Recent Advances in Rechargeable Metal-CO2 Batteries with Nonaqueous Electrolytes.

This review article discusses the recent advances in rechargeable metal-CO2 batteries (MCBs), which include the Li, Na, K, Mg, and Al-based rechargeable CO2 batteries, mainly with nonaqueous electrolytes. MCBs capture CO2 during discharge by the CO2 reduction reaction and release it during charging by the CO2 evolution reaction. MCBs are recognized as one of the most sophisticated artificial modes for CO2 fixation by electrical energy generation. However, extensive research and substantial developments are required before MCBs appear as reliable, sustainable, and safe energy storage systems. The rechargeable MCBs suffer from the hindrances like huge charging-discharging overpotential and poor cyclability due to the incomplete decomposition and piling of the insulating and chemically stable compounds, mainly carbonates. Efficient cathode catalysts and a suitable architectural design of the cathode catalysts are essential to address this issue. Besides, electrolytes also play a vital role in safety, ionic transportation, stable solid-electrolyte interphase formation, gas dissolution, leakage, corrosion, operational voltage window, etc. The highly electrochemically active metals like Li, Na, and K anodes severely suffer from parasitic reactions and dendrite formation. Recent research works on the aforementioned secondary MCBs have been categorically reviewed here, portraying the latest findings on the key aspects governing secondary MCB performances.

Inhibition of NKCC1 Ameliorates Anxiety and Autistic Behaviors Induced by Maternal Immune Activation in Mice.

Autism spectrum disorder (ASD) is thought to result from susceptibility genotypes and environmental risk factors. The offspring of women who experience pregnancy infection have an increased risk for autism. Maternal immune activation (MIA) in pregnant animals produces offspring with autistic behaviors, making MIA a useful model for autism. However, how MIA causes autistic behaviors in offspring is not fully understood. Here, we show that NKCC1 is critical for mediating autistic behaviors in MIA offspring. We confirmed that MIA induced by poly(I:C) infection during pregnancy leads to autistic behaviors in offspring. We further demonstrated that MIA offspring showed significant microglia activation, excessive dendritic spines, and narrow postsynaptic density (PSD) in their prefrontal cortex (PFC). Then, we discovered that these abnormalities may be caused by overexpression of NKCC1 in MIA offspring's PFCs. Finally, we ameliorated the autistic behaviors using PFC microinjection of NKCC1 inhibitor bumetanide (BTN) in MIA offspring. Our findings may shed new light on the pathological mechanisms for autism caused by pregnancy infection.

Melatonin attenuated chronic visceral pain by reducing Nav1.8 expression and nociceptive neuronal sensitization.

BACKGROUND: Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder, and its specific pathogenesis is still unclear. We have previously reported that TTX-resistant (TTX-R) sodium channels in colon-specific dorsal root ganglion (DRG) neurons were sensitized in a rat model of visceral hypersensitivity induced by neonatal colonic inflammation (NCI). However, the detailed molecular mechanism for activation of sodium channels remains unknown. This study was designed to examine roles for melatonin (MT) in sensitization of sodium channels in NCI rats. METHODS: Colorectal distention (CRD) in adult male rats as a measure of visceral hypersensitivity. Colon-specific dorsal root ganglion (DRG) neurons were labeled with DiI and acutely dissociated for measuring excitability and sodium channel current under whole-cell patch clamp configurations. Western blot and Immunofluorescence were employed to detect changes in expression of Nav1.8 and MT2. RESULTS: The results showed that rats exhibited visceral hypersensitivity after NCI treatment. Intrathecal application of melatonin significantly increased the threshold of CRD in NCI rats with a dose-dependent manner, but has no role in the control group. Whole-cell patch clamp recording showed that melatonin remarkably decreased the excitability and the density of TTX-R sodium channel in DRG neurons from NCI rats. The expression of MT2 receptor at the protein level was markedly lower in NCI rats. 8MP, an agonist of MT2 receptor, enhanced the distention threshold in NCI rats. Application of 8MP reversed the enhanced hypersensitivity of DRG neurons from NCI rats. 8MP also reduced TTX-R sodium current density and modulated dynamics of TTX-R sodium current activation. CONCLUSIONS: These data suggest that sensitization of sodium channels of colon DRG neurons in NCI rats is most likely mediated by MT2 receptor, thus identifying a potential target for treatment for chronic visceral pain in patients with IBS.

