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Background and Purpose: Urticaria is a prevalent recurrent skin allergic condition. Severe itching significantly impacts patients' quality of life. This paper aims to investigate the development status of urticaria through bibliometric analysis to predict future research hotspots and trends. Methods: On October 29, 2023, a literature search was conducted in the Web of Science (WOS) database to collect urticaria‐related publications. The top 100 most cited articles were charted, and VOSviewer software was utilized for the literature data analysis. A visual analysis was performed on the number of articles, journals, main researchers, keywords, and so on. Results: The research involved 415 authors from 28 countries, published across 25 journals, ranging from 1963 to 2023. Marcus Maurer was the leading author, with the United States being the foremost country in urticaria research. CEH Grattan received the most citations, and The Medical University of South Carolina had the highest number of publications. Key research focuses include epidemiology, pathogenesis, drug therapy, and quality of life assessments. "Anti‐high affinity IgE receptor α chain (FcεRIα)," "chronic idiopathic urticaria," "autoantibodies," "histamine‐release" emerged as the keywords with the highest prominence. Conclusion: The field of urticaria research has attracted substantial attention over the past few decades, witnessing rapid development. This study highlighted the top 100 articles by citation frequency within the urticaria field. Bibliometric analysis revealed a shift in treatment methods from traditional antihistamines to biological agents, with significant emphasis on improving the quality of life in chronic urticaria management. These areas represent the current research focal points and indicate future trends in urticaria research. [ABSTRACT FROM AUTHOR]

Oleanolic acid (OA) is a pentacyclic triterpene with reported protective effects against various diseases, including diabetes, hepatitis, and different cancers. However, the effects of OA on obesity‐induced muscle atrophy remain largely unknown. This study investigated the effects of OA on skeletal muscle production and proliferation of C2C12 cells. We report that OA significantly increased skeletal muscle mass and improved glucose intolerance and insulin resistance. OA inhibited dexamethasone (Dex)‐induced muscle atrophy in C2C12 myoblasts by regulating the PI3K/Akt signaling pathway. In addition, it also inhibited expression of MuRF1 and Atrogin1 genes in skeletal muscle of obese mice suffering from muscle atrophy, and increased the activation of PI3K and Akt, thereby promoting protein synthesis, and eventually alleviating muscle atrophy. Taken together, these findings suggest OA may have potential for the prevention and treatment of muscle atrophy. [ABSTRACT FROM AUTHOR]

In this paper, a metal–organic skeleton material MIL‐101‐NH2‐AL was prepared for loading the chemotherapeutic drug Oridonin (Ori) and photosensitizer Chlorin e6 (Ce6). A drug delivery system for synergistic chemotherapy and photodynamic therapy was constructed. At the same time, we evaluated MIL‐101‐NH2‐AL as a drug therapy carrier, including drug loading, cytotoxicity, and safety, verified the photodynamic efficiency of MIL‐101‐NH2‐AL@Ori@Ce6 in vitro, and studied the ability of MIL‐101‐NH2‐AL@Ori@Ce6 cancer cells to produce reactive oxygen species, cell uptake, cytotoxicity, and so on. Experiments have confirmed that MIL‐101‐NH2‐AL, as a nano‐carrier, encapsulated Oridonin and Ce6, the combination of PDT and chemotherapy showed enhanced tumor inhibition and high biosafety. The killing effect on cells was caused by reactive oxygen species produced by photosensitizers and apoptosis of tumor cells induced by Oridonin. The drug delivery system demonstrates enormous potential for synergistic anti‐tumor effects of photodynamic and chemotherapy. [ABSTRACT FROM AUTHOR]

