Ferroelectric materials can be utilized for fabricating photodetectors because of the photovoltaic effect. Enhancing the photovoltaic performance of ferroelectric materials is still a challenge. Here, a self-powered ultraviolet (UV) photodetector is designed based on the ferroelectric BiFeO (BFO) material, exhibiting a high current/voltage response to 365 nm light in heating/cooling states. The photovoltaic performance of the BFO-based device can be well modulated by applying different temperature variations, where the output current and voltage can be enhanced by 60 and 75% in heating and cooling states, respectively. The enhancement mechanism of the photocurrent is associated with both temperature effect and thermo-phototronic effect in the photovoltaic process. Moreover, a 4 × 4 matrix photodetector array has been designed for detecting the 365 nm light distribution in the cooling state by utilizing photovoltage signals. This study clarifies the role of the temperature effect and the thermo-phototronic effect in the photovoltaic process of the BFO material and provides a feasible route for pushing forward practical applications of self-powered UV photodetectors.

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seriously lowering the power conversion efficiency. [13][14][15][16] The photocurrent of ferroelectric devices is determined by the light adsorption process, dissociation efficiency of electron-hole pairs, lifetime and the mobility of charges. [17] As is known, most of the ferroelectric materials have small absorption coefficient and large bandgap of 2.6-4 eV, thus can only scavenge a little amount of solar energy in the UV range or near UV range of sunlight. According to the Glass model, driven by the noncentral symmetric potential well, the excited electrons only can shift several angstorms along the polarization direction before they decay, leading to very small photocurrent in ferroelectric-photovoltaic devices. Moreover, the lifetime of the photogenerated nonequilibrium charges was only in the picosecond scale, while the recombination lifetime was measured to be submicrosecond to tens of microseconds. [17] Therefore, owing to the very small photocurrent, it seems to be difficult for ferroelectric materials superior to classical semiconductor in mainstream usage of photovoltaic devices. However, these materials could be more appealing for some specific applications due to their multifunctionalities. For instance, most of the ferroelectric materials have bandgaps of 2.6-4 eV, which only can absorb a certain range of wavelength in sunlight with photons energies above bandgap energy. [17,18] Therefore, besides as nanogenerators for scavenging solar energy, ferroelectric photovoltaic devices may be more suitable for fabricating photodetectors to detect a certain wavelength light.Among the conventional ferroelectric materials, BiFeO 3 (BFO) has the narrowest bandgap of about 2.67 eV, which can absorb the light wavelengths of less than 465 nm. [19] Thus BFObased ferroelectric-photovoltaic devices could be well utilized to detect 450 nm light in the range of visible light. Moreover, as a multifunctional material, BFO possesses both the photovoltaic and pyroelectric effects, offering more opportunities for such applications. When 450 nm light is illuminating on BFO surface, electrical signals could be detected due to the generation and separation of electron-hole pairs. However, it is suggested that being different from traditional p-n junction based semiconductor, the photovoltaic effect of BFO may be associated with noncentral symmetric structure, domain wall, Schottky barrier, and depolarization field. [17] In addition, due to the noncentral symmetric crystal structure, pyroelectric signals can be generated by the light-induced temperature increase Ferroelectric material BiFeO 3 with narrow bandgap of 2.67 eV can be more suitable to fabricate photodetectors instead of solar energy harvesters because of low energy conversion efficiency. Herein, a BiFeO 3 film-based self-powered photodetector is reported by using the photovoltaic-pyroelectric coupled effect to enable a fast sensing of 450 nm light illumination. Compared with photovoltaic effect, the photosensitivity parameters including photoconductive gain, respons...

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Background and Purpose-Oxidative stress is known to be involved in ischemic stroke. Intense interest is drawn to the therapeutic potential of Chinese herbs on ischemic stroke because many of them contain antioxidant properties. Leonurine, 1 of the active compounds from purified Herba Leonuri, was studied to evaluate its possible therapeutic effects on ischemic stroke. Method-Middle cerebral artery occlusion was selected as our model of study. The animals were pretreated with Leonurine orally for 7 days and the surgery was done. One day after surgery, 2,3,5-triphenyltetrazolium chloride staining and neurological deficit score were carried out to evaluate the functional outcome of animals, whereas levels of superoxide dismutase, glutathione peroxidase, and malondialdehyde were analyzed for oxidative stress analysis. For mitochondrial studies, 3 hours after surgery, mitochondria were isolated for analysis of reactive oxygen species production, adenosine triphosphate biosynthesis, oxygen consumption, and respiratory control ratio value. Result-In in vivo experiments, Leonurine pretreatment reduced infarct volume, improved neurological deficit in stroke groups, increased activities of antioxidant enzymes superoxide dismutase and glutathione peroxidase, and decreased levels from the lipid peroxidation marker malondialdehyde. In terms of mitochondrial modulation, Leonurine inhibited mitochondrial reactive oxygen species production and adenosine triphosphate biosynthesis. Animal studies also demonstrated that the mitochondrial function and redox state were restored by Leonurine treatment. Conclusions-Leonurine has neuroprotective effects and carries a therapeutic potential of stroke prevention. (Stroke.