LncRNA NONRATT014888.2 contributes to cancer-induced bone pain through downregulation of natriuretic peptide receptor 3 in rats.

Long noncoding RNA (lncRNA) is implicated in both cancer development and pain process. However, the role of lncRNA in the development of cancer-induced bone pain (CIBP) is unclear. LncRNA NONRATT014888.2 is highly expressed in tibia related dorsal root ganglions (DRGs) in CIBP rats which function is unknown. CIBP was induced by injection of Walker 256 mammary gland tumor cells into the tibia canal of female SD rats. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) of rats were measured. Down-regulation of NONRATT014888.2 by siRNA in CIBP rats markedly attenuated hind-paw mechanical pain hypersensitivity. LncRNA-predicted target mRNAs analysis and mRNA sequencing results cued Socs3, Npr3 were related with NONRATT014888.2. Intrathecal injection of NONRATT014888.2-siR206 upregulated Npr3 both in mRNA and protein level. Npr3 was co-expressed in NONRATT014888.2-positive DRGs neurons and mainly located in cytoplasm, but not in Glial fibrillary acidic protein (GFAP)-positive cells. Intrathecal injection of ADV-Npr3 upregulated Npr3 expression and enhanced the PWT of CIBP rats. Our results suggest that upregulated lncRNA NONRATT014888.2 contributed to hyperalgesia in CIBP rats, and the mechanism may through downregulation of Npr3.

Downregulation of GRK6 in arcuate nucleus promotes chronic visceral hypersensitivity via NF-κB upregulation in adult rats with neonatal maternal deprivation.

AIMS: The arcuate nucleus is a vital brain region for coursing of pain command. G protein-coupled kinase 6 (GRK6) accommodates signaling through G protein-coupled receptors. Studies have demonstrated that GRK6 is involved in inflammatory pain and neuropathic pain. The present study was designed to explore the role and the underlying mechanism of GRK6 in arcuate nucleus of chronic visceral pain. METHODS: Chronic visceral pain of rats was induced by neonatal maternal deprivation and evaluated by monitoring the threshold of colorectal distension. Western blotting, immunofluorescence, real-time quantitative polymerase chain reaction techniques, and Nissl staining were employed to determine the expression and mutual effect of GRK6 with nuclear factor κB (NF-κB). RESULTS: Expression of GRK6 in arcuate nucleus was significantly reduced in neonatal maternal deprivation rats when compared with control rats. GRK6 was mainly expressed in arcuate nucleus neurons, but not in astrocytes, and a little in microglial cells. Neonatal maternal deprivation reduced the percentage of GRK6-positive neurons of arcuate nucleus. Overexpression of GRK6 by Lentiviral injection into arcuate nucleus reversed chronic visceral pain in neonatal maternal deprivation rats. Furthermore, the expression of NF-κB in arcuate nucleus was markedly upregulated in neonatal maternal deprivation rats. NF-κB selective inhibitor pyrrolidine dithiocarbamate suppressed chronic visceral pain in neonatal maternal deprivation rats. GRK6 and NF-κB were expressed in the arcuate nucleus neurons. Importantly, overexpression of GRK6 reversed NF-κB expression at the protein level. In contrast, injection of pyrrolidine dithiocarbamate once daily for seven consecutive days did not alter GRK6 expression in arcuate nucleus of neonatal maternal deprivation rats. CONCLUSIONS: Present data suggest that GRK6 might be a pivotal molecule participated in the central mechanisms of chronic visceral pain, which might be mediated by inhibiting NF-κB signal pathway. Overexpression of GRK6 possibly represents a potential strategy for therapy of chronic visceral pain.

