Advances in metabolic reprogramming of NK cells in the tumor microenvironment on the impact of NK therapy.

Natural killer (NK) cells are unique from other immune cells in that they can rapidly kill multiple neighboring cells without the need for antigenic pre-sensitization once the cells display surface markers associated with oncogenic transformation. Given the dynamic role of NK cells in tumor surveillance, NK cell-based immunotherapy is rapidly becoming a "new force" in tumor immunotherapy. However, challenges remain in the use of NK cell immunotherapy in the treatment of solid tumors. Many metabolic features of the tumor microenvironment (TME) of solid tumors, including oxygen and nutrient (e.g., glucose, amino acids) deprivation, accumulation of specific metabolites (e.g., lactate, adenosine), and limited availability of signaling molecules that allow for metabolic reorganization, multifactorial shaping of the immune-suppressing TME impairs tumor-infiltrating NK cell function. This becomes a key barrier limiting the success of NK cell immunotherapy in solid tumors. Restoration of endogenous NK cells in the TME or overt transfer of functionally improved NK cells holds great promise in cancer therapy. In this paper, we summarize the metabolic biology of NK cells, discuss the effects of TME on NK cell metabolism and effector functions, and review emerging strategies for targeting metabolism-improved NK cell immunotherapy in the TME to circumvent these barriers to achieve superior efficacy of NK cell immunotherapy.

Antibiotic prophylaxis with piperacillin-tazobactam reduces organ/space surgical site infection after pancreaticoduodenectomy: a retrospective and propensity score-matched analysis.

BACKGROUND: The occurrence of surgical site infection (SSI) after pancreaticoduodenectomy (PD) is still relatively high. The aim of this retrospective study is to evaluate the efficacy of piperacillin-tazobactam as perioperative prophylactic antibiotic on organ/space SSI for patients underwent PD. METHODS: Four hundred seven consecutive patients who underwent PD between January 2018 and December 2022 were enrolled and analyzed retrospectively. The univariate and multivariate analysis were used to identify independent risk factors of organ/space SSI. Postoperative complications were compared between the two groups according to the use of prophylactic antibiotics by a ratio of 1:1 propensity score-matched (PSM) analysis. RESULTS: Based on perioperative prophylactic antibiotic use, all 407 patients were divided into the ceftriaxone group (n = 192, 47.2%) and piperacillin-tazobactam group (n = 215, 52.8%). The rate of organ/space SSI was 31.2% with the choice of perioperative antibiotics (OR = 2.837, 95%CI = 1.802-4.465, P < 0.01) as one of independent risk factors. After PSM, there were similar baseline characteristics among the groups. Meanwhile, the piperacillin-tazobactam group had a significant lower rate of organ/space SSI compared to the ceftriaxone group both before and after PSM(P < 0.05). CONCLUSIONS: The adoption of piperacillin-tazobactam as perioperative prophylaxis for patients underwent PD reduced organ/space SSI significantly.

An Edge Computing System with AMD Xilinx FPGA AI Customer Platform for Advanced Driver Assistance System.

The convergence of edge computing systems with Field-Programmable Gate Array (FPGA) technology has shown considerable promise in enhancing real-time applications across various domains. This paper presents an innovative edge computing system design specifically tailored for pavement defect detection within the Advanced Driver-Assistance Systems (ADASs) domain. The system seamlessly integrates the AMD Xilinx AI platform into a customized circuit configuration, capitalizing on its capabilities. Utilizing cameras as input sensors to capture road scenes, the system employs a Deep Learning Processing Unit (DPU) to execute the YOLOv3 model, enabling the identification of three distinct types of pavement defects with high accuracy and efficiency. Following defect detection, the system efficiently transmits detailed information about the type and location of detected defects via the Controller Area Network (CAN) interface. This integration of FPGA-based edge computing not only enhances the speed and accuracy of defect detection, but also facilitates real-time communication between the vehicle's onboard controller and external systems. Moreover, the successful integration of the proposed system transforms ADAS into a sophisticated edge computing device, empowering the vehicle's onboard controller to make informed decisions in real time. These decisions are aimed at enhancing the overall driving experience by improving safety and performance metrics. The synergy between edge computing and FPGA technology not only advances ADAS capabilities, but also paves the way for future innovations in automotive safety and assistance systems.

