The present study aimed to evaluate the effects of two types of 9-month adapted physical activity (APA) program, based on a muscle reinforcement training and a postural training, respectively, on ...muscle mass, muscle strength, and static balance in moderate sarcopenic older women. The diagnosis of sarcopenia was done in accordance with measurable variables and cut-off points suggested by the European Working Group on Sarcopenia in Older People (EWGSOP). Seventy-two participants were randomly assigned to two groups: the muscle reinforcement training group (RESISTANCE) (n=35; 69.9 ± 2.7 years) and the postural training group (POSTURAL) (n=37; 70.0±2.8 years). Body composition, muscle mass, skeletal muscle mass index (SMI), and handgrip strength (HGS) were evaluated for sarcopenia assessment, whereas Sway Path, Sway Area, Stay Time, and Spatial Distance were evaluated for static balance assessment. Sixty-six participants completed the study (RESISTANCE group: n=33; POSTURAL group: n=33). Significant increases of muscle mass, SMI, and handgrip strength values were found in the RESISTANCE group, after muscle reinforcement program. No significant differences appeared in the POSTURAL group, after postural training. Furthermore, RESISTANCE group showed significant improvements in static balance parameters, whereas no significant differences appeared in the POSTURAL group. On the whole, the results of this study suggest that the APA program based on muscle reinforcement applied on moderate sarcopenic older women was able to significantly improve muscle mass and muscle strength, and it was also more effective than the applied postural protocol in determining positive effects on static balance.
Abstract Phosphocreatine–Mg-complex acetate (PCr-Mg-CPLX) is a creatine-derived compound that in previous in vitro research was able to increase neuronal creatine independently of the creatine ...transporter, thus providing hope to cure the hereditary syndrome of creatine transporter deficiency. In previous research we showed that it reproduces in vitro the known neuroprotective effect of creatine against anoxic damage. In the present paper we investigated if PCr-Mg-CPLX reproduces this neuroprotective effect in vivo, too. We used a mouse model of transient middle cerebral artery occlusion. Mice received PCr-Mg-CPLX or a mixture of the two separate compounds phosphocreatine (PCr) and MgSO4 , or vehicle. The injections were done 60 min and 30 min before ischemia. Forty-eight hours after ischemia neurological damage was evaluated with Clark's behavioural tests, then the infarct volume was measured. PCr-Mg-CPLX reduced the infarct volume by 48%, an effect that was not duplicated by the separate administration of PCr and MgSO4 and the neurological damage was decreased in a statistically significant way. We conclude that PCr-Mg-CPLX affords in vivo neuroprotection when administered before ischemia. These results are comparable to previous research on creatine administration in experimental stroke. PCr-Mg-CPLX maintains creatine-like neuroprotective effects in vivo as well as in vitro. Our study suggests that PCr-Mg-CPLX might have a therapeutic role in the treatment of hereditary creatine transporter deficiency and of conditions where there is a high risk of impending stroke or cerebral ischemic damage, like high-risk transient ischemic attacks, open heart surgery, and carotid surgery.
Hereditary creatine transporter deficiency causes brain damage, despite the brain having the enzymes to synthesize creatine. Such damage occurring despite an endogenous synthesis is not easily ...explained. This condition is incurable, because creatine may not be delivered to the brain without its transporter. Creatine-derived compounds that crossed the blood–brain barrier in a transporter-independent fashion would be useful in the therapy of hereditary creatine transporter deficiency, and possibly also in neuroprotection against brain anoxia or ischemia. We tested the double hypothesis that: (1) the creatine carrier is needed to make creatine cross the plasma membrane of brain cells and (2) creatine-derived molecules may cross this plasma membrane independently of the creatine carrier. In
in vitro mouse hippocampal slices, incubation with creatine increased creatine and phosphocreatine content of the tissue. Inhibition of the creatine transporter with 3-guanidinopropionic acid (GPA) dose-dependently prevented this increase. Incubation with creatine benzyl ester (CrOBzl) or phosphocreatine–Mg-complex acetate (PCr-Mg-CPLX) increased tissue creatine content, not phosphocreatine. This increase was not prevented by GPA. Thus, the creatine transporter is required for creatine uptake through the plasma membrane. Since there is a strong indication that creatine in the brain is mainly synthesized by glial cells and transferred to neurons, this might explain why hereditary transporter deficiency is attended by severe brain damage despite the possibility of an endogenous synthesis. CrOBzl and PCr-Mg-CPLX cross the plasma membrane in a transporter-independent way, and might be useful in the therapy of hereditary creatine transporter deficiency. They may also prove useful in the therapy of brain anoxia or ischemia.
