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With the growing adoption of battery energy storage systems in renewable energy sources, electric vehicles (EVs), and portable electronic devices, the effective management of battery systems has become increasingly critical. The advent of wireless battery management systems (wBMSs) represents a significant innovation in battery management technology. Traditional wired battery management systems (BMSs) face challenges, including complexity, increased weight, maintenance difficulties, and a higher chance of connection failure. In contrast, wBMSs offer a robust solution, eliminating physical connections. wBMSs offer enhanced flexibility, reduced packaging complexity, and improved reliability. Given that wBMSs are still in a preliminary stage, this review paper explores their evolution, current state, and future directions. A comprehensive survey of state-of-the-art wBMS technologies, including academic and commercial solutions, is elaborated in this paper. We compare wireless communication technologies like Bluetooth Low Energy (BLE), Zigbee, Near-Field Communication (NFC), Wi-Fi, and cellular networks in the context of wBMSs. We discuss their performance in terms of efficiency, reliability, scalability, and security. Despite its promising outlook, wBMSs still face challenges such as data security, signal interference, regulatory and standardization issues, and competition from the continued advancement of wired BMS technologies, making the advantages of wBMSs less evident. This paper concludes with guidelines for future research and development of wBMSs, aiming to address these challenges and pave the way for a broad adoption of wBMSs across various applications. This paper aims to inspire further research and innovation in the field, contributing to developing an industry-ready wBMS.

One strategy to address the variable effectiveness of many influenza vaccines is to induce antiviral resident memory T cells, which can mediate cross-protection against multiple substrains (heterosubtypic immunity). Unfortunately, such vaccines typically use attenuated active viruses, which may be unsafe for certain populations. Wang et al. report a vaccine using an inactivated virus that effectively induced heterosubtypic immunity in both mice and ferrets (see the Perspective by Herold and Sander). They coadministered the virus with 2′,3′-cyclic guanosine monophosphate–adenosine monophosphate (cGAMP), a potent activator of the innate immune system, encapsulated in pulmonary surfactant–biomimetic liposomes. This adjuvant was taken up by alveolar epithelial cells, whose activation resulted in effective antiviral T cell and humoral immune responses without accompanying immunopathology. Science , this issue p. eaau0810 ; see also p. 852 Biomimetic liposomes containing an innate immune adjuvant promote effective immunity using an inactivated influenza vaccine. Current influenza vaccines only confer protection against homologous viruses. We synthesized pulmonary surfactant (PS)–biomimetic liposomes encapsulating 2′,3′-cyclic guanosine monophosphate–adenosine monophosphate (cGAMP), an agonist of the interferon gene inducer STING (stimulator of interferon genes). The adjuvant (PS-GAMP) vigorously augmented influenza vaccine–induced humoral and CD8 + T cell immune responses in mice by simulating the early phase of viral infection without concomitant excess inflammation. Two days after intranasal immunization with PS-GAMP–adjuvanted H1N1 vaccine, strong cross-protection was elicited against distant H1N1 and heterosubtypic H3N2, H5N1, and H7N9 viruses for at least 6 months while maintaining lung-resident memory CD8 + T cells. Adjuvanticity was then validated in ferrets. When alveolar epithelial cells (AECs) lacked Sting or gap junctions were blocked, PS-GAMP–mediated adjuvanticity was substantially abrogated in vivo. Thus, AECs play a pivotal role in configuring heterosubtypic immunity.

Inflammation is likely a key contributor to the pathogenesis of Parkinson’s disease (PD), a progressively debilitating neurodegenerative disease that is accompanied by a pathological accumulation of the α-synuclein protein in a staged manner through the brain. What leads to the accumulation of α-synuclein in PD and how this relates to inflammatory pathways, however, is not entirely clear. Toll-like receptor (TLR) signaling is a major pathway mediating inflammation and, in particular, TLR2 is increasingly being implicated in PD. We have, therefore, examined the expression of TLR2 in postmortem brain tissue from PD patients and matched controls. We confirm that TLR2 is increased in PD brain, and find that levels of TLR2 correlate with the accumulation of pathological α-synuclein. TLR2 was expressed on neurons as well as microglia; however, the neuronal rather than glial expression of TLR2 was significantly increased in PD brain in accordance with disease staging, and TLR2 was strongly localized to α-synuclein positive Lewy bodies. In cell culture, activation of neuronal TLR2 induced an inflammatory response, including the secretion of inflammatory cytokines and microglial-activating chemokines, as well as the production of reactive oxygen species. Moreover, activation of neuronal TLR2 increased levels of endogenous α-synuclein protein, which was in turn associated with increased levels of the autophagy/lysosomal pathway marker p62. Finally, promoting autophagy with rapamycin or pharmacological inhibition of the TLR2 signaling pathway prevented the TLR2-mediated increase in α-synuclein in neuronal cell cultures. These results implicate neuronal TLR2 expression in human PD pathogenesis. In particular, the increased expression of TLR2 on neurons may provide new insight into disease pathogenesis and/or options for therapeutic intervention.

