Valutazione degli aggiustamenti cardiocircolatori nel motociclismo classe enduro

Hemodynamic parameters, such as Cardiac Output (CO) and Stroke Volume (SV), have never been studied in motorcycle racing. Probably because the measurement of these variables is hampered by difficulties related to the particular environment of motorcycle performance, which can be considered an extreme condition. Moreover, these parameters need the availability of a non-­‐‑invasive and reliable portable cardiovascular measurement systems. Indeed, the only data available are about Heart Rate (HR), which increases to about 90-­‐‑95% of maximum, despite the supposed low energy requirements of motorcycle riding. The aim of this study was to measure hemodynamics enduro -­‐‑ motorcycling pilots during real motorcycle race by means of portable impedance cardiograph. Fifteen male elite motorcycle riders performing regional and national competitions on enduro motorcycles were studied. Hemodynamics was assessed by means of a portable impedance cardiograph (New Core, 2C Technologies Inc., Cagliari, Italy). Data were collected at rest, throughout 10 minutes of motorcycle race at maximum speed possible and during passive recovery. Also the blood lactate was measured at rest and after motorcycle race. The comparison between rest and exercise showed a significant increase in hemodynamic parameters. In detail, increments in both HR and SV were observed, thereby leading to a CO elevation. Systemic Vascular Resistance (SVR) showed a significant reduction, while there was an increase in systolic (SV/VET) and diastolic (SV/DT) flow index. Blood lactate significantly increase after exercise. All parameters at recovery returned to rest levels, with the exception of HR and SV/VET. Data obtained show that enduro motorcycle riding leads to significant increments in both HR and SV. While the former fact was already known, the latter is a new finding of the present investigation. The significant CO response can be the consequence of a substantial increase in cardiac contractility which can be ascribed to a sympathetic activation, as testified by the contemporary increase in HR. It is possible to speculate that the heavy muscular work of the upper and lower limbs activates the exercise pressor reflex, thereby causing sympathetic activation

Valutazione degli aggiustamenti cardiocircolatori nel motociclismo classe enduro

Hemodynamic parameters, such as Cardiac Output (CO) and Stroke Volume (SV), have never been studied in motorcycle racing. Probably because the measurement of these variables is hampered by difficulties related to the particular environment of motorcycle performance, which can be considered an extreme condition. Moreover, these parameters need the availability of a non-­‐‑invasive and reliable portable cardiovascular measurement systems. Indeed, the only data available are about Heart Rate (HR), which increases to about 90-­‐‑95% of maximum, despite the supposed low energy requirements of motorcycle riding. The aim of this study was to measure hemodynamics enduro -­‐‑ motorcycling pilots during real motorcycle race by means of portable impedance cardiograph. Fifteen male elite motorcycle riders performing regional and national competitions on enduro motorcycles were studied. Hemodynamics was assessed by means of a portable impedance cardiograph (New Core, 2C Technologies Inc., Cagliari, Italy). Data were collected at rest, throughout 10 minutes of motorcycle race at maximum speed possible and during passive recovery. Also the blood lactate was measured at rest and after motorcycle race. The comparison between rest and exercise showed a significant increase in hemodynamic parameters. In detail, increments in both HR and SV were observed, thereby leading to a CO elevation. Systemic Vascular Resistance (SVR) showed a significant reduction, while there was an increase in systolic (SV/VET) and diastolic (SV/DT) flow index. Blood lactate significantly increase after exercise. All parameters at recovery returned to rest levels, with the exception of HR and SV/VET. Data obtained show that enduro motorcycle riding leads to significant increments in both HR and SV. While the former fact was already known, the latter is a new finding of the present investigation. The significant CO response can be the consequence of a substantial increase in cardiac contractility which can be ascribed to a sympathetic activation, as testified by the contemporary increase in HR. It is possible to speculate that the heavy muscular work of the upper and lower limbs activates the exercise pressor reflex, thereby causing sympathetic activation

Improvement in Hemodynamic Responses to Metaboreflex Activation after One Year of Training in Spinal Cord Injured Humans

Spinal cord injured (SCI) individuals show an altered hemodynamic response to metaboreflex activation due to a reduced capacity to vasoconstrict the venous and arterial vessels below the level of the lesion. Exercise training was found to enhance circulating catecholamines and to improve cardiac preload and venous tone in response to exercise in SCI subjects. Therefore, training would result in enhanced diastolic function and capacity to vasoconstrict circulation. The aim of this study was to test the hypothesis that one year of training improves hemodynamic response to metaboreflex activation in these subjects. Nine SCI individuals were enrolled and underwent a metaboreflex activation test at the beginning of the study (T0) and after one year of training (T1). Hemodynamics were assessed by impedance cardiography and echocardiography at both T0 and T1. Results show that there was an increment in cardiac output response due to metaboreflex activity at T1 as compared to T0 (545.4 ± 683.9 mL · min(-1) versus 220.5 ± 745.4 mL · min(-1), P < 0.05). Moreover, ventricular filling rate response was higher at T1 than at T0. Similarly, end-diastolic volume response was increased after training. We concluded that a period of training can successfully improve hemodynamic response to muscle metaboreflex activation in SCI subjects

