Background: The role of different diets and nutrients in the pathogenesis of cardiac dysfunction is controversial. However, it is well known that the Western diet has pro-inflammatory systemic effects, whereas Mediterranean-style diets have anti-inflammatory effects in all body systems. This study aimed to examine the effects of functional foods, omega-3 fatty acids and flavonoid-rich diets in patients with a high risk of Cardiovascular Diseases (CVDs) with reference to Heart Failure (HF).
The present study aimed to evaluate the effect of a progressive load of physical activity on a musculoskeletal injury in rats.Sixty-four rates were divided into two groups: experimental group (EG), which underwent physical activity (swimming) with a progressive load, and the control group (CG), which was not submitted to this program.The training was carried out according to an adapted version of the Gonçalves (1999) swimming system.Injuries were caused to the gastrocnemic muscle by inducing 40% NaOH.On days 2, 7, 14, and 21 after inducing muscle injury, the animals from both EC and CG were sacrificed.The injured area was removed and processed.The neutrophils, macrophages, lymphocytes, and plasmocytes were quantified by hematoxylin and eosin (H&E) stain.The percentage of the area of type I and type III collagen were quantified by a histological cut stained with picrosirius red stain (PSR) and submitted to polarization.A greater number of macrophages (GE=19.98±4.39;GC=2.48±1.00;p=0.006) and lymphocytes (GE=2.12±0.82;GC=0.06±0.82;p=0.037) after 2 days, and of macrophages (GE=15.74±3.00;GC=6.02±1.95;p=0.007) and lymphocytes (GE=2.01±0.78;GC=0.14±0.09;p=0.044) after 7 days, could be observed in the EG when compared to the CG; however, the opposite was true for neutrophils (GE=48.12±17.04;GC=105.54±12.25;p=0.005).After 14 days, a smaller quantity of neutrophils (GE= 32.70±10.26;GC= 90.96±17.62;p= 0.044) and a larger quantity of plasmocytes (GE=9.06±3.84;GC=0.68±0.53;p=0.028) could be observed in the EG as compared to the CG.A greater area of type III collagen could be observed in the EG when compared to the CG over a 14-day period (GE=44.90±16.15;GC=0.74±0.40;p=0.000) and a 21-day period (GE=13.19±9.09;GC=1.02±0.94;p=0.029), whereas the opposite could be observed for type I collagen.The physical activity promoted an increase in the deposition of type III collagen in the muscle injury.This activity accelerated the repair process after 14 days, possibly moderated by the larger number of inflammatory cells, while after 21 days, the lesion presented a lesser resistance.
The first cases of mucocutaneous lymph node syndrome (MLNS) were reported by Dr Tomisaku Kawasaki in 1967.His surname was later assigned to this new disease entity, and I was fortunate to meet him at the 100 th Annual Conference of the German Paediatric Association in Berlin in 2004 [1].According to our current understanding Kawasaki disease (KD) is a systemic autoimmune vasculitis which occurs in genetically susceptible people following an acute infection.Outside Japan KD has a low incidence and is notoriously difficult to diagnose because of its similarity to common infective childhood illnesses and a lack of specific and sensitive laboratory tests.The case report of KD by Bangert et al. [2] illustrates these difficulties aptly and calls for prompt diagnosis and treatment of this condition to avoid serious cardiovascular complications.
A diagnosis of Kawasaki disease (KD) is mainly based on clinical criteria.We discuss the case of a young boy who presented at the ages of 7 months and 13 months with signs and symptoms suggestive of Kawasaki disease.At the first episode he was treated for Kawasaki disease and at the second episode for lymphadenitis and fever.A diagnosis of recurrent KD was only made retrospectively when he developed thrombocytosis and desquamation of the extremities.Subsequent echocardiograms revealed no abnormalities.It is important that a diagnosis of KD is considered in any child presenting with a fever of more than 5 days irrespective of the previous medical history.
Current definition of inflammation by its cardinal signs is obsolete and unsuitable for guiding adequate therapeutic strategies.Furthermore, present theory of the inflammatory process regarding vascular phenomena as essential for generation of cardinal signs is invalid and unable to explain well established empirical facts, particularly the extent of the osmotic pressure and temperature variations within the inflamed tissue.From five cardinal signs, there is actually just one specific macroscopic sign of inflammation, namely localized edema.Further, the driving force for tissue fluid accumulation is defined in biochemical terms and as such taken for the definition of the inflammatory process.Inflammation may be defined as a degenerative process which is intense enough to cause local accumulation of low molecular weight catabolic products, which in turn elevates tissue osmotic pressure that attracts extra fluid, with or without heat release sufficient for significant elevation of tissue temperature.This process is in a sharp contrast to the pathogenesis of burns, where externally applied heat causes a process that is in essence opposite to inflammation, bearing only some superficial similarities with the latter.The inflammatory process is itself a pathological process, whereas the natural anti-inflammatory response that ensues after acute inflammation tends to reverse tissue homeostasis towards normality and should therefore be regarded as a true defensive reaction of the affected tissue.Based on the therapeutic principle of reverse thermodynamics, heat application to the inflamed tissue is an obvious, yet non-exclusive therapeutic choice that follows from the given universal definition of inflammation.