Background: Many observational epidemiology studies discovered that kidney cancer and impaired kidney function have a bidirectional relationship. However, it remains unclear whether these two kinds of traits are causally linked. In this study, we aimed to investigate the bidirectional causal relation between kidney cancer and kidney function biomarkers (creatinine‐based estimated glomerular filtration rate (eGFRcrea), cystatin C‐based estimated glomerular filtration rate (eGFRcys), blood urea nitrogen (BUN), serum urate, and urinary albumin‐to‐creatinine ratio (UACR)). Methods: For both directions, single‐nucleotide polymorphisms (SNPs), as genetic instruments, for the five kidney function traits were selected from up to 1,004,040 individuals, and SNPs for kidney cancer were from 408,786 participants(1338 cases). In the main analysis, we applied two state‐of‐the‐art MR methods, namely, contamination mixture and Robust Adjusted Profile Score to downweight the effect of weak instrument bias, pleiotropy, and extreme outliers. We additionally conducted traditional MR analyses as sensitivity analyses. Summary‐level data of European ancestry were extracted from UK Biobank, Chronic Kidney Disease Genetics Consortium, and Kaiser Permanente. Results: Based on 99 SNPs, we found that the eGFRcrea had a significant negative causal effect on the risk of kidney cancer (OR = 0.007, 95% CI:2.6 × 10−4–0.569, p = 0.041). After adjusting for body composition or diabetes, urate had a significant negative causal effect on kidney cancer (OR <1, p < 0.05). For UACR, it showed a strong causal effect on kidney cancer, after adjusting for body composition (OR = 14.503, 95% CI: 2.546–96.001, p = 0.032). Due to lacking significant signals and effect power for the reverse MR, further investigations are warranted. Conclusions: Our study suggested a potential causal effect of damaged kidney function on kidney cancer. EGFRcrea and UACR might be causally associated with kidney cancer, especially when patients were comorbid with obesity or diabetes. We called for larger sample‐size studies to further unravel the underlying causal relationship and the exact mechanism. [ABSTRACT FROM AUTHOR]

The precise control of monomer sequence and stereochemistry in copolymerization is of much interest and importance for the synthesis of high performance materials, but studies toward this goal have met with only limited success to date. The coordination polymerization of diphenylphosphinostyrene (p‐StPPh2 and o‐StPPh2) and its copolymerization with styrene (St) by (C5Me4SiMe3)Sc(CH2C6H4NMe2‐o)2 have been achieved for the first time to afford a new series of phosphine functionalized syndiotactic polystyrene. By the design of the polymer structure, the copolymer of o‐StPPh2 and St (poly(o‐StPPh2‐alt‐St)‐b‐sPS) containing o‐StPPh2 and St atactic alternating copolymer block and syndiotactic polystyrene block (sPS) showed excellent thermal stability and chemical resistance. The simple combination of the triphenylphosphine and syndiotactic polystyrene realized the stable immobilization of metal nanoparticles to afford highly robust metal@poly(o‐StPPh2‐alt‐St)‐b‐sPS nanocatalysts at high temperature and various atmospheres. The Cu@poly(o‐StPPh2‐alt‐St)‐b‐sPS catalyst can serve as a highly efficient heterogeneous catalyst for the synthesis of quinoline derivatives by acceptorless dehydrogenative coupling of o‐aminobenzylalcohol with ketones. [ABSTRACT FROM AUTHOR]

Background: Left atrial (LA) function and mechanical dispersion changes in breast cancer patients treated with chemotherapy remain unclear. Hypothesis: LA function and LA mechanical dispersion in breast cancer patients would be impaired after chemotherapy. Methods: This single‐center retrospective study included 91 consecutive breast cancer patients treated with chemotherapy and 30 controls. Patients were examined by echocardiography three times at intervals. Conventional parameters, left ventricular strain, LA strain, and LA mechanical dispersion were evaluated and compared. Results: LA strain during reservoir phase (LASr), conduit phase (LAScd), and contraction phase (LASct) all decreased markedly after chemotherapy and were lower than those of the controls (all p <.01). The standard deviation of time to peak positive strain during LA reservoir phase corrected by R‐R interval (LA SD‐TPSr) was significantly increased after chemotherapy and was higher than that of the controls (p <.001). The change of LA function was expressed as Δ. Multivariate linear regression analyses showed that LAVIp (0.399, 95% confidence interval [CI]: 0.610, 1.756, p =.000) was independently associated with ΔLASr, LAPEF (−0.325, 95% CI: −45.123, −10.676, p =.002) and age (0.227, 95% CI: 0.021, 0.350, p =.027) were independently associated with ΔLAScd, and LAVImax (0.341, 95% CI: 0.192, 0.723, p =.001) was independently associated with ΔLASct. LAVImax (0.505, 95% CI: 0.000, 0.001, p =.039) and mitral E (−0.256, 95% CI: 0.000, 0.000, p =.024）were independently associated with ΔLA SD‐TPSr. Conclusions: Mechanical function of LA declined after chemotherapy in breast cancer patients. With the decrease of LA mechanical function, LA mechanical dispersion assessed by two‐dimensional speckle‐tracking echocardiography increased significantly, and its clinical value needs to be further studied. [ABSTRACT FROM AUTHOR]

Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative-type fibers. However, the mechanism for coupling of mitochondrial function to the muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/ Myh7b and their intronic miR-208b/miR-499, parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1α-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, an AMP-activated protein kinase ( AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1α. Inhibition of Fnip1 reactivated AMPK/ PGC-1α signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy ( DMD) reduced the severity of DMD. Thus, we have identified a miR-499/Fnip1/ AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function. [ABSTRACT FROM AUTHOR]