Diving response after a one-week diet and overnight fasting

Background: We hypothesized that overnight fasting after a short dietary period, especially with carbohydrates, could allow performing breath-hold diving with no restraint for diaphragm excursion and blood shift and without any increase of metabolism, and in turn improve the diving response. Methods: During two separate sessions, 8 divers carried out two trials: (A) a 30-m depth dive, three hours after a normal breakfast and (B) a dive to the same depth, but after following a diet and fasting overnight. Each test consisted of 3 apnea phases: descent, static and ascent whose durations were measured by a standard chronometer. An impedance cardiograph, housed in an underwater torch, provided data on trans-thoracic fluid index (TFI), stroke volume (SV), heart rate (HR) and cardiac output (CO). Mean blood pressure (MBP), arterial O-2 saturation (SaO(2)), blood glucose (Glu) and blood lactate (BLa) were also collected. Results: In condition B, duration of the static phase of the dive was longer than A (37.8 +/- 7.4 vs. 27.3 +/- 8.4 s respectively, P < 0.05). In static phases, mean Delta SV value (difference between basal and nadir values) during fasting was lower than breakfast one (-2.6 +/- 5.1 vs. 5.7 +/- 7.6 ml, P < 0.05). As a consequence, since mean. HR values were equally decreased in both metabolic conditions, mean. CO value during static after fasting was lower than the same phase after breakfast (-0.4 +/- 0.5 vs. 0.4 +/- 0.5 L . min(-1) respectively, P < 0.05). At emersion, despite the greater duration of dives during fasting, SaO(2) was higher than A (92.0 +/- 2.7 vs. 89.4 +/- 2.9 % respectively, P < 0.05) and BLa was lower in the same comparison (4.2 +/- 0.7 vs. 5.3 +/- 1.1 mmol L-1, P < 0.05). Conclusions: An adequate balance between metabolic and splancnic status may improve the diving response during a dive at a depth of 30 m, in safe conditions for the athlete's healt

Profiles of VGF peptides in the rat brain and their modulations after Phencyclidine treatment

From the VGF precursor protein originate several low molecular weight peptides, whose distribution in the brain and blood circulation is not entirely known. Among the VGF peptides, those containing the N-terminus portion were altered in the cerebro-spinal fluid (CSF) and hypothalamus of schizophrenia patients. "Hence, we aimed to better investigate the involvement of the VGF peptides in schizophrenia by studying their localization in the brain regions relevant for the disease, and revealing their possible modulations in response to certain neuronal alterations occurring in schizophrenia". We produced antibodies against different VGF peptides encompassing the N-terminus, but also C-terminus-, TLQP-, GGGE- peptide sequences, and the so named NERP-3 and -4. These antibodies were used to carry out specific ELISA and immunolocalization studies while mass spectrometry (MS) analysis was also performed to recognize the intact brain VGF fragments. We used a schizophrenia rat model, in which alterations in the prepulse inhibition (PPI) of the acoustic startle response occurred after PCP treatment. In normal rats, all the VGF peptides studied were distributed in the brain areas examined including hypothalamus, prefrontal cortex, hippocampus, accumbens and amygdaloid nuclei and also in the plasma. By liquid chromatography-high resolution mass, we identified different intact VGF peptide fragments, including those encompassing the N-terminus and the NERPs. PCP treatment caused behavioral changes that closely mimic schizophrenia, estimated by us as a disruption of PPI of the acoustic startle response. The PCP treatment also induced selective changes in the VGF peptide levels within certain brain areas. Indeed, an increase in VGF C-terminus and TLQP peptides was revealed in the prefrontal cortex (p &lt; 0.01) where they were localized within parvoalbumin and tyrosine hydroxylase (TH) containing neurons, respectively. Conversely, in the nucleus accumbens, PCP treatment produced a down-regulation in the levels of VGF C-terminus-, N-terminus- and GGGE- peptides (p &lt; 0.01), expressed in GABAergic- (C-terminus/GGGE) and somatostatin- (N-terminus) neurons. These results confirm that VGF peptides are widely distributed in the brain and modulated in specific areas involved in schizophreni

A cascade of 24 histatins (histatin 3 fragments) in human saliva. Suggestions for a pre-secretory sequential cleavage pathway

