Triphenylamine-Based Covalent Organic Framework Films for Dopamine-Responsive Electrofluorochromism.

Covalent organic framework (COF) film with electrofluorochromic (EFC) and electrochromic (EC) properties has been synthesized by using triphenylamine-based monomers. The film exhibited a high maximum fluorescence contrast of 151 when subjected to a drive voltage of 0.75 V vs the Ag/AgCl electrode, causing the fluorescence to be quenched, which resulted in the EFC process's "fluorescence off" state. The switching times for the fluorescence on and off states were 0.51 and 7.79 s, respectively. Over the same voltage range, the COF film also displayed EC properties, achieving a contrast of 50.23% and a coloration efficiency of 297.4 cm2 C-1 at 532 nm, with switching times of 18.6 s for coloration and 0.7 s for bleaching. Notably, the quenched fluorescence of the COF film could be restored by adding dopamine as a reductant. This phenomenon enabled the implementation of a NAND logic gate using the applied potential as a physical input and dopamine addition as a chemical input. This study demonstrates the successful development of COF films with bifunctional EFC and EC properties, showcasing their potential for use in constructing advanced optoelectronic devices.

Exploration of ETV6::ABL1-positive AML with concurrent NPM1 and FLT3-ITD mutations.

ETV6::ABL1 is a rare fusion gene that found in MPN, ALL, and AML. It has a complex and diverse formation mechanism due to the reciprocal orientations of the ETV6 and ABL1 genes relative to the centromeres. NPM1 is frequently mutated in adult AML, often accompanied by FLT3-ITD, which suggests molecular synergisms in AML pathogenesis. Previous reports on ETV6::ABL1 mostly focus on FLT3-ITD. In this study, we present a case of AML with ETV6::ABL1, along with NPM1 and FLT3-ITD. The patient showed a rapid increase in primitive cells at the initial stage, along with the presence of immature granulocytes and erythrocytes. Through cytogenetic analysis, fluorescence in situ hybridization (FISH), and RNA-seq, we elucidated the mechanism behind the formation of the ETV6::ABL1 fusion gene. Despite conventional chemotherapy failure and rapid tumor proliferation, we attempted to add FLT3 inhibitor sorafenib to the treatment, along with chemotherapy bridging to haploidentical transplantation. After haplo-HSCT, a combination of sorafenib and dasatinib was administered as maintenance therapy. The patient achieved complete remission (CR) and maintained it for 11 months. The intricate genetic landscape observed in this case presents diagnostic dilemmas and therapeutic challenges, emphasizing the importance of a comprehensive understanding of its implications for disease classification, risk stratification, and treatment selection.

Targeting AGTPBP1 inhibits pancreatic cancer progression via regulating microtubules and ERK signaling pathway.

BACKGROUND: AGTPBP1 is a cytosolic carboxypeptidase that cleaves poly-glutamic acids from the C terminus or side chains of α/ß tubulins. Although its dysregulated expression has been linked to the development of non-small cell lung cancer, the specific roles and mechanisms of AGTPBP1 in pancreatic cancer (PC) have yet to be fully understood. In this study, we examined the role of AGTPBP1 on PC in vitro and in vivo. METHODS: Immunohistochemistry was used to examine the expression of AGTPBP1 in PC and non-cancerous tissues. Additionally, we assessed the malignant behaviors of PC cells following siRNA-mediated AGTPBP1 knockdown both in vitro and in vivo. RNA sequencing and bioinformatics analysis were performed to identify the differentially expressed genes regulated by AGTPBP1. RESULTS: We determined that AGTPBP1 was overexpressed in PC tissues and the higher expression of AGTPBP1 was closely related to the location of tumors. AGTPBP1 inhibition can significantly decrease cell progression in vivo and in vitro. Moreover, the knockdown of AGTPBP1 inhibited the expression of ERK1/2, P-ERK1/2, MYLK, and TUBB4B proteins via the ERK signaling pathway. CONCLUSION: Our research indicates that AGTPBP1 may be a putative therapeutic target for PC.

Severe Hypothermia Induces Ferroptosis in Cerebral Cortical Nerve Cells.