Rare, yet biologically critical, lipids that contain very long chain fatty acids (VLCFA-lipids) are synthesized in the brain by the enzyme ELOVL4. High levels of VLCFA-lipids are toxic to cells and excess VLCFA-lipids are actively removed by ABCD1 in an ATP-dependent manner. Virtually nothing is known about the impact of VLCFA-lipids in neurodegenerative diseases. Here, we investigated the possible role of VLCFA-lipids in frontotemporal dementia (FTD), which is a leading cause of younger-onset dementia. Using quantitative discovery lipidomics, we identified three VLCFA-lipid species that were significantly increased in FTD brain compared to controls, with strong correlations with ELOVL4. Increases in ELOVL4 expression correlated with significant decreases in the membrane-bound synaptophysin in FTD brain. Furthermore, increases in ABCD1 expression correlated with increases in VLCFA-lipids. We uncovered a new pathomechanism that is pertinent to understanding the pathogenesis of FTD.

The environmental effects of nanoparticles have attracted widespread attention. The removal and recycling of nanoparticles are crucial for both environmental protection and resource reuse. However, current removal and recycling methods are not yet mature, and there is a need to explore inexpensive materials for the efficient removal and recycling of nanoparticles. This study investigates the effects of pyrite species, thermal modification temperature, pH and ionic strength on the adsorption of gold nanoparticles (AuNPs) by pyrite. The experimental results demonstrate that the adsorption rate of artificially thermally modified pyrite is slightly faster than that of naturally thermally modified pyrite. However, the concentration of Fe ions dissolved from the artificially thermally modified pyrite is higher. Natural pyrite, when thermally modified at 400°C and 500°C, adsorbs 100% of AuNPs within 10 min. The lower the acidity of the system, the faster the adsorption rate. Conversely, an increase in ionic strength decreases the adsorption rate. Artificially thermally modified pyrite primarily adsorbs AuNPs through electrostatic gravitational attraction, which is supplemented by a significant amount of chemisorption. After four recycling cycles, the adsorption and desorption rates of AuNPs using artificially thermally modified pyrite were 92.1% and 94.2%, respectively, indicating excellent adsorption and recovery performance. The results of this study provide a new method for the recycling of nanoparticles and an experimental basis for the further application of thermally modified pyrite in environmental treatments.

Parkinson’s disease (PD) is a movement disorder characterized by the early loss of nigrostriatal dopaminergic pathways producing significant network changes impacting motor coordination. Recently three motor stages of PD have been proposed (a silent period when nigrostriatal loss begins, a prodromal motor period with subtle focal manifestations, and clinical PD) with evidence that motor cortex abnormalities occur to produce clinical PD[8]. We directly assess structural changes in the primary motor cortex and corticospinal tract using parallel analyses of longitudinal clinical and cross-sectional pathological cohorts thought to represent different stages of PD. 18F-FP-CIT positron emission tomography and subtle motor features identified patients with idiopathic rapid-eye-movement sleep behaviour disorder (n = 8) that developed prodromal motor signs of PD. Longitudinal diffusion tensor imaging before and after the development of prodromal motor PD showed higher fractional anisotropy in motor cortex and corticospinal tract compared to controls, indicating adaptive structural changes in motor networks in concert with nigrostriatal dopamine loss. Histological analyses of the white matter underlying the motor cortex showed progressive disorientation of axons with segmental replacement of neurofilaments with α-synuclein, enlargement of myelinating oligodendrocytes and increased density of their precursors. There was no loss of neurons in the motor cortex in early or late pathologically confirmed motor PD compared to controls, although there were early cortical increases in neuronal neurofilament light chain and myelin proteins in association with α-synuclein accumulation. Our results collectively provide evidence of a direct impact of PD on primary motor cortex and its output pathways that begins in the prodromal motor stage of PD with structural changes confirmed in early PD. These adaptive structural changes become considerable as the disease advances potentially contributing to motor PD.

