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Photoelectrochemical (PEC) carbon dioxide (CO2) reduction (CO2R) holds the potential to reduce the costs of solar fuel production by integrating CO2 utilization and light harvesting within one integrated device. However, the CO2R selectivity on the photocathode is limited by the lack of catalytic active sites and competition with the hydrogen evolution reaction. On the other hand, serious parasitic light absorption occurs on the front-side-illuminated photocathode due to the poor light transmittance of CO2R cocatalyst films, resulting in extremely low photocurrent density at the CO2R equilibrium potential. This paper describes the design and fabrication of a photocathode consisting of crystal phase-modulated Ag nanocrystal cocatalysts integrated on illumination-reaction decoupled heterojunction silicon (Si) substrate for the selective and efficient conversion of CO2. Ag nanocrystals containing unconventional hexagonal close-packed phases accelerate the charge transfer process in CO2R reaction, exhibiting excellent catalytic performance. Heterojunction Si substrate decouples light absorption from the CO2R catalyst layer, preventing the parasitic light absorption. The obtained photocathode exhibits a carbon monoxide (CO) Faradaic efficiency (FE) higher than 90% in a wide potential range, with the maximum FE reaching up to 97.4% at -0.2 V vs. reversible hydrogen electrode. At the CO2/CO equilibrium potential, a CO partial photocurrent density of -2.7 mA cm-2 with a CO FE of 96.5% is achieved in 0.1 M KHCO3 electrolyte on this photocathode, surpassing the expensive benchmark Au-based PEC CO2R system.
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The induction of ferroptosis in tumor cells is one of the most important mechanisms by which tumor progression can be inhibited; however, the specific regulatory mechanism underlying ferroptosis remains unclear. In this study, we found that transcription factor HBP1 has a novel function of reducing the antioxidant capacity of tumor cells. We investigated the important role of HBP1 in ferroptosis. HBP1 down-regulates the protein levels of UHRF1 by inhibiting the expression of the UHRF1 gene at the transcriptional level. Reduced levels of UHRF1 have been shown to regulate the ferroptosis-related gene CDO1 by epigenetic mechanisms, thus up-regulating the level of CDO1 and increasing the sensitivity of hepatocellular carcinoma and cervical cancer cells to ferroptosis. On this basis, we constructed metal-polyphenol-network coated HBP1 nanoparticles by combining biological and nanotechnological. MPN-HBP1 nanoparticles entered tumor cells efficiently and innocuously, induced ferroptosis, and inhibited the malignant proliferation of tumors by regulating the HBP1-UHRF1-CDO1 axis. This study provides a new perspective for further research on the regulatory mechanism underlying ferroptosis and its potential role in tumor therapy.
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Ferroptose , Neoplasias Hepáticas , Humanos , Fatores de Transcrição/metabolismo , Proteínas Repressoras/genética , Proteínas Repressoras/metabolismo , Regulação da Expressão Gênica , Proteínas de Grupo de Alta Mobilidade/metabolismo , Proteínas Estimuladoras de Ligação a CCAAT/genética , Proteínas Estimuladoras de Ligação a CCAAT/metabolismo , Ubiquitina-Proteína Ligases/genética , Ubiquitina-Proteína Ligases/metabolismoRESUMO
In Arabidopsis (Arabidopsis thaliana), stomatal closure mediated by abscisic acid (ABA) is redundantly controlled by ABA receptor family proteins (PYRABACTIN RESISTANCE 1 [PYR1]/PYR1-LIKE [PYLs]) and subclass III SUCROSE NONFERMENTING 1 (SNF1)-RELATED PROTEIN KINASES 2 (SnRK2s). Among these proteins, the roles of PYR1, PYL2, and SnRK2.6 are more dominant. A recent discovery showed that ABA-induced accumulation of reactive oxygen species (ROS) in mitochondria promotes stomatal closure. By analyzing stomatal movements in an array of single and higher order mutants, we revealed that the mitochondrial protein VOLTAGE-DEPENDENT ANION CHANNEL 3 (VDAC3) jointly regulates ABA-mediated stomatal closure with a specialized set of PYLs and SnRK2s by affecting cellular and mitochondrial ROS accumulation. VDAC3 interacted with 9 PYLs and all 3 subclass III SnRK2s. Single mutation in VDAC3, PYLs (except PYR1 and PYL2), or SnRK2.2/2.3 had little effect on ABA-mediated stomatal closure. However, knocking out PYR1, PYL1/2/4/8, or SnRK2.2/2.3 in vdac3 mutants resulted in significantly delayed or attenuated ABA-mediated stomatal closure, despite the presence of other PYLs or SnRK2s conferring redundant functions. We found that cellular and mitochondrial accumulation of ROS induced by ABA was altered in vdac3pyl1 mutants. Moreover, H2O2 treatment restored ABA-induced stomatal closure in mutants with decreased stomatal sensitivity to ABA. Our work reveals that VDAC3 ensures redundant control of ABA-mediated stomatal closure by canonical ABA signaling components.
