Bipolaris fujianensis sp. nov., an Emerging Pathogen of Sapling Shoot Blight on Chinese Fir, and Its Sensitivity to Fungicides.

Chinese fir is an extremely important economic tree species in southern China. In recent years, 74.5% of Chinese fir saplings suffered from shoot blight in Shunchang County, Nanping City, Fujian Province, China. Seventeen isolates were collected from rotten shoots, and their pathogenicity was confirmed following Koch's postulates. The five pathogenic isolates were identified as belonging to the genus Bipolaris based on morphological characteristics, including septate and geniculate conidiophores, smooth to slightly verruculose conidiogenous nodes, dematiaceous phragmospore conidia, oblong or fusiform conidia, and slightly protruding or truncate hilum on conidia, but the number of pseudosepta (3 to 11, mostly 5 to 8) and the size of conidia ([22.81 to 116.13] × [9.16 to 26.58] µm) are different from those of the known species of Bipolaris. A phylogenetic analysis based on ITS, GAPDH, and Tef1-α sequences determined that the five strains belong to a new species of Bipolaris, and the name Bipolaris fujianensis sp. nov. is proposed. The fungicide sensitivity of the pathogen strain Cfsb3 was further evaluated using eight fungicides. Flusilazole, difenoconazole, tebuconazole, and propiconazole exhibited high toxicity to Cfsb3, and the effective concentration inhibiting 50% (EC50) of mycelial growth was 0.08, 0.20, 0.34, and 0.36 µg/ml, respectively, for these four fungicides. Flusilazole, difenoconazole, and iprodione inhibited B. fujianensis by 100% on detached Chinese fir shoots at their recommended concentrations, but azoxystrobin and thiram were ineffective. In conclusion, this study reported an emerging pathogen of Chinese fir sapling shoot blight and proposed triazole and dicarboximide fungicides for disease control.

Role of macrophage polarization in periodontitis promoting atherosclerosis.

Periodontitis is a chronic inflammatory destructive disease occurring in periodontal supporting tissues. Atherosclerosis(AS) is one of the most common cardiovascular diseases. Periodontitis can promote the development and progression of AS. Macrophage polarization is closely related to the development and progression of the above two diseases, respectively. The purpose of this animal study was to evaluate the effect of periodontitis on aortic lesions in atherosclerotic mice and the role of macrophage polarization in this process. 45 ApoE-/-male mice were randomly divided into three groups: control (NC), atherosclerosis (AS), and atherosclerosis with periodontitis (AS + PD). Micro CT, serological testing and pathological testing(hematoxylin-eosin staining, oil red O staining and Masson staining) were used for Evaluate the modeling situation. Immunohistochemistry(IHC) and immunofluorescence(IF) were performed to evaluate macrophage content and macrophage polarization in plaques. Cytokines associated with macrophage polarization were analyzed using quantitative real-time polymerase chain reaction(qRT-PCR) and enzyme-linked immunosorbent assay(Elisa). The expression of macrophages in plaques was sequentially elevated in the NC, AS, and AS + PD groups(P < 0.001). The expression of M1 and M1-related cytokines showed the same trend(P < 0.05). The expression of M2 and M2-related cytokines showed the opposite trend(P < 0.05). The rate of M1/M2 showed that AS + PD > AS > NC. Our preliminary data support that experimental periodontitis can increase the content of macrophage in aortic plaques to exacerbate AS. Meanwhile, experimental periodontitis can increase M1 macrophages, and decrease M2 macrophages, increasing M1/M2 in the plaque.

Optimizing Molecular Crystallinity and Suppressing Electron-Phonon Coupling in Completely Non-Fused Ring Electron Acceptors for Organic Solar Cells.

