Porous ultrathin 2D catalysts are attracting great attention in the field of electro/photocatalytic hydrogen evolution reaction (HER) and overall water splitting. Herein, a universal pH‐controlled ...wet‐chemical strategy is reported followed by thermal and phosphorization treatment to prepare large‐size, porous and ultrathin bimetallic phosphide (NiCoP) nanosheets, in which graphene oxide is adopted as a template to determine the size of products. The thickness of the resultant NiCoP nanosheets ranges from 3.5 to 12.8 nm via delicately adjusting pH from 7.8 to 8.5. The thickness‐dependent electrocatalytic performance is evidenced experimentally and explained by computational studies. The prepared large‐size ultrathin NiCoP nanosheets show excellent bifunctional electrocatalytic activity for overall water splitting, with low overpotentials of 34.3 mV for HER and 245.0 mV for oxygen evolution reaction, respectively, at 10 mA cm−2. Furthermore, the NiCoP nanosheets exhibit superior photocatalytic HER performance, achieving a high HER rate of 238.2 mmol h−1 g−1 in combination with commonly used photocatalyst CdS, which is far superior to that of Pt/CdS (81.7 mmol h−1 g−1). All these results demonstrate large‐size porous ultrathin NiCoP nanosheets as an efficient and multifunctional electro/photocatalyst for water splitting.
A facile pH‐controlled wet‐chemical strategy is developed followed by thermal and phosphorization treatment to prepare large‐size porous and ultrathin NiCoP nanosheets. Such NiCoP nanosheets are controlled to ≈3.5 nm in thickness via delicately adjusting pH to balance the nucleation and growth of metal ions, which exhibit excellent electro/photocatalytic performance for water splitting, outperforming noble‐metal catalysts in electro/photocatalytic OER and HER.
The prefrontal cortex (PFC) serves as the chief executive officer of the brain, controlling the highest level cognitive and emotional processes. Its local circuits among glutamatergic principal ...neurons and GABAergic interneurons, as well as its long-range connections with other brain regions, have been functionally linked to specific behaviors, ranging from working memory to reward seeking. The efficacy of synaptic signaling in the PFC network is profundedly influenced by monoaminergic inputs via the activation of dopamine, adrenergic, or serotonin receptors. Stress hormones and neuropeptides also exert complex effects on the synaptic structure and function of PFC neurons. Dysregulation of PFC synaptic transmission is strongly linked to social deficits, affective disturbance, and memory loss in brain disorders, including autism, schizophrenia, depression, and Alzheimer's disease. Critical neural circuits, biological pathways, and molecular players that go awry in these mental illnesses have been revealed by integrated electrophysiological, optogenetic, biochemical, and transcriptomic studies of PFC. Novel epigenetic mechanism-based strategies are proposed as potential avenues of therapeutic intervention for PFC-involved diseases. This review provides an overview of PFC network organization and synaptic modulation, as well as the mechanisms linking PFC dysfunction to the pathophysiology of neurodevelopmental, neuropsychiatric, and neurodegenerative diseases. Insights from the preclinical studies offer the potential for discovering new medical treatments for human patients with these brain disorders.
We report a monometallic dysprosium complex, Dy(OtBu)2(py)5BPh4 (5), that shows the largest effective energy barrier to magnetic relaxation of Ueff=1815(1) K. The massive magnetic anisotropy is due ...to bis‐trans‐disposed tert‐butoxide ligands with weak equatorial pyridine donors, approaching proposed schemes for high‐temperature single‐molecule magnets (SMMs). The blocking temperature, TB , is 14 K, defined by zero‐field‐cooled magnetization experiments, and is the largest for any monometallic complex and equal with the current record for Tb2N2{N(SiMe3)2}4(THF)2.
Record‐breaking: A monometallic dysprosium complex, Dy(OtBu)2(py)5BPh4, displaying near‐perfect pentagonal bipyramid geometry defined by two strong axial tert‐butoxide ligands and five weak equatorial pyridine donors is reported. This complex displays massive magnetic anisotropy, approaching the limit of a two‐coordinate complex, with an energy barrier to magnetic relaxation of Ueff=1815(1) K and a blocking temperature of TB=14 K.
