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When building projects using a microcontroller there will come a time when you need to drive a load that exceeds the raw current capability of the device. Eric Wolf wrote a BJT Transistor article that will demonstrate how this can be done.
Intense in erectile that professionals staxyn . Intense in erectile that professionals...
Thats a perfect article about principles of electrical engineering. The Main point is that it is written very easy to understand, first of all for people who doesn't have a technical apprenticeship. Good work!
We used that simple cirquit (but omitted R1 and increades R2) to drive a superflux-LED at 30 mA using a PWM… the oszilloscope came up with a discharge-curve for the current flowing through the LED on the falling edge of the µC. No charging curve could be seen.
Tests showed that a Capacitator around 10µF produced a comparable discharging curve, but the LED-cirquit can't have more than a few pF.
Does anyone have an idea how to avoid this? More infos on demand if needed.


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Monday, February 10, 2014
Halloween: Magic, Mystery and the Macabre, by Paula Guran (ed.)
Edited by Paula Guran
Published by Prime Books
Publication Date: October 1, 2013
Source: NetGalley
View on Amazon
If only I'd had more time this Halloween, I would have lingered over these stories more! Unfortunately this has been a very busy month (couple of months actually) for me and it seems like I never have enough time to read, which is bad considering my hobby is writing book reviews. It's not that I'm not reading; it's just that I'm fitting it in when I can, speed-reading or sneaking in a chapter in between other chores. What I really miss is having the time to sit down and read--undisturbed--for hours on end.
And that's what this book would have been good for. Curling up on the cold nights leading to Halloween and getting lost in spooky stories. They reminded me a lot of the sort of horror fiction I read as a child, à la Stephen King. There are tales of haunted movie theatres, bodies that don't stay buried, and good old-fashioned ghosts and ghouls. Luckily, most of the stories were short enough that I could fit them in to my reading schedule without any trouble. But if you have the time, I'd recommend lingering over them, preferably at night with the lights low and the house creaking.
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The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis
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CHD8 directly regulates C/EBPα and PPARγ during adipogenesis
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CHD8 interacts with C/EBPβ and promotes its transactivity
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CHD8 ablation in preadipocytes results in a markedly reduced fat mass
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CHD8 is essential for not only neuronal development but also adipose development
The gene encoding the chromatin remodeler CHD8 is the most frequently mutated gene in individuals with autism spectrum disorder (ASD). Heterozygous mutations in CHD8 give rise to ASD that is often accompanied by macrocephaly, gastrointestinal complaints, and slender habitus. Whereas most phenotypes of CHD8 haploinsufficiency likely result from delayed neurodevelopment, the mechanism underlying slender habitus has remained unknown. Here, we show that CHD8 interacts with CCAAT/enhancer-binding protein β (C/EBPβ) and promotes its transactivation activity during adipocyte differentiation. Adipogenesis was impaired in Chd8-deleted preadipocytes, with the upregulation of C/EBPα and peroxisome-proliferator-activated receptor γ (PPARγ), two master regulators of this process, being attenuated in mutant cells. Furthermore, mice with CHD8 ablation in white preadipocytes had a markedly reduced white adipose tissue mass. Our findings reveal a mode of C/EBPβ regulation by CHD8 during adipogenesis, with CHD8 deficiency resulting in a defect in the development of white adipose tissue.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with a high prevalence (∼2% of the global population) (Schaaf and Zoghbi, 2011, Taylor et al., 2013). Recent exome-sequencing studies of individuals with ASD have identified many mutations, with the gene encoding the chromatin remodeler CHD8 (chromodomain helicase DNA-binding protein 8) being the most frequent site of such mutations (Neale et al., 2012, O'Roak et al., 2012a, O'Roak et al., 2012b, Talkowski et al., 2012). Many studies of CHD8 have thus focused on its role in neurogenesis and brain development (Cotney et al., 2015, Sugathan et al., 2014). CHD8 is expressed not only in neuronal tissues but also in many other organs, where it may also play an important developmental role (Ishihara et al., 2006, Nishiyama et al., 2009). Indeed, individuals with CHD8 mutations manifest not only ASD but also macrocephaly, distinct facial characteristics, gastrointestinal complaints, and a tall and slender habitus. Although psychological symptoms, macrocephaly, and gastrointestinal complaints resulting from CHD8 haploinsufficiency are likely attributable to defective neuronal development and associated responses, the mechanism by which CHD8 mutations give rise to slenderness has remained unclear (Bernier et al., 2014, Katayama et al., 2016). Such slenderness is an unexpected characteristic, given that ASD patients in general tend to be obese as a result of food selectivity, gastrointestinal symptoms, reduced physical activity, and medication use (Curtin et al., 2010, Curtin et al., 2014, Zheng et al., 2017). These observations suggest that CHD8 might also contribute to regulation of metabolism or adipogenesis.
CHD8 is a member of the CHD family of enzymes that belong to the SNF2 superfamily of ATP-dependent chromatin remodelers and are defined by the presence of two chromodomains: a helicase/ATPase domain and a DNA-binding domain (Hall and Georgel, 2007, Marfella and Imbalzano, 2007). Several members of this family play important roles during development and are implicated in various human diseases (Ho and Crabtree, 2010). For example, CHD1 is thought to contribute to the pluripotency of embryonic stem cells by maintaining an open chromatin state (Gaspar-Maia et al., 2009). Similarly, CHD5 is a key regulator of neurogenesis and plays a dual role in the activation of neuronal genes and the repression of Polycomb target genes (Egan et al., 2013). The CHD5 gene resides within a region of human chromosome 1p36 that shows loss of heterozygosity in individuals at high risk for the development of neuroblastoma (Bagchi et al., 2007). CHD7 is also required for neurogenesis and neural crest formation as a result of its direct binding to promoter or enhancer regions of fate-controlling transcription factor genes and consequent opening of chromatin structure (Bajpai et al., 2010, Feng et al., 2013). De novo mutations of human CHD7 give rise to CHARGE syndrome, a condition characterized by malformation of various organs (Vissers et al., 2004).
CHD8 was originally identified as a negative regulator of the Wnt/β-catenin signaling pathway (Nishiyama et al., 2012, Sakamoto et al., 2000). CHD8 generates two alternatively spliced transcripts that encode a 280-kDa full-length protein (CHD8L) or a 110-kDa protein (CHD8S) that contains only the NH2-terminal chromodomain (Ishihara et al., 2006, Nishiyama et al., 2009). Mutations identified in individuals with ASD are distributed throughout the CHD8 locus, with some expected to result in the loss of both CHD8 isoforms and others to affect only CHD8L. To recapitulate this situation, we generated two independent lines of mutant mice deficient in both CHD8 isoforms (ΔSL) or only CHD8L (ΔL), and we found that both heterozygous mutant strains manifest ASD-like behavioral characteristics (Katayama et al., 2016). CHD8 was also shown to regulate the expression of ASD-related neurodevelopmental genes in neurons, especially those targeted by RE1-silencing transcription factor (REST), which suppresses the transcription of many neuronal genes during development.
Adipogenesis is the strictly controlled cellular process by which preadipocytes differentiate into mature adipocytes. The expression of preadipogenic transcription factors such as CCAAT/enhancer-binding protein β (C/EBPβ) and C/EBPδ is induced during the early phase of adipogenesis and is followed by that of C/EBPα and peroxisome-proliferator-activated receptor γ (PPARγ), both of which are master regulators of adipogenesis. C/EBPα and PPARγ activate the expression of multiple adipogenic genes whose products mediate the final maturation process (Siersbæk et al., 2012). In response to adipogenic stimulation, chromatin structure undergoes substantial remodeling, resulting in the activation of a complex network of these transcription factors (Rosen and MacDougald, 2006). The mechanistic basis of such chromatin remodeling during adipogenesis has remained largely unknown, however.
