Anthropometric features and body composition of young athletes practicing karate at a high and medium competitive level

The aim of the study was to examine the anthropometric features and body composition of athletes practising karate at a high and medium competitive level. Our study was carried out on a sample of 35 subjects practising karate and aged from 16.0 to 32.5 years. This sample was divided into two groups: group 1 (n=14 elite athletes) and group 2 (n=21 amateur athletes). Various anthropometric measurements were taken (weight, height both standing and sitting, diameters, circumferences and skinfold thickness) from which different anthropometric indices were calculated (body mass index, Scelic and Grant indices, arm muscle circumference and area), and the somatotype was then determined. The body composition of each subject was assessed using the skinfold technique and the Jackson-Pollock (J-P) and Sloan-Weir (S-W) equations. The two groups of athletes showed very similar measurements regarding anthropometric characteristics. Only the Scelix index presented a significantly different value in the two groups (49.6±1.3 for group 1 vs. 51.1±1.3 for group 2; p<0.01). Group 1 showed a mesomorphic-ectomorphic somatotype, while the amateur athletes presented a balanced mesomorphic type. Moreover, a lower percentage of fat mass was more frequent in the first group (J-P=8.1±2.4%; S-W=8.9±3.3%) than in the second one (J-P=9.8±1.6%; S-W=11.2±3.7%), although the differences between the two groups were not significant. We conclude that group 1 is characterized by a slightly prominent vertical development of the skeletal frame. This could be an anthropometric characteristic that is best suited to meet the specific functional requirements of this sport. Moreover, both groups of athletes are characterized by a low percentage of fat mass, particularly the elite group

Cholesterol impairment contributes to neuroserpin aggregation

Intraneural accumulation of misfolded proteins is a common feature of several neurodegenerative pathologies including Alzheimer's and Parkinson's diseases, and Familial Encephalopathy with Neuroserpin Inclusion Bodies (FENIB). FENIB is a rare disease due to a point mutation in neuroserpin which accelerates protein aggregation in the endoplasmic reticulum (ER). Here we show that cholesterol depletion induced either by prolonged exposure to statins or by inhibiting the sterol regulatory binding-element protein (SREBP) pathway also enhances aggregation of neuroserpin proteins. These findings can be explained considering a computational model of protein aggregation under non-equilibrium conditions, where a decrease in the rate of protein clearance improves aggregation. Decreasing cholesterol in cell membranes affects their biophysical properties, including their ability to form the vesicles needed for protein clearance, as we illustrate by a simple mathematical model. Taken together, these results suggest that cholesterol reduction induces neuroserpin aggregation, even in absence of specific neuroserpin mutations. The new mechanism we uncover could be relevant also for other neurodegenerative diseases associated with protein aggregation.Comment: 7 figure

Neural responses to facial and vocal expressions of fear and disgust

Neuropsychological studies report more impaired responses to facial expressions of fear than disgust in people with amygdala lesions, and vice versa in people with Huntington's disease. Experiments using functional magnetic resonance imaging (fMRI) have confirmed the role of the amygdala in the response to fearful faces and have implicated the anterior insula in the response to facial expressions of disgust. We used fMRI to extend these studies to the perception of fear and disgust from both facial and vocal expressions. Consistent with neuropsychological findings, both types of fearful stimuli activated the amygdala. Facial expressions of disgust activated the anterior insula and the caudate-putamen; vocal expressions of disgust did not significantly activate either of these regions. All four types of stimuli activated the superior temporal gyrus. Our findings therefore (i) support the differential localization of the neural substrates of fear and disgust; (ii) confirm the involvement of the amygdala in the emotion of fear, whether evoked by facial or vocal expressions; (iii) confirm the involvement of the anterior insula and the striatum in reactions to facial expressions of disgust; and (iv) suggest a possible general role for the perception of emotional expressions for the superior temporal gyrus

Research of non-specific hyperreactivity of upper airways in subjects with gastro-esophageal reflux (G.E.R.): Preliminary reports