A Distinct Metabolically Defined Central Nucleus Circuit Bidirectionally Controls Anxiety-Related Behaviors.

Anxiety disorders are debilitating psychiatric diseases that affect ∼16% of the world's population. Although it has been proposed that the central nucleus of the amygdala (CeA) plays a role in anxiety, the molecular and circuit mechanisms through which CeA neurons modulate anxiety-related behaviors are largely uncharacterized. Soluble epoxide hydrolase (sEH) is a key enzyme in the metabolism of polyunsaturated fatty acids (PUFAs), and has been shown to play a role in psychiatric disorders. Here, we reported that sEH was enriched in neurons in the CeA and regulated anxiety-related behaviors in adult male mice. Deletion of sEH in CeA neurons but not astrocytes induced anxiety-like behaviors. Mechanistic studies indicated that sEH was required for maintaining the the excitability of sEH positive neurons (sEHCeA neurons) in the CeA. Using chemogenetic manipulations, we found that sEHCeA neurons bidirectionally regulated anxiety-related behaviors. Notably, we identified that sEHCeA neurons directly projected to the bed nucleus of the stria terminalis (BNST; sEHCeA-BNST). Optogenetic activation and inhibition of the sEHCeA-BNST pathway produced anxiolytic and anxiogenic effects, respectively. In summary, our studies reveal a set of molecular and circuit mechanisms of sEHCeA neurons underlying anxiety.SIGNIFICANCE STATEMENT Soluble epoxide hydrolase (sEH), a key enzyme that catalyzes the degradation of EETs, is shown to play a key role in mood disorders. It is well known that sEH is mostly localized in astrocytes in the prefrontal cortex and regulates depressive-like behaviors. Notably, sEH is also expressed in central nucleus of the amygdala (CeA) neurons. While the CeA has been studied for its role in the regulation of anxiety, the molecular and circuit mechanism is quite complex. In the present study, we explored a previously unknown cellular and circuitry mechanism that guides sEHCeA neurons response to anxiety. Our findings reveal a critical role of sEH in the CeA, sEHCeA neurons and CeA-bed nucleus of the stria terminalis (BNST) pathway in regulation of anxiety-related behaviors.

Analysis of T-cell receptor repertoire in peripheral blood of patients with pancreatic cancer and other pancreatic diseases.

Pancreatic cancer (PC) has been the fourth cancer-related death worldwide, diagnosed at an unresectable stage due to its rapid progression and few symptoms of this disease at early stages. The aim of this study was to determine the association between the diversity of T-cell receptor (TCR) repertoire and clinicopathological characteristics of patients with PC and other benign pancreatic diseases. In order to make a comprehensive analysis the TCR repertoire, high-throughput sequencing was used to differentiate complementarity determining region 3 (CDR3) of the TCR ß chain in peripheral blood samples from 3 PC, 3 chronic pancreatitis, 3 pancreatic cystic lesions and 3 pancreatic neuroendocrine tumour patients. We found that there were significant differences related to TCR repertoire between PC and other pancreatic diseases, and PC is a relatively immunosuppressive tumour. Changes of peripheral TCR repertoire may be used to predict the progression of PC and the response to immunotherapy. And there may exist novel-specific antigens in PC patients which could be used to design targeting immunotherapy in the nearly future.

An Astroglial Basis of Major Depressive Disorder: Molecular, Cellular, and Circuit Features.

