Electrochemical Biosensor for Protein Concentration Monitoring Using Natural Wood Evaporation for Power Generation.

A high-sensitivity, low-cost, self-powered biomass electrochemical biosensor based on the "evaporating potential" theory is developed for protein detection. The feasibility of experimental evaluation methods was verified with a probe protein of bovine serum albumin. The sensor was then used to detect lung cancer marker CYFRA21-1, and the potential of our sensor for clinical diagnosis was demonstrated by serum analysis. This work innovatively exploits the osmotic power generation capability of natural wood to construct a promising electrochemical biosensor that was driven by kinetics during testing. The detection methods used for this sensor, chronoamperometry and AC impedance, showed potential for quantitative analysis and specific detection, respectively. Furthermore, the sensor could facilitate new insights into the development of high-sensitivity, low-cost, and easy-to-use electrochemical biosensors.

Prolonged Early Exposure to a High-Fat Diet Augments the Adverse Effects on Neurobehavior and Hippocampal Neuroplasticity: Involvement of Microglial Insulin Signaling.

High-fat diet (HFD) consumption may contribute to the high prevalence of cognitive-emotional issues in modern society. Mice fed a HFD for a prolonged period develop more severe neurobehavioral disturbances when first exposed to a HFD in the juvenile period than in adulthood, suggesting an initial age-related difference in the detrimental effects of long-term HFD feeding. However, the mechanism underlying this difference remains unclear. Here, male C57BL/6J mice initially aged 4 (IA4W) or 8 (IA8W) weeks were fed a control diet (CD) or HFD for 6 months and then subjected to metabolic, neurobehavioral, and histomorphological examinations. Although the detrimental effects of long-term HFD feeding on metabolism and neurobehavior were observed in mice of both ages, IA4W-HFD mice showed significant cognitive inflexibility accompanied by significantly greater levels of anxiety-like behavior than age-matched controls. Hippocampal neuroplasticity and microglial phenotype were altered by HFD feeding, whereas significant morphological alterations were more frequently observed in IA4W-HFD mice than in IA8W-HFD mice. Additionally, significantly increased hippocampal microglial engulfment of postsynaptic proteins and elevated phospho-insulin-receptor levels were observed in IA4W-HFD, but not in IA8W-HFD, mice. These findings suggest that aberrant microglia-related histomorphological changes in the hippocampus underlie the exacerbated detrimental neurobehavioral effects of prolonged early HFD exposure and indicate that enhanced insulin signaling might drive microglial dysfunction after prolonged early HFD exposure.

Long-term exercise preserves pancreatic islet structure and ß-cell mass through attenuation of islet inflammation and fibrosis.

Islet fibrosis is associated with the disruption of islet structure and contributes to ß-cell dysfunction, playing an essential role in the pathogenesis of type 2 diabetes. Physical exercise has been shown to attenuate fibrosis in various organs; however, the effect of exercise on islet fibrosis has not been defined. Male Sprague-Dawley rats were divided into four groups: normal diet sedentary [N-Sed], normal diet + exercise [N-Ex], high-fat diet sedentary [H-Sed], and high-fat diet + exercise [H-Ex]. After 60 weeks of exercise, 4452 islets from Masson-stained slides were analyzed. Exercise led to a 68% and 45% reduction in islet fibrosis in the normal and high-fat diet groups and was correlated with a lower serum blood glucose. Fibrotic islets were characterized by irregular shapes and substantial loss of ß-cell mass, which were significantly reduced in the exercise groups. Remarkably, the islets from exercised rats at week 60 were morphologically comparable to those of sedentary rats at 26 weeks. In addition, the protein and RNA levels of collagen and fibronectin, and the protein levels of hydroxyproline in the islets were also attenuated by exercise. This was accompanied by a significant reduction in inflammatory markers in the circulation Interleukin-1 beta (IL-1ß)] and pancreas [IL-1ß, Tumor Necrosis Factor-alpha, Transforming Growth Factor-ß, and Phosphorylated Nuclear Factor Kappa-B p65 subunit], lower macrophage infiltration, and stellate cell activation in the islets of exercised rats. In conclusion, we have demonstrated that long-term exercise preserves pancreatic islet structure and ß-cell mass through anti-inflammatory and anti-fibrotic actions, suggesting additional rationales for the success of exercise training in the prevention and treatment of type 2 diabetes that should be further explored.

