DYNAMICAL FACTORS RELATED TO VERTICAL JUMP PERFOMANCE

INTRODUCTION - In most of sport exercises, the displacement of body Center of Mass (CM) is an important factor to de-terminate performance. And greater the velocity at takeoff phase, greater the height achieved by the body CM. High jumps are influenced by the net combination of different joints moments and its synchronization during this task. Thus, also the countermovement may influence high jump performance (HOCHMUTH & MARHOLD, 1978). To measure the effectiveness of training into increasing the height in vertical jump relays information to both coach and athlete in manner to adapt the training. The purpose of this study is to analyze temporal and frequencies factors of ground reaction force GRF and the effect of limitation of arms swing and trunk extension in vertical jump. METHODS AND EQUIPMENT - All the exercises were performed on a strain gauges force platform. The ground reaction force (GRF) had been sampled at 800 Hz frequency and after the determination of its frequency components by the use of FFT, the raw signals were low-pass filtered at 160 Hz. A video camera was exerted to control the set of jumps. The volunteer subject for this study was a male high jumper, 26 years old, 70.4f0.5 kg weight, 184.0k0.5 cm tall. Four different types of vertical jumps were performed (set of 5 trials) and analyzed in this study: 1) standard vertical jump; 2) jump with- out the elevation of upper limbs; 3) jump without the extension of trunk; and 4) jump without both the elevation of upper limbs and extension of trunk. All that jumps were preceded by countermovement. RESULTS AND DISCUSSION - Although four different techniques had been per- formed for high jumps, the temporal factors (DOWLINH & VAMOS, 1993) did not differ statistically (duration of major positive impulse and duration of major negative impulse). Eccentric and concentric phases was not different statistically. Power spectral analysis has showed that trunk mobility might be more influent than upper limb swing in the dynamic4 characteristics of the analyzed movement. Informations provided by spectral analysis probably relays important data to identify the influence of different body segments in vertical jump. It was not confirmed that the maintenance of a steady state just before the maximum vertical GRF or reducing the depression between the two positive peaks is related to the acceleration caused by arms swing. On the other hand, our results indicate that the first positive peak is probably exerted by trunk extension. In spite of the limitation of trunk and upper limb mobility, it is clear that is not possible to exclude their influence in total body moment of inertia. CONCLUSION - According to our results, despite different jumping exercises, restrictions to joints mobility changes the maxi- mum vertical GRF. Besides, tests that intend to measure the performance in high jumps according the use or not of parts of the human body may be reconsidered. REFERENCES Hochmuth G.; Marhold G. (1983) In Asmussen E. Jagenssen K. Biomechanics VI B. Dowling J.J.; Vamos L. (1 9933 J. Applied. Biornech. 9, 95-110

Biology and Role of Extracellular Vesicles (EVs) in the Pathogenesis of Thrombosis

Extracellular vesicles (EVs) are well-established mediators of cell-to-cell communication. EVs can be released by every cell type and they can be classified into three major groups according to their biogenesis, dimension, density, and predominant protein markers: exosomes, microvesicles, and apoptotic bodies. During their formation, EVs associate with specific cargo from their parental cell that can include RNAs, free fatty acids, surface receptors, and proteins. The biological function of EVs is to maintain cellular and tissue homeostasis by transferring critical biological cargos to distal or neighboring recipient cells. On the other hand, their role in intercellular communication may also contribute to the pathogenesis of several diseases, including thrombosis. More recently, their physiological and biochemical properties have suggested their use as a therapeutic tool in tissue regeneration as well as a novel option for drug delivery. In this review, we will summarize the impact of EVs released from blood and vascular cells in arterial and venous thrombosis, describing the mechanisms by which EVs affect thrombosis and their potential clinical applications

