Anti-IgLON5 disease: A case with intestinal obstruction and peripheral neuropathy.

IgLON5 autoimmunity is a novel antibody-mediated disorder characterized by serum and/or cerebrospinal fluid (CSF) positivity for IgLON5 antibody. Anti-IgLON5 disease mainly manifests as sleep disturbances, movement disorders and brainstem syndromes. In this study, we report the case of a patient with anti-IgLON5 disease who presented with abdominal distension, abdominal pain, intermittent dysuria and constipation, and intermittent lightning pain in the extremities, which are atypical of anti-IgLON5 disease and could easily lead to misdiagnosis. After performing autoantibody screening, we considered anti-IgLON5 disease. The patient was started on a course of immunotherapy with intravenous dexamethasone, intravenous immunoglobulin (IVIG) and oral azathioprine. Following treatment, the manifestations nearly resolved. The clinical manifestations of anti-IgLON5 disease are diverse and may present in different combinations, which can easily lead to misdiagnosis. Early recognition and treatment of this autoimmune disease with immunosuppressive agents may lead to better outcomes.

Structural Regulation of NiFe LDH under Spontaneous Corrosion to Enhance the Oxygen Evolution Properties.

Electrochemical water splitting holds promise for sustainable hydrogen production but restricted by the sluggish reaction kinetics at the anodic oxygen evolution. Herein, we present a room-temperature spontaneous corrosion strategy to convert inexpensive iron (Fe) on iron foam substrates into highly active and stable self-supporting nickel iron layered hydroxide (NiFe LDH) catalysts. The corrosion evolution mechanisms are elucidated combining ex-situ scanning electron microscopy (SEM) and X-ray photo electron spectroscopy (XPS) techniques, demonstrating precise control over the concentration of Ni2+ and reaction time to achieve controllable micro-structures of NiFe LDH. Taking advantage of the self-supporting morphology and hierarchical micro-/nano- structure, the NiFe LDH with optimized Ni2+ concentration and reaction time exhibits significant small overpotentials of 160 mV and 200 mV for the OER at current densities of 10 mA cm-2 and 100 mA cm-2 respectively, showcasing excellent OER activities. Furthermore, this catalyst demonstrates superior reaction kinetics, high electrochemical stability, and excellent integral water splitting performance when coupled with a commercial Pt/C cathode. The energy-efficient, cost-effective, and scalable spontaneous corrosion strategy opens new avenues for the development of high-electrochemical-interface catalysts.

MARCH1 negatively regulates TBK1-mTOR signaling pathway by ubiquitinating TBK1.

BACKGROUND: TBK1 positively regulates the growth factor-mediated mTOR signaling pathway by phosphorylating mTOR. However, it remains unclear how the TBK1-mTOR signaling pathway is regulated. Considering that STING not only interacts with TBK1 but also with MARCH1, we speculated that MARCH1 might regulate the mTOR signaling pathway by targeting TBK1. The aim of this study was to determine whether MARCH1 regulates the mTOR signaling pathway by targeting TBK1. METHODS: The co-immunoprecipitation (Co-IP) assay was used to verify the interaction between MARCH1 with STING or TBK1. The ubiquitination of STING or TBK1 was analyzed using denatured co-immunoprecipitation. The level of proteins detected in the co-immunoprecipitation or denatured co-immunoprecipitation samples were determined by Western blotting. Stable knocked-down cells were constructed by infecting lentivirus bearing the related shRNA sequences. Scratch wound healing and clonogenic cell survival assays were used to detect the migration and proliferation of breast cancer cells. RESULTS: We showed that MARCH1 played an important role in growth factor-induced the TBK1- mTOR signaling pathway. MARCH1 overexpression attenuated the growth factor-induced activation of mTOR signaling pathway, whereas its deficiency resulted in the opposite effect. Mechanistically, MARCH1 interacted with and promoted the K63-linked ubiquitination of TBK1. This ubiquitination of TBK1 then attenuated its interaction with mTOR, thereby inhibiting the growth factor-induced mTOR signaling pathway. Importantly, faster proliferation induced by MARCH1 deficiency was weakened by mTOR, STING, or TBK1 inhibition. CONCLUSION: MARCH1 suppressed growth factors mediated the mTOR signaling pathway by targeting the STING-TBK1-mTOR axis.