Abnormal shifts in global climate, leading to extreme weather, significantly threaten the safety of individuals involved in outdoor activities. Hypothermia-induced coma or death frequently occurs in clinical and forensic settings. Despite this, the precise mechanism of central nervous system injury due to hypothermia remains unclear, hindering the development of targeted clinical treatments and specific forensic diagnostic indicators. The GEO database was searched to identify datasets related to hypothermia. Post-bioinformatics analyses, DEGs, and ferroptosis-related DEGs (FerrDEGs) were intersected. GSEA was then conducted to elucidate the functions of the Ferr-related genes. Animal experiments conducted in this study demonstrated that hypothermia, compared to the control treatment, can induce significant alterations in iron death-related genes such as PPARG, SCD, ADIPOQ, SAT1, EGR1, and HMOX1 in cerebral cortex nerve cells. These changes lead to iron ion accumulation, lipid peroxidation, and marked expression of iron death-related proteins. The application of the iron death inhibitor Ferrostatin-1 (Fer-1) effectively modulates the expression of these genes, reduces lipid peroxidation, and improves the expression of iron death-related proteins. Severe hypothermia disrupts the metabolism of cerebral cortex nerve cells, causing significant alterations in ferroptosis-related genes. These genetic changes promote ferroptosis through multiple pathways.

dldhcri3 zebrafish exhibited altered mitochondrial ultrastructure, morphology and dysfunction partially rescued by probucol or thiamine.

Dihydrolipoamide dehydrogenase (DLD) deficiency is a recessive mitochondrial disease caused by variants in DLD, the E3 subunit of mitochondrial α-keto acid dehydrogenase complexes. DLD disease symptoms are multi-systemic, variably manifesting as Leigh syndrome, neurodevelopmental disability, seizures, cardiomyopathy, liver disease, fatigue and lactic acidemia. While most DLD disease symptoms are attributed to dysfunction of the pyruvate dehydrogenase complex, understanding the effects of other α-keto acid dehydrogenase deficiencies remain unclear. Current therapies for DLD deficiency are ineffective, with no vertebrate animal model available for preclinical study. We created a viable Danio rerio (zebrafish) KO model of DLD deficiency, dldhcri3. Detailed phenotypic characterization revealed shortened larval survival, uninflated swim bladder, hepatomegaly and fatty liver, and reduced swim activity. These animals displayed increased pyruvate and lactate levels, with severe disruption of branched-chain amino acid catabolism manifest as increased valine, leucine, isoleucine, α-ketoisovalerate, and α-ketoglutarate levels. Evaluation of mitochondrial ultrastructure revealed gross enlargement, severe cristae disruption and reduction in matrix electron density in liver, intestines, and muscle. Therapeutic modeling of candidate therapies demonstrated probucol or thiamine improved larval swim activity. Overall, this vertebrate model demonstrated characteristic phenotypic and metabolic alterations of DLD disease, offering a robust platform to screen and characterize candidate therapies.

Insulin sensitivity and insulin secretion in adults with Friedreich's Ataxia: the role of skeletal muscle.

INTRODUCTION: Friedreich's Ataxia (FRDA) is a multi-system disorder caused by frataxin deficiency. FRDA-related diabetes mellitus (DM) is common. Frataxin supports skeletal muscle mitochondrial oxidative phosphorylation (OXPHOS) capacity, a mediator of insulin sensitivity. Our objective was to test the association between skeletal muscle health and insulin sensitivity and secretion in adults with FRDA without DM. METHODS: Case-control study (NCT02920671). Glucose and insulin metabolism (stable-isotope oral glucose tolerance tests), body composition (dual-energy x-ray absorptiometry), physical activity (self-report), and skeletal muscle OXPHOS capacity (creatine chemical exchange saturation transfer MRI) were assessed. RESULTS: Participants included 11 individuals with FRDA (4 female), median age 27y (IQR 23, 39), BMI 26.9kg/m2 (24.1, 29.4), and 24 controls (11 female), 29y (26, 39), 24.4kg/m2 (21.8, 27.0). Fasting glucose was higher in FRDA (91 vs. 83mg/dL (5.0 vs. 4.6mmol/L), p<0.05). Individuals with FRDA had lower insulin sensitivity (WBISI 2.8 vs. 5.3, p<0.01), higher post-prandial insulin secretion (insulin secretory rate iAUC 30-180 minutes, 24,652 vs. 17,858, p<0.05), and more suppressed post-prandial endogenous glucose production (-0.9% vs. 26.9% of fasting EGP, p<0.05). In regression analyses, lower OXPHOS and inactivity explained some of the difference in insulin sensitivity. More visceral fat contributed to lower insulin sensitivity independent of FRDA. Insulin secretion accounting for sensitivity (disposition index) was not different. CONCLUSIONS: Lower mitochondrial OXPHOS capacity, inactivity, and visceral adiposity contribute to lower insulin sensitivity in FRDA. Higher insulin secretion appears compensatory, and when inadequate, could herald DM. Further studies are needed to determine if muscle- or adipose-focused interventions could delay FRDA-related DM.

