255 research outputs found
Direct Nucleophilic Substitution of Alcohols Using an Immobilized Oxovanadium Catalyst
Direct nucleophilic substitution of alcohols with thiols or carbon nucleophiles was achieved using a mesoporous silica-supported oxovanadium catalyst (VMPS4). Benzyl and allyl alcohols were compatible in this reaction under mild conditions, affording the products in high yields. The VMPS4 catalyst showed excellent chemoselectivity toward alcohols in the presence of acid-labile functional groups, which is in contrast to that observed for the commonly used Lewis acid catalysts, which exhibit poor selectivity. The VMPS4 catalyst could be recycled by simple centrifugation, and the catalytic activity was maintained over seven cycles.This is the pre-peer reviewed version of the following article:Nishio T., Yoshioka S., Hasegawa K., et al. Direct Nucleophilic Substitution of Alcohols Using an Immobilized Oxovanadium Catalyst. European Journal of Organic Chemistry 2021, 4417 (2021), which has been published in final form at https://doi.org/10.1002/ejoc.202100569. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archivin
The efficacy and safety of reduced-dose sulfamethoxazole-trimethoprim for chemoprophylaxis ofPneumocystispneumonia in patients with rheumatic diseases
Spectroscopic and theoretical investigation of the electronic states of layered perovskite oxyfluoride Sr2RuO3F2 thin films
LACTATE/MCT4/GPR81 AXIS IN BONE PAIN OF BREAST CANCER
Breast cancer (BC) bone metastasis causes bone pain (BP), which detrimentally damages the quality of life and outcome of patients with BC. However, the mechanism of BCâBP is poorly understood, and effective treatments are limited. The present study demonstrated a novel mechanism of BCâBP using a mouse model of bone pain, in which mouse (EO771) and human (MDAâMBâ231) BC cells were injected in the bone marrow cavity of tibiae. Western blot analysis using sensory nerves, in vivo assessment of cancer pain and in vitro calcium flux analysis were performed. These mice developed progressive BCâBP in tibiae in conjunction with an upregulation of phosphorylated pERK1/2 and cAMPâresponse elementâbinding protein (pCREB), which are molecular indicators of neuron excitation, in the dorsal root ganglia (DRG) of sensory nerves. Importantly, mice injected with BC cells, in which the expression of the lactic acid transporter monocarboxylate transporter 4 (MCT4) was silenced, exhibited decreased BCâBP with downregulated expression of pERK1/2 and pCREB in the DRG and reduced circulating levels of lactate compared with mice injected with parental BC cells. Further, silencing of the cellâsurface orphan receptor for lactate, G proteinâcoupled receptor 81 (GPR81), in the F11 sensory neuron cells decreased lactateâpromoted upregulation of pERK1/2 and Ca2+ influx, suggesting that the sensory neuro excitation was inhibited. These results suggested that lactate released from BC cells via MCT4 induced BCâBP through the activation of GPR81 of sensory neurons. In conclusion, the activation of GPR81 of sensory neurons by lactate released via MCT4 from BC was demonstrated to contribute to the induction of BCâBP, and disruption of the interactions among lactate, MCT4 and GPR81 may be a novel approach to control BCâBP
Impact of noncontrast PCI for ACS
Purpose : Contrast-induced acute kidney injury (CI-AKI) is one of the common serious complications of percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). This study aimed to assess the significance of noncontrast strategy in the setting of ACS. Methods : CI-AKI was defined as an increase in serum creatinine of â„ 0.5 mg / dL or â„ 1.25 times from the baseline. One-year worsening renal function (WRF) was defined as an increase of â„ 0.3 mg / dL in serum creatinine from the baseline after PCI. Results : Of 250 ACS patients, 81 were treated with noncontrast PCI. The average doses of contrast medium in the noncontrast and conventional groups were 17 (9â22) ml and 150 (120â200) ml, respectively. CI-AKI was observed in 4 patients (5%) in the noncontrast group and 29 patients (17%) in the conventional group. Noncontrast PCI was associated with a lower incidence of CI-AKI (adjusted odds ratio, 0.26 ; 95% confidence interval [CI], 0.08â0.82). The bootstrap method and inverse probability weighting led to similar results. CI-AKI was associated with a higher incidence of 1-year WRF (adjusted hazard ratio, 2.30 ; 95% CI, 1.12â4.69), while noncontrast PCI was not. Conclusions : Noncontrast PCI was associated with the lower incidence of CI-AKI in ACS patients
Specialized Pro-Resolving Mediators Do Not Inhibit the Synthesis of Inflammatory Mediators Induced by Tumor Necrosis Factor-α in Synovial Fibroblasts
