The increase of long noncoding RNA Fendrr in hepatocytes contributes to liver fibrosis by promoting IL-6 production.

Liver fibrosis/cirrhosis is a pathological state caused by excessive extracellular matrix deposition. Sustained activation of hepatic stellate cells (HSC) is the predominant cause of liver fibrosis, but the detailed mechanism is far from clear. In this study, we found that long noncoding RNA Fendrr is exclusively increased in hepatocytes in the murine model of CCl4- and bile duct ligation-induced liver fibrosis, as well as in the biopsies of liver cirrhosis patients. In vivo, ectopic expression of Fendrr aggravated the severity of CCl4-induced liver fibrosis in mice. In contrast, inhibiting Fendrr blockaded the activation of HSC and ameliorated CCl4-induced liver fibrosis. Our mechanistic study showed that Fendrr binds to STAT2 and enhances its enrichment in the nucleus, which then promote the expression of interleukin 6 (IL-6), and, ultimately, activates HSC in a paracrine manner. Accordingly, disrupting the interaction between Fendrr and STAT2 by ectopic expression of a STAT2 mutant attenuated the profibrotic response inspired by Fendrr in the CCl4-induced liver fibrosis. Notably, the increase of Fendrr in patient fibrotic liver is positively correlated with the severity of fibrosis and the expression of IL-6. Meanwhile, hepatic IL-6 positively correlates with the extent of liver fibrosis and HSC activation as well, thus suggesting a causative role of Fendrr in HSC activation and liver fibrosis. In conclusion, these observations identify an important regulatory cross talk between hepatocyte Fendrr and HSC activation in the progression of liver fibrosis, which might represent a potential strategy for therapeutic intervention.

Treatment Modalities and Outcomes in Brainstem Cavernous Malformations: A Large Multicenter Observational Cohort Study.

BACKGROUND: Symptomatic brainstem cavernous malformations (BSCMs) pose a high risk of morbidity and mortality due to recurrent hemorrhage, warranting aggressive management. However, few studies have compared the effectiveness of different treatment modalities for BSCMs. We aimed to assess the association of treatment modalities with recurrent hemorrhage and neurological outcomes in patients with BSCM. METHODS: We conducted a retrospective cohort study using an observational registry database covering population of southwest and southeast China. Adult patients with BSCM were included and followed up between March 1, 2011, to March 31, 2023. We compared outcomes between microsurgery and stereotactic radiosurgery (SRS) in propensity score-matched case pairs, incorporating demographic, medical history, and lesion characteristics. The outcomes studied included recurrent hemorrhage and poor prognosis (defined as a Glasgow Outcome Scale score, <4). Absolute rate differences and hazard ratios (HRs) with 95% CIs were calculated using Cox models. RESULTS: Among 736 diagnosed patients with BSCM, 96 (48 matched pairs) were included after exclusions and propensity score matching (mean age, 43.1 [SD, 12.1] years; 50% women). During the median 5-year follow-up, no significant differences in recurrent hemorrhage (4.2% [microsurgery] versus 14.6% [SRS], HR, 3.90 [95% CI, 0.46-32.65]; P=0.21) and poor prognosis (12.5% [microsurgery] versus 8.3% [SRS], HR, 0.29 [95% CI, 0.08-1.08]; P=0.07) were observed between microsurgery and SRS recipients. Furthermore, either microsurgery or SRS correlated with fewer recurrent hemorrhage (HR, 0.09 [95% CI, 0.02-0.39]; P=0.001; HR, 0.21 [95% CI, 0.07-0.69]; P=0.01) compared with conservative treatment. CONCLUSIONS: In this study, both microsurgery and SRS were safe and effective for BSCM, demonstrated comparable outcomes in recurrent hemorrhage and poor prognosis. However, interpretation should be cautious due to the potential for residual confounding. REGISTRATION: URL: https://www.chictr.org.cn/; Unique identifier: ChiCTR2300070907.

