Subjects. Twelve DBA/2J male mice, 13 DBA/2J female mice, 12 C57BL/6J male mice, and 12 C57BL/6J female mice were obtained from The Jackson Laboratories (Bar Harbor, ME). The animals were 9 to 10 weeks old at the beginning of discrimination training and were individually housed on a 12-h light/12-h dark cycle. The mice were weighed and allowed to acclimate to the laboratory for 2 weeks before training began. All mice were fed enough rodent chow (Harlan, Indianapolis, IN) at least 1 h postsession to maintain a body weight between 20 and 30 g. The Wake Forest University School of Medicine Animal Care and Use Committee approved all procedures involving these mice and procedures were conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals.. Apparatus. Drug discrimination sessions took place in standard two lever mouse operant-conditioning chambers (MED Associates, St. Albans, VT). Each chamber was equipped with two levers on the front wall of ...
Barski, G and Cassingena, R, Malignant transformation in vitro of cells from c57bl mouse normal pulmonary tissue. (1963). Subject Strain Bibliography 1963. 73 ...
Animals. The contractile performance was studied in five young (9-14 wk of age) male TR-α1-deficient mice and five wild-type control animals of the same age and weight (28-35 g). The force-frequency relationship (see below) was studied also in muscles from four female TR-α1-deficient mice and four wild-type control mice of the same age and weight. The TR-α1-deficient mice represent a cross between the SV-129/OLa and BALB/c (30). Contractile studies were performed on four male TR-β-deficient (12) and four control mice of the same age and weight as above. This group of mice has a mixed 129/Sv and C57Bl/6J genetic background, and was generated from TR-β+/ − heterozygote backcrosses. The wild-type mice were obtained from crosses of heterozygote TR-α1- or TR-β-deficient mice. The two homozygote wild-type strains were bred in parallel with the respective knockout strains. Thus the knockout strains have the same genetic background as their respective knockout strains: 129/Ola and BALB/c for ...
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Further information can be found in Supplemental Methods.. Mice, drugs, and tumor cell lines. C57BL/6 mice were purchased from Charles River Laboratories. Splenectomized and sham-operated C57BL/6, Batf3-/- (B6.129S(C)-Batf3tm1Kmm/J), zDC-DTR (B6(Cg)-Zbtb46tm1(HBEGF)Mnz/J), CD45.1, OT-I, OT-II, Gja1fl/fl (B6.129S7-Gja1tm1Dlg/J), CD11c-Cre (B6.Cg-Tg(Itgax-cre)1-1Reiz/J), B2m-/- (B6.129P2-B2mtm1Unc/J), MHCII-/- (B6.129S2-H2dlAb1-Ea/J), Ccr2-/- (B6.129S4-Ccr2tm1Ifc/J), and Ccr7-/- (B6.129P2(C)-Ccr7tm1Rfor/J) mice were from The Jackson Laboratory. zDC-DTR BM chimeras were generated by IV injection of 5 × 106 BM cells from zDC-DTR homozygous mice into CD45.1+ or CD45.2+ C57BL/6 recipient mice that had been myeloablated 4 weeks earlier as previously described (74) with some modifications. In brief, recipient mice were injected intraperitoneally (IP) with busulfan (25 μg/g; MilliporeSigma) on 2 consecutive days, followed by IV injection of donor BM cells 2 days later. DT (MilliporeSigma) was injected ...
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Analysis of polyclonal C57BL/6 repertoires. In 2 independent analyses, C57BL/6 splenocytes were sorted into CD4+GFP-Foxp3- and CD4+GFP-Foxp3+ populations and th
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TY - JOUR. T1 - CD34 expression on long-term repopulating hematopoietic stem cells changes during developmental stages. AU - Matsuoka, Sahoko. AU - Ebihara, Yasuhiro. AU - Xu, Ming Jiang. AU - Ishii, Takefumi. AU - Sugiyama, Daisuke. AU - Yoshino, Hiroshi. AU - Ueda, Takahiro. AU - Manabe, Atsushi. AU - Tanaka, Ryuhei. AU - Ikeda, Yasuo. AU - Nakahata, Tatsutoshi. AU - Tsuji, Kohichiro. PY - 2001/1/15. Y1 - 2001/1/15. N2 - The CD34 antigen serves as an important marker for primitive hematopoietic cells in therapeutic transplantation of hematopoietic stem cells (HSC) and gene therapy, but it has remained an open question as to whether or not most HSC express CD34. Using a competitive long-term reconstitution assay, the results of this study confirm developmental changes in CD34 expression on murine HSC. In fetuses and neonates, CD34 was expressed on Lin-c-Kit+ long-term repopulating HSC of bone marrow (BM), liver, and spleen. However, CD34 expression on HSC decreased with aging, and in mice older ...
The transplantation of spleen cells from old NZB/Bl mice with renal disease induced both the structural and the functional changes of membranous glomerulonephritis in young NZB/Bl mice within a few weeks and well in advance of its usual spontaneous occurrence. The development of hypergammaglobulinemia and lymphoid cell hyperplasia in the young mice indicated that immunologically competent cells, derived from either the transplant or the recipient, proliferated during this process. These experiments, together with other findings, provide further support for the view that membranous glomerulonephritis in NZB/Bl mice is produced by immunological, and probably autoimmune, mechanisms and that the renal disease is apparently almost wholly unrelated to the hemolytic process.. ...
The numbers of obese people and diabetic patients are ever increasing. Obesity and diabetes are high-risk conditions for chronic diseases, including certain types of cancer, such as colorectal cancer (CRC). The aim of this study was to develop a novel animal model in order to clarify the pathobiology of CRC development in obese and diabetic patients. We developed an animal model of obesity and colorectal cancer by breeding the C57BL/KsJ-db/db (db/db) mouse, an animal model of obesity and type II diabetes, and the C57BL/6J-ApcMin/+ (Min/+) mouse, a model of familial adenomatous polyposis. At 15 weeks of age, the N9 backcross generation of C57BL/KsJ-db/db-ApcMin/+ (db/db-Min/+) mice developed an increased incidence and multiplicity of adenomas in the intestinal tract when compared to the db/m-Min/+ and m/m-Min/+ mice. Blood biochemical profile showed significant increases in insulin (8.3-fold to 11.7-fold), cholesterol (1.2-fold to 1.7-fold), and triglyceride (1.2-fold to 1.3-fold) in the db/db-Min/+ mice
The CD105 MultiSort Kit (PE), mouse has been developed for the isolation of CD105+ cells or cell subsets, including vascular endothelial cells from mouse tissue or cell cultures long-term repopulating hematopoietic stem cells (LTR-HSCs) from mouse bone marrow when used in combination with the Anti-Sca-1 MicroBead Kit (FITC). - USA
This study characterizes the high-fat diet-fed mouse as a robust model for IGT and early type 2 diabetes. This model was initially described by Surwit et al. in 1988 (8), and the model has been shown to be most efficient in C57BL/6J mice compared with other strains (20-22). We show here by accumulated data on a large number of animals belonging to this strain that a high-fat diet results in increased body weight gain and over time a stable hyperglycemia but a progressively increased hyperinsulinemia, indicating progressive worsening of insulin resistance. Furthermore, already after 1 week on the diet, baseline plasma glucose and insulin were significantly elevated and IVGTTs showed reduced glucose elimination and impaired insulin secretion (particularly the AIR). The model thus shows two important mechanistic characteristics for IGT and type 2 diabetes: insulin resistance and islet dysfunction.. The growth curves for this 1-year study could be divided into two phases-one initial phase with more ...