Major depressive disorder is a common psychiatric disorder and a leading cause of disability worldwide. Astrocytes play a role in the maintenance of the function of the central nervous system, both physiologically and pathologically. Accumulated evidence indicates that the astrocyte is an important contributor to the pathophysiology of major depressive disorder including blood-brain barrier integrity, gap junctions, gliotransmission, glutamate homeostasis, and energy metabolism. Here, we comprehensively summarize an astroglial basis for major depressive disorder based on molecular, cellular, and circuit properties, suggesting that astrocytes appear to be highly sensitive to stress and are likely to be uniquely positioned to integrate peripheral and central stress responses.

Research progress on the role of tumor­associated macrophages in tumor development and their use as molecular targets (Review).

The tumor microenvironment (TME) is a complex system composed mainly of tumor cells, mesenchymal cells and immune cells. Macrophages, also known as tumor­associated macrophages (TAMs), among innate immune cells, are some of the most abundant components of the TME. They may influence tumor growth and metastasis through interactions with other cell populations in the TME and have been associated with poor prognosis in a variety of tumors. Therefore, a better understanding of the role of TAMs in the TME may provide new insight into tumor therapy. In the present review, the origin and classification of TAMs in the TME were outlined and their polarization and dual effects on tumor cells, as well as emerging strategies for cancer therapies targeting TAMs, were discussed.

Lysosomal TFEB-TRPML1 Axis in Astrocytes Modulates Depressive-like Behaviors.

Lysosomes are important cellular structures for human health as centers for recycling, signaling, metabolism and stress adaptation. However, the potential role of lysosomes in stress-related emotions has long been overlooked. Here, it is found that lysosomal morphology in astrocytes is altered in the medial prefrontal cortex (mPFC) of susceptible mice after chronic social defeat stress. A screen of lysosome-related genes revealed that the expression of the mucolipin 1 gene (Mcoln1; protein: mucolipin TRP channel 1) is decreased in susceptible mice and depressed patients. Astrocyte-specific knockout of mucolipin TRP channel 1 (TRPML1) induced depressive-like behaviors by inhibiting lysosomal exocytosis-mediated adenosine 5'-triphosphate (ATP) release. Furthermore, this stress response of astrocytic lysosomes is mediated by the transcription factor EB (TFEB), and overexpression of TRPML1 rescued depressive-like behaviors induced by astrocyte-specific knockout of TFEB. Collectively, these findings reveal a lysosomal stress-sensing signaling pathway contributing to the development of depression and identify the lysosome as a potential target organelle for antidepressants.

Astrocytic ALKBH5 in stress response contributes to depressive-like behaviors in mice.

Epigenetic mechanisms bridge genetic and environmental factors that contribute to the pathogenesis of major depression disorder (MDD). However, the cellular specificity and sensitivity of environmental stress on brain epitranscriptomics and its impact on depression remain unclear. Here, we found that ALKBH5, an RNA demethylase of N6-methyladenosine (m6A), was increased in MDD patients' blood and depression models. ALKBH5 in astrocytes was more sensitive to stress than that in neurons and endothelial cells. Selective deletion of ALKBH5 in astrocytes, but not in neurons and endothelial cells, produced antidepressant-like behaviors. Astrocytic ALKBH5 in the mPFC regulated depression-related behaviors bidirectionally. Meanwhile, ALKBH5 modulated glutamate transporter-1 (GLT-1) m6A modification and increased the expression of GLT-1 in astrocytes. ALKBH5 astrocyte-specific knockout preserved stress-induced disruption of glutamatergic synaptic transmission, neuronal atrophy and defective Ca2+ activity. Moreover, enhanced m6A modification with S-adenosylmethionine (SAMe) produced antidepressant-like effects. Our findings indicate that astrocytic epitranscriptomics contribute to depressive-like behaviors and that astrocytic ALKBH5 may be a therapeutic target for depression.

Plastic damage induced fracture behaviors of dental ceramic layer structures subjected to monotonic load.

