Recent progress in the extraction of terpenoids from essential oils and separation of the enantiomers by GC-MS.

Terpenoids possess significant physiological activities and are rich in essential oils. Some terpenoids have chiral centers and could form enantiomers with distinct physiological activities. Therefore, the extraction and separation of terpenoids enantiomers are very important and have attracted extensive attention in recent years. Meanwhile, the specific distribution and enantiomer excess results (the excess of one enantiomer over the other in a mixture of enantiomers) could be used as quality markers for illegitimate adulteration, origin identification, and exploring component variations and functional interrelations across different plant tissues. In this study, an overview of the progress in the extraction of terpenoids from essential oils and the separation of their enantiomers over the past two decades has been made. Extraction methods were retrieved by the resultant network visualization findings. The results showed that the predominant methods are hydrodistillation, solvent-free microwave extraction, headspace solid-phase microextraction and supercritical fluid extraction methods. GC-MS combined with chiral chromatography columns is commonly used for the separation of enantiomers, while 2D GC is found to have stronger resolution ability. Finally, some prospects for future research directions in the extraction and separation identification of essential oils are proposed.

Identification of potential drug targets for insomnia by Mendelian randomization analysis based on plasma proteomics.

Introduction: Insomnia, a common clinical disorder, significantly impacts the physical and mental well-being of patients. Currently, available hypnotic medications are unsatisfactory due to adverse reactions and dependency, necessitating the identification of new drug targets for the treatment of insomnia. Methods: In this study, we utilized 734 plasma proteins as genetic instruments obtained from genome-wide association studies to conduct a Mendelian randomization analysis, with insomnia as the outcome variable, to identify potential drug targets for insomnia. Additionally, we validated our results externally using other datasets. Sensitivity analyses entailed reverse Mendelian randomization analysis, Bayesian co-localization analysis, and phenotype scanning. Furthermore, we constructed a protein-protein interaction network to elucidate potential correlations between the identified proteins and existing targets. Results: Mendelian randomization analysis indicated that elevated levels of TGFBI (OR = 1.01; 95% CI, 1.01-1.02) and PAM ((OR = 1.01; 95% CI, 1.01-1.02) in plasma are associated with an increased risk of insomnia, with external validation supporting these findings. Moreover, there was no evidence of reverse causality for these two proteins. Co-localization analysis confirmed that PAM (coloc.abf-PPH4 = 0.823) shared the same variant with insomnia, further substantiating its potential role as a therapeutic target. There are interactive relationships between the potential proteins and existing targets of insomnia. Conclusion: Overall, our findings suggested that elevated plasma levels of TGFBI and PAM are connected with an increased risk of insomnia and might be promising therapeutic targets, particularly PAM. However, further exploration is necessary to fully understand the underlying mechanisms involved.

Targeting epigenetic and post-translational modifications regulating pyroptosis for the treatment of inflammatory diseases.

Inflammatory diseases, including infectious diseases, diabetes-related diseases, arthritis-related diseases, neurological diseases, digestive diseases, and tumor, continue to threaten human health and impose a significant financial burden despite advancements in clinical treatment. Pyroptosis, a pro-inflammatory programmed cell death pathway, plays an important role in the regulation of inflammation. Moderate pyroptosis contributes to the activation of native immunity, whereas excessive pyroptosis is associated with the occurrence and progression of inflammation. Pyroptosis is complicated and tightly controlled by various factors. Accumulating evidence has confirmed that epigenetic modifications and post-translational modifications (PTMs) play vital roles in the regulation of pyroptosis. Epigenetic modifications, which include DNA methylation and histone modifications (such as methylation and acetylation), and post-translational modifications (such as ubiquitination, phosphorylation, and acetylation) precisely manipulate gene expression and protein functions at the transcriptional and post-translational levels, respectively. In this review, we summarize the major pathways of pyroptosis and focus on the regulatory roles and mechanisms of epigenetic and post-translational modifications of pyroptotic components. We also illustrate these within pyroptosis-associated inflammatory diseases. In addition, we discuss the effects of novel therapeutic strategies targeting epigenetic and post-translational modifications on pyroptosis, and provide prospective insight into the regulation of pyroptosis for the treatment of inflammatory diseases.