MicroRNA (miRNA) molecules are potent mediators of post-transcriptional gene silencing that are emerging to be critical in the regulation of innate and adaptive immunity. Here we report that miR-155--an oncogenic miRNA with important function in the mammalian immune system--is induced in dendritic cells (DCs) upon maturation and potentially attenuates their ability to activate T cells. Biolistic epidermal transfection with DNA encoding miR-155 suppressed the induction of antigen-specific T cell-mediated immunity, whereas reduction of endogenous miR-155 by a partially complementary antisense sequence reversed this effect. Because DCs represent a significant component of epidermal tissue and are among the most potent of antigen-presenting cells, the inhibitory actions of miR-155 could be mediated through this subset of cells. These results suggest that miR-155 may repress the expression of key molecules involved in lymph node migration, antigen presentation, or T cell activation in DCs, and thus forms
LLN=lower limit of normal; ULN=upper limit of normal; BL=baseline. Sodium, serum (mEq/L):low if ,0.95*BL and BL,LLN or ,LLN and BL,ULN or ,0.95*LLN when BL missing or LLN ≤BL≤ULN, high if ,1.05*BL and BL,ULN or ,ULN and BL,LLN or ,1.05*ULN when BL missing or LLN≤BL≤ULN; potassium(mEq/L):low if ,0.90*BL and BL,LLN or ,LLN and BL,ULN or ,0.90*LLN if BL missing or LLN≤BL≤ULN, high if ,1.10*BL and BL,ULN or,ULN and BL,LLN or ,1.10*ULN when BL missing or LLN≤BL≤ULN; chloride(mEq/L):low if ,0.90*BL and BL,LLN or ,LLN and BL,ULN or ,0.90*LLN if BL missing or LLN≤BL ≤ULN, high if ,1.10*BL and BL,ULN or ,ULN and BL,LLN or ,1.10* ULN if BL missing or LLN≤BL≤ULN; calcium(mg/dL):low if ,0.75*BL and BL,LLN or ,LLN and BL,ULN or ,0.80*LLN if BL missing or LLN≤BL≤ULN, high if ,1.25*BL and BL,ULN or ,ULN if BL,LLN or ,1.20*ULN if BL missing or LLN≤BL≤ULN ; bicarbonate(mEq/L):low if ,0.75*BL when BL,LLN or ,LLN when BL,ULN or ,0.75*LLN if BL missing or LLN≤BL≤ULN, high if ...
LLN=lower limit of normal; ULN=upper limit of normal; BL=baseline. Sodium, serum (mEq/L):low if ,0.95*BL and BL,LLN or ,LLN and BL,ULN or ,0.95*LLN when BL missing or LLN ≤BL≤ULN, high if ,1.05*BL and BL,ULN or ,ULN and BL,LLN or ,1.05*ULN when BL missing or LLN≤BL≤ULN; potassium(mEq/L):low if ,0.90*BL and BL,LLN or ,LLN and BL,ULN or ,0.90*LLN if BL missing or LLN≤BL≤ULN, high if ,1.10*BL and BL,ULN or,ULN and BL,LLN or ,1.10*ULN when BL missing or LLN≤BL≤ULN; chloride(mEq/L):low if ,0.90*BL and BL,LLN or ,LLN and BL,ULN or ,0.90*LLN if BL missing or LLN≤BL ≤ULN, high if ,1.10*BL and BL,ULN or ,ULN and BL,LLN or ,1.10* ULN if BL missing or LLN≤BL≤ULN; calcium(mg/dL):low if ,0.75*BL and BL,LLN or ,LLN and BL,ULN or ,0.80*LLN if BL missing or LLN≤BL≤ULN, high if ,1.25*BL and BL,ULN or ,ULN if BL,LLN or ,1.20*ULN if BL missing or LLN≤BL≤ULN ; bicarbonate(mEq/L):low if ,0.75*BL when BL,LLN or ,LLN when BL,ULN or ,0.75*LLN if BL missing or LLN≤BL≤ULN, high if ...