PURPOSE: The aim of this study was to compare failure modes and fracture strength of ceramic structures using a combination of experimental and numerical methods. MATERIALS AND METHODS: Twelve specimens with flat layer structures were fabricated from two types of ceramic systems (IPS e.max ceram/e.max press-CP and Vita VM9/Lava zirconia-VZ) and subjected to monotonic load to fracture with a tungsten carbide sphere. Digital image correlation (DIC) and fractography technology were used to analyze fracture behaviors of specimens. Numerical simulation was also applied to analyze the stress distribution in these two types of dental ceramics. RESULTS: Quasi-plastic damage occurred beneath the indenter in porcelain in all cases. In general, the fracture strength of VZ specimens was greater than that of CP specimens. The crack initiation loads of VZ and CP were determined as 958 ± 50 N and 724 ± 36 N, respectively. Cracks were induced by plastic damage and were subsequently driven by tensile stress at the elastic/plastic boundary and extended downward toward to the veneer/core interface from the observation of DIC at the specimen surface. Cracks penetrated into e.max press core, which led to a serious bulk fracture in CP crowns, while in VZ specimens, cracks were deflected and extended along the porcelain/zirconia core interface without penetration into the zirconia core. The rupture loads for VZ and CP ceramics were determined as 1150 ± 170 N and 857 ± 66 N, respectively. CONCLUSIONS: Quasi-plastic deformation (damage) is responsible for crack initiation within porcelain in both types of crowns. Due to the intrinsic mechanical properties, the fracture behaviors of these two types of ceramics are different. The zirconia core with high strength and high elastic modulus has better resistance to fracture than the e.max core.

O-GlcNAc transferase in astrocytes modulates depression-related stress susceptibility through glutamatergic synaptic transmission.

Major depressive disorder is a common and devastating psychiatric disease, and the prevalence and burden are substantially increasing worldwide. Multiple studies of depression patients have implicated glucose metabolic dysfunction in the pathophysiology of depression. However, the molecular mechanisms by which glucose and related metabolic pathways modulate depressive-like behaviors are largely uncharacterized. Uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) is a glucose metabolite with pivotal functions as a donor molecule for O-GlcNAcylation. O-GlcNAc transferase (OGT), a key enzyme in protein O-GlcNAcylation, catalyzes protein posttranslational modification by O-GlcNAc and acts as a stress sensor. Here, we show that Ogt mRNA was increased in depression patients and that astroglial OGT expression was specifically upregulated in the medial prefrontal cortex (mPFC) of susceptible mice after chronic social-defeat stress. The selective deletion of astrocytic OGT resulted in antidepressant-like effects, and moreover, astrocytic OGT in the mPFC bidirectionally regulated vulnerability to social stress. Furthermore, OGT modulated glutamatergic synaptic transmission through O-GlcNAcylation of glutamate transporter-1 (GLT-1) in astrocytes. OGT astrocyte-specific knockout preserved the neuronal morphology atrophy and Ca2+ activity deficits caused by chronic stress and resulted in antidepressant effects. Our study reveals that astrocytic OGT in the mPFC regulates depressive-like behaviors through the O-GlcNAcylation of GLT-1 and could be a potential target for antidepressants.

The role of innate immune cells in the tumor microenvironment and research progress in anti-tumor therapy.

Innate immune cells in the tumor microenvironment (TME) mainly include macrophages, neutrophils, natural killer cells, dendritic cells and bone marrow derived suppressor cells. They play an anti-tumor or pro-tumor role by secreting various cytokines, chemokines and other factors, and determine the occurrence and development of tumors. Comprehending the role of innate immune cells in tumorigenesis and progression can help improve therapeutic approaches targeting innate immune cells in the TME, increasing the likelihood of favorable prognosis. In this review, we discussed the cell biology of innate immune cells, their role in tumorigenesis and development, and the current status of innate immune cell-based immunotherapy, in order to provide an overview for future research lines and clinical trials.