Extracellular vesicles from seminal plasma interact with T cells in vitro and drive their differentiation into regulatory T-cells.

Seminal plasma induces immune tolerance towards paternal allogenic antigens within the female reproductive tract and during foetal development. Recent evidence suggests a role for extracellular vesicles in seminal plasma (spEVs). We isolated spEVs from seminal plasma that was donated by vasectomized men, thereby excluding any contributions from the testis or epididymis. Previous analysis demonstrated that such isolated spEVs originate mainly from the prostate. Here we observed that when isolated fluorescently labelled spEVs were mixed with peripheral blood mononuclear cells, they were endocytosed predominantly by monocytes, and to a lesser extent also by T-cells. In a mixed lymphocyte reaction, T-cell proliferation was inhibited by spEVs. A direct effect of spEVs on T-cells was demonstrated when isolated T cells were activated by anti-CD3/CD28 coated beads. Again, spEVs interfered with T cell proliferation, as well as with the expression of CD25 and the release of IFN-γ, TNF, and IL-2. Moreover, spEVs stimulated the expression of Foxp3 and IL-10 by CD4+CD25+CD127- T cells, indicating differentiation into regulatory T-cells (Tregs). Prior treatment of spEVs with proteinase K revoked their effects on T-cells, indicating a requirement for surface-exposed spEV proteins. The adenosine A2A receptor-specific antagonist CPI-444 also reduced effects of spEVs on T-cells, consistent with the notion that the development of Tregs and their immune suppressive functions are under the influence of adenosine-A2A receptor signalling. We found that adenosine is highly enriched in spEVs and propose that spEVs are targeted to and endocytosed by T-cells, after which they may release their adenosine content into the lumen of endosomes, thus allowing endosome-localized A2A receptor signalling in spEVs targeted T-cells. Collectively, these data support the idea that spEVs can prime T cells directly for differentiation into Tregs.

Dietary salt promotes cognitive impairment through repression of SIRT3/PINK1-mediated mitophagy and fission.

Dietary salt is increasingly recognized as an independent risk factor for cognitive impairment. However, the exact mechanisms are not yet fully understood. Mitochondria, which play a crucial role in energy metabolism, are implicated in cognitive function through processes such as mitochondrial dynamics and mitophagy. While mitochondrial dysfunction is acknowledged as a significant determinant of cognitive function, the specific relationship between salt-induced cognitive impairment and mitochondrial health has yet to be fully elucidated. Here, we explored the underlying mechanism of cognitive impairment of mice and N2a cells treated with high-salt focusing on the mitochondrial homeostasis with western blotting, immunofluorescence, electron microscopy, RNA sequencing, and more. We further explored the potential role of SIRT3 in salt-induced mitochondrial dysfunction and synaptic alteration through plasmid transfection and siRNA. High salt diet significantly inhibited mitochondrial fission and blocked mitophagy, leading to dysfunctional mitochondria and impaired synaptic plasticity. Our findings demonstrated that SIRT3 not only promote mitochondrial fission by modulating phosphorylated DRP1, but also rescue mitophagy through promoting PINK1/Parkin-dependent pathway. Overall, our data for the first time indicate that mitochondrial homeostasis imbalance is a driver of impaired synaptic plasticity in a cognitive impairment phenotype that is exacerbated by a long-term high-salt diet, and highlight the protective role of SIRT3 in this process.

OLFM4 modulates intestinal inflammation by promoting IL-22+ILC3 in the gut.