Rab GTPases control intracellular membrane traffic by recruiting specific effector proteins to restricted membranes in a GTP-dependent manner. In this Cell Science at a Glance and the accompanying ...poster, we highlight the regulation of Rab GTPases by proteins that control their membrane association and activation state, and provide an overview of the cellular processes that are regulated by Rab GTPases and their effectors, including protein sorting, vesicle motility and vesicle tethering. We also discuss the physiological importance of Rab GTPases and provide examples of diseases caused by their dysfunctions.
Since its emergence in December 2019, corona virus disease 2019 (COVID-19) has impacted several countries, affecting more than 90 thousand patients and making it a global public threat. The routes of ...transmission are direct contact, and droplet and possible aerosol transmissions. Due to the unique nature of dentistry, most dental procedures generate significant amounts of droplets and aerosols, posing potential risks of infection transmission. Understanding the significance of aerosol transmission and its implications in dentistry can facilitate the identification and correction of negligence in daily dental practice. In addition to the standard precautions, some special precautions that should be implemented during an outbreak have been raised in this review.
Copy number variations (CNVs) of the human 16p11.2 genetic locus are associated with a range of neurodevelopmental disorders, including autism spectrum disorder, intellectual disability, and ...epilepsy. In this review, we delineate genetic information and diverse phenotypes in individuals with 16p11.2 CNVs, and synthesize preclinical findings from transgenic mouse models of 16p11.2 CNVs. Mice with 16p11.2 deletions or duplications recapitulate many core behavioral phenotypes, including social and cognitive deficits, and exhibit altered synaptic function across various brain areas. Mechanisms of transcriptional dysregulation and cortical maldevelopment are reviewed, along with potential therapeutic intervention strategies.
16p11.2 deletions or duplications predispose individuals to neurodevelopmental diseases, including autism spectrum disorder, intellectual disability, epilepsy/seizures, dysmorphic features, congenital anomalies, macrocephaly, and microcephaly.16p11.2 CNV mouse models recapitulate many of the human behavioral phenotypes, with distinct representation of social and cognitive deficits.Various forms of synaptic dysfunction are observed across distributed brain areas in 16p11.2 CNV mouse models.Broad transcriptional dysregulation is found in 16p11.2 CNV mouse models and human carriers, extending far beyond genes within the 16p11.2 region.Several 16p11.2 genes, including Mapk3, Kctd13, Taok2, are highly involved in abnormal cortical development in 16p11.2 CNVs.Possible therapeutic intervention strategies include the restoration of excitation–inhibition balance and synaptic plasticity by targeting glutamate and GABA systems.
Sealing holes in cellular membranes Zhen, Yan; Radulovic, Maja; Vietri, Marina ...
The EMBO journal,
01 April 2021, Letnik:
40, Številka:
7
Journal Article
Recenzirano
Odprti dostop
The compartmentalization of eukaryotic cells, which is essential for their viability and functions, is ensured by single or double bilayer membranes that separate the cell from the exterior and form ...boundaries between the cell’s organelles and the cytosol. Nascent nuclear envelopes and autophagosomes, which both are enveloped by double membranes, need to be sealed during the late stage of their biogenesis. On the other hand, the integrity of cellular membranes such as the plasma membrane, lysosomes and the nuclear envelope can be compromised by pathogens, chemicals, radiation, inflammatory responses and mechanical stress. There are cellular programmes that restore membrane integrity after injury. Here, we review cellular mechanisms that have evolved to maintain membrane integrity during organelle biogenesis and after injury, including membrane scission mediated by the endosomal sorting complex required for transport (ESCRT), vesicle patching and endocytosis.
This review provides an overview of the cellular mechanisms that have evolved to maintain membrane integrity during organelle biogenesis and after injury in eukaryotic cells.
