Sustainable, low-cost, high-contrast electrochromic displays via host-guest interactions.

Electrochromic (EC) displays with electronically regulating the transmittance of solar radiation offer the opportunity to increase the energy efficiency of the building and electronic products and improve the comfort and lifestyle of people. Despite the unique merit and vast application potential of EC technologies, long-awaited EC windows and related visual content displays have not been fully commercialized due to unsatisfactory production cost, durability, color, and complex fabrication processes. Here we develop a unique EC strategy and system based on the natural host and guest interactions to address the above issues. A completely reusable and sustainable EC device has been fabricated with potential advantages of extremely low cost, ideal user-/environment friendly property, and excellent optical modulation, which is benefited from the extracted biomass EC materials and reusable transparent electrodes involved in the system. The as-prepared EC window and nonemissive transparent display also show comprehensively excellent properties: high transmittance change (>85%), broad spectra modulation covering Ultraviolet (UV), Visible (Vis) to Infrared (IR) ranges, high durability (no attenuation under UV radiation for more than 1.5 mo), low open voltage (0.9 V), excellent reusability (>1,200 cycles) of the device's key components and reversibility (>4,000 cycles) with a large transmittance change, and pleasant multicolor. It is anticipated that unconventional exploration and design principles of dynamic host-guest interactions can provide unique insight into different energy-saving and sustainable optoelectronic applications.

Imaging of Carbonic Anhydrase Level in Epilepsy with an Environment-Sensitive Fluorescent Probe.

Carbonic anhydrases (CAs) participate in various physiological and pathological activities by catalyzing the interconversion between carbon dioxide and bicarbonate ions. Under normal circumstances, they guarantee that the relevant biological reactions in our body occur within an appropriate time scale. Abnormal expression or activity alteration of CAs is closely related to the pathogenesis of diverse diseases. This work reports an inhibitor-directed fluorescent probe FMRs-CA for the detection of CAs. Excellent selectivity, favorable biocompatibility, and desirable blood-brain barrier (BBB) penetration endow the probe with the ability to image the fluctuation of CAs in cells and mice. We achieved in situ visualization of the increased CAs in hypoxic cells with this probe. Additionally, probe FMRs-CA was mainly enriched within the liver and gradually metabolized by the liver. With the help of FMRs-CA, the increase of CAs in epileptic mouse brains was revealed first from the perspective of imaging, providing the mechanism connection between abnormal CA expressions and epilepsy.

Puromycin Prodrug Activation by Thioredoxin Reductase Overcomes Its Promiscuous Cytotoxicity.

Overexpression of the selenoprotein thioredoxin reductase (TrxR) has been documented in malignant tissues and is of pathological significance for many types of tumors. The antibiotic puromycin (Puro) is a protein synthesis inhibitor causing premature polypeptide chain termination during translation. The well-defined action mechanism of Puro makes it a useful tool in biomedical studies. However, the nonselective cytotoxicity of Puro limits its therapeutic applications. We report herein the construction and evaluation of two Puro prodrugs, that is, S1-Puro with a five-membered cyclic disulfide trigger and S2-Puro with a linear disulfide trigger. S1-Puro is selectively activated by TrxR and shows the TrxR-dependent cytotoxicity to cancer cells, while S2-Puro is readily activated by thiols. Furthermore, S1-Puro displays higher stability in plasma than S2-Puro. We expect that this prodrug strategy may promote the further development of Puro as a therapeutic agent.

Naphthalimide Fluorescent Skeleton for Facile and Accurate Quantification of Glutathione.

Glutathione (GSH), the most prevalent nonprotein thiol in biological systems, acts as both an antioxidant to manipulate intracellular redox homeostasis and a nucleophile to detoxify xenobiotics. The fluctuation of GSH is closely related to the pathogenesis of diverse diseases. This work reports the construction of a nucleophilic aromatic substitution-type probe library based on the naphthalimide skeleton. After an initial evaluation, the compound R13 was identified as a highly efficient GSH fluorescent probe. Further studies demonstrate that R13 could readily quantify GSH in cells and tissues via a straightforward fluorometric assay with a comparable accuracy to the results from the HPLC. We then used R13 to quantify the content of GSH in mouse livers after X-ray irradiation, revealing that irradiation-induced oxidative stress leads to the increase of oxidized GSH (GSSG) and depletion of GSH. In addition, probe R13 was also applied to investigate the alteration of the GSH level in the Parkinson's mouse brains, showing a decrease of GSH and an increase of GSSG in Parkinson's mouse brains. The convenience of the probe in quantifying GSH in biological samples facilitates further understanding of the fluctuation of the GSH/GSSG ratio in diseases.

Dynamic Metal-Ligand Interaction of Synergistic Polymers for Bistable See-Through Electrochromic Devices.