We now show that CHD8 is essential for adipogenesis and the development of white adipose tissue (WAT). We found that CHD8 cooperates with C/EBPβ to regulate transactivation of the genes for C/EBPα and PPARγ during adipogenesis. Generation of mice in which Chd8 is deleted specifically in mesenchymal stem cells revealed that these animals have a markedly reduced adipose tissue mass. Our results thus indicate that CHD8 plays an essential role not only in neuronal development but also in adipogenesis.
CHD8 Is Required for Adipogenesis
To investigate the role of CHD8 during adipogenesis, we established immortalized Chd8LF/F preadipocyte lines from inguinal WAT (iWAT) of 4-week-old mice and interscapular brown adipose tissue (BAT) of 2-day-old mice that were homozygous for a floxed (F) allele of Chd8 (Figure 1A). The cells were infected with a retrovirus encoding Cre recombinase to generate Chd8L−/− preadipocytes or with a control retrovirus encoding EGFP. We confirmed that Cre inactivated almost all floxed alleles in Chd8LF/F preadipocytes (Figures 1B and 1D). Ablation of Chd8 in preadipocytes resulted in a pronounced defect in adipogenesis in response to treatment with the combination of 3-isobutyl-1-methylxanthine, dexamethasone, and insulin (MDI) (Figures 1C and 1E). Consistent with this impairment of adipogenesis, RT-PCR and real-time PCR analysis showed that the induction of adipogenic marker genes such as Cebpa, Fabp4, Fas, Glut4, and Pparg was significantly attenuated in CHD8-deficient cells (Figure 1F). We also isolated preadipocytes from iWAT of wild-type (WT) or Chd8 heterozygous mutant (Chd8+/ΔL) mice (Katayama et al., 2016) (Figure 1G). Exposure of these cells to MDI revealed that the ability of Chd8+/ΔLpreadipocytes to undergo adipogenic differentiation was impaired compared with that of WT cells (Figure 1H). The induction of adipogenic marker genes was also attenuated in Chd8+/ΔL cells compared with WT cells (Figure 1I). Furthermore, we examined the effect of short hairpin RNA (shRNA)-mediated depletion of CHD8 on adipogenesis in the white preadipocyte cell line 3T3-L1 (Figure 1J). Adipogenesis and adipogenic gene expression were attenuated in these cells in a manner related to the extent of CHD8 depletion (Figures 1K and 1L), indicating that CHD8 is also important for adipocytic differentiation of 3T3-L1 cells. Together, these results showed that CHD8 plays an essential role in adipogenesis in vitro.
CHD8 Directly Regulates Cebpa and Pparg Expression during Adipogenesis
To explore the mechanism underlying the impairment of adipogenesis in CHD8-deficient preadipocytes, we compared the expression of several adipogenic transcription factors between Chd8L−/− and Chd8LF/F preadipocytes during adipogenesis. We first showed that the expression of CHD8 was markedly upregulated as early as day 1 or 2 after the onset of adipogenic induction in 3T3-L1 cells or in brown preadipocytes isolated from WT mice (Figures 2A and 2B ). Furthermore, ablation of CHD8 did not substantially affect the steady-state expression levels of preadipogenic genes such as Cebpb, Cebpd, Krox20, Pparg1, and Pref1 in Chd8LF/F preadipocytes or 3T3-L1 preadipocytes (Figures 2C and 2D). Whereas C/EBPβ, which functions upstream of Cebpa and Pparg, was induced normally at both mRNA and protein levels by MDI treatment in Chd8L−/−preadipocytes (Figures 2E and 2F), the deletion of Chd8 essentially prevented the activation of Cebpa and Pparg expression (Figures 2G and 2H).
We next investigated whether CHD8 might be associated with the promoter or enhancer regions of Cebpa or Pparg in preadipocytes of iWAT from WT mice using chromatin immunoprecipitation (ChIP) analysis (Guo et al., 2012, Wang et al., 2013). Endogenous CHD8 was indeed found to be associated with the promoter and enhancer regions of both Cebpa (Figure 3A) and Pparg (Figure 3B). No substantial association of CHD8 with the promoter region of Runx2 (control) was detected (Figure 3A). CHD8 binding to Cebpa and Pparg1 promoter regions was not affected by exposure of the cells to MDI, whereas that to the enhancer regions of both genes and to the Pparg2 promoter region was upregulated (Figure 3C). Deletion of Chd8 essentially abolished CHD8 association with the promoter and enhancer regions of Cebpa and Pparg (Figure 3D). Consistent with these results, forced expression of CHD8 increased Cebpa and Pparg2 promoter activities in a concentration-dependent manner (Figure 3E). We also infected Chd8L−/− preadipocytes with a retrovirus encoding PPARγ2. Such ectopic expression of PPARγ2 fully rescued adipogenesis in the CHD8-deficient preadipocytes (Figure 3F). Together, these results thus suggested that CHD8 interacts with the promoter and enhancer regions of Cebpa and Pparg and promotes transactivation of these genes during the early phase of adipogenesis.
CHD8 Interacts with C/EBPβ and Regulates Adipogenic Gene Induction
Given that C/EBPβ is an upstream transcription factor of C/EBPα and PPARγ, we speculated that CHD8 might function cooperatively with C/EBPβ. Consistent with this notion, co-immunoprecipitation analysis revealed that FLAG-epitope-tagged C/EBPβ interacted with endogenous CHD8 in HEK293T cells and that endogenous C/EBPβ interacted with endogenous CHD8, but not with cyclin A (a nuclear protein examined as a negative control), in MDI-treated 3T3-L1 cells (Figures 4A–4C). Furthermore, luciferase reporter assays showed that CHD8 and C/EBPβ acted cooperatively to activate Cebpa and Pparg2 promoters (Figure 4D). FAIRE (formaldehyde-assisted isolation of regulatory elements) analysis revealed a reduced extent of chromatin opening at the promoters of both Cebpa and Pparg in Chd8-deleted preadipocytes exposed to MDI compared with MDI-treated control cells (Figure 4E).
We next investigated whether the association of CHD8 with chromatin at Cebpa and Pparg loci is dependent on C/EBPβ. We depleted 3T3-L1 cells of C/EBPβ by shRNA-mediated RNAi and then examined whether the localization of CHD8 was affected. The amount of C/EBPβ protein in cells expressing the corresponding shRNA and exposed to MDI for 2 days was reduced to ∼30% of that in control cells expressing an EGFP shRNA, whereas the abundance of CHD8 was not affected by C/EBPβ knockdown (Figure 4F). The binding of C/EBPβ to the Pparg2 promoter was also correspondingly attenuated in the C/EBPβ-deficient cells (Figure 4G). ChIP analysis revealed that the extent of CHD8 binding to the Cebpa and Pparg2 promoters in C/EBPβ-depleted cells was reduced compared with that in control cells (Figure 4H). In contrast, CHD8 binding to the Pparg1 promoter, with which C/EBPβ does not interact (Siersbæk et al., 2011), was unaffected by the depletion of C/EBPβ (Figure 4H), suggesting that the attenuation of CHD8 binding to the Cebpa and Pparg2 promoters was specific. These results thus indicate that the genomic localization of CHD8 is dependent, at least in part, on C/EBPβ. Conversely, the localization of C/EBPβ also appeared to be dependent on CHD8 (Figure 4I), suggesting that CHD8 and C/EBPβ bind to genomic sites in a mutually dependent manner (Figure 4J).
CHD8 Colocalizes with C/EBPβ at the Genome-wide Level
To determine the extent of colocalization of CHD8 and C/EBPβ at the genome-wide level, we performed ChIP and sequencing (ChIP-seq) analysis with antibodies to CHD8 in 3T3-L1 cells at 4 hr after the onset of MDI treatment. The resulting data were then integrated with published ChIP-seq and DNaseI-hypersensitive site (DHS)-sequencing profiles (Siersbæk et al., 2011). A total of 71,830 CHD8 peaks were detected, and these peaks were annotated on the basis of genomic features. Most of the peaks localized to intergenic (34%), intron (26%), and transcription start site (TSS; 25%) regions (Figure 5A). Approximately half of genes (53%) had one or more CHD8 peaks within ±50 kbp from the TSS (Figure 5B). We found that 16% of CHD8 peaks overlapped with DHSs, and that 20% of these peaks colocalized with C/EBPβ peaks, including those associated with typical C/EBPβ target genes such as Cebpa, Klf5, Pparg2, and Wnt10b (Figures 5C–5E). The vast majority of CHD8 peaks that overlapped with C/EBPδ, the glucocorticoid receptor (GR), signal transducer and activator of transcription 5A (STAT5A), or the retinoid X receptor (RXR) were also occupied by C/EBPβ (Figure 5F), although the colocalization rate of CHD8 with these four transcription factors was low (Figure 5D). These results thus indicated that CHD8 mainly colocalizes with C/EBPβ at open chromatin sites and that the two proteins regulate the expression of adipogenic genes in a cooperative manner.
