text:
|Mutation Type
|11,283,849 bp (GRCm38)
|Base Change
|A ⇒ G (forward strand)
|Gene Name
|protein kinase C, theta
|PKC theta, PKC-0, PKCtheta, PKC-theta, A130035A12Rik, Pkcq
|Chromosomal Location
|11,172,108-11,301,222 bp (+)
|MGI Phenotype
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] Protein kinase C (PKC) is a family of serine- and threonine-specific protein kinases that can be activated by calcium and the second messenger diacylglycerol. PKC family members phosphorylate a wide variety of protein targets and are known to be involved in diverse cellular signaling pathways. PKC family members also serve as major receptors for phorbol esters, a class of tumor promoters. Each member of the PKC family has a specific expression profile and is believed to play a distinct role. The protein encoded by this gene is one of the PKC family members. It is a calcium-independent and phospholipid-dependent protein kinase. This kinase is important for T-cell activation. It is required for the activation of the transcription factors NF-kappaB and AP-1, and may link the T cell receptor (TCR) signaling complex to the activation of the transcription factors. [provided by RefSeq, Jul 2008]
PHENOTYPE: Homozygotes for targeted null mutations exhibit reduced T cell proliferative responses and interleukin 2 production and a lack of T cell receptor-initiated NF-kappaB activation in mature T lymphocytes. [provided by MGI curators]
|Accession Number
|Limits of the Critical Region
|11172113 - 11301226 bp
|Amino Acid Change
|Threonine changed to Alanine
|Institutional Source
|Beutler Lab
|Gene Model
|predicted gene model for protein(s): [ENSMUSP00000028118] [ENSMUSP00000100035]
|PDB Structure
|SMART Domains
Protein: ENSMUSP00000028118
Gene: ENSMUSG00000026778
AA Change: T538A
|Predicted Effect
|possibly damaging
PolyPhen 2 Score 0.753 (Sensitivity: 0.85; Specificity: 0.92)
|SMART Domains
Protein: ENSMUSP00000100035
Gene: ENSMUSG00000026778
AA Change: T538A
|Predicted Effect
|possibly damaging
PolyPhen 2 Score 0.822 (Sensitivity: 0.84; Specificity: 0.93)
|Phenotypic Category
|Alleles Listed at MGI
|Lab Alleles
|Mode of Inheritance
|Autosomal Recessive
|Local Stock
|Last Updated
|2018-01-18 9:48 AM by Anne Murray
|Record Created
|2015-10-22 11:43 PM by Jin Huk Choi
|Record Posted
|Phenotypic Description
The celina phenotype was identified among G3 mice of the pedigree R3402, some of which showed diminished T-dependent antibody responses to ovalbumin administered with aluminum hydroxide [OVA/alum] (Figure 1).
|Nature of Mutation
Whole exome HiSeq sequencing of the G1 grandsire identified 36 mutations. The diminished T-dependent antibody response to OVA/alum was linked by continuous variable mapping to a mutation in Prkcq. The Prkcq mutation is an A to G transition at base pair 11,283,849 (v38) on chromosome 2, or base pair 111,946 in the GenBank genomic region NC_000068 for Prkcq. Linkage was found with a recessive model of inheritance, wherein four variant homozygotes departed phenotypically from eight homozygous reference mice and 12 heterozygous mice with a P value of 2.844 x 10-6 (Figure 2).
The mutation corresponds to residue 1,700 in the mRNA sequence NM_008859 within exon 15 of 18 total exons.
The mutated nucleotide is indicated in red. The mutation results in a threonine (T) to alanine (A) substitution at position 538 (T538A) in the PKCθ protein, and is strongly predicted by PolyPhen-2 to be damaging (score = 0.753).
|Protein Prediction
Prkcq encodes protein kinase C theta (PKCθ), a member of the PKC family of serine threonine kinases. At least 11 mammalian PKC proteins are known with a wide range of tissue distribution, subcellular localization, and function. The PKC family belongs to the AGC-type kinase (protein kinase A/protein kinase G/protein kinase C) superfamily. PKC kinases share certain structural features including a highly conserved catalytic domain consisting of motifs required for ATP-substrate binding and catalysis, and a regulatory domain that maintains the enzyme in an inactive conformation (Figure 3). The regulatory and catalytic domains are attached to each other by a hinge region. PKC kinases can be split into three groups: conventional (α, βI, βII, and γ), novel (δ, ϵ, η, θ), and atypical (ζ and ι/λ). These classifications are based on the structural motifs in the regulatory domain that account for cofactor dependence and interactions during induction of catalytic activity. PKCθ is a novel PKC that requires diacylglycerol (but not calcium) to become activated.
PKCθ has a C2-like pTyr-binding domain (amino acids 8-123), a proline-rich motif in the V3 (hinge) domain that mediates CD28 interaction and immunological synapse translocation, two tandem cysteine-rich zinc finger C1 domains (amino acids 159-209 and 231-281) that bind diacylglycerol, and a kinase (C3/C4) domain (amino acids 380-634) (1).
The C2-like domain is approximately 130 amino acids long and binds to anionic phospholipids present in membranes in a Ca2+-dependent manner. Lck (see the record for iconoclast) phosphorylates PKCθ at Tyr90 upon antigen stimulation in T cells (2). Tyr90 phosphorylation is proposed to enhance PKCθ affinity for lipid membranes (3). PKCθ localization to the immunological synapse is dependent on its phosphorylation by Lck and germinal center kinase (GSK)-like kinase (GLK) as well as autophosphorylation (1;2;4).
C1 domains function as hydrophobic switches to anchor PKCs to the membrane (5). The upper third of the C1 domain forms a hydrophobic structure; the positively charged residues that interact with anionic phospholipids are in the middle third of the C1 domain. The bottom third of the C1 domain has two zinc-coordinating sites required for C1 domain folding. The C1 domains have a HX12CX2CXnCX2CX4HX2CX7C motif, where H is histidine, C is cysteine, X is any other amino acid, and n is 13 or 14. Diacylglycerol interacts with high affinity to the PKCθ C1B (but not C1A) domain (3). The difference in C1B domain binding affinity for diacylglycerol is attributed to an invariant tryptophan residue that is conserved in the lipid-binding surface of novel PKCs. Met267 within the C1B domain facilitates PKCθ localization to the Golgi complex where it functions in apoptosis (6).
The PKCθ kinase domain has a smaller N-terminal lobe that is comprised mainly of β-sheets. The kinase domain has a glycine-rich ATP-binding loop with a GXGXXG sequence (amino acids 387-392) that is found in protein kinases and nucleotide binding proteins. An invariant Lys (Lys409) structures the enzyme for phosphoryl-transfer. The C-terminal lobe of the kinase domain is predominantly α-helical and contains the activation loop. A hydrophobic methionine residue (Met458) within the sequence connecting the two lobes controls access to a cavity in the ATP binding pocket. Within the C-terminal catalytic domain is an ATP-binding site (C3) and a substrate-binding domain (C4). The V5 domain is C-terminal to the C3 and C4 domains, and contains a conserved turn and hydrophobic phosphorylation motifs. The V5 domain determines PKCθ targeting.
Autophosphorylation of Thr219 regulates the function of PKCθ. Thr219 is not phosphorylated in resting T cells, but phorbol 12,13-dibutryrate, vanadate, and antigen receptor cross-linking induce Thr219 phosphorylation. Mutation of Thr219 to alanine (Thr219Ala) caused a reduction in the ability of PKCθ to promote signaling that leads to the activation of NF-κB, NF-AT, and AP-1. The Thr219Ala mutation also prevented recruitment of PKCθ to the membrane in activated T cells (7). The hinge region of PKCθ undergoes caspase 3-dependent cleavage at a DEVD354K site in responses to apoptogenic stimuli (8), which releases a catalytic domain fragment from autoinhibition.
The celina mutation results in substitution of a threonine for an alanine at amino acid 538 located in the kinase domain.
PKCθ is the major PKC isoform in hematopoietic (9-12) and skeletal muscle cells (13;14). PKCθ is expressed at neuromuscular junctions (15) and is highly expressed in platelets (16-18). In their inactive conformations, most PKC proteins are localized in the cytosol and often associate with cytoskeletal proteins (19).
Many functions have been ascribed to PKC kinases due to their widespread expression and variety of substrates (see Table 1 for a list of PKCθ substrates). PKCs are involved in receptor desensitization, modulating membrane structure events, regulating transcription, mediating immune responses, regulating cell growth, and in learning and memory. PKCθ has roles in the regulation of migration, lymphoid cell motility, insulin signaling in skeletal muscle cells, insulin secretion and resistance, T cell activation, survival responses in adult T cells and T cell FasL-mediated apoptosis (see the record for riogrande), mast cell activation, neuronal differentiation and function, development of the peripheral and central nervous system (10;20-30). PKCθ also has putative functions in mitosis and the cell cycle (15;31-34).
Table 1. PKCθ substrates
TCR clustering and the IS
Activation of the T cell receptor results in cell proliferation, differentiation, cytokine production, and activation-induced cell death. Signaling through the T cell receptor (TCR) plays a critical role at multiple stages of thymocyte differentiation, T-cell activation, and homeostasis [reviewed in (42;43)]. TCRs are responsible for the recognition of major histocompatibility complex (MHC) class I and II, as well as other antigens found on the surface of antigen presenting cells (APCs). Binding of these ligands to the TCR initiates signaling and T cell activation (Figure 4). The TCR is composed of two separate peptide chains (TCRα/β for most T cells), and is complexed with a CD3 heterodimer (CD3εγ or CD3εδ; see the record for tumormouse) and a ζ homodimer (44). Signaling by the TCR complex depends on the phosphorylation of immunoreceptor tyrosine-based activation motifs (ITAMS) present on the CD3 and ζ chains [reviewed in (45;46)]. One of the first steps in TCR signaling is the recruitment of the tyrosine kinases Lck and Fyn to the receptor complex where they phosphorylate ITAMS. In the case of Lck, recruitment to the TCR complex depends on association with CD4, which recognizes MHC class II, or CD8, which recognizes MHC class I (47). Phosphorylation of the ITAM motifs results in recruitment of the ZAP-70 (ζ-chain-associated protein of 70 kDa) and Syk (spleen tyrosine kinase), which trans- and auto-phosphorylate, forming binding sites for SH2 domain- and protein tyrosine binding domain-containing proteins. ZAP-70 and Syk phosphorylate the linker for activation of T cells (LAT) and SH2 domain-containing leukocyte protein of 76 kDa (SLP-76). LAT serves as a docking site for a number of proteins including the adaptor proteins Src homologous and collagen (Shc) and growth factor receptor-bound (Grb) 2, phosphatidylinositol 3-kinase (PI3K), and phospholipase C (PLC). A number of these proteins also associate with and are activated by Lck (48). Eventually, the tyrosine phosphorylation cascade initiated by Lck culminates in the intracellular mobilization of calcium (Ca2+) ions and activation of important signaling cascades within the lymphocyte necessary for T cell activation and proliferation (45). These include the critical transcription factors NF-κB, NFAT (nuclear factor of activated T cells) and AP-1 (activator protein 1), which regulate the production of multiple cytokines, most notably interleukin-2 (IL-2).