Precursor-Dependent Photocatalytic Activity of Carbon Dots

This work systematically compares both structural features and photocatalytic performance of a series of graphitic and amorphous carbon dots (CDs) prepared in a bottom-up manner from fructose, glucose, and citric acid. We demonstrate that the carbon source and synthetic procedures diversely affect the structural and optical properties of the CDs, which in turn unpredictably influence their photo electron transfer ability. The latter was evaluated by studying the photo-reduction of methyl viologen. Overall, citric acid-CDs were found to provide the best photocatalytic performance followed by fructose- and glucose-CDs. However, while the graphitization of glucose- and citric acid-CDs favored the photo-reaction, a reverse structure-activity dependence was observed for fructose-CDs due to the formation of a large graphitic-like supramolecular assembly. This study highlights the complexity to design in advance photo-active bio-based carbon nanomaterials

Physical Exercise Affects Adipose Tissue Profile and Prevents Arterial Thrombosis in BDNF Val66Met Mice

Adipose tissue accumulation is an independent and modifiable risk factor for cardiovascular disease (CVD). The recent CVD European Guidelines strongly recommend regular physical exercise (PE) as a management strategy for prevention and treatment of CVD associated with metabolic disorders and obesity. Although mutations as well as common genetic variants, including the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism, are associated with increased body weight, eating and neuropsychiatric disorders, and myocardial infarction, the effect of this polymorphism on adipose tissue accumulation and regulation as well as its relation to obesity/thrombosis remains to be elucidated. Here, we showed that white adipose tissue (WAT) of humanized knock-in BDNFVal66Met (BDNFMet/Met) mice is characterized by an altered morphology and an enhanced inflammatory profile compared to wild-type BDNFVal/Val. Four weeks of voluntary PE restored the adipocyte size distribution, counteracted the inflammatory profile of adipose tissue, and prevented the prothrombotic phenotype displayed, per se, by BDNFMet/Met mice. C3H10T1/2 cells treated with the Pro-BDNFMet peptide well recapitulated the gene alterations observed in BDNFMet/Met WAT mice. In conclusion, these data indicate the strong impact of lifestyle, in particular of the beneficial effect of PE, on the management of arterial thrombosis and inflammation associated with obesity in relation to the specific BDNF Val66Met mutation

Patho- physiological role of BDNF in fibrin clotting

Circulating levels of Brain Derived Neurotrophic Factor (BDNF) are lower in coronary heart disease (CHD) than in healthy subjects and are associated with coronary events and mortality. However, the mechanism(s) underling this association is not fully understood. We hypothesize that BDNF may influence fibrin fiber structure and clot stability, favoring clot lysis and thrombus resolution. We showed that recombinant BDNF (rh-BDNF) influenced with clot formation in a concentration-dependent manner in both purified fibrinogen and plasma from healthy subjects. In particular, rh-BDNF reduced the density of fibrin fibers, the maximum clot firmness (MCF) and the maximum clot turbidity, and affected the lysis of clot. In addition, both thrombin and reptilase clotting time were prolonged by rh-BDNF, despite the amount of thrombin formed was greater. Intriguingly, CHD patients had lower levels of BDNF, greater fibrin fibers density, higher MCF than control subjects, and a negative correlation between BDNF and MCF was found. Of note, rh-BDNF markedly modified fibrin clot profile restoring physiological clot morphology in CHD plasma. In conclusion, we provide evidence that low levels of BDNF correlate with the formation of bigger thrombi (in vitro) and that this effect is mediated, at least partially, by the alteration of fibrin fibers formation

Anticancer activity of "Trigno M", extract of Prunus spinosa drupes, against in vitro 3D and in vivo colon cancer models

