Accurate 7Li(d,n)24He thermonuclear reaction rates are crucial for precise prediction of the primordial abundances of lithium and beryllium and to probe the mysteries beyond fundamental physics and ...the standard cosmological model. However, uncertainties still exist in current reaction rates of 7Li(d,n)24He widely used in big bang nucleosynthesis (BBN) simulations. In this work, we reevaluate the 7Li(d,n)24He reaction rate using the latest data on the three near-threshold 9Be excited states from experimental measurements. We present for the first time uncertainties that are directly constrained by experiments. Additionally, we take into account for the first time the contribution from the subthreshold resonance at 16.671 MeV of 9Be. We obtain a 7Li(d,n)24He rate that is overall smaller than the previous estimation by about a factor of 60 at the typical temperature of the onset of primordial nucleosynthesis. We implemented our new rate in BBN calculations, and we show that the new rates have a very limited impact on the final light element abundances in uniform density models. Typical abundance variations are in the order of 0.002%. For nonuniform density BBN models, the predicted 7Li production can be increased by 10% and the primordial production of light nuclides with mass number A > 7 can be increased by about 40%. Our results confirm that the cosmological lithium problem remains a long-standing unresolved puzzle from the standpoint of nuclear physics.
Abstract Several neuroimaging studies have revealed that the brains of schizophrenic patients exhibit abnormalities in white matter pathways. Using magnetic resonance imaging (MRI) methods, such as ...T2-weighted imaging and diffusion tensor imaging (DTI), it is possible to objectively quantify white matter structural properties in patients as well as the pharmacological effect on white matter. In the preclinical domain, these strategies, however, have been hindered by a lack of in vivo imaging assays. One preclinical approach that has been used to pharmacologically challenge the integrity of the white matter is the chronic administration of the copper chelator, cuprizone. In the present study, C57BL/6 mice were given 0.2% cuprizone in their diet for five weeks with or without the antipsychotic drug, quetiapine (10 mg/kg). In accordance with previous studies, myelin breakdown in cuprizone-exposed mice was measured by using T2-weighted MRI and DTI. Here, we demonstrate that cuprizone-induced white matter changes were attenuated by quetiapine treatment. These MRI-based results and trends were confirmed by histological and immunohistochemistry measures. This study suggests that the cuprizone-exposed C57BL/6 mouse is a potential animal model to investigate the impact of treatments on white matter abnormalities in schizophrenia.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
The changes in the mechanical properties of gas hydrate-bearing sediments (GHBS) induced by gas hydrate (GH) dissociation are essential to the evaluation of GH exploration and stratum instabilities. ...Previous studies present substantial mechanical data and constitutive models for GHBS at a given GH saturation under the non-dissociated condition. In this paper, GHBS was formed by the gas saturated method, GH was dissociated by depressurization until the GH saturation reached different dissociation degrees. The stress–strain curves were measured using triaxial tests at a same pore gas pressure and different confining pressures. The results show that the shear strength decreases progressively by 30%–90% of the initial value with GH dissociation, and the modulus decreases by 50% –75%. Simplified relationships for the modulus, cohesion, and internal friction angle with GH dissociated saturation were presented.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Circulating tumor cells (CTCs), as cells shed from solid tumor into the vasculature, play a significant role in tumor metastasis. In the peripheral blood, immune cells and stromal cells can interact ...with CTCs and influence their biological behaviors of survival, proliferation, dissemination, and immune evasion. These peripheral blood cells can evolve synergistically with CTCs to constitute the liquid microenvironment which is essential for tumor progression. Here, we review the mechanisms of peripheral blood cells interacting with CTCs and uncover their effects on both CTCs and tumor metastasis. Then, we introduce the applications of these CTC-associated peripheral blood cells in the clinical setting. Besides, some peripheral blood cell subsets are of additional clinical values to CTCs in cancer diagnosis and prognosis. To improve the clinical utility of CTCs, an integrative analysis of CTCs and associated peripheral blood cells should be advocated for, which could provide a novel insight into tumor biology and offer comprehensive information in cancer diagnosis, prognosis, and therapy efficacy evaluation.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OBVAL, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
In the high-light environment, young leaves accumulate anthocyanins as a photoprotection strategy. However, anthocyanin biosynthesis-related enzymes gene sequence is still unknown in the leaves of ...subtropical forest plants. There are thus few reports on the relationship between the expression level of these genes and photoprotection. In this study, Machilus chinensis and Castanopsis chinensis were taken as plant material in a subtropical forest. Non-full-length nucleotide sequences of chalcone synthase, dihydroflavonol 4-reductase, anthocyanin synthase, and β-tubulin gene were obtained by homologous and electronic cloning. The expression of those genes was verified and analyzed, and some physiological indicators were measured. The anthocyanin content and anthocyanin synthesis-related gene expression in the young leaves of C. chinensis were significantly higher than that of M. chinensis. Although young leaves of M. chinensis did not accumulate anthocyanins, they showed higher antioxidants and nonphotochemical quenching (NPQ). This study indicates that anthocyanins, antioxidants, and NPQ together mediate the positive effects on photoadaptation in young leaves.