High open-circuit voltage (Voc) organic solar cells (OSCs) have received increasing attention because of their promising application in tandem devices and indoor photovoltaics. However, the lack of a precise correlation between molecular structure and stacking behaviors of wide band gap electron acceptors has greatly limited its development. Here, we adopted an asymmetric halogenation strategy (AHS) and synthesized two completely non-fused ring electron acceptors (NFREAs), HF-BTA33 and HCl-BTA33. The results show that AHS significantly enhances the molecular dipoles and suppresses electron-phonon coupling, resulting in enhanced intramolecular/intermolecular interactions and decreased nonradiative decay. As a result, PTQ10 : HF-BTA33 realizes a power conversion efficiency (PCE) of 11.42 % with a Voc of 1.232 V, higher than that of symmetric analogue F-BTA33 (PCE=10.02 %, Voc=1.197 V). Notably, PTQ10 : HCl-BTA33 achieves the highest PCE of 12.54 % with a Voc of 1.201 V due to the long-range ordered π-π packing and enhanced surface electrostatic interactions thereby facilitating exciton dissociation and charge transport. This work not only proves that asymmetric halogenation of completely NFREAs is a simple and effective strategy for achieving both high PCE and Voc, but also provides deeper insights for the precise molecular design of low cost completely NFREAs.

Astrocyte-specific loss of lactoferrin influences neuronal structure and function by interfering with cholesterol synthesis.

Growing evidence indicates that circulating lactoferrin (Lf) is implicated in peripheral cholesterol metabolism disorders. It has emerged that the distribution of Lf changes in astrocytes of aging brains and those exhibiting neurodegeneration; however, its physiological and/or pathological role remains unknown. Here, we demonstrate that astrocyte-specific knockout of Lf (designated cKO) led to decreased body weight and cognitive abnormalities during early life in mice. Accordingly, there was a reduction in neuronal outgrowth and synaptic structure in cKO mice. Importantly, Lf deficiency in the primary astrocytes led to decreased sterol regulatory element binding protein 2 (Srebp2) activation and cholesterol production, and cholesterol content in cKO mice and/or in astrocytes was restored by exogenous Lf or a Srebp2 agonist. Moreover, neuronal dendritic complexity and total dendritic length were decreased after culture with the culture medium of the primary astrocytes derived from cKO mice and that this decrease was reversed after cholesterol supplementation. Alternatively, these alterations were associated with an activation of AMP-activated protein kinase (AMPK) and inhibition of SREBP2 nuclear translocation. These data suggest that astrocytic Lf might directly or indirectly control in situ cholesterol synthesis, which may be implicated in neurodevelopment and several neurological diseases.

Polysaccharide-Enriched Fraction from Amillariella Mellea Fruiting Body Improves Insulin Resistance.

Despite the edible fungus Amillariella mellea possessing a variety of biological activities, its effects on diabetes are still unclear. Polysaccharides are the main bioactive ingredients. In order to destroy the cell wall to obtain more polysaccharides, we used NaOH solution to extract Amillariella mellea fruiting bodies. The alkali extraction (AAMP) was identified as a polysaccharide-enriched fraction. Using type 2 diabetic rats induced by co-treatment of a high fat diet (HFD) and dexamethasone (DEX), we evaluated the hypoglycemic effects of AAMP. The results showed that oral administration of a high dose of AAMP markedly lowered fasting blood glucose, improving glucose intolerance and insulin resistance. AAMP also enhanced the level of LPL and the expressions of two critical lipases ATGL and HSL, leading to a decrease of serum triglyceride. In addition, AAMP specifically suppressed the expression of SREBP-1c, resulting in AAMP observably inhibiting lipid accumulation in the liver. These findings demonstrated that the improvement of AAMP on HFD/DEX-induced insulin resistance was correlated with its regulation of lipid metabolism. Our results indicated that AAMP could be a novel natural drug or health food used for the treatment of diabetes.

"Sketch and Peel" Lithography for High-Resolution Multiscale Patterning.

