571 research outputs found
The expression patterns of nogo-A, myelin associated glycoprotein and oligodendrocyte myelin glycoprotein in the retina after ocular hypertension : the expression of myelin proteins in the retina in glaucoma
Nogo-A, a major myelin inhibitory protein, inhibits axon growth and synaptic function in the central nervous system. Glaucoma is a progressive neuropathy as a result of retinal ganglion cell (RGC) death. Synaptic degeneration is thought to be an early pathology of neurodegeneration in glaucoma and precedes RGC loss. Here experimental ocular hypertension model was induced in adult rats with laser coagulation of the episcleral and limbal veins. The expression of Nogo-A, myelin-associated glycoprotein (MAG) and oligodendrocyte myelin glycoprotein (OMgp) in the retina was investigated using immunohistochemistry and Western blotting. We found that Nogo-A was expressed in the RGCs and upregulated after the induction of ocular hypertension. OMgp was only expressed in the inner plexiform layer. There was no MAG expression in the retina. Our data provided, for the first time, the expression patterns of three myelin proteins in the adult retina and suggested an important role of Nogo-A in the RGC death and synaptic degeneration in glaucoma. © 2011 Springer Science+Business Media, LLC.postprin
Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay
The decay channel
is studied using a sample of events collected
by the BESIII experiment at BEPCII. A strong enhancement at threshold is
observed in the invariant mass spectrum. The enhancement can be fit
with an -wave Breit-Wigner resonance function with a resulting peak mass of
and a
narrow width that is at the 90% confidence level.
These results are consistent with published BESII results. These mass and width
values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics
Loureirin B, an essential component of Sanguis Draxonis, inhibits Kv1.3 channel and suppresses cytokine release from Jurkat T cells
Sanguis draxonis (SD), also known as “Dragon’s Blood”, is a traditional herb medicine that has been used to treat a variety of complications with unknown mechanisms. Recent studies show that SD displays immunosuppressive activities and improves symptoms of type I diabetes in animal models. However, the mechanisms underlying SD’s immunosuppressive actions are not completely understood. The voltage-gated Kv1.3 channel plays a critical role in the pathogenesis of autoimmune diseases by regulating the functions of both T cells and B cells. Here we investigated the effect of SD and one of its active components loureirin B (LrB) on Kv1.3. Both SD and LrB inhibited Kv1.3-mediated currents, produced a membrane depolarization, and reduced Ca(2+) influx in Jurkat T cells. In addition, application of LrB inhibited phytohemagglutinin (PHA)-induced IL-2 release from activated Jurkat T cells. Furthermore, point mutations in the selective filter region significantly reduced the inhibitory effect of LrB on Kv1.3. The results of these experiments provide evidence that LrB is a channel blocker of Kv1.3 by interacting with amino acid residues in its selective filter region. Direct inhibition of Kv1.3 in T cells by SD and LrB might be the cellular and molecular basis of SD-mediated immunosuppression
Development of microspheres for biomedical applications: a review
An overview of microspheres manufactured for use in biomedical applications based on recent literature is presented in this review. Different types of glasses (i.e. silicate, borate, and phosphates), ceramics and polymer-based microspheres (both natural and synthetic) in the form of porous , non-porous and hollow structures that are either already in use or are currently being investigated within the biomedical area are discussed. The advantages of using microspheres in applications such as drug delivery, bone tissue engineering and regeneration, absorption and desorption of substances, kinetic release of the loaded drug components are also presented. This review also reports on the preparation and characterisation methodologies used for the manufacture of these microspheres. Finally, a brief summary of the existing challenges associated with processing these microspheres which requires further research and development are presented
Measurement of the matrix element for the decay η′→ηπ +π -
The Dalitz plot of η⊃′→ηπ⊃+π⊃- decay is studied using (225.2±2.8)×106 J/ψ events collected with the BESIII detector at the BEPCII e⊃+e⊃- collider. With the largest sample of η⊃′ decays to date, the parameters of the Dalitz plot are determined in a generalized and a linear representation. Also, the branching fraction of J/ψ→γη⊃′ is determined to be (4.84±0.03±0.24)×10⊃-3, where the first error is statistical and the second systematic. © 2011 American Physical Society.published_or_final_versio
Knockdown of TREML2 Alleviates Neuropathological Hallmarks and Cognitive Deficiency in a Model of Sporadic Alzheimer’s Disease