Cathelicidins such as the human 37-amino acid peptide (LL-37) are peptides that not only potently kill microbes but also trigger inflammation by enabling immune recognition of endogenous nucleic ...acids. Here, a detailed structure–function analysis of LL-37 was performed to understand the details of this process. Alanine scanning of 34-amino acid peptide (LL-34) showed that some variants displayed increased antimicrobial activity against Staphylococcus aureus and group A Streptococcus. In contrast, different substitutions clustered on the hydrophobic face of the LL-34 alpha helix inhibited the ability of those variants to promote type 1 interferon expression in response to U1 RNA or to present U1 to the scavenger receptor (SR) B1 on the keratinocyte cell surface. Small-angle X-ray scattering experiments of the LL-34 variants LL-34, F5A, I24A, and L31A demonstrated that these peptides form cognate supramolecular structures with U1 characterized by inter-dsRNA spacings of approximately 3.5 nm, a range that has been previously shown to activate toll-like receptor 3 by the parent peptide LL-37. Therefore, while alanine substitutions on the hydrophobic face of LL-34 led to loss of binding to SRs and the complete loss of autoinflammatory responses in epithelial and endothelial cells, they did not inhibit the ability to organize with U1 RNA in solution to associate with toll-like receptor 3. These observations advance our understanding of how cathelicidin mediates the process of innate immune self-recognition to enable inert nucleic acids to trigger inflammation. We introduce the term “innate immune vetting” to describe the capacity of peptides such as LL-37 to enable certain nucleic acids to become an inflammatory stimulus through SR binding prior to cell internalization.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Neutrophils are crucial for host defense but are notorious for causing sterile inflammatory damage. Activated neutrophils in inflamed tissue can liberate histone H4, which was recently shown to ...perpetuate inflammation by permeating membranes via the generation of negative Gaussian curvature (NGC), leading to lytic cell death. Here, we show that it is possible to build peptides or proteins that cancel NGC in membranes and thereby suppress pore formation, and demonstrate that they can inhibit H4 membrane remodeling and thereby reduce histone H4-driven lytic cell death and resultant inflammation. As a demonstration of principle, we use apolipoprotein A-I (apoA-I) mimetic peptide apoMP1. X-ray structural studies and theoretical calculations show that apoMP1 induces nanoscopic positive Gaussian curvature (PGC), which interacts with the NGC induced by the N-terminus of histone H4 (H4n) to inhibit membrane permeation. Interestingly, we show that induction of PGC can inhibit membrane-permeating activity in general and “turn off” diverse membrane-permeating molecules besides H4n. In vitro experiments show an apoMP1 dose-dependent rescue of H4 cytotoxicity. Using a mouse model, we show that tissue accumulation of neutrophils, release of neutrophil extracellular traps (NETs), and extracellular H4 all strongly correlate independently with local tissue cell death in multiple organs, but administration of apoMP1 inhibits histone H4-mediated cytotoxicity and strongly prevents organ tissue damage.