An association between asthma and gastro-esophageal reflux (GER) is well recognized but the underlying mechanism is still unclear. The authors suggest that could exist an association between GER and upper airways hyperreactivity and this association could represents the mechanism underlying the lower esophageal sphincter releasing, that determine the reflux. In fact they suppose that, the noxious injury of acid reflux follows a course that could be: pharynx → larynx → bronchi → 1/3 inferior of the esophagus → reflux. From these presuppositions the authors carried out a study on the possible relationship between GER and non-specific hyperreactivity of upper airways on 14 subjects, divided in 2 groups: 10 subjects with functional GER, 4 subjects suffering from GER caused by hiatus hernia as control group. All patients had a thorough medical history, ENT examination with rigid and flexible endoscope, anterior Rhinomanometry (RRM), skin-test for inhalant and alimentary allergens, RAST, audiometric exam, non-specific nasal provocation test (NSNPT) with histamine, using as control the number of sneezes. From a through analysis of objective examination and from the results of the NSNPT with histamine resulted that all subjects with functional GER were rhinopathics. In all tests both in vivo (Skin-test) and in vitro (RAST) for the most common allergens (pollens-inhalant-mycophites-alimentary) the results were negative. The authors also found an involvement of paranasal sinuses that raised: 91% in the patients with recurrents phlogosis due to non specific nasal hyperreactivity; 40.9% in the allergic subjects (20% in the Graminacee +; 32% in the Parietaria O. +; 76% in the Dermatophagoides Pt. +; others 4%); 100% in the ASA-intollerance subjects. The NSNSPT with histamine showed in the group with functional GER a hyperreactivity with sneezes in 6/10 subjects, and 1/4 subjects of the group with GER with hiatus hernia. The RRM variations showed an unilateral nasal hyperreactivity in 6/10, bilateral in 3/10 subjects of the group with functional GER. In the group with GER with hiatus hernia only 1/4 subject showed reliable unilateral RRM variation. From the analysis of data resulted that subjects with functional GER showed a completely involvement of the upper airways and not only of the pharynx and larynx, caused by non specific hyperreactivity at the NSNPT with histamine, associated with a chronic pathology

N-(3-Ethoxy-phenyl)-4-pyrrolidin-1-yl-3-trifluoromethyl-benzamide (EPPTB) prevents 3-iodothyronamine (T1AM)-induced neuroprotection against kainic acid toxicity

Thyroid hormone and thyroid hormone metabolites, including 3-iodothyronamine (T1AM) and 3-iodothyroacetic acid (TA1), activate AKT signaling in hippocampal neurons affording protection from excitotoxic damage. We aim to explore whether the mechanism of T1AM neuroprotection against kainic acid (KA)-induced excitotoxicity included the activation of the trace amine associated receptor isoform 1 (TAAR1), one of T1AM targets. Rat organotypic hippocampal slices were exposed to vehicle (Veh) or to 5 μM kA for 24 h in the absence or presence of 0.1, 1 and 10 μM T1AM or to 0.1, 1 and 10 μM T1AM and 1 μM N-(3-Ethoxy-phenyl)-4-pyrrolidin-1-yl-3-trifluoromethyl-benzamide (EPPTB), the only available TAAR1 antagonist, or to 1 μM T1AM in the absence or in the presence of 10 μM LY294002, an inhibitor of phosphoinositide 3-kinases (PI3Ks). Cell death was evaluated by measuring propidium iodide (PI) levels of fluorescence 24 h after treatment. In parallel, the expression levels of p-AKT and p-PKA were evaluated by Western blot analysis of slice lysates. The activity of mitochondrial monoamine oxidases (MAO) was assayed fluorimetrically. 24 h exposure of slices to T1AM resulted in the activation of AKT and PKA. KA exposure induced cell death in the CA3 region and significantly reduced p-AKT and p-PKA levels. The presence of 1 and 10 μM T1AM significantly protected neurons from death and conserved both kinase levels with the essential role of AKT in neuroprotection. Furthermore, EPPTB prevented T1AM-induced neuroprotection, activation of PKA and AKT. Of note, in the presence of EPPTB T1AM degradation by MAO was reduced. Our results indicate that the neuroprotection offered by T1AM depends, as for TA1, on AKT activation but do not allow to conclusively indicate TAAR1 as the target implicated. Graphical abstrac

Bursts of activity in collective cell migration

Dense monolayers of living cells display intriguing relaxation dynamics, reminiscent of soft and glassy materials close to the jamming transition, and migrate collectively when space is available, as in wound healing or in cancer invasion. Here we show that collective cell migration occurs in bursts that are similar to those recorded in the propagation of cracks, fluid fronts in porous media and ferromagnetic domain walls. In analogy with these systems, the distribution of activity bursts displays scaling laws that are universal in different cell types and for cells moving on different substrates. The main features of the invasion dynamics are quantitatively captured by a model of interacting active particles moving in a disordered landscape. Our results illustrate that collective motion of living cells is analogous to the corresponding dynamics in driven, but inanimate, systems