RIP3 regulates doxorubicin-induced intestinal mucositis via FUT2-mediated α-1,2-fucosylation.

OBJECTIVE: Intestinal mucositis is one of the common side effects of anti-cancer chemotherapy. However, the molecular mechanisms involved in mucositis development remain incompletely understood. In this study, we investigated the function of receptor-interacting protein kinase 3 (RIP3/RIPK3) in regulating doxorubicin-induced intestinal mucositis and its potential mechanisms. METHODS: Intestinal mucositis animal models were induced in mice for in vivo studies. Rat intestinal cell line IEC-6 was used for in vitro studies. RNA­seq was used to explore the transcriptomic changes in doxorubicin-induced intestinal mucositis. Intact glycopeptide characterization using mass spectrometry was applied to identify α-1,2-fucosylated proteins associated with mucositis. RESULTS: Doxorubicin treatment increased RIP3 expression in the intestine and caused severe intestinal mucositis in the mice, depletion of RIP3 abolished doxorubicin-induced intestinal mucositis. RIP3-mediated doxorubicin-induced mucositis did not depend on mixed lineage kinase domain-like (MLKL) but on α-1,2-fucosyltransferase 2 (FUT2)-catalyzed α-1,2-fucosylation on inflammation-related proteins. Deficiency of MLKL did not affect intestinal mucositis, whereas inhibition of α-1,2-fucosylation by 2-deoxy-D-galactose (2dGal) profoundly attenuated doxorubicin-induced inflammation and mucositis. CONCLUSIONS: RIP3-FUT2 pathway is a central node in doxorubicin-induced intestinal mucositis. Targeting intestinal RIP3 and/or FUT2-mediated α-1,2-fucosylation may provide potential targets for preventing chemotherapy-induced intestinal mucositis.

A diet-wide Mendelian randomization analysis: causal effects of dietary habits on type 2 diabetes.

Background: Traditional clinical studies have indicated a link between certain food intakes and type 2 diabetes (T2D), but the causal relationships between different dietary habits and T2D remain unknown. Using Mendelian randomization (MR) approaches, we investigated the potential causal association between dietary habits and T2D risk. Methods: We collected publicly available genome-wide association studies' summary statistics for 18 dietary habits from the UK Biobank and T2D data from the DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) consortium. We applied the inverse variance weighted (IVW) method, supplemented with the MR-Egger method, weighted median method (WMM), simple method, weighted mode, MR-Egger regression, and the MR pleiotropy residual sum and outlier test to determine whether a particular diet was causal for T2D. Results: Reliable and robust MR estimates demonstrated that poultry intake has a causal effect on a higher risk of T2D (IVW: OR 6.30, 95% CI 3.573-11.11, p = 2.02e - 10; WMM: OR 5.479, 95% CI 0.2758-10.88, p = 1.19e - 06). Conversely, dried fruit intake (IVW: OR 0.380, 95% CI 0.237-0.608, p = 5.57e - 05; WMM: OR 0.450, 95% CI 0.321-0.630, p = 3.33e - 06) and cereal intake (IVW: OR 0.455, 95% CI 0.317-0.653, p = 1.924e - 05; WMM: OR 0.513, 95% CI 0.379-0.694, p = 1.514e - 05) were causally associated with T2D as protective factors. Sensitivity analyses confirmed the reliability and robustness of these findings. Discussion: Our study established the causal effects of poultry intake, dried fruit intake, and cereal intake on T2D, identifying poultry intake as a risk factor and the other two as protective factors. Further research into potential mechanisms is required to validate these novel findings.

Short-term intermittent hypoxia exposure for dyspnea and fatigue in post-acute sequelae of COVID-19: A randomized controlled study.