Multi-Site Cation Control of Ultra-Broadband Near-Infrared Phosphors for Application in Light-Emitting Diodes.

Near-infrared (NIR) phosphors are fascinating materials that have numerous applications in diverse fields. In this study, a series of La3Ga5GeO14:Cr3+ phosphors, which was incorporated with Sn4+, Ba2+, and Sc3+, was successfully synthesized using solid-state reaction to explore every cationic site comprehensively. The crystal structures were well resolved by combining synchrotron X-ray diffraction and neutron powder diffraction through joint Rietveld refinements. The trapping of free electrons induced by charge unbalances and lattice vacancies changes the magnetic properties, which was well explained by a Dyson curve in electron paramagnetic resonance. Temperature and pressure-dependent photoluminescence spectra reveal various luminescent properties between strong and weak fields in different dopant centers. The phosphor-converted NIR light-emitting diode (pc-NIR LED) package demonstrates a superior broadband emission that covers the near-infrared (NIR) region of 650-1050 nm. This study can provide researchers with new insight into the control mechanism of multiple-cation-site phosphors and reveal a potential phosphor candidate for practical NIR LED application.

Sensitization of P2X3 receptors in insular cortex contributes to visceral pain of adult rats with neonatal maternal deprivation.

Aims Insular cortex is a brain region critical for processing of the sensation. Purinergic receptors are involved in the formation of chronic pain. The aim of the present study was to explore the role and mechanism of P2X3 receptors (P2X3Rs) in insular cortex in chronic visceral pain. Methods Chronic visceral pain in adult rats was induced by neonatal maternal deprivation and measured by detecting the threshold of colorectal distension. Western blotting, immunofluorescence, and real-time quantitative polymerase chain reaction techniques were used to detect the expression and distribution of P2X3Rs. Synaptic transmission in insular cortex was recorded in brain slices by patch clamp techniques. Results Expression of P2X3Rs both at mRNA and protein levels in right hemisphere of insular cortex was significantly increased in neonatal maternal deprivation rats. In addition, P2X3Rs were expressed with NeuN or synaptophysin but not with glial fibrillary acidic protein and CD11b. The co-localization of P2X3Rs with NeuN or synaptophysin was greatly enhanced in right hemisphere of insular cortex in neonatal maternal deprivation rats. Furthermore, neonatal maternal deprivation markedly increased both the frequency and amplitude of miniature excitatory postsynaptic current in right hemisphere of insular cortex. Incubation of A347091 significantly decreased the frequency of spontaneous excitatory postsynaptic current and miniature excitatory postsynaptic current of insular cortex neurons of neonatal maternal deprivation rats. Incubation of P2X3Rs agonists α,ß-mATP remarkably increased the frequency of spontaneous excitatory postsynaptic current and miniature excitatory postsynaptic current of the right hemisphere of insular cortex neurons of healthy control rats. Importantly, injection of A317491 significantly enhanced the colorectal distension threshold of neonatal maternal deprivation rats, while injection of α,ß-mATP into right but not left insular cortex markedly decreased the colorectal distension threshold in healthy control rats. Conclusions Overall, our data provide integrated pharmacological, biochemical, and functional evidence demonstrating that P2X3Rs are physically and functionally interconnected at the presynaptic level to control synaptic activities in the right insular cortex, thus contributing to visceral pain of neonatal maternal deprivation rats.

Vertically-aligned graphene nanowalls grown via plasma-enhanced chemical vapor deposition as a binder-free cathode in Li-O2 batteries.