Abstract In 2018 there were over 1.8 million new cases worldwide of colorectal cancer and relapses after clinical treatments. Many studies ascribe the risk of the appearance of this cancer to the Western life style : a sedentary life, obesity, and low -fiber, high -fat diets can promote the onset of disease. Several studies have shown supplement phytochemicals to have an inhibiting effect on the growth of various cancers through the activation of apoptosis. Our goal was to prove the effectiveness of a natural compound in the combined therapy of colorectal cancer. Trigno M supplement was an optimal candidate as anticancer product for its high concentrations of phenolic acids, flavonoids and anthocyanins. Our work showed the antitumor activity of Trigno M, extract of Prunus spinosa drupes combined with the nutraceutical activator complex (NAC), in 2D, 3D and in vivo colorectal cancer models. The cellular model we used both in vitro and in vivo was the HCT116 cell line, particularly suitable for engraftment after inoculation in mice. Trigno M inhibited the growth and colony formation of HCT116 cells (35%) as compared to the chemotherapy treatment with 5-fluorouracil (80%) used in clinical therapy. The reduction of the morphological dimensions in the spheroid cells after Trigno M, was compared with 5-fluorouracil demonstrating the efficacy of the Trigno M compound also in 3D models. Flow cytometric analysis on 3D cells showed a significant increase in the apoptotic cell fraction after Trigno M treatment (44.8%) and a low level of necrotic fraction (6.7%) as compared with control cells. Trigno M and 5-fluorouracil induced the apoptosis in a comparable percentage. Monotherapy with Trigno M in severely immunodeficient mice, carrying colon rectal cancer xenografts, significantly reduced tumor growth. The histopatological analysis of the ectopic tumors showed a lower level of necrosis after Trigno M treatment compared with the control. We conclude that Trigno M is well tolerated by mice, delays colorectal cancer growth in these animals and should be weighed up for integration of the current multi-drug protocols in the treatment of colon carcinoma

Fenretinide treatment accelerates atherosclerosis development in apoE-deficient mice in spite of beneficial metabolic effects

Background and Purpose Fenretinide, a synthetic retinoid derivative first investigated for cancer prevention and treatment, has been shown to ameliorate glucose tolerance, improve plasma lipid profile and reduce body fat mass. These effects, together with its ability to inhibit ceramide synthesis, suggest that fenretinide may have an anti-atherosclerotic action. Experimental Approach To this aim, nine-week-old apoE-knockout (EKO) female mice were fed for twelve weeks a Western diet, without (control) or with (0.1% w/w) fenretinide. As a reference, wild-type (WT) mice were treated similarly. Growth and metabolic parameters were monitored throughout the study. Atherosclerosis development was evaluated in the aorta and at the aortic sinus. Blood and lymphoid organs were further characterized with thorough cytological/histological and immunocytofluorimetric analyses. Key Results Fenretinide treatment significantly lowered body weight, glucose levels and plasma levels of total cholesterol, triglycerides, and phospholipids. In the liver, fenretinide remarkably reduced hepatic glycogenosis and steatosis driven by the Western diet. Treated spleens were abnormally enlarged, with severe follicular atrophy and massive extramedullary haematopoiesis. Severe renal hemosiderin deposition was observed in treated EKO mice. Treatment resulted in a threefold increase of total leukocytes (WT and EKO) and raised the activated/resting monocyte ratio in EKO mice. Finally, atherosclerosis development was markedly increased at the aortic arch, thoracic and abdominal aorta of fenretinide-treated mice. Conclusions and Implications We provide the first evidence that, despite beneficial metabolic effects, fenretinide treatment may enhance the development of atherosclerosis

An update on methods for Sarcopenia Diagnosis: From bench to bedside

Sarcopenia has been recognized as an age-related syndrome characterized by low muscle mass, low muscle strength, and low physical performance that is associated with increased likelihood of adverse outcomes including falls, fractures, hospitalization, frailty and mortality. Therefore, it is necessary to identify the condition early for applying intervention and prevention of the disastrous consequences of sarcopenia if left untreated. Clinical definition and diagnostic criteria for sarcopenia have been developed in the last years and different tools have been proposed for screening subjects with sarcopenia, evaluating the muscle mass, the muscle strength and the physical performance. In this review we analyzed the diagnostic criteria of sarcopenia and examined the current assessment tools used for the diagnosis and screening of sarcopenia