BACKGROUND: Post-acute sequelae of COVID-19 (PASC) is incurring a huge health and economic burden worldwide. There is currently no effective treatment or recommended drug for PASC. METHODS: This prospective randomized controlled study was conducted in a hospital in China. The effect of intermittent hypoxia exposure (IHE; 5-min hypoxia alternating with 5-min normal air, repeated five times) on dyspnea and fatigue was investigated in patients meeting the NICE definition of PASC. Patients were computationally randomized to receive normoxia exposure (NE) and routine therapy or IHE and routine therapy. Six-minute walk distance (6MWD) and spirometry were tested before and after the interventions; the Borg Dyspnea Scale (Borg) and the modified Medical Research Council Dyspnea Scale (mMRC) were used to assess dyspnea; and the Fatigue Assessment Scale (FAS) and the Chalder Fatigue Scale-11 (CFQ-11) were used to assess fatigue. The study was registered in the Chinese Clinical Trial Registry (ChiCTR2300070565). FINDINGS: Ninety-five participants (33 males and 62 females) were recruited between March 1, 2023 and December 30, 2023. Forty-seven patients in the IHE group received 10.0 (9.0, 15.0) days of IHE, and 48 patients in NE group received 10.0 (8.0, 12.0) days of NE. 6MWD, forced vital capacity (FVC), FVC %pred, forced expiratory volume in 1 s (FEV1), FEV1 %pred, tidal volume (VT), and dyspnea and fatigue scales markedly improved after IHE (p < 0.05), and improvements were greater than in the NE group (all p < 0.05). Furthermore, participants in IHE group had better subjective improvements in dyspnea and fatigue than those in the NE group (p < 0.05). Compared with <10 days of IHE, ≥10 days of IHE had a greater impact on 6MWD, FVC, FEV1, FEV1 %pred, VT, FAS, and CFQ-11. No severe adverse events were reported. INTERPRETATION: IHE improved spirometry and 6MWD and relieved dyspnea and fatigue in PASC patients. Larger prospective studies are now needed to verify these findings.

Development and Evaluation of a Shrimp Virus (IHHNV)-Mediated Gene Transfer and Expression System for Shrimps.

An efficient gene transfer and expression tool is lacking for shrimps and shrimp cells. To solve this, this study has developed a shrimp DNA virus-mediated gene transfer and expression system, consisting of insect Sf9 cells for viral packaging, the shrimp viral vector of pUC19-IHHNV-PH-GUS and the baculoviral vector of Bacmid or Bacmid-VP28 encoding the shrimp WSSV envelope protein VP28. The pUC19-IHHNV-PH-GUS vector was constructed by assembling the genomic DNA of shrimp infectious hypodermal and hematopoietic necrosis virus (IHHNV), which has shortened inverted terminal repeats, into a pUC19 backbone, and then an expression cassette of baculoviral polyhedron (PH) promoter-driven GUS (ß-glucuronidase) reporter gene was inserted immediately downstream of IHHNV for proof-of-concept. It was found that the viral vector of pUC19-IHHNV-PH-GUS could be successfully packaged into IHHNV-like infective virions in the Sf9 cells, and the gene transfer efficiency of this system was evaluated and verified in three systems of Sf9 cells, shrimp hemolymph cells and tissues of infected shrimps, but the GUS expression could only be detected in cases where the viral vector was co-transfected or co-infected with a baculovirus of Bacmid or Bacmid-VP28 due to the Bacmid-dependence of the PH promoter. Moreover, the packaging and infection efficiencies could be significantly improved when Bacmid-VP28 was used instead of Bacmid.

Au-modified ceria nanozyme prevents and treats hypoxia-induced pulmonary hypertension with greatly improved enzymatic activity and safety.

BACKGROUND: Despite recent advances the prognosis of pulmonary hypertension remains poor and warrants novel therapeutic options. Extensive studies, including ours, have revealed that hypoxia-induced pulmonary hypertension is associated with high oxidative stress. Cerium oxide nanozyme or nanoparticles (CeNPs) have displayed catalytic activity mimicking both catalase and superoxide dismutase functions and have been widely used as an anti-oxidative stress approach. However, whether CeNPs can attenuate hypoxia-induced pulmonary vascular oxidative stress and pulmonary hypertension is unknown. RESULTS: In this study, we designed a new ceria nanozyme or nanoparticle (AuCeNPs) exhibiting enhanced enzyme activity. The AuCeNPs significantly blunted the increase of reactive oxygen species and intracellular calcium concentration while limiting proliferation of pulmonary artery smooth muscle cells and pulmonary vasoconstriction in a model of hypoxia-induced pulmonary hypertension. In addition, the inhalation of nebulized AuCeNPs, but not CeNPs, not only prevented but also blunted hypoxia-induced pulmonary hypertension in rats. The benefits of AuCeNPs were associated with limited increase of intracellular calcium concentration as well as enhancement of extracellular calcium-sensing receptor (CaSR) activity and expression in rat pulmonary artery smooth muscle cells. Nebulised AuCeNPs showed a favorable safety profile, systemic arterial pressure, liver and kidney function, plasma Ca2+ level, and blood biochemical parameters were not affected. CONCLUSION: We conclude that AuCeNPs is an improved reactive oxygen species scavenger that effectively prevents and treats hypoxia-induced pulmonary hypertension.

