Effects of hypopressive exercises on pelvic floor and abdominal muscles in adult women: A systematic review of randomized clinical trials.

INTRODUCTION: Hypopressive exercises (HE) are postural and breathing exercises that activate deep muscles in the abdomen and pelvic floor. Despite this, there is still no consensus in the literature on its real effectiveness. The objective was to analyze the effects of HE on the abdominal and pelvic floor muscles in women with or without dysfunctions in these regions. METHODS: This is a systematic review of randomized clinical trials found in the PEDro, PubMed, Cochrane, LILACS, and Embase databases. We include studies that evaluate the effects of HE (with or without other techniques) on the pelvic floor and abdominal region for 8 weeks or more, in women over 18 years old, with or without dysfunction in these regions, with the presence of a control group (active or passive). RESULTS: HE were effective in improving strength, tone, and reducing symptoms of pelvic floor dysfunctions, in magnitude less than (in two studies) or equal (in one study) to the pelvic floor muscle training (PFMT). When HE were performed with PFMT in the same group, no additional benefits were found. Only one study evaluated abdominal muscles activation, where HE were effective in improving postural control and activation of the transversus abdominis muscle. CONCLUSIONS: The HE presented positive results to the evaluated parameters. However, the information is still preliminary and scarce. There are methodological divergences regarding the execution, follow-up and standardization of the method, which could affect the results. According to the existing information, HE cannot yet be reliably indicated for the treatment of the pelvic floor, despite pointing out relevant results in some studies. More randomized clinical trials and long-term studies are needed to analyze the effects of HE not only for pelvic floor, but also for other regions, such as abdominal muscles and related dysfunctions.

Human apoCIII transgenic mice with epicardial adipose tissue inflammation and PRESERVATION of the cardiac plexus.

Hypertriglyceridemia is a result of the increase in the serum levels of lipoproteins, which are responsible for the transport of triglycerides and can be caused by genetic and/or metabolic factors. Animal models which either express or lack genes related to changes in the lipoproteins profile are useful to understand lipid metabolism. Apolipoprotein CIII (apoCIII) is an important modulator of hepatic production and peripheral removal of triglycerides. Mice that overexpress the apoCIII gene become hypertriglyceridemic, showing high concentrations of free fatty acids in the blood. Since hypertriglyceridemia is related to atherosclerosis, and the latter refers to cardiac alterations, this study aimed at evaluating the morphological, morphometric and quantitative profiles of the cardiac plexus, as well as the morphometric and histopathological aspects of the epicardial adipose tissue in human apoCIII transgenic mice. Therefore, 8-12-month-old male C57BL/6 mice that overexpressed human apoCIII (CIII) and their respective controls were used. Our results showed that overexpression of human apoCIII did not modify morphological or quantitative parameters of cardiac plexus neurons; however, age increased both, the area and the number of such cells. Furthermore, there was a direct correlation of this dyslipidemia to the thickening of periganglionar type 1 collagens. On the other hand, this overexpression caused epicardial adipose tissue inflammation and an increase in the area of the adipocytes, thus, favoring the recruitment of inflammatory cells in this tissue. In conclusion, this overexpression is harmful since it is related to an increase in cardiac adiposity, as well as to a predisposition to an inflammatory environment in the epicardial fat and to the incidence of cardiovascular diseases.

Efeitos do estresse físico e psicológico juvenil sobre a glândula suprarrenal em ratos adultos / Effects of juvenile physical and psychological stress on the suprarenal gland in adult rats

Estresse é a resposta aos diferentes estímulos que o organismo sofre em busca de adaptação à homeostasia. Devido à sua alta incidência, diversos modelos experimentais estão sendo desenvolvidos para a melhor compreensão de sua inter-relação com outros órgãos. Neste contexto, o objetivo deste estudo foi avaliar os efeitos em longo prazo do estresse físico e psicológico juvenil agudo sobre as glândulas suprarrenais de ratos, no que se refere aos aspectos morfológicos, pois tais glândulas apresentam relação direta com situações de estresse. Para tanto, as glândulas suprarrenais destes animais foram processadas e análises morfológicas da medula e do córtex foram realizadas por meio de morfometria e quantificação por planimetria. Os resultados obtidos demonstraram que o estresse tanto físico quanto psicológico não provocaram alterações significativas em relação à área de superfície e espessura das suprarrenais, indicando adaptação dos animais aos fatores estressantes aqui estudados.