High-Voltage Na0.76Ni0.25-x/2Mgx/2Mn0.75O2-xFx Cathode Improved by One-Step In Situ MgF2 Doping with Superior Low-Temperature Performance and Extra-Stable Air Stability.

P2-NaxMnO2 has garnered significant attention due to its favorable Na+ conductivity and structural stability for large-scale energy storage fields. However, achieving a balance between high energy density and extended cycling stability remains a challenge due to the Jahn-Teller distortion of Mn3+ and anionic activity above 4.1 V. Herein, we propose a one-step in situ MgF2 strategy to synthesize a P2-Na0.76Ni0.225Mg0.025Mn0.75O1.95F0.05 cathode with improved Na-storage performance and decent water/air stability. By partially substituting cost-effective Mg for Ni and incorporating extra F for O, the optimized material demonstrates both enhanced capacity and structure stability via promoting Ni2+/Ni4+ and oxygen redox activity. It delivers a high capacity of 132.9 mA h g-1 with an elevated working potential of ≈3.48 V and maintains ≈83.0% capacity retention after 150 cycles at 100 mA g-1 within 2-4.3 V, compared to the 114.9 mA h g-1 capacity and 3.32 V discharging potential of the undoped Na0.76Ni0.25Mn0.75O2. While increasing the charging voltage to 4.5 V, 133.1 mA h g-1 capacity and 3.55 V discharging potential (vs Na/Na+) were achieved with 72.8% capacity retention after 100 cycles, far beyond that of the pristine sample (123.7 mA h g-1, 3.45 V, and 43.8%@100 cycles). Moreover, exceptional low-temperature cycling stability is achieved, with 95.0% after 150 cycles. Finally, the Na-storage mechanism of samples employing various doping strategies was investigated using in situ EIS, in situ XRD, and ex situ XPS techniques.

Circadian rhythm response and its effect on photosynthetic characteristics of the Lhcb family genes in tea plant.

BACKGROUND: The circadian clock, also known as the circadian rhythm, is responsible for predicting daily and seasonal changes in the environment, and adjusting various physiological and developmental processes to the appropriate times during plant growth and development. The circadian clock controls the expression of the Lhcb gene, which encodes the chlorophyll a/b binding protein. However, the roles of the Lhcb gene in tea plant remain unclear. RESULTS: In this study, a total of 16 CsLhcb genes were identified based on the tea plant genome, which were distributed on 8 chromosomes of the tea plant. The promoter regions of CsLhcb genes have a variety of cis-acting elements including hormonal, abiotic stress responses and light response elements. The CsLhcb family genes are involved in the light response process in tea plant. The photosynthetic parameter of tea leaves showed rhythmic changes during the two photoperiod periods (48 h). Stomata are basically open during the day and closed at night. Real-time quantitative PCR results showed that most of the CsLhcb family genes were highly expressed during the day, but were less expressed at night. CONCLUSIONS: Results indicated that CsLhcb genes were involved in the circadian clock process of tea plant, it also provided potential references for further understanding of the function of CsLhcb gene family in tea plant.

Stabilizing the Bulk-Phase and Solid Electrolyte Interphase of Silicon Microparticle Anode by Constructing Gradient-Hierarchically Ordered Conductive Networks.

The poor bulk-phase and interphase stability, attributable to adverse internal stress, impede the cycling performance of silicon microparticles (µSi) anodes and the commercial application for high-energy-density lithium-ion batteries. In this work, a groundbreaking gradient-hierarchically ordered conductive (GHOC) network structure, ingeniously engineered to enhance the stability of both bulk-phase and the solid electrolyte interphase (SEI) configurations of µSi, is proposed. Within the GHOC network architecture, two-dimensional (2D) transition metal carbides (Ti3C2Tx) act as a conductive "brick", establishing a highly conductive inner layer on µSi, while the porous outer layer, composed of one-dimensional (1D) Tempo-oxidized cellulose nanofibers (TCNF) and polyacrylic acid (PAA) macromolecule, functions akin to structural "rebar" and "concrete", effectively preserves the tightly interconnected conductive framework through multiple bonding mechanisms, including covalent and hydrogen bonds. Additionally, Ti3C2Tx enhances the development of a LiF-enriched SEI. Consequently, the µSi-MTCNF-PAA anode presents a high discharge capacity of 1413.7 mAh g-1 even after 500 cycles at 1.0 C. Moreover, a full cell, integrating LiNi0.8Mn0.1Co0.1O2 with µSi-MTCNF-PAA, exhibits a capacity retention rate of 92.0% following 50 cycles. This GHOC network structure can offer an efficacious pathway for stabilizing both the bulk-phase and interphase structure of anode materials with high volumetric strain.