We next performed RNA sequencing (RNA-seq) analysis in CHD8-depleted and control 3T3-L1 cells at 12 h after the onset of MDI treatment and then integrated the resulting data with those of our ChIP-seq analysis with antibodies to CHD8. RNA-seq analysis revealed that the expression of 11% of genes was upregulated and that of 11% of genes was downregulated in the CHD8-depleted cells (Figure 5G; Data S1). We also examined our ChIP-seq and RNA-seq data for 43 key adipogenesis-associated genes highlighted in recent reviews (Siersbæk et al., 2012, Stephens, 2012). Gene set enrichment analysis (GSEA) revealed a significant decrease in the expression of pro-adipogenic genes in the cells depleted of CHD8 compared with control cells, whereas anti-adipogenic genes did not show enrichment (Figure 5H). ChIP-seq analysis revealed that all 43 adipogenic genes had CHD8 peaks, with these peaks in 39 of the genes overlapping with DHSs, whereas 47% of all genes did not have CHD8 peaks (Figures 5B and 5I). We identified 19 genes at which CHD8 and C/EBPβ colocalized, including Cebpa and Pparg, suggesting that the two proteins cooperate to promote the expression of these adipogenic genes. Collectively, our results thus suggested that CHD8 regulates the expression of many adipogenic genes in association with C/EBPβ and thereby promotes adipogenesis.
CHD8 Is Essential for WAT Development
To investigate CHD8 function in vivo, we generated Prx1-Cre/Chd8LF/F mice by crossing Chd8LF/F mice with Prx1-Cre mice. Expression of Prx1-Cre in adipose tissue is limited to preadipocytes of iWAT, rendering Prx1-Cre-dependent recombination useful for depot-restricted genetic manipulation (Figure 6A) (Krueger et al., 2014, Sanchez-Gurmaches et al., 2015). To examine whether Prx1-Cre-dependent deletion of Chd8 inhibits adipogenesis, we fed Prx1-Cre/Chd8LF/F mice and Chd8LF/F (control) mice either a low-fat diet (LFD) or a high-fat diet (HFD) for 11 weeks beginning at 4 weeks of age. Although body weight was similar in Prx1-Cre/Chd8LF/F mice and Chd8LF/F mice fed either diet (Figure 6B), the gross appearance of iWAT was substantially affected in the former animals (Figures 6C, 6D, and S1A). Computed tomography (CT) also revealed that subcutaneous fat mass was markedly reduced in Prx1-Cre/Chd8LF/F mice fed either diet compared with control mice, whereas visceral fat mass did not differ between the two genotypes (Figures 6E and 6F). Although gonadal WAT (gWAT) weight and interscapular BAT weight were similar in Prx1-Cre/Chd8LF/F mice and Chd8LF/F mice (Figures 6G, 6H, and S1B), iWAT weight was significantly smaller in the former animals fed either an LFD or HFD (Figure 6I).
CHD8 Controls Adipogenesis and Adipocyte Hypertrophy in Vivo
Histological analysis showed that the area of vascular tissue in iWAT was increased in Prx1-Cre/Chd8LF/F mice fed an LFD compared with control animals, whereas adipocyte size did not differ between the two genotypes (Figure 6J). In contrast, the size of adipocytes in iWAT of Prx1-Cre/Chd8LF/F mice fed an HFD was reduced compared with that in control mice (Figures 6K and 6L). The amounts of mRNAs for preadipogenic genes were increased, whereas those of mRNAs for adipogenic genes were greatly reduced, in iWAT of Prx1-Cre/Chd8LF/F mice fed an LFD compared with control mice (Figure 6M), suggesting that the smaller fat mass of Prx1-Cre/Chd8LF/F mice maintained on such a diet was attributable to reduced adipogenesis. The expression levels of adipogenic genes in iWAT of Prx1-Cre/Chd8LF/F mice fed an HFD were also reduced compared with those in control mice, suggesting that the smaller fat mass of the mutant animals fed an HFD is attributable to reduced adipogenesis and adipocyte hypertrophy (Figure 6N). Consistent with these observations, preadipocytes isolated from Prx1-Cre/Chd8LF/Fmice were impaired in the ability to form mature adipocytes (Figures S1C–S1E).
To examine whether CHD8 is essential for HFD-induced adipocyte hypertrophy, we generated CAG-CreERT2/Chd8LF/F mice by crossing Chd8LF/F mice with CAG-CreERT2 mice. We then administered tamoxifen to 6-week-old CAG-CreERT2/Chd8LF/F mice by oral gavage for five consecutive days and confirmed that almost all floxed alleles were inactivated in preadipocytes derived from iWAT of the treated animals (Figure 7A). Tamoxifen-treated CAG-CreERT2/Chd8LF/F mice fed an HFD beginning after the end of tamoxifen administration showed a significantly reduced body weight, fat mass, and WAT weight compared with Chd8LF/F (control) mice (Figures 7B–7F). Moreover, the size of adipocytes (Figure 7G) as well as the expression levels of adipogenic genes (Figure 7H) in iWAT of tamoxifen-treated CAG-CreERT2/Chd8LF/F mice fed an HFD were reduced compared with those in control mice. Collectively, these results suggested that CHD8 is required in a cell-autonomous manner for both adipogenesis and adipocyte hypertrophy during WAT development.
We have shown that CHD8 interacts with C/EBPβ and positively regulates C/EBPα and PPARγ gene expression during adipogenesis. Deletion of Chd8 specifically in preadipocytes of iWAT resulted in a marked reduction in corresponding adipose tissue mass, suggesting that impairment of adipogenesis occurs in a cell-autonomous manner. Although individuals with ASD in general tend to be overweight or prone to obesity (Curtin et al., 2010, Curtin et al., 2014, Zheng et al., 2017), those with CHD8 mutations tend to be slender (Bernier et al., 2014). We now conclude that this latter phenotype is not the result of a neurodevelopmental defect but is instead due to impairment of adipogenesis.
Adipogenesis is controlled by a complex network of transcription factors that mediate the differentiation of preadipocytes into mature adipocytes (Rosen and MacDougald, 2006). In the early phase of adipogenesis, multiple adipogenic signals activate a variety of preadipogenic transcription factors, including C/EBPβ, C/EBPδ, GR, and STAT5A, that colocalize at transcriptional regulatory regions of the genome and coordinate the assembly of functional "hotspots," resulting in transcriptional activation of target genes such as Cebpa and Pparg via DNA looping and interaction with promoter regions (Siersbæk et al., 2014). Our results now identify CHD8 as an important coactivator of C/EBPβ in this process, with the extent of CHD8 association with transcriptional regulatory regions of Cebpa and Pparg increasing in response to adipogenic stimulation. Our results thus suggest that adipogenic stimulation induces binding of CHD8 to transcription regulatory regions or to preadipogenic transcription factors, including C/EBPβ, and that such association is required for proper adipogenesis. Given that dynamic chromatin loops that link promoter and enhancer regions are implicated in regulation of the expression of specific genes during adipogenesis (Siersbaek et al., 2017), we speculate that CHD8 might play a role in mediating such interactions. The molecular mechanism underlying these promoter-enhancer interactions and the identity of transcription factors that may function with CHD8 remain to be elucidated.
An increase in both adipocyte cell size (hypertrophy) and number (hyperplasia) is required for adipose tissue growth. We have shown that both the formation of adipocytes (adipogenesis) and subsequent adipocyte hypertrophy were abrogated in WAT of CHD8-deficient mice (Figure 6), whereas cells in which Chd8 was deleted by retroviral expression of Cre recombinase in vitro showed only a defect in adipogenesis (Figure 1E). One possible explanation for these findings is that although CHD8 is indispensable for both adipogenesis and adipocyte hypertrophy, Chd8L deletion due to Cre expression driven by the Prx1 promoter in vivo is not complete during adipogenesis, with the result that some cells undergo delayed Chd8 deletion after adipogenesis and then manifest a defect in adipocyte hypertrophy. In contrast, the efficiency of Chd8L deletion due to retrovirus-mediated Cre expression in Chd8LF/F preadipocytes in vitro appears to be ∼100%, with the resulting almost complete block of adipogenesis precluding manifestation of the effect of CHD8 loss on adipocyte hypertrophy (Figure S2).
Adipocytes play a central role in energy storage, lipid metabolism, and glucose homeostasis (Rosen and Spiegelman, 2006). Given that excessive adipocyte hypertrophy and hyperplasia lead to obesity and obesity-related disorders such as type 2 diabetes, hypertension, hyperlipidemia, and arteriosclerosis, a full understanding of adipogenesis is important for elucidation of the mechanisms underlying these various conditions (Muir et al., 2016). Our identification of the role of CHD8 in this process provides a basis for the development of potential treatments for obesity and type 2 diabetes.
We thank T. Kitamura and T. Akagi for providing vectors and DNA; N. Nishimura, K. Tsunematsu, and other laboratory members for technical assistance; and A. Ohta for help in preparation of the manuscript. This study was funded in part by KAKENHI grants (2522130, 26640080, and 17H06301) from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan. It was also supported in part by a Japan Society for the Promotion of Science (JSPS) fellowship (13J04520) to Y. Kita.
Author Contributions
Y. Kita planned and performed all experiments. Y. Katayama created Chd8+/ΔL and Chd8LF/F mice, performed experiments, and provided intellectual support. T. Shiraishi, K.M., and T.O. assisted with experiments. Y. Ohkawa, M. Suyama and T. Sato performed sequencing and data analysis. M.N. and M. Shirane provided materials and intellectual support. Y. Oike provided intellectual support. K.I.N. coordinated the study, oversaw the results and wrote the manuscript. All authors discussed the results and commented on the manuscript.