Stress is a response to different stimuli experienced by the organism for its adaption to homeostasis. Due to its high occurrence, several experimental models are being developed to understand better the interrelationships between these organs. Current paper evaluates long-term effects of juvenile physical and psychological stress on the suprarenal glands of rats with regard to morphological aspects. In fact, these glands have a direct relationship with stress conditions. Rats´ suprarenal glands were processed and their medulla and cortex were morphologically investigated through planimetry. Results show that physical and psychological stress failed to cause significant changes on the surface area and thickness of the glands. This fact showed adaptation of animals to the type of stress under analysis.

Toxoplasma gondii causes lipofuscinosis, collagenopathy and spleen and white pulp atrophy during the acute phase of infection.

In this study, we evaluated homeostatic and functional disorders of the spleen in mice inoculated with Toxoplasma gondii. The kinetics of megakaryocyte and leukocyte production, body and spleen mass and certain histopathological aspects were analyzed. There was increased (P < 0.05) the accumulation of lipofuscin in the red pulp of the spleen, in the periods of 30 and 60 dpi of the infection, that is, in the chronification stage of the disease and decrease of the white pulp area. In addition, we observed (from 7dpi) a quantitative and qualitative increase (P < 0.05) in the deposition of collagen fibers in the spleen of all infected mice. Since resolution of the inflammatory process resulted in pathophysiological changes, we can suggest that the T. gondii invaded and multiplied in the cells of the white and red pulps of the spleen. Although we did not find the parasite in the spleen, this hypothesis is supported by the presence of diffuse inflammatory infiltrate, which extended through the spleen parenchyma of all inoculated mice. Taken together, our results suggest that T. gondii causes severe homeostatic disorders that have altered spleen physiology, including diffuse parenchymal inflammation, lipofuscinosis in histiocytes, early aging, collagenopathy, systemic sclerosis and spleen and white pulp atrophy.

Effects of Ezetimibe, Simvastatin, and their Combination on Inflammatory Parameters in a Rat Model of Adjuvant-Induced Arthritis.

Statins are hypocholesterolemic drugs that are prescribed for patients with an increased risk of cardiovascular and cerebrovascular complications. Ezetimibe has an atheroprotective activity through inhibition of the expression of vascular adhesion molecule-I and vascular CD14, a marker of the infiltration of mononuclear leukocytes. Ezetimibe reduces the amount of chemoattractant protein-1 that is available for monocytes and macrophages and alters the activity of nuclear factor κB in leukocytes. The mechanisms of action of statins complement those of ezetimibe. Previous studies have demonstrated that the combination of statins and ezetimibe has beneficial effects, including antiinflammatory activity. The present study evaluated the effects of monotherapy with ezetimibe and simvastatin compared with ezetimibe + simvastatin combined on the evolution of the inflammatory response in a rat model of Complete Freund's Adjuvant-induced arthritis. The animals were treated with 10 mg/kg ezetimibe, 40 mg/kg simvastatin, or 10 mg/kg ezetimibe + 40 mg/kg simvastatin for 1, 7, 14, or 28 days. We analyzed leukocyte rolling behavior, leukocyte adhesion to the endothelium, the number of leukocytes that were recruited to the knee joint cavity, and the concentration of cytokines that are involved in the inflammatory response. The data were analyzed using paired t tests or analysis of variance followed by Bonferroni post hoc test. The treatments reduced leukocyte rolling behavior and leukocyte adhesion. The monotherapies did not change the number of leukocytes that were recruited to the knee joint cavity, whereas the ezetimibe + simvastatin combination significantly reduced this parameter. The treatments reduced the levels of proinflammatory cytokines and increased the levels of the antiinflammatory cytokine IL-10, indicating antiinflammatory properties of these drugs in this experimental model of inflammation.