High-fat diet consumption promotes adolescent neurobehavioral abnormalities and hippocampal structural alterations via microglial overactivation accompanied by an elevated serum free fatty acid concentration.

Mounting evidence suggests that high-fat diet (HFD) consumption increases the risk for depression, but the neurophysiological mechanisms involved remain to be elucidated. Here, we demonstrated that HFD feeding of C57BL/6J mice during the adolescent period (from 4 to 8 weeks of age) resulted in increased depression- and anxiety-like behaviors concurrent with changes in neuronal and myelin structure in the hippocampus. Additionally, we showed that hippocampal microglia in HFD-fed mice assumed a hyperactive state concomitant with increased PSD95-positive and myelin basic protein (MBP)-positive inclusions, implicating microglia in hippocampal structural alterations induced by HFD consumption. Along with increased levels of serum free fatty acids (FFAs), abnormal deposition of lipid droplets and increased levels of HIF-1α protein (a transcription factor that has been reported to facilitate cellular lipid accumulation) within hippocampal microglia were observed in HFD-fed mice. The use of minocycline, a pharmacological suppressor of microglial overactivation, effectively attenuated neurobehavioral abnormalities and hippocampal structural alterations but barely altered lipid droplet accumulation in the hippocampal microglia of HFD-fed mice. Coadministration of triacsin C abolished the increases in lipid droplet formation, phagocytic activity, and ROS levels in primary microglia treated with serum from HFD-fed mice. In conclusion, our studies demonstrate that the adverse influence of early-life HFD consumption on behavior and hippocampal structure is attributed at least in part to microglial overactivation that is accompanied by an elevated serum FFA concentration and microglial aberrations represent a potential preventive and therapeutic target for HFD-related emotional disorders.

Adult mice with noise-induced hearing loss exhibited temporal ordering memory deficits accompanied by microglia-associated neuroplastic changes in the medial prefrontal cortex.

Acquired peripheral hearing loss in midlife is considered the primary modifiable risk factor for dementia, while the underlying pathological mechanism remains poorly understood. Excessive noise exposure is the most common cause of acquired peripheral hearing loss in modern society. This study was designed to investigate the impact of noise-induced hearing loss (NIHL) on cognition, with a focus on the medial prefrontal cortex (mPFC), a brain region that is involved in both auditory and cognitive processes and is highly affected in patients with cognitive impairment. Adult C57BL/6 J mice were randomly assigned to a control group and seven noise groups: 0HPN, 12HPN, 1DPN, 3DPN, 7DPN, 14DPN, and 28DPN, which were exposed to broadband noise at a 123 dB sound pressure level (SPL) for 2 h and sacrificed immediately (0 h), 12 h, or 1, 3, 7, 14, or 28 days post-noise exposure (HPN, DPN), respectively. Hearing assessment, behavioral tests, and neuromorphological studies in the mPFC were performed in control and 28DPN mice. All experimental animals were included in the time-course analysis of serum corticosterone (CORT) levels and mPFC microglial morphology. The results illustrated that noise exposure induced early-onset transient serum CORT elevation and permanent moderate-to-severe hearing loss in mice. 28DPN mice, in which permanent NIHL has been verified, exhibited impaired performance in temporal order object recognition tasks concomitant with reduced structural complexity of mPFC pyramidal neurons. The time-course immunohistochemical analysis in the mPFC revealed significantly higher morphological microglial activation at 14 and 28 DPN, preceded by a remarkably higher amount of microglial engulfed postsynaptic marker PSD95 at 7 DPN. Additionally, lipid accumulation in microglia was observed in 7DPN, 14DPN and 28DPN mice, suggesting a driving role of lipid handling deficits following excessive phagocytosis of synaptic elements in delayed and sustained microglial abnormalities. These findings provide fundamentally novel information concerning mPFC-related cognitive impairment in mice with NIHL and empirical evidence suggesting the involvement of microglial malfunction in the mPFC neurodegenerative consequences of NIHL.

