Distributed thermal monitoring of lithium ion batteries with optical fibre sensors

Real-time temperature monitoring of li-ion batteries is widely regarded within the both the academic literature and by the industrial community as being a fundamental requirement for the reliable and safe operation of battery systems. This is particularly evident for larger format pouch cells employed in many automotive or grid storage applications. Traditional methods of temperature measurement, such as the inclusion of individual sensors mounted at discrete locations on the surface of the cell may yield incomplete information. In this study, a novel Rayleigh scattering based optical fibre sensing technology is proposed and demonstrated to deliver a distributed, real-time and accurate measure of temperature that is suitable for use with Li-ion pouch cells. The thermal behaviour of an A5-size pouch cell is experimentally investigated over a wide range of ambient temperatures and electrical load currents, during both charge and discharge. A distributed fibre optical sensor (DFOS) is used to measure both the in-plane temperature difference across the cell surface and the movement of the hottest region of the cell during operation, where temperature difference is the difference of temperature amongst different measuring points. Significantly, the DFOS results highlight that the maximum in-plane temperature difference was found to be up to 307% higher than that measured using traditional a thermocouple approach

Microparticles as regulators of cardiovascular inflammation

Microparticles are a heterogeneous group of membrane-coated vesicles that can act as signaling elements in the inflammatory processes. Once released from cells by membrane blebbing, microparticles become efficient vectors that exchange biological information between cells. Detectable in small amounts in peripheral blood of healthy individuals, elevated concentrations of microparticles originating from platelet, leukocyte, erythrocyte, and endothelial lineages are associated with a variety of pathophysiological conditions, including thrombosis, inflammation, sepsis, and metabolic disorders. This review summarizes the role of microparticles in modulating inflammation during cardiovascular diseases

Microparticles Harboring Sonic Hedgehog Morphogen Improve the Vasculogenesis Capacity of Endothelial Progenitor Cells Derived from Myocardial Infarction Patients.

Endothelial progenitor cells (EPC) play a role in endothelium integrity maintenance and regeneration. Decreased numbers of EPC or their impaired function correlates with an increase in cardiovascular events. Thus, EPC are important predictors of cardiovascular mortality and morbidity. Microparticles carrying Sonic hedgehog (Shh) morphogen (MPShhþ) trigger pro-angiogenic responses, both in endothelial cells and in ischaemic rodent models. Here, we propose that MPShhþ regulates EPC function, thus enhancing vasculogenesis, and correcting the defects in dysfunctional EPC obtained from acute myocardial infarction (AMI) patients

Switching from TDF to TAF or dual therapy (DT)-based regimens in HIV-infected individuals with viral load <=50 copies/ml: does eGFR matter?

Our aim was to evaluate the association between most recent eGFR values and the risk of switching from TDF to TAF or to dual therapy (DT) separately for the two strategies in a real-life setting. HIV-positive patients, achieving HIV-RNA≤50 copies/ml for the first time after starting a TDF-based regimen (baseline) were included. Kaplan-Meier (KM) curves and Cox regression models were used to estimate the time from TDF to switch to TAF or DT. A total of 1,486 participants were included: median (IQR) age 36y(30-42), baseline CKD-EPI eGFR 99.92 (86.47,111.4) mL/min/1.73m2. We observed a consistently higher proportion of people with a HIV-RNA≤50copies/mL who have switched from TDF to TAF rather than to DT. By competing risk analysis, the 2 years from baseline, the probability of switching was 3.5% (95% CI 2.6-4.7) to DT and 46.7% (95% CI 42.8-48.5) to TAF. A significant higher probability of switching to TAF was found for patients receiving INSTI at baseline versus NNRTIs and PI/b (KM: 65.6%, 95%CI 61.7, 69.4; vs. 4.0%, 95%CI 1.8, 6.1 and 59.9%, 95%CI 52.7, 67.2, respectively; p<.0001). A eGFR<60 ml/min/1.73m2 both as time-fixed covariate at baseline or as current value, was associated with a higher risk of switching to DT [aHR 6.68, 95%CI 2.69, 16.60 and 8.18, 95% CI 3.54, 18.90; p-value <0.001] but not to TAF-based cART [aHR= 0.94, 95%CI 0.39, 2.31, p=0.897 and 1.19, 95%CI 0.60, 2.38, p=0.617)]. In conclusion, counter to our original hypothesis, current eGFR value is used by clinician to guide switches to DT but does not seems to be a key determinant for switching to TAF. This should be taken into account when managing people on TAF-based regimens

PPARα regulates endothelial progenitor cell maturation and myeloid lineage differentiation through a NADPH oxidase-dependent mechanism in mice

Peroxisome proliferator-activated receptor-alpha (PPARα) is a key modulator of lipid metabolism. Here, we propose that PPARα regulates the maturation and function of bone marrow (BM) progenitor cells. Although PPARα deletion increased the number of BM-resident cells and the differentiation of endothelial progenitor cells (EPCs) and monocytic progenitor cells, it impaired re-endothelization of injured carotid artery that was associated with reduced circulating EPCs. Also, PPARα deletion diminished the in vivo pro-angiogenic effect of PPARα agonist without affecting EPC differentiation markers. Macrophage colony-stimulating factor (M-CSF) treatment increased the population of monocytic progenitor cells as well as secretome of BM-derived cells in PPARα wild-type but not in knock-out mice. In addition, PPARα-null mice displayed reduced lymphocytes and increased monocytes and neutrophils in the blood. Furthermore, PPARα-null mice exhibited increments in the number of total cells (as well as of phenotypically distinct subpopulations of lymph node cells) but also a significant alteration in the number of various subpopulations of splenocytes and thymocytes. Finally, PPARα negatively regulated reactive oxygen species (ROS) derived by NADPH oxidase in BM-resident progenitor cells. Taken together, our data provide evidence that PPARα is a critical regulator of recruitment, homing and maturation of BM-derived progenitor cells