Synergistic Effects of In-Situ Exsolved Ni-Ru Bimetallic Catalyst on High-Performance and Durable Direct-Methane Solid Oxide Fuel Cells.

Direct-methane solid oxide fuel cells (CH4-SOFCs) have gained significant attention as methane, the primary component of natural gas (NG), is cheap and widely available and the natural gas infrastructures are relatively mature. However, at intermediate temperatures (e.g., 600-650 °C), current CH4-SOFCs suffer from low performance and poor durability under a low steam-to-carbon ratio (S/C ratio), which is ascribed to the Ni-based anode that is of low catalytic activity and prone to coking. Herein, with the guidance of density functional theory (DFT) studies, a highly active and coking tolerant steam methane reforming (SMR) catalyst, Sm-doped CeO2-supported Ni-Ru (SCNR), was developed. The synergy between Ni and Ru lowers the activation energy of the first C-H bond activation and promotes CHx decomposition. Additionally, Sm doping increases the oxygen vacancy concentration in CeO2, facilitating H2O adsorption and dissociation. The SCNR can therefore simultaneously activate both CH4 and H2O molecules while oxidizing the CH* and improving coking tolerance. We then applied SCNR as the CH4-SOFC anode catalytic reforming layer. A peak power density of 733 mW cm-2 was achieved at 650 °C, representing a 55% improvement compared to that of pristine CH4-SOFCs (473 mW cm-2). Moreover, long-term durability testing, with >2000 h continuous operation, was performed under almost dry methane (5% H2O). These results highlight that CH4-SOFCs with a SCNR catalytic layer can convert NG to electricity with high efficiency and resilience.

Unraveling a Concerted Proton-Coupled Electron Transfer Pathway in Atomically Precise Gold Nanoclusters.

Metal nanoclusters (MNCs) represent a promising class of materials for catalytic carbon dioxide and proton reduction as well as dihydrogen oxidation. In such reactions, multiple proton-coupled electron transfer (PCET) processes are typically involved, and the current understanding of PCET mechanisms in MNCs has primarily focused on the sequential transfer mode. However, a concerted transfer pathway, i.e., concerted electron-proton transfer (CEPT), despite its potential for a higher catalytic rate and lower reaction barrier, still lacks comprehensive elucidation. Herein, we introduce an experimental paradigm to test the feasibility of the CEPT process in MNCs, by employing Au18(SR)14 (SR denotes thiolate ligand), Au22(SR)18, and Au25(SR)18- as model clusters. Detailed investigations indicate that the photoinduced PCET reactions in the designed system proceed via an CEPT pathway. Furthermore, the rate constants of gold nanoclusters (AuNCs) have been found to be correlated with both the size of the cluster and the flexibility of the Au-S framework. This newly identified PCET behavior in AuNCs is prominently different from that observed in semiconductor quantum dots and plasmonic metal nanoparticles. Our findings are of crucial importance for unveiling the catalytic mechanisms of quantum-confined metal nanomaterials and for the future rational design of more efficient catalysts.

Effect of Automated Real-Time Feedback on Early-Sepsis Care: A Pragmatic Clinical Trial.

