Disease relevance of CELP

• Results showed that (a) nine scale items were consistently and reliably rated by the listeners; (b) all coders degraded speech quality on these nine scales, with the GSM and CELP coders providing the better quality speech; and (c) interactions between coders and individual voices did occur on several voice quality scales [1].
• Osteopontin thus appears to regulate T helper cell-1 (TH1)-mediated demyelinating disease, and it may offer a potential target in blocking development of progressive MS [2].
• T helper cell 1-type CD4+ T cells, but not B cells, mediate colitis in interleukin 10-deficient mice [3].
• Helicobacter pylori modulates the T helper cell 1/T helper cell 2 balance through phase-variable interaction between lipopolysaccharide and DC-SIGN [4].
• Pretreatment with HDACi at nontoxic doses, followed by incubation with TRAIL, resulted in a marked increase in TRAIL-induced apoptosis of T24 cells but showed no significant increase in toxicity to SV40 immortalized normal human uroepithelial cell-1 [5].

High impact information on CELP

• Activation of human CD4+ cells with CD3 and CD46 induces a T-regulatory cell 1 phenotype [6].
• The Fc receptor type III (Fc gamma R III, CD 16), present in 135,000 sites per cell 1 on neutrophils and accounting for most of FcR in blood, unexpectedly has a phosphatidylinositol glycan (PIG) membrane anchor [7].
• OVA-specific CD4+ T cells were induced by nCT and by mCTs, and quantitative analysis of secreted cytokines and mRNA revealed a T helper cell 2 (Th2)-type response [8].
• Therapy of murine tumors with tumor peptide-pulsed dendritic cells: dependence on T cells, B7 costimulation, and T helper cell 1-associated cytokines [9].
• Because her E had expressed 173 sites/cell 2 yr before, the CR1 deficiency was considered to be acquired and a possible mechanism was sought [10].

Chemical compound and disease context of CELP

• NFkappaBD also mitigates disease activity in the T helper cell 2-like oxazolone colitis and epithelial injury-related acute dextran sodium sulphate colitis models [11].
• In the T helper cell 1-driven trinitrobenzene sulphonic acid-induced colitis model, mice receiving NFkappaBD treatment exhibit a dose-dependent reduction in disease severity and a more rapid recovery to normal body weight, similar to a clinically relevant dose of budesonide [11].
• CONCLUSION: The study describes a delayed hypersensitivity to suxamethonium, driven by an oligoclonal T helper cell 1-skewed CD4+ memory T cell population, expressing the skin homing receptors CLA and CCR4 [12].
• The average toxicity of the cultures was 8.8 and 11.0 pg saxitoxin equiv. cell-1 with acetic acid or HCl extraction, respectively [13].
• In human D384 astrocytoma cells, cyclic AMP accumulation can be conveniently studied after labelling of the adenosine triphosphate pool (15 fmol cell-1) with [3H]adenine [14].

Biological context of CELP

• No correlation of plasma cell 1 overexpression with insulin resistance in diabetic rats and 3T3-L1 adipocytes [15].
• A survival curve showed an initial shoulder and became steeper beyond 200-250 pCi cell-1 (low linear energy transfer type) [16].
• According to the calibration, the mean biomass of planktonic bacteria from the North Sea in August 1998 was 24 fg of protein cell-1 [17].
• It is suggested that a T-helper cell 2 (Th2) shift and Th2 spreading of autoimmunity following immunization with beta-cell antigen causes diabetes protection [18].
• The intracellular microcystin content was similarly correlated to the cell density, but the cellular quota was slightly higher (0.3-0.7 pg cell-1) than in the natural population [19].

Anatomical context of CELP

• Lymphocytes in the human gastric mucosa during Helicobacter pylori have a T helper cell 1 phenotype [20].
• Both macro- (HUVEC) and microvascular endothelial cells derived from human skin (human dermal microvascular endothelial cell 1) and human colon (human intestinal microvascular endothelial cells) were found to express high constitutive amounts of TLR5 mRNA and protein [21].
• Because the proteoglycans that are present in the secretory granules of different types of rat and mouse mast cells possess small peptide cores that are rich in serine and glycine, we propose that this HL-60 cell-3 derived cDNA encodes the peptide core of the proteoglycan that is expressed in the secretory granules of this human promyelocytic cell [22].
• It acts downstream of interleukin-13; inhibition of AMCase leads to an abrogated T-helper cell 2 inflammation, less bronchial hyperreactivity, and fewer eosinophils [23].
• Equivalent functional nuclear factor of activated T cell 1 mRNA and protein expression in cord blood and adult T cells [24].