We report a unique lithographic process, termed "Sketch and Peel" lithography (SPL), for fast, clean, and reliable patterning of metallic structures from tens of nanometers to submillimeter scale using direct writing technology. The key idea of SPL process is to define structures using their presketched outlines as the templates for subsequent selective peeling of evaporated metallic layer. With reduced exposure area, SPL process enables significantly improved patterning efficiency up to hundreds of times higher and greatly mitigated proximity effect compared to current direct writing strategy. We demonstrate that multiscale hierarchical metallic structures with arbitrary shapes and minimal feature size of ∼15 nm could be defined with high fidelity using SPL process for potential nanoelectronic and nano-optical applications.

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy.

Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation.

Effects of Ni Content and Heat Treatment on the Properties, Microstructures, and Precipitates of Cu-0.2 wt% Be-x wt% Ni Alloys.

Cu-Be alloys exhibit excellent comprehensive performance in electrics, thermotics, and mechanics, and hence, they attract much attention. Among them, low-Be copper alloys are more environmentally friendly and promising. This study explores the effects of different Ni contents and heat treatment parameters on the properties, microstructures, and precipitates of Cu-0.2 wt% Be-x wt% Ni (0 < x < 2.0) alloys. The experimental results demonstrate that the fast cooling rate of cast alloys during solidification contributes to retention of the solute atoms in the copper matrix, which is beneficial for subsequent solid solution treatment. Furthermore, solid solution treatment slightly reduces the electrical conductivities, microhardness values, and compressive yield strengths of Cu-0.2 wt% Be-1.0/1.6 wt% Ni alloys. The optimal solution temperature and time are about 925 ℃ and 60 min, respectively. Aging treatment significantly increases the electrical conductivities, microhardness values, and compressive yield strengths of Cu-0.2 wt% Be-1.0/1.6 wt% Ni alloys. The best aging temperature is around 450 ℃. However, the properties of Cu-0.2 wt%Be-0.4 wt%Ni alloys remain unaffected by solution and aging treatments. Around x = 1.0, Cu-0.2 wt% Be-x wt% Ni alloys possess the best comprehensive properties, which are about 72%IACS of electrical conductivity, 241 HV of microhardness, and 281MPa of compressive yield strength, respectively. TEM and EDS analyses reveal that the precipitate evolution of Cu-0.2 wt% Be-1.0 wt% Ni alloys with aging time is GP zones → γ″ → γ'. Notably, a distinct double-peak age strengthening phenomenon emerges with Cu-0.2 wt% Be-1.0/1.6 wt% Ni alloys. The precipitation of plenty of GP zones at the early stage of aging should account for the first strengthening peak, and the strengthening mechanism transformation of the γ″ or γ' phase from shear to Orowan should induce the second strengthening peak. This work may help to design new low-Be copper alloys and their preparation processes.

Beyond Immune Balance: The Pivotal Role of Decidual Regulatory T Cells in Unexplained Recurrent Spontaneous Abortion.

Recurrent spontaneous abortion (RSA) is defined as two or more consecutive pregnancy failures, which brings tremendous stress to women of childbearing age and seriously affects family well-being. However, the reason in about 50% of cases remains unknown and is defined as unexplained recurrent spontaneous abortion (URSA). The immunological perspective in URSA has attracted widespread attention in recent years. The embryo is regarded as a semi-allogeneic graft to the mother. A successful pregnancy requires transition to an immune environment conducive to embryo survival at the maternal-fetal interface. As an important member of regulatory immunity, regulatory T (Treg) cells play a key role in regulating immune tolerance at the maternal-fetal interface. This review will focus on the phenotypic plasticity and lineage stability of Treg cells to illustrate its relationship with URSA.

Efficient CsPbBr3 Perovskite Light-Emitting Diodes via Novel Multi-Step Ligand Exchange Strategy Based on Zwitterionic Molecules.