Group 3 innate lymphoid cells (ILC3s) play key roles in intestinal inflammation. Olfactomedin 4 (OLFM4) is highly expressed in the colon and has a potential role in dextran sodium sulfate-induced colitis. However, the detailed mechanisms underlying the effects of OLFM4 on ILC3-mediated colitis remain unclear. In this study, we identify OLFM4 as a positive regulator of IL-22+ILC3. OLFM4 expression in colonic ILC3s increases substantially during intestinal inflammation in humans and mice. Compared to littermate controls, OLFM4-deficient (OLFM4-/-) mice are more susceptible to bacterial infection and display greater resistance to anti-CD40 induced innate colitis, together with impaired IL-22 production by ILC3, and ILC3s from OLFM4-/-mice are defective in pathogen resistance. Besides, mice with OLFM4 deficiency in the RORγt compartment exhibit the same trend as in OLFM4-/-mice, including colonic inflammation and IL-22 production. Mechanistically, the decrease in IL-22+ILC3 caused by OLFM4 deficiency involves the apoptosis signal-regulating kinase 1 (ASK1)- p38 MAPK signaling-dependent downregulation of RAR-related orphan receptor gamma (RORγt) protein. The OLFM4-metadherin (MTDH) complex upregulates p38/RORγt signaling, which is necessary for IL-22+ILC3 activation. The findings indicate that OLFM4 is a novel regulator of IL-22+ILC3 and essential for modulating intestinal inflammation and tissue homeostasis.

Revisiting the Charging Mechanism of α-MnO2 in Mildly Acidic Aqueous Zinc Electrolytes.

In recent years, there have been extensive debates regarding the charging mechanism of MnO2 cathodes in aqueous Zn electrolytes. The discussion centered on several key aspects including the identity of the charge carriers contributing to the overall capacity, the nature of the electrochemical process, and the role of the zinc hydroxy films that are reversibly formed during the charging/discharging. Intense studies are also devoted to understanding the effect of the Mn2+ additive on the performance of the cathodes. Nevertheless, it seems that a consistent explanation of the α-MnO2 charging mechanism is still lacking. To address this, a step-by-step analysis of the MnO2 cathodes is conducted. Valuable information is obtained by using in situ electrochemical quartz crystal microbalance with dissipation (EQCM-D) monitoring, supplemented by solid-state nuclear magnetic resonance (NMR), X-ray diffraction (XRD) in Characterization of Materials, and pH measurements. The findings indicate that the charging mechanism is dominated by the insertion of H3O+ ions, while no evidence of Zn2+ intercalation is found. The role of the Mn2+ additive in promoting the generation of protons by forming MnOOH, enhancing the stability of Zn/α-MnO2 batteries is thoroughly investigated. This work provides a comprehensive overview on the electrochemical and the chemical reactions associated with the α-MnO2 electrodes, and will pave the way for further development of aqueous cathodes for Zn-ion batteries.

[Medium- and long-term effectiveness of hip revision with SL-PLUS MIA stem in patients with Paprosky type â - â ¢ femoral bone defect].

Objective: To investigate the medium- and long-term effectiveness of hip revision with SL-PLUS MIA stem in patients with Paprosky typeⅠ-Ⅲ femoral bone defect. Methods: Between June 2012 and December 2018, 44 patients with Paprosky typeⅠ-Ⅲ femoral bone defect received hip revision using SL-PLUS MIA stem. There were 28 males and 16 females, with an average age of 57.7 years (range, 31-76 years). Indications for revision comprised aseptic loosening (27 cases) and periprosthetic joint infection (17 cases). The Harris hip scores were 54 (48, 60) and 43 (37, 52) in patients with aseptic loosening and periprosthetic joint infection, respectively. The preoperative femoral bone defects were identified as Paprosky type Ⅰ in 32 cases, type Ⅱ in 9 cases, type ⅢA in 2 cases, and type ⅢB in 1 case. Operation time and intraoperative blood transfusion volume were recorded. During follow-up after operation, the hip joint function were evaluated by Harris hip score and X-ray films, the femoral stem survival was analyzed, and the surgical related complications were recorded. Results: The operation time of infected patients was 95-215 minutes, with an average of 125.0 minutes. The intraoperative blood transfusion volume was 400-1 800 mL, with an average of 790.0 mL. The operation time of patients with aseptic loosening was 70-200 minutes, with an average of 121.0 minutes. The intraoperative blood transfusion volume was 400-1 400 mL, with an average of 721.7 mL. All patients were followed up 5.3-10.0 years (mean, 7.4 years). At last follow-up, the Harris hip scores were 88 (85, 90) and 85 (80, 88) in patients with aseptic loosening and periprosthetic joint infection, respectively, both of which were significantly higher than those before operation ( P<0.05). Radiological examination results showed that the distal end of the newly implanted femoral stem did not cross the distal end of the original prosthesis in 25 cases, and all femoral stems obtained bone fixation. Two cases experienced femoral stem subsidence and 1 case had a translucent line on the lateral side of the proximal femoral stem. When aseptic loosening was defined as the end event, the 10-year survival rate of the SL-PLUS MIA stem was 100%. When treatment failure due to any reason was defined as the end event, the survival time of the prosthesis was (111.70±3.66) months, and the 7-year survival rate was 95.5%. The 7-year survival rates were 94.1% and 96.3% in patients with aseptic loosening and periprosthetic joint infection, respectively. The incidence of postoperative complications was 9.1% (4/44), among which the prosthesis related complications were 4.5% (2/44), 1 case of dislocation and 1 case of infection recurrence. Conclusion: Hip revision with SL-PLUS MIA stem has the advantages of simple operation and few postoperative complications in the patients with Paprosky type Ⅰ-Ⅲ femoral bone defect, and the medium- and long-term effectiveness is reliable.