Complete genome sequence of the 4-hydroxybenzoate-degrading bacterium Gymnodinialimonas sp. 57CJ19, a potential novel species from intertidal sediments.

A bacterium Gymnodinialimonas sp. 57CJ19, was isolated from the intertidal sediments of Aoshan Bay, and further assays showed that it has the ability to degrade the antibacterial preservative 4-hydroxybenzoate. The complete genome sequence was sequenced, and phylogenomic analyses indicated that strain 57CJ19 represents a potential novel species in the genus Gymnodinialimonas (family Rhodobacteraceae). Its genome contains a 3,861,607-bp circular chromosome with 61.25% G + C content. Gene prediction revealed 3716 protein-encoding genes, 41 tRNA genes, 3 rrn operons, and 3 non-coding RNA genes. Functional annotation revealed a complete metabolic pathway for 4-hydroxybenzoate. The genome sequence of strain 57CJ19 provides new insights into the potential and underlying genomic basis of aromatic compound pollutant degradation by marine bacteria.

Deciphering internal and external factors influencing intestinal junctional complexes.

The intestinal barrier, an indispensable guardian of gastrointestinal health, mediates the intricate exchange between internal and external environments. Anchored by evolutionarily conserved junctional complexes, this barrier meticulously regulates paracellular permeability in essentially all living organisms. Disruptions in intestinal junctional complexes, prevalent in inflammatory bowel diseases and irritable bowel syndrome, compromise barrier integrity and often lead to the notorious "leaky gut" syndrome. Critical to the maintenance of the intestinal barrier is a finely orchestrated network of intrinsic and extrinsic factors that modulate the expression, composition, and functionality of junctional complexes. This review navigates through the composition of key junctional complex components and the common methods used to assess intestinal permeability. It also explores the critical intracellular signaling pathways that modulate these junctional components. Lastly, we delve into the complex dynamics between the junctional complexes, microbial communities, and environmental chemicals in shaping the intestinal barrier function. Comprehending this intricate interplay holds paramount importance in unraveling the pathophysiology of gastrointestinal disorders. Furthermore, it lays the foundation for the development of precise therapeutic interventions targeting barrier dysfunction.

Hydrogen Atom Abstraction and Reduction Study of 21-Thiaporphyrin and 21,23-Dithiaporphyrin.

The metal-free porphyrins protonation has gained interest over five decades because its structure modification and hardly monoacid intermediate isolation. Here, upon the hydrogen atom abstraction processes, one step diproptonated H3STTP(BF4)2 (STTP = 5,10,15,20-tetraphenyl-21-thiaporphyrin) (3) and stepwise protonated HS2TTPSbCl6 (5) and diprotonated H2S2TTP(BF4)2 (6) (S2TTP = 5,10,15,20-tetraphenyl-21,23-thiaporphyrin) compounds were obtained using HSTTP and S2TTP with oxidants. The closed-shell protonated compounds were fully characterized using XRD, UV-vis, IR and NMR spectra. In addition, the reduced 19π compounds [K(2,2,2)]HSTTP (2) and [K(2,2,2)]S2TTP (7) were synthesized by the ligands with reductant KC8 in THF solution. These two open-shell compounds were characterized with UV-vis, IR and EPR spectroscopies. The semiempirical ZINDO/S method was employed to analyze the HOMO/LUMO gap lever and identify the electronic transitions of the UV-vis spectra of the closed- and open-shell porphyrin compounds.

Near-infrared light-driven biomass conversion.