Perovskite nanocrystals have absorbed increasing interest, especially in the field of optoelectronics, owing to their unique characteristics, including their tunable luminescence range, robust solution processability, facile synthesis, and so on. However, in practice, due to the inherent instability of the traditional long-chain insulating ligands surrounding perovskite quantum dots (PeQDs), the performance of the as-fabricated QLED is relatively disappointing. Herein, the zwitterion 3-(decyldimethylammonio)propanesulfonate (DLPS) with the capability of double passivating perovskite quantum dots could effectively replace the original long-chain ligand simply through a multistep post-treatment strategy to finally inhibit the formation of defects. It was indicated from theexperimental results that the DLPS, as one type of ligand with the bimolecular ion, was very adavntageous in replacing long-chain ligands and further suppressing the formation of defects. Finally, the perovskite quantum dots with greatly enhanced PLQY as high as 98% were effectively achieved. Additionally, the colloidal stability of the corresponding PeQDs has been significantly enhanced, and a transparent colloidal solution was obtained after 45 days under ambient conditions. Finally, the as-fabricated QLEDs based on the ligand-exchanged PeQDs exhibited a maximum brightness of 9464 cd/m2 and an EQE of 12.17%.

Estrogen promotes the growth of decidual stromal cells in human early pregnancy.

Interleukin-24 (IL-24) is a novel tumor suppressor gene, which has suppressor activity in a broad spectrum of human cancer cells. The present study aimed to elucidate the biological function of IL-24 and its receptors (IL-20R1, IL-20R2 and IL-22R1) in decidual stromal cells (DSCs) at human maternal-fetal interface. The DSCs behaviors in vitro were verified by viability (MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and apoptosis assay, respectively. Additionally, the effects of pregnancy-associated hormones on IL-24 and the effect of IL-24 on the correspondent functional molecules were investigated by ELISA, in-cell western and flow cytometry, respectively. Here we found that DSCs expressed IL-24 and its receptors, and IL-24 obviously suppressed the viability and stimulated the apoptosis in DSCs. On the contrary, both anti-IL-24 and IL-22R1 neutralizing antibodies markedly promoted growth and reduced the apoptosis. Estrogen but not progesterone could significantly decrease IL-24 but not its receptors, and these effects could be abolished by the antagonist of estrogen receptor beta (ERß). IL-24 significantly restricted the stimulatory effect of estrogen on the viability, anti-apoptosis, anti-apoptosis gene Bcl-2 and proliferation relative gene Ki-67 in DSCs. Our study has demonstrated that IL-24/IL-20R2/IL-22R1 axis is involved in the regulation of estrogen/ERß signaling on the growth of DSCs through up-regulating the expression of Bcl-2 and Ki67, which suggests that estrogen plays an important role in DSC growth of the early pregnancy through down-regulating IL-24.

NME1 suppression promotes growth, adhesion and implantation of endometrial stromal cells via Akt and MAPK/Erk1/2 signal pathways in the endometriotic milieu.

STUDY QUESTION: Is Nometastatic gene 23-H1 (NME1, also known as nm23-H1) involved in regulating the biological behavior of endometrial stromal cells (ESCs), and does it participate in the pathogenesis of endometriosis? SUMMARY ANSWER: NME1 suppression induces ESC dysfunction in the endometriotic milieu. WHAT IS KNOWN ALREADY: NME1 is a wide-spectrum tumor metastasis suppressor gene that plays an important role in suppressing the invasion and metastasis of tumor cells. STUDY DESIGN, SIZE, DURATION: An in vitro investigation of the effect of NME1 on the proliferation, adhesion and invasion of eutopic ESCs from patients with endometriosis. PARTICIPANTS/MATERIALS, SETTING, METHODS: Primary ESCs were prepared from 12 samples of ectopic endometrial tissue (6 peritoneal and 6 ovarian lesions), 18 samples of eutopic endometrial tissues (16 from women with ovarian and 2 from women with pelvic endometriomas) and 12 samples of normal endometrial tissue from women without endometriosis, after the tissues had been analyzed histologically. The growth, invasiveness and adhesion of ESCs were studied by the 5-bromo-2'-deoxyuridine cell proliferation assay and by the Matrigel invasion and adhesion assay. Additionally, the effects of NME1 on the activation or expression of related regulatory proteins were investigated by in-cell Western and flow cytometry assays. MAIN RESULTS AND THE ROLE OF CHANCE: Expression of NME1 in ESCs derived from eutopic or ectopic endometrium from women with endometriosis is lower than in ESCs from women without endometriosis. Estrogen could down-regulate NME1 expression in ESCs. Silencing NME1 in ESCs promoted the expression of proliferating cell nuclear antigen (PCNA), the anti-apoptotic molecule, survivin, and the adhesion-related molecules, integrin ß1 and integrin ανß3. Silencing NME1 also stimulated ESC proliferation, adhesion and invasion but these effects were inhibited by MAPK/Erk and/or Akt blockers. LIMITATIONS, REASONS FOR CAUTION: Further studies are needed to examine the regulatory mechanism of estrogen on NME1 expression of ESCs. WIDER IMPLICATIONS OF THE FINDINGS: Abnormally low expression of NME1 in ESCs may be involved in the pathogenesis of endometriosis by up-regulating growth, adhesion and invasion of ESCs via activating the Akt and MAPK/Erk1/2 signal pathways. STUDY FUNDING/COMPETING INTEREST(S): This work was supported by National Natural Science Foundation of China (NSFC) (31270969, 31101064 and 81270677) and Program for ZhouXue of Fudan University. None of the authors has any conflict of interest to declare.