OBJECTIVES: To determine if a real-time monitoring system with automated clinician alerts improves 3-hour sepsis bundle adherence. DESIGN: Prospective, pragmatic clinical trial. Allocation alternated every 7 days. SETTING: Quaternary hospital from December 1, 2020 to November 30, 2021. PATIENTS: Adult emergency department or inpatients meeting objective sepsis criteria triggered an electronic medical record (EMR)-embedded best practice advisory. Enrollment occurred when clinicians acknowledged the advisory indicating they felt sepsis was likely. INTERVENTION: Real-time automated EMR monitoring identified suspected sepsis patients with incomplete bundle measures within 1-hour of completion deadlines and generated reminder pages. Clinicians responsible for intervention group patients received reminder pages; no pages were sent for controls. The primary analysis cohort was the subset of enrolled patients at risk of bundle nonadherent care that had reminder pages generated. MEASUREMENTS AND MAIN RESULTS: The primary outcome was orders for all 3-hour bundle elements within guideline time limits. Secondary outcomes included guideline-adherent delivery of all 3-hour bundle elements, 28-day mortality, antibiotic discontinuation within 48-hours, and pathogen recovery from any culture within 7 days of time-zero. Among 3,269 enrolled patients, 1,377 had reminder pages generated and were included in the primary analysis. There were 670 (48.7%) at-risk patients randomized to paging alerts and 707 (51.3%) to control. Bundle-adherent orders were placed for 198 intervention patients (29.6%) versus 149 (21.1%) controls (difference: 8.5%; 95% CI, 3.9-13.1%; p = 0.0003). Bundle-adherent care was delivered for 152 (22.7%) intervention versus 121 (17.1%) control patients (difference: 5.6%; 95% CI, 1.4-9.8%; p = 0.0095). Mortality was similar between groups (8.4% vs 8.3%), as were early antibiotic discontinuation (35.1% vs 33.4%) and pan-culture negativity (69.0% vs 68.2%). CONCLUSIONS: Real-time monitoring and paging alerts significantly increased orders for and delivery of guideline-adherent care for suspected sepsis patients at risk of 3-hour bundle nonadherence. The trial was underpowered to determine whether adherence affected mortality. Despite enrolling patients with clinically suspected sepsis, early antibiotic discontinuation and pan-culture negativity were common, highlighting challenges in identifying appropriate patients for sepsis bundle application.

TRIM26 inhibits clear cell renal cell carcinoma progression through destabilizing ETK and thus inactivation of AKT/mTOR signaling.

BACKGROUND: Tripartite motif-containing 26 (TRIM26), a member of the TRIM protein family, exerts dual function in several types of cancer. Nevertheless, the precise role of TRIM26 in clear cell renal cell carcinoma (ccRCC) has not been investigated. METHODS: The expression of TRIM26 in ccRCC tissues and cell lines were examined through the use of public resources and experimental validation. The impacts of TRIM26 on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) process were determined via CCK-8, colony formation, EdU incorporation, wound healing, Transwell invasion, Western blot, and Immunofluorescence assays. RNA-seq followed by bioinformatic analyses were used to identify the downstream pathway of TRIM26. The interaction between TRIM26 and ETK was assessed by co-immunoprecipitation, qRT-PCR, Western blot, cycloheximide (CHX) chase, and in vivo ubiquitination assays. RESULTS: We have shown that TRIM26 exhibits a downregulation in both ccRCC tissues and cell lines. Furthermore, this decreased expression of TRIM26 is closely linked to unfavorable overall survival and diseases-free survival outcomes among ccRCC patients. Gain- and loss-of-function experiments demonstrated that increasing the expression of TRIM26 suppressed the proliferation, migration, invasion, and EMT process of ccRCC cells. Conversely, reducing the expression of TRIM26 had the opposite effects. RNA sequencing, coupled with bioinformatic analysis, revealed a significant enrichment of the mTOR signaling pathway in the control group compared to the group with TRIM26 overexpression. This finding was then confirmed by a western blot assay. Subsequent examination revealed that TRMI26 had a direct interaction with ETK, a non-receptor tyrosine kinase. This interaction facilitated the ubiquitination and degradation of ETK, resulting in the deactivation of the AKT/mTOR signaling pathway in ccRCC. ETK overexpression counteracted the inhibitory effects of TRIM26 overexpression on cell proliferation, migration, and invasion. CONCLUSION: Our results have shown a novel mechanism by which TRIM26 hinders the advancement of ccRCC by binding to and destabilizing ETK, thus leading to the deactivation of AKT/mTOR signaling. TRIM26 shows promise as both a therapeutic target and prognostic biomarker for ccRCC patients.