Among the multiple components of propolis, flavonoids contribute greatly to the antioxidant activities of propolis. Flavonoids mainly exist in the form of sugar-conjugated derivatives. Quercetin ...glycosides represent the predominant flavonoid fraction in propolis. In this work, density functional theory (DFT) calculations were applied to analyze the antioxidative properties of quercetin and its glucosides in the gas and in the liquid phase (ethanol, water). Three main antioxidant mechanisms, hydrogen atom transfer (HAT), single electron transfer followed by proton transfer (SET-PT) and sequential proton loss electron transfer (SPLET) were used to analyze the antioxidative capacity of the investigated compounds. Solvent effects dominantly affect SET-PT and SPLET. Thus, the thermodynamically preferred mechanism can be altered. HAT and SPLET are the thermodynamically dominant mechanisms in gas and solvent phases, respectively. Therefore, in the gas phase, the sequence of the antioxidative capacity is similar with the bond dissociation enthalpy values: quercetin > quercetin-5-O-glucoside > quercetin-7-O-glucoside > quercetin-3-O-glucoside > quercetin-3'-O-glucoside > quercetin-4'-O-glucoside. While, in the solvent phases, the sequence is similar with the proton affinity values: quercetin-4'-O-glucoside > quercetin-5-O-glucoside > quercetin > quercetin-3-O-glucoside > quercetin-7-O-glucoside > quercetin-3'-O-glucoside. OH groups in B-ring and C-ring contribute mainly to the antioxidative activities of quercetin and glucosides compared with A-ring.
Nonalcoholic fatty liver disease (NAFLD) is a prevalent and complex disease that confers a high risk of severe liver disorders. Despite such public and clinical health importance, very few effective ...therapies are currently available for NAFLD. We report a protective function and the underlying mechanism of dual‐specificity phosphatase 14 (DUSP14) in NAFLD and related metabolic disorders. Insulin resistance, hepatic lipid accumulation, and concomitant inflammatory responses, key pathological processes involved in NAFLD development, were significantly ameliorated by hepatocyte‐specific DUSP14 overexpression (DUSP14‐HTG) in high‐fat diet (HFD)‐induced or genetically obese mouse models. By contrast, specific DUSP14 deficiency in hepatocytes (DUSP14‐HKO) aggravated these pathological alterations. We provided mechanistic evidence that DUSP14 directly binds to and dephosphorylates transforming growth factor β–activated kinase 1 (TAK1), resulting in the reduced activation of TAK1 and its downstream signaling molecules c‐Jun N‐terminal kinase 1 (JNK), p38, and nuclear factor kappa B NF‐κB. This effect was further evidenced by the finding that inhibiting TAK1 activity effectively attenuated the deterioration of glucolipid metabolic phenotype in DUSP14‐HKO mice challenged by HFD administration. Furthermore, we identified that both the binding domain and the phosphatase activity of DUSP14 are required for its protective role against hepatic steatosis, because interruption of the DUSP14‐TAK1 interaction abolished the mitigative effects of DUSP14. Conclusion: Hepatocyte DUSP14 is required for maintaining hepatic metabolic homeostasis and for suppressing inflammation, a novel function that relies on constraining TAK1 hyperactivation. (Hepatology 2018;67:1320‐1338).
Hepatic ischemia‐reperfusion (IR) injury is the leading cause of liver dysfunction and failure after liver resection or transplantation and lacks effective therapeutic strategies. Here, we applied a ...systematic proteomic analysis to identify the prominent contributors to IR‐induced liver damage and promising therapeutic targets for this condition. Based on an unbiased proteomic analysis, we found that toll‐interacting protein (Tollip) expression was closely correlated with the hepatic IR process. RNA sequencing analysis and phenotypic examination showed a dramatically alleviated hepatic IR injury by Tollip deficiency both in vivo and in hepatocytes. Mechanistically, Tollip interacts with apoptosis signal‐regulating kinase 1 (ASK1) and facilitates the recruitment of tumor necrosis factor receptor–associated factor 6 (TRAF6) to ASK1, leading to enhanced ASK1 N‐terminal dimerization and the subsequent activation of downstream mitogen‐activated protein kinase (MAPK) signaling. Furthermore, the Tollip methionine and phenylalanine motif and TRAF6 ubiquitinating activity are required for Tollip‐regulated ASK1–MAPK axis activation. Conclusion: Tollip is a regulator of hepatic IR injury by facilitating ASK1 N‐terminal dimerization and the resultant c‐Jun N‐terminal kinase/p38 signaling activation. Inhibiting Tollip or its interaction with ASK1 might be promising therapeutic strategies for hepatic IR injury.
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