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all things makeup
There is something so wonderful about weddings, isn't there? Its a magical time in a persons life and I truly love being a small part of it. The getting ready part is sometimes better then the getting married part, right?! Just kidding, it comes second to that!
Having trouble with picking the right foundation? Have no idea how to shape your brows? Or you just want to learn how to turn your day look into a night time smokey eye?! My favorite thing to do is talk makeup, so let me teach you!


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Yumbii needed to reimagine their inventory process and take a deep dive into recipe costing, plating procedures and portioning protocols.Read More
Blackberry Farm sought guidance on creating a new butcher program as well as in the development of a proprietary line of charcuterie.Read More
The Queso Truck needed menu and recipe guidance to identify flavor profiles and test out menus.Read More
Saint Leo needed start up guidance and we provided them with a full suite of start up tools and recipe/menu development. In 2017, they became a James Beard winner.Read More
Opening Chef for 2nd and 3rd Atlanta units and 1st Asheville, NC Unit.
Embedded consultant for multiple culinary projects and lead consultant on recipe database implementation across 10 units.Read More


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Chocolate | Saintly or Sinful?
Over the years, chocolate has attracted a bad reputation for being a 'naughty' or 'unhealthy' food, due – for the most part – to its high sugar and fat content.
But did you know that eating the right types of chocolate can actually have positive effects on your health and wellbeing? But before you go reaching for a spoon and a jar of Nutella; as a general rule, the higher the cocoa content, the more health benefits it is reported to contain.
This is thanks to increasing levels of flavonoids and flavanols – also known as antioxidants – responsible for destroying 'free radicals' in the body – chemicals that can cause damage to DNA and other cell compounds, accelerating ageing and contributing to heart disease, cancer and other illnesses.
Be sure to always check nutrition labels on chocolate before consumption, as brands vary widely and always consult your doctor on health conditions before vastly changing your diet.
Take a look at some of the ways chocolate can be beneficial for your body…
Staying heart-healthy
The presence of plant sterols (PS) and cocoa flavanols (CF) in chocolate have been studied in relation to their effect on 'bad cholesterol' in the body. Research concluded that dark chocolate, consumed regularly in small amounts, may support cardiovascular health by lowering cholesterol and improving blood pressure.
Decreasing risk of stroke or stroke-related death
A study involving over 44,000 people found that people who regularly consumed chocolate were 22 percent less likely to suffer from a stroke; and those who had had a stroke were 46 percent less likely to die as a result.
Weight loss
Nope, eating an entire sharing box of Maltesers isn't going to make you drop pounds overnight. But studies show that small daily amounts of dark chocolate can help stabilise blood sugar levels; controlling appetite and reducing cravings. It can also improve your mood, curbing the desire to eat comfort foods and help you make better food choices.
Feeling good!
Speaking of good mood, cocoa beans contain dopamine and serotonin – compounds known to enhance mood and promote feelings of happiness, similar to those experienced after exercising. They also contain phenylethylamine, a compound known for increasing libido and energy levels.
Excerpts from Medical News Today


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Sensation + Non-reactivity
When we can learn to breathe through a long hold in a Warrior 2, or we pause at the bottom of the exhale and hold Chaturanga, we're training our nervous system and our mind to breathe through an intense physical sensation. The practice of this, this training if you will, pays off when we're faced with obstacles off the mat. Maybe it's a person who does or says something thoughtless, or someone who cuts us off on the highway or in a conversation. Maybe we're feeling anxious, impatient, jealous, ashamed, full of guilt or maybe we're mildly depressed. The thing is, when we address these emotions, we're really bringing awareness to the uncomfortable physical sensations they create in the body. When we're enraged, our blood pressure goes up, our heart rate increases, maybe our shoulders tighten or our jaw clenches - or maybe all of the above! When someone says they're lonely, they're talking about the ache in their heart. When someone says they're down or bummed out, they're referring to the listlessness, the heaviness that's settled over everything. They're talking about sensation.
Developing a practice where we learn to breathe and remain curious when challenging physical sensations arise, gives us back our power. Instead of walking through the world feeling triggered when people do things that seem incomprehensible or hurtful, we pause + breathe + stay present. In that space we've created to breathe, there's also the possibility that understanding and empathy might surface. A little patience, compassion, or the benefit of the doubt can go a long way.
We're all faced with ups and downs. That's a part of the adventure of life. It's the normal flow of things. However, there's no need to travel through the world feeling like a victim of circumstance, or be on a crazy high when things are going well, and super low when they aren't working out the way we intended them to. There's no power in that. Feel into what's real. Take a breath. And take your power back.


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Champion trainer John Size is having easily the best Happy Valley season of his career and House Of Fun can snare him the final race of the term there on Wednesday night in the Sweet Orange Handicap (1,200m).
There was a time when Happy Valley meetings barely featured on the Size resume but this record-breaking term has been completely different, with the Australian handler taking 29 winning photos there as he steams towards his ninth championship in 16 attempts.
House Of Fun (Joao Moreira) has been a part of that, winning five of his 11 starts for the season and has been a model of consistency even in defeat, with another four first four finishes as well.
Now he looks to go into rarefied territory if he can make it six wins in a season, as very few horses ever manage that, but House Of Fun should get every chance on Wednesday night.
Karis Teetan eyes off a late surge up the jockeys' championship table
In a race without a lot of pace, Happy Meteor might well be the leader at just a comfortable speed. Even from what looks an awkward draw on paper, House Of Fun has the natural speed to stay in touch with him and should be in advance of some of his main rivals.
That should see Moreira sending him clear as the field straightens and it will be a case of whether the run on horses can get past him in the final 100m.
For danger, lightly weighted Dragon General (Umberto Rispoli) looks to find an opportunity here.
He is going much better than his form looks on paper and his latest ninth at Sha Tin was a worthwhile effort despite being beaten more than seven lengths.
That finishing position was Dragon General's own fault as he stood there when the gates opened and was no hope by the time the race had gone 20 metres but closed the race off well and doesn't have a history of missing away so he can be forgiven that lapse.


