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Fluorescence/luminescence bioimaging, utilizing rare‐earth doped nanocrystals (RENCs) within the NIR‐IIb (1500–1700 nm) sub‐window, has drawn interest for its deep penetration depth and superior resolution. Herein, Er3+/Yb3+ couple is rationally designed in topologically arranged RENCs that facilitate a boosted 1530 nm emission of Er3+ via premeditated Yb3+‐mediated energy transfer processes under 808 nm excitation. To maximize this modulation effect for boosting 1530 nm emission, a regional active ions concentration and spatial regulation strategy is explored in the optimized concentration and core–shell–shell structure (NaErF4:20%Yb@NaYbF4:20%Er@NaYF4 with a quantum yield of 16.46% in NIR‐IIb region). Leveraging the superior emission and multi‐wavelength excitation characteristics of the as‐obtained nanocrystals, a NIR‐IIb‐based ratiometric fluorescence imaging measurement is achieved under 808 and 980 nm excitation, which cannot only show the 2D distribution of probes but also provide spatial depth information (range from 0 to 2.8 mm with a tissue depth resolution of 66 µm). The findings hold significant potential for advancing both vascular science and clinical medicine. [ABSTRACT FROM AUTHOR]

Urological malignancy (UM) is among the leading threats to health care worldwide. Recent years have seen much investment in fundamental UM research, including mechanistic investigation, early diagnosis, immunotherapy, and nanomedicine. However, the results are not fully satisfactory. Bioprinted research models (BRMs) with programmed spatial structures and functions can serve as powerful research tools and are likely to disrupt traditional UM research paradigms. Herein, a comprehensive review of BRMs of UM is presented. It begins with a brief introduction and comparison of existing UM research models, emphasizing the advantages of BRMs, such as modeling real tissues and organs. Six kinds of mainstream bioprinting techniques used to fabricate such BRMs are summarized with examples. Thereafter, research advances in the applications of UM BRMs, such as culturing tumor spheroids and organoids, modeling cancer metastasis, mimicking the tumor microenvironment, constructing organ chips for drug screening, and isolating circulating tumor cells, are comprehensively discussed. At the end of this review, current challenges and future development directions of BRMs and UM are highlighted from the perspective of interdisciplinary science. [ABSTRACT FROM AUTHOR]

As an alternative to hydrogen peroxide (H2O2) production by complex anthraquinone oxidation process, photosynthesis of H2O2 from water and oxygen without sacrificial agents is highly demanded. Herein, a covalently connected molecular heterostructure is synthesized via sequential C−H arylation and Knoevenagel polymerization reactions for visible‐light and sacrificial‐agent‐free H2O2 synthesis. The subsequent copolymerization of the electron‐deficient benzodithiophene‐4,8‐dione (BTD) and the electron‐rich biphenyl (B) and p‐phenylenediacetonitrile (CN) not only expands the π‐conjugated domain but also increases the molecular dipole moment, which largely promotes the separation and transfer of the photoinduced charge carriers. The optimal heterostructured BTDB‐CN0.2 manifested an impressive photocatalytic H2O2 production rate of 1920 μmol g−1 h−1, which is 2.2 and 11.6 times that of BTDB and BTDCN. As revealed by the femtosecond transient absorption (fs‐TA) and theoretical calculations, the linkage serves as a channel for the rapid transfer of photogenerated charge carriers, enhancing the photocatalytic efficiency. Further, in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) uncovers that the oxygen reduction reaction occurs through the step one‐electron pathway and the mutual conversion between C=O and C−OH with the anchoring of H+ during the catalysis favored the formation of H2O2. This work provides a novel perspective for the design of efficient organic photocatalysts. [ABSTRACT FROM AUTHOR]

Background: There are very few cosmetic ingredients that can target oil control and extend the wear time. Fullerenes have been reported to have excellent antioxidant capacity and a variety of biological activities, such as quenching free radicals, inhibiting lipid peroxidation, and promoting lipid flocculation. Objective: The purpose of applying foundation makeup on the face is to make the skin color even, but the secretion and oxidation of skin oil will make the makeup mottled and dull. In order to solve this problem, a fullerene composite material that can directionally absorb oil and resist oil oxidation has been developed. Methods: Fullerenes and hydroxyapatite composite was prepared by high pressure homogenization under alkaline condition. The indicated morphology and structure were characterized by SEM, UV–Vis, Raman, and XRD. The oil absorption capacity was determined by adding the C60‐hydroxyapatite composite to a mixed solution of hexane and oil, shaking for 1 h, filtering, analyzed by GC–MS, and calculating the oil absorption by external standard method. Artificial sebum was prepared by adding different mass of water and oleic acid to screen the optimum ratio. C60‐hydroxyapatite mixture and C60‐hydroxyapatite composite were added to the artificial sebum to test the oil‐absorbing capacity of the materials. The hydroxyl radical scavenging ability of C60‐hydroxyapatite composite containing different fullerene contents was measured by X‐band ESR spectroscopy, and the long‐term radical scavenging ability of the composites was tested in comparison with VC. Antioxidant experiment is adding C60‐hydroxyapatite composite material, and hydroxyapatite to oleic acid, then the UV light irradiation is aimed to accelerate the oxidation of oleic acid. Oleic acid act as a control group, and make the detection of oleic acid peroxide value after 7 days. The safety of the materials was tested by using culture media to soak the C60‐hydroxyapatite composite for 24 h and then used to culture cells. Results: The characterization of SEM, UV–Vis, Raman, and XRD showed that fullerene clusters were dispersed on the surface of hydroxyapatite stably, and they formed a stable composite. The adsorption rates of C60‐hydroxyapatite composites for oleic acid, phenyl trimethicone, caprylic capric glyceride, isooctyl palmitate, mineral oil, olive oil, and dimethicone were 60.5%, 9.3%, 9.15%, 5.24%, 2.94%, 1.01%, and 0%, respectively. The flocculation amount of artificial sebum was 5.9 g per gram of C60‐hydroxyapatite mixture and 24.2 g per gram of C60‐hydroxyapatite composite. C60‐hydroxyapatite composites have excellent quenching ability for hydroxyl radicals. When the fullerene content is 1, 2, 3, and 4 mg/kg, the quenching rates are 25.02%, 39.57%, 49.75%, and 62.24%, respectively. The quenching effect was enhanced with the increase of fullerene content, and it had strong long‐term antioxidant properties. It can also be proved that C60‐hydroxyapatite composites have strong antioxidant capacity through antioxidant experiments. The peroxide value of oleic acid on Day 0 was 2.8, and after 7 days of UV irradiation, the peroxide values of blank control, hydroxyapatite group, C60‐hydroxyapatite composite containing 0.5% and 1% fullerenes four groups of materials were 8.02 meq O2/kg, 7.98 meq O2/kg, 7.11 meq O2/kg, and 6.87 meq O2/kg, respectively. The cell activity was 20.94% and 99.2% after the cells were cultured for 24 h using C60‐hydroxyapatite composite and hydroxyapatite extracts, respectively, and the addition of fullerene was able to significantly increase the cell activity. Conclusion: Fullerene hydroxyapatite complex has excellent directional oil absorption characteristics, which can effectively remove free radicals and reduce skin oil oxidation. [ABSTRACT FROM AUTHOR]