Folate receptor-positive circulating tumor cells predict survival and recurrence patterns in patients undergoing resection for pancreatic cancer.

Objective: To evaluate the prognostic impact of folate receptor (FR)-positive circulating tumor cells (FR+ CTCs) for patients with pancreatic cancer (PC). Background: Risk stratification before surgery for PC patients remains challenging as there are no reliable prognostic markers currently. FR+ CTCs, detected by ligand-targeted polymerase chain reaction (LT-PCR), have shown excellent diagnostic value for PC in our previous study and prognostic value in a variety of cancer types. Methods: Peripheral blood samples from 44 consecutive patients diagnosed with PC were analyzed for FR+ CTCs. 25 patients underwent tumor resection and were assigned to the surgical group. 19 patients failed to undergo radical resection because of local advance or distant metastasis and were assigned to the non-surgical group. The impact of CTCs on relapse and survival were explored. Results: For the prognostic stratification, the optimal cut-off value of CTCs analyzed by receiver operating characteristic (ROC) curve was 14.49 folate units (FU)/3 ml. High CTC levels (> 14.49 FU/3 ml) were detected in 52.0% (13/25) of the patients in the surgical group and 63.2% (12/19) in the non-surgical group. In the surgical group, median disease-free survival (DFS) for patients with high CTC levels versus low CTC levels (< 14.49 FU/3 ml) was 8.0 versus 26.0 months (P = 0.008). In multivariable analysis, CTCs were an independent risk factor for DFS (HR: 4.589, P = 0.012). Concerning the recurrence patterns, patients with high CTC levels showed a significantly frequent rate of distant and early recurrence (P = 0.017 and P = 0.011). CTC levels remained an independent predictor for both distant (OR: 8.375, P = 0.014) and early recurrence (OR: 8.412, P = 0.013) confirmed by multivariable logistic regression. However, CTCs did not predict survival in the non-surgical group (P = 0.220). Conclusion: FR+ CTCs in resected PC patients could predict impaired survival and recurrence patterns after surgery. Preoperative CTC levels detected by LT-PCR may help guide treatment strategies and further studies in a larger cohort are warranted.

P2X2 receptors in pyramidal neurons are critical for regulating vulnerability to chronic stress.

Rationale: Stress is a major risk factor for the development of depression. However, the underlying molecular mechanisms of stress vulnerability in depression are largely uncharacterized. Methods: P2X2 receptors (a major receptor for gliotransmitter-ATP) in the medial prefrontal cortex (mPFC) were identified by real-time qPCR, western blots and RNAscope in situ hybridization in chronic social defeat stress model (CSDS). We generated P2X2 conditional knockout mice and overexpressed AAV-P2X2 in CamkIIα-Cre mice. The depression-like behaviors were assessed via CSDS, subthreshold social defeat stress (SSDS), social interaction test (SI), forced interaction test (FIT), forced swimming test (FST), sucrose preference test (SPT), novel stressed feeding (NSF) and open field test (OFT). The neuronal activity and synapse function of P2X2 receptors in the mPFC were detected by in vivo fiber-photometry, patch-clamp techniques and neuronal morphometric analysis. Results: We identified that P2X2 receptors were increased in the mPFC of susceptible mice in CSDS. Conditional knockout of P2X2 receptors in pyramidal neurons promoted resilience of chronic stress-induced depressive-like behaviors, whereas pyramidal neurons - specific gain of P2X2 in the mPFC increased vulnerability to depressive-like behaviors. In vivo fiber-photometry, electrophysiology and neuronal morphometric analysis showed P2X2 receptors regulated neuronal activity and synapse function in the mPFC. Conclusions: Overall, our studies reveal a critical role of P2X2 in mediating vulnerability to chronic stress and identify P2X2 as a potential therapeutic target for treatment of stress-related mood disorders.

Characterization of the Estrogen Response Helps to Predict Prognosis and Identify Potential Therapeutic Targets in Cholangiocarcinoma.