In the present report, vertically-aligned graphene nanowalls are grown on Ni foam (VA-G/NF) using plasma-enhanced chemical vapor deposition method at room temperature. Optimization of the growth conditions provides graphene sheets with controlled defect sites. The unique architecture of the vertically-aligned graphene sheets allows sufficient space for the ionic movement within the sheets and hence enhancing the catalytic activity. Further modification with ruthenium nanoparticles (Ru NPs) drop-casted on VA-G/NF improves the charge overpotential for lithium-oxygen (Li-O2) battery cycles. Such reduction we believe is due to the easier passage of ions between the perpendicularly standing graphene sheets thereby providing ionic channels.

Hyperexcitability and sensitization of sodium channels of dorsal root ganglion neurons in a rat model of lumber disc herniation.

PURPOSE: Low back pain and sciatica are the most common symptoms of patients with lumbar disc herniation (LDH). The pathophysiology of lumbocrural pain and sciatica is not fully understood. The aim of the present study was to define the membrane properties and activities of voltage-gated sodium channels of dorsal root ganglion (DRG) neurons in a rat model of LDH. METHODS: LDH was established by transplantation of autologous nucleus pulposus (NP) to lumbar 5 and 6 spinal nerves (L5-L6 DRG) of adult male rats. Mechanical paw withdrawal threshold (PWT) and thermal paw withdrawal latency (PWL) were measured 1 day before and through 35 days after transplantation of NP. Changes in expression of VGSCs were determined by western blotting. L5-L6 DRGs neurons innervating the hindpaw were labeled with DiI and acutely dissociated for measuring excitability and sodium channel currents under whole-cell patch clamp configurations. RESULTS: NP transplantation significantly reduced the PWT and PWL in association with a significant reduction in rheobase and an increase in numbers of action potentials evoked by 2X and 3X rheobase current stimulation. Voltage-gated sodium current density was significantly enhanced in L5-L6 DRG neurons from LDH rats. The inactivation curve showed a leftward shift in LDH rats while activation curve did not significantly alter. However, NP transplantation remarkably enhanced expression of NaV1.7 and NaV1.8 in L5-L6 DRGs but not in T10-12 DRGs. CONCLUSION: These data suggest that NP application produces pain-related behavior and potentiates sodium current density of DRG neurons, which is most likely mediated by enhanced expression of NaV1.7 and NaV1.8.

Adrenergic signaling mediates mechanical hyperalgesia through activation of P2X3 receptors in primary sensory neurons of rats with chronic pancreatitis.

The mechanism of pain in chronic pancreatitis (CP) is poorly understood. The aim of this study was designed to investigate roles of norepinephrine (NE) and P2X receptor (P2XR) signaling pathway in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced in male adult rats by intraductal injection of trinitrobenzene sulfonic acid (TNBS). Mechanical hyperalgesia was assessed by referred somatic behaviors to mechanical stimulation of rat abdomen. P2XR-mediated responses of pancreatic dorsal root ganglion (DRG) neurons were measured utilizing calcium imaging and whole cell patch-clamp-recording techniques. Western blot analysis and immunofluorescence were performed to examine protein expression. TNBS injection produced a significant upregulation of P2X3R expression and an increase in ATP-evoked responses of pancreatic DRG neurons. The sensitization of P2X3Rs was reversed by administration of ß-adrenergic receptor antagonist propranolol. Incubation of DRG neurons with NE significantly enhanced ATP-induced intracellular calcium signals, which were abolished by propranolol, and partially blocked by protein kinase A inhibitor H-89. Interestingly, TNBS injection led to a significant elevation of NE concentration in DRGs and the pancreas, an upregulation of ß2-adrenergic receptor expression in DRGs, and amplification of the NE-induced potentiation of ATP responses. Importantly, pancreatic hyperalgesia was markedly attenuated by administration of purinergic receptor antagonist suramin or A317491 or ß2-adrenergic receptor antagonist butoxamine. Sensitization of P2X3Rs, which was likely mediated by adrenergic signaling in primary sensory neurons, contributes to pancreatic pain, thus identifying a potential target for treating pancreatic pain caused by inflammation.

Heterostructure of Si and CoSe2: A Promising Photocathode Based on a Non-noble Metal Catalyst for Photoelectrochemical Hydrogen Evolution.

Development of a solar water splitting device requires design of a low-cost, efficient, and non-noble metal compound as alternative to noble metals. For the first time, we showed that CoSe2 can function as co-catalyst in phototoelectrochemical hydrogen production. We designed a heterostructure of p-Si and marcasite-type CoSe2 for solar-driven hydrogen production. CoSe2 successively coupled with p-Si can act as a superior photocathode in the solar-driven water splitting reaction. Photocurrents up to 9 mA cm(-2) were achieved at 0 V vs. reversible hydrogen electrode. Electrochemical impedance spectroscopy showed that the high photocurrents can be attributed to low charge transfer resistance between the Si and CoSe2 interfaces and that between the CoSe2 and electrolyte interfaces. Our results suggest that this CoSe2 is a promising alternative co-catalyst for hydrogen evolution.

Promoted interaction of nuclear factor-κB with demethylated cystathionine-ß-synthetase gene contributes to gastric hypersensitivity in diabetic rats.

Patients with long-standing diabetes frequently demonstrate gastric hypersensitivity with an unknown mechanism. The present study was designed to investigate roles for nuclear factor-κB (NF-κB) and the endogenous H2S-producing enzyme cystathionine-ß-synthetase (CBS) signaling pathways by examining cbs gene methylation status in adult rats with diabetes. Intraperitoneal injection of streptozotocin (STZ) produced gastric hypersensitivity in female rats in response to gastric balloon distention. Treatment with the CBS inhibitor aminooxyacetic acid significantly attenuated STZ-induced gastric hypersensitivity in a dose-dependent fashion. Aminooxyacetic acid treatment also reversed hyperexcitability of gastric-specific dorsal root ganglion (DRG) neurons labeled by the dye DiI in diabetic rats. Conversely, the H2S donor NaHS enhanced neuronal excitability of gastric DRG neurons. Expression of CBS and p65 were markedly enhanced in gastric DRGs in diabetic rats. Blockade of NF-κB signaling using pyrrolidine dithiocarbamate reversed the upregulation of CBS expression. Interestingly, STZ treatment led to a significant demethylation of CpG islands in the cbs gene promoter region, as determined by methylation-specific PCR and bisulfite sequencing. STZ treatment also remarkably downregulated the expression of DNA methyltransferase 3a and 3b. More importantly, STZ treatment significantly enhanced the ability of cbs to bind DNA at the p65 consensus site, as shown by chromatin immunoprecipitation assays. Our findings suggest that upregulation of cbs expression is attributed to cbs promoter DNA demethylation and p65 activation and that the enhanced interaction of the cbs gene and p65 contributes to gastric hypersensitivity in diabetes. This finding may guide the development and evaluation of new treatment modalities for patients with diabetic gastric hypersensitivity.

Upregulation of cystathionine-ß-synthetase expression contributes to inflammatory pain in rat temporomandibular joint.

BACKGROUND: Hydrogen sulfide (H2S), an endogenous gaseotransmitter/modulator, is becoming appreciated that it may be involved in a wide variety of processes including inflammation and nociception. However, the role for H2S in nociceptive processing in trigeminal ganglion (TG) neuron remains unknown. The aim of this study was designed to investigate whether endogenous H2S synthesizing enzyme cystathionine-ß-synthetase (CBS) plays a role in inflammatory pain in temporomandibular joint (TMJ). METHODS: TMJ inflammatory pain was induced by injection of complete Freund's adjuvant (CFA) into TMJ of adult male rats. Von Frey filaments were used to examine pain behavioral responses in rats following injection of CFA or normal saline (NS). Whole cell patch clamp recordings were employed on acutely isolated TG neurons from rats 2 days after CFA injection. Western blot analysis was carried out to measure protein expression in TGs. RESULTS: Injection of CFA into TMJ produced a time dependent hyperalgesia as evidenced by reduced escape threshold in rats responding to VFF stimulation. The reduced escape threshold was partially reversed by injection of O-(Carboxymethyl) hydroxylamine hemihydrochloride (AOAA), an inhibitor for CBS, in a dose-dependent manner. CFA injection led to a marked upregulation of CBS expression when compared with age-matched controls. CFA injection enhanced neuronal excitability as evidenced by depolarization of resting membrane potentials, reduction in rheobase, and an increase in number of action potentials evoked by 2 and 3 times rheobase current stimulation and by a ramp current stimulation of TG neurons innervating the TMJ area. CFA injection also led to a reduction of IK but not IA current density of TG neurons. Application of AOAA in TMJ area reduced the production of H2S in TGs and reversed the enhanced neural hyperexcitability and increased the IK currents of TG neurons. CONCLUSION: These data together with our previous report indicate that endogenous H2S generating enzyme CBS plays an important role in TMJ inflammation, which is likely mediated by inhibition of IK currents, thus identifying a specific molecular mechanism underlying pain and sensitization in TMJ inflammation.

Homogeneous Catalytic Process of a Heterogeneous Ru Catalyst in Li-O2 via X-ray Nanodiffraction Observation.

In recent years, lithium oxygen batteries (Li-O2) have received considerable research attention due to their extremely high energy density. However, the poor conductivity and ion conductivity of the discharge product lithium peroxide (Li2O2) result in a high charging overpotential, poor cycling stability, and low charging rate. Therefore, studying and improving catalysts is a top priority. This study focuses on the commonly used heterogeneous catalyst ruthenium (Ru). The local distribution of this catalyst is controlled by using sputtering technology. Moreover, X-ray nanodiffraction is applied to observe the relationship between the decomposition of Li2O2 and the local distribution of Ru. Results show that Li2O2 decomposes homogeneously in liquid systems and heterogeneously in solid-state systems. This study finds that the catalytic effect of Ru is related to electrolyte decomposition and that its soluble byproducts act as electron acceptors or redox mediators, effectively reducing charging overpotential but also shortening the cycle life.

Improvement strategy of citrate and biochar assisted nano-palladium/iron composite for effective dechlorination of 2,4-dichlorophenol.

Rapid passivation and aggregation of nanoscale zero-valent iron (nZVI) seriously limit its performance in the remediation of different contaminants from wastewater. To overcome such issues, in the present study, nano-palladium/iron (nPd/Fe) was simultaneously improved by biochar (BC) prepared from discarded peanut shells and green complexing agent sodium citrate (SC). For this purpose, a composite (SC-nPd/Fe@BC) was successfully synthesized to remove 2,4-dichlorophenol (2,4-DCP) from wastewater. In the SC-nPd/Fe@BC, BC acts as a carrier with dispersed nPd/Fe particles to effectively prevent its agglomeration, and increased the specific surface area of the composite, thereby improving the reactivity and stability of nPd/Fe. Characterization results demonstrated that the SC-nPd/Fe@BC composites were well dispersed, and the agglomeration was weakened. The formation of the passivation layer on the surface of the particles was inhibited, and the mechanism of SC and BC improving the reactivity of nPd/Fe was clarified. Different factors were found to influence the reductive dichlorination of 2,4-DCP, including Pd loading, Fe:C, SC addition, temperature, initial pH, and initial pollutant concentration. The dechlorination results revealed that the synergistic effect of the BC and SC made the removal efficiency and dechlorination rate of 2,4-DCP by SC-nPd/Fe@BC reached to 96.0 and 95.6%, respectively, which was better than that of nPd/Fe (removal: 46.2%, dechlorination: 45.3%). Kinetic studies explained that the dechlorination reaction of 2,4-DCP and the data were better represented by the pseudo-first-order kinetic model. The reaction rate constants followed the order of SC-nPd/Fe@BC (0.0264 min-1) > nPd/Fe@BC (0.0089 min-1) > SC-nPd/Fe (0.0081 min-1) > nPd/Fe (0.0043 min-1). Thus, SC-nPd/Fe@BC was capable of efficiently reducing 2,4-DCP and the dechlorination efficiency of BC and SC synergistically assisted composite on 2,4-DCP was much better than that of SC-nPd/Fe, nPd/Fe@BC and nPd/Fe. Findings suggested that SC-nPd/Fe@BC can be promising for efficient treatment of chlorinated pollutants.