OBJECTIVES The extent of autophagy in myocardium following persistent ischemia and the effects of insulin resistance and diabetes on cardiac autophagy following myocardial infarction (MI) have not been well elucidated. It is generally thought that autophagy reflects the nutritional status of cells, presumably alterable by diabetes. It has been conjectured that diminution of autophagy early after the onset of MI may preserve jeopardized myocardium thereby improving prognosis. METHODS Ten-week-old nondiabetic C57BL6 mice, 20-week-old diabetic and nondiabetic C57BL6 mice were subjected to MI for 4 weeks. Hearts from these mice were harvested and assayed for markers of autophagy. RESULT Hearts of 10-week-old C57BL6 mice subjected to 4 weeks of MI had similar levels of LC3-II, a protein indicator of autophagy, as measured by western blotting compared with hearts from sham operated controls. In 20-week-old C57BL6 mice rendered diabetic by feeding a high-fat diet, the amounts of autophagy were comparable
Toll-like receptor 2 (TLR2) is implicated in various pathologies, mainly in terms of its function within innate immune cells. However, TLR2 is also present in endothelial cells. Here, we explored the physiological and pathophysiological roles of endothelial TLR2 signaling. We found that TLR2 was highly abundant in the endothelium within various tissues using TLR2-IRES-EGFP reporter mice and was required for proinflammatory endothelial cell function. Endothelial cells lacking TLR2 exhibited reduced proinflammatory potential at the protein, cell, and tissue levels. Loss of endothelial TLR2 blunted the inflammatory response to both exogenous and endogenous danger signals in endothelial cells in culture and in vivo. Endothelial TLR2 promoted tumor growth, angiogenesis, and protumorigenic immune cell recruitment in a mouse model of prostate cancer. Furthermore, the cell surface localization of P-selectin and the subsequent production of other critical cell adhesion molecules (such as E-selectin, ...
Toll-like receptor 2 (TLR2) is implicated in various pathologies, mainly in terms of its function within innate immune cells. However, TLR2 is also present in endothelial cells. Here, we explored the physiological and pathophysiological roles of endothelial TLR2 signaling. We found that TLR2 was highly abundant in the endothelium within various tissues using TLR2-IRES-EGFP reporter mice and was required for proinflammatory endothelial cell function. Endothelial cells lacking TLR2 exhibited reduced proinflammatory potential at the protein, cell, and tissue levels. Loss of endothelial TLR2 blunted the inflammatory response to both exogenous and endogenous danger signals in endothelial cells in culture and in vivo. Endothelial TLR2 promoted tumor growth, angiogenesis, and protumorigenic immune cell recruitment in a mouse model of prostate cancer. Furthermore, the cell surface localization of P-selectin and the subsequent production of other critical cell adhesion molecules (such as E-selectin, ...
Incidence and severity of K/BxN serum transfer-induced arthritis are not reduced in IL-36 receptor (R) knockout (KO) mice. Incidence of arthritis (A), arthritis
Rodents of an inbred strain display large variations in several behaviors: sucrose preference (Strekalova & Steinbusch, 2010), fear conditioning (Siegmund, Kaltwasser, Holsboer, Czisch, & Wotjak., 2009), decrease in social interaction after social defeat (Krishnan et al., 2007), ambulation in the open-field and the elevated plus-maze (Vidal, 2015). Variations of physiological variables (weight, course of infection, stress response) in inbred animals have also been reported (Gärtner, 2012). This variability, which is not readily explained by genetics or environment, has been termed intangible variation, developmental noise (Blewitt, Chong, & Whitelaw, 2004; Falconer, 1989) or third component (Gärtner, 2012). The author of the present report could not find studies documenting individual differences in the antibody response within an inbred mouse strain; therefore, one goal of this report was to find out if such differences occurred in mice of the C57Bl/6J inbred strain.. A set of correlated ...
Integrated scheme of the kinetics of prothymocyte gating, occupation of microenvironmental niches, and generation of thymocytes in normal mice. Clusters of vertical arrows represent receptive periods (open gate) and horizontal black bars represent refractory periods (closed gate) for importation of hematogenous prothymocytes. Shaded triangles represent filling/equilibration (up slope) and emptying (down slope) phases of occupation of a finite number of intrathymic niches by prothymocytes and their immediate descendants. Dashed, dotted, and mixed symbol curves represent sequential waves of thymocytopoiesis, each generated by the gated importation of a saturating wave of prothymocytes. The lag period of thymocytopoiesis corresponds roughly to the filling/equilibration phase of occupation of the intrathymic niches. The duration of each wave of thymocytopoiesis exceeds the periodicity of gate-opening by twofold, so as to maintain relatively constant levels of total thymocytes. Gate closing appears ...
Certain pathogens, including HIV and hepatitis viruses, that lead to persistent infections are often associated with suboptimal antibody responses. Using LCMV infection in mice, Fallet et al., Moseman et al., and Sammicheli et al. report that up-regulation of type I interferon (IFN-I) in the early phase of infection is a key contributor to premature deletion of virus-specific B cells. Blockade of IFN-I prevents B cell deletion. Although the studies agree that IFN-I does not act directly on B cells, they found that distinct immune cells mediate IFN-I-dependent deletion of B cells, depending on the system examined. Targeting of the IFN-I pathway could be used to restore B cell responses during persistent viral infections in humans. ...