Cholangiocarcinoma (CCA) is an aggressive malignancy originating from the epithelium of the bile duct. The prognosis of patients is poor regardless of radical resection and chemoradiotherapy. The current classification and prognostic model of CCA are unable to satisfy the requirements for predicting the clinical outcome and exploring therapeutic targets. Estrogen signaling is involved in diverse cancer types, and it has long been established that CCA could be regulated by estrogen. In our study, estrogen response was identified to be significantly and stably correlated with poor prognosis in CCA. Employing several algorithms, CCA was classified into ES cluster A and B. ES cluster B was mainly composed of patients with fluke infection and overlapped with CCA cluster 1/2, and ES cluster A was mainly composed of patients without fluke infection and overlapped with CCA cluster 3/4. COMT and HSD17B1 were identified to be responsible for the differential estrogen response between ES clusters A and B, and the estrogen response may be correlated with the differentiation and cancer stemness of CCA at the single-cell level. Complement activation and the expression of C3 and C5, which are mainly expressed by CCA cells, were significantly downregulated in ES cluster B. An estrogen response risk score (ESRS) model was constructed to predict the prognosis of CCA, followed by a nomogram integrating ESRS and clinical features. Finally, altered pathways, applicable drugs and sensitivity to chemical drugs were analyzed specific to the estrogen response. In summary, our results provide insights into the role of the estrogen response in CCA progression as well as applicable drugs and potential therapeutic targets in estrogen metabolism, the complement system and ESRS-related pathways.

Glucocorticoid Receptor-Dependent Astrocytes Mediate Stress Vulnerability.

BACKGROUND: Major depressive disorder is a devastating psychiatric illness that affects approximately 17% of the population worldwide. Astrocyte dysfunction has been implicated in its pathophysiology. Traumatic experiences and stress contribute to the onset of major depressive disorder, but how astrocytes respond to stress is poorly understood. METHODS: Using Western blotting analysis, we identified that stress vulnerability was associated with reduced astrocytic glucocorticoid receptor (GR) expression in mouse models of depression. We further investigated the functions of astrocytic GRs in regulating depression and the underlying mechanisms by using a combination of behavioral studies, fiber photometry, biochemical experiments, and RNA sequencing methods. RESULTS: GRs in astrocytes were more sensitive to stress than those in neurons. GR absence in astrocytes induced depressive-like behaviors, whereas restoring astrocytic GR expression in the medial prefrontal cortex prevented the depressive-like phenotype. Furthermore, we found that GRs in the medial prefrontal cortex affected astrocytic Ca2+ activity and dynamic ATP (adenosine 5'-triphosphate) release in response to stress. RNA sequencing of astrocytes isolated from GR deletion mice identified the PI3K-Akt (phosphoinositide 3-kinase-Akt) signaling pathway, which was required for astrocytic GR-mediated ATP release. CONCLUSIONS: These findings reveal that astrocytic GRs play an important role in stress response and that reduced astrocytic GR expression in the stressed subject decreases ATP release to mediate stress vulnerability.

The effects of adhesive type and thickness on stress distribution in molars restored with all-ceramic crowns.

PURPOSE: This study investigated the effects of luting cement type and thickness on the stress distribution within all-ceramic crowns using finite element analysis. MATERIALS AND METHODS: An all-ceramic crown restoration of the mandibular right first molar was prepared according to standard dental processes and scanned using micro-computed tomography. Eight 3D FE models were then developed that accounted for two adhesive systems, each with cement thickness of 60 µm, 90 µm, 120 µm, and 150 µm. The models were subjected to four loading conditions, and stresses in the veneer and core layers were evaluated. RESULTS: The stress distribution and maximum stresses in the veneer, core, and cement are presented in corresponding loading conditions. The cement with higher elastic modulus resulted in lower tensile stresses in the veneer and core layers, and the shear strength of the cement was critical to the intactness of the all-ceramic crown. CONCLUSION: The cement thickness acts as a cushion between the crown and dentin substrate. Although there is an optimal thickness (approximately 90 µm) that can reduce the stress level in ceramic crowns, cement thickness is not very important to stresses in the core or veneer in most cases when compared to the influence of loading conditions or cement moduli.