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Proteínas de Arabidopsis , Arabidopsis , Ácido Abscísico/farmacologia , Ácido Abscísico/metabolismo , Proteínas de Arabidopsis/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Peróxido de Hidrogênio/metabolismo , Estômatos de Plantas/metabolismo , Arabidopsis/metabolismo , Canais de Ânion Dependentes de Voltagem/metabolismo , Mitocôndrias/metabolismoRESUMO
Long interspersed element 1 (LINE-1) is the only active autonomous mobile element in the human genome. Its transposition can exert deleterious effects on the structure and function of the host genome and cause sporadic genetic diseases. Tight control of LINE-1 mobilization by the host is crucial for genetic stability. In this study, we report that MOV10 recruits the main decapping enzyme DCP2 to LINE-1 RNA and forms a complex of MOV10, DCP2, and LINE-1 RNP, exhibiting liquid-liquid phase separation (LLPS) properties. DCP2 cooperates with MOV10 to decap LINE-1 RNA, which causes degradation of LINE-1 RNA and thus reduces LINE-1 retrotransposition. We here identify DCP2 as one of the key effector proteins determining LINE-1 replication, and elucidate an LLPS mechanism that facilitates the anti-LINE-1 action of MOV10 and DCP2.
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Grânulos Citoplasmáticos , RNA Helicases , Humanos , Grânulos Citoplasmáticos/metabolismo , Endorribonucleases/genética , Elementos Nucleotídeos Longos e Dispersos , RNA/metabolismo , RNA Helicases/metabolismoRESUMO
Blue quantum dot (QD) light-emitting diodes (QLEDs) exhibit unsatisfactory operational stability and electroluminescence (EL) properties due to severe nonradiative recombination induced by large numbers of dangling bond defects and charge imbalance in QD. Herein, dipolar aromatic amine-functionalized molecules with different molecular polarities are employed to regulate charge transport and passivate interfacial defects between QD and the electron transfer layer (ETL). The results show that the stronger the molecular polarity, especially with the -CF3 groups possessing a strong electron-withdrawing capacity, the more effective the defect passivation of S and Zn dangling bonds at the QD surface. Moreover, the dipole interlayer can effectively reduce electron injection into QD at high current density, enhancing charge balance and mitigating Joule heat. Finally, blue QLEDs exhibit a peak external quantum efficiency (EQE) of 21.02% with an operational lifetime (T50 at 100 cd m-2) exceeding 4000 h.