The synthesis of polycyclic compounds is of high interest due to the prevalence of these motifs in drugs and natural products. Herein, we report on the stereoselective construction of 3D bicyclic scaffolds and azetidine derivatives by modulation of N‐sulfonylimines to achieve either [4+2]‐ or [2+2]‐cycloaddition reactions. The utility of the method was established by further modulation of the product. Mechanistic studies are also included, which support reaction via Dexter energy transfer. [ABSTRACT FROM AUTHOR]

Inorganic arsenic (iAs) has been a human health concern and is associated with intestinal malignancies. However, the molecular mechanisms of the iAs‐induced oncogenic process in intestine epithelial cells remain elusive, partly because of the known hormesis effect of arsenic. Here, we established that six‐month exposure to iAs at a concentration similar to those found in contaminated drinking water could promote malignant characteristics, including enhanced proliferation and migration, resistance to apoptosis, and mesenchymal‐like transition in Caco‐2 cells. Transcriptome analysis and mechanism study revealed that key genes and pathways involved in cell adhesion, inflammation and oncogenic regulation were altered during chronic iAs exposure. Specifically, we uncovered that down‐regulation of HTRA1 was essential for the iAs‐induced acquisition of the cancer hallmarks. Further, we evidenced that the loss of HTRA1 during iAs‐exposure could be restored by HDAC6 inhibition. Caco‐2 cells with chronic exposure to iAs exhibited enhanced sensitivity to WT‐161, a specific inhibitor of HDAC6, when used alone than in combination with a chemotherapeutic agent. These findings provide valuable information for understanding the mechanisms of arsenic‐induced carcinogenesis and facilitating the health management of populations in arsenic‐polluted areas. This study explored the molecular mechanism associated with long‐term inorganic arsenic exposure in the colon epithelial Caco‐2 cell model. Our findings revealed that the down‐regulation of HTRA1 was essential for the malignant progression induced by chronic arsenic exposure, which could be restored by HDAC6 inhibition. These findings provide valuable information for understanding the key regulators of arsenic‐induced carcinogenesis. [ABSTRACT FROM AUTHOR]

Islet autoantibodies, including autoantibodies directed against the 65kDa isoform of glutamate decarboxylase (GAD65Ab), are present in the majority of patients with newly diagnosed type 1 diabetes (T1D). Whereas these autoantibodies are historically viewed as an epiphenomenon of the autoimmune response with no significant pathogenic function, we consider in this study the possibility that they impact the major islet function, namely glucose‐stimulated insulin secretion. Two human monoclonal GAD65Ab (GAD65 mAb) (b78 and b96.11) were investigated for uptake by live rat beta cells, subcellular localization and their effect on glucose‐stimulated insulin secretion. The GAD65 mAbs were internalized by live pancreatic beta cells, where they localized to subcellular structures in an epitope‐specific manner. Importantly, GAD65 mAb b78 inhibited, while GAD65 mAb b96.11 enhanced, glucose‐stimulated insulin secretion (GSIS). These opposite effects on GSIS rule out non‐specific effects of the antibodies and suggest that internalization of the antibody leads to epitope‐specific interaction with intracellular machinery regulating insulin granule release. The most likely explanation for the alteration of GSIS by GAD65 Abs is via changes in GABA release due to inhibition or change in GAD65 enzyme activity. This is the first report indicating an active role of GAD65Ab in the pathogenesis of T1D. [ABSTRACT FROM AUTHOR]

Background: Chenxiang Huaqi tablets (CXHQTs) are a traditional Chinese medicine (TCM) commonly used to treat stomach‐related diseases. Currently, the ministerial standards do not provide detailed guidance and regulations on the content determination of CXHQTs, and the reported studies only use individual active components as indicators for determining effective ingredients. Objective: The present study aimed to propose a methodology for quality control of CXHQTs based on high‐performance liquid chromatography (HPLC) fingerprinting combined with the quantitative analysis of multi‐components by single marker (QAMS) method. Methods: HPLC method was used to determine seven active ingredients and performed fingerprint analysis of CXHQTs. To further process chemometric assessment, technical analysis‐model including similarity analysis (SA), hierarchical clustering analysis (HCA), principal components analysis (PCA) and orthogonal partial least squares discrimination analysis (OPLS‐DA) was set up to differentiate and classify the 20 batches of samples. Results: After comparing the results of QAMS method with the external standard method (ESM), we found there is no significant difference. Besides, the fingerprint of CXHQT was also established. Conclusion: HPLC fingerprint combined with the QAMS could be an efficient and selective analysis technique to achieve a qualitative and quantitative evaluation of executing quality processes. Chenxiang Huaqi tablets (CXHQTs) are a traditional Chinese medicine commonly used to treat stomach‐related diseases. The present study aimed to propose a methodology for batch‐to‐batch quality control of CXHQTs based on high‐performance liquid chromatography (HPLC) fingerprinting combined with the quantitative analysis of multi‐components by single marker (QAMS) method. [ABSTRACT FROM AUTHOR]