Voluntary wheel exercise ameliorates cognitive impairment, hippocampal neurodegeneration and microglial abnormalities preceded by demyelination in a male mouse model of noise-induced hearing loss.

Acquired peripheral hearing loss (APHL) in midlife has been identified as the greatest modifiable risk factor for dementia; however, the pathophysiological neural mechanisms linking APHL with an increased risk of dementia remain to be elucidated. Here, in an adult male mouse model of noise-induced hearing loss (NIHL), one of the most common forms of APHL, we demonstrated accelerated age-related cognitive decline and hippocampal neurodegeneration during a 6-month follow-up period, accompanied by progressive hippocampal microglial aberrations preceded by immediate-onset transient elevation in serum glucocorticoids and delayed-onset sustained myelin disruption in the hippocampus. Pretreatment with the glucocorticoid receptor antagonist RU486 before stressful noise exposure partially mitigated the early activation of hippocampal microglia, which were present at 7 days post noise exposure (7DPN), but had no impact on later microglial aberrations, hippocampal neurodegeneration, or cognitive decline exhibited at 1 month post noise exposure (1MPN). One month of voluntary wheel exercise following noise exposure barely affected either the hearing threshold shift or hippocampal myelin changes but effectively countered cognitive impairment and the decline in hippocampal neurogenesis in NIHL mice at 1MPN, paralleled by the normalization of microglial morphology, which coincided with a reduction in microglial myelin inclusions and a restoration of microglial hypoxia-inducible factor-1α (HIF1α) expression. Our results indicated that accelerated cognitive deterioration and hippocampal neuroplastic decline following NIHL are most likely driven by the maladaptive response of hippocampal microglia to myelin damage secondary to hearing loss, and we also demonstrated the potential of voluntary physical exercise as a promising and cost-effective strategy to alleviate the detrimental impact of APHL on cognitive function and thus curtail the high and continuously increasing global burden of dementia. Furthermore, the findings of the present study highlight the contribution of myelin debris overload to microglial malfunction and identify the microglial HIF1α-related pathway as an attractive candidate for future comprehensive investigation to obtain a more definitive picture of the underlying mechanisms linking APHL and dementia.

Tunable Aggregation-induced Emission and Emission Colors of Imidazolium and Pyridinium Based Hydrazones.

Aggregation-induced emission (AIE) materials have drawn great attention for their wide applications as optical materials. The applications of AIE materials, however, are restricted by the complicated syntheses, hydrophobic properties and short emission wavelengths. Herein, an imidazolium based hydrazone (E)-1-(4-methoxyphenyl)-2-((1-methyl-1H-imidazol-2-yl)methylene)hydrazine hydrochloride (1) and a pyridinium based hydrazone (E)-1-(4-methoxyphenyl)-2-(pyridin-4-ylmethylene)hydrazine hydrochloride (2) have been synthesized. Notably, 1 and 2 in crystals show distinct green and near-infrared (NIR) fluorescence, with emission peaks at 530 and 688 nm, and Stokes shifts of 176 and 308 nm, respectively. After grinding the crystals to powder, the absolute fluorescence quantum yield (ΦF) of 1 is increased from 4.2% to 10.6%, and the ΦF of 2 is increased from 0.2% to 0.7%. X-ray crystallography studies together with theoretical calculations indicate that the enhanced emission of 1 arises from hydrogen bonding induced rigid network, and the fluorescence in the NIR region and large Stokes shift of 2 are attributed to its twisted molecular structure and strong push-pull effect.

Effects of Prolonged High-Fat Diet Consumption Starting at Different Ages on Behavioral Parameters and Hippocampal Neuroplasticity in Male Mice.