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Quantum-dot light-emitting diodes (QLEDs), a kind of promising optoelectronic device, demonstrate potential superiority in next-generation display technology. Thermal cross-linked hole transport materials (HTMs) have been employed in solution-processed QLEDs due to their excellent thermal stability and solvent resistance, whereas the unbalanced charge injection and high cross-linking temperature of cross-linked HTMs can inhibit the efficiency of QLEDs and limit their application. Herein, a low-temperature cross-linked HTM of 4,4'-bis(3-(((4-vinylbenzyl)oxy)methyl)-9H-carbazol-9-yl)-1,1'-biphenyl (DV-CBP) with a flexible styrene side chain is introduced, which reduces the cross-linking temperature to 150 °C and enhances the hole mobility up to 1.01 × 10-3 cm2 V-1 s-1. More importantly, the maximum external quantum efficiency of 21.35% is successfully obtained on the basis of the DV-CBP as a cross-linked hole transport layer (HTL) for blue QLEDs. The low-temperature cross-linked high-mobility HTL using flexible side chains could be an excellent alternative for future HTL development.
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The performance of blue quantum dot light-emitting diodes (QLEDs) is limited by unbalanced charge injection, resulting from insufficient holes caused by low mobility or significant energy barriers. Here, we introduce an angular-shaped heteroarene based on cyclopentane[b]thiopyran (C8-SS) to modify the hole transport layer poly-N-vinylcarbazole (PVK), in blue QLEDs. C8-SS exhibits high hole mobility and conductivity due to the π···π and S···π interactions. Introducing C8-SS to PVK significantly enhanced hole mobility, increasing it by 2 orders of magnitude from 2.44 × 10-6 to 1.73 × 10-4 cm2 V-1 s-1. Benefiting from high mobility and conductivity, PVK:C8-SS-based QLEDs exhibit a low turn-on voltage (Von) of 3.2 V. More importantly, the optimized QLEDs achieve a high peak power efficiency (PE) of 7.13 lm/W, which is 2.65 times that of the control QLEDs. The as-proposed interface engineering provides a novel and effective strategy for achieving high-performance blue QLEDs in low-energy consumption lighting applications.
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Cholecystokinin (CCK) enables excitatory circuit long-term potentiation (LTP). Here, we investigated its involvement in the enhancement of inhibitory synapses. Activation of GABA neurons suppressed neuronal responses in the neocortex to a forthcoming auditory stimulus in mice of both sexes. High-frequency laser stimulation (HFLS) of GABAergic neurons potentiated this suppression. HFLS of CCK interneurons could induce the LTP of their inhibition toward pyramidal neurons. This potentiation was abolished in CCK knock-out mice but intact in mice with both CCK1R and 2R knockout of both sexes. Next, we combined bioinformatics analysis, multiple unbiased cell-based assays, and histology examinations to identify a novel CCK receptor, GPR173. We propose GPR173 as CCK3R, which mediates the relationship between cortical CCK interneuron signaling and inhibitory LTP in the mice of either sex. Thus, GPR173 might represent a promising therapeutic target for brain disorders related to excitation and inhibition imbalance in the cortex.SIGNIFICANCE STATEMENT CCK, the most abundant and widely distributed neuropeptide in the CNS, colocalizes with many neurotransmitters and modulators. GABA is one of the important inhibitory neurotransmitters, and much evidence shows that CCK may be involved in modulating GABA signaling in many brain areas. However, the role of CCK-GABA neurons in the cortical microcircuits is still unclear. We identified a novel CCK receptor, GPR173, localized in the CCK-GABA synapses and mediated the enhancement of the GABA inhibition effect, which might represent a promising therapeutic target for brain disorders related to excitation and inhibition imbalance in the cortex.
