In the the double-slit experiment, nonclassical paths are Feynman paths that go through both slits. Prior work with atom cavities as which-way detectors in the double-slit experiment has shown these ...paths to be experimentally inaccessible. In this paper, we show how such a setup can indeed detect nonclassical paths with 1% probability if one considers a different type of nonclassical path than previously investigated. We also show how this setup can be used to erase and restore the coherence of the nonclassical paths. Finally, we also show how atom cavities may be used to implement a exact measure of Born-rule violation Quach, Which-way double-slit experiments and Born-rule violation, Phys. Rev. A 95, 042129 (2017), which up until now has only been a formal construct.
This study examines intracellular signaling events associated with the activation of chondrocytes by the cytokine interleukin-17 (IL-17). Stimulation of normal human articular chondrocytes with IL-17 ...induced nitric oxide (NO) production, concomitant with an increase in transcripts and de novotranslation products of the inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) genes. Several other genes associated with inflammation and cartilage degradation, such as IL-1β, IL-6, and stromelysin, were also up-regulated in IL-17-treated chondrocytes. Among signaling events displaying early response to IL-17 in chondrocytes were the mitogen-activated protein (MAP) kinases ERK1, ERK2, JNK, and p38. DNA binding activity of NF-κB was also significantly induced. IL-17 effects on NO release, as well as iNOS, COX-2, and IL-6 protein expression, were inhibited by the anti-inflammatory drug dexamethasone. Importantly, dexamethasone blunted IL-17-dependent activation of MAP kinases, suggesting a mechanistic relationship between these activities and the aforementioned gene expression responses. Similar effects of a lesser extent were observed with the p38-specific inhibitor SB203580. These results suggest that IL-17 activation of chondrocytes is associated with and depends at least in part on the activation of MAP kinases and NF-κB.
Articular cartilage chondrocytes have the unique ability to elaborate large amounts of extracellular pyrophosphate (PPi), and transforming growth factor β (TGFβ) appears singular among cartilage ...regulatory factors in stimulating PPiproduction. TGFβ caused a time and dose-dependent increase in intracellular and extracellular PPiin human articular chondrocyte cultures. TGFβ and interleukin 1β (IL-1β) antagonistically regulate certain chondrocyte functions. IL-1β profoundly inhibited basal and TGFβ-induced PPielaboration. To address mechanisms involved with the regulation of PPisynthesis by IL-1β and TGFβ, we analyzed the activity of the PPi-generating enzyme NTP pyrophosphohydrolase (NTPPPH) and the PPi-hydrolyzing enzyme alkaline phosphatase. Human chondrocyte NTPPPH activity was largely attributable to plasma cell membrane glycoprotein 1, PC-1. Furthermore, TGFβ induced comparable increases in the activity of extracellular PPi, intracellular PPi, and cellular NTPPPH and in the levels of PC-1 protein and mRNA in chondrocytes as well as a decrease in alkaline phosphatase. All of these TGFβ-induced responses were completely blocked by IL-1β. Thus, IL-1β may be an important regulator of mineralization in chondrocytes by inhibiting TGFβ-induced PPiproduction and PC-1 expression.
IL-18, a cytokine originally identified as IFN-gamma-inducing factor, is a member of the IL-1 family of proteins. Because IL-1alpha and IL-1beta are important mediators in the pathogenesis of ...arthritis, the present study addresses the expression of IL-18 and its role in regulating in articular chondrocytes. IL-18 mRNA was induced by IL-1beta in chondrocytes. Chondrocytes produced the IL-18 precursor and in response to IL-1 stimulation secreted the mature form of IL-18. Studies on IL-18 effects on chondrocytes showed that it inhibits TGF-beta-induced proliferation and enhances nitric oxide production. IL-18 stimulated the expression of several genes in normal human articular chondrocytes including inducible nitric oxide synthase, inducible cyclooxygenase, IL-6, and stromelysin. Gene expression was associated with the synthesis of the corresponding proteins. Treatment of normal human articular cartilage with IL-18 increased the release of glycosaminoglycans. These finding identify IL-18 as a cytokine that regulates chondrocyte responses and contributes to cartilage degradation.
The rate at which matter emits or absorbs light can be modified by its environment, as dramatically exemplified by the widely-studied phenomenon of superradiance. The reverse process, ...superabsorption, is harder to demonstrate due to the challenges of probing ultrafast processes, and has only been seen for small numbers of atoms. Its central idea - superextensive scaling of absorption meaning larger systems absorb faster - is also the key idea underpinning quantum batteries. Here we implement experimentally a paradigmatic model of a quantum battery, constructed of a microcavity enclosing a molecular dye. Ultrafast optical spectroscopy allows us to observe charging dynamics at femtosecond resolution to demonstrate superextensive charging rates and storage capacity, in agreement with our theoretical modelling. We find that decoherence plays an important role in stabilising energy storage. Our work opens new opportunities for harnessing collective effects in light-matter coupling for nanoscale energy capture, storage, and transport technologies.
Chondrocytes exposed to nitric oxide (NO) or antibody to Fas undergo cell death by apoptosis. This study examines structural and functional properties of chondrocyte-derived apoptotic bodies. In NO ...treated cartilage, the dense pericellular matrix that normally surrounds the cells is degraded and apoptotic bodies accumulate within and in the vicinity of the chondrocyte lacunae. Functional analysis shows that apoptotic bodies isolated from NO-treated chondrocytes or cartilage produce pyrophosphate. The levels of pyrophosphate produced by apoptotic bodies are increased by pretreatment of the chondrocytes with transforming growth factor β and decreased by interleukin 1. Apoptotic bodies contain alkaline phosphatase and NTP pyrophosphohydrolase activities and can precipitate calcium. These results suggest that chondrocyte-derived apoptotic bodies express functional properties that may contribute to the pathologic cartilage calcification observed in aging and osteoarthritis.
Gold sodium thiomalate (GST), chloroquine (CQ), and methotrexate have been widely used in the therapy of rheumatoid arthritis and other inflammatory conditions. Using the human monocytic cell line ...THP-1 we have analyzed effects of these drugs on cytokine production and intracellular signaling. GST and CQ were equally effective in reducing lipopolysaccharide (LPS)-induced IL-1 beta release while CQ was a more effective inhibitor of TNF-alpha production than GST. Methotrexate did not affect production of these cytokines. CQ reduced IL-1 beta mRNA expression and strongly inhibited phosphorylation of mitogen-activated protein kinase (MAPK) p38, and to a lesser extent c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2. In contrast, GST did not affect cytokine mRNA expression or MAPK activation. However, GST selectively inhibited the activity of the interleukin-1 converting enzyme (ICE)/caspase-1. These data demonstrate that CQ inhibits IL-1 beta release from monocytes by interfering with pretranscriptional signaling and TNF-alpha release by posttranslational events whereas GST downregulates IL-1 beta secretion by interfering with posttranslational IL-1 beta processing.
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