BACKGROUND: The overconsumption of a high-fat diet (HFD) has been repeatedly blamed as being a possible contributor to the global prevalence of emotional problems in modern society. Our group recently demonstrated the deleterious effect of a chronic HFD throughout adulthood on both emotional behavior and neuroplasticity markers in mice. As a heightened preference for palatable HFDs from the time of the juvenile period (when the brain is particularly vulnerable to environmental insults) is universal among populations around the world, a comparison of the consequences of chronic HFDs starting from juveniles or adults will assist in obtaining better knowledge of the impact that chronic HFDs have on mental health, thus potentially leading to the discovery of more effective strategies for reducing the incidence of psychiatric disorders. METHODS: In the present study, male C57BL/6J mice with an initial age of 4 weeks (IA-4 W) or 8 weeks (IA-8 W) were separately assigned to two subgroups and fed either a control diet (CD, 10 kJ% from fat) or HFD (60 kJ% from fat) for 9 months followed by an analysis focused on metabolic, emotional behavioral, and neuroplastic profiles. RESULTS: The results illustrated that, in addition to abnormal glucolipid metabolism and insulin sensitivity, mice on a chronic HFD exhibited increased levels of anxiety and depression-like behaviors and aberrant hippocampal neuroplasticity. When compared with IA-8 W mice, several changes indicating systemic metabolic disturbance and neurobehavioral disorder after chronic HFD consumption were aggravated in IA-4 W mice, accompanied by exaggerated impairments in hippocampal insulin sensitivity and neurogenesis. CONCLUSIONS: These results not only provide in vivo evidence that the juvenile stage is a critical period of vulnerability to detrimental effects of HFD consumption on metabolic and neuronal function but also suggest dampened hippocampal insulin signaling as a potential link between prolonged HFD consumption and negative neurobehavioral outcomes. Considering the substantial burden posed by psychiatric disorders and the high prevalence of HFD among youth, these observations are meaningful for raising awareness of the harmful effects of excessive dietary fat intake and developing strategy for preventing mental disorders.

Recent progress on the construction and application of dithienylethene-based photochromic AIEgens.

Photochromic fluorescent materials have rapidly developed as a new class of intelligent materials, offering a unique combination of traditional photochromic and organic fluorescent materials. These materials possess remarkable photoresponsiveness that can be observed by the naked eye and exhibit fluorescence color change. Consequently, they have found widespread applications in various domains, including molecular switches, logic encryption, medical diagnosis and treatment, and biosensors. Among the multitude of photochromic systems, those based on dithienylethenes (DTEs) have garnered significant attention due to their exceptional photochromic efficiency, commendable reversible photoresponse and fatigue resistance, as well as excellent photostability and thermal stability. Nevertheless, these photochromic fluorescent materials continue to grapple with the issue of aggregation-caused quenching (ACQ), a common problem faced by traditional fluorescent materials. Therefore, the integration of DTE systems with aggregation-induced emission (AIE) systems presents a promising solution to tackle this predicament, enabling an improved quantum yield for photochromic fluorescent materials in their aggregated state and broadening their range of applications. This review comprehensively summarizes and evaluates the construction strategies and application prospects of DTE-based photochromic AIE luminogens (AIEgens) in recent years, while also providing an outlook on their future development.

High-Fat Diet Consumption Induces Neurobehavioral Abnormalities and Neuronal Morphological Alterations Accompanied by Excessive Microglial Activation in the Medial Prefrontal Cortex in Adolescent Mice.

The association between a high-fat diet (HFD) consumption and emotional/cognitive disorders is widely documented. One distinctive feature of the prefrontal cortex (PFC), a kernel emotion- and cognition-related brain region, is its protracted adolescent maturation, which makes it highly vulnerable to the detrimental effects of environmental factors during adolescence. Disruption of the PFC structure and function is linked to emotional/cognitive disorders, especially those that emerge in late adolescence. A HFD consumption is common among adolescents, yet its potential effects on PFC-related neurobehavior in late adolescence and any related underlying mechanisms are yet to be established. In the present study, adolescent (postnatal days 28-56) male C57BL/6J mice were fed a control diet (CD) or a HFD and underwent behavioral tests in addition to Golgi staining and immunofluorescence targeting of the medial PFC (mPFC). The HFD-fed adolescent mice exhibited anxiety- and depression-like behavior and abnormal mPFC pyramidal neuronal morphology accompanied by alterations in microglial morphology indicative of a heightened state of activation and increased microglial PSD95+ inclusions signifying excessive phagocytosis of the synaptic material in the mPFC. These findings offer novel insights into the neurobehavioral effects due to adolescent HFD consumption and suggest a contributing role in microglial dysfunction and prefrontal neuroplasticity deficits for HFD-associated mood disorders in adolescents.