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GABAérgicos , Receptores da Colecistocinina , Masculino , Feminino , Camundongos , Animais , GABAérgicos/farmacologia , Células Piramidais/fisiologia , Sinapses/fisiologia , Neurônios GABAérgicos/fisiologia , Camundongos Knockout , Interneurônios , Colecistocinina , Ácido gama-Aminobutírico/fisiologia , Potenciação de Longa Duração/fisiologia , Receptores Acoplados a Proteínas G/genéticaRESUMO
Early detection plays a critical role in mitigating mortality rates linked to gastric cancer. However, current clinical screening methods exhibit suboptimal efficacy. Methylation alterations identified from cell-free DNA (cfDNA) present a promising biomarker for early cancer detection. Our study focused on identifying gastric cancer-specific markers from cfDNA methylation to facilitate early detection. We enrolled 150 gastric cancer patients and 100 healthy controls in this study, and undertook genome-wide methylation profiling of cfDNA using cell-free methylated DNA immunoprecipitation and high-throughput sequencing. We identified 21 differentially methylated regions (DMRs) between the gastric tumor and nontumor groups using multiple algorithms. Subsequently, using the 21 DMRs, we developed a gastric cancer detection model by random forest algorithm in the discovery set, and validated the model in an independent set. The model was able to accurately discriminate gastric cancer with a sensitivity and specificity of 93.90% and 95.15% in the discovery set, respectively, and 88.38% and 94.23% in the validation set, respectively. These results underscore the efficacy and accuracy of cfDNA-derived methylation markers in distinguishing early stage gastric cancer. This study highlighted the significance of cfDNA methylation alterations in early gastric cancer detection.
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A cost-effective method to achieve a 2-3 µm wavelength light source on silicon represents a major challenge. In this study, we have developed a novel approach that combines an epitaxial growth and the ion-slicing technique. A 2.1â µm wavelength laser on a wafer-scale heterogeneous integrated InP/SiO2/Si (InPOI) substrate fabricated by ion-slicing technique was achieved by epitaxial growth. The performance of the lasers on the InPOI are comparable with the InP, where the threshold current density (Jth) was 1.3â kA/cm2 at 283â K when operated under continuous wave (CW) mode. The high thermal conductivity of Si resulted in improved high-temperature laser performance on the InPOI. The proposed method offers a novel means of integrating an on-chip light source.
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Depression is a common and severe mental disorder. Evidence suggested a substantial causal relationship between stressful life events and the onset of episodes of major depression. However, the stress-induced pathogenesis of depression and the related neural circuitry is poorly understood. Here, we investigated how cholecystokinin (CCK) and CCKBR in the basolateral amygdala (BLA) are implicated in stress-mediated depressive-like behavior. The BLA mediates emotional memories, and long-term potentiation (LTP) is widely considered a trace of memory. We identified that the cholecystokinin knockout (CCK-KO) mice impaired LTP in the BLA, while the application of CCK4 induced LTP after low-frequency stimulation (LFS). The entorhinal cortex (EC) CCK neurons project to the BLA and optogenetic activation of EC CCK afferents to BLA-promoted stress susceptibility through the release of CCK. We demonstrated that EC CCK neurons innervate CCKBR cells in the BLA and CCK-B receptor knockout (CCKBR-KO) mice impaired LTP in the BLA. Moreover, the CCKBR antagonists also blocked high-frequency stimulation (HFS) induced LTP formation in the BLA. Notably, CCKBR antagonists infusion into the BLA displayed an antidepressant-like effect in the chronic social defeat stress model. Together, these results indicate that CCKBR could be a potential target to treat depression.
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Complexo Nuclear Basolateral da Amígdala , Humanos , Camundongos , Animais , Potenciação de Longa Duração/fisiologia , Receptor de Colecistocinina B/fisiologia , Depressão/tratamento farmacológico , Colecistocinina/farmacologia , Colecistocinina/fisiologiaRESUMO
BACKGROUND: There is a lack of research on the relationship between pain catastrophizing, kinesiophobia, and physical activity (PA) in people with haemophilia (PWH), and the underlying mechanisms connecting these variables remain unclear. AIM: The study's aim was to clarify the roles of kinesiophobia and self-efficacy in the relationship between pain catastrophizing and PA in PWH. METHODS: This cross-sectional study included adult PWH at the Haemophilia Centre of a Tertiary hospital in Beijing, China. The following questionnaires were used to collect data: the general information, the International Physical Activity Short Questionnaire, the Pain Catastrophizing Scale, the Tampa Scale of Kinesiophobia Scale, and the Exercise Self-Efficacy Scale. RESULTS: The study included a total of 187 PWH, including 154 having haemophilia A and 33 having haemophilia B. The median interquartile range of PA was 594 (198, 1554) MET-min/wk. There were significant differences in PA of patients based on age stage, treatment modality, highest pain score within the last seven days, and presence of haemophilic arthropathy (p < .05). It was showed that pain catastrophizing could directly predict PA (p < .001), accounting for 38.13% of the total effect. Pain catastrophizing also had indirect effects on PA through the mediating factors of kinesiophobia or self-efficacy, and through the chain-mediating effect of kinesiophobia and self-efficacy, accounting for 38.40%, 17.07%, and 6.40%, respectively. CONCLUSION: The study discovered that PWH have limited PA due to pain catastrophizing. This not only directly affects their activity but also indirectly influences it through kinesiophobia and self-efficacy.