PKCθ functions in T cell signaling at the immunological synapse. TCR activation promotes the translocation of PKCθ to the center of the immunological synapse (termed the central supramolecular activation cluster (cSMAC)). A high concentration of diacylglycerol at the cSMAC is required for PKCθ recruitment, and signals from CD28 are essential for PKCθ localization to the cSMAC (49). Activation of Vav, Rac and/or Cdc42, results in actin polymerization and TCR capping, which promotes PKCθ translocation to the TCR in the immunological synapse (50;51). PKCθ phosphorylates effector molecules that transduce signals and activate NF-κB, NFAT, and AP-1 (25;52-54). Upon activation, PKCθ-deficient T cells showed impaired proliferation, IL-2 production, and CD25 expression (52;53). At the immunological synapse, PKCθ-induced phosphorylation of Wiskott–Aldrich syndrome protein (WASP)-interacting protein (WIP) induces dissociation of WASP from the CrkL-WIP-WASP adaptor complex (38). WASP is subsequently activated by binding to GTP-bound Cdc42. Binding to Cdc42 induces a conformation change in WASP, which facilitates binding and activation of the Arp2/3 complex, which initiates actin polymerization.
T cell activation
CARMA1 (see the record for king) belongs to the membrane-associated guanylate kinase (MAGUK) protein family, whose members function as molecular scaffolds for the localized assembly of multiprotein complexes at the immunological synapse. Upon T cell activation by TCR and costimulatory molecule engagement, CARMA1 associates with a complex containing Bcl10 and MALT1 (Mucosa-Associated Lymphoid tissue lymphoma Translocation-associated gene 1; also known as MLT or Paracaspase; see the record for mousebird) and recruits these proteins to lipid rafts of the immunological synapse, where they activate the IKK complex, leading to degradation of IκB and subsequent activation of NF-κB (55-58). Upon lymphocyte activation, the linker domain of CARMA1 is phosphorylated at several sites (including Ser552, 555, 564, 565, 649, and 657) by PKCβ or PKCθ. These phosphorylation events are required for release of the inhibitory intramolecular CARD domain-linker domain interactions within CARMA1, allowing CARMA1 to assemble the CARMA1/Bcl10/MALT1 complex required to activate NF-κB (36;59). TCR stimulation also leads to CARMA1-dependent activation of c-Jun N-terminal kinase 2 (JNK2) (60).
LFA-1 (CD11a/CD18) signaling
PKCθ also mediates LFA-1 (CD11a/CD18)-associated signal transduction to the actin cytoskeleton (see the record joker for more information about CD18). LFA-1 and its ligands ICAM-1, -2, and -3 on antigen-presenting cells stabilize antigen-specific interactions between the T cell and the antigen presenting cell (61). PKCθ association with RapGEF2, and subsequent RapGEF2 phosphorylation, promote Rap1 activation. Activated Rap1 increases LFA-1 adhesiveness to ICAM-1 and an overall increase in T cell adhesiveness to the endothelium and antigen presenting cell (62).
T cell polarity
PKCθ functions in the establishment of T cell polarity. During formation of the immunological synapse, the microtubule-organizing center polarizes adjacent to the synapse. Polarization of the microtubule-organizing center establishes the axis of polarization and facilitates directional release of cytokines and cytolytic factors toward the antigen presenting cell (63). Diacylglycerol-mediated recruitment of PKCϵ and PKCη promotes the recruitment of PKCθ to the immune synapse, which is required for proper microtubule organizing center reorientation (64). PKCθ also regulates the formation of the distal pole complex, which is an immune synapse membrane projection containing cytoskeleton components (e.g., ezrin and moeisin) that is formed during T cell—antigen presenting cell recognition (65). PKCθ phosphorylates moesin, which is required for interaction of the ezrin-moiesing-radixin proteins with actin (66).
PKCθ is sequestered from the Treg immunological synapse, which inhibits suppressive function (67). Blockade of PKCθ results in increased Treg function, protected Tregs from TNF-α (see the record for Panr1)-associated inactivation, restored the activity of defective Tregs from rheumatoid arthritis patients, and increased protection from inflammatory colitis in mice. PKCθ-deficient mice exhibited reduced numbers of CD4+Foxp3+ Treg cells (12). The loss in Treg number was not due to changes in cell survival. PKCθ is proposed to promote the development of Treg cells by increasing Foxp3 expression through activation of the calcineurin/NFAT pathway.
Th17 cells
PKCθ stabilizes the Th17 cell phenotype by suppressing the STAT4/IFN-γ/T-bet axis at the onset of differentiation and upregulating STAT3 (68;69). PKCθ-deficient CD4+ T cells displayed defective Th17 differentiation; forced expression of STAT3 resulted in rescue of Th17 differentiation (69). The PKCθ-deficient CD4+ T cells had normal Th17 marker gene expression (i.e., IL17a and RORγt [see the record for chestnut]) with increased production of Th1-typical markers (e.g., IFN-γ [see the record for marigold] and T-bet) (68).
Platelet activation and aggregation
PKCθ positively regulates the 'outside-in' signal transduction pathway associated with the platelet αIIbβ3 integrin receptor (70). Upon fibrinogen binding to the αIIbβ3 receptor on platelets, the platelets are activated, aggregate, and adhere to the site of vascular damage. Fibrinogen binding promotes an 'outside-in' signal that promotes actin polymerization and cytoskeleton alterations that are necessary for efficient platelet aggregation and spreading (71). Upon fibrinogen binding to the αIIbβ3 receptor, PKCθ associates and activates the protein tyrosine kinases Btk and Syk (see the record for poppy). PKCθ-mediated phosphorylation of WIP facilitates the uncoupling of WASP from the WIP—WASP complex, and the subsequent WASP-induced stimulation of Cdc42 and the activation of the Arp2/3 complex (72;73). In PKCθ-deficient mice, platelet aggregation and secretion were impaired (11).
Insulin resistance and obesity susceptibility
PKCθ mediates fat-induced insulin resistance in skeletal muscle (24). Accumulation of fat metabolites in skeletal muscle is proposed to activate PKCθ, and lead to defects in insulin signaling and glucose transport in the muscle. Loss of PKCθ expression prevented fat-induced defects in insulin signaling and glucose transport in skeletal muscle (24). A transgenic mouse expressing a muscle-specific dominant-negative PKCθ exhibited age- and obesity-associated glucose intolerance (74). PKCθ-deficient mice do not exhibit changes in body weight and food intake on normal chow diet (75). However, body fat content was increased with a corresponding decrease in body lean mass. PKCθ-deficient mice exhibited reduced energy expenditure and spontaneous physical activity. On a high fat diet, the body weight and fat content increased quickly in the PKCθ-deficient mice. After eight weeks on the high fat diet, the PKCθ-deficient mice exhibited insulin resistance.
Neuromuscular synapse
PKCθ-deficient mice did not exhibit defects in endplate morphology or the density of synaptic vesicles, but the myelin sheath in intramuscular nerve fibers was thinner than that in wild type mice (30). The PKCθ-deficient mice exhibited reduction in the size of evoked endplate potentials as well as in the frequency of spontaneous, asynchronous, miniature endplate potentials.
PKCθ regulates cytoskeleton rearrangements during myogenesis. PKCθ also regulates myogenic signaling through IRS1 and ERK1/2 phosphorylation. During myogenesis, cytoskeletal actin is reorganized to promote the function of enzymatic and contractile apparatuses (76). PKCθ forms a complex with the transcription factor Nfix (NF one X-type) and MEF2A (myocyte-specific enhancer factor 2A). The PKCθ/Nfix/MEF2A complex controls the transcription of factors associated with fetal myogenesis, including MCK and β-enolase (77). PKCθ also promotes the phosphorylation of MARCKS (myristoylated alanine-rich C-kinase substrate 1), a protein that anchors the actin cytoskeleton to the plasma membrane (78;79). PKCθ-mediated phosphorylation of MARCKS modulates the interaction between MARCKS and the membrane, and indirectly affects the arrangement of the undermembrane actin cytoskeleton.
Mammary tumorigenesis
PKCθ activation inhibits the Foxo3a/ERalpha/p27 axis and induces c-Rel target genes to promote proliferation, survival, and more invasive breast cancer (80)
Mutations in PRKCQ are linked to type 1 diabetes, rheumatoid arthritis, and celiac disease.
|Putative Mechanism
B cell responses are classified as T-dependent (T-D) or T-independent (T-I) based on their requirement for T cell help in antibody production. T cell-dependent antigens are processed and presented to helper T cells via the MHC class II molecules, whereas T cell-independent antigens are typically polysaccharides that cannot be processed and presented by MHC molecules. These antigens are often expressed on the surface of pathogens in an organized, highly repetitive form that can activate specific B cells by cross-linking of antigen receptors. The formation of antigen receptor clusters can recruit and activate multiple Btk molecules, resulting in long-term mobilization of intracellular ionized Ca2+, gene transcription and B cell activation and proliferation. Toll-like receptor (TLR) engagement provides a second signal that allows the secretion of antibody in response to these antigens. The T-D B cell response is mediated by conventional (follicular B-2) B cells, while T-I B cell responses are mediated by peritoneal B-1 and marginal zone (MZ) B cells [reviewed by (81;82)]. The reduction of B cell antibody responses to OVA-alum in the celina mice suggests that the function of antigen processing may be impaired.