Reversible Near-Infrared Fluorescent Probe for Rapid Sensing Sulfur Dioxide and Formaldehyde: Recognition and Photoactivation Mechanism and Applications in Bioimaging and Encryption Ink.

A novel near-infrared (NIR) fluorescent Probe 1 was successfully developed for the reversible detection of sulfur dioxide derivatives and formaldehyde. The purple solution of Probe 1 faded to colorless in 1.8 s with the addition of HSO3-. Meanwhile, its fluorescence signal disappeared instantaneously with a 39 nM detection limit. The probe exhibited excellent selectivity toward HSO3- over other potential interfering agents. Then, its absorption and fluorescence bands were able to effectively recover in response to formaldehyde. Remarkably, this reverse process was able to accelerate 84 times under UV light in 122 s and achieved a recovery rate of 98% by UV light, the photoactivation mechanism was fully determined by HRMS and theoretical calculation. Furthermore, we demonstrated that Probe 1 was successfully applied for the detection of sulfur dioxide derivatives and formaldehyde in living cells and data encryption.

Long-term high-fat diet consumption by mice throughout adulthood induces neurobehavioral alterations and hippocampal neuronal remodeling accompanied by augmented microglial lipid accumulation.

High-fat diet (HFD) consumption is generally associated with an increased risk of cognitive and emotional dysfunctions that constitute a sizeable worldwide health burden with profound social and economic consequences. Middle age is a critical time period that affects one's health later in life; pertinently, the prevalence of HFD consumption is increasing among mature adults. Given the growing health-related economic burden imposed globally by increasing rates of noncommunicable diseases in rapidly aging populations, along with the pervasive but insidious health impairments associated with HFD consumption, it is critically important to understand the effects of long-term HFD consumption on brain function and to gain insights into their potential underlying mechanisms. In the present study, adult male C57BL/6J mice were randomly assigned a control diet (CD, 10 kJ% from fat) or an HFD (60 kJ% from fat) for 6 months (6 M) or 9 months (9 M) followed by behavioral tests, serum biochemical analysis, and histological examinations of both the dorsal and ventral regions of the hippocampus. In both the 6 M and 9 M cohorts, mice that consumed an HFD exhibited poorer memory performance in the Morris water maze test (MWM) and greater depression- and anxiety-like behavior during the open field test (OFT), sucrose preference test (SPT) and forced swim test (FST) than control mice. Compared with age-matched mice in the CD group, mice in the HFD group showed abnormal hippocampal neuronal morphology, which was particularly evident in the ventral hippocampus. Hippocampal microglia in mice in the HFD group generally had a more activated phenotype evidenced by a smaller microglial territory area and increased cluster of differentiation 68 (CD68, a marker of phagocytic activity) immunoreactivity, while the microglial density in the dentate gyrus (DG) was decreased, indicating microglial decline. The engulfment of postsynaptic density 95 (PSD95, a general postsynaptic marker) puncta by microglia was increased in the HFD groups. Histological analysis of neutral lipids using a fluorescent probe (BODIPY) revealed that the total neutral lipid content in regions of interests (ROIs) and the lipid load in microglia were increased in the HFD group relative to the age-matched CD group. In summary, our results demonstrated that chronic HFD consumption from young adulthood to middle age induced anxiety- and depression-like behavior as well as memory impairment. The negative influence of chronic HFD consumption on behavioral and hippocampal neuroplasticity appears to be linked to a change in microglial phenotype that is accompanied by a remarkable increase in cellular lipid accumulation. These observations highlighting the potential to target lipid metabolism deficits to reduce the risk of HFD-associated emotional dysfunctions.

METTL3 is a key regulator of milk synthesis in mammary epithelial cells.