A variety of pseudorutaecarpine derivatives were prepared in good to excellent yields through a gold(I)‐catalyzed selective cyclization and 1,2‐shift of N‐alkynyl quinazolinone‐tethered indoles. Mechanistic study revealed that spiroindolenines generated in situ by cyclization at the the indole C3 position underwent an alkenyl 1,2‐shift to generate pseudorutaecarpine. The reaction proceeds under mild reaction conditions, has a broad substrate scope, good functional group tolerance, and gram‐scalable application. Furthermore, biological evaluation showed that most of the pseudorutaecarpine scaffolds prepared exhibit anti‐inflammatory activity. [ABSTRACT FROM AUTHOR]

The resulting interfacial stress in heteroepitaxial nanocomplex usually has negligible influence on its performance, but at high pressures (HP) the effect can be significantly amplified. In order to unravel the underlying mechanism and search for high quality pressure sensors, a simple object is employed, NaErF4@NaLnF4 (Ln = Y, Lu, Gd) and its Tm3+‐doped derivatives, to comparatively study the effect of interfacial stress on upconversion (UC) luminescence. Specifically, the doping enhances greatly mechanosensitivity because of the anisotropic local geometry of the dopant ions of which the structural distortion is amplified by HP. The generated compressive strain does extend into the core as witnessed by the effect of tensile strain in the shell on the core and the fact that Lu‐shelled nanoparticles are the most sensitive to external force among Tm3+‐doped system. This compressive strain in concert with the external HP intensifies the coupling between Er3+ and Tm3+, making the attenuation of green UC emission more pronounced. The red to green UC emission ratio of this material, robust both in structural and optical properties, increases linearly with pressure in the range from ambient to 9 GPa. The study opens a new horizon for understanding the effect of interfacial stress on UC luminescence. [ABSTRACT FROM AUTHOR]

Osteoporosis is a systemic bone metabolism disorder, which increases the risk of fractures, and in severe cases it may cause disability or even death. An important factor contributing to osteoporosis is the imbalance between bone formation and resorption. Naringin was reported to promote osteoblast differentiation, thus enhancing bone formation and alleviating osteoporosis development. However, the signalling pathways related to the regulatory mechanism of naringin in osteoporosis development are not clear. Proliferation of bone mesenchymal stem cells (BMSCs) treated with naringin in vitro was detected by CCK‐8. An osteogenesis differentiation medium supplemented with naringin was applied to explore the effects of naringin on BMSC osteogenic differentiation, as detected by Alizarin red staining. Ovariectomy (OVX)‐induced postmenopausal osteoporosis (PMOP) rats were orally administered with naringin. Dual‐energy X‐ray absorptiometry (DEXA) and micro‐CT were applied to measure bone mineral density (BMD), bone volume/total volume (BV/TV), trabecula thickness (Tb.Th), trabecula number (Tb.N), trabecular separation (Tb.Sp) and bone surface/bone volume (BS/BV). H&E staining was performed to show pathological changes of the femur in PMOP rats after naringin treatment. Bone metabolism indicators were assessed by ELISA. We found that naringin suppressed the activation of the JAK2/STAT3 pathway. Naringin promoted BMSC proliferation and osteogenic differentiation. Furthermore, naringin alleviates bone loss and improves abnormal bone metabolism of PMOP rats. Collectively, naringin promotes BMSC osteogenic differentiation to ameliorate osteoporosis development by targeting JAK2/STAT3 signalling. [ABSTRACT FROM AUTHOR]

Gallic acid (GA) is a natural ingredient in functional foods, which has various health‐promoting and antitumour effects. Peptidyl‐prolyl cis/trans isomerase Pin1 plays an important role in preventing the development of some malignant tumours. However, whether there was an interaction between Pin1 and GA remains unknown. In this work, the binding information of GA and Pin1 was investigated systematically using multiple spectral and computational methods. GA bound to Pin1 directly with moderate binding affinity in the order of 104 mol/L, therefore decreasing the activity of Pin1. Also, the binding process of GA to Pin1 was driven through weak van der Waals forces, hydrogen bonds, and electrostatic forces. In addition, the important residues Lys63, Arg68, and Arg69 played a significant role in maintaining the binding stability between Pin1 and GA. Interestingly, GA reduced the activity of Pin1 by affecting its conformational characteristics. Our present work showed that GA binds to Pin1 and inhibits its activity, affecting its structural and functional properties, which may contribute to the therapy of Pin1‐related diseases. [ABSTRACT FROM AUTHOR]

Reactions of polycarboxylate ligand (2,2′‐H2bpdc or H3OABDC), N‐donor auxiliary ligand (4‐bpmh) with Cd(II) salts under solvothermal conditions resulted in two coordination polymers formulated as [Cd(2,2′‐bpdc)(4‐bpmh)(H2O)]n·n(H2O) (1) and [Cd3(OABDC)2(4‐bpmh)2(H2O)4]n·2n(H2O) (2) (2,2′‐H2bpdc = diphenic acid, H3OABDC = 5‐oxyacetate isophthalic acid, and 4‐bpmh is N,N‐bis‐pyridin‐4‐ylmethylene‐hydrazine). Meanwhile, the investigations of luminescent performances and thermal stabilities suggest that the two compounds are candidate materials for the fluorescent emitting material. The assessment of their application values on the infantile bronchial pneumonia was carried out and their specific mechanism was investigated in the meantime. [ABSTRACT FROM AUTHOR]