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Catastrofização , Exercício Físico , Hemofilia A , Cinesiofobia , Autoeficácia , Adolescente , Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto Jovem , Catastrofização/psicologia , Estudos Transversais , Exercício Físico/psicologia , Hemofilia A/psicologia , Hemofilia A/complicações , Cinesiofobia/psicologia , Inquéritos e QuestionáriosRESUMO
BACKGROUND: A cost-effective Escherichia coli expression system has gained popularity for producing virus-like particle (VLP) vaccines. However, the challenge lies in balancing the endotoxin residue and removal costs, as residual endotoxins can cause inflammatory reactions in the body. RESULTS: In this study, porcine parvovirus virus-like particles (PPV-VLPs) were successfully assembled from Decreased Endotoxic BL21 (BL21-DeE), and the effect of structural changes in the lipid A of BL21 on endotoxin activity, immunogenicity, and safety was investigated. The lipopolysaccharide purified from BL21-DeE produced lower IL-6 and TNF-α than that from wild-type BL21 (BL21-W) in both RAW264.7 cells and BALB/c mice. Additionally, mice immunized with PPV-VLP derived form BL21-DeE (BL21-DeE-VLP) showed significantly lower production of inflammatory factors and a smaller increase in body temperature within 3 h than those immunized with VLP from BL21-W (BL21-W-VLP) and endotoxin-removed VLP (ReE-VLP). Moreover, mice in the BL21-DeE-VLP immunized group had similar levels of serum antibodies as those in the BL21-W-VLP group but significantly higher levels than those in the ReE-VLP group. Furthermore, the liver, lungs, and kidneys showed no pathological damage compared with the BL21-W-VLP group. CONCLUSION: Overall, this study proposes a method for producing VLP with high immunogenicity and minimal endotoxin activity without chemical or physical endotoxin removal methods. This method could address the issue of endotoxin residues in the VLP and provide production benefits.
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Endotoxinas , Escherichia coli , Lipídeo A , Camundongos Endogâmicos BALB C , Parvovirus Suíno , Vacinas de Partículas Semelhantes a Vírus , Animais , Camundongos , Escherichia coli/genética , Escherichia coli/metabolismo , Parvovirus Suíno/imunologia , Parvovirus Suíno/genética , Vacinas de Partículas Semelhantes a Vírus/imunologia , Endotoxinas/imunologia , Células RAW 264.7 , Lipídeo A/imunologia , Lipídeo A/análogos & derivados , Interleucina-6/imunologia , Fator de Necrose Tumoral alfa/metabolismo , Feminino , Suínos , Lipopolissacarídeos/imunologiaRESUMO
BACKGROUND AND AIMS: The Triglyceride-Glucose Index (TyG) has been proposed as a predictor to mortality, yet its association remains incompletely understood for individuals with or without chronic kidney disease (CKD). METHODS AND RESULTS: We analyzed data from the National Health and Nutrition Examination Survey spanning the years 1999-2018. CKD was defined as eGFR level <60 ml/min/1.73 m2 or urinary albumin creatinine ratio ≥30 mg/g. We employed the Cox proportional-hazards model to evaluate the incident risk of mortality associated with TyG among both non-CKD and CKD individuals. In the current analysis, 19,426 individuals were without CKD, while 2975 individuals had CKD. The overall mean TyG was 8.65, with significant difference between non-CKD and CKD individuals (8.60 vs 8.95, P < 0.001). The TyG index exhibited linear associations with incident cardiovascular disease (CVD) mortality and all-cause mortality among non-CKD and CKD individuals, respectively. A per-unit increase in the TyG index was significantly associated with CVD mortality for both non-CKD (HR = 1.24, 95%CI = 1.09-1.41) and CKD participants (HR = 1.19, 95%CI = 1.04-1.36), with no significant difference in the associations between the two groups (P = 0.091). For both non-CKD and CKD participants, TyG index was significantly associated with CVD mortality and all-cause mortality among those with age <65, but not for those with age ≥65. CONCLUSIONS: Our findings underscore the TyG index's as a valuable predictive tool for assessing the risk of all-cause and CVD mortality in both individuals with and without CKD.