PCR Primer
celina(F):5'- TGATGACACAGCTGCCACAC -3'
celina(R):5'- CACTCAAATGGAATCTAGTCACAG -3'
Sequencing Primer
celina_seq(F):5'- TGCCACACCCCATGAGAATTTC -3'
celina_seq(R):5'- TGTTAGTTGTAAAACTCAAAAGACCC -3'
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35. Li, Y., Hu, J., Vita, R., Sun, B., Tabata, H., and Altman, A. (2004) SPAK Kinase is a Substrate and Target of PKCtheta in T-Cell Receptor-Induced AP-1 Activation Pathway. EMBO J. 23, 1112-1122.
36. Matsumoto, R., Wang, D., Blonska, M., Li, H., Kobayashi, M., Pappu, B., Chen, Y., Wang, D., and Lin, X. (2005) Phosphorylation of CARMA1 Plays a Critical Role in T Cell Receptor-Mediated NF-kappaB Activation. Immunity. 23, 575-585.
37. Pietromonaco, S. F., Simons, P. C., Altman, A., and Elias, L. (1998) Protein Kinase C-Theta Phosphorylation of Moesin in the Actin-Binding Sequence. J Biol Chem. 273, 7594-7603.
38. Sasahara, Y., Rachid, R., Byrne, M. J., de la Fuente, M. A., Abraham, R. T., Ramesh, N., and Geha, R. S. (2002) Mechanism of Recruitment of WASP to the Immunological Synapse and of its Activation Following TCR Ligation. Mol Cell. 10, 1269-1281.
39. Li, Y., Soos, T. J., Li, X., Wu, J., Degennaro, M., Sun, X., Littman, D. R., Birnbaum, M. J., and Polakiewicz, R. D. (2004) Protein Kinase C Theta Inhibits Insulin Signaling by Phosphorylating IRS1 at Ser(1101). J Biol Chem. 279, 45304-45307.
40. Marino, J. S., Hinds, T. D.,Jr, Potter, R. A., Ondrus, E., Onion, J. L., Dowling, A., McLoughlin, T. J., Sanchez, E. R., and Hill, J. W. (2013) Suppression of Protein Kinase C Theta Contributes to Enhanced Myogenesis in Vitro Via IRS1 and ERK1/2 Phosphorylation. BMC Cell Biol. 14, 39-2121-14-39.
41. Park-York, M., Boghossian, S., Oh, H., and York, D. A. (2013) PKCtheta Expression in the Amygdala Regulates Insulin Signaling, Food Intake and Body Weight. Obesity (Silver Spring). 21, 755-764.
42. Zamoyska, R., Basson, A., Filby, A., Legname, G., Lovatt, M., and Seddon, B. (2003) The Influence of the Src-Family Kinases, Lck and Fyn, on T Cell Differentiation, Survival and Activation. Immunol Rev. 191, 107-118.
43. Palacios, E. H., and Weiss, A. (2004) Function of the Src-Family Kinases, Lck and Fyn, in T-Cell Development and Activation. Oncogene. 23, 7990-8000.
44. Klausner, R. D., Lippincott-Schwartz, J., and Bonifacino, J. S. (1990) The T Cell Antigen Receptor: Insights into Organelle Biology. Annu Rev Cell Biol. 6, 403-431.
45. Pitcher, L. A., and van Oers, N. S. (2003) T-Cell Receptor Signal Transmission: Who Gives an ITAM? Trends Immunol. 24, 554-560.
46. Love, P. E., and Shores, E. W. (2000) ITAM Multiplicity and Thymocyte Selection: How Low can You Go? Immunity. 12, 591-597.
47. Turner, J. M., Brodsky, M. H., Irving, B. A., Levin, S. D., Perlmutter, R. M., and Littman, D. R. (1990) Interaction of the Unique N-Terminal Region of Tyrosine Kinase p56lck with Cytoplasmic Domains of CD4 and CD8 is Mediated by Cysteine Motifs. Cell. 60, 755-765.
48. Mustelin, T., and Tasken, K. (2003) Positive and Negative Regulation of T-Cell Activation through Kinases and Phosphatases. Biochem J. 371, 15-27.
49. Isakov, N., and Altman, A. (2012) PKC-Theta-Mediated Signal Delivery from the TCR/CD28 Surface Receptors. Front Immunol. 3, 273.
50. Villalba, M., Bi, K., Hu, J., Altman, Y., Bushway, P., Reits, E., Neefjes, J., Baier, G., Abraham, R. T., and Altman, A. (2002) Translocation of PKC[Theta] in T Cells is Mediated by a Nonconventional, PI3-K- and Vav-Dependent Pathway, but does Not Absolutely Require Phospholipase C. J Cell Biol. 157, 253-263.
51. Villalba, M., Coudronniere, N., Deckert, M., Teixeiro, E., Mas, P., and Altman, A. (2000) A Novel Functional Interaction between Vav and PKCtheta is Required for TCR-Induced T Cell Activation. Immunity. 12, 151-160.
52. Sun, Z., Arendt, C. W., Ellmeier, W., Schaeffer, E. M., Sunshine, M. J., Gandhi, L., Annes, J., Petrzilka, D., Kupfer, A., Schwartzberg, P. L., and Littman, D. R. (2000) PKC-Theta is Required for TCR-Induced NF-kappaB Activation in Mature but Not Immature T Lymphocytes. Nature. 404, 402-407.
53. Pfeifhofer, C., Kofler, K., Gruber, T., Tabrizi, N. G., Lutz, C., Maly, K., Leitges, M., and Baier, G. (2003) Protein Kinase C Theta Affects Ca2+ Mobilization and NFAT Cell Activation in Primary Mouse T Cells. J Exp Med. 197, 1525-1535.
54. Baier-Bitterlich, G., Uberall, F., Bauer, B., Fresser, F., Wachter, H., Grunicke, H., Utermann, G., Altman, A., and Baier, G. (1996) Protein Kinase C-Theta Isoenzyme Selective Stimulation of the Transcription Factor Complex AP-1 in T Lymphocytes. Mol Cell Biol. 16, 1842-1850.
55. Gaide, O., Favier, B., Legler, D. F., Bonnet, D., Brissoni, B., Valitutti, S., Bron, C., Tschopp, J., and Thome, M. (2002) CARMA1 is a Critical Lipid Raft-Associated Regulator of TCR-Induced NF-Kappa B Activation. Nat Immunol. 3, 836-843.
56. Egawa, T., Albrecht, B., Favier, B., Sunshine, M. J., Mirchandani, K., O'Brien, W., Thome, M., and Littman, D. R. (2003) Requirement for CARMA1 in Antigen Receptor-Induced NF-Kappa B Activation and Lymphocyte Proliferation. Curr Biol. 13, 1252-1258.
57. Che, T., You, Y., Wang, D., Tanner, M. J., Dixit, V. M., and Lin, X. (2004) MALT1/paracaspase is a Signaling Component Downstream of CARMA1 and Mediates T Cell Receptor-Induced NF-kappaB Activation. J Biol Chem. 279, 15870-15876.
58. Wang, D., You, Y., Case, S. M., McAllister-Lucas, L. M., Wang, L., DiStefano, P. S., Nunez, G., Bertin, J., and Lin, X. (2002) A Requirement for CARMA1 in TCR-Induced NF-Kappa B Activation. Nat Immunol. 3, 830-835.
59. Sommer, K., Guo, B., Pomerantz, J. L., Bandaranayake, A. D., Moreno-Garcia, M. E., Ovechkina, Y. L., and Rawlings, D. J. (2005) Phosphorylation of the CARMA1 Linker Controls NF-kappaB Activation. Immunity. 23, 561-574.
60. Blonska, M., Pappu, B. P., Matsumoto, R., Li, H., Su, B., Wang, D., and Lin, X. (2007) The CARMA1-Bcl10 Signaling Complex Selectively Regulates JNK2 Kinase in the T Cell Receptor-Signaling Pathway. Immunity. 26, 55-66.
61. Sims, T. N., and Dustin, M. L. (2002) The Immunological Synapse: Integrins Take the Stage. Immunol Rev. 186, 100-117.
62. Letschka, T., Kollmann, V., Pfeifhofer-Obermair, C., Lutz-Nicoladoni, C., Obermair, G. J., Fresser, F., Leitges, M., Hermann-Kleiter, N., Kaminski, S., and Baier, G. (2008) PKC-Theta Selectively Controls the Adhesion-Stimulating Molecule Rap1. Blood. 112, 4617-4627.
63. Huse, M. (2012) Microtubule-Organizing Center Polarity and the Immunological Synapse: Protein Kinase C and Beyond. Front Immunol. 3, 235.
64. Quann, E. J., Liu, X., Altan-Bonnet, G., and Huse, M. (2011) A Cascade of Protein Kinase C Isozymes Promotes Cytoskeletal Polarization in T Cells. Nat Immunol. 12, 647-654.
65. Billadeau, D. D., Nolz, J. C., and Gomez, T. S. (2007) Regulation of T-Cell Activation by the Cytoskeleton. Nat Rev Immunol. 7, 131-143.
66. Delon, J., Kaibuchi, K., and Germain, R. N. (2001) Exclusion of CD43 from the Immunological Synapse is Mediated by Phosphorylation-Regulated Relocation of the Cytoskeletal Adaptor Moesin. Immunity. 15, 691-701.
67. Zanin-Zhorov, A., Ding, Y., Kumari, S., Attur, M., Hippen, K. L., Brown, M., Blazar, B. R., Abramson, S. B., Lafaille, J. J., and Dustin, M. L. (2010) Protein Kinase C-Theta Mediates Negative Feedback on Regulatory T Cell Function. Science. 328, 372-376.
68. Wachowicz, K., Hermann-Kleiter, N., Meisel, M., Siegmund, K., Thuille, N., and Baier, G. (2014) Protein Kinase C Theta Regulates the Phenotype of Murine CD4+ Th17 Cells. PLoS One. 9, e96401.
69. Kwon, M. J., Ma, J., Ding, Y., Wang, R., and Sun, Z. (2012) Protein Kinase C-Theta Promotes Th17 Differentiation Via Upregulation of Stat3. J Immunol. 188, 5887-5897.
70. Soriani, A., Moran, B., de Virgilio, M., Kawakami, T., Altman, A., Lowell, C., Eto, K., and Shattil, S. J. (2006) A Role for PKCtheta in Outside-in Alpha(IIb)beta3 Signaling. J Thromb Haemost. 4, 648-655.
71. Shattil, S. J., and Newman, P. J. (2004) Integrins: Dynamic Scaffolds for Adhesion and Signaling in Platelets. Blood. 104, 1606-1615.
72. Shcherbina, A., Cooley, J., Lutskiy, M. I., Benarafa, C., Gilbert, G. E., and Remold-O'Donnell, E. (2010) WASP Plays a Novel Role in Regulating Platelet Responses Dependent on alphaIIbbeta3 Integrin Outside-in Signalling. Br J Haematol. 148, 416-427.
73. Li, Z., Kim, E. S., and Bearer, E. L. (2002) Arp2/3 Complex is Required for Actin Polymerization during Platelet Shape Change. Blood. 99, 4466-4474.
74. Serra, C., Federici, M., Buongiorno, A., Senni, M. I., Morelli, S., Segratella, E., Pascuccio, M., Tiveron, C., Mattei, E., Tatangelo, L., Lauro, R., Molinaro, M., Giaccari, A., and Bouche, M. (2003) Transgenic Mice with Dominant Negative PKC-Theta in Skeletal Muscle: A New Model of Insulin Resistance and Obesity. J Cell Physiol. 196, 89-97.
75. Gao, Z., Wang, Z., Zhang, X., Butler, A. A., Zuberi, A., Gawronska-Kozak, B., Lefevre, M., York, D., Ravussin, E., Berthoud, H. R., McGuinness, O., Cefalu, W. T., and Ye, J. (2007) Inactivation of PKCtheta Leads to Increased Susceptibility to Obesity and Dietary Insulin Resistance in Mice. Am J Physiol Endocrinol Metab. 292, E84-91.
76. Wozniak, M. A., and Chen, C. S. (2009) Mechanotransduction in Development: A Growing Role for Contractility. Nat Rev Mol Cell Biol. 10, 34-43.
77. Messina, G., Biressi, S., Monteverde, S., Magli, A., Cassano, M., Perani, L., Roncaglia, E., Tagliafico, E., Starnes, L., Campbell, C. E., Grossi, M., Goldhamer, D. J., Gronostajski, R. M., and Cossu, G. (2010) Nfix Regulates Fetal-Specific Transcription in Developing Skeletal Muscle. Cell. 140, 554-566.
78. Uberall, F., Giselbrecht, S., Hellbert, K., Fresser, F., Bauer, B., Gschwendt, M., Grunicke, H. H., and Baier, G. (1997) Conventional PKC-Alpha, Novel PKC-Epsilon and PKC-Theta, but Not Atypical PKC-Lambda are MARCKS Kinases in Intact NIH 3T3 Fibroblasts. J Biol Chem. 272, 4072-4078.
79. Kim, S. S., Kim, J. H., Kim, H. S., Park, D. E., and Chung, C. H. (2000) Involvement of the Theta-Type Protein Kinase C in Translocation of Myristoylated Alanine-Rich C Kinase Substrate (MARCKS) during Myogenesis of Chick Embryonic Myoblasts. Biochem J. 347 Pt 1, 139-146.
80. Belguise, K., and Sonenshein, G. E. (2007) PKCtheta Promotes c-Rel-Driven Mammary Tumorigenesis in Mice and Humans by Repressing Estrogen Receptor Alpha Synthesis. J Clin Invest. 117, 4009-4021.
81. Alugupalli, K. R. (2008) A Distinct Role for B1b Lymphocytes in T Cell-Independent Immunity. Curr Top Microbiol Immunol. 319, 105-130.
|Science Writers
|Anne Murray
|Katherine Timer
|Jin Huk Choi, James Butler, Bruce Beutler