Amnion‐derived prostaglandin E2 (PGE2) and cortisol are key to labor onset. Identification of a common transcription factor driving the expression of both cyclooxygenase‐2 (COX‐2) and 11β‐hydroxysteroid dehydrogenase 1 (11β‐HSD1), the key enzymes in their production, may hold the key to the treatment of pre‐term labor. Here, we have found that the CCAAT enhancer binding protein δ (C/EBPδ) is such a transcription factor which underlies the feed‐forward induction of COX‐2 and 11β‐HSD1 expression by their own products PGE2 and cortisol in human amnion fibroblasts so that their production would be ensured in the amnion for the onset of labor. Moreover, the abundance of C/EBPδ in the amnion increases along with COX‐2 and 11β‐HSD1 at term and further increases at parturition. Knockout of C/EBPδ in mice delays the onset of labor further supporting the concept. In conclusion, C/EBPδ pathway may be speculated to serve as a potential pharmaceutical target in the amnion for treatment of pre‐term labor. [ABSTRACT FROM AUTHOR]

The nickel‐catalyzed arylboration of conjugated dienes is reported. Good 1,4‐regioselectivity and (E)‐stereoselectivity were obtained using isoprene, together with very good 1,2‐regioselectivity and (E)‐stereoselectivity using 1‐arylbutadienes. The high reactivity and selectivity of this process were dependent on the use of the appropriate nitrogen‐based ligand. Moreover, wide functional group tolerance was observed under mild reaction conditions. This protocol provides a path to allyl or homoallyl boronic ester derivatives starting from 1,3‐dienes, aryl bromides, and B2pin2. The downstream transformation of allyl boronic esters was also achieved, suggesting a strategy for the diastereoselective 1,2‐difunctionalization of isoprene and demonstrating the potential for the synthesis of complex molecules. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation is a key feature of many neurodegenerative diseases, however its regulation is not well understood. MicroRNAs (miRNAs) are small, non‐coding RNAs that involve in the regulation of many biological and pathological pathways including inflammation. MiR‐223‐3p is macrophage/microglia enriched miRNA that involves in inflammation and immunity. However, the role of miR‐223‐3p in neurodegeneration is unknown. Method: MiR‐223‐3p knockout (KO) and genetic background matched wildtype (WT), female and male young (12‐14‐week) or aged (18‐20‐month) mice were used in the studies. CD11b+ cells were isolated from brain tissues of KO and WT, female and male naïve mice and RT‐qPCR was used to quantify inflammatory markers. Immunofluorescent studies using anti‐IBA1 was used to determine the number of activated microglia in brain sections of aged KO and WT female mice following a CCI. To evaluate the impact of miR‐223‐3p on cognitive and behavior, young (12‐14‐week) or old (18‐20‐month) mice were subjected to CCI followed by a radio arm water maze (RAWM) test (young mice) or Y‐maze test (aged mice) 2 weeks after controlled cortical impact (CCI). Result: Our preliminary studies reveal that deficiency of miR‐223‐3p resulted in a female‐biased elevation of inflammatory transcripts including such as NLRP3, TRAF6, TNFα, NFκB, and ITGAM in brain CD11b+ cells. In addition, immunofluorescent analysis demonstrated that a greater number of IBA1 staining microglia in KO than that of WT mice brains. Furthermore, deficiency of miR‐223‐3p seemed to associate with a deficit in cognitive function in aged female mice following CCI. We also examined the level of CCAAT‐enhancer‐binding protein beta (CEBPβ), an important transcription factor regulating inflammation and a validated target of miR‐223‐3p. Our preliminary data showed that CEBPβ protein was increased in the brain of miR‐223‐3p KO mice brain tissue relative to that of WT. Conclusion: Our preliminary data suggest that miR‐223‐3p may regulate a sexually dimorphic neuroinflammation and cognitive function, likely via regulating inflammation transcription factor CEBPβ. [ABSTRACT FROM AUTHOR]

Neointimal hyperplasia remains an obstacle after vascular interventions. Programmed death‐1 (PD‐1) antibody treatment decreases tumor cell proliferation and secretion of inflammatory factors, and several antineoplastic drugs show efficacy against neointimal hyperplasia. We hypothesized that inhibition of PD‐1 inhibits neointimal hyperplasia in a rat patch angioplasty model. In a rat aorta patch angioplasty model, four groups were compared: the control group without treatment, a single dose of humanized PD‐1 antibody (4 mg/kg) injected immediately after patch angioplasty, PD‐1 antibody‐coated patches, and BMS‐1 (PD‐1 inhibitor)‐coated patches. Patches were harvested (Day 14) and analyzed. After patch angioplasty, PD‐1‐positive cells were present. Inhibition of PD‐1 using both intraperitoneal injection of humanized PD1 antibody as well as using patches coated with humanized PD1 antibody significantly decreased neointimal thickness (p = 0.0199). There were significantly fewer PD‐1 (p = 0.0148), CD3 (p = 0.0072), CD68 (p = 0.0001), CD45 (p = 0.001), and PCNA (p < 0.0001)‐positive cells, and PCNA/α‐actin dual positive cells (p = 0.0005), in the treated groups. Patches coated with BMS‐1 showed similarly decreased neointimal thickness and accumulation of inflammatory cells. Inhibition of PD‐1 using PD‐1 antibody or its inhibitor BMS‐1 can significantly decrease neointimal thickness in vascular patches. Inhibition of the PD‐1 pathway may be a promising therapeutic strategy to inhibit neointimal hyperplasia. [ABSTRACT FROM AUTHOR]