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This time of year is special for our community. We all get the oppurtunity to test our fitness on a worldwide level. For every person this means something different - some of us are competitors, some of us are coming back from injury, some first time participants, and some simply want to prove they have put in a year of hard work and are better than they were last year. Wherever you stand on that spectrum, this time of year should mean a lot to you.
There is no doubt it can get hectic and stressful. You have been in class all year, studying material, taking practice tests.... but when it "counts", it counts! That whole concept can be nerve wracking. As the sport grows, there are more and more "strategy videos" and "tips for success" popping up all over the place during this time of year. As a nutrition coach year round, I thought it would be a fun idea to chime in with some Open Nutrition Strategy each week in hopes to clear up that space in your brain in order to use it on more important aspects of life in March - like perfect lockouts, getting below parallel, and making sure your heels are over that evil piece of tape on the wall.
After the workouts are released on Thursday evening, I will go home and issue a brief update on how I recommend fueling for that week's particular workout. I will get it posted sometime between the end of the release show and the time I go to bed - which hopefully isn't too late. In addition to helping you, this will be fun for me, because 1) it will take my mind off of the workout for about as long as it takes me to write the piece, and 2) it will help to hold myself and my team accountable in making sure we are properly fueled each week as well. I will simply add to this blog piece and reissue the link every week (you can also bookmark it if you're a smarty pants!).
Hopefully, the points I make and recommendations I issue are not that much different than your typical training day nutrition. As my coach and team captain explained yesterday -- goals aren't just attained. You will not be able to just set a goal and then turn around and make it happen. Daily habits performed over periods of time allow goals to be attained. If your nutrition has been completely off leading up to now, it is very probable that your training has been suffering and your biggest goals may be difficult to attain in the next few weeks. There is simply nothing I can recommend to change that. However, if you have been practicing good habits with your nutrition leading up to now, my recommendations should be easy to adjust to and should contribute significantly to you achieving your goals.
Let's take the stress out of the next couple of weeks. It is a test that we all knew was coming and have all prepared for. Here is to realistic expectations, performing great reps, staying honorable, moving fast, being consistent, having fun. In the end, it is still only exercise.
#honoryournutrition #HONORYOURGIFTS
16.1 Nutrition Strategy
As soon as I sat at my computer to start this, I was reminded how much of a nerd I am and how much I wanted to go off on a tangent about a ton of exercise science madness about energy systems and the proper fueling for each system and purpose behind it. Although interesting (to me), this is not the place for that each week as I would like this to be fairly short, to the point - and APPLICABLE. Not just a ramble of science.
As you all have figured out by now, 16.1 is an aerobic workout. This means first and foremost it is a workout requiring optimal oxygen uptake. So, BREATHE! Because of the aerobic nature of this workout, your body is going to be running in the Oxidative Energy System (also known as the Kreb's Cycle) for the majority of the time. The other two energy systems (ATP-PC system and Glycolysis) that are primary utilized in short burst, high intensity workouts require carbohydrates as their main fuel source. When we exercise, a shift from those two systems into the Kreb's Cycle can happen anywhere from 3-8 minutes in (depending on threshold of the individual). It is important to understand that as activity becomes longer in duration (like 16.1) and we spend more time in the Kreb's Cycle, our bodies will shift from the use of carbohydrates as the main fuel source, to the use of fats. If fats are not easily accessible for use, our bodies will have a hard time efficently fueling past the aerobic threshold and performance will suffer. This is not a time where I would recommend a refeed (high carb, low fat) day before or on game day. This is a workout that is going to require a great balance of both carbohydrates and fats as energy.
So, what does this mean for an athlete about to take on 16.1?
The day before: The main thing here is going to be making sure you get ample calories in the day before you take on 16.1. Now is not a time to under eat! If you are currently following macro numbers, I suggest increasing your carbs by 25-60g for the day, and fats by about 8-12g (this will vary by size of athlete). Although an increase in fats and carbs may look like an invitation for a few more donuts and cupcakes, hold off from that until after. It would be wise to stay with clean, whole, nutrient dense food sources leading up to this workout. There is a lot to be said for the acute, negative effects of processed foods on performance. If I had to recommend a dinner for 16.1 eve, it would be a nice 4-8oz lean cut steak (varying on the size of human you are) with a side of 100-300g of potato (same variance) and a fancy spinach salad (eat your iron!). Hydration is going to be HUGE here as it always is - work toward that gallon!
If you workout in the morning: By "morning" I am referring to those working out after only their first meal. I recommend having breakfast about 2.5 hours before you are set to "3..2..1..GO". Be a responsible athlete and get up with enough time to accommodate this and get your day going correctly. Your breakfast should be about 30% protein, 40% carbs, 30% fats. This will give you a relatively bigger meal and a solid source of fuel for your body to tap into. About 20-30 mins before tip off, I recommend getting some "quick carbs" in your system (about 30-80g depending on size) in the form of liquid or fruit.
If you workout in the afternoon: I will refer to afternoon as late enough to have to eat two meals before #StormDeCastro. In this case, I recommend a breakfast of about the same size as the morning exercisers, however I would recommend a slightly different breakdown. Because this group has a bit more time before GO, it would make sense to have a breakfast with a breakdown of about 35% protein, 30% carbs, 35% fats. Depending on how late in the "afternoon" you are going, you may need a snack between here and second meal. If that is the case, I recommend a bar with a similar macro breakdown to that of an RX Bar (12p/23c/9f). Your second meal should look more like 30% protein, 45% carbs, 25% fats - as you have already had a higher fat meal earlier. Same pre workout carb strategy as above, about 20-30 mins before GO, get some "quick carbs" in your system (about 30-80g depending on size) in the form of liquid or fruit.
If you workout in the evening: Here I reccomend following a similar plan to the afternoon exercisers, while adding another smaller meal about an hour and a half before GO. That meal should carry a pretty standard 30% protein, 40% carb, 30% fat ratio, but be a bit smaller in size than your first two meals. The most important concept in this group is to understand that it is crucial we do not go into this workout hungry. Twenty minutes is a long time and your body is going to need reserve fuel sources to tap into - especially fats. If you are going in hungry, your energy levels are going to take a hit. Everyone is different, and as an athlete you should understand what portions will be most beneficial to you in this situation. As with the first two groups, use the pre workout carb strategy - about 20-30 mins before GO, get some "quick carbs" in your system (about 30-80g depending on size) in the form of liquid or fruit.
As for "intra-workout" nutrition, I really do not recommend it here, even with the long duration. This is a 20 minute piece where you should go in and do nothing but lunge, burpee, and pullup until the clock beeps. Fuel properly beforehand and you will not have to stop to take a sip from your shaker bottle. That being said, if you are someone who is prone to getting lightheaded or feeling weak during workouts (email me if this is the case, because it should not happen) then I would suggest having a shaker nearby with some juice in it for easy access to a quick carb source.
Through this whole series, it is important to remember that nutrition is a very individualized process. What works for some people may not work for others. Some people generally respond better to carbohydrates, and some to fats - there are many factors that contribute to that. Now is really not the time to try something completely different from your normal routine. Finding the best gameday nutrition practices for you will be an ongoing process. These strategy tips should simply be some education on what your body is going through during the workout and get you thinking how to properly fuel yourself to perform at your best. Have fun out there y'all! See you next week!


