Leucine-rich glioma-inactivated protein 1 antibody-associated encephalitis in a 22-month-old girl: a case report.

BACKGROUND: LGI-1 antibody-associated encephalitis is a type of autoimmune encephalitis with a lower prevalence than NMDAR antibody-associated encephalitis. LGI-1 antibody-associated encephalitis is the second most prevalent of all autoimmune encephalitides. LGI-1 antibodies interfere with the interactions of inter-synaptic proteins to produce clinical manifestations (N Engl J Med 378:840-851, 2018). CASE PRESENTATION: Leucine-rich glioma-inactivated protein 1 (LGI-1) antibody-associated encephalitis is a subtype of autoimmune encephalitis with a low incidence. We report a case of a girl aged 22 months with convulsive seizures, psycho-behavioral abnormalities, sleep disorders, and limb tremors. This patient was diagnosed with LGI-1 antibody-associated encephalitis based on electroencephalography (EEG) examinations and autoimmune encephalitis antibody analyses. A combined therapy of anti-epileptic and immunosuppressant drugs was effective in controlling the patient's neurological symptoms. CONCLUSIONS: The incidence of LGI-1 antibody-associated encephalitis is low and it occurs mostly in middle-aged and elderly patients, although it occasionally occurs in pediatric patients. To the best of our knowledge, this report describes the youngest patient with LGI-1 antibody-associated encephalitis. Following timely diagnosis, administration of anti-epileptic and immunosuppressant therapy was remarkably effective.

A High-Performance Alginate Hydrogel Binder for Aqueous Zn-Ion Batteries.

The binder is an indispensable battery component that maintains the integrity of the electrode. Polyvinylidene fluoride (PVDF) is most commonly used as a binder in rechargeable batteries; however, it is associated with the toxic and expensive N-methyl-2-pyrrolidone organic solvent. Here, through the cross-linking of sodium alginate (SA) with metal cations, a high-performance hydrogel binder is developed that maintains the stability of MnO2 cathodes in an aqueous electrolyte. Owing to the strong adhesion, high hydrophilicity, and good mechanical stability resulting from the strong bonding of Ca2+ with SA, a commercial microsized MnO2 cathode with a Ca-SA binder delivered a capacity above 300 mAh/g at 1 C, which was larger than those of Mn-SA and Zn-SA (∼200 mAh/g) and PVDF (∼150 mAh/g) binders, and a capacity of 250 mAh/g at 3 C for over 200 cycles. These encouraging results could unlock the enormous potential of aqueous binders for practical applications in aqueous batteries.

Transportin-3 Facilitates Uncoating of Influenza A Virus.

Influenza A viruses (IAVs) are a major global health threat and in the future, may cause the next pandemic. Although studies have partly uncovered the molecular mechanism of IAV-host interaction, it requires further research. In this study, we explored the roles of transportin-3 (TNPO3) in IAV infection. We found that TNPO3-deficient cells inhibited infection with four different IAV strains, whereas restoration of TNPO3 expression in knockout (KO) cells restored IAV infection. TNPO3 overexpression in wild-type (WT) cells promoted IAV infection, suggesting that TNPO3 is involved in the IAV replication. Furthermore, we found that TNPO3 depletion restrained the uncoating in the IAV life cycle, thereby inhibiting the process of viral ribonucleoprotein (vRNP) entry into the nucleus. However, KO of TNPO3 did not affect the virus attachment, endocytosis, or endosomal acidification processes. Subsequently, we found that TNPO3 can colocalize and interact with viral proteins M1 and M2. Taken together, the depletion of TNPO3 inhibits IAV uncoating, thereby inhibiting IAV replication. Our study provides new insights and potential therapeutic targets for unraveling the mechanism of IAV replication and treating influenza disease.

Autophagy Promotes Replication of Influenza A Virus In Vitro.