Effects of simvastatin, ezetimibe, and their combination on histopathologic alterations caused by adjuvant-induced arthritis.

The objective of the present study was to investigate the effects of monotherapy with simvastatin or ezetimibe compared with those of an ezetimibe + simvastatin combination on the histopathologic aspects of arthritis induced by Complete Freund's Adjuvant in rats. The characteristics of diarthrosis were analyzed 7 and 28 days after arthritis induction with regard to the regularity and integrity of articular cartilage, the presence of leukocytes in blood vessels at the inflammation site, and the cytokine levels in articular tissue. Monotherapy with simvastatin or ezetimibe and the ezetimibe + simvastatin combination effectively reduced the cytokine levels (interleukin-6 and tumor necrosis factor) and articular lesions that are characteristic of this experimental disease. Although the results did not reveal significant differences between the monotherapy and the combined therapy, they suggest that these drugs have considerable antiinflammatory properties, as reflected by an attenuation of articular cartilage lesions mediated by a reduction in the levels of proinflammatory cytokines.

Anti-arthritic effect of eugenol on collagen-induced arthritis experimental model.

This study was designed to test the efficacy of eugenol, a compound obtained from the essential oil of cloves (Syzygium aromaticum) in collagen-induced arthritis (CIA), a well characterized murine model of rheumatoid arthritis. Macroscopic clinical evidence of CIA manifests first as periarticular erythema and edema in the hind paws. Treatment with eugenol starting at the onset of arthritis (day 25) ameliorated these clinical signs of CIA. Furthermore, eugenol inhibited mononuclear cell infiltration into the knee joints of arthritic mice and also lowered the levels of cytokines (tumor necrosis factor (TNF)-α, interferon (IFN)-γ and tumor growth factor (TGF)-ß) within the ankle joints. Eugenol treatment did not affect the in vitro cell viability as assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Therefore, eugenol ameliorates experimental arthritis and could be useful as a beneficial supplement in treating human arthritis.

Effects of simvastatin, atorvastatin, ezetimibe, and ezetimibe + simvastatin combination on the inflammatory process and on the liver metabolic changes of arthritic rats.

In this study, simvastatin, atorvastatin, ezetimibe, and ezetimibe + simvastatin combination were administered to arthritic rats, first to determine their effects on the inflammatory response, employing a low-dose adjuvant-induced arthritis model in rats. Arthritis was induced by the subcutaneous injection of a suspension of Mycobacterium tuberculosis (100 µg) in mineral oil [complete Freund's adjuvant used (CFA)] into the plantar surface of the hind paws. Simvastatin(40 mg/kg), atorvastatin(10 mg/kg), ezetimibe(10 mg/kg), ezetimibe(10 mg/kg) + simvastatin(20 mg/kg or 40 mg/kg) were given intragastrically and the treatment began on the day of CFA injection and continued daily up to the 28th day after arthritis induction. The ezetimibe + simvastatin combination was more effective in reducing the inflammatory response in arthritic rats than in atorvastatin, simvastatin, or ezetimibe monotherapy. The observed effect seems to be cholesterol-independent as there were no changes in plasma cholesterol levels. In spite of the benefits on joint lesions, treatment with ezetimibe + simvastatin combination caused a marked increment in liver, kidneys, spleen size, and plasma transaminases activities. Therefore, animals treated with the ezetimibe(10 mg/kg) + simvastatin(40 mg/kg) combination were also submitted to liver perfusion experiments. In this regard, ezetimibe + simvastatin did not improve the liver metabolic alterations seen in control arthritic rats, on the contrary, a worsening was observed in liver production of glucose from alanine, as well as in oxygen uptake. All of these metabolic changes appear to be induced by treatment with ezetimibe + simvastatin combination, as the same metabolic effects were observed in normal and treated arthritic animals.