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Officers arrested a Hutchinson teenager Friday night in connection to another round of church burglaries.
An employee of First Church of God, 704 N. Jefferson St., reported shortly after 7 p.m. that 17-year-old Richard Grissom Jr. broke a window of the church to gain access to the building. Officers arrived at the scene and arrested Grissom. Although nothing was reported stolen from the church, another local house of worship was not so fortunate.
Police Sgt. Tyson Meyers said Grissom took $26 in cash from Riverside Baptist Church, 114 E. Eighth Ave., less than an hour before trying to break into First Church of God. Officers also found on Grissom an allegedly stolen handgun, as well as marijuana and drug paraphernalia.
In addition to the church burglaries, Meyers said Grissom also is being held in the Reno County Juvenile Detention Center on suspicion of three counts of auto burglary believed to have been committed in the past week.
Investigators do not believe the incidents are related to the rash of church burglaries that occurred in 2012.

subset: commoncrawl


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Working Tax Credit is designed to top up your earnings if you work and you're on a low income.
You could get Working Tax Credit if:
- you're aged 16-24 and have a child or a qualifying disability, or
- you're aged 25 or over, with or without children
You must:
- work a certain number of hours a week
- get paid, or expect to get paid, for the work you do
- have an income below a certain level
The amount you are paid will depend on your your age, your income, and how many hours of paid work you do a week.
How to make a claim
You can only make a new claim for Working Tax Credit if you don't live in a Universal Credit area or you or your partner qualify for Pension Credit.
If you're new to tax credits you can order a claim form on-line or you can contact the Tax Credit Helpline on Telephone 0345 300 3900 (Textphone 0345 300 3909) between 8am-8pm Monday-Friday, 8am-4pm Saturday or 9am-5pm Sunday.
For more information, visit the GOV.UK website.
Universal Credit
Universal Credit (UC) is being phased in by the Government which will replace six existing benefits, including Working Tax Credit, with a single payment. For information vist the GOV.UK website.


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CORDAID, Netherlands
To ensure income generating resource to the children affected and persons with disability cauesed by tsunami or otherwise in Kanyakumari District.
CSR provided vocational support for income generation to 80 persons with disabilities and parents of children with disabilities. The main aim of this programme was to support the persons with disabilities to earn a regular income of atleast Rs.2500 by the end of each month . The major activities are:
Medicines Sans Frontiers (MSF).
To provide support and counselling to the following groups.
16 Tsunami affected villages of Kanyakumari District
Counseling in a disaster simply means extending an emotional support to the affected people. This is done by Showing empathy, Listening actively, Allowing them ventilation, Extending social and medical support, Externalization of interest and Telling them the value of relaxation and spirituality.
To facilitate the smooth functioning and effective management of Anganwadi centres in the coastal blocks of Kanykumari and provide support adhering to mutually agreed tools and techniques and help the district ICDS systems to follow up closely on the nutritional status of children in the temporary AWCs.
The specific objectives of the project is
5 Tsunami affected Blocks of Kanyakumari District.
Target Group:
CSR with the help of District Administration conducted five days TOT Programme to a team of 20 staffs from 9 NGOs to performstreet theatre performances on Disaster Awareness. Supported byGoI-UNDP, theprogrammewas designed to performstreet plays on disaster preparedness in the Coastal villages of Kanyakumari district. The songs and script for the Training were prepared by the R&TC Team. Each participating NGOs after the TOT underwent similar training at their level and conducted awareness events in their respective working areas.After the training 10 community based teams performed more than 100 plays. Each NGO covered 10 villages.


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The deadline is approaching to submit nominations for hometown heroes from Nebraska and Iowa who will be recognized during the Huskers-versus-Hawkeyes football game next month.
Tammy Lee, with the American Red Cross, says it's become an annual tradition, singling out valuable local leaders in both states.
Lee says, "We're looking for people who have given of themselves either in a lifesaving act or through service to their communities, gifts to others, that have been unrecognized largely."
She encourages residents in both states to fill out the simple online form and nominate someone for the award.
"We want you to look around to your friends and neighbors and see who is deserving of recognition," Lee says. "If they're selected, one person from Iowa, one person from Nebraska, they will be honored at the Heroes Game on the 24th of November."
That game will be played in Lincoln this year. Some of the previous years' honorees have been recognized for heroic, life-saving acts.
Lee says, "We also have recognized folks who have taken on a number of children in their community, that have taken on special projects, that over time maybe haven't done anything that would seem significant in terms of a single event, but people recognize they're genuinely good people and that their community is a better place for having them in it."
The two heroes will receive tickets to the game at Memorial Stadium and on-field recognition. They will also have their names and hometowns inscribed on the Hy-Vee Heroes Game trophy.
The entry deadline is October 23rd. The winners will be made public on or around November 20th. Nominations can be made here.


