968 research outputs found
Frustrated minority spins in GeNi2O4
Recently, two consecutive phase transitions were observed, upon cooling, in
an antiferromagnetic spinel GeNiO at K and
K, respectively \cite{matsuno, crawford}. Using unpolarized and polarized
elastic neutron scattering we show that the two transitions are due to the
existence of frustrated minority spins in this compound. Upon cooling, at
the spins on the \kagome planes order ferromagnetically in the
plane and antiferromagnetically between the planes (phase I), leaving the spins
on the triangular planes that separate the \kagome planes frustrated
and disordered. At the lower , the triangular spins also order in the
plane (phase II). We also present a scenario involving exchange
interactions that qualitatively explains the origin of the two purely magnetic
phase transitions
Characteristics of Japanese wrestlers with respect to function and structure of limbs
It is well known that hypertrophy and strength gain of the human skeletal muscle are induced by muscle training. It has also been shown that the training effect on size and strength of the skeletal muscle are altered the different athletic training protocols (1, 4). From these findings, it seems possible that wrestlers possess the hypertrophied muscle and stronger muscle strength by specific training.
In the present study, we assess the functional and structural characteristics of the skeletal muscle in Japanese wrestlers
Analysis of adam12-mediated ephrin-a1 cleavage and its biological functions
Accumulating evidence indicates that an elevated ephrin-A1 expression is positively correlated with a worse prognosis in some cancers such as colon and liver cancer. The detailed mechanism of an elevated ephrin-A1 expression in a worse prognosis still remains to be fully elucidated. We previously reported that ADAM12-cleaved ephrin-A1 enhanced lung vascular permeability and thereby induced lung metastasis. However, it is still unclear whether or not cleaved forms of ephrin-A1 are derived from primary tumors and have biological activities. We identified the ADAM12-mediated cleavage site of ephrin-A1 by a Matrix-assisted laser desorption ionization mass spectrometry and checked levels of ephrin-A1 in the serum and the urine derived from the primary tumors by using a mouse model. We found elevated levels of tumor-derived ephrin-A1 in the serum and the urine in the tumor-bearing mice. Moreover, inhibition of ADAM-mediated cleavage of ephrin-A1 or antagonization of the EphA receptors resulted in a significant reduction of lung metastasis. The results suggest that tumor-derived ephrin-A1 is not only a potential biomarker to predict lung metastasis from the primary tumor highly expressing ephrin-A1 but also a therapeutic target of lung metastasis
Vibrational properties of phonons in random binary alloys: An augmented space recursive technique in the k-representation
We present here an augmented space recursive technique in the
k-representation which include diagonal, off-diagonal and the environmental
disorder explicitly : an analytic, translationally invariant, multiple
scattering theory for phonons in random binary alloys.We propose the augmented
space recursion (ASR) as a computationally fast and accurate technique which
will incorporate configuration fluctuations over a large local environment. We
apply the formalism to , Ni_{88}Cr_12} and
alloys which is not a random choice. Numerical results on spectral functions,
coherent structure factors, dispersion curves and disordered induced FWHM's are
presented. Finally the results are compared with the recent itinerant coherent
potential approximation (ICPA) and also with experiments.Comment: 20 pages, LaTeX, 23 figure
Phase transition in the collisionless regime for wave-particle interaction
Gibbs statistical mechanics is derived for the Hamiltonian system coupling
self-consistently a wave to N particles. This identifies Landau damping with a
regime where a second order phase transition occurs. For nonequilibrium initial
data with warm particles, a critical initial wave intensity is found: above it,
thermodynamics predicts a finite wave amplitude in the limit of infinite N;
below it, the equilibrium amplitude vanishes. Simulations support these
predictions providing new insight on the long-time nonlinear fate of the wave
due to Landau damping in plasmas.Comment: 12 pages (RevTeX), 2 figures (PostScript
Overexpression of the JmjC histone demethylase KDM5B in human carcinogenesis: involvement in the proliferation of cancer cells through the E2F/RB pathway.