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Biomarcadores , Glicemia , Doenças Cardiovasculares , Inquéritos Nutricionais , Insuficiência Renal Crônica , Triglicerídeos , Humanos , Insuficiência Renal Crônica/mortalidade , Insuficiência Renal Crônica/sangue , Insuficiência Renal Crônica/diagnóstico , Masculino , Feminino , Estados Unidos/epidemiologia , Pessoa de Meia-Idade , Triglicerídeos/sangue , Medição de Risco , Adulto , Biomarcadores/sangue , Glicemia/metabolismo , Idoso , Doenças Cardiovasculares/mortalidade , Doenças Cardiovasculares/sangue , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/epidemiologia , Fatores de Tempo , Prognóstico , Incidência , Fatores de Risco , Valor Preditivo dos Testes , Causas de Morte , Taxa de Filtração GlomerularRESUMO
BACKGROUND: Tumor mutational burden (TMB) is one of the most significant predictive biomarkers of immunotherapy efficacy in non-small cell lung cancer (NSCLC). Radiomics allows high-throughput extraction and analysis of advanced and quantitative medical imaging features. This study develops and validates a radiomic model for predicting TMB level and the response to immunotherapy based on CT features in NSCLC. METHOD: Pre-operative chest CT images of 127 patients with NSCLC were retrospectively studied. The 3D-Slicer software was used to outline the region of interest and extract features from the CT images. Radiomics prediction model was constructed by LASSO and multiple logistic regression in a training dataset. The model was validated by receiver operating characteristic (ROC) curves and calibration curves using external datasets. Decision curve analysis was used to assess the value of the model for clinical application. RESULTS: A total of 1037 radiomic features were extracted from the CT images of NSCLC patients from TCGA. LASSO regression selected three radiomics features (Flatness, Autocorrelation and Minimum), which were associated with TMB level in NSCLC. A TMB prediction model consisting of 3 radiomic features was constructed by multiple logistic regression. The area under the curve (AUC) value in the TCGA training dataset was 0.816 (95% CI: 0.7109-0.9203) for predicting TMB level in NSCLC. The AUC value in external validation dataset I was 0.775 (95% CI: 0.5528-0.9972) for predicting TMB level in NSCLC, and the AUC value in external validation dataset II was 0.762 (95% CI: 0.5669-0.9569) for predicting the efficacy of immunotherapy in NSCLC. CONCLUSION: The model based on CT radiomic features helps to achieve cost effective improvement in TMB classification and precise immunotherapy treatment of NSCLC patients.