Editorial: Management of PJI/SSI after joint arthroplasty.

The management of periprosthetic joint infection (PJI) and surgical site infection (SSI) after joint arthroplasty poses a major challenge in orthopedic surgery. This Editorial provides an overview of the studies published in the special issue "Management of PJI/SSI after Joint Arthroplasty", summarizing the key findings from these studies, which cover a wide range of topics, including stringent preventive strategies, comprehensive diagnostic methods, and personalized treatment modalities. The authors concluded the editorial with their perspectives regarding the status quo of research in this field and future directions for research, such as the development of novel antibiotics, biofilm research, patient-specific risk factors, and the integration of technological advancements (such as machine learning and artificial intelligence) into clinical practice. The authors emphasized the need for continued research, interdisciplinary collaboration, and the application of innovative technologies to enhance patient outcomes and mitigate the burden of these infections on healthcare systems.

Conservative femoral revision using short cementless stems with a tapered rectangular shape for selected Paprosky II-IV bone defects: an average seven-year follow-up.

BACKGROUND: The use of long stems for severe femoral bone defects is suggested by many scholars, but it is associated with further bone loss, intraoperative fracture, increased surgical trauma, and complications. With better bone retention, simple and quick surgical procedures, and minimal complications, the short cementless stems with a tapered rectangular shape may be an alternative for femoral revision. This study aimed to evaluate the results of this type of stem in treating selected Paprosky II-IV bone defects. METHODS: This retrospective study included 73 patients (76 hips involved) who underwent conservative femoral revision using the short cementless stems with a tapered rectangular shape between January 2012 and December 2020. The preoperative femoral bone defects were identified as follows: 54 cases of type II, 11 cases of type IIIA, 7 cases of type IIIB, and 4 cases of type IV. Indications for revision included aseptic loosening (76.3%) and prosthetic joint infection (23.7%). Six cementless stems with a tapered rectangular shape from three companies were used in all patients. Among them, SLR-Plus, SL-Plus MIA, and Corail stems were employed in most patients (40.8%, 23.7%, and 17.1%, respectively). The average length of these stems measured 171.7 mm (SD 27 mm; 122-215 mm). Radiographic results, Harris hip scores (HHS), complications, and survivorship were analyzed. The follow-up lasted for 7 years on average (range 3-11 years). RESULTS: The subsidence was observed in three hips (3.9%), and all stems achieved stable bone ingrowth. Proximal femoral bone restoration in the residual osteolytic area was found in 67 hips (88.2%), constant defects in nine hips (11.8%), and increasing defects in 0 cases. There was no evidence of stem fractures and stem loosening in this series. The mean HHS significantly improved from 32 (range 15-50) preoperatively to 82 (range 68-94) at the last follow-up (t = - 36.297, P < 0.001). Five hips developed prosthesis-related complications, including three infection and two dislocation cases. The mean 5- and 10-year revision-free survivorships for any revision or removal of an implant and reoperation for any reason were 94.6% and 93.3%, respectively. Both mean 5- and 10-year revision-free survivorships for aseptic femoral loosening were 100%. CONCLUSION: Conservative femoral revision using short cementless stems with a tapered rectangular shape can provide favorable radiographic outcomes, joint function, and mid-term survivorship with minimal complications. Of note, a sclerotic proximal femoral bone shell with continued and intact structure and enough support strength is the indication for using these stems.

