139,197 research outputs found
Infrared properties of single crystal SrTiO3, a substrate for high temperature superconducting films
No full textParticipation of c-FLIP in NLRP3 and AIM2 inflammasome activation
No full textCellular FLICE-inhibitory protein (c-FLIP) is an inhibitor of caspase-8 and is required for macrophage survival. Recent studies have revealed a selective role of caspase-8 in noncanonical IL-1 beta production that is independent of caspase-1 or inflammasome. Here we demonstrated that c-FLIPL is an unexpected contributor to canonical inflammasome activation for the generation of caspase-1 and active IL-1 beta. Hemizygotic deletion of c-FLIP impaired ATP-and monosodium uric acid (MSU)-induced IL-1 beta production in macrophages primed through Toll-like receptors (TLRs). Decreased IL-1 beta expression was attributed to a reduced activation of caspase-1 in c-FLIP hemizygotic cells. In contrast, the production of TNF-alpha was not affected by downregulation in c-FLIP. c-FLIPL interacted with NLRP3 or procaspase-1. c-FLIP is required for the full NLRP3 inflammasome assembly and NLRP3 mitochondrial localization, and c-FLIP is associated with NLRP3 inflammasome. c-FLIP downregulation also reduced AIM2 inflammasome activation. In contrast, c-FLIP inhibited SMAC mimetic-, FasL-, or Dectin-1-induced IL-1 beta generation that is caspase-8-mediated. Our results demonstrate a prominent role of c-FLIPL in the optimal activation of the NLRP3 and AIM2 inflammasomes, and suggest that c-FLIP could be a valid target for treatment of inflammatory diseases caused by over-activation of inflammasomes
Measurement of the ratio of prompt χ c to J / ψ production in pp collisions at √s = 7 TeV
Full text linkThe prompt production of charmonium χ c and J / ψ states is studied in proton-proton collisions at a centre-of-mass energy of √s = 7 TeV at the Large Hadron Collider. The χ c and J / ψ mesons are identified through their decays χ c → J / ψ γ and J / ψ → μ + μ - using 36 pb - 1 of data collected by the LHCb detector in 2010. The ratio of the prompt production cross-sections for χ c and J / ψ, σ (χ c → J / ψ γ) / σ (J / ψ), is determined as a function of the J / ψ transverse momentum in the range 2 < p T J / ψ < 15 GeV / c. The results are in excellent agreement with next-to-leading order non-relativistic expectations and show a significant discrepancy compared with the colour singlet model prediction at leading order, especially in the low p T J / ψ region
The Effect of Stress, BCG Vaccination,and Combination of Stress-BCG Vaccination to The Ability of Macrophage to Bind with CD4+ T Cells in BALB/c Mice
Full text linkThe Effect of Stress, BCG Vaccination,and Combination of Stress-BCG Vaccination to The Ability of Macrophage to Bind with CD4+ T Cells in BALB/c Mice
Rahajeng N. Tunjung*, Dwi Pudjonarko**
Background. BCG has been recognized as potentiator for cellular immune system, while stress has been reported to suppress it.
Objective. This research was emphasized on the effect of electric foot shock as stressor and BCG vaccination in cellular immune alteration through the evaluation of CD4+ T cells bound to macrophage.
Methods. This research adopted Laboratory Experimental and Post-Test Only Group Design. The 24 female BALB/c mice (6-8 week old with average weight of 21.88 ± 1.75 grams) were obtained from PUSVETMA (Pusat Veterinaria Farma Surabaya). All mice were then divided into four groups and received standard lab diet daily. The first group (control group=C) received no other additional treatment. The second group (BCG group=B) received intraperitoneal injection of 0.1 cc BCG on day 1 and 11. The third group (electric foot shock group=E) received electric foot shock (EFS) with increasing amount and length of sessions for ten days. The fourth group received intraperitoneal injection of 0.1 cc BCG on day 1 and day 11 along with electric foot shock with increasing amount and length of sessions for ten days (EFS+BCG group=EB). At day 21 all groups received intravenous injection of 104 live Listeria monocytogenes (LD50=2x105 bacteria) and terminated on day 26.
Results. The result showed significant differences in the amount of CD4+ T cells bound to macrophage (p < 0.05) among the groups. The lowest number of binding was found in group E. The significant difference was found between group BE and both group C and E (p < 0.05).
Conclusion. It can be concluded that stress caused suppression of the macrophage ability to bind with CD4+ T cells, while the BCG caused its enhancement. The BCG vaccination may prevent the decrease of macrophage ability to bind with CD4+ T cells in BALB/c mice caused by stress.
Keywords: Stress, BCG, CD4+ T cells bindin
Letter from Carl T. Hayden to C. H. Gensler, Havasupai Reservation
No full textLetter from Carl T. Hayden to C. H. Gensler, Havasupai Indian Reservation, regarding Hualapai and Cataract Canyons geography
Mellin-Transform-Based Performance Analysis of FFH -ary FSK Using Product Combining for Combatting Partial-Band Noise Jamming
No full text
Conversion of Surface Energy and Manipulation of Single Droplet across Micro Textured Surfaces
No full textHeterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
Full text linkIFN-γ and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4(+) and CD8(+) T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN-γ(-/-) mice during P. berghei ANKA infection. The expansion of splenic CD4(+) and CD8(+) T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-γ(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-γ(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN-γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended on active IFN-γ-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells
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