To overcome the low external quantum efficiency of ultraviolet light‐emitting diodes (UV LEDs) in the technologically significant wavelength range of 300–350 nm, a change of approach to device design may be required. Herein, room‐temperature electroluminescence (EL) at 335 nm is achieved from simple aluminum gallium nitride (AlGaN)‐based metal–insulator–semiconductor (MIS) light‐emitting diodes (LEDs), which do not contain any p‐doped material. Current–voltage and capacitance–voltage measurements indicate that electrons in the valence band of the n‐Al0.14Ga0.86 N layer efficiently tunnel via localized states in the thin, sputter‐deposited aluminum nitride (AlN) barrier of the MIS device to provide the source of holes needed for near‐band‐edge luminescence. The full width at half maximum (FWHM) in the UV emission peak is only around 18 nm and it is very close to the photoluminescence (PL) peak of the active n‐Al0.14Ga0.86N layer, confirming that the EL is derived from band‐to‐band radiative transitions in the simple non‐p‐doped MIS diode. This design is a potential option to overcome the problem of the poor thermal excitation of holes in the AlGaN‐based pn junction devices. [ABSTRACT FROM AUTHOR]

The oceans are natural sources of atmospheric methane (CH4), but the origin of excess CH4 at the surface remains enigmatic. Incubation experiments were conducted in the western North Pacific (WNP) and its marginal seas (i.e., Yellow Sea and South China Sea [SCS]) to identify the degradation of methylphosphonate (MPn) to CH4 in the oceans and the microbes associated with MPn‐driven CH4 production. In the coastal seawater of the Yellow Sea, CH4 was observed to accumulate after MPn enrichment with a high MPn to CH4 conversion efficiency (approximately 60%). Dissolved inorganic phosphorus (Pi) did not effectively restrict the microbial utilization of MPn in the eutrophic coastal waters. The results of 16S rRNA gene sequencing showed that Vibrio spp. were the dominant bacteria in the MPn‐amended treatments. Moreover, several Vibrio isolates isolated from the coastal waters were found to produce CH4 while growing in culture using MPn as the sole P source, thereby indicating that Vibrio spp. might be the major contributors to MPn‐dependent CH4 production. In oligotrophic areas, such as the SCS and WNP, CH4 production from MPn metabolism was also observed in the surface seawater. In contrast to coastal waters, this pathway in oligotrophic areas is regulated by dissolved Pi availability. This work confirms that aerobic CH4 formation from MPn degradation can occur both in eutrophic coastal waters and oligotrophic oceans driven by MPn‐utilizing microorganisms (especially heterotrophic bacteria), which may have a significant impact on our understanding of the CH4 and P cycles in global oceans. [ABSTRACT FROM AUTHOR]

Although the science of implantable materials has advanced therapeutic options in vascular surgery, graft failure is still a problem in need of a durable solution. With the development of coating and decellularization techniques, coated prosthetic grafts have become an option; however, whether decellularized human saphenous vein can be conjugated and implanted is not known. Human great saphenous vein (GSV) was harvested and decellularized and hyaluronic acid (HA)–heparin was conjugated to the GSV; water contact angles (WCA), morphology, and sulfur element change were measured before and after heparin bonding. GSV patches were implanted into the rat inferior vena cava and aorta; patches were harvested (Day 14) and analyzed. HA–heparin was successfully conjugated to the decellularized human GSV with altered morphology and reduced WCA. The HA–heparin coated decellularized GSV patch was anti‐thrombotic in vitro, and significantly decreased neointimal thickness both in patch venoplasty and angioplasty in a rat model. Both CD90 and nestin positive cells participated in neointima formation. These data show that HA–heparin coated human GSV patches decrease neointimal thickness when used both in venoplasty and arterioplasty. Tissue engineered decellularized human GSV is a promising vascular prosthesis. [ABSTRACT FROM AUTHOR]

Current dogma holds that the heart balances energy demand and supply effectively and sustainably by sequestering enough Ca2+ into mitochondria during heartbeats to stimulate metabolic enzymes in the tricarboxylic acid (TCA) cycle and electron transport chain (ETC). This process is called excitation‐contraction‐bioenergetics (ECB) coupling. Recent breakthroughs in identifying the mitochondrial Ca2+ uniporter (MCU) and its associated proteins have opened up new windows for interrogating the molecular mechanisms of mitochondrial Ca2+ homeostasis regulation and its role in ECB coupling. Despite remarkable progress made in the past 7 years, it has been surprising, almost disappointing, that germline MCU deficiency in mice with certain genetic background yields viable pups, and knockout of the MCU in adult heart does not cause lethality. Moreover, MCU deficiency results in few adverse phenotypes, normal performance, and preserved bioenergetics in the heart at baseline. In this review, we briefly assess the existing literature on mitochondrial Ca2+ homeostasis regulation and then we consider possible explanations for why MCU‐deficient mice are spared from energy crises under physiological conditions. We propose that MCU and/or mitochondrial Ca2+ may have limited ability to set ECB coupling, that other mitochondrial Ca2+ handling mechanisms may play a role, and that extra‐mitochondrial Ca2+ may regulate ECB coupling. Since the heart needs to regenerate a significant amount of ATP to assure the perpetuation of heartbeats, multiple mechanisms are likely to work in concert to match energy supply with demand. [ABSTRACT FROM AUTHOR]

An unprecedented nickel‐catalyzed 1,1‐alkylboration of electronically unbiased alkenes has been developed, providing straightforward access to secondary aliphatic boronic esters from readily available materials under very mild reaction conditions. The regioselectivity of this reaction is governed by a unique pyridyl carboxamide ligated catalyst, rather than the substrates. Moreover, this transformation shows excellent chemo‐ and regio‐selectivity and remarkably good functional‐group tolerance. We also demonstrate that under balloon pressure, ethylene can also be utilized as a substrate. Additionally, competence experiments indicate that selective bond formation is favored at the α‐position of boron and preliminary mechanistic studies indicate that the key step in this three‐component reaction involves a 1,2‐nickel migration. [ABSTRACT FROM AUTHOR]