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Damn I missed it. I meant to have my iPhone in recording mode for the great moment. Figure 26 in the first movement of Mahler's Sym. No 1.
It's the first climax in the symphony after a long build up. Anyway, technically we're not supposed to have iPhones in rehearsals. At least not if you're a string player.
The second rehearsal I had my iPhone ready but this time it didn't happen. It only happens the first time, the first rehearsal, with a fresh conductor.
There is a huge roar as the orchestra open their throats and let it all out. It's an amazing phenomenum. And it's lovely to see the shock on the face of the maestro. It's probably why we do it.
That was the rehearsal on Tuesday for the concert on Thursday at the Barbican. It didn't happen again.
In June 1985 we were in Watford Town Hall. The maestro was Claudio Abbado and the piece Ravel's Bolero.
When the climax finally comes it is after one of the longest crescendos ever written.
Claudio was suitably shocked, amazed, and thought it wonderful.
It was a recording session for Deutsche Grammophon. Claudio enjoyed the roaring cheer so much that he wanted it include in the final recording.
He disappeared into the box (control room). That's where the record producer listens.
Rainer Brock the DG producer was not keen on the idea at all.
. . . Claudio was insistent.
Eventually it was agreed that we could try it. The red light went on. We recorded from the beginning. And when the moment came, we summoned up our second climactic roar of the day.
The red light went off and Claudio disappeared back into the box.
. . . Claudio came out of the box. The record producer wasn't happy. Too messy. Only perhaps acceptable if it more could be more organised.
We were to do it again. This time in a more controlled fashion.
Still not happy.
After lengthy discussions "in camera" it was finally agreed that we could do it, but should be only if it were in unison with the trombones.
Another recording.
Still not happy. There was a problem.
At that time there were few women in the orchestra.
You could hear one female voice sticking out. It was first violinist, Gilly Findlay.
The women were asked to tacet.
You can hear the final version on the Deutsche Grammophon recording.
It's an historic moment. The only commercial recording of the LSO roar.
Even if we did fake it.


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If you've read my blog previously, you've probably noticed that I'm not really funny.
But I'm thankful that people around me are.
They give me something interesting to post for you fine folks to enjoy.
So for today's tale from Street Road I feel I must highlight my youngest son, Gavin.
He brought a little entertainment into my morning, not once, but 3 times.
1.) At 6:30, while eating breakfast, he said:
"Daddy you actually look even older with those glasses, cause old people wear glasses." I couldn't help but laugh, then immediately posted my sons bash on me onto the Twitter. I like that he can sound so sweet and put someone down at the same time.
2.) At 7:10, while getting into my car for me to take him to my mother in law's house, he paused before climbing all the way in and said "Daddy, your car smells like cheese sticks.". I just laughed on the outside, but on the inside I was thinking "No son. That's cheeseburgers."
(Side bar: Since she is the mother of The Lovely Kristi, I just considered calling my mother in law "The Lovely Mother in Law" but that just didn't seem appropriate. Your thoughts?)
3.) At 7:15, after we fed the dogs, Gavin told me he needed to warm up his voice for the day and began doing this....
So of course I made him do it again for the camera.
So within 45 minutes, Gavin made me laugh at least 3 memorable times. I gotta admit, it made me wish I could have hung out with this cool kid even longer.


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It's been a hot minute since I posted an article on fitness, but it's finally here. For those of you who aren't following me on Instagram, then you probably don't know that I've finally launched my YouTube channel. I'm super excited about it because it had been a huge dream of mine for years and now it's finally here!
So what is my YouTube channel going to be about? My channel will give you lots of fitness tips, food/recipe tips, fashion tips, beauty tips, and life tips. So go and subscribe!
My first fitness YouTube video is now live on my channel and it's about growing your chest and shoulders. Now I know a lot of women are reluctant when it comes to training chest because they're afraid it's going to flatten their breasts. Well, it's not. Trust me. Training chest alone will not decrease the size of breasts. What might (and I say might) affect their size is weight loss. So if your ultimate goal is losing weight and your training and meal plan are tailored to meet that goal then you'll lose fat. You'll lose fat throughout your entire body, which will also include your tatas (because tatas are FAT). However, don't forget that you can't spot reduce. In other words, you can't control where your body will lose fat.
Training chest is actually very beneficial for women. Here are a couple of reasons why:
1) Imagine if you were to train everything except chest. Don't you think that would develop muscular imbalances in your body? Well, it would. And you don't want to do that because you want to avoid injury.
2) When training chest you are building your pectoral muscles, which will lift up your breasts and make them sit higher on your chest. Yey to a sexier cleavage!
3) Did you know that you're using your chest muscles on a daily basis? Just think about grocery shopping, lawn mowing, or moving things. A stronger chest will make those pain-in-the-ass chores a little easier.
And having nice round shoulders to go with a killer-looking chest has never hurt anyone. So here's my entire chest-shoulder workout. Enjoy!
Thank you guys for watching!!!