Current photocatalytic technologies mainly rely on the input of high-energy ultraviolet-visible (UV-vis) light to obtain the desired excited states with adequate energy to drive redox reactions, precluding the use of low-energy near-infrared (NIR) light that occupies ~50% of the solar spectrum. Here, we report the efficient utilization of NIR light by coupling the low-energy NIR photons with reactive biomass conversion. A unique mechanism of photothermally synergistic photocatalysis was revealed for the selective biomass conversion under NIR light. Using biomass-derived 5-hydroxymethylfurfural (HMF) conversion as a model reaction, it was found that NIR and UV-vis light featured markedly different reaction patterns. 5-Formyl-2-furancarboxylic acid (FFCA) was almost exclusively produced under NIR light, whereas UV-vis light favored the formation of 2,5-diformylfuran (DFF) as the major product. This work provides a paradigm for sustainable and selective chemical synthesis using the Earth's abundant resources, sunlight and biomass.

A Glycoprotein-Based Surface-Enhanced Raman Spectroscopy-Lateral Flow Assay Method for Abrin and Ricin Detection.

Abrin and ricin, both type II ribosome-inactivating proteins, are toxins of significant concern and are under international restriction by the Chemical Weapons Convention and the Biological and Toxin Weapons Convention. The development of a rapid and sensitive detection method for these toxins is of the utmost importance for the first emergency response. Emerging rapid detection techniques, such as surface-enhanced Raman spectroscopy (SERS) and lateral flow assay (LFA), have garnered attention due to their high sensitivity, good selectivity, ease of operation, low cost, and disposability. In this work, we generated stable and high-affinity nanotags, via an efficient freezing method, to serve as the capture module for SERS-LFA. We then constructed a sandwich-style lateral flow test strip using a pair of glycoproteins, asialofetuin and concanavalin A, as the core affinity recognition molecules, capable of trace measurement for both abrin and ricin. The limit of detection for abrin and ricin was 0.1 and 0.3 ng/mL, respectively. This method was applied to analyze eight spiked white powder samples, one juice sample, and three actual botanic samples, aligning well with cytotoxicity assay outcomes. It demonstrated good inter-batch and intra-batch reproducibility among the test strips, and the detection could be completed within 15 min, indicating the suitability of this SERS-LFA method for the on-site rapid detection of abrin and ricin toxins.

Interleukin receptor therapeutics attenuate inflammation in canine synovium following cruciate ligament injury.

OBJECTIVE: In the knee, synovial fibrosis after ligamentous injury is linked to progressive joint pain and stiffness. The objective of this study was to evaluate changes in synovial architecture, mechanical properties, and transcriptional profiles following naturally occurring cruciate ligament injury in canines and to test potential therapeutics that target drivers of synovial inflammation and fibrosis. DESIGN: Synovia from canines with spontaneous cruciate ligament tears and from healthy knees were assessed via histology (n = 10/group) and micromechanical testing (n = 5/group) to identify changes in tissue architecture and stiffness. Additional samples (n = 5/group) were subjected to RNA-sequencing to define the transcriptional response to injury. Finally, synovial tissue samples from injured animals (n = 6 (IL1) or n = 8 (IL6)/group) were assessed in vitro for response to therapeutic molecules directed against interleukin (IL) signaling (IL1 or IL6). RESULTS: Cruciate injury resulted in increased synovial fibrosis, vascularity, inflammatory cell infiltration, and intimal hyperplasia. Additionally, the stiffness of both the intima and subintima regions were higher in diseased compared to healthy tissue. Differential gene expression analysis showed that diseased synovium had an upregulation of immune response and cell adhesion pathways and a downregulation of Rho protein transduction pathways. In vitro application of small molecule therapeutics targeting IL1 (anakinra) or IL6 (tocilizumab) dampened expression of inflammatory and matrix deposition mediators. CONCLUSION: Spontaneous cruciate ligament injury in canines is associated with synovial inflammation and fibrosis in a relevant model for testing emerging intra-articular treatments. Small molecule therapeutics targeting IL pathways may be ideal interventions for delivery to the joint space after injury.

Chromosome-level genome assembly and sex chromosome identification of the pink stem borer, Sesamia inferens (Lepidoptera: Noctuidae).