Music and movement therapy improves quality of life and attention and associated electroencephalogram changes in patients with attention-deficit/hyperactivity disorder.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is the most common neurobehavioral disorder. Treatments for ADHD include pharmacological and nonpharmacological therapy. However, pharmacological treatments have side effects such as poor appetite, sleep disturbance, and headache. Moreover, nonpharmacological treatments are not effective in ameliorating core symptoms and are time-consuming. Hence, developing an alternative and effective treatment without (or with fewer) side effects is crucial. Music therapy has long been used to treat numerous neurological diseases. Although listening to music is beneficial for mood and cognitive functions in patients with ADHD, research on the effects of music and movement therapy in children with ADHD is lacking. METHODS: The present study investigated the effects of an 8-week music and movement intervention in 13 children with ADHD. The Pediatric Quality of Life Inventory (PedsQL) was used to evaluate changes in participants' quality of life. Conners' Kiddie Continuous Performance Test (K-CPT 2) and the Swanson, Nolan, and Pelham rating scale (SNAP-IV) were used to assess core symptoms. Electroencephalogram (EEG) recordings were analyzed to determine neurophysiological changes. RESULTS: The results revealed that the participants' quality of life increased significantly after the 8-week intervention. Furthermore, the participants' hit reaction times in the block 1 and block 2 tests of K-CPT 2 decreased significantly after the intervention. EEG analysis demonstrated an increase in alpha power and Higuchi's fractal dimension and a decrease in delta power in certain EEG channels. CONCLUSION: Our music and movement intervention is a potential alternative and effective tool for ADHD treatment and it can significantly improve patients' quality of life and attention.

Completely Non-Fused Low-Cost Acceptor Enables Organic Photovoltaic Cells with 17 % Efficiency.

To meet the industrial requirements of organic photovoltaic (OPV) cells, it is imperative to accelerate the development of cost-effective materials. Thiophene-benzene-thiophene central unit-based acceptors possess the advantage of low synthetic cost, while their power conversion efficiency (PCE) is relatively low. Here, by incorporating a para-substituted benzene unit and 1st-position branched alkoxy chains with large steric hindrance, a completely non-fused non-fullerene acceptor, TBT-26, was designed and synthesized. The narrow band gap of 1.38 eV ensures the effective utilization of sunlight. The favorable phase separation morphology of TBT-26-based blend film facilitates the efficient exciton dissociation and charge transport in corresponding OPV cell. Therefore, the TBT-26-based small-area cell achieves an impressive PCE of 17.0 %, which is the highest value of completely non-fused OPV cells. Additionally, we successfully demonstrated the scalability of this design by fabricating a 28.8 cm2 module with a high PCE of 14.3 %. Overall, our work provides a practical molecular design strategy for developing high-performance and low-cost acceptors, paving the way for industrial applications of OPV technology.

Molecular Design of Fully Nonfused Acceptors for Efficient Organic Photovoltaic Cells.

The nonfused thiophene-benzene-thiophene (TBT) unit offers advantages in obtaining low-cost organic photovoltaic (OPV) materials due to its simple structure. However, OPV cells, including TBT-based acceptors, exhibit significantly lower energy conversion efficiencies. Here, we introduce a novel approach involving the design and synthesis of three TBT-based acceptors by substituting different position-branched side chains on the TBT unit. In comparison to TBT-10 and TBT-11, TBT-13, which exclusively incorporates α-position branched side chains with a large steric hindrance, demonstrates a more planar and stable conformation. When blended with the donor PBQx-TF, TBT-13-based blend film achieves favorable π-π stacking and aggregation characteristics, resulting in excellent charge transfer performance in the corresponding device. Due to the simultaneous enhancements in short-circuit current density and fill factor, the TBT-13-based OPV cell obtains an outstanding efficiency of 16.1%, marking the highest value for the cells based on fully nonfused acceptors. Our work provides a practical molecular design strategy for high-performance and low-cost OPV materials.