Xin-Xin Fu,1,2,* Zhi-Hang Huang,1,* Shi-Yao Wang,1,* Jing-Wen Qi,1 Zi-Jian Luo,3 Yan E,1 Ying-Dong Zhang,1 Teng Jiang1 1Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People’s Republic of China; 2Department of Pharmacology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People’s Republic of China; 3The First School of Clinical Medicine, Nanjing Medical University, Nanjing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Teng Jiang, Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, People’s Republic of China, Email [email protected]: Recently, we revealed that triggering receptor expressed on myeloid cells-like 2 (TREML2) modulated inflammation by regulating microglial polarization and NLRP3 inflammasome activation. However, the role of TREML2 in Alzheimer’s disease (AD) pathogenesis remains poorly understood. In this study, we tried to observe the impact of TREML2 on neuropathological hallmarks (including amyloid-β (Aβ) pathology, hyperphosphorylated tau and neuroinflammation) and cognitive deficiency in senescence-accelerated mouse prone substrain 8 (SAMP8) mice, an animal model of sporadic AD.Methods: A lentiviral-based strategy was employed to manipulate TREML2 levels in the brain of SAMP8 mice. Enzyme-linked immunosorbent assay was used to detect the protein levels of inflammatory cytokines, Aβ42 and hyperphosphorylated tau. The mRNA levels of microglial polarization markers were assessed by qRT-PCR. Morris water maze test was performed to evaluate the spatial cognitive functions.Results: TREML2 overexpression elevated inflammatory cytokines levels, induced microglial M1-type polarization, and exacerbated Aβ and tau pathology in SAMP8 mice. Contrastingly, knocking down TREML2 mitigated inflammatory cytokines release, promoted microglial M2-type polarization, ameliorated Aβ and tau pathology, and rescued cognitive deficiency in SAMP8 mice.Conclusion: This study offers the first in vivo evidence that TREML2 contributes to the pathogenesis of AD. Furthermore, this study also proves that inhibition of TREML2 signaling may represent a potential treatment strategy for this disease.Keywords: TREML2, neuroinflammation, Alzheimer’s disease, microglia, cognitive deficienc
First observation of the decays χcJ→π0π0π0π0
We present a study of the P-wave spin-triplet charmonium χ cJ decays (J=0, 1, 2) into π0π0π0π0. The analysis is based on 106×106 ψ⊃′ decays recorded with the BESIII detector at the BEPCII electron positron collider. The decay into the π0π0π0π0 hadronic final state is observed for the first time. We measure the branching fractions B(χ c0→π0π0π0π0)=(3.34±0. 06±0.44)×10⊃-3, B(χ c1→π0π0π0π0) =(0.57±0.03±0.08)×10⊃-3, and B(χ c2→π0π0π0π0)=(1.21±0.05±0.16) ×10⊃-3, where the uncertainties are statistical and systematical, respectively. © 2011 American Physical Society.published_or_final_versio
Branching fraction measurements of χc0 and χc2 to π0π0 and ηη
Using a sample of 1.06×108 ψ ′ decays collected by the BESIII detector, χc0 and χc2 decays into π0π0 and ηη are studied. The branching fraction results are Br(χc0→π 0π0)=(3.23±0.03±0.23±0.14)×10 -3, Br(χc2→π0π0)=(8.8±0.2±0.6±0.4)×10 -4, Br(χc0→ηη)=(3.44±0.10±0. 24±0.2)×10 -3, and Br(χc2→ηη)=(6. 5±0.4±0.5±0.3)×10 -4, where the uncertainties are statistical, systematic due to this measurement, and systematic due to the branching fractions of ψ ′→ γχcJ. The results provide information on the decay mechanism of χc states into pseudoscalars. © 2010 The American Physical Society.published_or_final_versio
Study of a00(980)-f0(980) mixing
Using samples of 2.25×108 J/ψ events and 1.06×108 ψ ′ events collected with the BES III detector, we study the f 0(980)→a00(980) and a00(980)→f 0(980) transitions in the processes J/ψ→φf 0(980) →φa00(980) and χ c1→π0a00(980)→π0f 0(980), respectively. Evidence for f 0(980)→a00(980) is found with a significance of 3.4σ, while in the case of a00(980)→f 0(980) transition, the significance is 1.9σ. Measurements and upper limits of both branching ratios and mixing intensities are determined. © 2011 American Physical Society.published_or_final_versio
Planck 2015 results. XIII. Cosmological parameters
We present results based on full-mission Planck observations of temperature and polarization anisotropies of the CMB. These data are consistent with the six-parameter inflationary LCDM cosmology. From the Planck temperature and lensing data, for this cosmology we find a Hubble constant, H0= (67.8 +/- 0.9) km/s/Mpc, a matter density parameter Omega_m = 0.308 +/- 0.012 and a scalar spectral index with n_s = 0.968 +/- 0.006. (We quote 68% errors on measured parameters and 95% limits on other parameters.) Combined with Planck temperature and lensing data, Planck LFI polarization measurements lead to a reionization optical depth of tau = 0.066 +/- 0.016. Combining Planck with other astrophysical data we find N_ eff = 3.15 +/- 0.23 for the effective number of relativistic degrees of freedom and the sum of neutrino masses is constrained to < 0.23 eV. Spatial curvature is found to be |Omega_K| < 0.005. For LCDM we find a limit on the tensor-to-scalar ratio of r <0.11 consistent with the B-mode constraints from an analysis of BICEP2, Keck Array, and Planck (BKP) data. Adding the BKP data leads to a tighter constraint of r < 0.09. We find no evidence for isocurvature perturbations or cosmic defects. The equation of state of dark energy is constrained to w = -1.006 +/- 0.045. Standard big bang nucleosynthesis predictions for the Planck LCDM cosmology are in excellent agreement with observations. We investigate annihilating dark matter and deviations from standard recombination, finding no evidence for new physics. The Planck results for base LCDM are in agreement with BAO data and with the JLA SNe sample. However the amplitude of the fluctuations is found to be higher than inferred from rich cluster counts and weak gravitational lensing. Apart from these tensions, the base LCDM cosmology provides an excellent description of the Planck CMB observations and many other astrophysical data sets
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