384,122 research outputs found
Yizhou Li shi cong ke : [7 zhong] /
No full textEach work has special t. p., the last without imprint.Title from folded edge of v. 4.On double leaves, oriental style, in case.[1] Chong jiao wu yi you yi zhai du hua shi 2 juan ; Haiwang cun suo jian shu hua lu can gao -- [2] Jin bu lian yin ji / Wu Chongxi, Li Baoxun zhu -- [3] Hong ying shan guan yi chao -- [4] Jiu xue an bi ji -- [5] San yong cui mo yi ti ba 4 juan.Mode of access: Internet
SPECIFIC RECOGNITION OF N-ACETYLNEURAMINIC ACID IN THE G(M2) EPITOPE BY HUMAN G(M2) ACTIVATOR PROTEIN
No full textG(M2) Activator is a low molecular weight protein cofactor that stimulates the enzymatic conversion of G(M2) into G(M3) by human beta-hexosaminidase A and also the conversion of G(M2) into G(A2) by clostridial sialidase (Wu, Y.-Y., Lockyer, J. M., Sugiyama, E., Pavlova, N. V., Li, Y.-T., and Li, S.- C. (1994) J. Biol. Chem. 269, 16276-16283). Among the five known activator proteins for the enzymatic hydrolysis of glycosphingolipids, only G(M2) activator is effective in stimulating the hydrolysis of G(M2). However, the mechanism of action of G(M2) activator is still not well understood, Using a unique disialosylganglioside, GalNAc-G(D1a), as the substrate, we were able to show that in the presence of G(M2) activator, GalNAc-G(D1a) was specifically converted into GalNAc-G(M1a) by clostridial sialidase, while in the presence of saposin B, a nonspecific activator protein, GalNAc-G(D1a) was converted into both GalNAc-G(M1a) and GalNAc-G(M1b). individual products generated from GalNAc-G(D1a) by clostridial sialidase were identified by thin layer chromatography, negative secondary ion mass spectrometry, and immunostaining with a monoclonal IgM that recognizes the G(M2) epitope. Our results clearly show that G(M2) activator recognizes the G(M2) epitope in GalNAc-G(D1a). Thus, G(M2) activator may interact with the trisaccharide structure of the G(M2) epitope and render the GalNAc and NeuAc residues accessible to beta-hexosaminidase A and sialidase, respectively
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
Kwalita’ tal-ħajja għat-tarbija li se titwieled
No full textFl-aħħar ħmistax-il sena psikologi ewlenin ikkonfermaw permezz ta’riċerka medika u l-esperjenza klinika li t-tarbija fil-ġuf tisma ', ittiegħem,
tħoss, u titgħallem; u dak li tesperjenza jibda jifforma l-attitudnijiet u l-aspettattivi tagħha dwarha nnifisha. Huwa ta 'importanza kbira allura, li
aħna nifhmu dan is-suġġett tajjeb biżżejjed, biex inkunu nistgħu nipprovdu l-aħjar ambjent u ħajja ta’ kwalita’ għat-tarbija fil-ġuf.
Iżda ħa niehdu pass wieħed wara l-ieħor ... Nixtieq li naqsam dawn il-ftit ħsibijiet magħkom, liebsa l-kpiepel differenti tiegħi ta’ social worker u
akkademika fil-qasam, ħaddiema volontarja maż-żgħażagħ u adulti għal ħafna snin, chairperson tal-kummissjoni nazzjonali familja - fejn aħna
nikkonċernaw ruhna dwar il-benesseri tal-membri kollha tal-familja – u fl-aħħar u mhux l-inqas omm ta 'żewġt itfal u omm li esperjenzajt it-telfa u
l-uġigħ ta’ miscarriage. Dan ma kienx sempliċiment esperjenza medika, iżda esperjenza profondament emozzjonali!