15-Lipoxygenase-2 (ALOX15B), an oxidoreductase in the metabolism of arachidonic acid, is a functional tumor suppressor whose expression is reduced in a variety of human cancers. To determine the roles of ALOX15B in carcinogenesis, we generated transgenic mice with ALOX8, the murine homolog of ALOX15B, knocked out. ALOX8 expression at mRNA level was abolished in homozygous knockout mice and reduced to half of wild type in heterozygous knockout mice. Its observed that homozygous female ALOX8 knockout mice are infertile but male ALOX8 knockout mice are fertile. Increased incidence of tumor as uni or multimass was found in the lung, prostate and in the mesentery region of homozygous and heterozygous ALOX8 knockout mice, when compared with little mate wild type mice. Histological evaluations showed an increase in secondary tumors and inflammation in different tissues like lung and large intestine in mice with ALOX8 knocked out. The transgenic mice could be a good model to study the role of ...
In this report, we show that overexpression of scurfin in FoxP3 Tg mice results in the inability to mount an effective humoral immune response. FoxP3 Tg mice displayed lower levels of circulating IgG when compared with their nontransgenic littermates, and had a dramatically reduced response when challenged with a specific Ag. However, B cells from FoxP3 Tg mice produced normal levels of Ig when stimulated in vitro, suggesting that a defect in T cell-derived help was responsible for the phenotype seen in these mice. Three additional lines of evidence support this hypothesis. First, T cells from FoxP3 Tg mice failed to provide help to B cells from NLC mice. Second, CD4+ T cells from FoxP3 Tg mice failed to up-regulate CD40L and CD69 expression when stimulated. Finally, significantly fewer IL-4- and IFN-γ-producing splenic T cells were generated in immunized FoxP3 Tg mice as compared with NLC mice. Overall, these findings suggest that the poor Ag-specific Ab response generated by FoxP3 Tg mice ...
TY - JOUR. T1 - Gene transfer of AIMP1 and B7.1 into epitope-loaded, fibroblasts induces tumor-specific CTL immunity, and prolongs the survival period of tumor-bearing mice. AU - Kim, Tae S.. AU - Lee, Byeong C.. AU - Kim, Eugene. AU - Cho, Daeho. AU - Cohen, Edward P.. N1 - Funding Information: We would like to thank Drs. I.J. Fidler, M. Bevan and R. Mulligan for providing valuable reagents. This work was supported by grants from the National R&D Program for Cancer Control, Ministry of Health & Welfare (070335), and from the Research Center for Womens Diseases, Science Research Center Program, Ministry of Science & Technology, Republic of Korea (R11-2005-017).. PY - 2008/11/5. Y1 - 2008/11/5. N2 - T helper type 1 (Th1) cell-mediated immune responses play various roles in cellular immunity, including inducing cytotoxic T lymphocytes (CTLs) and they have been shown to be crucial in cancer immunotherapy. Previously, we found that aminoacyl-tRNA synthetase-interacting multifunctional protein 1 ...
Cancer immunotherapy is emerging as a treatment option for patients with late-stage tumors (23, 24). Modulating tumor microenvironments by antagonizing tumor-associated negative immune regulators such as PD-1, TGFβ, or adenosine has been viewed as an attractive treatment strategy (25, 26). In the current study, we found that myeloid-selective deletion of Adora2a slowed tumor growth and significantly increased activation markers, IL12 and MHCII, on macrophages without affecting ex vivo cytotoxicity. Myeloid-selective deletion of the A2AR also decreased ,90% IL10 production by tumor-associated macrophages, DCs, and MDSCs. This was associated with increased NK and CD8+ T-cell numbers, CD44 expression, and T-cell IFNγ production in the tumor.. Deletion of A2ARs from T cells causes T-cell activation, but reduces T-cell survival and memory cell differentiation in the solid tumor environment (27). Consequently, selective deletion of T-cell Adora2a sometimes reduces T-cell numbers and enhances the ...