Influenza A virus (IAV) infection could induce autophagosome accumulation. However, the impact of the autophagy machinery on IAV infection remains controversial. Here, we showed that induction of cellular autophagy by starvation or rapamycin treatment increases progeny virus production, while disruption of autophagy using a small interfering RNA (siRNA) and pharmacological inhibitor reduces progeny virus production. Further studies revealed that alteration of autophagy significantly affects the early stages of the virus life cycle or viral RNA synthesis. Importantly, we demonstrated that overexpression of both the IAV M2 and NP proteins alone leads to the lipidation of LC3 to LC3-II and a redistribution of LC3 from the cytosol to punctate vesicles indicative of authentic autophagosomes. Intriguingly, both M2 and NP colocalize and interact with LC3 puncta during M2 or NP transfection alone and IAV infection, leading to an increase in viral ribonucleoprotein (vRNP) export and infectious viral particle formation, which indicates that the IAV-host autophagy interaction plays a critical role in regulating IAV replication. We showed that NP and M2 induce the AKT-mTOR-dependent autophagy pathway and an increase in HSP90AA1 expression. Finally, our studies provided evidence that IAV replication needs an autophagy pathway to enhance viral RNA synthesis via the interaction of PB2 and HSP90AA1 by modulating HSP90AA1 expression and the AKT-mTOR signaling pathway in host cells. Collectively, our studies uncover a new mechanism that NP- and M2-mediated autophagy functions in different stages of virus replication in the pathogenicity of influenza A virus.IMPORTANCE Autophagy impacts the replication cycle of many viruses. However, the role of the autophagy machinery in IAV replication remains unclear. Therefore, we explored the detailed mechanisms utilized by IAV to promote its replication. We demonstrated that IAV NP- and M2-mediated autophagy promotes IAV replication by regulating the AKT-mTOR signaling pathway and HSP90AA1 expression. The interaction of PB2 and HSP90AA1 results in the increase of viral RNA synthesis first; subsequently the binding of NP to LC3 favors vRNP export, and later the interaction of M2 and LC3 leads to an increase in the production of infectious viral particles, thus accelerating viral progeny production. These findings improve our understanding of IAV pathogenicity in host cells.

Facile synthesis of Sb2S3/MoS2 heterostructure as anode material for sodium-ion batteries.

A novel Sb2S3/MoS2 heterostructure in which Sb2S3 nanorods are coated with MoS2 nanosheets to form a core-shell structure has been fabricated via a facile two-step hydrothermal process. The Sb2S3/MoS2 heterostructure utilized as the anode of sodium-ion batteries (SIBs) shows higher capacity, superior rate capability and better cycling performance compared with individual Sb2S3 nanorods and MoS2 nanosheets. Specifically, the Sb2S3/MoS2 electrode shows an initial reversible capacity of 701 mAh g-1 at a current density of 100 mA g-1, which then remains at 80.1% of the initial performance after 100 cycles at the same current density. This outstanding electrochemical performance indicates that the Sb2S3/MoS2 heterostructure is a very promising anode material for high-performance SIBs.

Manipulating the Solvation Structure and Interface via a Bio-Based Green Additive for Highly Stable Zn Metal Anode.

The practical application of aqueous zinc-ion batteries (AZIBs) is limited by serious side reactions, such as the hydrogen evolution reaction and Zn dendrite growth. Here, the study proposes a novel adoption of a biodegradable electrolyte additive, γ-Valerolactone (GVL), with only 1 vol.% addition (GVL-to-H2 O volume ratio) to enable a stable Zn metal anode. The combination of experimental characterizations and theoretical calculations verifies that the green GVL additive can competitively engage the solvated structure of Zn2+ via replacing a H2 O molecule from [Zn(H2 O)6 ]2+ , which can efficiently reduce the reactivity of water and inhibit the subsequent side reactions. Additionally, GVL molecules are preferentially adsorbed on the surface of Zn to regulate the uniform Zn deposition and suppress the Zn dendrite growth. Consequently, the Zn anode exhibits boosted stability with ultralong cycle lifespan (over 3500 h) and high reversibility with 99.69% Coulombic efficiency. The Zn||MnO2 full batteries with ZnSO4 -GVL electrolyte show a high capacity of 219 mAh g-1 at 0.5 A g-1 and improved capacity retention of 78% after 550 cycles. This work provides inspiration on bio-based electrolyte additives for aqueous battery chemistry and promotes the practical application of AZIBs.

Facile synthesis of nanosized Mn3O4 powder anodes for high capacity Lithium-Ion battery via flame spray pyrolysis.

Mn3O4 powders with nanometer size are successfully synthesized by a simple one-step method via flame spray pyrolysis. The precursor droplet is generated by heating under high temperature flame with fixed flow rate, and the exothermic reaction is induced to form nanosized Mn3O4 powders. When used as anode material for lithium-ion battery, the Mn3O4 exhibits good cycling capacity and rate performance. It delivers a specific capacity of 1,182 mA h g-1 over 110 cycles at a current density of 200 mA g-1, and has a high capacity of 140 mA h g-1 at 5,000 mA g-1.