HDAC9-mediated calmodulin deacetylation induces memory impairment in Alzheimer's disease.

AIMS: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive dysfunction and memory impairment. AD pathology involves protein acetylation. Previous studies have mainly focused on histone acetylation in AD, however, the roles of nonhistone acetylation in AD are less explored. METHODS: The protein acetylation and expression levels were detected by western blotting and co-immunoprecipitation. The stoichiometry of acetylation was measured by home-made and site-specific antibodies against acetylated-CaM (Ac-CaM) at K22, K95, and K116. Hippocampus-dependent learning and memory were evaluated by using the Morris water maze, novel object recognition, and contextual fear conditioning tests. RESULTS: We showed that calmodulin (CaM) acetylation is reduced in plasma of AD patients and mice. CaM acetylation and its target Ca2+ /CaM-dependent kinase II α (CaMKIIα) activity were severely impaired in AD mouse brain. The stoichiometry showed that Ac-K22, K95-CaM acetylation were decreased in AD patients and mice. Moreover, we screened and identified that lysine deacetylase 9 (HDAC9) was the main deacetylase for CaM. In addition, HDAC9 inhibition increased CaM acetylation and CaMKIIα activity, and hippocampus-dependent memory in AD mice. CONCLUSIONS: HDAC9-mediated CaM deacetylation induces memory impairment in AD, HDAC9, or CaM acetylation may become potential therapeutic targets for AD.

Neonatal stress disrupts the glymphatic system development and increases the susceptibility to Parkinson's disease in later life.

INTRODUCTION: Neonatal stress disrupts brain development and increases the risk of neurological disorders later in life. However, the impact of neonatal stress on the development of the glymphatic system and susceptibility to Parkinson's disease (PD) remains largely unknown. METHODS: Neonatal maternal deprivation (NMD) was performed on mice for 14 consecutive days to model chronic neonatal stress. Adeno-associated virus expressing A53T-α-synuclein (α-syn) was injected into the substantia nigra to establish PD model mice. Glymphatic activity was determined using in vivo magnetic resonance imaging, ex vivo fluorescence imaging and microplate assay. The transcription and expression of aquaporin-4 (AQP4) and other molecules were evaluated by qPCR, western blotting, and immunofluorescence. Animal's responses to NMD and α-syn overexpression were observed using behavioral tests. RESULTS: Glymphatic activity was impaired in adult NMD mice. AQP4 polarization and platelet-derived growth factor B (PDGF-B) signaling were reduced in the frontal cortex and hippocampus of both young and adult NMD mice. Furthermore, exogenous α-syn accumulation was increased and PD-like symptoms were aggravated in adult NMD mice. CONCLUSION: The results demonstrated that NMD could disrupt the development of the glymphatic system through PDGF-B signaling and increase the risk of PD later in life, indicating that alleviating neonatal stress could be beneficial in protecting the glymphatic system and reducing susceptibility to neurodegeneration.

Neonatal maternal deprivation sensitizes voltage-gated sodium channel currents in colon-specific dorsal root ganglion neurons in rats.