Cascaded multicore fiber interferometers for enhanced bending sensing based on the Vernier effect.

In this paper, cascaded modal interferometers constructed by strongly-coupled seven-core fiber (SC-SCF) with different lengths are demonstrated for enhanced bending sensing based on Vernier effect. The free spectral range (FSR) of a single SC-SCF interferometer is determined by the length of SC-SCF. Two SC-SCF interferometers with different FSRs are cascaded, in which, one functions as the sensor while the other functions as the reference. The wavelength shift of the envelope of the output spectrum is much larger than that of a single SC-SCF interferometer due to the Vernier effect. Therefore, enhanced sensing can be achieved. Experimental results show that the bending sensitivity of the proposed sensor is improved from -2.20 nm/m-1 (single SC-SCF interferometer) to 42.32 nm/m-1 (cascaded SC-SCF interferometers). The temperature response of the sensor is also investigated. Our proposed cascaded SC-SCF sensor has advantages of high sensitivity, ease of fabrication, and low cost. It is attractive for high precision bending sensing applications.

Efficient Initialization of Fluxonium Qubits based on Auxiliary Energy Levels.

Fast and high-fidelity qubit initialization is crucial for low-frequency qubits such as fluxonium, and in applications of many quantum algorithms and quantum error correction codes. In a circuit quantum electrodynamics system, the initialization is typically achieved by transferring the state between the qubit and a short-lived cavity through microwave driving, also known as the sideband cooling process in atomic system. Constrained by the selection rules from the parity symmetry of the wave functions, the sideband transitions are only enabled by multiphoton processes which require multitone or strong driving. Leveraging the flux tunability of fluxonium, we circumvent this limitation by breaking flux symmetry to enable an interaction between a noncomputational qubit transition and the cavity excitation. With single-tone sideband driving, we realize qubit initialization with a fidelity exceeding 99% within a duration of 300 ns, robust against the variation of control parameters. Furthermore, we show that our initialization scheme has a built-in benefit in simultaneously removing the second-excited state population of the qubit, and can be easily incorporated into a large-scale fluxonium processor.

Native Approach to Controlled-Z Gates in Inductively Coupled Fluxonium Qubits.

The fluxonium qubits have emerged as a promising platform for gate-based quantum information processing. However, their extraordinary protection against charge fluctuations comes at a cost: when coupled capacitively, the qubit-qubit interactions are restricted to XX interactions. Consequently, effective ZZ or XZ interactions are only constructed either by temporarily populating higher-energy states, or by exploiting perturbative effects under microwave driving. Instead, we propose and demonstrate an inductive coupling scheme, which offers a wide selection of native qubit-qubit interactions for fluxonium. In particular, we leverage a built-in, flux-controlled ZZ interaction to perform qubit entanglement. To combat the increased flux-noise-induced dephasing away from the flux-insensitive position, we use a continuous version of the dynamical decoupling scheme to perform noise filtering. Combining these, we demonstrate a 20 ns controlled-z gate with a mean fidelity of 99.53%. More than confirming the efficacy of our gate scheme, this high-fidelity result also reveals a promising but rarely explored parameter space uniquely suitable for gate operations between fluxonium qubits.

Temperature-responsive optogenetic probes of cell signaling.

We describe single-component optogenetic probes whose activation dynamics depend on both light and temperature. We used the BcLOV4 photoreceptor to stimulate Ras and phosphatidyl inositol-3-kinase signaling in mammalian cells, allowing activation over a large dynamic range with low basal levels. Surprisingly, we found that BcLOV4 membrane translocation dynamics could be tuned by both light and temperature such that membrane localization spontaneously decayed at elevated temperatures despite constant illumination. Quantitative modeling predicted BcLOV4 activation dynamics across a range of light and temperature inputs and thus provides an experimental roadmap for BcLOV4-based probes. BcLOV4 drove strong and stable signal activation in both zebrafish and fly cells, and thermal inactivation provided a means to multiplex distinct blue-light sensitive tools in individual mammalian cells. BcLOV4 is thus a versatile photosensor with unique light and temperature sensitivity that enables straightforward generation of broadly applicable optogenetic tools.