Multi-core yolk-shell-structured Bi2Se3@C nanocomposite as an anode for high-performance lithium-ion batteries.

Emerging Bi2Se3-based anode materials are attracting great interest for lithium storage because of their high theoretical capacity. Although quite attractive, Bi2Se3 still faces the problem of large volume expansion during lithiation/delithiation, leading to poor cycling stability. Herein, a multi-core yolk-shell Bi2Se3@C nanocomposite was designed and synthesized via a solvothermal method followed by heat treatment. The as-prepared yolk-shell nanocomposite consists of two parts: several Bi2Se3 nanospheres (diameter of approximately 100 nm) as a core, and carbon (thickness of approximately 16 nm) as the shell. Owing to its unique structural features, multi-core yolk-shell Bi2Se3@C nanocomposite demonstrates excellent cycling stability with a capacity of 392.2 mA h g-1 at 0.2 A g-1 after 100 cycles for lithium-ion batteries (LIBs). A reversible capacity of 416.9 mA h g-1 can be maintained even at a higher current density of 1 A g-1 after 1200 cycles. The reason for the superior electrochemical performance was further explored through electrochemical kinetic analysis and theoretical calculations. This work provides an effective strategy for the preparation of multi-core yolk-shell anode materials, and also affords a new method by which to prepare high-performance LIBs.

BiSbS3@N-doped carbon core-shell nanorods as efficient anode materials for sodium-ion batteries.

BiSbS3@N-doped carbon (NC) core-shell nanorods were prepared through a simple preparation process. As anode materials for sodium-ion batteries (SIBs), BiSbS3@NC core-shell nanorods present excellent electrochemical performance with higher specific capacity and better rate capability compared with the unmodified pristine BiSbS3 nanorods. The BiSbS3@NC electrode delivers high sodium storage capacity (771.5 mA h g-1 in the 2nd cycle) and excellent rate performance (capacity of 518.4 mA h g-1 at 1000 mA g-1). The improvement in electrochemical performance results from the coated conductive NC layer which brings about fast ion/electron transfer and buffers volume expansion. The BiSbS3@NC core-shell nanorods are thus promising high performance anode materials for SIBs.

Influenza M2 protein regulates MAVS-mediated signaling pathway through interacting with MAVS and increasing ROS production.

Influenza A virus can evade host innate immune response that is involved in several viral proteins with complicated mechanisms. To date, how influenza A M2 protein modulates the host innate immunity remains unclear. Herein, we showed that M2 protein colocalized and interacted with MAVS (mitochondrial antiviral signaling protein) on mitochondria, and positively regulated MAVS-mediated innate immunity. Further studies revealed that M2 induced reactive oxygen species (ROS) production that was required for activation of macroautophagy/autophagy and enhancement of MAVS signaling pathway. Importantly, the proton channel activity of M2 protein was demonstrated to be essential for ROS production and antagonizing the autophagy pathway to control MAVS aggregation, thereby enhancing MAVS signal activity. In conclusion, our studies provided novel insights into mechanisms of M2 protein in modulating host antiviral immunity and uncovered a new mechanism into biology and pathogenicity of influenza A virus. Abbreviations: AKT/PKB: AKT serine/threonine kinase; Apo: apocynin; ATG5: autophagy related 5; BAPTA-AM: 1,2-Bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetrakis; BECN1: beclin 1; CARD: caspase recruitment domain; CCCP: carbonyl cyanide m-chlorophenylhydrazone; CQ: chloroquine; DCF: dichlorodihyd-rofluorescein; DPI: diphenyleneiodonium; DDX58: DExD/H-box helicase 58; eGFP: enhanced green fluorescent protein; EGTA: ethylene glycol-bis(2-aminoethylether)-N,N,N',N'-tetraacetic acid; ER: endoplasmic reticulum; hpi: hours post infection; IAV: influenza A virus; IFN: interferon; IP: immunoprecipitation; IRF3: interferon regulatory factor 3; ISRE: IFN-stimulated response elements; LIR: LC3-interacting region; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MAVS: mitochondrial antiviral signaling protein; MMP: mitochondrial membrane potential; MOI, multiplicity of infection; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; NC: negative control; NFKB/NF-κB: nuclear factor kappa B; PI3K: class I phosphoinositide 3-kinase; RLR: RIG-I-like-receptor; ROS: reactive oxygen species; SEV: sendai virus; TM: transmembrane; TMRM: tetramethylrhodamine methylester; VSV: vesicular stomatitis virus.