Adsorption of nanoparticles on minerals affects the fate and transport of nanoparticles directly and is of great significance to many fields, including research into ore deposits, geochemistry, the environment and mineral materials. Whereas many previous studies have been conducted under the equilibrium pH and low solid (mineral) to liquid (nanoparticle suspension) ratio conditions, adsorption processes under initial pH and high solid/liquid ratio conditions may represent many important yet underexamined complex scenarios. To fill in this research gap, the adsorption of gold nanoparticles on illite was investigated experimentally at a relatively high solid/liquid ratio of 5 g L-1 and the effects of initial pH, ionic strength, citrate concentration, temperature and illite particle size were evaluated. The adsorbed amount of gold nanoparticles (from <5% to nearly 100%) increased with increasing ionic strength, temperature and citrate concentration and decreased with increasing pH and illite particle size. The presence of illite resulted in the dynamic evolution of the pH of the suspension, which, along with solution chemistry parameters, controlled the electrostatic interaction of illite and gold nanoparticles. The adsorption results, scanning electron microscopy observations and surface properties of illite suggest that the negatively charged gold nanoparticles were adsorbed predominantly on the positive illite edges through electrostatic interaction. The electrostatic attraction between illite and gold nanoparticles appeared to be strong, supported by the minor amount of desorption. These research findings are expected to provide a valuable reference regarding many critical issues in the geosciences as well as for industrial applications.

In karst regions, the majority of studies have focused on ecosystem carbon sequestration in the same lithology, but no studies in different lithologies. In this study, actual measurements were used to reveal carbon sequestration characteristics of two plantation forest ecosystems ( Bodinieri cinnamon and Cupressus funebris ) with different lithologies of karst. The results showed that the tree layer showed the highest vegetation biomass, carbon content, carbon density, and ratio of aboveground biomass to belowground biomass. The carbon density of B . cinnamon plantation and C . funebris plantation was high in dolomite and in limestone respectively. The soil quality and carbon density of bare ground and plantation varied across different lithologies. The carbon density of various ecosystem components was in the order of vegetation>soil>litterfall. The carbon density and net carbon density of plantation varied across different lithologies. In B . cinnamon plantation, the carbon sequestration rate of vegetation and ecosystem was high in dolomite, moderate in limestone, and low in dolomitic sandstone. In Cupressus funebris plantation, the carbon sequestration rate was in the order of limestone>dolomite>dolomitic sandstone. These findings revealed that lithology is an important factor affecting ecosystem carbon pools, and plantation ecosystems have low biomass and low carbon density in karst areas.

Parkinson’s disease (PD) is an age-related neurodegenerative disorder affecting millions of people worldwide. The disease is characterized by the progressive loss of dopaminergic neurons and spread of Lewy pathology (α-synuclein aggregates) in the brain but the pathogenesis remains elusive. PD presents substantial clinical and genetic variability. Although its complex etiology and pathogenesis has hampered the breakthrough in targeting disease modification, recent genetic tools advanced our approaches. As such, mitochondrial dysfunction has been identified as a major pathogenic hub for both familial and sporadic PD. In this review, we summarize the effect of mutations in 11 PARK genes ( SNCA, PRKN, PINK1, DJ-1, LRRK2, ATP13A2, PLA2G6, FBXO7, VPS35, CHCHD2 , and VPS13C ) on mitochondrial function as well as their relevance in the formation of Lewy pathology. Overall, these genes play key roles in mitochondrial homeostatic control (biogenesis and mitophagy) and functions (e.g., energy production and oxidative stress), which may crosstalk with the autophagy pathway, induce proinflammatory immune responses, and increase oxidative stress that facilitate the aggregation of α-synuclein. Thus, rectifying mitochondrial dysregulation represents a promising therapeutic approach for neuroprotection in PD.

Alpha-synuclein (αSyn) is one of the most abundant proteins in the nervous system and is currently associated with devastating synucleinopathies, yet its biology extends far beyond this. In this review, we suggest that αSyn-driven disease emerges within specific neural circuits through the combined effects of cell-type-specific roles, subcellular environments, post-translational modifications (PTMs), and co-pathology. These interacting and additive dimensions, rather than αSyn alone, generate the pathological diversity, shaping whether pathology manifests as Parkinson’s disease (PD), Parkinson’s disease dementia (PDD), dementia with Lewy bodies (DLB), multiple system atrophy (MSA), or mixed dementia phenotypes. We integrate recent advances on the physiological roles of αSyn in neurons and glia (astrocytes, oligodendrocytes, and microglia), its compartment-dependent (e.g., synaptic and nuclear) functions, and the molecular transitions (e.g., mediated by pS129) that convert functional assemblies into pathogenic conformers. Building on this foundation, we outline mechanisms through which these factors contribute to disease-specific vulnerability, progression, and clinical heterogeneity. Finally, we highlight how this multidimensional perspective on αSyn biology can inform the development of next-generation biomarkers that support precision therapies across distinct disorders.