The pink stem borer, Sesamia inferens Walker (Lepidoptera: Noctuidae), is one of the most notorious pest insects of rice and maize crops in the world. Here, we generated a high-quality chromosome-level genome assembly of S. inferens, using a combination of Illumina, PacBio HiFi and Hi-C technologies. The total assembly size was 973.18 Mb with a contig N50 of 33.39 Mb, anchored to 31 chromosomes, revealing a karyotype of 30 + Z. The BUSCO analysis indicated a high completeness of 98.90% (n = 5286), including 5172 (97.8%) single-copy BUSCOs and 58 (1.1%) duplicated BUSCOs. The genome contains 58.59% (564.58 Mb) repeat elements and 26628 predicted protein-coding genes. The chromosome-level genome assembly of S. inferens provides in-depth knowledge and will be a helpful resource for the Lepidoptera and pest control research communities.

Novel cathodic and anodic dual-emitting electrochemiluminescence of Ru(bpy)32+/α-keto acid system.

Novel cathodic and anodic dual-emitting electrochemiluminescence (ECL) of Ru(bpy)32+ and α-keto acids system are studied for the first time. Based on their cathodic and anodic ECL intensity, α-keto acids including oxalate, glyoxylic acid, pyruvic acid, and phenylglyoxylic acid can be directly sensitively detected. The limits of detection (LOD) of oxalate, glyoxylic acid, pyruvic acid, and phenylglyoxylic acid are 31.25 nM, 23.26 µM, 36.36 µM, and 18.52 µM, respectively. Possible mechanism of ECL produced is also proposed. Electrochemical results show that the reduction of oxygen at the cathode to produce ·OH is a vital step for cathodic and anodic dual-emitting ECL. Furthermore, using the enhancement strategy of S2O82-/Ag+ as coreactant accelerators is proposed considering that decarboxylation of α-keto acids to produce acyl radical can be achieved via S2O82- or Ag+. Using the S2O82-/Ag+ enhancement strategy, the LOD of oxalate, glyoxylic acid, pyruvic acid, and phenylglyoxylic acid are improved and are 2.12 nM, 0.37 µM, 3.23 µM, and 0.28 µM, respectively. Coreactants of Ru(bpy)32+ with dual-emitting ECL are expanded, which includes additional substances with organic carboxylic acid characterized by the keto group in α-position. It also provides an effective way to enhance ECL and improve sensitivity. More importantly, cathodic and anodic dual-emitting ECL greatly improves the selectivity.

Personality traits and co-occurrence of depressive symptoms and high BMI: a prospective cohort study.

We assess the associations between personality traits and co-occurrence of depressive symptoms and high BMI from adolescence to early adulthood. We employed a nationally representative cohort in China from 2010 to 2020 year. We included adolescents aged 10-19 years without depressive symptoms and unhealthy weight status (obesity, overweight, or thinness) at baseline and excluded those without any measurement of depressive symptoms or BMI at follow-ups. We assessed baseline personality traits in 7 dimensions of conscientiousness, openness, neuroticism, agreeableness, extraversion, self-esteem, and responsibility. We also assessed the combined effects of these 7 dimensions of personality traits by generating individual-level personality trait risk scores based on the weighted sum of all these 7 dimensions of personality traits. We measured the co-occurrence of depressive symptoms and high BMI using both a single measurement of depressive symptoms and BMI at the last follow-up and repeated measurements of them over 10 years. We used the multinomial logistic regression models to examine the exposure-outcome associations. At baseline, we included 1778 individuals (mean age: 14.4 year; female: 853 (48.0%)). At follow-ups, we observed increased risk of co-occurrence of depressive symptoms and high BMI per 1-SD increase in neuroticism score (1.95-2.38 odds ratio) or 1-SD decrease in self-esteem and conscientiousness (0.63-0.80 odds ratio; all P values < 0.05); we observed no evidence of associations between openness, agreeableness, extraversion, or responsibility and the risk of co-occurrence of depressive symptoms and high BMI (all P values > 0.05). For the combined effects of the 7 dimensions of personality traits, we found an elevated risk of co-occurrence of depressive symptoms and high BMI per 1-SD increase in the personality trait risk scores (OR (95% CI), single measurement at the last follow-up: 2.01, 1.66 to 2.43; trajectory classification using the repeated measurements 2.30, 1.55 to 3.42; average level using the repeated measurements: 2.27, 1.93 to 2.67). In this national cohort in China, personality traits were found to be associated with the co-occurrence of depressive symptoms and high BMI from adolescence to early adulthood. These findings highlight the importance of stratifying individuals based on their personality traits and providing targeted interventions for those at risk of comorbid depression and obesity.