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What do extended low interest rates mean for you?
Interest rates are low and according to the federal reserve our slow-moving economy means that rates may not be going up during the next two years. How might this affect you? A prolonged low rate environment has several implications for people at different stages of life. Some are positive, but others aren't so rosy. The good news is that it makes borrowing money cheaper, which is great if you're considering making a major purchase like a car or home. On the other hand, it indicates a slow economic recovery, which may negatively affect unemployment and the real estate market. If you're saving for retirement, lower-than-expected yields on investments could impede your ability to meet your retirement goals if you don't revisit and adjust your financial plan.
What it means: The economic recovery is slower than expected.
The Federal Open Market committee's decision to keep interest rates low indicates that the Fed is not particularly optimistic about the economy and expects a slow recovery. If we continue to be plagued with high unemployment rates, sluggish consumer confidence and lackluster growth, consumers will have no real motivation to spend, and it may be slow going if you're looking for a new job or trying to increase your savings.
The good news: It's cheaper to borrow.
The Federal Funds rate is the interest rate that banks charge each other for overnight loans, and acts as the federal government's primary tool for stimulating the economy. The idea behind it is that low interest rates encourage spending. In theory, consumers who have access to credit at low rates are more likely to borrow money for mortgages, cars or other purchases, and then use additional capital for spending, which stimulates the economy and creates growth.
If you're looking to buy a house or car, or to finance student loans, you have a great advantage. With long-term loans like these, the cost savings from locking in a low interest rate loan can have a significant impact on your bottom line over time. If you'd like to see how this works for yourself, run two mortgage scenarios on an online calculator using the same amount and length of the loan, and compare a 4 percent to a 7 percent rate.
This doesn't mean that you should rush out to borrow simply because rates are low; everyone should only take on an appropriate amount of debt as part of a well-constructed financial plan. Interestingly, the economic environment also has made lending standards stricter - so even though it's less expensive to borrow, it may be tougher to qualify.
The bad news: It may affect your retirement.
Investors have long looked to bonds as a part of their overall asset allocation or as investment vehicles to produce retirement income. If you are planning for retirement - regardless of your age - the current economic environment may prove challenging.
In the past, financial planners and investment professionals have looked at historical interest rates to create assumptions for return models. In plain English, that means they used interest rate numbers from the past to calculate how much invested money might grow, or how much income bonds would generate. Today, traditional investment strategies, which typically have moderate interest rate assumptions behind them, are unlikely to enable investors to meet their goals. With rates at all-time lows, consumers may find themselves rethinking their allocations or looking for guaranteed income elsewhere.
Low interest rates may impact your financial goals positively or negatively - or possibly both ways. Consider meeting with a professional financial planner who can help you put together a plan to achieve your financial goals while taking into consideration the current low interest rate environment.
Byron W. Ellis, CFP, CLU, ChFC, CRPC, is a private wealth adviser with Ellis & Ellis, a financial advisory practice of Ameriprise Financial. Call or write for a free copy of "The Dream Book, Planning Beyond the Numbers." www.byronwellis.com © 2012 Ameriprise Financial, Inc. All rights reserved.


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This article has 946 Comments
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Rockstone Surfacing Ltd become the newest customer to sign up to Evolution M
For over 22 years, Rockstone Surfacing Ltd in Swindon have been providing high quality Asphalt and Bitumen Macadam surfacing solutions to clients including, government, local authorities, civil engineering and ground working contractors, agricultural and large scale commercial property developers.
15th February 2017 published by Integrity Software Webmaster
After a strong referral from Blaze Construction in Hampshire, Rockstone Surfacing Ltd requested a demonstration of Evolution M. Having seen some of the other providers in the marketplace, it was clear to the team at Rockstone that Evolution M would give them the integrated solution they required. Evolution M will enable them to move away from their current generic accounting solution and numerous spreadsheets to deliver a seamless integrated product without the need for bolt-on's or extra third party software.
A key factor in their decision to sign up for Evolution M was the number of well-established customers who already work with Evolution M in Rockstone's region. This established presence in the market place gives Rockstone confidence in the package they have purchased, safe in the knowledge that they are buying a respected and trusted solution for their business.
We look forward to developing a long-term partnership with Rockstone and working with them for a successful implementation in the coming weeks and months.
If you would like a demonstration on how Evolution M can help you implement integrated construction job costing and account management software for your business, call us today on 03453 40 30 40 or email us here.
Stevens Homes Ltd purchase Evolution M
Devon based Stevens Homes Ltd, yesterday became the latest customer to purchase the specialist construction accounting and job costing software Evolution M securing a fully integrated solution for their business. Read more
Kenaidan Contractors upgrade to construction specific software
Kenaidan Contractors Ltd are a Building and Civil Engineering company based near Kilkelly, Co Mayo who have been trading since 1974. Read more
Bellwood Homes upgrade to Evolution M
Oxfordshire housing developer Bellwood Homes today cemented their partnership with Integrity Software by upgrading their current construction specific accounting and job costing software to Evolution M. Read more


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Really? Hrithik to Romance Deepika in Kabir Khan's next?
Media has been abuzz with reports of Hrithik Roshan and Deepika Padukone pairing up together for a film since a long time. Initially, there were reports that two actors would be seen opposite each other in Vijay Krishna Acharya's film, but things didn't seem to have moved ahead. However, now there are reports that Hrithik would be seen romancing the Bajirao Mastani actor in Kabir Khan's next, which would be produced by Sajid Nadiadwala. According to a leading daily, a source told them, "Sajid has been quite keen to work with Deepika. But that hasn't worked out due to several issues. However, there are chances that Deepika might sign up for his next production with Kabir." Well, we are quite excited to see Duggu and Dippy together. What about you? CREDITS: DNA


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Data Link partners Jiangsu University
Data Link Institute (DLI) has signed a deal with Jiangsu University of Science and Technology (JUST) in China to run Bachelor and Master of Science Computer Science programmes relevant to industry.
The agreement formed part of the Institute's commitment to deliver quality tertiary education in the country and contribute to building strong human resource faculty of the nation for accelerated social and economic growth.
Mrs Ingrid Ansha, Vice President and Head of Institutional Advancement at DLI, told journalists at a press briefing on Monday that the respective academic programmes have been planned to commence in January 2017.
"It is of great importance to note that these programmes are unique in terms of content which makes them industry-relevant," she said.
"The programme structure will offer students first class knowledge in the subject areas, and convenient study sessions," he said.
"For master students, there is one year scholarship to study in China with a monthly payment of stipend and partial scholarship for undergraduate students who are expected to do two years of their programme duration in China per the arrangement.
The Institute with nearly 2000 student population says it is in the process of also establishing collaborations with several other universities in Ghana and abroad.
The institute already runs professional programmes with the Chartered Institute of Logistics and Transport, UK for certificates, Diploma and Advanced Diploma Programmes and serves as an accredited centre for ICM and ACCA programmes.
Institute established and inaugurated in 2006, has operated as an accredited higher education body and duly recognised by National Accreditation Board (NAB).
The DLI is affiliated to Kwame Nkrumah University of Science and Technology in collaboration with University of Education, Winneba.
It is committed to the delivery of a holistic higher education that focuses on the physical, social, spiritual and mental development of students for service to communities.


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The Montana round crib bedding set combines Blue Denim (Dark Denim) and Ticking to echo the simple elegance of Americana. It is luxurious, stately, and a timeless creation only from Little Miss Liberty.
Consider making your own group like this sample - Canopy Set (Bumper, Dust Ruffle, 1 Contour Sheet, 4 Canopy Valances plus 4 Canopy Drapes and 4 Ties)
Heart-Shaped Crib Bedding Set also available, same price.
Montana can also be purchased by individually-selected pieces.
Desired Canopy Covers must be purchased separately.
FREE SHIPPING on orders of $300+
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Note: All prices in US Dollars