High-dose sinomenine attenuates ischemia/reperfusion-induced hepatic inflammation and oxidative stress in rats with diabetes mellitus.

INTRODUCTION: Ischemia-reperfusion (I/R) injury, resulting from blood flow interruption and its subsequent restoration, is a prevalent complication in liver surgery. The liver, as a crucial organ for carbohydrate and lipid metabolism, exhibits decreased tolerance to hepatic I/R in patients with diabetes mellitus (DM), resulting in a significant increase in hepatic dysfunction following surgery. This may be attributed to elevated oxidative stress and inflammation. Our prior research established sinomenine's (SIN) protective role against hepatic I/R injury. Nevertheless, the impact of SIN on hepatic I/R injury in DM rats remains unexplored. OBJECTIVE AND METHODS: This study aimed to investigate the therapeutic potential of SIN in hepatic I/R injury in DM rats and elucidate its mechanism. Diabetic and hepatic I/R injury models were established in rats through high-fat/sugar diet, streptozotocin injection, and hepatic blood flow occlusion. Liver function, oxidative stress, inflammatory reaction, histopathology, and Nrf-2/HO-1 signaling pathway were evaluated by using UV spectrophotometry, biochemical assays, enzyme-linked immunosorbent assay, hematoxylin-eosin staining, and Western blot analysis. RESULTS: High-dose SIN (300 mg/kg) significantly attenuated hepatic I/R injury in DM rats, reducing serum activities of ALT and AST, decreasing the AST/ALT ratio, enhancing tissue contents of SOD and GSH-Px, suppressing the levels of TNF-α and IL-6, improving the liver histopathology, and activating Nrf-2/HO-1 signaling by promoting Nrf-2 trans-location from cytoplasm to nucleus. Low-dose SIN (100 mg/kg) was ineffective. CONCLUSIONS: This study demonstrates that high-dose sinomenine's mitigates hepatic I/R-induced inflammation and oxidative stress in diabetes mellitus (DM) rats via Nrf-2/HO-1 activation, suggesting its potential as a preventive strategy for hepatic I/R injury in DM patients.

Sea Urchin-Like NiCo-LDH Hollow Spheres Anchored on 3D Graphene Aerogel for High-Performance Supercapacitors.

To enhance the inherent poor conductivity and low cycling stability of dimetallic layered double hydroxides (LDHs) materials, designing a synergistic effect between EDLC capacitors and pseudocapacitors is an efficient strategy. In this paper, we utilized a solvothermal technique employing Co-glycerate as a precursor to prepare sea urchin-like NiCo-LDH hollow spheres anchored on a 3D graphene aerogel. The unique morphology of these hollow microspheres significantly expand the specific surface area and exposes more active sites, while reducing the volume changes of materials during long-term charging and discharging processes. The 3D graphene aerogel serves as a conductive skeleton, improving the material's electrical conductivity and buffering high current. The sea urchin-like NiCo-LDH hollow spheres anchored on 3D graphene aerogel (H-NiCo-LDH@GA) has a specific surface area of 51 m2 g-1 and the ID/IG value is 1.02. The H-NiCo-LDH@GA demonstrate a significant specific capacitance of 236.8 mAh g-1 at 1 A g-1, with a remarkable capacity retention rate of 63.1 % even at 20 A g-1. Even after 8000 cycles at 10 A g-1, the capacity retention still remains at 96.3 %, presenting excellent cycling stability.

Determination of vancomycin and meropenem in serum and synovial fluid of patients with prosthetic joint infections using UPLC-MS/MS.