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Bilbo Baggins
Bilbo Baggins is the title character and protagonist of J. R. R. Tolkien's 1937 novel The Hobbit, as well as a supporting character in The Lord of the Rings. In Tolkien's narrative conceit, in which all the writings of Middle-earth are translations from the fictitious volume of the Red Book of Westmarch, Bilbo is the author of The Hobbit and translator of various "works from the elvish" (as mentioned in the end of The Return of the King).
|Bilbo Baggins
|Tolkien character
J. R. R. Tolkien's illustration of Bilbo Baggins
|First appearance
|The Hobbit
|Last appearance
|The Lord of the Rings
|Bilba Labingi
The HobbitEdit
In The Hobbit, Bilbo Baggins, a hobbit in comfortable middle age, was hired as a "burglar" –despite his initial objections– by the wizard Gandalf and 13 Dwarves led by their king, Thorin Oakenshield. The Dwarves were on a quest to reclaim the Lonely Mountain and its treasures from the dragon Smaug. The adventure took Bilbo and his companions through the wilderness, to the elf haven of Rivendell, across the Misty Mountains, through the black forest of Mirkwood, to Lake-town in the middle of Long Lake, and eventually to the Mountain itself. There, after Smaug was killed and the Mountain was reclaimed, the Battle of Five Armies took place. In that battle, a host of Elves, Men, and Dwarves - with the help of Eagles and Beorn the shapeshifter -defeated a host of Goblins and Warg. At the end of the story, Bilbo returned to his home in the Shire to find that several of his relatives - believing him to be dead - were trying to claim his home and possessions.
During his journey, Bilbo encountered other fantastic creatures, including Trolls, Elves, giant spiders, Beorn (a man who could change into a bear), Goblins, Eagles, Warg, and a murderous creature named Gollum. Underground, near Gollum's lair under the Misty Mountains, Bilbo accidentally found a magic ring of invisibility that, unbeknownst to him, belonged to Gollum. After playing a riddle game with Bilbo, Gollum planned to use the Ring to kill and eat Bilbo. Upon discovering that he lost the Ring, Gollum deduced that Bilbo had it from his last riddle - "What have I got in my pocket?" - and chased after him, but by then Bilbo had discovered the Ring's power and disappeared. Bilbo at first thought to kill Gollum, but spared his life out of pity and leaped over him to escape.
By the end of the journey, Bilbo had become wiser and more confident, having saved the day in many precarious situations. Bilbo's journey has been compared to a pilgrimage of grace. The Hobbit can be characterized as a "Christian bildungsroman which equates progress to wisdom gained in the form of a rite of passage".[1] He rescued the Dwarves from giant spiders with the magic ring and a short Elven-sword that he had acquired. He used the magic ring to sneak around in dangerous places, and he used his wits to smuggle the 13 Dwarves out of the Wood-elves' prison. When tensions arose over ownership of the treasures beneath the Lonely Mountain, Bilbo used the Arkenstone, a stolen heirloom jewel, as leverage in an unsuccessful attempt to negotiate a compromise between the Dwarves, the Wood-elves, and the Men of Lake-town. In so doing, Bilbo strained his relationship with Thorin; however, the two were reconciled at Thorin's deathbed following the Battle of the Five Armies. In addition to becoming wealthy from his share of the Dwarves' treasure, Bilbo found that he had traded respectability for experience and wisdom. At the end of the book, Gandalf proclaimed that Bilbo was no longer the Hobbit that he had been.[1]
The Lord of the RingsEdit
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The Fellowship of the Ring, the first volume of The Lord of the Rings, begins with Bilbo's "eleventy-first" (111th) birthday, 60 years after the beginning of The Hobbit. The main character of the novel is Frodo Baggins, Bilbo's cousin,[nb 1] who celebrates his 33rd birthday and legally comes of age on the same day.
In T.A. 2989 (S.R. 1389), Bilbo, a lifelong bachelor, adopted Frodo, the orphaned son of his first cousin Primula Brandybuck and his second cousin Drogo Baggins, and made him his heir. Though Frodo was actually "his first and second cousin once removed either way",[2] the two regarded each other as uncle and nephew.
All this time Bilbo had kept his magic ring, with no idea of its significance, using it mostly to hide from his obnoxious cousins, the Sackville-Bagginses, when they came to visit. Gandalf's investigations revealed it to be the One Ring forged by the Dark Lord Sauron. The Ring had prolonged Bilbo's life beyond the normal hobbit span, and at 111 he still looked 50. While the Ring did not initially corrupt him as it had its previous owners, it was beginning to affect him; over the years, it had begun to prey on his mind when out of his sight, and he lost sleep and felt "thin, sort of stretched … like butter that has been scraped over too much bread".[2]
On the night of his and Frodo's birthday, Bilbo threw himself a party and invited all of the Shire. He signed his home, Bag End, and estate over to Frodo. He then gave a farewell address to his neighbours, at the end of which he put on the Ring and vanished from sight. As Bilbo prepared finally to leave the house, he reacted with panic and suspicion when Gandalf tried to persuade him to leave the Ring with Frodo. Bilbo refused to give up the Ring, referring to it as his "precious" – just as Gollum had. Gandalf lost his temper with his old friend and talked some sense into him. Bilbo admitted he would have liked to be rid of the Ring, and he left it behind, becoming the first person to do so voluntarily. He left the Shire that night, and was never seen in Hobbiton again.
His earlier adventure, his eccentric habits as a hobbit, and his sudden disappearance led to the enduring figure of "Mad Baggins" in hobbit folklore, who disappeared with a flash and a bang and returned with gold and jewels.
Freed of the Ring's power over his senses, Bilbo travelled first to Rivendell, and then on to visit the dwarves of the Lonely Mountain. After he returned to Rivendell he spent much of the next 17 years living a pleasant life of retirement: eating, sleeping, writing poetry, and working on his memoirs, There and Back Again, known as The Hobbit. He became a scholar of Elven lore, leaving behind the Translations from the Elvish, which forms the basis of what is known to us as The Silmarillion.
When Frodo and his friends Samwise Gamgee, Meriadoc Brandybuck and Peregrin Took stopped in Rivendell on their quest to destroy the Ring, Bilbo was still alive but now visibly aged, the years having caught up with him after he surrendered the Ring. Upon seeing the Ring again, he suddenly tried to take it from Frodo; he returned to his senses when a terrified Frodo backed away, and he broke down in tears, apologizing for bringing the burden of the Ring onto Frodo.
After the quest to destroy the Ring was fulfilled in The Return of the King, Gandalf and the four Hobbits visited Rivendell on their way back to the Shire and found Bilbo still living there. He gave Frodo a set of manuscripts that later became Translations from the Elvish, and also gave Sam a small bag of gold that represented the last of his share from Smaug's vast hoard. Two years later Bilbo accompanied Gandalf, Elrond, Galadriel, and Frodo to the Grey Havens, there to take ship for Tol Eressëa across the sea, on 29th 'September' T.A. 3021. He had already celebrated his 131st birthday by this time, surpassing the Old Took by one year and becoming the oldest Hobbit ever in Middle-earth. (The natural lifespan of Hobbits is about 100 years.)[3]
The AppendicesEdit
According to Appendix C of The Lord of the Rings, Bilbo was born to Bungo Baggins and Belladonna Took in T.A. 2890, or S.R. 1290. The Lord of the Rings gives the date of Bilbo's birthday as 22 September,[2] but the actual date in the Shire calendar was Halimath 22; Tolkien tells us in Appendix D that he "used our modern names" for the months "to avoid confusion, while the seasonal implications of our names are more or less the same", so that Halimath is translated as September, but that "the Shire dates were actually in advance of ours by some ten days, and our New Year's Day corresponded more or less to the Shire January 9".[4]
The Bagginses of Bag End were one of the oldest, wealthiest, and most respectable Hobbit families in Hobbiton until the year 2941 (SR 1341), when Bilbo inexplicably disappeared on his adventure and was thought dead.
Poems and songs written by BilboEdit
- "A Walking Song"
- "All that is gold does not glitter"
- "The Man in the Moon Stayed Up Too Late"
- "The Road Goes Ever On"
Bilbo's Last SongEdit
Tolkien's posthumously published poem "Bilbo's Last Song", illustrated by Pauline Baynes, describes Bilbo's contemplation of his forthcoming voyage to the Undying Lands. The illustrations evoke his last ride in the company of Elrond from Rivendell to the Grey Havens, as described in The Lord of the Rings.
In the 1955–1956 BBC Radio serialisation of The Lord of the Rings, Bilbo was played by Felix Felton.
In the 1968 BBC Radio serialisation of The Hobbit, Bilbo was played by Paul Daneman.
Nicol Williamson portrayed Bilbo with a light West Country accent in the 1974 performance released on Argo Records.[5]
In the 1977 Rankin/Bass animated version of The Hobbit, Bilbo was voiced by Orson Bean. Bean also voiced both the aged Bilbo and Frodo in the same company's 1980 adaptation of The Return of the King.
In Ralph Bakshi's 1978 animated version of The Lord of the Rings, Bilbo was voiced by Norman Bird. Billy Barty was the model for Bilbo, as well as Frodo and Sam, in the live-action recordings Bakshi used for rotoscoping.
The 3000th story to be broadcast in the BBC's long-running children's programme Jackanory was The Hobbit, in 1979. Four narrators told the story, with Bilbo's part being played by Bernard Cribbins.
In the BBC's 1981 radio serialisation of The Lord of the Rings, Bilbo is played by John Le Mesurier.
In the 1993 television miniseries Hobitit by Finnish broadcaster Yle, Bilbo is portrayed by Martti Suosalo.
Throughout the 2003 video game the players control Bilbo, voiced by Michael Beatie. The game follows the plot of the book, but adds the elements of platform gameplay and various side-objectives along the main quests.
In The Lord of the Rings Online (2007) Bilbo resides in Rivendell, mostly playing riddle games with the Elf Lindir in the Hall of Fire. The game also includes multiple storylines about Bilbo's adventures.
In Peter Jackson's films The Fellowship of the Ring (2001) and The Return of the King (2003) Bilbo is played by Ian Holm, who had played Frodo in the BBC radio series 20 years earlier. The movies omit the 17-year gap between Bilbo's 111th birthday and Frodo's departure from the Shire; as a result, Bilbo mentions in Rivendell that he was unable to revisit the Lonely Mountain before his retirement.
In Peter Jackson's The Hobbit film series, a prequel to The Lord of the Rings, the young Bilbo is portrayed by Martin Freeman[6] while Ian Holm reprises his role as an older Bilbo in An Unexpected Journey (2012) and The Battle of the Five Armies (2014).
Family treeEdit
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|Balbo Baggins
|Berylla Boffin
|Laura Grubb
|Fastolph Bolger
|Mimosa Bunce
|Togo Goodbody
|Tanta Hornblower
|Belladonna Took
|Rudigar Bolger
|Camellia Sackville
|Bodo Proudfoot
|Chica Chubb
|Ruby Bolger
|Bilbo Baggins
|Otho Sackville-Baggins
|Lobelia Bracegirdle
|Falco Chubb-Baggins
|Primula Brandybuck
|Filibert Bolger
|Griffo Boffin
The International Astronomical Union names all colles (small hills) on Saturn's moon Titan after characters in Tolkien's work.[7] In 2012, they named a hilly area "Bilbo Colles" after Bilbo Baggins.[8]
See alsoEdit
Notes and referencesEdit
- ^ Although Frodo referred to Bilbo as his "uncle", they were in fact first and second cousins, once removed either way (his paternal great-great-uncle's son's son and his maternal great-aunt's son).
- ^ a b Pearce, Joseph (2012). Bilbo's Journey: Discovering the Hidden Meaning of the Hobbit. Charlotte, NC: Saint Benedict Press. ISBN 978-1618900586.
- ^ a b c Tolkien, J. R. R. (1954), The Fellowship of the Ring, The Lord of the Rings, Boston: Houghton Mifflin (published 1987), "A Long-expected Party", ISBN 0-395-08254-4
- ^ Tolkien, J.R.R. "Prologue, Of the Ordering of the Shire". The Lord of the Rings.
- ^ The Lord of the Rings, Appendix D.
- ^ Nicol Williamson on IMDB
- ^ White, James (22 October 2010). "Martin Freeman Confirmed As Bilbo!". Empire. Retrieved 28 November 2010.
- ^ "Categories for Naming Features on Planets and Satellites". Gazetteer of Planetary Nomenclature. International Astronomical Union. Retrieved 29 December 2012.
- ^ "Bilbo Colles". Gazetteer of Planetary Nomenclature. International Astronomical Union. Retrieved 14 November 2012.
External linksEdit
- "Bilbo Baggins". Tolkien Gateway.
- Bilbo Baggins on IMDb
- For an alternate, fuller, version of Bilbo's family tree see Rodovid Engine.
- A brief character study of Bilbo Baggins