The enzyme m6 A methyltransferase-like 3 (METTL3) catalyzes N6 -methyladenosine (m6 A) modification in eukaryotic messenger RNAs (mRNAs). However, the physiological function and molecular mechanism of METTL3 in mammalian cells have not been fully understood. Here we showed that METTL3 was highly expressed in mouse mammary gland of the lactation period. METTL3 was located in the nucleus of bovine mammary epithelial cells (MECs), and methionine (Met) and ß-estrodial (E2) upregulated METTL3 protein level. METTL3 knockdown decreased milk protein and fat synthesis, whereas its overexpression had the opposite effects. METTL3 overexpression stimulated mRNA expression and protein phosphorylation of the mechanistic target of rapamycin (mTOR) and mRNA and protein expression of sterol regulatory element binding protein 1 (SREBP1), whereas METTL3 knockdown blocked the stimulatory effects of Met and E2 on these processes. Furthermore, METTL3 overexpression led to increased mRNA m6 A methylation of mTOR and SREBP1, whereas METTL3 knockdown suppressed the stimulatory effects of Met and E2 on these processes. The interaction between METTL3 and glycyl-tRNA synthetase (GlyRS) was confirmed by Co-immunoprecipitation and fluorescence resonance energy transfer approaches, and colocalization observation further showed that Met and E2 treatment increased this interaction. GlyRS knockdown abolished METTL3 protein levels upregulated by Met and E2, and METTL3 knockdown markedly decreased the effects of GlyRS overexpression on mTOR expression and phosphorylation and SREBP1 expression. In summary, we demonstrate that METTL3 is a key positive regulator of Met and E2-stimulated and GlyRS-mediated mTOR and SREBP1 signaling pathways and milk protein and fat synthesis in mammary epithelial cells.

Preparative chromatography behavior of palmitoleic acid on octadecyl stationary phases with different densities.

The availability of various high-purity unsaturated fatty acids has a wide range of needs due to their different activities. The nonlinear preparative chromatography behavior and principle for purification of palmitoleic acid with octadecyl bonded stationary phases were studied. The peak broadening and the concentration distribution of the target compounds were used to compare different C18 stationary phases. In preparative liquid chromatography, the C18 stationary phases with low, medium, and high bonding density showed different peak broadening and concentration distribution results. Medium bonding density C18 was suitable for the purification of ethyl palmitoleic acid. The forward broadening was much greater than the backward broadening on medium bonding density C18 column. And the highest concentration distribution of impurities and the main peak was not crossed in this column. Due to the low content of crude ethyl palmitoleic acid sample, a two-step purified method yields an oily product with purity of 96.57% in the GC method. This method would be universal and extensible for constructing purification method for other unsaturated fatty acids.

High-Fat Diet Consumption in Adolescence Induces Emotional Behavior Alterations and Hippocampal Neurogenesis Deficits Accompanied by Excessive Microglial Activation.

Adolescence is a developmental epoch characterized by massive neural circuit remodeling; thus, the brain is particularly vulnerable to environmental influences during this period. Excessive high-fat diet (HFD) consumption, which is very common among adolescents, has long been recognized as a potent risk factor for multiple mood disorders, including depression and anxiety. However, the precise mechanisms underlying the influences of HFD consumption in adolescence on emotional health are far from clear. In the present study, C57BL/6 mice were fed a control diet (CD) or HFD for about 4 weeks from postnatal day (P) 28 to P60, spanning most of the adolescence period, and then subjected to behavioral assessments and histological examinations. HFD mice exhibited elevated levels of depression and anxiety, decreased hippocampal neurogenesis, and excessive microglial activation in the ventral hippocampus. Furthermore, in HFD-fed mice, microglia showed increased DCX+ inclusions, suggesting aberrant microglial engulfment of newborn neurons in HFD-fed adolescents. To our knowledge, this is the first observation suggesting that the negative effects of HFD consumption in adolescence on emotion and neuroplasticity may be attributed at least in part to aberrant microglial engulfment of nascent neurons, extending our understanding of the mechanism underlying HFD-related affective disorders in young people.