Numerous studies have suggested that intra-articular administration of antibiotics following primary revision surgery may be one of the methods for treating prosthetic joint infection (PJI). Vancomycin and meropenem are the two most commonly used antibiotics for local application. Determining the concentrations of vancomycin and meropenem in the serum and synovial fluid of patients with PJI plays a significant role in further optimizing local medication schemes and effectively eradicating biofilm infections. This study aimed to establish a rapid, sensitive, and accurate ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method for determining the concentrations of vancomycin and meropenem in human serum and synovial fluid. Serum samples were processed using acetonitrile precipitation of proteins and dichloromethane extraction, while synovial fluid samples were diluted before analysis. Chromatographic separation was achieved in 6 min on a Waters Acquity UPLC BEH C18 column, with the mobile phase consisting of 0.1% formic acid in water (solvent A) and acetonitrile (solvent B). Quantification was carried out using a Waters XEVO TQD triple quadrupole mass spectrometer with an electrospray ionization (ESI) source in positive ion mode. The multiple reaction monitoring (MRM) mode was employed to detect the following quantifier ion transitions: 717.95-99.97 (norvancomycin), 725.90-100.04 (vancomycin), 384.16-67.99 (meropenem). The method validation conformed to the guidelines of the FDA and the Chinese Pharmacopoeia. The method demonstrated good linearity within the range of 0.5-50 µg/ml for serum and 0.5-100 µg/ml for synovial fluid. Selectivity, intra-day and inter-day precision and accuracy, extraction recovery, matrix effect, and stability validation results all met the required standards. This method has been successfully applied in the pharmacokinetic/pharmacodynamic (PK/PD) studies of patients with PJI.

Astragaloside IV inhibits angiotensin II-induced atrial fibrosis and atrial fibrillation by SIRT1/PGC-1α/FNDC5 pathway.

Aims and objectives: Astragaloside IV (AS-IV) has been found to possess anti-oxidative, anti-inflammatory, and anti-apoptotic properties, but its effect on atrial fibrosis is yet to be determined. This research investigates the protective role of AS-IV in angiotensin II (Ang II)-induced atrial fibrosis and atrial fibrillation (AF). Methods: C57BL/6 male mice aged 8-10 weeks (n = 40) were subcutaneously administered Ang II (2.0 mg/kg/day) or saline, with AS-IV (80 mg/kg) intraperitoneally administered 2 h before Ang II infusion for 4 weeks. Biochemical, histological, and morphological analyses were carried out. Using transesophageal burst pacing, AF was generated in vivo. Results: Here, we report that AS-IV treatment inhibited Ang II-induced AF development in mice (58 ± 5.86 vs 15.13 ± 2.16 %, p < 0.001). Ang II + AS-IV therapy was effective in reducing the atrial fibrotic area and decreasing the increase in smooth muscle alpha-actin (α-SMA)-positive myofibroblasts brought on by Ang II treatment (fibrotic area: 26.25 ± 3.81 vs 8.62 ± 1.83 %, p < 0.001 and α-SMA: 65.62 ± 10.63 vs 17.25 ± 1.78 %, p < 0.001). The reactive oxygen species (ROS) production was reduced by pretreatment with Ang II + AS-IV (9.20 ± 0.92 vs 2.63 ± 0.22 %/sec, p < 0.001). In addition, Ang II + AS-IV treatment suppressed oxidative stress in Ang II-induced atrial fibrosis (malondialdehyde: 701.78 ± 85.01 vs 504.07 ± 25.62 pmol/mg protein, p < 0.001; superoxide dismutase: 13.82 ± 1.25 vs 29.54 ± 2.45 U/mg protein, p < 0.001 and catalase: 11.43 ± 1.19 vs 20.83 ± 3.29 U/mg protein, p < 0.001, respectively). Moreover, Ang II + AS-IV decreased the expression of α-SMA, collagen III and collagen I (3.32 ± 0.53 vs 1.41 ± 0.20 fold, p < 0.001; 3.41 ± 0.55 vs 1.48 ± 0.18 fold, p < 0.001; 2.34 ± 0.55 vs 0.99 ± 0.17 fold, p < 0.001, respectively) while increasing the protein expression of sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α), and fibronectin type III domain-containing protein 5 (FNDC5) in Ang II-treated mice (0.22 ± 0.02 vs 0.57 ± 0.08 fold, p < 0.001; 0.28 ± 0.04 vs 0.72 ± 0.05 fold, p < 0.001; 0.38 ± 0.03 vs 0.68 ± 0.06 fold, p < 0.001, respectively). Conclusion: Our data led us to speculate that AS-IV may protect against Ang II-induced atrial fibrosis and AF via upregulation of the SIRT1/PGC-1α/FNDC5 pathway.