Hypoxia not only promotes tumor metastasis but also strengthens tumor resistance to therapies that demand the involvement of oxygen, such as radiation therapy and photodynamic therapy (PDT). Herein, taking advantage of the high reactivity of manganese dioxide (MnO2) nanoparticles toward endogenous hydrogen peroxide (H2O2) within the tumor microenvironment to generate O2, multifunctional chlorine e6 (Ce6) loaded MnO2 nanoparticles with surface polyethylene glycol (PEG) modification (Ce6@MnO2-PEG) are formulated to achieve enhanced tumor-specific PDT. In vitro studies under an oxygen-deficient atmosphere uncover that Ce6@MnO2-PEG nanoparticles could effectively enhance the efficacy of light-induced PDT due to the increased intracellular O2 level benefited from the reaction between MnO2 and H2O2, the latter of which is produced by cancer cells under the hypoxic condition. Owing to the efficient tumor homing of Ce6@MnO2-PEG nanoparticles upon intravenous injection as revealed by T1-weighted magnetic resonance imaging, the intratumoral hypoxia is alleviated to a great extent. Thus, in vivo PDT with Ce6@MnO2-PEG nanoparticles even at a largely reduced dose offers remarkably improved therapeutic efficacy in inhibiting tumor growth compared to free Ce6. The results highlight the promise of modulating unfavorable tumor microenvironment with nanotechnology to overcome current limitations of cancer therapies. [ABSTRACT FROM AUTHOR]

The preparation of tropical wood surface sections for time-of-flight secondary ion mass spectrometry imaging is described, and the use of delayed extraction of secondary ions and its interest for the analysis of vegetal surface are shown. The method has been applied to the study by time-of-flight secondary ion mass spectrometry imaging with a resolution of less than one micron of a tropical wood species, Dicorynia guianensis, which is one of the most exploited wood in French Guiana for its durable heartwood. The heartwood of this species exhibits an economical importance, but its production is not controlled in forestry. Results show an increase of tryptamine from the transition zone and a concomitant decrease of inorganic ions and starch fragment ions. These experiments lead to a better understanding of the heartwood formation and the origin of the natural durability of D. guianensis. Copyright © 2016 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

A one-pot procedure for the synthesis of unsymmetrical ketones utilizing a pyrrole-bearing carbonyl linchpin reagent (carbonyl linchpin N, O-dimethylhydroxylamine pyrrole; CLAmP) is reported. In contrast to other carbonyl dielectrophile equivalents, CLAmP enables the synthesis of ketones from a variety of organolithium and Grignard reagents. The electrophilic nature of CLAmP enables the addition of less reactive as well as thermally unstable nucleophiles. CLAmP was designed to form kinetically stable tetrahedral intermediates upon the addition of organometallic nucleophiles. Evidence for the existence of persistent tetrahedral intermediates was obtained through in situ IR studies. [ABSTRACT FROM AUTHOR]

A novel methodology for the creating C-P bond via the oxidative coupling of a wide range of arylboronic acids with various H-phosphine oxides in the presence of palladium catalyst under dry air as the green oxidant is described. [ABSTRACT FROM AUTHOR]

Upon adaption of skeletal muscle to physiological and pathophysiological stimuli, muscle fiber type and mitochondrial function are coordinately regulated. Recent studies have identified pathways involved in control of contractile proteins of oxidative-type fibers. However, the mechanism for coupling of mitochondrial function to the muscle contractile machinery during fiber type transition remains unknown. Here, we show that the expression of the genes encoding type I myosins, Myh7/Myh7b and their intronic miR-208b/miR-499, parallels mitochondrial function during fiber type transitions. Using in vivo approaches in mice, we found that miR-499 drives a PGC-1α-dependent mitochondrial oxidative metabolism program to match shifts in slow-twitch muscle fiber composition. Mechanistically, miR-499 directly targets Fnip1, an AMP-activated protein kinase (AMPK)-interacting protein that negatively regulates AMPK, a known activator of PGC-1α. Inhibition of Fnip1 reactivated AMPK/PGC-1α signaling and mitochondrial function in myocytes. Restoration of the expression of miR-499 in the mdx mouse model of Duchenne muscular dystrophy (DMD) reduced the severity of DMD Thus, we have identified a miR-499/Fnip1/AMPK circuit that can serve as a mechanism to couple muscle fiber type and mitochondrial function., (© 2016 The Authors. Published under the terms of the CC BY 4.0 license.)