Primary Sjögrens syndrome (pSS) is characterized by a panel of autoantbodies, while it is not clear whether B cells and autoantibodies play an essential role in pathogenesis of the disease. Here we report a novel mouse model for pSS which is induced by immunization with the Ro60_316-335 peptide containing a predominant T cell epitope. After immunization, mice developed several symptoms mimicking pSS, including a decreased secretion of tears, lymphocytic infiltration into the lacrimal glands, autoantibodies and increased levels of inflammatory cytokines. Disease susceptibility to this novel mouse model varies among strains, where C3H/HeJ (H2-k) and C3H/HeN (H2-k) are susceptible while DBA/1 (H2-q) and C57BL/6 (H2-b) are resistant. Depletion of B cells using anti-CD20 monoclonal antibodies prevented C3H/HeN mice from development of the pSS-like disease. In addition, HLA-DRB1*0803, a pSS risk allele, was predicted to bind to the hRo60_308-328 which contains a predominant T cell epitope of human Ro60.
Results The wild-derived mouse strain PWD/Ph was highly susceptible to CAIA induced arthritis, whereas the classical laboratory strain C57BL/6J was resistant. Mice carrying chromosomes 5 or 12 from PWD on a B6 background display a B6-like phenotype in the CAIA model as well as the F1 hybrids (B6xPWD and PWDxB6) implicating the presence of dominant resistance modifiers in the C57BL/6J genetic background. The two mouse strains differ highly in their autoantigenic profile. Injecting specific monoclonal ACPAs reactive with the citrullintated H1 and H4 were able to block the CAIA induced arthritis. This inhibition can be explained in part by a Toll 9 dependent inhibition of osteoclasts. Moreover TLR2 activation via P.gingivalis LPS and lipomannan treated animals show a 80% reduction of arthritis score compared to E. coli LPS in a C57BL/6J CAIA model. Anti-collagen specific antibodies are increased in both strains B6 and PWD when arthritis is induced. Commercial CCP2 ELISA detected ACPA in animals ...
It is generally viewed that the effects of IFN-I on clonal expansion in vivo are related largely via their actions on APCs and to some extent via skewing activated T cells toward a type I cytokine response (6-15). Our studies highlight a previously unappreciated role for IFN-I in causing clonal expansion via direct action on antigen-specific CD8 T cells. We think this effect was not appreciated in previous experiments that analyzed T cell responses directly in virally infected IFN-IR0 mice (16), in which neither T cells nor APCs can respond to IFN-I, possibly because (a) the infected IFN-IR0 mice may elicit altered innate responses and (b) the IFN-IR0 mice have a high persistent viral load that makes it difficult to dissociate effects because of the absence of IFN-I action from effects related to overwhelming viral loads (16, 17). For example, IFN-IR0 mice are known to elicit elevated levels of IL-12 (which may overcome the defect caused by IFN-IR0 deficiency on CD8 T cells; Fig. 8) because of ...
Figure 5. Pretreatment of donor T cells with a c-Rel antagonist does not impair GVT activity. A, lethally irradiated C57BL/6 recipients received C57BL/6 TCD BM cells with 2 × 106 C57BL/6 WT or c-Rel−/− T cells (syngeneic HSCT). Control mice received BM only. All groups received 1 × 105 luciferase-expressing EL4-TGL tumor cells on day 0. Survival curve is shown (n = 5-8). B, lethally irradiated C57BL/6 recipients received 5 × 106 C57BL/6 WT or c-Rel−/− T cells (syngeneic HSCT). All groups received 1 × 106 EL4 tumor cells on day 0. Expression level of CD25 in donor-derived splenic CD8+ T cells on day 7 is shown. C, lethally irradiated BALB/c recipients were transplanted with C57BL/6 TCD BM cells with 2 × 106 C57BL/6 WT or c-Rel−/− T cells (allo-HSCT). Expression level of CD25 in donor-derived splenic CD8+ T cells on day 7 is shown. D, lethally irradiated C57BL/6 recipients received C57BL/6 TCD BM cells with 1 × 106 C57BL/6 Pmel1+/+ T cells (syngeneic HSCT). T cells were ...