Flexible Thermoelectric Device Based on Protrusion-Structured Liquid Metal Elastomer for Gravity Heat Pipe.

Monitoring the temperature of the coal gangue mountains is fundamental to preventing their spontaneous combustion. However, the existing temperature monitoring systems fail to achieve stable, pollution-free temperature monitoring without affecting vegetation growth in these mountains. To address this issue, this work proposes a flexible thermoelectric device (FTD) based on a protrusion-structured liquid metal elastomer (LME). Utilizing a high-thermal-conductivity LME, the FTD adheres closely to the surface of the gravity heat pipe (GHP), ensuring compatibility between FTD and the curved surface of the GHP. Simultaneously, employing a low-thermal-conductivity elastomer helps concentrate heat onto FTD, thereby enhancing thermoelectric power generation efficiency. Additionally, the impact of the shape, size, and height of the protrusion structure at the cold end of the GHP on its efficiency was also investigated. The practical application of FTD on GHP was demonstrated.

Laparoscopic-assisted full-sized liver transplantation with magnetically fast portal vein anastomosis: An initial cohort study.

BACKGROUND: Some cases of laparoscopic-assisted liver transplantation (LA-LT) with utilization of reduced-size grafts has been reported. We here introduced successful utilization of LA-LT with whole liver grafts and magnetic portal vein anastomosis. METHODS: Eight patients with liver cirrhosis were included for LA-LT using donor organs after cardiac death. The surgical procedures included purely laparoscopic explant hepatectomy and whole-liver graft implantation via the midline incision. After explant removal, the whole-liver graft was then placed in situ, and a side-to-side cavo-caval anastomosis with 4-5 cm oval opening was performed. The magnetic rings were everted on the donor and recipient portal vein, respectively, and the instant attachment of the two magnets at the donor and recipient portal vein allowed fast blood reperfusion, followed by continuous suturing on the surface of the magnets. RESULTS: The median operation time was 495 (range 420-630). The median time of explant hepatectomy and IVC anastomosis was 239 (range 150-300) min and 14.5 (range 10-19) min, respectively. Of note, the median anhepatic time was 25 (range 20-35) min. All the patients were discharged home with no major complications after more than six months follow-up. CONCLUSION: LA-LT with full-size graft is feasible and utilization of magnetic anastomosis would further simplify the procedure.

Promoted Reaction Reversibility by Dual-Effect 15-Crown-5 Ether Additive for High-Performance Li-O2 Batteries.

The practical application of lithium-oxygen batteries (LOBs) with ultrahigh theoretical energy density faces the problems of poor kinetics and deficient reversibility. The electrolyte is of vital significance to the electrochemical stability and reaction pathway of LOBs due to the formation of soluble products. Here, a 15-crown-5 ether (15C5) is employed to regulate the solvation structure of Li+ and manipulate the reaction mechanism through regulating the binding ability toward Li+. The promoted dissociation of LiNO3 by 15C5 increases the catalytical active anions in the electrolyte and stabilizes the Li-containing reduced oxygen species to promote the solution pathway of discharge product growth. Besides, 15C5 also facilitates the kinetics of the electrochemical decomposition of Li2O2 and prolongs the cycle life to 178 cycles. This work inspires a novel approach to improve the battery performance through electrolyte component design.

SLIT3 promotes cardiac fibrosis and differentiation of cardiac fibroblasts by RhoA/ROCK1 signaling pathway.