As the progress of electrification for the public transportation sector is accelerated, it becomes more and more important to integrated planning charging infrastructure for public transportation, while emerging technologies such as distributed renewable generation and energy storage system should be accounted. Here, an integrated resource planning framework is proposed where both planning investment cost and operational cost are considered. An aggregation strategy is also proposed to optimise the charging decisions for electric bus on different routes, which could effectively improve the planning and operation efficiency. To address the uncertainties involved in this process, a scenario-based chance-constrained programming approach is adopted. A numerical case study is also included to demonstrate the effectiveness of this proposed resource planning model. [ABSTRACT FROM AUTHOR]

As the progress of electrification for the public transportation sector is accelerated, it becomes more and more important to integrated planning charging infrastructure for public transportation, while emerging technologies such as distributed renewable generation and energy storage system should be accounted. Here, an integrated resource planning framework is proposed where both planning investment cost and operational cost are considered. An aggregation strategy is also proposed to optimise the charging decisions for electric bus on different routes, which could effectively improve the planning and operation efficiency. To address the uncertainties involved in this process, a scenario‐based chance‐constrained programming approach is adopted. A numerical case study is also included to demonstrate the effectiveness of this proposed resource planning model. [ABSTRACT FROM AUTHOR]

An unprecedented arylboration of unactivated terminal alkenes, featuring 1,n‐regioselectivity, has been achieved by nickel catalysis. The nitrogen‐based ligand plays an essential role in the success of this three‐component reaction. This transformation displays good regioselectivity and excellent functional‐group tolerance. In addition, the incorporation of a boron group into the products provides substantial opportunities for further transformations. Also demonstrated is that the products can be readily transformed into pharmaceutically relevant molecules. Unexpectedly, preliminary mechanistic studies indicate that although the metal migration favors the α‐position of boron, selective and decisive bond formation is favored at the benzylic position. An unprecedented arylboration of unactivated terminal alkenes, featuring 1,n‐regioselectivity (n>2), has been achieved by nickel catalysis. An array of valuable alkylboronic esters are prepared with this method. Mechanism studies indicate that a nickel migration and a selective bond‐formation step are involved in this reaction. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction is an early feature of Alzheimer's disease (AD). Accumulated damaged mitochondria, which are associated with impaired mitophagy, contribute to neurodegeneration in AD. We show levels of Disrupted‐in‐schizophrenia‐1 (DISC1), which is genetically associated with psychiatric disorders and AD, decrease in the brains of AD patients and transgenic model mice and in Aβ‐treated cultured cells. Disrupted‐in‐schizophrenia‐1 contains a canonical LC3‐interacting region (LIR) motif (210FSFI213), through which DISC1 directly binds to LC3‐I/II. Overexpression of DISC1 enhances mitophagy through its binding to LC3, whereas knocking‐down of DISC1 blocks Aβ‐induced mitophagy. We further observe overexpression of DISC1, but not its mutant (muFSFI) which abolishes the interaction of DISC1 with LC3, rescues Aβ‐induced mitochondrial dysfunction, loss of spines, suppressed long‐term potentiation (LTP). Overexpression of DISC1 via adeno‐associated virus (serotype 8, AAV8) in the hippocampus of 8‐month‐old APP/PS1 transgenic mice for 4 months rescues cognitive deficits, synaptic loss, and Aβ plaque accumulation, in a way dependent on the interaction of DISC1 with LC3. These results indicate that DISC1 is a novel mitophagy receptor, which protects synaptic plasticity from Aβ accumulation‐induced toxicity through promoting mitophagy. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are highly prevalent aging‐related diseases associated with significant morbidity and mortality. Some findings in human and animal models have linked T2DM to AD‐type dementia. Despite epidemiological associations between the T2DM and cognitive impairment, the interrelational mechanisms are unclear. The preponderance of evidence in longitudinal studies with autopsy confirmation have indicated that vascular mechanisms, rather than classic AD‐type pathologies, underlie the cognitive decline often seen in self‐reported T2DM. T2DM is associated with cardiovascular and cerebrovascular disease (CVD), and is associated with increased risk of infarcts and small vessel disease in the brain and other organs. Neuropathological examinations of post‐mortem brains demonstrated evidence of cerebrovascular disease and little to no correlation between T2DM and β‐amyloid deposits or neurofibrillary tangles. Nevertheless, the mechanisms upstream of early AD‐specific pathology remain obscure. In this regard, there may indeed be overlap between the pathologic mechanisms of T2DM/"metabolic syndrome," and AD. More specifically, cerebral insulin processing, glucose metabolism, mitochondrial function, and/or lipid metabolism could be altered in patients in early AD and directly influence symptomatology and/or neuropathology. [ABSTRACT FROM AUTHOR]

In this study, the biosorption of heavy metal ions such as Cd(II), Cu(II), Zn(II), and Pb(II), was investigated using a new bacterial species isolated from the soil of the industrial zone of Xuzhou city. Sequence analysis of the 16S rRNA gene showed that the bacteria were Pectobacterium sp., denoted as ND2. In order to optimize the conditions for the biosorption of heavy metal ions, the effects of various physico‐chemical parameters were assessed, including pH value, contact time, initial metal ion concentration, biosorbent dose, and temperature. Under the optimal condition, the maximum ion biosorption capacity (mg/g) of Pectobacterium sp. ND2 was ranked in the order of Cd(II)(44.9 mg/g) > Cu(II)(38.6 mg/g) > Zn(II)(34.2 mg/g) > Pb(II)(31.2 mg/g). Both Langmuir and Freundlich isotherm models were used to explain this adsorption phenomenon. The FTIR analysis of surface chemical functional groups of Pectobacterium sp. ND2, revealed the involvement of carboxyl, amino and phosphate groups in the adsorption process. In addition, adsorption–desorption studies indicated that 0.1M nitric acid is an efficient desorbent for Cd(II), Cu(II), Zn(II), and Pb(II) ions, with maximum recovery rates of more than 90%. © 2017 American Institute of Chemical Engineers Environ Prog, 37: 968–974, 2018 [ABSTRACT FROM AUTHOR]