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder characterized by abdominal pain in association with altered bowel movements. The underlying mechanisms of visceral hypersensitivity remain elusive. This study was designed to examine the role for sodium channels in a rat model of chronic visceral hyperalgesia induced by neonatal maternal deprivation (NMD). Abdominal withdrawal reflex (AWR) scores were performed on adult male rats. Colon-specific dorsal root ganglion (DRG) neurons were labeled with DiI and acutely dissociated for measuring excitability and sodium channel current under whole-cell patch-clamp configurations. The expression of Na(V)1.8 was analyzed by Western blot and quantitative real-time PCR. NMD significantly increased AWR scores, which lasted for ~6 wk in an association with hyperexcitability of colon DRG neurons. TTX-resistant but not TTX-sensitive sodium current density was greatly enhanced in colon DRG neurons in NMD rats. Compared with controls, activation curves showed a leftward shift in NMD rats whereas inactivation curves did not differ significantly. NMD markedly accelerated the activation time of peak current amplitude without any changes in inactivation time. Furthermore, NMD remarkably enhanced expression of Na(V)1.8 at protein levels but not at mRNA levels in colon-related DRGs. The expression of Na(V)1.9 was not altered after NMD. These data suggest that NMD enhances TTX-resistant sodium activity of colon DRG neurons, which is most likely mediated by a leftward shift of activation curve and by enhanced expression of Na(V)1.8 at protein levels, thus identifying a specific molecular mechanism underlying chronic visceral pain and sensitization in patients with IBS.

Synergistic Effect of the Anode Interface of Garnet-Type All-Solid-State Batteries.

Next-generation lithium-ion batteries must have high energy density and safety, making the development of all-solid-state batteries imperative. One of the biggest advantages of an all-solid-state lithium-ion battery (ASSLIB) is that its alloy uses lithium metal as an anode while ignoring its flammability and other dangers. Herein, high-conductivity garnet-type Li6.75La3Zr1.75Ta0.25O12 (LLZTO) was chosen as the solid electrolyte part of an all-solid-state battery. A composite anode was formed by melting Li and MXene-MAX together, reducing the interface impedance from 566 to 55 Ω cm2. The Li-MXene|LLZTO|LFP full battery displayed a high initial discharge capacity of 163.0 mAh g-1 and a Coulombic efficiency of 97.0% and maintained 90.2% of its discharge capacity over 100 cycles, but it did not maintain a good overpotential. Therefore, the synergistic effect of Li-MXene-Pt will highly improve the performance of the full battery because of its high initial discharge capacity of 150.0 mAh g-1 and Coulombic efficiency of 95.5%, discharge capacity maintained at 93.3% over 100 cycles, and low overpotential of 0.04 V.

In Situ and Low-Cost Improvement of the Lithium Anode Interface in Garnet-Type Solid-State Electrolytes.

In recent years, the development of electric vehicles and environmental concerns have made necessary improvements in the energy density and safety of lithium-ion batteries. Therefore, the development of all-solid-state lithium-ion batteries (ASSLIBs) has become imperative. One advantage of ASSLIBs is their potential for downsizing with the use of lithium metal as the anode. However, in this study, a garnet-type solid electrolyte (Li6.75La3Zr1.75Ta0.25O12) was used, which has low reactivity with lithium metal. Thus, interface modification using CaCl2 was employed to form a Li-Ca-Cl composite anode. The interfacial resistance was remarkably reduced to 7 Ω cm2, and the symmetric cell exhibited stable cycling for 1200 h at room temperature and a current density of 0.1 mA cm-2. The voltage ranged from ±15 to ±16 mV. The full cell demonstrated a high initial discharge capacity of 149.2 mA h g-1 and a Coulombic efficiency of 98.0% while maintaining a discharge capacity retention of 91.3% after 100 cycles. These findings lay a solid foundation for future commercial applications as interface modification was achieved through a simple spin-coating process using low-cost CaCl2 (0.7 USD g-1).