Network pharmacology and molecular docking analysis on Shenfu Qiangxin indicate mTOR is a potential target to treat heart failure.

BACKGROUND: Heart failure (HF) is one of the major causes of mortality worldwide with high recurrence rate and poor prognosis. Our study aimed to investigate potential mechanisms and drug targets of Shenfu Qiangxin (SFQX), a cardiotonic-diuretic traditional Chinese medicine, in treating HF. METHODS: An HF-related and SFQX-targeted gene set was established using disease-gene databases and the Traditional Chinese Medicine Systems Pharmacology database. We performed gene function and pathway enrichment analysis and constructed protein-protein interaction (PPI) network to investigate the potential mechanisms. We also performed molecular docking to analyze the interaction patterns between the active compounds and targeted protein. RESULTS: A gene set with 217 genes was identified. The gene function enrichment indicated that SFQX can regulate apoptotic process, inflammatory response, response to oxidative stress and cellular response to hypoxia. The pathway enrichment indicated that most genes were involved in PI3K-Akt pathway. Eighteen hub target genes were identified in PPI network and subnetworks. mTOR was the key gene among hub genes, which are involved in PI3K-Akt pathway. The molecular docking analysis indicated that 6 active compounds of SFQX can bind to the kinase domain of mTOR, which exerted potential therapeutic mechanisms of SFQX in treating HF. CONCLUSIONS: The results of network pharmacology analysis highlight the intervention on PI3K-Akt pathway of SFQX in the treatment of HF. mTOR is a key drug target to help protect myocardium.

Tumor Homing Chimeric Peptide Rhomboids to Improve Photodynamic Performance by Inhibiting Therapy-Upregulated Cyclooxygenase-2.

Negative therapeutic feedback of inflammation would extensively attenuate the antitumor effect of photodynamic therapy (PDT). In this work, tumor homing chimeric peptide rhomboids (designated as NP-Mel) are fabricated to improve photodynamic performance by inhibiting PDT-upregulated cyclooxygenase-2 (COX-2). The hydrophobic photosensitizer of protoporphyrin IX (PpIX) and palmitic acid are conjugated onto the neuropilin receptors (NRPs) targeting peptide motif (CGNKRTR) to obtain tumor homing chimeric peptide (Palmitic-K(PpIX)CGNKRTR), which can encapsulate the COX-2 inhibitor of meloxicam. The well dispersed NP-Mel not only improves the drug stability and reactive oxygen species (ROS) production ability, but also increase the breast cancer targeted drug delivery to intensify the PDT effect. In vitro and in vivo studies verify that NP-Mel will decrease the secretion of prostaglandin E2 (PGE2) after PDT treatment, inducing the downregulation of IL-6 and TNF-α expressions to suppress PDT induced inflammation. Ultimately, an improved PDT performance of NP-Mel is achieved without inducing obvious systemic toxicity, which might inspire the development of sophisticated nanomedicine in consideration of the feedback induced therapeutic resistance.

DHCR24 Insufficiency Promotes Vascular Endothelial Cell Senescence and Endothelial Dysfunction via Inhibition of Caveolin-1/ERK Signaling.

Endothelial cells (ECs) senescence is critical for vascular dysfunction, which leads to age-related disease. DHCR24, a 3ß-hydroxysterol δ 24 reductase with multiple functions other than enzymatic activity, has been involved in age-related disease. However, little is known about the relationship between DHCR24 and vascular ECs senescence. We revealed that DHCR24 expression is chronologically decreased in senescent human umbilical vein endothelial cells (HUVECs) and the aortas of aged mice. ECs senescence in endothelium-specific DHCR24 knockout mice was characterized by increased P16 and senescence-associated secretory phenotype, decreased SIRT1 and cell proliferation, impaired endothelium-dependent relaxation, and elevated blood pressure. In vitro, DHCR24 knockdown in young HUVECs resulted in a similar senescence phenotype. DHCR24 deficiency impaired endothelial migration and tube formation and reduced nitric oxide (NO) levels. DHCR24 suppression also inhibited the caveolin-1/ERK signaling, probably responsible for increased reactive oxygen species production and decreased eNOS/NO. Conversely, DHCR24 overexpression enhanced this signaling pathway, blunted the senescence phenotype, and improved cellular function in senescent cells, effectively blocked by the ERK inhibitor U0126. Moreover, desmosterol accumulation induced by DHCR24 deficiency promoted HUVECs senescence and inhibited caveolin-1/ERK signaling. Our findings demonstrate that DHCR24 is essential in ECs senescence.

An all-inorganic lead-free metal halide double perovskite for the highly selective detection of norfloxacin in aqueous solution.

Lead-based perovskites are highly susceptible to environmental influences, and their application in analytical chemistry, especially in aqueous solution, has been reported rarely. All-inorganic lead-free metal halide perovskites have been considered as a substitute for lead-based perovskites. Herein, a Cs2RbTbCl6 perovskite microcrystal (PMCs), which emits strong yellow-green fluorescence with a maximum emission wavelength at 547 nm, was for the first time  synthesized and characterized. The Cs2RbTbCl6 PMCs could be well dispersed in N,N-dimethylacetamide (DMF), and its fluorescence could be significantly enhanced by the addition of norfloxacin (NOR) in the aqueous solution. We found that the Cs2RbTbCl6 PMCs can be used as fluorescent probes (excitation, 365 nm; emission, 547 nm) to selectively detect NOR in a concentration range from 10.0 to 200.0 µM with the limit of detection (LOD) being 0.04 µM. The Cs2RbTbCl6 PMCs could also be adsorbed on filter paper to fabricate as a fluorescent test paper for visual detection of NOR under 365-nm ultraviolet (UV) lamp irradiation. The proposed method has the potential to establish a new analytical method to visualize the detection of NOR in aqueous environments and also promotes the application of all-inorganic lead-free perovskites for analytical detection in aqueous environments.

Metabolic clues to aging: exploring the role of circulating metabolites in frailty, sarcopenia and vascular aging related traits and diseases.

Background: Physical weakness and cardiovascular risk increase significantly with age, but the underlying biological mechanisms remain largely unknown. This study aims to reveal the causal effect of circulating metabolites on frailty, sarcopenia and vascular aging related traits and diseases through a two-sample Mendelian Randomization (MR) analysis. Methods: Exposures were 486 metabolites analyzed in a genome-wide association study (GWAS), while outcomes included frailty, sarcopenia, arterial stiffness, atherosclerosis, peripheral vascular disease (PAD) and aortic aneurysm. Primary causal estimates were calculated using the inverse-variance weighted (IVW) method. Methods including MR Egger, weighted median, Q-test, and leave-one-out analysis were used for the sensitive analysis. Results: A total of 125 suggestive causative associations between metabolites and outcomes were identified. Seven strong causal links were ultimately identified between six metabolites (kynurenine, pentadecanoate (15:0), 1-arachidonoylglycerophosphocholine, androsterone sulfate, glycine and mannose) and three diseases (sarcopenia, PAD and atherosclerosis). Besides, metabolic pathway analysis identified 13 significant metabolic pathways in 6 age-related diseases. Furthermore, the metabolite-gene interaction networks were constructed. Conclusion: Our research suggested new evidence of the relationship between identified metabolites and 6 age-related diseases, which may hold promise as valuable biomarkers.

Mitochondrial dysfunction mediated by thioredoxin-interacting protein: A crucial determinant in di(2-ethylhexyl) phthalate-induced liver failure.

Di(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer that can interfere with the endocrine system and cause liver damage. However, the molecular mechanism of DEHP-induced liver injury is unclear. This study aimed to investigate the effects of DEHP on liver function and its relationship with thioredoxin-interacting protein (TXNIP) and mitochondrial oxidative stress pathway. We used C57BL/6 J mice and THLE-2 liver cells as in vivo and in vitro models, respectively, and treated them with different doses of DEHP, and measured the relevant biochemical indicators and molecular markers. We found that DEHP significantly increased the expression of TXNIP and NLRP3, while decreasing the expression of mitochondrial functional proteins, such as PGC-1α, TFAM, NRF1, NDUHA9, SDHA, MFN1. This resulted in mitochondrial dysfunction, manifested by reduced ATP generation, increased inflammatory factor release, elevated liver enzyme indicators, decreased mitochondrial membrane potential and increased oxidative stress. We further demonstrated that TXNIP upregulation activated NF-κB and MAPK signaling pathways, such as NF-κB, IκB, TAB2, TRAF6, ERK1, JNK, p38 MAPK, MEK1, which exacerbated oxidative stress and inflammation, leading to liver damage. Additionally, we found that treatment with the antioxidant MitoQ partially alleviated DEHP-induced liver toxicity, while silencing TXNIP more effectively restored mitochondrial function. Our study supports the hypothesis that DEHP induces mitochondrial oxidative stress through the TXNIP signaling pathway, resulting in liver dysfunction in mice, and suggests possible links between endocrine-disrupting chemicals and human diseases.

Differential Response of MYB Transcription Factor Gene Transcripts to Circadian Rhythm in Tea Plants (Camellia sinensis).

The circadian clock refers to the formation of a certain rule in the long-term evolution of an organism, which is an invisible 'clock' in the body of an organism. As one of the largest TF families in higher plants, the MYB transcription factor is involved in plant growth and development. MYB is also inextricably correlated with the circadian rhythm. In this study, the transcriptome data of the tea plant 'Baiyeyihao' were measured at a photoperiod interval of 4 h (24 h). A total of 25,306 unigenes were obtained, including 14,615 unigenes that were annotated across 20 functional categories within the GO classification. Additionally, 10,443 single-gene clusters were annotated to 11 sublevels of metabolic pathways using KEGG. Based on the results of gene annotation and differential gene transcript analysis, 22 genes encoding MYB transcription factors were identified. The G10 group in the phylogenetic tree had 13 members, of which 5 were related to the circadian rhythm, accounting for 39%. The G1, G2, G8, G9, G15, G16, G18, G19, G20, G21 and G23 groups had no members associated with the circadian rhythm. Among the 22 differentially expressed MYB transcription factors, 3 members of LHY, RVE1 and RVE8 were core circadian rhythm genes belonging to the G10, G12 and G10 groups, respectively. Real-time fluorescence quantitative PCR was used to detect and validate the expression of the gene transcripts encoding MYB transcription factors associated with the circadian rhythm.

FTO attenuates LPS-induced acute kidney injury by inhibiting autophagy via regulating SNHG14/miR-373-3p/ATG7 axis.

N6-methyladenosine (m6A) is a master driver of RNA function and implicates in the pathogenesis of renal injury. LncRNA SNHG14 is highly expressed in sepsis patients with acute kidney injury (AKI) and aggravates kidney cell dysfunction. This study aimed to explore whether demethylase FTO affect m6A methylation of SNHG14 in AKI injury and its underlying mechanism. The expression level of FTO was obviously downregulated in sepsis-associated AKI patients compared with normal controls. Mechanistically, FTO overexpression impeded SNHG14 expression by decreasing the stability of SNHG14 in an m6A-dependent manner in LPS-induced HK-2 cells. Additionally, FTO overexpression inhibited cell autophagy and apoptosis while promoting cell viability of LPS-induced HK-2 cells. Moreover, overexpression of FTO inhibited SNHG14 expression and autophagy in LPS-induced AKI mice. Functionally, SNHG14 acts as a competing endogenous RNA (ceRNA) via directly sponging miR-373-3p in LPS induced HK-2 cells. Additionally, miR-373-3p directly targets ATG7. Inhibition of SNHG14 suppresses NF-κB signaling pathway and production of inflammatory cytokines (TNF-α, IL-6, and IL-1ß) via miR-373-3p/ATG7 in LPS-induced HK-2 cells. Furthermore, the SNHG14/miR-373-3p/ATG7 interaction network contributes to the regulatory effect of FTO on LPS-induced HK-2 cell viability, apoptosis and autophagy. These results suggested demethylase FTO suppressed the m6A modification of lncRNA SNHG14 and inhibits autophagy in LPS-induced AKI via regulating miR-373-3p/ATG7, which provided an important novel perspective for understanding sepsis-associated AKI and is conducive for developing new therapeutic targets and strategies.

Increased Circulating IL-32 Is Associated With Placenta Macrophage-derived IL-32 and Gestational Diabetes Mellitus.