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Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Humanos , Carcinoma Pulmonar de Células não Pequenas/diagnóstico por imagem , Carcinoma Pulmonar de Células não Pequenas/terapia , Carcinoma Pulmonar de Células não Pequenas/patologia , Neoplasias Pulmonares/diagnóstico por imagem , Neoplasias Pulmonares/terapia , Neoplasias Pulmonares/patologia , Estudos Retrospectivos , Radiômica , Tomografia Computadorizada por Raios X/métodos , Biomarcadores Tumorais , ImunoterapiaRESUMO
Schlafen-5 (SLFN5) is an interferon-induced protein of the Schlafen family, which are involved in immune responses and oncogenesis. To date, little is known regarding its anti-HIV-1 function. Here, the authors report that overexpression of SLFN5 inhibits HIV-1 replication and reduces viral mRNA levels, whereas depletion of endogenous SLFN5 promotes HIV-1 replication. Moreover, they show that SLFN5 markedly decreases the transcriptional activity of HIV-1 long terminal repeat (LTR) via binding to two sequences in the U5-R region, which consequently represses the recruitment of RNA polymerase II to the transcription initiation site. Mutagenesis studies show the importance of nuclear localization and the N-terminal 1-570 amino acids fragment in the inhibition of HIV-1. Further mechanistic studies demonstrate that SLFN5 interacts with components of the PRC2 complex, G9a and Histone H3, thereby promoting H3K27me2 and H3K27me3 modification leading to silencing HIV-1 transcription. In concert with this, they find that SLFN5 blocks the activation of latent HIV-1. Altogether, their findings demonstrate that SLFN5 is a transcriptional repressor of HIV-1 through epigenetic modulation and a potential determinant of HIV-1 latency.
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Proteínas de Ciclo Celular , Epigênese Genética , Infecções por HIV , HIV-1 , Proteínas de Ciclo Celular/genética , Regulação Viral da Expressão Gênica , Repetição Terminal Longa de HIV/genética , HIV-1/genética , HIV-1/fisiologia , Histonas/genética , Humanos , Ativação Viral , Latência Viral/genética , Replicação Viral/genéticaRESUMO
OBJECTIVE: To describe the status of return to work and identify predictors of return to work among Chinese postoperative patients with colorectal cancer. DESIGN: A cross-sectional study. SETTING: Conducted in two tertiary hospitals in China. PARTICIPANTS: A total of 210 postoperative patients with colorectal cancer were included in the study. MAIN MEASURES: Two hundred and ten postoperative patients with colorectal cancer who were working at the time of their diagnosis were assessed with the Perceived Social Support Scale, the Return-To-Work Self-Efficacy Questionnaire, Kessler Psychological Distress Scale, Cancer Fatigue Scale, and Social Impact Scale. Descriptive statistics, univariate logistic regression analysis, and multivariate logistic regression analysis were used for data analysis in SPSS 26.0. RESULTS: Around a third of participants (n = 74, 35.2%) returned to work after surgery. Multiple stepwise regression analysis indicated that more family income (odds ratio (OR) = 5.769, 95% confidence interval (CI) = 1.666-19.972), time span after surgery 5-10 months, and ≥10 months (OR = 3.546, 95% CI = 1.084-11.598; OR = 3.077, 95% CI = 1.074-8.818), with a stoma (OR = 0.221, 95% CI = 0.075-0.653), psychological distress (OR = 0.912, 95% CI = 0.843-0.987), cancer fatigue (OR = 0.924, 95% CI = 0.872-0.978), and stigma (OR = 0.928, 95% CI = 0.886-0.971) were significantly associated with return to work. CONCLUSIONS: A high proportion of patients with colorectal cancer did not return to work within 1 year after diagnosis. Those with shorter postoperative time, lower family income, stoma, greater psychological stress, higher level of cancer fatigue, and more stigma may have a higher risk in delayed work resumption.