Effects of acetate-producing Blautia wexlerae on oxidative stress and NLRP3 inflammasome in obesity-associated male infertility.

BACKGROUND: Obesity-associated male infertility is a common complication of obesity and has been increasing in prevalence. Blautia wexlerae has modulation effects on obesity. However, the action of B. wexlerae on obesity-associated male infertility is unclear. The nod-like receptor protein 3 (NLRP3) inflammasome has become a major target for addressing many diseases, including obesity-associated male infertility. This study aims to investigate the action of B. wexlerae on obesity-associated male infertility and the influence of B. wexlerae on NLRP3 inflammasome. MATERIALS AND METHODS: The fecal samples were collected from 60 infertile men with or without obesity and 30 healthy men. The obesity mice model was established through high-fat diet (HFD) induction. The mating assays evaluated the male infertility of obese mice. A mouse-derived spermatogonia (GC-1 spg) cell viability was detected using the Cell Counting Kit-8 assay. The reactive oxygen species (ROS) were assessed using flow cytometry. Furthermore, immunofluorescence, enzyme-linked immunosorbent assay, and western blotting were applied to measure the gene expressions. RESULTS: Blautia wexlerae was decreased and negatively correlated with interleukin-1 beta (IL-1ß) or IL-18 levels in infertile men with obesity. On the other hand, B. wexlerae improved the mating capability of obese male mice and suppressed oxidative stress and NLRP3 inflammasome via the activation of the acetate receptor. Furthermore, sodium acetate regulated oxidative stress and NLRP3 inflammasome via the activation of the acetate receptor in GC-1 spg cells in vitro. CONCLUSION: The administration of Blautia wexlerae improved obesity-associated male infertility and regulated oxidative stress and NLRP3 inflammasome activities. In general, its administration may be an effective strategy for the treatment of obesity-associated male infertility.

Construction and Validation of a Prognostic Model Based on Mitochondrial Genes in Prostate Cancer.

This study attempted to build a prostate cancer (PC) prognostic risk model with mitochondrial feature genes. PC-related MTGs were screened for Cox regression analyses, followed by establishing a prognostic model. Model validity was analyzed via survival analysis and receiver operating characteristic (ROC) curves, and model accuracy was validated in the GEO dataset. Combining risk score with clinical factors, the independence of the risk score was verified by using Cox analysis, followed by generating a nomogram. The Gleason score, microsatellite instability (MSI), immune microenvironment, and tumor mutation burden were analyzed in two risk groups. Finally, the prognostic feature genes were verified through a q-PCR test. Ten PC-associated MTGs were screened, and a prognostic model was built. Survival analysis and ROC curves illustrated that the model was a good predictor for the risk of PC. Cox regression analysis revealed that risk score acted as an independent prognostic factor. The Gleason score and MSI in the high-risk group were substantially higher than in the low-risk group. Levels of ESTIMATE Score, Immune Score, Stromal Score, immune cells, immune function, immune checkpoint, and immunopheno score of partial immune checkpoints in the high-risk group were significantly lower than in the low-risk group. Genes with the highest mutation frequencies in the two groups were SPOP, TTN, and TP53. The q-PCR results of the feature genes were consistent with the gene expression results in the database. The 10-gene model based on MTGs could accurately predict the prognosis of PC patients and their responses to immunotherapy.

Photocatalytic Reduction of Perrhenate and Pertechnetate in a Strongly Acidic Aqueous Solution.