BACKGROUND: Although an increasing number of histone demethylases have been identified and biochemically characterized, their biological functions largely remain uncharacterized, particularly in the context of human diseases such as cancer. We investigated the role of KDM5B, a JmjC histone demethylase, in human carcinogenesis. Quantitative RT-PCR and microarray analyses were used to examine the expression profiles of histone demethylases in clinical tissue samples. We also examined the functional effects of KDM5B on the growth of cancer cell lines treated with small interfering RNAs (siRNAs). Downstream genes and signal cascades induced by KDM5B expression were identified from Affymetrix Gene Chip experiments, and validated by real-time PCR and reporter assays. Cell cycle-dependent characteristics of KDM5B were identified by immunofluorescence and FACS. RESULTS: Quantitative RT-PCR analysis confirmed that expression levels of KDM5B are significantly higher in human bladder cancer tissues than in their corresponding non-neoplastic bladder tissues (P < 0.0001). The expression profile analysis of clinical tissues also revealed up-regulation of KDM5B in various kinds of malignancies. Transfection of KDM5B-specific siRNA into various bladder and lung cancer cell lines significantly suppressed the proliferation of cancer cells and increased the number of cells in sub-G1 phase. Microarray expression analysis indicated that E2F1 and E2F2 are downstream genes in the KDM5B pathway. CONCLUSIONS: Inhibition of KDM5B may affect apoptosis and reduce growth of cancer cells. Further studies will explore the pan-cancer therapeutic potential of KDM5B inhibition.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are
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Exploring the Role of Platelets in Virus-Induced Inflammatory Demyelinating Disease and Myocarditis
Data Availability Statement:
The data generated for this study can be found in the GEO at the NCBI (accession no. GSE253385, https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE253385 (accessed on 15 March 2024)).Supplementary Materials:
The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/ijms25063460/s1 .Theiler’s murine encephalomyelitis virus (TMEV) infection has been used as a mouse model for two virus-induced organ-specific immune-mediated diseases. TMEV-induced demyelinating disease (TMEV-IDD) in the central nervous system (CNS) is a chronic inflammatory disease with viral persistence and an animal model of multiple sclerosis (MS) in humans. TMEV infection can also cause acute myocarditis with viral replication and immune cell infiltration in the heart, leading to cardiac fibrosis. Since platelets have been reported to modulate immune responses, we aimed to determine the role of platelets in TMEV infection. In transcriptome analyses of platelets, distinct sets of immune-related genes, including major histocompatibility complex (MHC) class I, were up- or downregulated in TMEV-infected mice at different time points. We depleted platelets from TMEV-infected mice by injecting them with platelet-specific antibodies. The platelet-depleted mice had significantly fewer viral antigen-positive cells in the CNS. Platelet depletion reduced the severities of TMEV-IDD and myocarditis, although the pathology scores did not reach statistical significance. Immunologically, the platelet-depleted mice had an increase in interferon (IFN)-γ production with a higher anti-TMEV IgG2a/IgG1 ratio. Thus, platelets may play roles in TMEV infection, such as gene expression, viral clearance, and anti-viral antibody isotype responses.This work is supported by the Ministry of Education, Culture, Sports, Science and Technology, Japan, through the Monbukagakusho (MEXT, 2021-2025) Scholarship (I.A.), Grant-in Aid for Scientific Research KAKENHI from the Japan Society for the Promotion of Science (JSPS) (JP22K07527 (S.O.), JP23K06493 (F.S.), JP21K07167 (H.T.), and JP22K18378 and JP23K08901 (I.T.)), Novartis Pharma Research Grants (S.O. and I.T.), the Royal Society Wolfson Foundation (RSWF\R3\183001, (F.N.E.G.)), the Hokkaido Lawyer Association for Hepatitis B (Orange funding) (H.T.), and Hokkaido Organization for Translational Research (A seeds) (H.T.)
Long-time discrete particle effects versus kinetic theory in the self-consistent single-wave model
The influence of the finite number N of particles coupled to a monochromatic
wave in a collisionless plasma is investigated. For growth as well as damping
of the wave, discrete particle numerical simulations show an N-dependent long
time behavior resulting from the dynamics of individual particles. This
behavior differs from the one due to the numerical errors incurred by Vlasov
approaches. Trapping oscillations are crucial to long time dynamics, as the
wave oscillations are controlled by the particle distribution inhomogeneities
and the pulsating separatrix crossings drive the relaxation towards thermal
equilibrium.Comment: 11 pages incl. 13 figs. Phys. Rev. E, in pres
Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium
Several deleterious intra-acinar phenomena are simultaneously triggered on initiating acute pancreatitis. These culminate in acinar injury or inflammatory mediator generation in vitro and parenchymal damage in vivo. Supraphysiologic caerulein is one such initiator which simultaneously activates numerous signaling pathways including non-receptor tyrosine kinases such as of the Src family. It also causes a sustained increase in cytosolic calcium- a player thought to be crucial in regulating deleterious phenomena. We have shown Src to be involved in caerulein induced actin remodeling, and caerulein induced changes in the Golgi and post-Golgi trafficking to be involved in trypsinogen activation, which initiates acinar cell injury. However, it remains unclear whether an increase in cytosolic calcium is necessary to initiate acinar injury or if injury can be initiated at basal cytosolic calcium levels by an alternate pathway. To study the interplay between tyrosine kinase signaling and calcium, we treated mouse pancreatic acinar cells with the tyrosine phosphatase inhibitor pervanadate. We studied the effect of the clinically used Src inhibitor Dasatinib (BMS-354825) on pervanadate or caerulein induced changes in Src activation, trypsinogen activation, cell injury, upstream cytosolic calcium, actin and Golgi morphology. Pervanadate, like supraphysiologic caerulein, induced Src activation, redistribution of the F-actin from its normal location in the sub-apical area to the basolateral areas, and caused antegrade fragmentation of the Golgi. These changes, like those induced by supraphysiologic caerulein, were associated with trypsinogen activation and acinar injury, all of which were prevented by Dasatinib. Interestingly, however, pervanadate did not cause an increase in cytosolic calcium, and the caerulein induced increase in cytosolic calcium was not affected by Dasatinib. These findings suggest that intra-acinar deleterious phenomena may be initiated independent of an increase in cytosolic calcium. Other players resulting in acinar injury along with the Src family of tyrosine kinases remain to be explored. © 2013 Mishra et al
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Metallothionein I as a direct link between therapeutic hematopoietic stem/progenitor cells and cerebral protection in stroke
National Institutes of Health/National Heart, Lung, and blood Institute (NIH/NHLBI (HL125572-01A1)); Malcolm Feist Cardiovascular Fellowship program; National Institute of General Medical Sciences COBRE Grant (P30-
GM110703) and Japan Society for the Promotion of Science (Grants-in-Aid for Scientific Research-
KAKENHI, 16H07356)
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