OBJECTIVE: Placenta-derived inflammation plays a vital role in the pathophysiology of gestational diabetes mellitus (GDM). IL-32 is a novel pro-inflammatory cytokine and metabolic regulator involved in the development of metabolic disease. We investigated the effect of IL-32 in GDM. MATERIALS AND METHODS: First-trimester C-reactive protein (CRP) level was monitored in a case-control study of 186 women with GDM and 186 women without. Placental tissue was lysed and analyzed by high-resolution liquid chromatography-tandem mass spectrometry. Circulating level of inflammatory cytokines IL-32, IL-6, and TNF-α were measured by ELISA kits. The expression of placenta-derived macrophages, inflammatory cytokines, and related pathway proteins were assessed by reverse transcriptase-quantitative PCR, western blot, immunohistochemistry, or immunofluorescence. RESULTS: First-trimester CRP level in peripheral blood was closely associated with glucose and insulin resistance index and was an independent correlation with the development of GDM. High-resolution liquid chromatography-tandem mass spectrometry revealed that placenta-derived CRP expression was dramatically elevated in women with GDM. Interestingly, the expression of placenta-derived IL-32 was also increased and located in the macrophages of placental tissue. Meanwhile, the expression of IL-6, TNF-α, and p-p38 were up-regulated in the placental tissues with GDM. Either IL-6 or TNF-α was colocated with IL-32 in the placental tissue. Importantly, circulating IL-32 throughout pregnancy was increased in GDM and was related to placental-derived IL-32 expression, circulating IL-6, and TNF-α, glucose and insulin resistance index. CONCLUSION: Increased circulating IL-32 throughout pregnancy was closely associated with placenta macrophage-derived IL-32 expression and GDM. First trimester IL-32 level in peripheral blood may serve to predict the development of GDM.

An Ortho-Bisalkyloxylated Benzene-Based Fully Non-fused Electron Acceptor for Efficient Organic Photovoltaic Cells.

To develop the low-cost nonfullerene acceptors (NFAs), two fully non-fused NFAs (TBT-2 and TBT-6) with ortho-bis((2-ethylhexyl)oxy)benzene unit and different side chains onto thiophene-bridges are synthesized through highly efficient synthetic procedures. Both acceptors show good planarity, low optical gaps (≈1.51 eV), and deep highest occupied molecular orbital levels (≤-5.77 eV). More importantly, the single-crystal structure of TBT-2 shows compact molecular arrangement due to the existence of intramolecular interactions between adjacent aromatic units and strong π-π stacking between intermolecular terminal groups. When the two acceptors are fabricated organic photovoltaic (OPV) cells by combining with a wide optical gap polymer donor, the TBT-6 with strong crystallization forms large domain sizes in bulk heterojunction (BHJ) blend. As a result, the TBT-6-based OPV cell shows a low power conversion efficiency (PCE) of 9.53%. In contrast, the TBT-2 with proper crystallization facilitates morphological optimization in the BHJ blend. Consequently, the TBT-2-based OPV cell gives an outstanding PCE of 13.25%, which is one of the best values among OPV cells with similar optical gaps. Overall, this work provides a practical molecular design strategy for developing high-performance and low-cost electron acceptors.

Morphology Control for Efficient Nonfused Acceptor-Based Organic Photovoltaic Cells.

Non-fused electron acceptors have huge advantages in fabricating low-cost organic photovoltaic (OPV) cells. However, morphology control is a challenge as non-fused C─C single bonds bring more molecular conformations. Here, by selecting two typical polymer donors, PBDB-TF and PBQx-TF, the blend morphologies and its impacts on the power conversion efficiencies (PCEs) of non-fused acceptor-based OPV cells are studied. A selenium-containing non-fused acceptor named ASe-5 is designed. The results suggest that PBQx-TF has a lower miscibility with ASe-5 when compared with PBDB-TF. Additionally, the polymer networks may form earlier in the PBQx-TF:ASe-5 blend film due to stronger preaggregation performance, leading to a more obvious phase separation. The PBQx-TF:ASe-5 blend film shows faster charge transfer and suppressed charge recombination. As a result, the PBQx-TF:ASe-5-based device records a good PCE of 14.7% with a higher fill factor (FF) of 0.744, while the PBDB-TF:ASe-5-based device only obtains a moderate PCE of 12.3% with a relatively low FF of 0.662. The work demonstrates that the selection of donors plays a crucial role in controlling the blend morphology and thus improving the PCEs of non-fused acceptor-based OPV cells.