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This is a list of quotes for the solo character Devilotte. Like the other solo characters, she has a unique pre-battle dialog with all the paired characters and additionally, around five post-battle dialogs with select paired characters.
- If you don't perform up to spec, I'll use you for parts in one of my creations!
- I see, I see. That sounds fun ♪
- Behod the glory of Princess Devilotte, the beautiful flower of evil!
- Oh just shut up and get on with it!
- There's no stopping now, even if I wanted to!
- I'll show you what it means to be bad!
- That's acceptable. Shall we play with them a bit?
- Go ahead and get excited while you still can.
- Do good here and I may even take you in as one of my minions.
- I'll make an exception this time and let you off with a punch from Blodia.
Solo BeginEdit
- Make way, idiots! You're in the way!
- Reality is brutal, isn't it!
- And now, some secret weapons!
- Fool! A Princess is in your presence!
- I will show you!
- I forbid this world's justice!
- Take a gander at this!
- Ho ho ho ho! Get outta my way!
- Think of this as an honor!
- Princess Devilotte makes her appearance!
Solo FinishEdit
- A-aah!
- Tsk!
- N-wha?
- Ngh...
- Wh-what?
- Oh wha--?
- Heh?!
- Hyaa!
- Ahhh?
- Being bad always makes me feel so good ♪
- That was a pretty shabby performance. I think you could use some more time in the fire.
- That felt great! I'm going to sleep well tonight.
- I'll stoop as far as I have to in order to win!
- Yes, that's acceptable. You are now free to praise me too.
- You could never beat me, even in 1 million years and 4 months!
Paired CharactersEdit
Akira Yuki & Pai ChanEdit
Devilotte: The armies of my kingdom are full of soldiers as strong as this enemy!
Akira: That's pretty impressive. I'd like to go and take a few of them on.
Pai: And just how are you going to get into space, not to mention the future?
Chris Redfield & Jill ValentineEdit
Devilotte: You soldiers should be soldierly and get out there on the frontline!
Chris: Don't get the wrong idea. We aren't soldiers.
Jill: Even though our work is sometimes more difficult than military missions...
Chun-Li & MorriganEdit
Devilotte: Perform well enough, and I may even recruit you as one of my minions.
Morrigan: Well, it sounds like we wouldn't be bored at least. What do you think, Chun-Li?
Chun-Li: A member of law enforcement shouldn't become a minion of evil.
Dante & Demitri MaximoffEdit
Dante: I guess I should probably try to show what I can do in front of a princess.
Devilotte: I like your attitude. I'll you remake you two as a gorgeous devil and a muscle-bound onion!
Demitri: Would you care to try repeating that, little girl?
Frank West & Hsien-KoEdit
Devilotte: You'd better make me look good! Do it well enough and you may even get a reward!
Frank: Well then, I'll just have to do my best work, princess.
Hsien-Ko: I think you'd better find out what she means by a "reward" before we get started…
Gemini Sunrise & Erica FontaineEdit
- Devilotte: Fight well and I may even rebuild you two as a patchwork monster!
Gemini: Oh my god! But wait, what's a patchwork monster?
Erica: We'd probably be called Gerica Fonrise.
Haken Browning & Kaguya NanbuEdit
Devilotte: Kaguya, I'm willing to convert some of your "excess baggage" you're carrying around into weaponry.
Kaguya: E-Excess baggage? And what do you mean by weaponry?
Haken: Don't worry princess. They already look explosive enough to me.
Devilotte: Very well. I suppose that was satisfactory.
Kaguya: Is that the proper way for a princess is supposed to speak?
Haken: I'm not sure if I would consider her a good standard to learn from.
Ichiro Ogami & Sakura ShingujiEdit
- Ichiro: Now is the time to stand up for justice! Let's go!
Devilotte: In that case I will fight for the glory of evil! Right, Sakura?
Sakura: U-Um, I'm actually on the side of justice, too!
- Devilotte: Too weak! I think Ogami here needs some upgrades...
Sakura: Maybe you can fix his brain first so he doesn't have such a dirty mind...
Ichiro: Eep! W-What are you asking her about, Sakura?!
Jin Kazama & Ling XiaoyuEdit
Devilotte: You know, Jin, I wouldn't mind rebuilding you as a monster with beam vision.
Jin: Sorry, but I'll pass.
Xiaoyu: Yeah, beam vision... That would be pretty cool!
Kite & BlackRoseEdit
Devilotte: The World, a realm in cyberspace... Someday, it will be mine as well!
BlackRose: I wouldn't try it if I were you. That would make us enemies.
Kite: A quest to defeat the princess... That sounds pretty innovative, actually.
Kogoro & MiiEdit
- Devilotte: You might have money, but a peasant will always be a peasant! What the hell are you wearing?
Mii: H-Hey let go of me! Kogoro!
Kogoro: Let's save the fun stuff for after the battle.
KOS-MOS & T-elosEdit
T-elos: Fool! I'll crush you like an insect!
Devilotte: I haven't seen such pure evil in years. You have my permission to join the Four Heavenly Kings!
KOS-MOS: That does not fall within the purpose for which we were constructed, so we must decline, Devilotte.
Kurt & RielaEdit
Devilotte: Don't let me catch you two messing up! Otherwise it's the flame pits for you!
Riela: What?! She's crazy Kurt!
Kurt: Calm down. Nobody uses such inhumane punishments.
Reiji Arisu & XiaomuEdit
Xiaomu: Your techniques are the ultimate fusion of dreams, hope, and friendship, right?
Devilotte: Sorry, but I'm not really into ultimate fusion.
Reiji: I have absolutely no idea what they're talking about.
Reiji: You both should start taking things more seriously.
Devilotte: How dare you insult my multitude of top caliber skills!
Xiaomu: They call that getting carried away.
Ryu & Ken MastersEdit
Devilotte: Fight well enough and I might even consider remaking you two into one of my patchwork creations!
Ryu: P-Patchwork creations?!
Ken: We'd probably be able to pull off a Metsu Shinryuken.
Soma Schicksal & Alisa AmiellaEdit
Soma: What do you want, little princess. Quit staring at me.
Devilotte: That devouring mechanism... Maybe I can get the doctor to make me one.
Alisa: It's not something you can just go and make as simple as that.
Toma & CyrilleEdit
Devilotte: Even our foes fear the glory of the Deathsatan family! Hahaha!
Toma: Why do people from royalty always have to be such a pain?
Cyrille: Quiet! She'll be even more of a pain if she hears you!
X & ZeroEdit
Devilotte: Now my Maverick Hunters, go forth and defeat our foes!
Zero: I don't recall joining the service of the Deathsatan Royal Family.
X: Just think of it as protecting a member of the royal family.
Devilotte: At this rate I will soon have the power to rule the entire galaxy!
X: She's started raving about some pretty serious ambitions here...
Zero: Don't get carried away, kid, or we might be forced to take you down.
Yuri Lowell & Estellise Sidos HeurasseinEdit
Estelle: The punishment for defying us is being burnt alive…I guess!
Devilotte: Not good enough! You've got to look down on them more like the scum they are!
Yuri: Don't try to give Estelle any bad ideas. Flynn will get mad at me.
Devilotte: The final form of a princess is the Evil Empress of the Heavens!
Estelle: Empress of the Heavens…! The one rules all of creation!
Yuri: It'll never happen, so don't let her bad example rub off on you…
Zephyr & LeanneEdit
Zephyr: Leanne, doing your makeup is fine, but don't fall behind!
Devilotte: If you're hoping to become one of my female minions, then you need thicker eye shadow.
Leanne: I'm not trying to become one of your followers...


text:
1/30/14 Thursday at Kissimmee, FL (Sherwood Forest RV Resort-Encore)
Spent our morning getting caught up on computer dealings. We had a special treat lined up for the afternoon: Dinner and Show at Capone's. Through the Internet or a small coupon book you can get the discounted price of $29.99/person. You will have to add tips. Well worth it. Fun Chicago style characters welcome you to your table and invite you to the buffet line. Great food and plenty of it. Oh, I forgot to mention that you get free drinks (including alcohol) – no limits. Wonderful performances with song and comedy and lots of audience participation. Memorable. We definitely recommend enjoying this. Bonus: it just happened to be only 2.6 miles from our campground.


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Pictured working inside Soigneur bike shop in Copenhagen is co-owner Jacob Lindsel. The store provides high quality bikes and equipment to serious riders, especially those who take part in the sport of Cyclocross.
- Copyright
- © 2014 Photography by Matthew James
- Image Size
- 4172x2776 / 6.8MB
- Contained in galleries
- Portraits Portfolio