Pertechnetate (99TcO4-), a physiologically toxic radioactive anion, is of great concern due to its high mobility in environmental contamination remediation. Although the soluble oxyanion can be photoreduced to sparingly soluble TcO2·nH2O, its effective removal from a strongly acidic aqueous solution remains a challenge. Here, we found that low-crystalline nitrogen-doped titanium oxide (N-TiO2, 0.6 g L-1) could effectively uptake perrhenate (ReO4-, 10 mg L-1, a nonradioactive surrogate for TcO4-) with 50.8% during 360 min under simulated sunlight irradiation at pH 1.0, but P25 and anatase could not. The nitrogen active center formed by trace nitrogen doping in N-TiO2 can promote the separation and transfer of photogenerated carriers. The positive valence band value of N-TiO2 is slightly higher than those of P25 and anatase, which means that the photogenerated holes have a stronger oxidizability. These holes are involved in the formation of strong reducing •CO2- radicals from formic acid oxidation. The active radicals convert ReO4- to Re(VI), which is subsequently disproportionated to Re(IV) and Re(VII). Effective photocatalytic reduction/removal of Re(VII)/Tc(VII) is performed on the material, which may be considered a potential and convenient strategy for technetium decontamination and extraction in a strongly acidic aqueous solution.

A colorimetric sensing strategy based on chitosan-stabilized platinum nanoparticles for quick detection of α-glucosidase activity and inhibitor screening.

α-Glucosidase (α-Glu) is implicated in the progression and pathogenesis of type II diabetes (T2D). In this study, we developed a rapid colorimetric technique using platinum nanoparticles stabilized by chitosan (Ch-PtNPs) to detect α-Glu activity and its inhibitor. The Ch-PtNPs facilitate the conversion of 3,3',5,5'-tetramethylbenzidine (TMB) into oxidized TMB (oxTMB) in the presence of dissolved O2. The catalytic hydrolysis of 2-O-α-D-glucopyranosyl-L-ascorbic acid (AA-2G) by α-Glu produces ascorbic acid (AA), which reduces oxTMB to TMB, leading to the fading of the blue color. However, the presence of α-Glu inhibitors (AGIs) hinders the generation of AA, allowing Ch-PtNPs to re-oxidize colorless TMB back to blue oxTMB. This unique phenomenon enables the colorimetric detection of α-Glu activity and AGIs. The linear range for α-Glu was found to be 0.1-1.0 U mL-1 and the detection limit was 0.026 U mL-1. Additionally, the half-maximal inhibition value (IC50) for acarbose, an α-Glu inhibitor, was calculated to be 0.4769 mM. Excitingly, this sensing platform successfully detected α-Glu activity in human serum samples and effectively screened AGIs. These promising findings highlight the potential application of the proposed strategy in clinical diabetes diagnosis and drug discovery.

Panaxadiol carbamate derivatives: Synthesis and biological evaluation as potential multifunctional anti-Alzheimer agents.

It is reported that panaxadiol has neuroprotective effects. Previous studies have found that compound with carbamate structure introduced at the 3-OH position of 20 (R) -panaxadiol showed the most effective neuroprotective activity with an EC50 of 13.17 µM. Therefore, we designed and synthesized a series of ginseng diol carbamate derivatives with ginseng diol as the lead compound, and tested their anti-AD activity. It was found that the protective effect of compound Q4 on adrenal pheochromocytoma was 80.6 ±â€¯10.85 % (15 µM), and the EC50 was 4.32 µM. According to the ELISA results, Q4 reduced the expression of Aß25-35 by decreasing ß-secretase production. Molecular docking studies revealed that the binding affinity of Q4 to ß-secretase was -49.67 kcal/mol, indicating a strong binding affinity of Q4 to ß-secretase. Western blotting showed that compound Q4 decreased IL-1ß levels, which may contribute to its anti-inflammatory effect. Furthermore, compound Q4 exhibits anti-AD activities by reducing abnormal phosphorylation of tau protein and activation of the mitogen activated protein kinase pathway. The learning and memory deficits in mice treated with Q4in vivo were significantly alleviated. Therefore, Q4 may be a promising multifunctional drug for the treatment of AD, providing a new way for anti-AD drugs.

