540 research outputs found
IMU-based classification of resistive exercises for real-time training monitoring on board the international space station with potential telemedicine spin-off
The microgravity exposure that astronauts undergo during space missions lasting up to 6 months induces biochemical and physiological changes potentially impacting on their health. As a countermeasure, astronauts perform an in-flight training program consisting in different resistive exercises. To train optimally and safely, astronauts need guidance by on-ground specialists via a real-time audio/video system that, however, is subject to a communication delay that increases in proportion to the distance between sender and receiver. The aim of this work was to develop and validate a wearable IMU-based biofeedback system to monitor astronauts in-flight training displaying real-time feedback on exercises execution. Such a system has potential spin-offs also on personalized home/remote training for fitness and rehabilitation. 29 subjects were recruited according to their physical shape and performance criteria to collect kinematics data under ethical committee approval. Tests were conducted to (i) compare the signals acquired with our system to those obtained with the current state-of-the-art inertial sensors and (ii) to assess the exercises classification performance. The magnitude square coherence between the signals collected with the two different systems shows good agreement between the data. Multiple classification algorithms were tested and the best accuracy was obtained using a MultiLayer Perceptron (MLP). MLP was also able to identify mixed errors during the exercise execution, a scenario that is quite common during training. The resulting system represents a novel low-cost training monitor tool that has space application, but also potential use on Earth for individuals working-out at home or remotely thanks to its ease of use and portability
Control of the urban pigeon Columba livia population and the preservation of common swift Apus apus and bats Chiroptera during the restoration of the Ghirlandina tower in the city of Modena (Italy)
Ferri, M., Ferraresi, M., Gelati, A., Zannetti, G., Domenichini, A., Ravizza, L., Cadignani, R
Evidence for weathering and volcanism during the PETM from Arctic Ocean and Peri-Tethys osmium isotope records
Sudden global warming during the Paleocene–Eocene Thermal Maximum (PETM, 55.9 Ma) occurred because of the rapid release of several thousand gigatonnes of isotopically light carbon into the oceans and atmosphere; however, the cause of this release is not well understood. Some studies have linked carbon injection to volcanic activity associated with the North Atlantic Igneous Province (NAIP), while others have emphasised carbon cycle feedbacks associated with orbital forcing. This study presents the osmium isotope compositions of mudrocks that were deposited during the PETM at four locations (one from the Arctic Ocean, and three from the Peri-Tethys). The Os-isotope records all exhibit a shift of similar magnitude towards relatively radiogenic values across the PETM. This observation confirms that there was a transient, global increase in the flux of radiogenic Os from the weathering of continental rocks in response to elevated temperatures at that time. The tectonic effects of NAIP volcanic emplacement near the onset of the PETM is recorded by anomalously radiogenic Os-isotope compositions of PETM-age Arctic Ocean samples, which indicate an interval of hydrographic restriction that can be linked tectonic uplift due to hotspot volcanism in the North Atlantic seaway. The Peri-Tethys data also document a transient, higher flux of unradiogenic osmium into the ocean near the beginning of the PETM, most likely from the weathering of young mafic rocks associated with the NAIP. These observations support the hypothesis that volcanism played a major role in triggering the cascade of environmental changes during the PETM, and highlight the influence of paleogeography on the Os isotope characteristics of marine water masses
Role of the p53/p21 system in the response of human colon carcinoma cells to Doxorubicin
BACKGROUND: Colon adenocarcinomas are refractory to a number of widely used anticancer agents. Multifactorial mechanisms have been implicated in this intrinsically resistant phenotype, including deregulation of cell death pathways. In this regard, the p53 protein has a well established role in the control of tumor cell response to DNA damaging agents; however, the relationship between p53-driven genes and drug sensitivity remains controversial. The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels. METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells. We then assessed the effects of DOX in two isogenic cell lines derived from HCT116 by abrogating the expression and/or function of p53 and p21 (HCT116-E6 and HCT116 p21-/-, respectively). Finally, we evaluated the effect of pre-treatment with the piperidine nitroxide Tempol (TPL), an agent that was reported to induce p21 expression irrespective of p53 status, on the cytotoxicity of DOX in the four cell lines. Comparisons of IC50 values and apoptotic cell percentages were performed by ANOVA and Bonferroni's test for independent samples. C.I. calculations were performed by the combination Index method. RESULTS: Our results indicate that, in the colon carcinoma cell lines tested, sensitivity to DOX is associated with p21 upregulation upon drug exposure, and DOX cytotoxicity is potentiated by pre-treatment with TPL, but only in those cell lines in which p21 can be upregulated. CONCLUSIONS: p21 induction may significantly contribute to the response of colon adenocarcinomas cells to DOX treatment; and small molecules that can exploit p53-independent pathways for p21 induction, such as TPL, may find a place in chemotherapeutic protocols for the clinical management of colorectal cancer, where p53 function is often lost, due to genetic or epigenetic defects or to post-transcriptional inactivating mechanisms