The systematic search by tandem mass spectrometry of human saliva from four different subjects, of 136 possible fragments originated from histatin 3, allowed the detection of 24 different peptides. They include, with the exception of histatin 4, all the known histatin 3 fragments, namely histatins 5-12 and the peptides corresponding to 15-24, 26-32, 29-32 residues, and 13 new fragments corresponding to 1-11, 1-12, 1-13, 5-13, 6-11, 6-13, 7-11, 7-12, 7-13, 14-24, 14-25, 15-25, and 28-32 residues of histatin 3. On the contrary, none of 119 possible fragments of histatin 1, including histatin 2, was detected. The results suggest that the genesis of histatin 3-related peptides, being under the principal action of trypsin-like activities, is probably not a random process but rather follows a sequential fragmentation pathway. Lack of detection of C-terminal fragments, with the exception of 26-32, 28-32, and 29-32 fragments, suggested that arginine 25 should be the first cleavage site, generating histatin 6 and 26-32 fragments. The genesis of 28-32 and 29-32 fragments and histatin 5 should implicate a subsequent exo-protease action. Similarly, lack of detection of fragments having Lys-5 and Arg-6 at the N terminus and Arg-25 at the C terminus strongly suggested that sequences KRKF (11-14 residues) and AKR (4-6 residues) should be the second and the third cleavage sites, respectively. Lys-17 and Arg-22 are not cleaved at all

Sex-Specific Parental Effects on Offspring Lipid Levels

Background: Plasma lipid levels are highly heritable traits, but known genetic loci can only explain a small portion of their heritability. Methods and Results: In this study, we analyzed the role of parental levels of total cholesterol (TC), low‐density lipoprotein cholesterol (LDL‐C), high‐density lipoprotein cholesterol (HDL‐C), and triglycerides (TGs) in explaining the values of the corresponding traits in adult offspring. We also evaluated the contribution of nongenetic factors that influence lipid traits (age, body mass index, smoking, medications, and menopause) alone and in combination with variability at the genetic loci known to associate with TC, LDL‐C, HDL‐C, and TG levels. We performed comparisons among different sex‐specific regression models in 416 families from the Framingham Heart Study and 304 from the SardiNIA cohort. Models including parental lipid levels explain significantly more of the trait variation than models without these measures, explaining up to ≈39% of the total trait variation. Of this variation, the parent‐of‐origin effect explains as much as ≈15% and it does so in a sex‐specific way. This observation is not owing to shared environment, given that spouse‐pair correlations were negligible (\u3c1.5% explained variation in all cases) and is distinct from previous genetic and acquired factors that are known to influence serum lipid levels. Conclusions: These findings support the concept that unknown genetic and epigenetic contributors are responsible for most of the heritable component of the plasma lipid phenotype, and that, at present, the clinical utility of knowing age‐matched parental lipid levels in assessing risk of dyslipidemia supersedes individual locus effects. Our results support the clinical utility of knowing parental lipid levels in assessing future risk of dyslipidemia

Synthesis, cytotoxicity and antiviral evaluation of new series of imidazo[4,5-g]quinoline and pyrido[2,3-g]quinoxalinone derivatives

Linear aromatic N-tricyclic compounds with promising antiviral activity and minimal cytotoxicity were prepared and analyzed in the last years. Specifically, the pyrido[2,3-g]quinoxalinone nucleus was found endowed with high potency against several pathogenic RNA viruses as etiological agents of important veterinary and human pathologies. Following our research program on new antiviral agents we have designed, synthesized and assayed new series of imidazo[4,5-g]quinoline and pyrido[2,3-g]quinoxalinone derivatives. Lead compounds 1-4 were further modified to enhance their antiviral activity and reduce their cytotoxicity. Thus, different substituents were introduced on N atom at position 1 or the O atom at position 2 of the leads; contextually, several groups were inserted on the nitrogen atom at position 7 of diaminoquinoline intermediates. Title compounds were tested in cell-based assays for cytotoxicity and antiviral activity against RNA virus families containing single-stranded (either positive-sense (ssRNA+) or negative-sense (ssRNA-)), and double-stranded genomes (dsRNA), and against two representatives of DNA virus families. Some derivatives emerged as potential leads for further development as antiviral agents against some viruses of public health significance, such as RSV, Reo, BVDV and HCV. Particularly, compounds 4, 11b, 11c, 13c, 15a, 18 and 21 resulted active against BVDV at concentrations ranging from 1.3 to 5\ua0\u3bcM. Compound 21 was also evaluated for its activity on the BVDV RdRp. Compound 4 was also tested as potential anti-HCV compound in a subgenomic replication assay. Molecular simulation results provided a molecular rationale for the anti-BVDV activity of these compounds

Evidence of Innovative Assessment : Literature Review and Case Studies

Non peer reviewe