[Research progress on the role of TANK-binding kinase 1 in PINK1/Parkin-dependent and -independent mitophagy].

Mitophagy is a process that selectively removes excess or damaged mitochondria and plays an important role in regulating intracellular mitochondrial mass and maintaining mitochondrial energy metabolism. TANK-binding kinase 1 (TBK1) is a multifunctional serine/threonine protein kinase, which is involved in the regulation of PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent and -independent mitophagy. Recent studies have shown that TBK1 phosphorylates the autophagy related proteins, such as optineurin (OPTN), p62/sequestosome-1, Ras-related GTP binding protein 7 (Rab7), and mediates the binding of nuclear dot protein 52 (NDP52) to UNC-51 like autophagy activating kinase 1 (ULK1) complex, as well as the binding of TAX1-binding protein 1 (TAX1BP1) to microtubule-associated protein 1 light chain 3 (LC3), thereby enhancing PINK1/Parkin-dependent mitophagy. In addition, TBK1 is a direct substrate of AMP-activated protein kinase (AMPK)/ULK1 pathway, and its activation phosphorylates dynamin-related protein 1 (Drp1) and Rab7 to promote PINK1/Parkin-independent mitophagy. This article reviews the role and mechanism of TBK1 in regulating PINK1/Parkin-dependent and -independent mitophagy.

Site-Isolated Rhodium(II) Metalloradicals Catalyze Olefin Hydrofunctionalization.

Rh(II) porphyrin complexes display pronounced metal-centered radical character and the ability to activate small molecules under mild conditions, but catalysis with Rh(II) porphyrins is extremely rare. In addition to facile dimerization, Rh(II) porphyrins readily engage in kinetically and thermodynamically facile reactions involving two Rh(II) centers to generate stable Rh(III)-X intermediates that obstruct turnover in thermal catalysis. Here we report site isolation of Rh(II) metalloradicals in a MOF host, which not only protects Rh(II) metalloradicals against dimerization, but also allows them to participate in thermal catalysis. Access to PCN-224 or PCN-222 in which the porphyrin linkers are fully metalated by Rh(II) in the absence of any accompanying Rh(0) nanoparticles was achieved via the first direct MOF synthesis with a linker containing a transition-metal alkyl moiety, followed by Rh(III)-C bond photolysis.

Synergy of Ultrathin CoOx Overlayer and Nickel Single Atoms on Hematite Nanorods for Efficient Photo-Electrochemical Water Splitting.

To solve surface carrier recombination and sluggish water oxidation kinetics of hematite (α-Fe2 O3 ) photoanodes, herein, an attractive surface modification strategy is developed to successively deposit ultrathin CoOx overlayer and Ni single atoms on titanium (Ti)-doped α-Fe2 O3 (Ti:Fe2 O3 ) nanorods through a two-step atomic layer deposition (ALD) and photodeposition process. The collaborative decoration of ultrathin CoOx overlayer and Ni single atoms can trigger a big boost in photo-electrochemical (PEC) performance for water splitting over the obtained Ti:Fe2 O3 /CoOx /Ni photoanode, with the photocurrent density reaching 1.05 mA cm-2 at 1.23 V vs. reversible hydrogen electrode (RHE), more than three times that of Ti:Fe2 O3 (0.326 mA cm-2 ). Electrochemical and electronic investigations reveal that the surface passivation effect of ultrathin CoOx overlayer can reduce surface carrier recombination, while the catalysis effect of Ni single atoms can accelerate water oxidation kinetics. Moreover, theoretical calculations evidence that the synergy of ultrathin CoOx overlayer and Ni single atoms can lower the adsorption free energy of OH* intermediates and relieve the potential-determining step (PDS) for oxygen evolution reaction (OER). This work provides an exemplary modification through rational engineering of surface electrochemical and electronic properties for the improved PEC performances, which can be applied in other metal oxide semiconductors as well.