Apocynin Prevents Abnormal Megakaryopoiesis and Platelet Activation Induced by Chronic Stress

Environmental chronic stress (ECS) has been identified as a trigger of acute coronary syndromes (ACS). Changes in redox balance, enhanced reactive oxygen species (ROS) production, and platelet hyperreactivity were detected in both ECS and ACS. However, the mechanisms by which ECS predisposes to thrombosis are not fully understood. Here, we investigated the impact of ECS on platelet activation and megakaryopoiesis in mice and the effect of Apocynin in this experimental setting. ECS induced by 4 days of forced swimming stress (FSS) treatment predisposed to arterial thrombosis and increased oxidative stress (e.g., plasma malondialdehyde levels). Interestingly, Apocynin treatment prevented these alterations. In addition, FSS induced abnormal megakaryopoiesis increasing the number and the maturation state of bone marrow megakaryocytes (MKs) and affecting circulating platelets. In particular, a higher number of large and reticulated platelets with marked functional activation were detected after FSS. Apocynin decreased the total MK number and prevented their ability to generate ROS without affecting the percentage of CD42d+ cells, and it reduced the platelet hyperactivation in stressed mice. In conclusion, Apocynin restores the physiological megakaryopoiesis and platelet behavior, preventing the detrimental effect of chronic stress on thrombosis, suggesting its potential use in the occurrence of thrombosis associated with ECS

Fenretinide treatment accelerates atherosclerosis development in apolipoprotein e-deficient mice in spite of beneficial metabolic effects

Aim. Fenretinide, a synthetic retinoid derivative first investigated for cancer prevention and treatment, has been shown to ameliorate glucose tolerance and the plasma lipid profile, and to reduce body fat mass. These effects, together with its ability to inhibit ceramide synthesis, have suggested that fenretinide may display anti-atherosclerotic effects. Methods. To this aim, 9-weeks-old apoE-knockout (EKO) female mice were fed for 12 weeks a Western diet, without (EKO-Ctrl) or with (0.1% w/w) fenretinide (EKO-Fen). As a reference, wild-type (WT) mice were likewise treated. Growth and metabolic parameters were monitored throughout the study. Atherosclerosis development was evaluated in the aorta and at the aortic sinus. Blood and lymphoid organs were further characterized with thorough cytological/histological and immunocytofluorimetric analyses. Results. Fenretinide treatment significantly lowered body weight, glucose levels and plasma levels of total cholesterol, triglycerides and phospholipids. In the liver, fenretinide remarkably reduced hepatic glycogenosis and steatosis driven by the Western diet. Treated spleens were abnormally enlarged, with severe follicular atrophy and massive extramedullary hematopoiesis. Severe renal hemosiderin deposition was observed in EKO-Fen. Treatment resulted in a threefold increase of total leukocytes (WT and EKO) and raised the activated/resting monocyte ratio in EKO-Fen. Finally, atherosclerosis development was markedly increased at the aortic arch (34.4\uc5}7.3% vs 26.1\uc5}5.8%, +32%), thoracic (14.3\uc5}4.9% vs 4.9\uc5}2.1%, +191%) and abdominal aorta (7.6\uc5}3.3% vs 3.3\uc5}1.8%,+130%) of fenretinide-treated mice. Plaque extent was further quantified at the aortic sinus and provided similar results (810.000 \u3bcm2 vs. 540.000 \u3bcm2, +50% in EKO-Fen). Plaques of treated mice were characterized by an increased collagen content and a larger necrotic core, whereas the area occupied by macrophages, foam cells and neutral lipids was comparable between EKO-Fen and EKO-Ctrl. Conclusion. We provide the first evidence that, despite beneficial metabolic effects, fenretinide treatment may prove detrimental for atherosclerosis development