Bistable electrochromic materials are a promising alternative solution to reduce energy consumption in displays. Limited by the mechanism and lack of a design strategy, only a few electrochromic materials have truly been able achieve bistability. Herein, a novel strategy is proposed to design bistable electrochromic materials based on polymer-assisted dynamic metal-ligand coordination. The mechanism and materials of such unconventional electrochromic systems are proved by sufficient characterization. Synergistic stabilization of polymerized switchable dyes and the ionic ligand polymer are attracted to each other by supramolecular forces. The color states of the dye molecules are controlled and stabilized by valence changes of the metal ions. Meanwhile, through the polymerization of the electrochromic material and the nearby metal-ligand material, the metal ions of the electroinduced valence change are tightly fixed, and the related diffusion problem of the active EC component is also almost completely suppressed. This strategy successfully enables preparation of the corresponding transparent electrochromic displays with good performances, such as, the display information is clearly visible for more than 1.5 h without consuming energy. Furthermore, the new way of dynamic coordination or dissociation bistable displays could likely prosper the development of the electrochromic area and inspire other fields.

A fatal case of hypothermia caused by dog bites.

Death from hypothermia usually *We presented a fatal case of hypothermia after being bitten by dog in this article. occurs among people exposed to cold and humid environmental conditions when they are homeless, aged, suffering from natural or psychiatric diseases and drug or alcohol intoxication. A normal healthy person dying from hypothermia due to dog bites is unusual and rare. Here, we present a fatal case of hypothermia following dog bites causing blood loss and multiple wounds on the body. A 56-year-old man was found dead in a remote roadside puddle of a small village, early in the morning. He was naked, and his body trunk and limbs had multiple irregular wounds. Gray animal hairs could be seen in parts of the wound cavities and surrounding areas. In addition, there was a kennel near the scene. Family members argued that the deceased was bitten to death by a dog. However, autopsy revealed several findings which were strongly supportive of fatal hypothermia. Moreover, we saw no obvious changes caused by blood loss, either on the body surface or internal organs. Accordingly, we concluded the true cause of his death was fatal hypothermia; bites from a dog was a necessary causative factor.

Effects of Ketamine on Levels of Inflammatory Cytokines IL-6, IL-1ß, and TNF-α in the Hippocampus of Mice Following Acute or Chronic Administration.

Ketamine is an injectable anesthetic and recreational drug of abuse commonly used worldwide. Many experimental studies have shown that ketamine can impair cognitive function and induce psychotic states. Neuroinflammation has been suggested to play an important role in neurodegeneration. Meanwhile, ketamine has been shown to modulate the levels of inflammatory cytokines. We hypothesized that the effects of ketamine on the central nervous system are associated with inflammatory cytokines. Therefore, we set out to establish acute and chronic ketamine administration models in C57BL/6 mice, to evaluate spatial recognition memory and emotional response, to analyze the changes in the levels of the inflammatory cytokines interleukin-6 (IL-6), interleukin-1ß (IL-1ß), and tumor necrosis factor-α (TNF-α) in the mouse hippocampus, employing behavioral tests, Western blot, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) and immunohistochemistry. Our results showed that ketamine at the dose of 60 mg/kg induced spatial recognition memory deficit and reduced anxiety-like behaviors in mice after chronic administration. Moreover, we found that ketamine increased the hippocampal levels of IL-6 and IL-1ß after single, multiple and long-term administration in a dose-dependent manner. However, the expression level of TNF-α differed in the mouse hippocampus under different conditions. Single administration of ketamine increased the level of TNF-α, whereas multiple and long-term administration decreased it significantly. We considered that TNF-α expression could be controlled by a bi-directional regulatory pathway, which was associated with the dose and duration of ketamine administration. Our results suggest that the alterations in the levels of inflammatory cytokines IL-6, IL-1ß, and TNF-α may be involved in the neurotoxicity of ketamine.

Changes in hippocampal AMPA receptors and cognitive impairments in chronic ketamine addiction models: another understanding of ketamine CNS toxicity.

Ketamine has been reported to impair human cognitive function as a recreational drug of abuse. However, chronic effects of ketamine on central nervous system need to be further explored. We set out to establish chronic ketamine addiction models by giving mice a three or six month course of daily intraperitoneal injections of ketamine, then examined whether long-term ketamine administration induced cognition deficits and changed hippocampal post-synaptic protein expression in adult mice. Behavior tests results showed that mice exhibited dose- and time-dependent learning and memory deficits after long-term ketamine administration. Western blot results showed levels of GluA1, p-S845 and p-S831 proteins demonstrated significant decline with ketamine 60 mg/kg until six months administration paradigm. But levels of p-S845 and p-S831 proteins exhibited obvious increase with ketamine 60 mg/kg three months administration paradigm. NR1 protein levels significantly decrease with ketamine 60 mg/kg three and six months administration paradigm. Our results indicate that reduced expression levels and decreased phosphorylation levels of hippocampal post-synaptic membrane GluA1- containing AMPA receptors maybe involved in cognition impairment after long-term ketamine administration. These findings provide further evidence for the cognitive damage of chronic ketamine addiction as a recreational drug.