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IJS, KILJ, NUK, PNG, UL, UM
The heavy rare-earth GdFeO3-type RFeO3 (R = Dy, Ho and Er) orthoferrites (space group Pnma, N 62) show spin reorientation transition characterized by a turning point on the magnetization curves. The ...basic Arrott plots curves showing positive slopes confirm the second-order nature of the spin reorientation and the transition temperature TSR is estimated to be ∼45 K, ∼53 K and ∼94 K for DyFeO3, HoFeO3 and ErFeO3, respectively. In addition, magnetic entropy change −ΔSM of the three samples is calculated to be 11.4, 9.8 and 7.4 J kg−1 K−1 at 10 K and 50 kOe, respectively. The field sensitive antiferromagnetic state and competitive magnetocaloric performances in RFeO3 have been attracting considerable interest for the possible applications in spintronic devices.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
•The sample of Co(Cr0.9Fe0.1)2O4 with various crystallite size is prepared by annealing at different temperatures.•Compensation effect and negative magnetization are observed in samples S3-S6 with ...larger crystallite size.•The critical temperature of positive and negative magnetic states can be manipulated by changing the crystallite size.•Both normal and inverse magnetocaloric effects are realized in Co(Cr0.9Fe0.1)2O4.
The effect of annealing temperature on crystalline structure and magnetic behaviors are experimentally investigated for Co(Cr0.9Fe0.1)2O4 with cubic spinel structure (space group Fd3¯m, No. 227). The average crystallite size shows an increase with the increased annealing temperature (700–1200 ºC). Magnetic compensation effect and negative magnetization are observed in temperature dependent magnetization M(T) curves of samples S3-S6 with larger crystallite size, which are respectively characterized by M(T) = 0 and M(T) < 0 under a stable positive magnetic field of 100 Oe. However, the phenomena are absent in S1-S2 due to the reduction of spontaneous magnetization in samples with smaller crystallite size. Furthermore, magnetization reversal occurs to be almost the same as compensation temperature Tcomp characterized by an abrupt change in M(T) curves under a higher magnetic field. This work provides a route for the manipulation of magnetism or magnetization state by annealing the sample at different temperatures.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Background
Diabetes can result in pathological changes to enteric nervous system. Our aim was to test the dynamic changes of enteric neurons and identify the role of enteric glial cells (EGCs) in ...regulating enteric neuron expression in diabetic rats.
Methods
A single injection of streptozotocin (STZ) was used to establish diabetic rats. Animals were randomly distributed into diabetic 1‐, 4‐, 8‐, and 16‐week groups, as well as age‐matched control groups. The PGP9.5‐ and glial fibrillary acidic protein (GFAP)‐immunopositive cells were quantified by immunohistochemistry. The protein levels of PGP9.5, ChAT, nNOS, S‐100β, and c‐fos were determined by western blotting. The levels of nerve growth factor (NGF), neurotrophin 3 (NT‐3), and glial cell‐derived neurotrophic factor (GDNF) were tested by ELISA.
Key Results
An increase in blood glucose and a decrease in body weight were observed following STZ administration. PGP9.5 expression did not change in the diabetic ileum. However, ChAT increased after 16 weeks, and nNOS decreased after 8 and 16 weeks in the ilea of diabetic rats. The absence of degeneration of enteric neurons during the acute stage of the disease could be the consequence of the up‐regulation of GFAP, S‐100β, and c‐fos. Moreover, the content of NGF, NT‐3, and GDNF in the ileum increased by varying degrees after 1 and/or 4 weeks of diabetes. Using 2 co‐culture models of EGCs and SH‐SY5Y cells in a high glucose condition, the supportive role of EGCs was further confirmed.
Conclusions & Inferences
Enteric glial cell activation can protect enteric neurons from damage due to diabetes in the acute stage of the disease, in part via the promotion of neurotrophin release.
Diabetes can result in pathological changes to the enteric nervous system. However, the dynamic changes of enteric neurons and the role of EGCs in regulating enteric neuron expression in rats with diabetes have not been elucidated.
We found that EGC activation protected enteric neurons from damage due to diabetes in the acute stage of the disease, in part via the promotion of neurotrophin release.
The protective effect of EGCs in diabetic neuropathy provides further direction on disease intervention in humans.
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DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK