A triplet biradical with double bidentate sites based on tert-butyl pyridyl nitroxide as a candidate for strong ferromagnetic couplers

We synthesised a new biradical, 34bpybNO, having two chelating radical sites and demonstrated its crystal structure and ground triplet nature. Frozen-solution magnetic measurement and electron spin resonance results revealed a strong intramolecular ferromagnetic coupling reaching 2J/kB = ∼+170 K, which is supported by density functional theory calculations

Minor element chemistry of low-Ca pyroxene in Allan Hills-77252, an L3-6 regolith breccia

Allan Hills (ALH-) 77252 is a regolith breccia consisting of various types of clasts differing in metamorphic grades (L3-6). Titanium/aluminum ratios of low-Ca pyroxene in ALH-77252 are bimodally distributed. In equilibrated clasts, Ti/Al ratios of low-Ca pyroxene are ∿0.5 which are quite different from those in unequilibrated clasts of ∿0.07. Among equilibrated and unequilibrated clasts, the Ti/Cr ratio of low-Ca pyroxene also shows large differences. Because titanium and aluminum are not diffusive elements in the pyroxene crystal structure, diffusional redistribution of titanium and aluminum in low-Ca pyroxene requires significantly higher metamorphic temperature than Fe-Mg homogenization, possibly above ∿800℃. Alternatively, if the source materials of L-group chondrites were initially different, the fingerprints of mineral properties resistant to thermal metamorphism remain unchanged. If this was the case, the distinctly higher Ti/Al ratios of low-Ca pyroxene in equilibrated clasts originated from the primary signatures of low-Ca pyroxene prior to thermal metamorphism

Mouse 3T3-L1 cells acquire resistance against oxidative stress as the adipocytes differentiate via the transcription factor FoxO

Repression of excessive increase and enlargement of adipocytes that is closely associated with obesity is effective in the prevention and treatment of metabolic syndrome. Generally, apoptosis is induced in cells via a wide variety of intracellular or extracellular substances, and recently, it has been suggested that the FoxO subfamily is involved in the induction of apoptosis. We aimed to elucidate the mechanism of FoxO-mediated apoptosis-induction in the adipocytes under the reactive oxygen species (ROS) stimulus. The treatment of differentiated and undifferentiated 3T3-L1 cells with glucose oxidase (GOD), an enzyme that generates H2O2, induced apoptosis and led to the accumulation of 8-OHdG. Apoptosis analysis revealed that GOD treatment induced apoptosis in differentiated 3T3-L1 cells less efficiently than in undifferentiated preadipocytes. GOD remarkably increased the levels of Bad, Bax, and Bim—the genes that are actively involved in cell apoptosis. GOD treatment also increased the expression of FoxO3a mRNA and protein. The introduction of FoxO3a-siRNA into 3T3-L1 cells suppressed the oxidative stress-induced expression of Bim mRNA, as well as the GOD-induced apoptosis. Furthermore, the expression of MnSOD, Cu/ZnSOD, and catalase, as well as of FoxO, increased significantly along with the progression of adipocyte differentiation. These results indicated that ROS-induced apoptosis in undifferentiated 3T3-L1 cells via the expression of FoxO3a, whereas FoxO expression suppressed the ROS-induced apoptosis in differentiated 3T3-L1 cells via the expression of ROS-scavenging enzymes

All APOBEC3 family proteins differentially inhibit LINE-1 retrotransposition

Approximately 17% of the human genome is comprised of long interspersed nuclear element 1 (LINE-1, L1) non-LTR retrotransposons. L1 retrotransposition is known to be the cause of several genetic diseases, such as hemophilia A, Duchene muscular dystrophy, and so on. The L1 retroelements are also able to cause colon cancer, suggesting that L1 transposition could occur not only in germ cells, but also in somatic cells if innate immunity would not function appropriately. The mechanisms of L1 transposition restriction in the normal cells, however, are not fully defined. We here show that antiretroviral innate proteins, human APOBEC3 (hA3) family members, from hA3A to hA3H, differentially reduce the level of L1 retrotransposition that does not correlate either with antiviral activity against Vif-deficient HIV-1 and murine leukemia virus, or with patterns of subcellular localization. Importantly, hA3G protein inhibits L1 retrotransposition, in striking contrast to the recent reports. Inhibitory effect of hA3 family members on L1 transposition might not be due to deaminase activity, but due to novel mechanism(s). Thus, we conclude that all hA3 proteins act to differentially suppress uncontrolled transposition of L1 elements

Hepatocellular Carcinoma with Foamy Histiocyte-Like Appearance: A Deceptively Clear Cell Carcinoma Appearing Variant

Hepatocellular carcinoma (HCC) shows many pathological features, and it varies architecturally and cytologically. There have been many reports and discussions of the morphological features of HCC. A 63-year-old man was found to have a solitary tumor in liver segment 7 that was diagnosed as HCC. A partial resection of liver segment 7 was performed. Microscopically, the tumor lesion showed a moderately differentiated HCC. There was also a lesion with foamy histiocyte-like cells corresponding to the white lesion in the face of the cut tumor. Immunohistochemical staining showed that they were negative for CD68, S-100, vimentin, and HMB-45. The cytoplasm itself was negative on periodic acid Schiff (PAS) and Sudan staining. Without immunohistological analysis, it is difficult to distinguish this HCC variant from clear cell carcinoma or metastases of renal cell carcinoma. It is important to recognize this type as a specific cytological variant of HCC that requires confirmation by immunohistochemistry. This report describes the case of a patient with a morphologically distinctive pattern of HCC with prominent cell cytoplasm that had a foamy histiocyte-like appearance. To the best of our knowledge, this is the first report of this HCC variant

Peripheral Administration of Morphine Attenuates Postincisional Pain by Regulating Macrophage Polarization through COX-2-Dependent Pathway

BACKGROUND: Macrophage infiltration to inflammatory sites promotes wound repair and may be involved in pain hypersensitivity after surgical incision. We recently reported that the development of hyperalgesia during chronic inflammation is regulated by macrophage polarity, often referred to as proinflammatory (M1) or anti-inflammatory (M2) macrophages. Although opioids such as morphine are known to alter the inflammatory milieu of incisional wounds through interactions with immunocytes, the macrophage-mediated effects of morphine on the development of postincisional pain have not been well investigated. In this study, we examined how morphine alters pain hypersensitivity through phenotypic shifts in local macrophages during the course of incision-induced inflammation. RESULTS: Local administration of morphine in the early phase, but not in the late phase alleviated mechanical hyperalgesia, and this effect was reversed by clodronate-induced peripheral depletion of local macrophages. At the morphine-injected incisional sites, the number of pro-inflammatory F4/80(+)iNOS(+)M1 macrophages was decreased during the course of pain development whereas increased infiltration of wound healing F4/80(+)CD206(+)M2 macrophages was observed during the early phase. Morphine increased the gene expression of endogenous opioid, proenkephalin, and decreased the pronociceptive cytokine, interleukin-1β. Heme oxygenase (HO)-1 promotes the differentiation of macrophages to the M2 phenotype. An inhibitor of HO-1, tin protoporphyrin reversed morphine-induced analgesic effects and the changes in macrophage phenotype. However, local expression levels of HO-1 were not altered by morphine. Conversely, cyclooxygenase (COX)-2, primarily produced from peripheral macrophages in acute inflammation states, was up-regulated in the early phase at morphine-injected sites. In addition, the analgesic effects and a phenotype switching of infiltrated macrophages by morphine was reversed by local administration of a COX inhibitor, indomethacin. CONCLUSIONS: Local administration of morphine alleviated the development of postincisional pain, possibly by altering macrophage polarity at the incisional sites. A morphine-induced shift in macrophage phenotype may be mediated by a COX-2-dependent mechanism. Therefore, μ-opioid receptor signaling in macrophages may be a potential therapeutic target during the early phase of postincisional pain development

コウシュウハ イオンプレーティング ホウ ニ ヨル ハクマク ケイセイ ニ カンスル ケンキュウ

The nanostructural hydrogenated graphite (CnanoHx) was synthesized from graphite by ball milling under hydrogen (H2) atmosphere. In this product, characteristic hydrogenated states in the form of polarized hydrocarbon groups (―CH, ―CH2, and ―CH3) are realized in the nanoscale. By synthesizing the composite of CnanoHx and lithium hydride (LiH), known as the Li―C―H system, hydrogen was desorbed at 350 °C, which is a lower temperature compared to the decomposition temperature of each component. It is considered that this hydrogen desorption would be induced by destabilization of each hydrogen absorbed state due to an interaction between the polarized C―H groups in CnanoHx and LiH. Therefore, in order to understand the hydrogen absorption/desorption mechanism of the Li―C―H system, it is an important issue to investigate the change in the C―H groups during hydrogen absorption/desorption reactions in the composite. The correlations among atoms contained in this composite are examined by neutron diffraction measurements, where the protium/deuterium (H/D) isotopic substitution was used to clarify the location of hydrogen atoms in this composite. Some C―D and Li―D correlations are found from the radial distribution function [RDF(r)] obtained by the neutron diffraction for the CnanoDx and LiD composite. After dehydrogenation, C―C triple bond and Li―C bond, ascribed to lithium carbide (Li2C2), are observed. Furthermore, the RDF(r) corresponding to rehydrogenated composite indicates the presence of not only the Li―D correlation but also the C―D one