Comparing carbon nanoparticles and indocyanine green for sentinel lymph node mapping in endometrial cancer: A randomized-controlled single-center trial.

BACKGROUND AND OBJECTIVES: To compare the feasibility and diagnostic value of sentinel lymph node (SLN) mapping with carbon nanoparticles (CNPs) and indocyanine green (ICG) in endometrial cancer (EC). METHODS: This was a single-center, open-label, randomized controlled trial. Between August 1, 2020 and April 30, 2022, patients with early-stage EC were assessed for enrollment. All patients underwent SLN mapping with ICG or CNPs ± pelvic and/or para-aortic lymphadenectomy. The detection rate (DR), its impact factors, the sensitivity and the negative predictive value (NPV) of SLN mapping were analyzed. RESULTS: In total, 206 patients, with 103 per group, were included. The overall and bilateral DRs of the two groups were comparable without significant differences. There was no difference regarding the distribution of mapped SLNs. The sensitivity was 66.7% for both groups, and the NPVs were not significantly different. Furthermore, the sensitivity and NPV reached 100% when calculated either per hemipelvis or only in patients with bilateral SLN detection. CONCLUSIONS: SLN mapping by CNPs in EC is feasible with high DRs and diagnostic accuracy compared with ICG. CNPs might be an alternative to ICG for SLN mapping when near-infrared imaging equipment is lacking, especially in stage IA patients.

KIF2C promotes clear cell renal cell carcinoma progression via activating JAK2/STAT3 signaling pathway.

BACKGROUND: Clear cell renal cell carcinoma (ccRCC) is one of the most common malignant tumors that can be highly aggressive. Despite advances in the exploration of its underlying molecular biology, the clinical outcome for advanced ccRCC is still unsatisfied. Recently, more attention was paid to the functions of Kinesin family member 2C (KIF2C) in cancer progression, while the specific function of KIF2C in ccRCC has not been sufficiently elucidated. The present study aims to investigate the role of KIF2C in the progression of ccRCC and reveal potential mechanisms. METHODS: Expression of KIF2C in ccRCC tissues and adjacent normal tissue was compared and the association of KIF2C expression level with tumor grade, stage, and metastasis were analyzed using online web tool. Kaplan-Meier survival was performed to detect the association of KIF2C expression and patient' prognosis. Stably cell lines with KIF2C knockdown or overexpression were constructed by lentivirus infection. CCK-8, colony formation, scratch healing, and transwell invasion assays were carried out to explore the effect of KIF2C knockdown or overexpression on the proliferation, migration, and invasion of ccRCC cells. Gene set enrichment analysis (GSEA) was conducted to reveal signaling pathways associated with KIF2C expression. The effect of KIF2C on JAK2/STAT3 signaling pathway were explored by western blot assay. RESULTS: KIF2C expression was significantly upregulated in ccRCC tissues and was higher with the increase of tumor grade, stage, and metastasis. Higher expression of KIF2C was correlated with worse overall survival and diseases free survival in ccRCC patients. Silence of KIF2C inhibited proliferation, migration, and invasion in ccRCC cells. Conversely, overexpression of KIF2C had the opposite effect. GSEA results showed that JAK/STAT signaling pathway was markedly enriched in KIF2Chigh group. Pearson' correlation revealed that KIF2C expression was significantly associated with genes in JAK2/STAT3 signaling. Western blot results showed that KIF2C knockdown decreased protein expression of p-JAK2 and p-STAT3, and KIF2C overexpression increased the phosphorylation of JAK2 and STAT3. AG490, a JAK2/STAT3 signaling inhibitor, could partly impair the tumor-promoting effects of KIF2C in ccRCC. CONCLUSION: KIF2C expression was significantly upregulated in ccRCC and correlated with tumor grade, stage, metastasis, and patients' prognosis. KIF2C promoted ccRCC progression via activating JAK2/STAT3 signaling pathway, and KIF2C might be a novel target in ccRCC therapy.