Background : Tumor necrosis factor (TNF)-α, a proinflammatory cytokine, is involved in the pathogenesis of rheumatoid arthritis (RA). The omega-3 unsaturated fatty acid-derived metabolites resolvin (Rv) D1, RvE1, and maresin-1 (MaR1) have been reported as anti-inflammatory lipid mediators and are known as specialized pro-resolving mediators (SPMs). In this study, we aimed to investigate the anti-inflammatory effects of SPMs on TNF-α-induced responses in synovial fibroblasts. Methods: We investigated the effects of SPMs on gene expression and/or production of cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase-1 (mPGES-1), interleukin (IL)-6, and matrix metalloproteinase (MMP)-3, which are involved in TNF-α-induced synovitis in RA or OA synovial fibroblasts, by quantitative real-time PCR. We also investigated the effects of SPMs on the mitogen-activated protein kinase (MAPK) signaling pathway by western blotting. Anti-inflammatory effects of SPMs were evaluated by applying SPMs to cultured synovial fibroblasts, followed by TNF-α stimulation. Results: The induction of COX-2, mPGES-1, IL-6, and MMP-3 by TNF-α in synovial fibroblasts was not suppressed by omega 3-derived SPMs regardless of their origin such as RA or OA. SPMs had no effect on lipid mediator receptor gene expression induce by TNF-α and did not inhibit the TNF-α-activated MAPK signaling pathway. The production of COX-2 and IL-6 protein was significantly decreased by p38 inhibitor. Conclusion: Despite reports on the anti-inflammatory effect of omega 3-derived SPMs, its anti-inflammatory effect on TNF-α-induced responses was not observed in synovial fibroblasts. The reason may be that SPMs have no suppressive effect on p38 activation, which plays an important role in the production of inflammatory cytokines in synovial fibroblasts
High mobility group box 1 induces bone pain associated with bone invasion in a mouse model of advanced head and neck cancer
Advanced head and neck cancer (HNC) can invade facial bone and cause bone pain, thus posing a significant challenge to the quality of life of patients presenting with advanced HNC. The present study was designed to investigate HNC bone pain (HNCâBP) in an intratibial mouse xenograft model that utilized an HNC cell line (SAS cells). These mice develop HNCâBP that is associated with an expression of phosphorylated ERK1/2 (pERK1/2), which is a molecular indicator of neuron excitation in dorsal root ganglia (DRG) sensory neurons. Our experiments demonstrated that the inhibition of high mobility group box 1 (HMGB1) by short hairpin (shRNA) transduction, HMGB1 neutralizing antibody, and HMGB1 receptor antagonist suppressed the HNCâBP and the pERK1/2 expression in DRG. It was also observed that HNCâderived HMGB1 increased the expression of the acidâsensing nociceptor, transient receptor potential vanilloid 1 (TRPV1), which is a major cause of osteoclastic HNCâBP in DRG. Collectively, our results demonstrated that HMGB1 originating in HNC evokes HNCâBP via direct HMGB1 signaling and hypersensitization for the acid environment in sensory neurons
A marine phytoplankton (Prymnesium parvum) up-regulates ABC transporters and several other proteins to acclimatize with Fe-limitation
Iron (Fe) is one of the vital limiting factors for phytoplankton in vast regions of the contemporary oceans, notably the high nutrient low chlorophyll regions. Therefore, it is apparent to be acquainted with the Fe uptake strategy of marine phytoplankton under Fe-limited condition. In the present study, marine phytoplankton Prymnesium parvum was grown under Fe-deplete (0.0025 ΌM) and Fe-rich (0.05 ΌM) conditions, and proteomic responses of the organism to Fe conditions were compared. In sodium dodecyl sulfate (SDS) gel electrophoresis, 7 proteins (16, 18, 32, 34, 75, 82, and 116. kDa) were highly expressed under Fe-deplete condition, while one protein (23. kDa) was highly expressed under Fe-rich condition. These proteins were subjected to 2-dimensional gel electrophoresis (2-D DIGE) to differentiate individual proteins, and were identified by matrix-assisted laser desorption-ionization-time of flight-mass spectrometer (MALDI-TOF-MS) analysis. The results showed that under Fe-deplete condition P. parvum increases the biosynthesis of ATP binding cassette (ABC) transporters, flagellar associated protein (FAP), and Phosphoribosylaminoimidazole-succinocarboxamide synthase. These proteins are assumed to be involved in a number of cellular biochemical processes that facilitate Fe acquisition in phytoplankton. Under Fe-deplete condition, P. parvum increases the synthesis of ribulose biphosphate carboxylase (RuBisCo), malate dehydrogenase, and two Fe-independent oxidative stress response proteins, manganese superoxide dismutase (MnSOD) and Serine threonine kinase (STK). Thus, marine phytoplankton may change their Fe acquisition strategy by altering the biosynthesis of several proteins in order to cope with Fe-limitation. © 2013 Elsevier Ltd
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