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Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide, mainly affecting the elderly. The disease progresses gradually, with core motor presentations and a multitude of non-motor manifestations. There are two neuropathological hallmarks of PD, the dopaminergic neuronal loss and the alpha-synuclein-containing Lewy body inclusions in the substantia nigra. While the exact pathomechanisms of PD remain unclear, genetic investigations have revealed evidence of the involvement of mitochondrial function, alpha-synuclein (α-syn) aggregation, and the endo-lysosomal system, in disease pathogenesis. Due to the high energy demand of dopaminergic neurons, mitochondria are of special importance acting as the cellular powerhouse. Mitochondrial dynamic fusion and fission, and autophagy quality control keep the mitochondrial network in a healthy state. Should defects of the organelle occur, a variety of reactions would ensue at the cellular level, including disrupted mitochondrial respiratory network and perturbed calcium homeostasis, possibly resulting in cellular death. Meanwhile, α-syn is a presynaptic protein that helps regulate synaptic vesicle transportation and endocytosis. Its misfolding into oligomeric sheets and fibrillation is toxic to the mitochondria and neurons. Increased cellular oxidative stress leads to α-syn accumulation, causing mitochondrial dysfunction. The proteasome and endo-lysosomal systems function to regulate damage and unwanted waste management within the cell while facilitating the quality control of mitochondria and α-syn. This review will analyze the biological functions and interactions between mitochondria, α-syn, and the endo-lysosomal system in the pathogenesis of PD.

As one of the most important photocatalysts, TiO 2 has triggered broad interest and intensive studies for decades. Observation of the interfacial reactions between water and TiO 2 at microscopic scale can provide key insight into the mechanisms of photocatalytic processes. Currently, experimental methodologies for characterizing photocatalytic reactions of anatase TiO 2 are mostly confined to water vapor or single molecule chemistry. Here, we investigate the photocatalytic reaction of anatase TiO 2 nanoparticles in water using liquid environmental transmission electron microscopy. A self-hydrogenated shell is observed on the TiO 2 surface before the generation of hydrogen bubbles. First-principles calculations suggest that this shell is formed through subsurface diffusion of photo-reduced water protons generated at the aqueous TiO 2 interface, which promotes photocatalytic hydrogen evolution by reducing the activation barrier for H 2 (H–H bond) formation. Experiments confirm that the self-hydrogenated shell contains reduced titanium ions, and its thickness can increase to several nanometers with increasing UV illuminance. Photocatalytic water splitting on TiO 2 is a promising route to H 2 fuel production, but the mechanistic pathway at the water–TiO 2 interface remains poorly understood. Here, using liquid environmental TEM and first-principles calculations, the authors unveil the formation of a self-hydrogenated shell on the TiO 2 surface that further promotes H 2 production.

A non-faradaic label-free cortisol biosensor was demonstrated using MoS 2 nanosheets integrated into a nanoporous flexible electrode system. Low volume (1–5 μL) sensing was achieved through use of a novel sensor stack design comprised of vertically aligned metal electrodes confining semi-conductive MoS 2 nanosheets. The MoS 2 nanosheets were surface functionalized with cortisol antibodies towards developing an affinity biosensor specific to the physiological relevant range of cortisol (8.16 to 141.7 ng/mL) in perspired human sweat. Sensing was achieved by measuring impedance changes associated with cortisol binding along the MoS 2 nanosheet interface using electrochemical impedance spectroscopy. The sensor demonstrated a dynamic range from 1–500 ng/mL with a limit of detection of 1 ng/mL. A specificity study was conducted using a metabolite expressed in human sweat, Ethyl Glucuronide. Continuous dosing studies were performed during which the sensor was able to discriminate between four cortisol concentration ranges (0.5, 5, 50, 500 ng/mL) for a 3+ hour duration. Translatability of the sensor was shown with a portable form factor device, demonstrating a comparable dynamic range and limit of detection for the sensor. The device demonstrated a R 2 correlation value of 0.998 when comparing measurements to the reported impedance values of the benchtop instrumentation.

Plant oils have been utilized for a variety of purposes throughout history, with their integration into foods, cosmetics, and pharmaceutical products. They are now being increasingly recognized for their effects on both skin diseases and the restoration of cutaneous homeostasis. This article briefly reviews the available data on biological influences of topical skin applications of some plant oils (olive oil, olive pomace oil, sunflower seed oil, coconut oil, safflower seed oil, argan oil, soybean oil, peanut oil, sesame oil, avocado oil, borage oil, jojoba oil, oat oil, pomegranate seed oil, almond oil, bitter apricot oil, rose hip oil, German chamomile oil, and shea butter). Thus, it focuses on the therapeutic benefits of these plant oils according to their anti-inflammatory and antioxidant effects on the skin, promotion of wound healing and repair of skin barrier.

Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique modality of cell death, ferroptosis is mediated by iron-dependent phospholipid peroxidation. The mechanisms of ferroptosis inhibitors enhance antioxidative capacity to counter the oxidative stress from lipid peroxidation, such as through the system xc−/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis and the coenzyme Q10 (CoQ10)/FSP1 pathway. Another means to reduce ferroptosis is with iron chelators. To date, there is no disease-modifying therapy to cure or slow PD progression, and a recent topic of research seeks to intervene with the development of PD via regulation of ferroptosis. In this review, we provide a discussion of different cell death pathways, the molecular mechanisms of ferroptosis, the role of ferroptosis in blood–brain barrier damage, updates on PD studies in ferroptosis, and the latest progress of pharmacological agents targeting ferroptosis for the intervention of PD in clinical trials.

Nonreciprocal transport refers to charge transfer processes that are sensitive to the bias polarity. Until recently, nonreciprocal transport was studied only in dissipative systems, where the nonreciprocal quantity is the resistance. Recent experiments have, however, demonstrated nonreciprocal supercurrent leading to the observation of a supercurrent diode effect in Rashba superconductors. Here we report on a supercurrent diode effect in NbSe 2 constrictions obtained by patterning NbSe 2 flakes with both even and odd layer number. The observed rectification is a consequence of the valley-Zeeman spin-orbit interaction. We demonstrate a rectification efficiency as large as 60%, considerably larger than the efficiency of devices based on Rashba superconductors. In agreement with recent theory for superconducting transition metal dichalcogenides, we show that the effect is driven by the out-of-plane component of the magnetic field. Remarkably, we find that the effect becomes field-asymmetric in the presence of an additional in-plane field component transverse to the current direction. Supercurrent diodes offer a further degree of freedom in designing superconducting quantum electronics with the high degree of integrability offered by van der Waals materials. The supercurrent diode effect was recently observed in a Nb/V/Ta superlattice thin film with Rashba-type spin-orbit coupling. Here, the authors observe this effect in few-layer NbSe 2 crystals driven by valley-Zeeman-type spin-orbit coupling and find that the effect is proportional to out-of-plane magnetic field.

Banana (Musa sp.) is cultivated worldwide and is one of the most popular fruits. The soil-borne fungal disease Fusarium wilt of banana (FWB), commonly known as Panama disease, is caused by Fusarium oxysporum f. sp. cubense (Foc) and is a highly lethal vascular fungal disease in banana plants. Raman spectroscopy, an emerging laser-based technology based on Raman scattering, has been used for the qualitative characterization of biological tissues such as foodborne pathogens, cancer cells, and melamine. In this study, we describe a Raman spectroscopic technique that could potentially be used as a method for diagnosing FWB. To that end, the Raman fingerprints of Foc (including mycelia and conidia) and Foc-infected banana pseudostems with varying levels of symptoms were determined. Our results showed that eight, eleven, and eleven characteristic surface-enhanced Raman spectroscopy peaks were observed in the mycelia, microconidia, and macroconidia of Foc, respectively. In addition, we constructed the Raman spectroscopic fingerprints of banana pseudostem samples with varying levels of symptoms in order to be able to differentiate Foc-infected bananas from healthy bananas. The rate at which FWB was detected in asymptomatic Foc-infected samples by using the spectral method was 76.2%, which was comparable to the rates previously reported for other FWB detection methods based on real-time PCR assays, suggesting that the spectral method described herein could potentially serve as an alternative tool for detecting FWB in fields. As such, we hope that the developed spectral method will open up new possibilities for the on-site diagnosis of FWB.