3‐Amino‐2‐benzenesulfonyl‐1‐alkyl/aryl‐1H‐pyrazolo[1,2‐b]phthalazine‐5,10‐dione derivatives were synthesized by the one‐pot, three‐component condensation of phthalhydrazide, aldehydes, and (phenylsulfonyl)acetonitrile in EtOH using 2‐hydroxyethylammonium acetate as catalyst. The advantages of this method include environmental friendliness, easy work‐up, and excellent yields. The reduction of some products and photophysical properties were also investigated. [ABSTRACT FROM AUTHOR]

ABSTRACT This article presents research results showing that the property of fused deposition modeling (FDM) products is obtained jointly by careful control of processing parameters, structure of products, and the composition of material. In this manuscript, poly(lactic acid) (PLA) was incorporated with graphene or carbon nanotube (CNT) through repeated melt blending. Filament of the PLA/graphitic nano-filler was prepared and used in FDM. Rheological and thermal analysis were conducted to assess the suitability of the composite as FDM feedstock, and mechanical and electrical property were tested subsequently. Research results demonstrate that filament diameter-regarded as processing-related parameter-was positively correlated with mechanical stiffness and strength of FDM products. Tensile elongation at break of FDM products exhibited significant increase at a raster angle of 45° compared with the filament before FDM, showing in certain cases, material property depends more on the structure than the composition. And when incorporated with graphene or CNT, the electrical conductivity of the PLA-based composite increased drastically. The electrical conductivity of the best experiment sample reached ∼10−1 S m−1, demonstrating that composition is the key to functionalizing material. © 2017 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2017, 134, 44703. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is a persistent environmental toxin and occupational pollutant that is considered to be a potential risk factor in the development of neurodegenerative diseases. Abnormal mitochondrial dynamics are increasingly implicated in mitochondrial damage in various neurological pathologies. The aim of this study was to investigate whether the disturbance of mitochondrial dynamics contributed to Cd-induced neurotoxicity and whether melatonin has any neuroprotective properties. After cortical neurons were exposed to 10 μM cadmium chloride (CdCl2) for various periods (0, 3, 6, 12, and 24 hr), the morphology of their mitochondria significantly changed from the normal tubular networks into punctuated structures within 3 hr. Following this pronounced mitochondrial fragmentation, Cd treatment led to signs of mitochondrial dysfunction, including excess reactive oxygen species ( ROS) production, decreased ATP content, and mitochondrial membrane potential (▵Ψm) loss. However, 1 mM melatonin pretreatment efficiently attenuated the Cd-induced mitochondrial fragmentation, which improved the turnover of mitochondrial function. In the brain tissues of rats that were intraperitoneally given 1 mg/kg CdCl2 for 7 days, melatonin also ameliorated excessive mitochondrial fragmentation and mitochondrial damage in vivo. Melatonin's protective effects were attributed to its roles in preventing cytosolic calcium ([Ca2+]i) overload, which blocked the recruitment of Drp1 from the cytoplasm to the mitochondria. Taken together, our results are the first to demonstrate that abnormal mitochondrial dynamics is involved in cadmium-induced neurotoxicity. Melatonin has significant pharmacological potential in protecting against the neurotoxicity of Cd by blocking the disbalance of mitochondrial fusion and fission. [ABSTRACT FROM AUTHOR]

Introduction Chronic thromboembolic pulmonary hypertension ( CTEPH) is a life-threatening condition characterized by single or recurrent pulmonary embolisms, which promotes pulmonary vascular remodeling. There is significant relationship between red cell distribution width ( RDW) and pulmonary hypertension; however, the usefulness of RDW as biomarker for the diagnosis of CTEPH remains poorly defined. Objective This study sought to assess the change and the diagnostic value of RDW in CTEPH. Methods This retrospective study included 56 CTEPH patients and 56 sex- and age-matched healthy controls treated at Beijing Chao- Yang Hospital. Correlations between RDW and hematological and hemodynamic parameters were assessed. A logistic regression model was applied to test independent parameters in relation to the diagnosis of CTEPH, and receiver operating characteristic curve was plotted to determine the diagnostic value of RDW in CTEPH. Results RDW values were significantly higher in CTEPH patients (13.82% ± 1.14%) compared with healthy controls (12.75% ± 0.49%) and in World Health Organization ( WHO), functional class III- IV cases (14.39% ± 1.24%) compared with class I- II cases (13.32% ± 0.78%) (both P = 0.000). RDW levels in CTEPH patients showed negative correlations with hemoglobin ( r = −0.357, P = 0.007) and cardiac index ( r = −0.288, P = 0.031), and positive correlations with pulmonary vascular resistance ( r = 0.292, P = 0.029) and WHO functional class ( r = 0.450, P = 0.001). Moreover, RDW was an independent parameter in the diagnosis of CTEPH (95% confidence interval: 2.866-13.698, P = 0.000); in particular, an RDW level ≥ 13.05% was the most useful cut-off value, with a sensitivity of 82.1% and a specificity of 71.4%. Conclusion Increased RDW level may be an acceptable diagnostic parameter for CTEPH. [ABSTRACT FROM AUTHOR]

ABCC9 genetic polymorphisms are associated with increased risk for various human diseases including hippocampal sclerosis of aging. The main goals of this study were 1 > to detect the ABCC9 variants and define the specific 3′ untranslated region (3′ UTR) for each variant in human brain, and 2 > to determine whether a polymorphism (rs704180) associated with risk for hippocampal sclerosis of aging pathology is also associated with variation in ABCC9 transcript expression and/or splicing. Rapid amplification of ABCC9 cDNA ends (3′ RACE) provided evidence of novel 3′ UTR portions of ABCC9 in human brain. In silico and experimental studies were performed focusing on the single nucleotide polymorphism, rs704180. Analyses from multiple databases, focusing on rs704180 only, indicated that this risk allele is a local expression quantitative trait locus ( eQTL). Analyses of RNA from human brains showed increased ABCC9 transcript levels in individuals with the risk genotype, corresponding with enrichment for a shorter 3′ UTR which may be more stable than variants with the longer 3′ UTR. Micro RNA transfection experiments yielded results compatible with the hypothesis that miR-30c causes down-regulation of SUR2 transcripts with the longer 3′ UTR. Thus we report evidence of complex ABCC9 genetic regulation in brain, which may be of direct relevance to human disease. [ABSTRACT FROM AUTHOR]