The rate of neutrino-electron elastic scattering interactions from 862 keV Be7 solar neutrinos in Borexino is determined to be 46.0±1.5(stat)-1.6+1.5(syst)counts/(day*100ton). This corresponds to a ...νe-equivalent Be7 solar neutrino flux of (3.10±0.15)×109cm-2s-1 and, under the assumption of νe transition to other active neutrino flavours, yields an electron neutrino survival probability of 0.51±0.07 at 862 keV. The no flavor change hypothesis is ruled out at 5.0σ. A global solar neutrino analysis with free fluxes determines Φpp=6.06-0.06+0.02×1010cm-2s-1 and ΦCNO<1.3×109cm-2s-1 (95% C.L.). These results significantly improve the precision with which the Mikheyev-Smirnov-Wolfenstein large mixing angle neutrino oscillation model is experimentally tested at low energy.
Although a large body of evidence shows that pretreatment of brain tissue with creatine protects against anoxic injury in vitro, only a couple of papers have investigated creatine protection in vivo, ...and they yielded conflicting results. We attempted to clarify how creatine may be protective in an in vivo model of global cerebral ischemia (GCI). We administered creatine either before of after GCI. We decided to administer it by intracerebroventricular infusion, to maximize its bioavailability to the brain. Our findings show that creatine is clearly protective in vivo when administered before ischemia. In that case, histological evaluation of damage was consistently improved in all regions examined, and neurological score was better in creatine-treated rats than in controls. When administered after ischemia, histology was improved in the hippocampus, while only a not significant trend toward improvement was observed in the cerebral cortex and in the caudo-putamen. Neurological score was not improved by creatine administration after GCI. Our findings show that creatine administration is protective in vivo. Such protection was clear in the case of pretreatment, and was present, to a lesser degree, when treatment was started after ischemia. Our results should encourage further research in the possible role of creatine therapy in neuroprotection.
AstrO: A portable cosmic ray telescope Grazzi, S.; Assandri, L.; Battaglieri, M. ...
Nuclear instruments & methods in physics research. Section A, Accelerators, spectrometers, detectors and associated equipment,
10/2020, Letnik:
976, Številka:
C
Journal Article
Recenzirano
Odprti dostop
This paper describes the design and performances of the AstrO (Astroparticle Outreach) cosmic muon telescope. The detector, contained in a trolley, is transportable and simple enough to be used by ...high-school students. The sophisticated data acquisition system is based on advanced DAQ technology and thanks to a simple interface is suitable for non-expert users. The detector is capable of measuring an integrated cosmic muon rate of 1–2 Hz with a precision (statistical and systematic) of a few percent in few hours of data taking. It can be used to detect variations induced by the solar activity, to determine the rate dependence on the geographical location (altitude and latitude) and to measure the cosmic muon rate attenuation due to surrounding high-density shielding such as rocks or concrete walls.
Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine ...increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.
Some derivatives more lipophylic than creatine, thus theoretically being capable to better cross the blood-brain barrier, were studied for their neuroprotective effect in mouse hippocampal slices. In ...mouse hippocampal slices we found that EM2 I is ineffective, EM"" weakly increased the latency to population spike disapperance during anoxia. Creatine, Creatine-MG-complex (acetate) and Phosphocreatine-Mg-complex (acetate) increased more effectively the latency to population spike disappearance during anoxia. Moreover, Phosphocreatine-Mg-complex (acetate) significantly reduced neuronal hyperexcitability during anoxia, an effect that no other compound (including creatine itself) showed. Summing up, EM2 I is not useful for brain protection, while EM22 and cgelates of both creatine and phosphocreatine di replicate some of the knownn protective effects of creatine. In addition, Phosphocreatine-Mg-complex (acetate) also reduced neuronal hyperexcitability during anoxia.
PDF