Jiena ħdimt u għadni naħdem ma' żgħażagħ u adulti li jkunu qed jesperjenzaw sens profond ta' rifjut, ansjetà, sens li qatt ma jistgħu jogħġbu lil
ħadd, wisq inqas lilhom infushom. Permezz ta’ ħidma intensiva, spiss jirnexxielna nittraċċaw l-għeruq ta 'dawn il-kwistjonijiet, għall-ħajja
tagħhom fil-ġuf. Tfal mhux mixtieqa, tfal mhux ippjanati; tfal li ommhom riedu jabortixxu; tfal li baqgħu ħajjin wara attentat ta’ abort ... it-taqlib
psikoloġiku u emozzjonali li jkunu qed jesperjenzaw fil-ħajja tagħhom huwa ta’ qsim il-qalb. Qrajt u qsamt hafna stejjer kliniċi ta' psikoterapewti u
ta' counsellors li esperjenzaw sitwazzjonijiet simili. Ir-riċerka fil-qasam qed tindika b'mod ċar li t-tarbija fil-ġuf hija sensittiva, tħoss, hija konxja u
tista’ tiftakar. Psikologi prenatali huma konvinti li l-qofol tal-personalità tal-bniedem tifforma fil-ġuf. Studji juru li din il-formazzjoni tal-personalità
isseħħ permezz ta' komunikazzjoni intensiva bejn il-ġenituri - speċjalment l-omm - u t-tarbija fil-ġuf. Hija l-kombinazzjoni ta' dawn ir-realtajiet li wassluni biex nagħżel li nitkellem dwar dan is-suġġett. Nemmen bis-sħiħ li nistgħu niżguraw li t-tfal
jikbru f’ambjent kemm jista’ jkun pożittiv, mill-mument tal-konċepiment. Il-ġuf huwa d-dinja ewlenija tat-tfal – u dawn it-tfal jistgħu jesperjenzaw
din id-dinja bħala faċli jew bħala ostili. Huwa inkontestabbli li l-kwalità tal-ambjent u l-kwalita’ tal-ħajja fil-ġuf, hija determinata prinċipalment millġenituri.peer-reviewe
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
No full textIFN-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
An Investigation of Transitional Phenomena from Laminar to Turbulent Natural Convection using Compressible Direct Numerical Simulation
No full textThe transitional phenomena from laminar to turbulent natural convection and the development process inside the channel are investigated using compressible direct numerical simulation (DNS). Numerical method of Roe scheme with preconditioning and dual time stepping are used for addressing natural convection flows with large temperature differences, which are low speed but the densities are variable. The results are qualitatively well consistent with the experimental data [1] and the transition point can be accurately captured. In addition, the development process respected to time can be clearly identified for four stages, which are laminar, unstable process, reliminarization and turbulence. After reaching the quasi-steady state, it can be observed that the laminar, transition and turbulence coexist in the same flow filed. Most important of all, the transitional phenomena are naturally induced by the effects of interactions between the buoyancy and shear stress without adding any fluctuations at inlet. It means that the numerical scheme and physical model adopted in this study has the potential to be a universal case for estimating the accuracy of turbulence model because the characteristics of parameters-free and independence from inlet condition
Early Growth Response genes 2 and 3 play a role in chronic inflammation pathology and are essential for the differentiation of T follicular helper cells
No full textThis thesis was submitted for the award of Doctor of Philosophy and was awarded by Brunel University LondonThe Early Growth Response genes 2 and 3 (Egr2/3) are zinc finger transcription factors that play an important role in the immune system. These transcription factors have reported functions in T cell receptor signaling, differentiation of effector T cell subsets and the development of lupus-like autoimmune diseases. Using CD2-Egr2-/- Egr3-/- mouse model, I investigate the development of inflammation pathology, differentiation of T follicular helper (Tfh) cells and the formation of germinal centers (GC) following viral challenge within these mice. The onset of inflammation pathology in CD2-Egr2-/- Egr3-/- mice was discovered to correlate with high levels of pro-inflammatory cytokines in the serum and the development of autoimmune diseases as previously reported by Li et al, 2012. Most importantly, a novel role for the Egr2/3 genes in the differentiation of T follicular helper (Tfh) cells was identified. Tfh cells are responsible for T cell dependent antibody immune response in the GC. They support the differentiation of GC B cells into plasma cells producing long lived high-affinity isotype-switched antibodies and memory B cells. Tfh cell differentiation is regulated by Bcl6 however; the regulators of Bcl6 during Tfh differentiation remain largely unknown. We have now discovered that Egr2/3 genes are required for Bcl6 expression during Tfh cell differentiation. In the absence of the Egr2 and 3 genes, Tfh cell differentiation is severely impaired and GC formation and functions were defective in response to Vaccinia Virus Western Reserve strain (VVWR) infection. Further investigation revealed that Egr2 regulated Bcl6 expression in a Tfh-specific manner as adoptive transfer of WT CD4+ T cells into Egr2-/- Egr3-/- mice was able to rescue Bcl6 expression, Tfh differentiation and GC formation. When the molecular mechanism of how Egr2 regulated Bcl6 was investigated, it was uncovered that Egr2 directly bound to the promoter region of Bcl6 gene in CD4 T cells to regulated Bcl6 expression. Indeed constitutive expression of either Egr2 or Bcl6 in CD2-Egr2-/- Egr3-/- CD4+ T cells rescued Tfh cell differentiation and GC formation. Our results inferred that the Egr2/3 genes are essential for Tfh differentiation and GC formation by regulating Bcl6 expression in CD4 T cells under Tfh condition. Our studies thus suggest that the Egr2/3 genes are paramount for minimising immunopathology and are also critical for efficient antibody production by regulating Tfh cell differentiation
Modulation of antigen-specific T-cells as immune therapy for chronic infectious diseases and cancer
No full textCopyright: © 2014 Li, Symonds, Miao, Sanderson and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.This article has been made available through the Brunel Open Access Publishing Fund.T-cell responses are induced by antigen presenting cells (APC) and signals from the microenvironment. Antigen persistence and inflammatory microenvironments in chronic infections and cancer can induce a tolerant state in T-cells resulting in hyporesponsiveness, loss of effector function, and weak biochemical signaling patterns in response to antigen stimulation. Although the mechanisms of T-cell tolerance induced in chronic infection and cancer may differ from those involved in tolerance to self-antigen, the impaired proliferation and production of IL-2 in response to antigen stimulation are hallmarks of all tolerant T cells. In this review, we will summarize the evidence that the immune responses change from non-self to “self”-like in chronic infection and cancer, and will provide an overview of strategies for re-balancing the immune response of antigen-specific T cells in chronic infection and cancer without affecting the homeostasis of the immune system.Arthritis Research UK and Medical Research Council UK
NanoAPC deliver antigen, IL-2 and co-stimulatory molecules to antigen specific T cells and activate viral specific T cells in chronic infections
No full textThis thesis was submitted for the degree of Doctor of Philosophy and awarded by Brunel University.The study of the immune system has provided insight in the mechanism of protection induced by vaccination; primarily that most clinically protective vaccines are potent in generating neutralizing antibody responses. However, vaccination fails to protect against a wide range of acquired chronic infections caused by viruses, such as HIV, HBV and HCV. One of the major reasons for weak responses to therapeutic vaccine is the impaired function of effector T cells resulting from viral persistence. Although IL-2 can potently increase effect function of viral specific T cells, systemic administration of IL-2 induces organ pathology and expansion of Treg cells.
In this study, we have now developed a novel vaccine delivery system IL-2-nanoAPC delivering antigen-MHC complexes (pMHC), co-stimulatory molecules and IL-2 to antigen specific T cells. NanoAPC are derived from the endoplasmic reticulum (ER) membranes of human B cell line 721.221 engineered with selected HLA allele and IL-2 as the ER retention proteins. The IL-2-nanoAPC interacted with antigen specific T cells, induced immune synapses and expression of high affinity
IL-2 receptor and enhanced effector function of antigen specific T cells, but did not affect bystander T cells and Foxp3+ Treg cells. Together with pMHC, co-stimulatory molecules, the selective delivery of IL-2 not only increased the CD4 and CD8 T cell responses to viral antigens but also enhanced TCR proximal signalling and suppressed expression of PD1 molecules on IFNγ producing effector CD8 T cells. We also found that the co-induction of T helper responses by IL-2-nanoAPC in a mixed culture could increase CD8 T cell responses to viral antigen. The IL-2-nanoAPC effectively induced responses of CD4 and CD8 T cells from chronic HBV patients. The results demonstrate that selective delivery of IL-2, together with pMHC and co-stimulatory molecules, by nanoAPC to antigen specific T cells has potential to recover anti-viral immune responses in chronic HBV patients
GABI-Kat SimpleSearch: an Arabidopsis thaliana T-DNA mutant database with detailed information for confirmed insertions
No full textLi Y, Rosso MG, Viehöver P, Weisshaar B. GABI-Kat SimpleSearch: an Arabidopsis thaliana T-DNA mutant database with detailed information for confirmed insertions. Nucleic Acids Research. 2007;35(Database):D874-D878
- …