Parkinson disease (PD) is the second most common neurodegenerative disease without known disease modification therapy to slow down disease progression. This disease has pathological features of Lewy bodies with α-synuclein aggregation being the major component and selective dopaminergic neuronal loss over the substantia nigra. Although the exact etiology is still unknown, mitochondrial dysfunction has been shown to be central in PD pathophysiology. Type 2 diabetes mellitus has recently been connected to PD, and anti-diabetic drugs, such as glucagon-like peptide-1 receptor agonists (GLP-1RAs), have been shown to possess neuroprotective effects in PD animal models. The GLP-1RA liraglutide is currently under a phase 2 clinical trial to measure its effect on motor and non-motor symptoms in PD patients. In this study, we used an acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD to test the possible mechanism of the GLP-1RA liraglutide in the pathogenesis of PD. We show that the neurobehavioral and motor dysfunction caused by the mitochondrial complex I inhibitor, MPTP, can be partially reversed by liraglutide. The GLP-1RA can protect mice from apoptosis of substantia nigra neurons induced by MPTP. MPTP treatment led to imbalanced mitochondrial fusion and fission dynamics, altered mitochondrial morphology, impeded autophagy flux, increased α-synuclein accumulation, and elevated oxidative stress. Specifically, the normalizing of mitochondrial fusion-fission dynamic-related proteins and enhancement of autophagy flux after administration of liraglutide is associated with improving neuronal survival. This suggests that GLP-1RAs may provide potential beneficial effects for PD caused by mitochondrial dysfunction through improvement of mitochondrial morphology balance and enhancing damaged organelle degradation.

Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease affecting more than 1% of the population over 65 years old. The etiology of the disease is unknown and there are only symptomatic managements available with no known disease-modifying treatment. Aging, genes, and environmental factors contribute to PD development and key players involved in the pathophysiology of the disease include oxidative stress, mitochondrial dysfunction, autophagic–lysosomal imbalance, and neuroinflammation. Recent epidemiology studies have shown that type-2 diabetes (T2DM) not only increased the risk for PD, but also is associated with PD clinical severity. A higher rate of insulin resistance has been reported in PD patients and is suggested to be a pathologic driver in this disease. Oral diabetic drugs including sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and dipeptidyl peptidase-4 (DPP-4) inhibitors have been shown to provide neuroprotective effects in both PD patients and experimental models; additionally, antidiabetic drugs have been demonstrated to lower incidence rates of PD in DM patients. Among these, the most recently developed drugs, SGLT2 inhibitors may provide neuroprotective effects through improving mitochondrial function and antioxidative effects. In this article, we will discuss the involvement of mitochondrial-related oxidative stress in the development of PD and potential benefits provided by antidiabetic agents especially focusing on sglt2 inhibitors.

This work presents the viability of passive eccrine sweat as a functional biofluid toward tracking the human body's inflammatory response. Cytokines are biomarkers that orchestrate the manifestation and progression of an infection/inflammatory event. Hence, noninvasive, real‐time monitoring of cytokines can be pivotal in assessing the progression of infection/inflammatory event, which may be feasible through monitoring of host immune markers in eccrine sweat. This work is the first experimental proof demonstrating the ability to detect inflammation/infection such as fever, FLU directly from passively expressed sweat in human subjects using a wearable “SWEATSENSER” device. The developed SWEATSENSER device demonstrates stable, real‐time monitoring of inflammatory cytokines in passive sweat. An accuracy of >90% and specificity >95% was achieved using SWEATSENSER for a panel of cytokines (interleukin‐6, interleukin‐8, interleukin‐10, and tumor necrosis factor‐α) over an analytical range of 0.2–200 pg mL−1. The SWEATSENSER demonstrated a correlation of Pearson's r > 0.98 for the study biomarkers in a cohort of 26 subjects when correlated with standard reference method. Comparable IL‐8 levels (2–15 pg mL−1) between systemic circulation (serum) and eccrine sweat through clinical studies in a cohort of 15 subjects, and the ability to distinguish healthy and sick (infection) cohort using inflammatory cytokines in sweat provides pioneering evidence of the SWEATSENSER technology for noninvasive tracking of host immune response biomarkers. Such a wearable device can offer significant strides in improving prognosis and provide personalized therapeutic treatment for several inflammatory/infectious diseases.