Placental exosomal miR-125b triggered endothelial barrier injury in preeclampsia.

INTRODUCTION: Preeclampsia (PE) is an elusive life-threatening complication of pregnancy, and maternal endothelial dysfunction induced by components from the impaired placenta is a key hallmark of PE. Placenta-derived exosomes in maternal circulation have been correlated with risk of PE, however, the role of exosomes in PE remains to be determined. We hypothesized that placenta-released exosomes link the placental abnormalities with maternal endothelial dysfunction in PE. METHODS: Circulating exosomes were collected from plasma samples of preeclamptic patients and normal pregnancies. Endothelial barrier function was examined by transendothelial electrical resistance (TEER) and cell permeability to FITC-dextran assays in human umbilical vein endothelial cells (HUVECs). miR-125b and VE-cadherin gene expression in exosomes and endothelial cells were assessed by qPCR and Western, and the possible post-transcriptional regulation of miR-125b on VE-cadherin was detected by luciferase assay. RESULTS: We isolated placenta-derived exosomes in the maternal circulation and found that placenta-derived exosomes from preeclamptic patients (PE-exo) leads to endothelial barrier dysfunction. We then identified decreased expression of VE-cadherin in endothelial cells contribute to the breakdown of the endothelial barrier. Further investigations revealed increased exosomal miR-125b in PE-exo directly inhibited VE-cadherin in HUVECs, thereby mediating the adverse effect of PE-exo on endothelial barrier function. DISCUSSION: Placental exosomes link impaired placentation and endothelial dysfunction, thus providing new insight into the pathophysiology of preeclampsia. Exosomal miRNAs derived from placenta contribute to the endothelial dysfunction in PE and could be a promising therapeutic target for PE.

The interrelation of galectins and autophagy.

Autophagy is a vital physiological process that maintains intracellular homeostasis by removing damaged organelles and senescent or misfolded molecules. However, excessive autophagy results in cell death and apoptosis, which will lead to a variety of diseases. Galectins are a type of animal lectin that binds to ß-galactosides and can bind to the cell surface or extracellular matrix glycans, affecting a variety of immune processes in vivo and being linked to the development of many diseases. In many cases, galectins and autophagy both play important regulatory roles in the cellular life course, yet our understanding of the relationship between them is still incomplete. Galectins and autophagy may share common etiological cofactors for some diseases. Hence, we summarize the relationship between galectins and autophagy, aiming to draw attention to the existence of multiple associations between galectins and autophagy in a variety of physiological and pathological processes, which provide new ideas for etiological diagnosis, drug development, and therapeutic targets for related diseases.

RANKL up-regulated by progesterone aggravates lipopolysaccharide-induced acute lung injury during pregnancy.