Due to their unique architectures and outstanding electrical properties, three dimensional graphene-based frameworks (3DGFs) have attracted extensive attention in wide fields. However, recently reported techniques always require complex processes and high cost, which severely limit their large-scale application. In this study, the massive preparation of macroscopically porous 3DGFs from the inherently inexpensive graphite paper is for the first time realized by simply combining the modified Hummer's method with freezing technique. The as-prepared 3DGFs that consist of well exfoliated, high-quality reduced graphene oxide (RGO) exhibit a mesoporous structure and superior conductivity. Such unique features enable the 3DGFs to be directly used as a supercapacitor electrode and as ideal 3D scaffolds to create PANI@3DGFs, Pd@3DGFs, and Pt@3DGFs composites, which hold great potential applications in supercapacitors and catalysts. [ABSTRACT FROM AUTHOR]

The effect of air exposure on antioxidant activities in Pacific white shrimpLitopenaeus vannameiwas studied. The behavioral changes in the shrimp and the levels of superoxide dismutase (SOD), malondialdehyde (MDA), and total antioxidant competence (T-AOC) in the muscles and hepatopancreas were determined after the shrimp were exposed to air and then resubmersed in water. Results showed that the duration of air exposure significantly influenced shrimp survival. The maximum air exposure period during which the shrimp could remain alive was 30 min. After 10 min of air exposure, the shrimp could survive when they were resubmersed in water. The T-AOC in the hepatopancreas and muscles was significantly decreased in shrimp that were exposed to air for 20 min. The MDA content in the hepatopancreas was significantly higher for the 20-, 30-, and 40-min air exposure groups than for the control group. During the resubmersion period, the MDA content in the shrimp hepatopancreas and muscles increased. For shrimp that were exposed to air for 10 min, SOD activities in the hepatopancreas and muscles were restored after 3 h of resubmersion in water. Our results indicate that air exposure can cause oxidative damage to Pacific white shrimp, but the damage can be reversed after the shrimp are resubmersed. Received June 13, 2014; accepted August 6, 2014 [ABSTRACT FROM PUBLISHER]

Hypoxia-induced pulmonary hypertension (HPH) is a clinical syndrome associated with high morbidity and mortality. However, the underlying mechanisms remain unclear. Both the mammalian target of rapamycin (mTOR) and the Notch3 signaling pathways have been reported to be involved in HPH; however, it is unknown whether there is a connection between these two signaling pathways in HPH. This study was designed to investigate the relationship between mTOR and Notch3 in HPH. After treatment with 10% O2 for 4 weeks, male C57BL/6 mice developed HPH with gradually increased right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), and pulmonary arteriolar remodeling accompanied by the activation of mTOR complex 1 (mTORC1) and Notch3 in the lung tissue and pulmonary arterioles. Pretreatment with the mTORC1 inhibitor rapamycin not only alleviated pulmonary arterial pressure and pulmonary arteriolar remodeling but also suppressed hypoxia-induced mTORC1 and Notch3 activation. Prophylactic N-[ N-(3,5-difluorophenacetyl)- L-alanyl]- S-phenylglycine t-butyl ester (DAPT) administration, a Notch signaling inhibitor, protected against the effects of hypoxia. These in vivo data were confirmed by in vitro experiments on human pulmonary arterial smooth muscle cell (PASMC) exposed to 3% O2. Furthermore, overexpression of Notch3 intracellular domain partially abrogated the inhibitory effects of rapamycin on human PASMC proliferation. These data indicate that both mTORC1 and Notch3 signaling are involved in HPH and the downstream effects of mTORC1 activation in HPH are partially dependent on the activation of Notch3 signaling. J. Cell. Physiol. 229: 2117-2125, 2014. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Up-regulation of G-protein-coupled receptors (GPCR) plays key roles in renal hypertension and cardiovascular disease pathogenesis. The present study was designed to examine if lipid-soluble cigarette smoking particles (DSP), nicotine and endotoxin (LPS), induce GPCR up-regulation for thromboxane A2 (TP), endothelin type A (ETA) and type B (ETB) receptors in renal artery, and if intracellular signal mechanisms are involved. Renal artery segments of rats were exposed to DSP, nicotine or LPS, in organ culture for up to 24 hr. The GPCR-mediated contractions were recorded by using a myograph system. Expression of the GPCR was examined by real-time PCR and immunohistochemistry at mRNA and protein levels. Sarafatoxin 6c (S6c, selective ETB receptor agonist), endothelin-1 (ET-1, non-selective ETA and ETB receptor agonist) and 9,11-Dideoxy-9a,11a-methanoepoxy prostaglandin F2a (U46619, a TP receptor agonist) induced contractions were significantly increased after the arterial segments exposed to DSP in a concentration-dependent (0.1-0.4 μl/ml) manner, and S6c also induced a time-dependent contraction, compared to control (dimethyl sulfoxide). This was in parallel with enhanced mRNA expression for ETB receptor but not ETA and TP receptors, while increased protein expression for ETA, ETB and TP receptors was seen. The specific nuclear factor-kappa B (NF-κB) signal pathway inhibitor BMS345541 was applied to link DSP effects to the GPCR up-regulation. It totally abolished ETB receptor up-regulation, but not ETA and TP receptor up-regulations. Our results suggest that DSP transcriptionally up-regulated ETB receptor expression in rat renal artery via NF-κB signal pathways, whereas up-regulation of ETA and TP receptor-mediated contraction may involve post-transcriptional mechanisms. [ABSTRACT FROM AUTHOR]