Objectives: Slit guidance ligand 3 (SLIT3) has been identified as a potential therapeutic regulator against fibroblast activity and fibrillary collagen production in an autocrine manner. However, this research aims to investigate the potential role of SLIT3 in cardiac fibrosis and fibroblast differentiation and its underlying mechanism. Materials and Methods: C57BL/6 mice (male, 8-10 weeks, n=47) were subcutaneously infused with Ang II (2.0 mg/kg/day) for 4 weeks. One to two-day-old Sprague-Dawley (SD) rats were anesthetized by intraperitoneal injection of 1% pentobarbital sodium (60 mg/kg) and ketamine (50 mg/kg) and the cardiac fibroblast was isolated aseptically. The mRNA and protein expression were analyzed using RT-qPCR and Western blotting. Results: The SLIT3 expression level was increased in Ang II-induced mice models and cardiac fibroblasts. SLIT3 significantly increased migrated cells and α-smooth muscle actin (α-SMA) expression in cardiac fibroblasts. Ang II-induced increases in mRNA expression of collagen I (COL1A1), and collagen III (COL3A1) was attenuated by SLIT3 inhibition. SLIT3 knockdown attenuated the Ang II-induced increase in mRNA expression of ACTA2 (α-SMA), Fibronectin, and CTGF. SLIT3 suppression potentially reduced DHE expression and decreased malondialdehyde (MDA) content, and the superoxide dismutase (SOD) and catalase (CAT) levels were significantly increased in cardiac fibroblasts. Additionally, SLIT3 inhibition markedly decreased RhoA and ROCK1 protein expression, whereas ROCK inhibitor Y-27632 (10 µM) markedly attenuated the migration of cardiac fibroblasts stimulated by Ang II and SLIT3. Conclusion: The results speculate that SLIT3 could significantly regulate cardiac fibrosis and fibroblast differentiation via the RhoA/ROCK1 signaling pathway.

High-Area-Capacity Cathode by Ultralong Carbon Nanotubes for Secondary Binder-Assisted Dry Coating Technology.

Thick electrodes with high mass loading and increased content of active materials are critical for achieving higher energy density in contemporary lithium-ion batteries (LIBs). Nonetheless, producing thick electrodes through the commonly used slurry coating technology remains a formidable challenge. In this study, we have addressed this challenge by developing a dry electrode technology by using ultralong multiwalled carbon nanotubes (MWCNT) as a conductive additive and secondary binder. The mixing process of electrode compositions and the fibrillation process of the polytetrafluoroethylene (PTFE) binder were optimized. The resulting LiCoO2 (LCO) electrode exhibited a remarkable mass loading of 48 mg cm-2 and an active material content of 95 wt %. Notably, the thick LCO electrode demonstrated a superior mechanical strength and electrochemical performance. After 100 cycles at a current density of 1/3 C, the electrode still exhibited a capacity retention of 91% of its initial capacity. This dry electrode technology provides a practicable and scalable approach to the powder-to-film LIB electrode manufacturing process.

Crocetin preconditioning attenuates ischemia reperfusion-induced hepatic injury by disrupting Keap1/Nrf2 interaction and activating Nrf2/HO-1 pathway.

BACKGROUND: Ischemia reperfusion (I/R) injury is a frequent occurrence during liver transplantation surgery, resulting from the temporary cessation of blood flow and subsequent restoration of blood flow. Serious I/R injury is a significant factor causing transplant failure. Hepatic I/R process is characterized by excessive inflammation, oxidation, and apoptosis. Crocetin (Crt) is a natural compound exhibiting beneficial roles in various I/R-induced organ damages. However, Crt's potential role in hepatic I/R remains unexplored. OBJECTIVE AND METHODS: In order to reveal the impact of Crt on hepatic I/R and the associated signaling pathway, we utilized a syngeneic orthotopic liver transplantation rat model to induce hepatic I/R injury. RESULTS: Pretreatment with Crt significantly mitigated hepatic I/R injury. This was evident by decreased activities of serum ALT, AST and LDH, indicating improved liver function. Crt treatment also alleviated oxidative stress, as demonstrated by decreased serum MDA content and elevated serum SOD and GSH-Px activities. Furthermore, Crt suppressed inflammatory responses by downregulating both the serum and liver IL-1ß, IL-6 and TNF-α while upregulating IL-10 expression. Additionally, Crt reduced apoptosis by decreasing pro-apoptotic Bax, cleaved caspase-3 and cleaved caspase-9, while increasing anti-apoptotic Bcl2 expression. Notably, these protective effects of Crt were dose-dependent. Moreover, our data indicates that Crt plays protective functions during hepatic I/R via disrupting Keap1/Nrf2 interaction and activating Nrf2/HO-1 signaling. This was further supported by observations of alleviated hepatic histopathological changes in I/R rats treated with Crt. CONCLUSIONS: Crt shows potential as a therapeutic agent for preventing hepatic I/R injury during clinical liver transplantation.