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OBJECTIVE: To evaluate the validity of intraoperative evoked potential (EP) including motor evoked potential (MEP) and somatosensory evoked potentials (SEP) as a biomarker for predicting neural function changes after thoracic spinal decompression (TSD) surgery. METHOD: A consecutive series of 336 TSD surgeries were reviewed between 2010 and 2021 from four spine center. All patients with TSD were divided into 3 groups according to different intraoperative EP results: group 1, EP alerts; group 2, no obvious EP deterioration; group 3, EP improvement compared with baselines. The lower limb Japanese Orthopedic Association (JOA) scores (as well as early and long-term JOA recovery rate) were utilized to quantitatively assess pre- and postoperative neural function change. RESULTS: Among the 3 subgroups according to the different EP changes, the early JOA recovery rate (RR%) in the EP improvement group was significantly better than the other two groups (51.3 ± 58.6* vs. 27.5 ± 31.2 and 33.3 ± 43.1; p < 0.01) after 3-month follow-up. The mean MEP and SEP amplitude were from 116 ± 57 µV to 347 ± 71 µV (p < 0.01) and from 1.86 ± 0.24 µV to 2.65 ± 0.29 µV (p < 0.01) between spinal cord pre-decompression and post-decompression. Moreover, multivariate logistic regression analysis revealed that risk factors of EP improvement were duration of symptom (p < 0.001, OR 10.9) and Preop. neurologic deficit degree (p = 0.013, OR 7.46). CONCLUSION: The intraoperative EP can predict postoperative neural function changes as a biomarker during TSD. Patient with EP improvement probably has better prognosis for early neural function recovery. The duration of symptom and preoperative neurologic deficit degree may be related to intraoperative EP improvement.
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Potencial Evocado Motor , Potenciais Somatossensoriais Evocados , Humanos , Potenciais Somatossensoriais Evocados/fisiologia , Potencial Evocado Motor/fisiologia , Coluna Vertebral , Biomarcadores , Descompressão , Estudos RetrospectivosRESUMO
OBJECTIVE: To report a "critical phase" (between osteotomy completion and correction beginning) that will frequently lead to the reversible intraoperative neurophysiological monitoring (IOM) change during posterior vertebral column resection (PVCR) surgery. METHODS: The study sample consisted of 120 patients with severe spine deformity who underwent PVCR and deformity correction surgeries. Those patients were recruited consecutively from 2010 to 2018 January in our spine center. The detailed IOM data (the amplitude of MEP & SEP) and its corresponding surgical points were collected prospectively. Early and long-term postoperative neurologic outcomes were assessed for the following functions: motor, sensory, and pain at immediate postoperative and 1-year post-operation in this cases series. RESULTS: A total of 105 (105/120) patients presented varying degrees of IOM reduction in the critical phase; the mean IOM amplitude retention vs rescue rate was 27% ± 11.2 versus 58% ± 16.9, P < 0.01 (MEP) & 34% ± 8.3 versus 66% ± 12.4 P < 0.01 (SEP). Patients with postoperative spinal deficits often had a significantly longer IOM-alerting duration than the patients without (p < 0.01, Mann-Whitney U-test), and IOM-alerting duration greater than 39.5 min was identified as an independent predictor of the risk of postoperative spinal deficits. CONCLUSIONS: The reversible IOM events probably often appear in the critical phase during PVCR surgery. The new postoperative spinal deficits are possible for patients without satisfied IOM recovery or alerting duration greater than 39.5 min. Timely and suitable surgical interventions are useful for rescuing the IOM alerts.
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Hydrogen is an essential energy carrier which will address the challenges posed by the energy crisis and climate change. Photoelectrochemical water splitting (PEC) is an important method for producing solar-powered hydrogen. The PEC tandem configuration harnesses sunlight as the exclusive energy source to drive both the hydrogen (HER) and oxygen evolution reactions (OER), simultaneously. Therefore, PEC tandem cells have been developed and gained tremendous interest in recent decades. This review describes the current status of the development of tandem cells for unbiased photoelectrochemical water splitting. The basic principles and prerequisites for constructing PEC tandem cells are introduced first. We then review various single photoelectrodes for use in water reduction or oxidation, and highlight the current state-of-the-art discoveries. Second, a close look into recent developments of PEC tandem cells in water splitting is provided. Finally, a perspective on the key challenges and prospects for the development of tandem cells for unbiased PEC water splitting are given.