Acute lung injury (ALI) is a common acute respiratory disease with high morbidity and mortality rate in pregnant women. Receptor activator of NF-κB ligand (TNFSF11, also known as RANKL) exerts either pro-inflammatory or anti-inflammatory effects on the immune response. LPS administration reduced the survival time (n = 10, p < 0.01), increased wet/dry ratio (n = 10, p < 0.001) and lung injury score (n = 10, p < 0.001), the elevated proportions of plasmacytoid dendritic cells (pDCs) (n = 10, p < 0.0001), tissue-resident DCs (resDCs) (n = 10, p < 0.0001), macrophages (n = 10, p < 0.0001), and neutrophils (n = 10, p < 0.0001), and the expressions of costimulatory molecules and inflammation cytokines (n = 10, p < 0.05) in lungs of pregnant mice, compared with non-pregnant mice. In vitro, progesterone up-regulated the expression of RANKL (n > 6, p < 0.05) on pulmonary fibroblasts. The results of cytokine arrays showed that the cytokines associated with inflammatory response and leukocyte differentiation were decreased in pulmonary fibroblasts after treatment with anti-RANKL neutralizing antibody, compared with control pulmonary fibroblasts. More notably, we found that Tnfsf11-/- pregnant mice had longer survival durations (n = 10, p < 0.01), lower lung injury scores (n = 10, p < 0.05), and lower immune cell infiltration (n = 10, p < 0.05). These data imply that the RANKL/RANK axis plays an essential role in LPS-induced ALI during pregnancy possibly through a variety of pathways.

CXCL8 enhances proliferation and growth and reduces apoptosis in endometrial stromal cells in an autocrine manner via a CXCR1-triggered PTEN/AKT signal pathway.

BACKGROUND: Chemokine CXCL8 (also known as IL-8) has been identified as a potential regulator of endometrial stromal cells (ESCs), but it is unclear how CXCL8 regulates the survival of ESCs in the pathogenesis of endometriosis. METHODS: We assessed the secretion of CXCL8 by enzyme-linked immunosorbent assays and the expression of its receptors, CXCR1 and CXCR2, by in-cell Western assay and immunohistochemistry. The effects of CXCL8 on the activation or expression of various cell mediators were also investigated by in-cell Western assay. The effects of CXCL8 on the proliferation, growth and apoptosis of ESCs in vitro were assessed by BrdU assays, cell counts and annexin V labeling, respectively. RESULTS: Secretion of CXCL8 and expression of CXCR1 in the eutopic ESCs from women with endometriosis were significantly higher than that in control ESCs, but the expression of CXCR2 showed no significant difference between these two cell types. CXCL8 stimulated proliferation and growth and reduced apoptosis of ESCs in an autocrine manner, and these effects were abolished by anti-human CXCL8 and CXCR1 neutralizing antibodies and by a PI3K/Akt inhibitor. Moreover, CXCL8 up-regulated the expression of the anti-apoptotic proteins, survivin and Bcl-2, inhibited the expression of the Phosphatase and tensin homolog (PTEN) and activated the phosphorylation of Akt. CONCLUSIONS: This study suggests that CXCL8 and CXCR1 are involved in the pathogenesis of endometriosis by up-regulating proliferation and growth and restricting apoptosis in ESCs by activating the PTEN/Akt pathway and mediating the expression of survivin and Bcl-2.

Ginsenoside Compound K Protects against Obesity through Pharmacological Targeting of Glucocorticoid Receptor to Activate Lipophagy and Lipid Metabolism.

(1) Background: The glucocorticoid receptor (GR) plays a key role in lipid metabolism, but investigations of GR activation as a potential therapeutic approach have been hampered by a lack of selective agonists. Ginsenoside compound K (CK) is natural small molecule with a steroid-like structure that offers a variety of therapeutic benefits. Our study validates CK as a novel GR agonist for the treatment of obesity. (2) Methods: By using pulldown and RNA interference, we determined that CK binds to GR. The anti-obesity potential effects of CK were investigated in obese mice, including through whole-body energy homeostasis, glucose and insulin tolerance, and biochemical and proteomic analysis. Using chromatin immunoprecipitation, we identified GR binding sites upstream of lipase ATGL. (3) Results: We demonstrated that CK reduced the weight and blood lipids of mice more significantly than the drug Orlistat. Proteomics data showed that CK up-regulated autophagy regulatory proteins, enhanced fatty acid oxidation proteins, and decreased fatty acid synthesis proteins. CK induced lipophagy with the initial formation of the phagophore via AMPK/ULK1 activation. However, a blockade of autophagy did not disturb the increase in CK on lipase expression, suggesting that autophagy and lipase are independent pathways in the function of CK. The pulldown and siRNA experiments showed that GR is the critical target. After binding to GR, CK not only activated lipophagy, but also promoted the binding of GR to the ATGL promoter. (4) Conclusions: Our findings indicate that CK is a natural food candidate for reducing fat content and weight.

Carboxylate-Containing Wide-Bandgap Polymers for High-Voltage Non-Fullerene Organic Solar Cells.

As one of the polymer modification strategies, carboxylate functionalization has proved effective in downshifting the energy levels and enhancing polymer crystallinity and aggregation. However, high-performance carboxylate-containing polymers are still limited for organic solar cells (OSCs), especially with open-circuit voltage (VOC) above 1.0 V. Herein, we utilize two carboxylate-functionalized wide-band gap (WBG) donor polymers (TTC-F and TTC-Cl) to pair with two WBG electron acceptors (BTA5 and F-BTA5) for high-voltage OSCs. Due to the deeper molecular energy levels, chlorinated polymer TTC-Cl shows higher VOC than fluorinated polymer TTC-F. Furthermore, because of the stronger aggregation in the film, the TTC-Cl-based devices attain suppressed energetic disorders and trap-assisted recombination, decreasing voltage loss and JSC loss. Finally, the TTC-Cl: F-BTA5 blend achieves a higher VOC of 1.17 V and an excellent PCE of 10.98%, one of the best results for high-voltage carboxylate-containing polymers. In addition, the TTC-Cl: BTA5 combination demonstrates the highest VOC of 1.25 V with an ultralow nonradiative energy loss of 0.17 eV. Our results indicate that the carboxylate-containing polymer donors have significant application potential for high-voltage OSCs due to reduced energy loss and improved charge transport and dissociation. Furthermore, the matched absorption spectra with the indoor light sources and low voltage loss promote these material combinations to construct high-performance indoor photovoltaics.

Decidual macrophages in recurrent spontaneous abortion.

Recurrent spontaneous abortion (RSA) is defined as two or more pregnancy loss, affecting the happiness index of fertility couples. The mechanisms involved in the occurrence of RSA are not clear to date. The primary problem for the maternal immune system is how to establish and maintain the immune tolerance to the semi-allogeneic fetuses. During the pregnancy, decidual macrophages mainly play an important role in the immunologic dialogue. The purpose of this study is to explore decidual macrophages, and to understand whether there is a connection between these cells and RSA by analyzing their phenotypes and functions. Pubmed, Web of Science and Embase were searched. The eligibility criterion for this review was evaluating the literature about the pregnancy and macrophages. Any disagreement between the authors was resolved upon discussion and if required by the judgment of the corresponding author. We summarized the latest views on the phenotype, function and dysfunction of decidual macrophages to illuminate its relationship with RSA.

Uterine natural killer cells and recurrent spontaneous abortion.

Recurrent spontaneous abortion (RSA), termed as two or more consecutive pregnancy loss is a great problem for some women of childbearing age. A large number of evidence confirm that there may be an immune background of RSA. As a member of the innate immune system, uterine natural killer (uNK) cells account for about 70% of total lymphocytes during pregnancy and play a critical role in the establishment and maintenance of pregnancy. This review mainly introduces the phenotype, origin, receptor, and function of uNK cells to illuminate its relationship with RSA.