High levels of trim5a are associated with xenophagy in hiv‐1‐infected long‐term nonprogressors

Autophagy is a lysosomal‐dependent degradative mechanism essential in maintaining cellular homeostasis, but it is also considered an ancient form of innate eukaryotic fighting against invading microorganisms. Mounting evidence has shown that HIV‐1 is a critical target of autoph-agy that plays a role in HIV‐1 replication and disease progression. In a special subset of HIV‐1‐infected patients that spontaneously and durably maintain extremely low viral replication, namely, long‐term nonprogressors (LTNP), the resistance to HIV‐1‐induced pathogenesis is ac-companied, in vivo, by a significant increase in the autophagic activity in peripheral blood mon-onuclear cells. Recently, a new player in the battle of autophagy against HIV‐1 has been identified, namely, tripartite motif protein 5α (TRIM5α). In vitro data demonstrated that TRIM5α directly recognizes HIV‐1 and targets it for autophagic destruction, thus protecting cells against HIV‐1 in-fection. In this paper, we analyzed the involvement of this factor in the control of HIV‐1 infection through autophagy, in vivo, in LTNP. The results obtained showed significantly higher levels of TRIM5α expression in cells from LTNP with respect to HIV‐1‐infected normal progressor patients. Interestingly, the colocalization of TRIM5α and HIV‐1 proteins in autophagic vacuoles in LTNP cells suggested the participation of TRIM5α in the autophagy containment of HIV‐1 in LTNP. Al-together, our results point to a protective role of TRIM5α in the successful control of the chronic viral infection in HIV‐1‐controllers through the autophagy mechanism. In our opinion, these findings could be relevant in fighting against HIV‐1 disease, because autophagy inducers might be employed in combination with antiretroviral drugs

Genotypic HIV-1 tropism determination might help to identify people with exhausted treatment options and advanced disease

Objectives: To evaluate HIV-1 tropism in 1382 combined antiretroviral therapy (cART)-experienced patients failing therapy to characterize those with exhausted therapeutic options. Methods: HIV-1 genotypic tropism was inferred through Geno2Pheno by estimating the false-positive-rate (FPR) values. Cumulative resistance and drug activity were evaluated by Stanford algorithm. Results: Overall, median (IQR) CD4 count (cells/mm3) nadir and at last genotypic resistance test (GRT) available were 98 (33-211) and 312 (155-517), respectively. Considering HIV-1 tropism, 30.5% had X4/dual-mixed strains (FPR ≤5%: 22.2%; FPR 5%-10%: 8.3%). By stratifying according to tropism, by decreasing FPR, a significant decrease of CD4 nadir and at last GRT was observed. The proportion of individuals with CD4 count &lt;200 cells/mm3, who were perinatally infected and with a long treatment history significantly increased as FPR levels decreased. Regarding resistance, 933 (67.5%) individuals accumulated at least one class resistance, with 52.7%, 48.2%, 23.5% and 13.2% of individuals showing resistance to NRTIs, NNRTIs, PIs and INIs; while 23.2%, 27.2%, 14.3% and 2.8% harboured resistance to 1, 2, 3 and 4 classes, respectively. Individuals with FPR ≤5% showed a significantly higher level of resistance to PIs, NRTIs and INIs compared with others. The proportion of individuals harbouring strains susceptible to ≤2 active drugs was only about 2%; nonetheless, this proportion doubled (4.6%) in patients infected with FPR ≤5%. Conclusions: Our findings showed that a small proportion of cART failing individuals have limited therapeutic options. However, tropism determination might help to identify people who have accumulated a high level of resistance and have a greater risk of advanced disease

No Efficacy of the Combination of Lopinavir/Ritonavir Plus Hydroxychloroquine Versus Standard of Care in Patients Hospitalized With COVID-19: A Non-Randomized Comparison

Objectives: No specific treatment has been approved for COVID-19. Lopinavir/ritonavir (LPV/r) and hydroxychloroquine (HCQ) have been used with poor results, and a trial showed advantages of combined antiviral therapy vs. single antivirals. The aim of the study was to assess the effectiveness of the combination of antivirals (LPV/r and HCQ) or their single use in COVID-19 hospitalized patients vs. standard of care (SoC). Methods: Patients ≥18 years with SARS-CoV-2 infection, defined as positive RT-PCR from nasal/oropharyngeal (NP/OP) swab or positive serology, admitted at L. Spallanzani Institute (Italy) were included. Primary endpoint: time to invasive ventilation/death. Secondary endpoint: time to two consecutive negative SARS-CoV-2 PCRs in NP/OP swabs. In order to control for measured confounders, a marginal Cox regression model with inverse probability weights was used. Results: A total of 590 patients were included in the analysis: 36.3% female, 64 years (IQR 51-76), and 91% with pneumonia. Cumulative probability of invasive ventilation/death at 14 days was 21.2% (95% CI 17.6, 24.7), without difference between SOC, LPV/r, hydroxychloroquine, HCQ + LPV/r, and SoC. The risk of invasive ventilation/death in the groups appeared to vary by baseline ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO2/FiO2). Overall cumulative probability of confirmed negative nasopharyngeal swabs at 14 days was 44.4% (95% CI 38.9, 49.9), without difference between groups. Conclusion: In this retrospective analysis, we found no difference in the rate of invasive ventilation/death or viral shedding by different strategies, as in randomized trials performed to date. Moreover, even the combination HCQ + LPV/r did not show advantages vs. SoC