Background: In recent years, there has been growing evidence that vitamin D deficiency is associated with the development and progression of chronic heart failure (CHF). Hypothesis: Additional supplementation of vitamin D may have protective effects in patients with CHF. Methods: We searched PubMed, Embase, and Cochrane databases through June 2015 and included 7 randomized controlled trials that investigated the effects of vitamin D on cardiovascular outcomes in patients with CHF. Then, we performed a meta-analysis of clinical trials to confirm whether vitamin D supplementation is beneficial in CHF patients. The weighted mean difference (WMD) and 95% confidence interval (CI) were calculated using fixed-or random-effects models. Results: Our pooled results indicated that additional supplementation of vitamin D was not superior to conventional treatment in terms of left ventricular ejection fraction, N-terminal pro-B-type natriuretic peptide, and 6-minute walk distance. Moreover, vitamin D supplementation was associated with significant decreases in the levels of tumor necrosis factor-α (WMD: −2.42 pg/mL, 95% CI: −4.26 to −0.57, P < 0.05), C-reactive protein (WMD: −0.72 mg/L, 95% CI: −1.42 to −0.02, P < 0.05), and parathyroid hormone (WMD: −13.44 pg/mL, 95% CI: −21.22 to −5.67, P < 0.05). Conclusions: Vitamin D supplementation may decrease serum levels of parathyroid hormone and inflammatory mediators in CHF patients, whereas it has no beneficial effects on improvement of left ventricular function and exercise tolerance.

Cisplatin chemotherapy often causes acute kidney injury (AKI) in cancer patients. There is increasing evidence that mitochondrial dysfunction plays an important role in cisplatin-induced nephrotoxicity. Degradation of damaged mitochondria is carried out by mitophagy. Although mitophagy is considered of particular importance in protecting against AKI, little is known of the precise role of mitophagy and its molecular mechanisms during cisplatin-induced nephrotoxicity. Also, evidence that activation of mitophagy improved mitochondrial function is lacking. Furthermore, several evidences have shown that mitochondrial fission coordinates with mitophagy. The aim of this study was to investigate whether activation of mitophagy protects against mitochondrial dysfunction and renal proximal tubular cells injury during cisplatin treatment. The effect of mitochondrial fission on mitophagy was also investigated. In cultured human renal proximal tubular cells, we observed that 3-methyladenine, a pharmacological inhibitor of autophagy, blocked mitophagy and exacerbated cisplatin-induced mitochondrial dysfunction and cells injury. In contrast, autophagy activator rapamycin enhanced mitophagy and protected against the harmful effects of cisplatin on mitochondrial function and cells viability. Suppression of mitochondrial fission by knockdown of its main regulator dynamin-related protein-1 (Drp1) decreased cisplatin-induced mitophagy. Meanwhile, Drp1 suppression protected against cisplatin-induced cells injury by inhibiting mitochondrial dysfunction. Our results provide evidence that Drp1-depedent mitophagy has potential as renoprotective targets for the treatment of cisplatin-induced AKI.

Background The novel coronavirus disease (2019-nCoV) has been affecting global health since the end of 2019 and there is no sign that the epidemic is abating . The major issue for controlling the infectious is lacking efficient prevention and therapeutic approaches. Chloroquine (CQ) and Hydroxychloroquine (HCQ) have been reported to treat the disease, but the underlying mechanism remains controversial. Purpose The objective of this study is to investigate whether CQ and HCQ could be ACE2 blockers and used to inhibit 2019-nCoV virus infection. Methods In our study, we used CCK-8 staining, flow cytometry and immunofluorescent staining to evaluate the toxicity and autophagy of CQ and HCQ, respectively, on ACE2 high-expressing HEK293T cells (ACE2 h cells). We further analyzed the binding character of CQ and HCQ to ACE2 by molecular docking and surface plasmon resonance (SPR) assays, 2019-nCoV spike pseudotyped virus was also used to observe the viropexis effect of CQ and HCQ in ACE2 h cells. Results Results showed that HCQ is slightly more toxic to ACE2 h cells than CQ. Both CQ and HCQ could bind to ACE2 with K D = (7.31 ± 0.62) e −7 M and (4.82 ± 0.87) e −7 M, respectively. They exhibit equivalent suppression effect for the entrance of 2019-nCoV spike pseudotyped virus into ACE2 h cells. Conclusions CQ and HCQ both inhibit the entrance 2019-nCoV into cells by blocking the binding of the virus with ACE2. Our findings provide novel insights into the molecular mechanism of CQ and HCQ treatment effect on virus infection.