Associations of CELP with chemical compounds

• Initial rates of one-way efflux as a function of [vinblastine] at 25 degrees C +/- glucose give the maximum rate of this component of pumping as 0.59 x 10(6) molecules s-1 cell-1 [25].
• Combined diesel exhaust particulate and ragweed allergen challenge markedly enhances human in vivo nasal ragweed-specific IgE and skews cytokine production to a T helper cell 2-type pattern [26].
• The initial rate of norepinephrine uptake was saturable, with Vmax and KM of 197 +/- 17 amol min-1 cell-1 and 1.64 +/- 0.46 microM, respectively [27].
• Estimated cell-specific nitrite oxidation rates were 1.2-2.7 fmol NO2- cell-1 h-1 [28].
• The swim motor pattern is generated by a network formed of four groups of premotor interneurons: cerebral cell 2 (C2), dorsal swim interneurons (DSIs), and two types of ventral swim interneurons (VSI-A and VSI-B) [29].

Regulatory relationships of CELP

• Instead, human mast cell-1 supernatants induced enhanced fibroblast growth factor 7 secretion from dermal fibroblasts, with phorbol-myristate-acetate-stimulated supernatants being more effective [30].
• The addition of Ang II (200 ng/ml) to human dermal microvessel endothelial cell-1 for 16 hr resulted in a significant (P < 0.05) reduction of GSH contents control endothelial cells but not in endothelial cells transduced with HO-1 gene [31].
• The oxygen affinity of the CPD blood was less influenced by the red cell 2, 3-DPG than was that of the ACD blood [32].

Other interactions of CELP

• A previously unknown gene with a striking homology to the human CEL gene, here called the CEL-like gene (CELL), has also been isolated and characterized, including 1724 bp of the 5'-flanking region [33].
• Akira et al. discovered a new molecule of TLR family, TLR9, recognizing unmethylated bacterial CpG-DNA, whose clinical use is expected for cancer therapy as a potent inducer of a helper T cell 1 (Th1)-type T-cell response [34].
• Acutely infected children showed a distinct T helper cell-1 (Th1)-type (IFN-gamma) cytokine response to infection [35].
• The P-gp- and MRP1-mediated pump coefficient (k v a), Michealis-Menten's constant (K V m), and maximal pumping rate (V V max) values of those located on vesicular membranes were 1.87 +/- 0.30 pL x cell-1 x s-1, 1.63 +/- 0.21 microM, and 4.95 +/- 0.45 nM x s-1</sup>, respectively [36].
• Cord blood (CB) cells are now an important source of stem cells for bone marrow reconstitution as a result of the decreased risk of graft-versus-host disease that was attributed to previously reported absent or diminished nuclear factor of activated T (NFAT) cell 1 expression by CB T cells [24].

Analytical, diagnostic and therapeutic context of CELP

• Genomic organization, sequence analysis, and chromosomal localization of the human carboxyl ester lipase (CEL) gene and a CEL-like (CELL) gene [33].
• Immune receptor expressed by myeloid cell-3 cDNA was cloned from a PHA-activated PBMC library and RT-PCR revealed the gene to be expressed preferentially in cells of myeloid origin [37].
• The nature of antigen presenting cells, T-cell receptors, adhesion molecules between inflammatory cells and myelinated fibers and the apparent predominance of T helper cell 1-related cytokines need to be explored to design more specific immunotherapies [38].
• In situ hybridization experiments using the 35S-labeled rat ovary 3 beta-HSD cDNA probe show that the inhibitory effect of PRL is exerted primarily on luteal cell 3 beta-HSD expression and activity [39].
• When it is given to the donor, G-CSF polarizes T cells to produce T-helper cell-2 cytokines, which reduce GVHD after transplantation [40].

References