In the present study, we show that anti-CD40 can synergize with class B CpG in activating tumoricidal Mφ, which, in turn, mediated antitumor effects in vitro and in vivo. Class B CpGs are potent activators of both murine and human mononuclear phagocytes, and Mφ in particular (30, 33, 34, 44). Although CpG and LPS share many immunostimulatory properties, CpG seems to be less toxic in vivo due to stimulation of mononuclear phagocytes in a much more restricted manner (33, 34). Our data suggest that CpG and LPS might synergize with anti-CD40 in activating Mφ via different mechanisms, because CpG, but not LPS, synergized with anti-CD40 in C3H/HeJ mice. Our results also show that anti-CD40 synergized with CpG in activation of cytotoxic Mφ in a time- and order-dependent manner. The observed time-dependent up-regulation of TLR9 in response to anti-CD40 could account, at least in part, for the synergy between anti-CD40 and CpG. Thus, CD40-ligation of B cells resulted in augmented expression of TLR9 ...
CD4 and CD8 T cells are constantly exposed to inflammatory signals that influence diverse functional outcomes during infections and certain autoimmune disorders. One of the signals controlling CD4 and CD8 T cell functions is the inflammatory cytokine IL-12. Previous studies have focused on how IL-12 regulates CD4 and CD8 T cell functions when present during or after the activation of the T cell receptor (TCR). However, based on murine studies, we have only recently begun to appreciate that exposure to inflammatory signals, driven in part by IL-12, could alter how CD4 and CD8 T cells respond to TCR stimulation. Although intriguing, these studies have left several questions unanswered. Does IL-12 similarly regulate the function of human T cells? If so, what is the exact molecular mechanism by which IL-12 mediates these effects? To address these critical questions, we examined how IL-12 pretreatment altered human CD4 and CD8 T cell responses to subsequent TCR stimulation. In CHAPTER III, we examined how
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Immune cells constantly circulate in the body in search of pathogens or tissue damage. Because they move autonomously, immune cell trafficking must be tightly controlled and coordinated by extracellular cues. The main signals that guide immune cells are chemokines, small polypeptides that modulate the migratory behavior of cells. Remarkably, most chemokines are not only sensed but also secreted by immune cells, indicating that immune cells might either attract more of their own kind or trigger complex patterns of feedbacks between different cell populations. Such cascades might allow different immune cell types to orchestrate their sequential arrival at a site of infection (1). On page 1071 of this issue, Lim et al. (2) show that this is indeed the case with neutrophils and cytotoxic T cells, the former leaving a trail of cues for the latter to follow during the eradication of a viral infection. ...
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Format of Logitech Mouse parameter table: Offset Size Description ) 00h WORD baud rate divided by 100 (serial mouse only) 02h WORD emulation (serial mouse only) 04h WORD report rate (serial mouse only) 06h WORD firmware revision (serial mouse only) 08h WORD 00h (serial mouse only) 0Ah WORD port (serial mouse only) 0Ch WORD physical buttons 0Eh WORD logical buttons ...
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chr6:40953984-40975892, + strand. Annotation of mouse strain C57BL/6NJ genome assembly provided by GENCODE consortium. Distributed via Ensembl Release 92. Gene type: protein coding gene; Gene Name: Prss1 ...
chr15:106010884-106040265, + strand. Annotation of mouse strain C57BL/6NJ genome assembly provided by GENCODE consortium. Distributed via Ensembl Release 92. Gene type: protein coding gene; Gene Name: Tmprss12 ...
Whether expected to be key contributors or free agency afterthoughts, these NBA players did not measure up during the 2011-2012 season. Disappointment comes in many various forms...
In the Cardiology Masters section of European Cardiology Review we bring you an insight into the career of a key contributor to the field of cardiology.
acquired change in the genetic material to cells other than those involved in reproduction, caused by radiation, chemicals and drugs acquired change in the genetic material to cells other than those involved in reproduction, caused by radiation, chemicals and drugs acquired change in the genetic material to cells other than those involved in reproduction, caused by radiation, chemicals and drugs ...
Validate the conditional Knockout efficacy by measuring a reporter gene expression and quantify the deletion in a specific tissue or cell.