Membrane-Bound EMC10 Is Required for Sperm Motility via Maintaining the Homeostasis of Cytoplasm Sodium in Sperm.

Endoplasmic reticulum membrane protein complex subunit 10 (EMC10) is an evolutionarily conserved and multifunctional factor across species. We previously reported that Emc10 knockout (KO) leads to mouse male infertility. Emc10-null spermatozoa exhibit multiple aspects of dysfunction, including reduced sperm motility. Two subunits of a Na/K-ATPase, ATP1A4 and ATP1B3, are nearly absent in Emc10 KO spermatozoa. Here, two isoforms of EMC10 were characterized in the mouse testis and epididymis: the membrane-bound (mEMC10) and secreted (scEMC10) isoforms. We present evidence that mEMC10, rather than scEMC10, is required for cytoplasm sodium homeostasis by positively regulating ATP1B3 expression in germ cells. Intra-testis mEMC10 overexpression rescued the sperm motility defect caused by Emc10 KO, while exogenous recombinant scEMC10 protein could not improve the motility of spermatozoa from either Emc10 KO mouse or asthenospermic subjects. Clinically, there is a positive association between ATP1B3 and EMC10 protein levels in human spermatozoa, whereas no correlation was proven between seminal plasma scEMC10 levels and sperm motility. These results highlight the important role of the membrane-bound EMC10 isoform in maintaining cytoplasm sodium homeostasis and sperm motility. Based on the present results, the mEMC10-Na, K/ATPase α4ß3 axis is proposed as a novel mechanism underlying the regulation of cytoplasmic sodium and sperm motility, and its components seem to have therapeutic potential for asthenospermia.

Effects of Vallisneria natans on H2S and S2- releases in black-odorous waterbody under additional nitrate: Comprehensive performance and microbial community structure.

Releases of hydrogen sulphide (H2S) and sulphur ions (S2-) through sulphate reduction in black-odorous waterbody is a great environmental health concern. Aquatic planting for blackening and odour controls has received great attention in research and practice. Nitrate concentration in black-odorous waterbody can vary significantly but little is known about the responses of aquatic plants on H2S and S2- releases under different nitrate levels. This controlled laboratory study explored the changes of H2S and S2- releases in simulated black-odorous waterbody planted with Vallisneria natans and artificial plants (control). V. natans growth was stimulated by additional nitrate (6.6 mg/L NO3--N), resulting in an increase of dissolved oxygen (DO) and pH in overlying water and an 11.0% decrease in removal efficiency of chemical oxygen demand (COD). At relatively low nitrate level (i.e., 2.0 mg/L NO3--N in the absence of additional nitrate), V. natans after the 48th day inhibited H2S and S2- releases by 81.5% and 66.8%, respectively, and their inhibition efficiencies were improved to 95.7% and 98.8% by the presence of additional nitrate. Additional nitrate reduced the relative abundance of sulphate-reducing bacteria (SRB) in the sediments while increased the relative abundance of sulphur-oxidizing bacteria (SOB) and nitrate-reducing sulphur-oxidizing bacteria (NR-SOB) in the leaf biofilms of V. natans and artificial plants. Genus compositions in leaf biofilms showed host specificity. Pearson correlation analysis showed that DO, pH, and nitrate concentration had a positive correlation with the relative abundance of SOB (Aeromonas) and NR-SOB (Hydrogenophaga), while were negatively correlated with the relative abundance of SRB (MSBL7). These results indicated that V. natans under additional nitrate altered microbial community to be unfavourable for H2S and S2- releases. This study clarified the inhibition of H2S and S2- releases by aquatic planting under additional nitrate and provided theoretical basis for improving black-odorous waterbody restoration technology.

Multi-Stimuli-Induced Mechanical Bending and Reversible Fluorescence Switching in a Single Organic Crystal.