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01 "Black Blood Brothers" "Kuroki chi no kyōdai" (黒き血の兄弟)
Ten years after the Kowloon Shock, Jiro Mochizuki and his little brother, Kotaro, return to Japan so they can go to the Special Zone. Inside the ship, Kotaro sneaks out, despite the fact that Jiro told him not to. He then meets a girl name Chan. Chan promises to keep their encounter a secret. On the ship, Kotaro is caught in the middle of a fight between the Special Zone Supression Team and a group of refugees. Jiro is awakened by the fighting and punishes Kotaro for disobeying him. Jiro asks why is everyone fighting. The leader of the refugees introduces herself as Kelly Wong. She accuses The Suppression Team for being nothing but homicidal maniacs. The Suppression Team then explain that they won't allow Jiro, Kelly, and the refugees to enter the Special Zone illegally. However, if they have premission from the owners of the Special Zone then the Special Zone, they will be accepted. Jiro comfirms that he is unfamiliar with the concept. The Suppresion Team attack Jiro, but Jiro uses Hide-Hand to defend himself During the fight, the ship's deck explodes. As a result, Kotaro falls into the ocean and Jiro jumps in to save him. Kelly and the rest of the refugees escape through a small boat. Meanwhile, Mimiko Katsuragi, a Compromiser from the Company, receives a call from Jinnai.
02 "Compromiser" "Conpuromaizā" (調停員(コンプロマイザー))
Mimiko is dispatched to a beach to investigate.There, Jiro and Kotaro are washed up into a beach where they are saved by Mimiko. Mimiko agrees to show them how to reach the Special Zone. They are approached by Kelly Wong and Johan Tsang, the two vampires from before. They want Jiro to aid them while the Suppression team set out to to destroy them. Kelly is shot in the arm, so Johan helps her escape. Jiro plays decoy with the Suppression team so that Kotaro can escape. Kotaro makes it out safely, but Jiro is captured by the Suppression team.
03 "Kowloon Child" "Kūron chairudo" (九龍の血統(クーロンチャイルド))
Kotaro meets up with Johan. Johan tells Kotaro to come with him and Kelly so that they can help him find Jiro. Mimiko arrives and comes along woth them. Jiro is questioned by the head of the Suppression team, Badrick. Badrick explains that one of the refugees may be a Kowloon Child. For that reason, the Suppression Team must exterminate them all. At Chinatown, Kotaro and Chan are playing with plane airplanes. Kelly explains to Mimiko that if she would have let him drink her blood, Jiro would've easily escaped the Suppression team earlier. Mimiko explains to Kelly that Kowloon children can turn people just by drinking their blood and can even turn other vampires. Kelly explains that Kowloon Children are similar to all other vampires because they are all seen as monsters. Mimiko then explains that Kowloon Children kill the people they feed on. Thus, Kowloon Children are nothing like other vampires. Chan appears before Kotaro as a Kowloon Child. Meanwhile, Rinsuke releases Jiro. Back at Chinatown, the Suppression Team once again attack the refugees. It is then revealed that Johan is the kowloon child and has infected the remaining refugees. Jiro, finding out, goes to save Kotaro and Mimiko who are with them. Kotaro is kidnapped by Johan, along with Chan, and Kelly's friends, who became Kowloon children.
04 "Old Blood" "Ōrudo buraddo" (古血(オールド·ブラッド))
Jiro is weakened after everything that happened. Despite this, Jiro still wants to save his brother. Mimiko tries to convince him not to. So she decides to let him drink her blood. After drinking Mimiko's blood, Jiro recovers his strength. Badrick gives Kelly premission to enter the Special Zone. Jiro sets out to save Kotaro. Jiro defeats Johan's allies and arrives at the twilight brige, where Johan is trying to enter the Special Zone. Jiro uses Hide-Hand to shake the entire bridge which causes Johan to drop his guard, but Chan protects Johan. Kelly then shoots Cham in the neck, killing her. Johan tries to kill Kotaro, but Jiro kills him. In the end, Jiro and Kotaro are invited by Mimiko to come stay with her in the Special Zone. Jinnai is notified of the situation regarding Jiro. Mimiko invites Jiro and Kotaro to spend the night with her.
05 "Special Zone" "Tokku" (経済特別解放区(トック))
Mimiko helps Jiro and Kotaro look for a place to live in. Hibari, another Compromiser from the Company, discovers that Mimiko is traveling with the Silver Blade. The Company discuss the issue of having Jiro in the Special Zone while a vampire named Zelman sets out to meet him. Jiro, Mimiko, and Kotaro are attacked by the Coven and their leader, August.
06 "Coven" "Coven" (夜会(カヴン))
After defeating their attackers, Jiro and company go to meet Zelman. After meeting Zelman, the group bump into Rinsuke, Sei, and Kain and they have a picinc. Kain explains that both he and Sei can't allow Jiro to stay in the Special Zone. On the way home, they are attacked by the Coven once again. As an act of revenge, August bombs Mimiko's apartment.
07 "Silver Blade" "Gintō" (銀刀)
Jiro, Mimikko and Kotaro are standing in front of Mimiko's burning apartment. Jiro was extremely agitated that August went on to Blew up Mimiko's place. Mimiko said that it's okay and that their new plan is to go to the office of the Order Coffin Company to make sure that Jiro and Kotaro can stay safe in the Special Zone. Elsewhere, Zaza is seen on a boat at the river. He suddenly notices that Yafuri sneaked out. To make matters worse, he recives a call from Cassandra. Upon reaching the office, all the leader of the 3 Bloodlines in the special zone came together with a former vampire hunter, Jinnai, Kain and the president of OCC. Mimiko speaks to them regarding Jiro's situtation while the brothers wait outside the room. Kain decides that August must be punished by his action and that no one else mus take his place after he's gone. Meanwhile, Sayuka was seen with several men, one of which was trying to carry a seemed to be lifeless body. However, as one of them started carrying the dead guy, he suddenly woke up and bit the the guy carrying him. The other quickly threw him to the ground and started kicking him until he turns to dust. They were all shocked by what happened but only after a few seconds, the guy who was bitten seemed to have transformed and started biting and killing the other men. Back at the meeting, Kain made it clear that he and Sei are not gonna let Jiro stay in the Special Zone since he only brings trouble. However, Zelman said that if no one is willing to accept Jiro into their place he will. Kain again expressed his concern with his decision. Shortly after, Kotaro was heard talking to the guard outside looking for Mimiko. Kain allowed Kotaro to come to the room. Kotaro came bursting into the room and informed Mimiko that Jiro has left the building and told Kotaro that he will teach someone a lesson. Kotaro said that he was smiling but the look in his eyes is very scary and that he was worried. Kain immediately ordered to call the Suppression Team of the company to stop Jiro. Mimiko made her objection about the matter but Kain explained that no red blood can know that old bloods are fighting as this may result into bigger conflilcts. Jinnai then talks to Mimiko who was crying and gave her a mission: to find Jiro and make sure no commosion happens since that is the job of a compromiser. After Mimiko and Kotaro left, Jinnai changes the subject of the meeting from Jiro to the Kowloon Children. Sei was asked if there was a way to detect if a Kowloon Child enter the Special Zone. He said the barrier he built was not made to detect them. Zelman commented that the Special Zone will act as a prison to any Kowloon Child who entered since it's technically impossible to get out as the barrier is controoled by Sei. Back in the office, Zelman receives a call from Sayuka. Zelman then put his phone on speakers and let the others listen to Sayuka. Sayuka explained exactlly what happen and confirmed that the first guy was bitten by August. Kain then ordered to have the Suppression Team change their gear to the one specifically manufactured for fighting the Kowloon Children. Jiro is now seen attacking the mansion, impaling every vampire that stands in his way. As Mimiko and Kotaro arrived at the mansion, Jiro was seen standing in front of the door waiting for them. Mimiko immediately threw fits at Jiro saying that what he did will compromise his situation at the Special Zone. Jiro said that he just wants the others to know what will happen to them if they mess with him. Mimiko again promised that they will stay in Special Zone but Jiro wants to leave. He said that that is that only way for Mimiko to be safe but Mimiko objected. Mimiko was then attacked by August who is now a Kowloon Child. However, she was saved by Jiro and they started to fight. Jiro asked him who bit him to become what he is. August said he wasn't bitten but instead drank the blood of a Kowloon Child. Jiro defeats August when two other Coven vampires attacked both him and Mimiko and Kotaro. Jiro saved himself but did not have time to save Mimiko and Kotaro. Fortunately, they were saved by Yafuri. Although he save the two, Jiro quickly went in between them and confirmed with Yafuri that he is a direct descendant of the Kowloon King. Yafuri informed Jiro that he was turned into Kowloon Child before Jiro defeated the Kowloon King. Yafuri also told Jiro that in the past 10 years, his sister Cassa has said nothing but she wants to see Jiro again. Jiro was deeply upset.
08 "Protector" "Goeimono" (護衛者)
Jiro fights Yafuri, but Yafuri seems to have the advantage. Their battle is interupted by the arrival of the suppresion team. Jiro leaves Mimiko. The Company discuss how they will handle the case of Kowloon contamination in the Special Zone. Kain explains his history with Cassandra Jill Warlock, explaining that she may be involved. Zaza tells Yafuri that he shouldn't confront the Silver Blade by himself, but Yafuri ignores his warnings. Kotaro leaves Jiro so he can say good-bye to Mimiko. Mimiko wakes up in a hotel where she meets Hibari and Kelly. Kelly encourages Mimiko to find Jiro. Kain explains to Jiro that Cassa and the Kowloon children aren't after him or his brother.
09 "Eleventh Yard" "Irebun yādo" (第十一地区(イレブン·ヤード))
Mimiko and Kelly try to look for Jiro. Kotaro is rescued by Zelman. Kotaro continues to look for Mimiko. Zelman joins him. The Suppression team discover a bunch of vampire bodies. Rinsuke tells Jiro that he'll help him find Kotaro, but he wants Jiro to find Mimiko so that he can apologize to her. Kain battles Yafuri. Kain is badly injured, but is able to defeat Yafuri by turning to Kain the blue wolf. Mimiko and Kelly discover illegal inventory of vampire blood. Also, Mimiko learns a dark secret about Kelly.
10 "Order Coffin Company" "Ōdā Fofin Kanpanī" (オーダー·コフィン·カンパニー)
The false Kelly Wong is actually Cassa, who is holding Mimiko captive so that she can see Jiro again. Rinsuke become unconcsious due to hypnotic suggestion by Kain. As Cassa prepares to turn Mimiko into a Kowloon child, Kotaro and Zelman comes to her rescue. Hibari tells Jiro where he can find her. After her fight with Zelman, Cassa decides to leave, but not before giving a message about the Coven. The Company discover that the vampires that the Suppression team rescued in the previous episode are actually Kowloon children as they start infecting others with their blood. Jinnai learns that it was because of the blood packs that Mimiko discovered. Sei is confronted by Zaza, who tells him that if he doesn't tell him the location of the Eleventh Yard, he will destroy the OCC building with a hidden bomb. Before he could, he was impaled by Zhang. Zaza then steals a body of one of the Suppression team members, then helps Yafuri escape.
11 "The Ocean" "Umi" (海)
The Special Zone is plunging into disaster. Kain discovers that Yafuri has escaped. Sei sets out to end the outbreak of Kowloon children. Yafuri and Zaza start searching for Cassa, but are attacked by Kain. The Suppresion team are having trouble maintaning the outbreak, but are rescued by Sei. Zelman is seen killing members of the Coven, due to the fact that they're Kowloon children. Meanwhile, Kotaro convinces Mimiko to talk to Jiro so that that they can live in the Special Zone. Jiro finds Kotaro, but he still wants to leave the Special Zone. Kain is catching up with Yafuri and Zaza, but is stopped by Cassa. After a long conversation with Jiro, Mimiko is finally able to convince him to stay with her. Shortly after, Zaza appears as a Kowloon child and shots Jiro multiple times with a gun. Jiro falls into the river, with Zaza jumping in and stabbing Jiro mltiple times. Mimiko jumps in an attempt to save Jiro's life.
12 "For the Eternal Pulse of Mine Bloodline, I Would Offer This Blood in Totality" "Waga kettō no eien naru kodō ga tame kono chi no subete o sasage n koto o" (我が血統の永遠なる鼓動がためこの血の総てを捧げんことを)
Jiro stops Zaza from killing Mimiko, but he is severely injured. Mimiko, however, allows him to drink her blood. Now fully healed, Jiro defeats Zaza and heads toward his final battle with Cassa. Sei clears the way for Jiro so he can get there faster. On the way, Jiro explains that he and Kotaro came to the Special Zone so that Kotaro can make new friends. Jiro doesn't want Kotaro to be alone when he's not around anymore. The vampire that turned Jiro was Alice Eve, the Sage. She was a source blood, and one of the most ancient black bloods. She never wanted to share her blood with anyone, except for Jiro, who is the only person she shared her blood with. As her protector, it's Jiro's responsibility to keep her body and her blood safe. Unfortunetly, she was killed in Hong Kong, but was reborn as a child: Kotaro. Once Kotaro fully matures, Jiro will return Ailce's blood to her. Afterwards, he will live on through her. Jiro concludes his explanation saying that this is what it means to be a vampire, that it's their destiny to sacrifice anything for the sake of their bloodline. Jiro finally catches up with Cassa, and they both have their final battle. Kain confronts Yafuri, but is defeated. Zelman uses eye ignite to slow down Zaza and Yafuri, but when he notices that they made it through, he lets them escape. Yafuri notices that Cassa is having trouble with her fight with Jiro. He tries to help, but Jiro kills him. Jiro prepares to finish off Cassa, but it starts raining, which makes him weak. However, he managed to overcome this weakness and charges towards Cassa. Zaza tries to stop Jiro, but Jiro kills him. Jiro and Cassa both impale each other, but they both survive. Cassa escapes the Special Zone. Sei closes the barrier so that no more Kowloon children can enter the Special Zone. Peace has finally returned to the Special Zone. Mimiko wakes up in a hotel, where Kotaro gives her money for rent. Meanwhile, Jinnai explains to Jiro that it wasn't August who bombed Mimiko's apartment(see episode 6). The bomb was placed by his command. It was so that Jiro would stay in the Special Zone. Jinnai tells Jiro that there's a old building that the Company once use as a warehouse. It's really old, but more than big enough for three people. Jiro asks Jinnai about the Eleventh Yard. Jinnai said that the Eleventh Yard contains ashes of the Kowloon king. Cassa and the Kowloon children came to the Special Zone to retrieve the ashes. They wanted to resurrect him. Jinnai explains to Jiro that he is the Special Zone's only chance of survival due to the fact that Jiro killed the Kowloon king in the past. Jinnai concludes by saying that he is no longer capable of fighting along side Jiro, so he must protect the special Zone, Mimiko, and Kotaro(aka the Lord Sage, as Jinnai calls him) alone. The next day, Jiro tells Mimiko that she can't tell Kotaro what Jiro told her yesterday. Mimiko, Jiro, and Kotaro receive their first assignment and head straight for work. Mimiko notices the look on Jiro's face, but believes everything will work out.