Proteomic Profiling of Astrocytic O-GlcNAc Transferase-Related Proteins in the Medial Prefrontal Cortex.

The medial prefrontal cortex (mPFC), a key part of the brain networks that are closely related to the regulation of behavior, acts as a key regulator in emotion, social cognition, and decision making. Astrocytes are the majority cell type of glial cells, which play a significant role in a number of processes and establish a suitable environment for the functioning of neurons, including the brain energy metabolism. Astrocyte's dysfunction in the mPFC has been implicated in various neuropsychiatric disorders. Glucose is a major energy source in the brain. In glucose metabolism, part of glucose is used to convert UDP-GlcNAc as a donor molecule for O-GlcNAcylation, which is controlled by a group of enzymes, O-GlcNAc transferase enzyme (OGT), and O-GlcNAcase (OGA). However, the role of O-GlcNAcylation in astrocytes is almost completely unknown. Our research showed that astrocytic OGT could influence the expression of proteins in the mPFC. Most of these altered proteins participate in metabolic processes, transferase activity, and biosynthetic processes. GFAP, an astrocyte maker, was increased after OGT deletion. These results provide a framework for further study on the role of astrocytic OGT/O-GlcNAcylation in the mPFC.

Combinations of V2C and Ti3C2 MXenes for Boosting the Hydrogen Storage Performances of MgH2.

Two-dimensional vanadium carbide (V2C) and titanium carbide (Ti3C2) MXenes were first synthesized by exfoliating V2AlC or Ti3AlC2 and then introduced jointly into magnesium hydride (MgH2) to tailor the hydrogen desorption/absorption performances of MgH2. The as-prepared MgH2-V2C-Ti3C2 composites show much better hydrogen storage performances than pure MgH2. MgH2 with addition of 10 wt % of 2V2C/Ti3C2 initiates hydrogen desorption at around 180 °C; 5.1 wt % of hydrogen was desorbed within 60 min at 225 °C, while 5.8 wt % was desorbed within 2 min at 300 °C. Under 6 MPa H2, the dehydrided MgH2-2V2C/Ti3C2 can start to recover hydrogen at room temperature, and 5.1 wt % of H2 is obtained within 20 s at a constant temperature of 40 °C. The reversible capacity (6.3 wt %) does not decline for up to 10 cycles, which shows excellent cycling stability. The addition of 2V2C/Ti3C2 can remarkably lower the activation energy for the hydrogen desorption reaction of MgH2 by 37% and slightly reduce the hydrogen desorption reaction enthalpy by 2 kJ mol-1 H2. It was demonstrated that the combination of V2C and Ti3C2 promotes the hydrogen-releasing process of MgH2 compared with addition of only V2C or Ti3C2, while Ti3C2 impacts MgH2 more significantly than V2C in the hydrogen absorption process of MgH2 at ambient temperatures. A possible mechanism in the hydrogen release and uptake of the MgH2-V2C-Ti3C2 system was proposed as follows: hydrogen atoms or molecules may preferentially transfer through the MgH2/V2C/Ti3C2 triple-grain boundaries during the desorption process and through the Mg/Ti3C2 interfaces during the absorption process. Microstructure studies indicated that V2C and Ti3C2 mainly act as efficient catalysts for MgH2. This work provides an insight into the hydrogen storage behaviors and mechanisms of MgH2 boosted by a combination of two MXenes.

Erratum: Cenicriviroc ameliorates the severity of graft-versus host disease through inhibition of CCR5 in a rat model of liver transplantation.

[This corrects the article on p. 3438 in vol. 11, PMID: 31312356.].