Fluorescent single crystals that respond to multiple external stimuli are of great interest in molecular machines, sensors, and displays. The integration of photo- or acid-induced fluorescence enhancement and bending in one organic crystal, however, has not been reported yet. Herein, we report the interesting plastic photomechanical bending and switching on of the fluorescence of an azine crystal in a single-crystal transformation, due to extended π-conjugation and molecular slippage. Moreover, the fluorescent plastic bending driven by multiple volatile acid vapors was firstly observed, and attributed to the synergistic effect of push-pull electronic structure and hydrogen bonding. The single crystal also shows high elasticity under external force. In addition, reversible fluorescence switching can be triggered by grinding and solvent fuming, as well as by the adsorption and desorption of HCl vapor. The integration of plastic, elastic bending and switch-on fluorescence into one single crystal provides a new strategy for next-generation smart materials.

How Do Molecular Motions Affect Structures and Properties at Molecule and Aggregate Levels?

Molecular motions are essential natures of matter and play important roles in their structures and properties. However, owing to the diversity and complexity of structures and behaviors, the study of motion-structure-property relationships remains a challenge, especially at all levels of structural hierarchy from molecules to macro-objects. Herein, luminogens showing aggregation-induced emission (AIE), namely, 9-(pyrimidin-2-yl)-carbazole (PyCz) and 9-(5-R-pyrimidin-2-yl)-carbazole [R = Cl (ClPyCz), Br (BrPyCz), and CN (CyPyCz)], were designed and synthesized, to decipher the dependence of materials' structures and properties on molecular motions at the molecule and aggregate levels. Experimental and theoretical analysis demonstrated that the active intramolecular motions in the excited state of all molecules at the single-molecule level endowed them with more twisted structural conformations and weak emission. However, owing to the restriction of intramolecular motions in the nano/macroaggregate state, all the molecules assumed less twisted conformations with bright emission. Unexpectedly, intermolecular motions could be activated in the macrocrystals of ClPyCz, BrPyCz, and CyPyCz through the introduction of external perturbations, and synergic strong and weak intermolecular interactions allowed their crystals to undergo reversible deformation, which effectively solved the problem of the brittleness of organic crystals, while endowing them with excellent elastic performance. Thus, the present study provided insights on the motion-structure-property relationship at each level of structural hierarchy and offered a paradigm to rationally design multifunctional AIE-based materials.

Long noncoding RNA LINC00982 upregulates CTSF expression to inhibit gastric cancer progression via the transcription factor HEY1.

Upregulating the expression of long noncoding RNA LINC00982 controlled cell proliferation in gastric cancer, but the regulatory molecular mechanisms are yet to be expounded. We here aimed to elaborate how LINC00982 regulated the malignancy of gastric cancer cells. RT-qPCR and Western blot analysis were used to detect the expression of LINC00982 and cathepsin F (CTSF) in gastric cancer tissues and cells. Modulatory effect of LINC00982 on gastric cancer cells was assessed by CCK-8, colony formation, Transwell migration, and invasion assays. The relationship between LINC00982, YRPW motif 1 (HEY1), and CTSF was examined by RNA-binding protein immunoprecipitation, luciferase assay, and chromatin immunoprecipitation, and their interaction in the regulation of gastric cancer cellular functions was analyzed by performing gain-of-function and rescue assays. The nude mouse model of tumor formation was developed to examine the effects of LINC00982 on tumorigenesis. LINC00982 was lowly expressed in gastric cancer tissues, whereas its overexpression impaired the proliferative, migratory, and invasive properties of gastric cancer cells. Furthermore, LINC00982 could bind to transcription factor HEY1 and inhibited its expression. Through blocking the binding of HEY1 to CTSF promoter, LINC00982 promoted the expression of CTSF. Overexpression of HEY1 or inhibition of CTSF could reverse the antitumor effects of LINC00982 on gastric cancer, which were further demonstrated in vivo. All these taken together, LINC00982 acted as a tumor suppressor in gastric cancer, which is therefore suggested to be a potential antitumor target for gastric cancer.NEW & NOTEWORTHY We identified LINC00982 as a promising antitumor target for the treatment of patients with gastric cancer. We also determined a regulatory network involved in the pathophysiology of gastric cancer wherein LINC00982 could bind to HEY1 to impair its binding to cathepsin F (CTSF) promoter and hence promote CTSF expression, which aids in better understanding of molecular mechanisms related to gastric tumorigenesis.