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A complete makeover for Skyrim's citizens. New faces, hairs, and bodies, designed for the lore-friendly adventurer.
I owe a lot of people praise and credit for their assets in helping make this mod. You must contact both me and the mod authors listed below if you wish to modify Diversity in any way. Thank you.
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22/07/2012 European Commission Access City Award, Third Edition, 2013
The European Commission opened the competition on 22 May for the third "Access City Award", the European Award for Accessible Cities. The annual prize recognises and celebrates cities that are dedicated to providing an accessible environment for all, and for persons with disabilities in particular. 0 comments
05/06/2012 Transport accessibility for all users under threat in Council discussions on new TEN-T guidelines
Representing a wide coalition of European organisations acting on behalf of the transport industry and the transport passengers, we call upon the Council of the European Union and the European Parliament to uphold article 43 of the Commission's proposal for the development of the trans-European transport network. 0 comments
24/11/2011 A special ENAT offer on two essential Accessible Tourism books
Order these two new textbooks on Accessible Tourism from Channel View Publications and make great savings, thanks to this deal arranged with ENAT. The offer closes on 31 January 2012. 0 comments
17/11/2011 EU Access Cities Award competition advances towards the December final
Eight cities have been shortlisted for the prestigious European Access City Award 2012. With 114 entries from 23 EU countries, the jurors had a challenging task identifying the finalists. 0 comments
29/10/2011 Call for Abstracts, Interdependence 2012 Conference, Vancouver, Canada
Co-hosted by the Rick Hansen Foundation and the Rick Hansen Institute, Interdependence 2012 is an international four-day conference and exposition with a focus on creating accessible communities and furthering spinal cord injury (SCI) research for a cure. Abstracts are now invited for presentations in the theme session on "Making Communities Accessible for All". The two sub-themes are "Accessible and Inclusive Tourism" and "UN Convention on the Rights of Persons with Disabilities". 0 comments
01/02/2011 Coming Soon - Access to all in Europe: A Study About 11 Cities
This spring, Certu (the Centre for Studies on Urban planning, Transport and Public facilities, France) will publish a study about practices improving access for all in 11 European cities. This analysis is part of a comprehensive review led by Certu to identify interesting examples of accessibility practices in Europe. 0 comments
20/08/2010 European Passengers' Rights - a New Campaign Takes Off
This summer the European Commission has launched a new campaign to raise awareness of passengers' rights. Although the European Union has made great strides in establishing common passenger rights for those travelling by air or rail, not every European is yet aware of what he or she is entitled to. This campaign sets out to make all air and rail passengers aware of what rights they enjoy under European legislation and how to make use of them. 2 comments
16/03/2010 Three UK West Country Attractions in line for Accessible Tourism Awards
Three West Country businesses have been shortlisted for the first UK tourism award recognising attractions with access for disabled visitors. The new Rough Guide to Accessible Britain Awards named the Totnes Rare Breeds Farm, alongside the South Devon Railway and the Eden Project in Cornwall. 0 comments
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01/06/2010 Sport and leisure for all in Vuokatti, Finland
For long Vuokatti is known worldwide for its superb sports and leisure facilities. It has been a regular host for all levels of athletes and individuals who enjoy practicing a physical activity in a purely natural and friendly setting. The Elma project is focussed on developing a sustainable, Universally Accessible destination for all. 0 comments
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26/03/2010 Take Charge of Your Travel. A Guide for Persons with Disabilities
This guide was written to provide advance travel information for persons with mobility, sensory and/or cognitive disabilities.
23/01/2010 European Disability Forum Comments on AFNOR Feasibility Study on Accessibility to Tourism and Transport Services to Disabled People
EDF considers that the developments of terminology and classification standards are necessary in these areas as a pre-requisite for any future initiative on access to transport and tourism services. Clarifying the definition of disability on one hand, and of accessibility to transport and tourism services on the other, is crucial. EDF underlines the importance of basing all standardisation initiatives on the social model of disability and on a human rights approach.
02/12/2009 Accessible Tourism. Good Practice Guide, Catalonia
This Guide presents a selection of 19 destinations which offer a full range of adapted tourist resources so that everyone has the chance to enjoy Catalonia's important cultural heritage, its impressive landscapes, its rich gastronomy, and even sporting activities.


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Ideas For Baby Shower Gifts – Gone will be the full days when baby showers were designed on generic, age-old clichés and ideas. Today, most expectant father and mother design the baby shower around a theme with most of these styles revolving around the gender of the child to be. Everything is designed and planned in line with the theme. There happen to be three directions or broader styles around which any baby shower celebration get together would revolve- boy, twins or girl. So, if you know that the shower party is certainly inclined towards a specific gender of the child to be, then you ought to choose a gift that suits the theme and the overall mood of the get together.
On the right section of the parents as well, it becomes all the more vital that you design and set their get together up in such a way that it speaks volumes about the themes of the get together. For a ongoing get together set around a boy, from shower favors, to the centerpiece and the cake should be in consonance with the theme. Darker and soberer colors, such as for example blue and black should be used appropriately. The choice of baby shower celebration favors boys-type should be kept in brain. Guests also needs to prepare the gifts appropriately, which might contain diapers, pacifiers, and boys-toys such as for example cars, trfavoursnd toy weapons.
Be careful that you are not presenting anything that has a probable choking hazard connected with it. Again, if you know that you are going to become blessed with a baby female, you should keep carefully the theme more women centric. From using liberal levels of pink in décor apart, foodstuff, beverages, and cakes, you ought to be certain that you have narrowed down your choice of favor to baby shower celebration favors girls would love to cherish after searching at their shower images and photographs, couple of years after their birth. Friends should choose their presents as well accordingly.
Clothes containing more shades of red and pink, with frills and ribbons all over should suffice. To add an additional flavor, you can amalgamate your gift with a choice of selected baby-edible chocolates, which girls would adore just. Finally, you may be one of those lucky few to have been blessed by twin babies. The selection of baby shower celebration favors twins want becomes all the more important in this instance, day that a few is blessed by twins because it will not happen every. Of one cake instead, centerpiece and diaper cake, you could have a pair.
As another addition, you could orient the get together towards the gender of you twin babies, if you happen to know it before delivery. The very best circumstance arises if among the babies will be a female and the other one would become a boy. In such a situation, the prospects you have while developing the whole baby shower celebration party are limitless. From colours to cakes to diapers and foodstuff and favors even, you can contain a complete gamut of supplies, and never have to worry too much about the appropriateness of the plain thing being used in accordance with the theme.


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What You Need:
-1 Box of Cupcake Mix (eggs, oil, water)
-1 Can of Frosting
-Bag of Candy Corn
-Halloween Platter/Dish/Tray
Follow the simple instructions on the back of the cupcake mix box. Once baked and cooled, frost each cupcake and place (1) candy corn on top. Then, position them on your serving tray and sprinkle the remaining candy corn around the cupcakes so you have a festive, colorful, Halloween treat!
[Cupcakes are ready to be frosted]
[Vanilla icing is the best]
[Candy corn time]
[Decorated & ready to go]


text: Fog lights wont turn on [Archive] - GrandAmGT.com Forum GrandAmGT.com Forum > GAGT - Technical - Sponsored by www.MilzyMotorSports.com > Technical Q&A > Fog lights wont turn on PDA View Full Version : Fog lights wont turn on icecats8710-18-2009, 04:00 PMJust replaced both fog bulbs and they still wont turn on, any ideas why? lone_wolf02510-18-2009, 10:25 PMCheck the usual stuff of fuse and switch. If the light on the switch comes on the fuse and switch should be good. If they still dont come on push the wires further into the plug and see if that does it. icecats8710-18-2009, 10:32 PMill try it but when i flip the switch to turn it on the light doesnt even come on is it the fuse or loose wire? Malaclypse10-19-2009, 07:54 AMNo guarantees this is your problem, but I've seen a bad BCM cause the foglamps not to work before. aiixon10-19-2009, 12:23 PMtake a test light to the power wire and that will let you know if you are getting power or not. If not, it is probably a fuse. If you are getting power then it's the switch at fault since you just changed your bulbs. Haughee10-19-2009, 07:13 PMDo you hear a click when you flip the switch? You should hear a click which is the relay switching the lights on. Mine went bad and the switch light would not turn on. Try replacing the relay its in one of the fuse boxes by the doors. I'm pretty sure that is your problem. vBulletin® v3.7.2, Copyright ©2000-2019, Jelsoft Enterprises Ltd.