced 403030 with caloric restriction, should be considered as a form of gene silencing technology, in particular the silencing of the genes involved in the generation of silent inflammation. To this anti-inflammatory diet foundation supplemental omega-3 fatty acids at the level of 2-3 g of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) per day should be added. Finally, a diet rich in colorful, nonstarchy vegetables would contribute adequate amounts of polyphenols to help not only to inhibit nuclear factor (NF)-κB (primary molecular target of inflammation) but also activate AMP kinase. Understanding the impact of an anti-inflammatory diet on silent inflammation can elevate the diet from simply a source of calories to being on the cutting edge of gene-silencing technology.Chronic inflammation negatively impacts all physiological functions, causing an array of degenerative conditions including diabetes; cancer; cardiovascular, osteo-articular, and neurodegenerative diseases; autoimmunity disorders; and aging. In particular, there is a growing knowledge of the role that gene transcription factors play in the inflammatory process. Obesity, metabolic syndrome, and diabetes represent multifactorial conditions resulting from improper balances of hormones and gene expression. In addition, these conditions have a strong inflammatory component that can potentially be impacted by the diet. It can reduce pro-inflammatory eicosanoids that can alter hormonal signaling cascades to the modulation of the innate immune system and gene transcription factors. Working knowledge of the impact of how nutrients, especially dietary fatty acids and polyphenols, can impact these various molecular targets makes it possible to develop a general outline of an anti-inflammatory diet that offers a unique, nonpharmacological approach in treating obesity, metabolic syndrome, and diabetes. Several important bioactive dietary components can exert their effect through selected inflammatory pathways that can affect metabolic and genetic changes. In fact, dietary components that can modulate glucose and insulin levels, as well as any other mediator that can activate nuclear factor-kB, can also trigger inflammation through common pathway master switches.This article introduces the subjective side of quality of life as it has evolved within the discipline of psychology. Subjective well-being is also of special interest within medicine due to its links to pathology and the fact that it is managed by a homeostatic system. This form of management offers an explanation for the unusual properties of subjective well-being, including its normal positivity, stability, and nonlinear relationship to objective variables, such as physical health. Central to understanding is the proposition that subjective well-being mainly consists of a specific form of trait mood. This homeostatically protected mood has a genetic set point and it is the experience of this set-point mood that homeostasis is defending. The resources required to maintain normal homeostatic control are described. If these resources are inadequate to protect the experience of set-point mood, mood positivity falls, and there is a high probability of depression. In this article, the process of homeostasis is shown to assist understanding of intervention effectiveness within both psychology and medicine. This concerns matters of resilience, the nonlinear relationship between levels of subjective well-being, and the strength of challenging agents, and the important understanding that interventions designed to raise subjective well-being are critically dependent on its level at baseline. Key teaching points The physiological process of homeostasis has a parallel in psychology in the homeostatic management of subjective well-being. Subjective well-being is a more globally informative construct than health-related quality of life. How people feel about themselves and their lives cannot be simply predicted through measures of health. When subjective well-being homeostasis is defeated, there is a high probability of depression.

In comparative examinations of kinematics of the knees of humans and pigs in flexional/extensional motion under compressive loads, the significant differential geometric essentials of articular guidance are elaborated to criticise the shaping of the articular surfaces of conventional knee-endoprostheses and to suggest constructional outlines that allow the endoprosthesis to adopt natural knee kinematics. Implantation is discussed with regard to the remaining ligamentous apparatus.

Twelve fresh pig knee joints and 19 preserved human knee joints were moved into several flexional/extensional positions. In each joint, the tibia and femur were repeatably caught by metal plates. After removing all ligaments, the tibia and femur were again caught in these positions, and their points of contact were marked on both articular surfaces. Along the marker points, a thin lead wire was glued onto each surface. The positions and shapes of the four contact lines were mapped by teleradiography.

All contact lines were found to be plane curves. The medial and lateral planes were parallel, thus defining the joint's sagittal plane. In the human knee, as compared to the lateral, the medial femoral contact line was always shifted anteriorly by several millimetres. The tibial contact curve was laterally convex and medially concave. In the pig knees, the lateral and medial contact lines were asymmetrically placed. Both tibial curves were convex.

Both knees represent cam mechanisms (with one degree of freedom) that produce rolling of the articular surfaces during the stance phase. Implantation requires preservation of the anterior cruciate ligament, and ligamentous balancing is disadvantageous.

Both knees represent cam mechanisms (with one degree of freedom) that produce rolling of the articular surfaces during the stance phase. Implantation requires preservation of the anterior cruciate ligament, and ligamentous balancing is disadvantageous.Primary total knee arthroplasty is the treatment for end-stage arthritis of the knee; in the last years, it is becoming more common and reliable, due to technical and implant improvement. With larger implant rates, the overall complications will increase and pain is the most common sign of implant failure. Pain can be related to a lot of different clinical findings, and the surgeon has to be aware of the various etiologies that can lead to failure. Pain does not always mean revision, and the patient has to be fully evaluated to have a correct diagnosis; if surgery is performed for the wrong reason, this will surely lead to a failure. In this paper, the authors revised the more common causes of failure that can have a painful onset proposing an approach for diagnosis and treatment.Charcot-Marie-Tooth disease type 4H (CMT4H) is an autosomal recessive demyelinating subtype of peripheral enuropathies caused by mutations in the FGD4 gene. Most CMT4H patients are in consanguineous Mediterranean families characterized by early onset and slow progression. We identified two CMT4H patients from a Korean CMT cohort, and performed a detailed genetic and clinical analysis in both cases. Both patients from nonconsanguineous families showed characteristic clinical manifestations of CMT4H including early onset, scoliosis, areflexia, and slow disease progression. Exome sequencing revealed novel compound heterozygous mutations in FGD4 as the underlying cause in both families (p.Arg468Gln and c.1512-2A>C in FC73, p.Met345Thr and c.2043+1G>A (p.Trp663Trpfs*30) in FC646). The missense mutations were located in highly conserved RhoGEF and PH domains which were predicted to be pathogenic in nature by in silico modeling. The CMT4H occurrence frequency was calculated to 0.7% in the Korean demyelinating CMT patients.