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Downstream Intensification Effects Associated with CO2 Laser Mitigation of Fused Silica
Mitigation of 351nm laser-induced damage sites on fused silica exit surfaces by selective CO{sub 2} treatment has been shown to effectively arrest the exponential growth responsible for limiting the lifetime of optics in high-fluence laser systems. However, the perturbation to the optical surface profile following the mitigation process introduces phase contrast to the beam, causing some amount of downstream intensification with the potential to damage downstream optics. Control of the laser treatment process and measurement of the associated phase modulation is essential to preventing downstream 'fratricide' in damage-mitigated optical systems. In this work we present measurements of the surface morphology, intensification patterns and damage associated with various CO{sub 2} mitigation treatments on fused silica surfaces. Specifically, two components of intensification pattern, one on-axis and another off-axis can lead to damage of downstream optics and are related to rims around the ablation pit left from the mitigation process. It is shown that control of the rim structure around the edge of typical mitigation sites is crucial in preventing damage to downstream optics
Toll-like receptor 4 and high-mobility group box-1 are involved in ictogenesis and can be targeted to reduce seizures
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Pregnancy Loss in Women with HIV is not Associated with HIV Markers: Data from a National Study in Italy, 2001-2018.
BACKGROUND:
There is limited information on pregnancy loss in women with HIV, and it is still debated whether HIV-related markers may play a role.Objectives: To explore potential risk factors for pregnancy loss in women with HIV, with particular reference to modifiable risk factors and markers of HIV disease.
METHODS:
Multicenter observational study of HIV-positive pregnant women. The main outcome measure was pregnancy loss, including both miscarriage (<22 weeks) and stillbirth ( 6522 weeks). Possible associations of pregnancy loss were evaluated in univariate and multivariate analyses.
RESULTS:
Among 2696 eligible pregnancies reported between 2001 and 2018, 226 (8.4%) ended in pregnancy loss (miscarriage 198, 7.3%; stillbirth 28, 1.0%). In multivariate analyses, only older age (adjusted odds ratio [AOR] per additional year of age: 1.079, 95% confidence interval [CI] 1.046-1.113), HIV diagnosis before pregnancy (AOR: 2.533, 95%CI 1.407-4.561) and history of pregnancy loss (AOR: 1.625, 95%CI 1.178-2.243) were significantly associated with pregnancy loss. No significant association with pregnancy loss was found for parity, coinfections, sexually transmitted diseases, hypertension, smoking, alcohol and substance use, CD4 cell count, HIV-RNA viral load, and CDC HIV stage.
CONCLUSIONS:
Older women and those with a previous history of pregnancy loss should be considered at higher risk of pregnancy loss. The severity of HIV disease and potentially modifiable risk factors did not increase the risk of pregnancy loss
Molecular isoforms of high-mobility group box 1 are mechanistic biomarkers for epilepsy
Approximately 30% of epilepsy patients do not respond to antiepileptic drugs, representing an unmet medical need. There is evidence that neuroinflammation plays a pathogenic role in drug-resistant epilepsy. The high-mobility group box 1 (HMGB1)/TLR4 axis is a key initiator of neuroinflammation following epileptogenic injuries, and its activation contributes to seizure generation in animal models. However, further work is required to understand the role of HMGB1 and its isoforms in epileptogenesis and drug resistance. Using a combination of animal models and sera from clinically well-characterized patients, we have demonstrated that there are dynamic changes in HMGB1 isoforms in the brain and blood of animals undergoing epileptogenesis. The pathologic disulfide HMGB1 isoform progressively increased in blood before epilepsy onset and prospectively identified animals that developed the disease. Consistent with animal data, we observed early expression of disulfide HMGB1 in patients with newly diagnosed epilepsy, and its persistence was associated with subsequent seizures. In contrast with patients with well-controlled epilepsy, patients with chronic, drug-refractory epilepsy persistently expressed the acetylated, disulfide HMGB1 isoforms. Moreover, treatment of animals with antiinflammatory drugs during epileptogenesis prevented both disease progression and blood increase in HMGB1 isoforms. Our data suggest that HMGB1 isoforms are mechanistic biomarkers for epileptogenesis and drug-resistant epilepsy in humans, necessitating evaluation in larger-scale prospective studies
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