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How to Get Involved
The Youth Council meetings are always open to the public; youth do not need to be a Council member to participate in meetings and activities.
Currently there are 5 vacant alternate positions in the following Districts:
Baboquivari – 2 positions
Gu Achi- 2 Positions
Sif Oidag – 1 Position
To apply for these vacant positions, submit a letter of interest to your District or District Youth Council. The process of appointment through the District will occur.
For help during this process contact the Youth Council Office.


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Antiphospholipid antibody syndrome (APS) is an autoimmune disorder characterized by vascular thrombosis, complications during pregnancy, and the presence of antiphospholipid antibodies (APL) in plasma. Continue reading
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Revised Diagnostic Criteria for Neurocysticercosis
This simplified revised set of diagnostic criteria may facilitate its more uniform and widespread applicability in different clinical scenarios and environments. Continue reading
Revised IMWG Diagnostic Criteria for Multiple Myeloma
The International Myeloma Working Group (IMWG) consensus updates the disease definition of multiple myeloma to include validated biomarkers in addition to existing requirements of attributable CRAB features (hypercalcaemia, renal failure, anaemia, and bone lesions). Continue reading
Revised Diagnostic Criteria for Rett Syndrome (RTT)
Rett syndrome (RTT) is a severe neurodevelopmental disease that affects approximately 1 in 10,000 live female births and is often caused by mutations in Methyl-CpG-binding protein 2 (MECP2).
Continue reading
Revised Diagnostic Criteria for Neuromyelitis Optica (NMO)
Neuromyelitis optica (NMO; Devic syndrome) is a clinically defined, severe CNS demyelinating syndrome characterized by optic neuritis (ON) and acute myelitis; the presence of CNS symptoms outside the optic nerves and spinal cord has until recently excluded the diagnosis.
Continue reading
Revised International Classification Criteria for Sjögren's Syndrome (SS)
I. Ocular symptoms: a positive response to at least one of the following questions:
Have you had daily, persistent, troublesome dry eyes for more than 3 months?
Do you have a recurrent sensation of sand or gravel in the eyes?
Do you use tear substitutes more than 3 times a day?


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I have used Winforms and WPF earlier and I am not sure if this is the right way to achieve the result I am working on.
I put my activity in a android c# library (xamarin.android) and create a android project. The code is not working
Java.Lang.RuntimeException: Binary XML file line #1: You must supply a layout_width attribute.
[Activity(Label = "MainActivity", MainLauncher = true)] public class MainActivity : Activity { protected override void OnCreate(Bundle savedInstanceState) { base.OnCreate(savedInstanceState); SetContentView(Resource.Layout.MainActivity); // Create your application here } }
`<?xml version="1.0" encoding="utf-8"?>
Someone please tell me what is going wrong in my code. I read on stackoverflow.com that I need to register my acitivity in mainfest. If I need to do that how I can do it in xamarin. If I am wrong please help me to use activity and code from a library.
Why are you tagging user names on your post? Do you know these people? Seems rude if not...
Does the layout referenced here exist in your project? SetContentView(Resource.Layout.MainActivity);
If you have WPF experience and you are new to Xamarin, i would recommend a Forms PCL project project, not an Android project. I would start here: https://developer.xamarin.com/guides/xamarin-forms/getting-started/
You'll find Forms very familiar to what you're used to in WPF, while simultaneously getting exposure / an education on mobile app dev in general.
Actually layout is stored in the library itself. Should I add them in Mainfest. if yes, how?
Is my code broken because my layout files are in the library.


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The Cadillac XLR was a high-performance, luxury roadster built from 2004 to 2009 on the same platform as the Chevrolet Corvette C6. The nameplate could return when GM introduces the mid-engined, C8-generation Corvette.
Although there's no official confirmation from Cadillac, leaked photos of a key fob suggest that the luxury brand will soon unveil a mid-engined sports car with a retractable roof. More specifically, the drawings on the fob look like the upcoming mid-engined Corvette, but also show a convertible roof. The C8-generation Corvette will break cover in 2019, so the Cadillac might follow sometime in 2020, for the 2021 model year. That's a long wait, so here's a rendering of the luxury roadster and everything we already know about it.
Video Rating: / 5


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Heads up! Come check out our new forums, CurlTalk.
Why does my hair seem to not grow even though i have stopped perming?
I am African American and I always braid my hair to protect it. But it seems even though I have stopped perming it, every time I take it out of the braid in like a few months It breaks when i comb it and I feel its getting shorter.
3 Answers
Im not an expert but aren't the braids bad for the permed part? I bet that is the part of the hair breaking, I would say you need to be able to fully treat the permed part and in braids the task is difficult. Why don't you try other kind of protective styles while transitioning?
I do that same thing but I just don't comb my hair as much because it shields a lot and it can cause breakage to my ends so I mostly brush and oil my hair as often as possible. When needed.
Maybe the tension is causing some of your hair to shed from the root. If the braids are done too tight this can cause that problem. Maybe instead u should corn row & stitch in a medium/bob length weave......that why u can protect your natural hair maybe with less tension
This Q&A section is soo last year... Talk curls at the all new CurlTalk!


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Undergraduate study in Drama
What you can study in Drama
As part of a Bachelor of Arts majoring in Drama you will combine the literary study of drama with experience in all aspects of performance.
Advanced Drama courses provide training in acting and involve a full-scale, public production.
As you proceed with your study you can concentrate on areas such as acting, writing or directing; or you might choose to focus on the historical or theoretical study of drama.
Structuring your BA major in Drama
You can take a major in Drama as one of your two BA majors (a double major). You will need to pass at least 120 points (eight courses) towards each of your majors, including at least 45 points (three courses) at Stage III.
If you first enrolled in a BA prior to 2018
- For a single major you must pass at least 135 points, including at least 60 points above Stage II.
- For a double major you must pass at least 120 points in each of two majors, including at least 45 points above Stage II in each major.
- For a BA minor you must pass at least 90 points, including at least 60 points above Stage I.
BA courses in Drama
Explore the undergraduate courses you can take as part of a Bachelor of Arts majoring in Drama. You would normally take Stage I courses in your first year, Stage II in your second and Stage III in your third.
Required courses
You must pass the following courses as part of the Drama major:
- DRAMA 202, 301 and 302
Scholarships and awards
Help and advice
For help with planning your BA and enrolling in your courses, please contact the Arts Students' Centre.
If you would like to find out more about studying Drama, you can contact our Undergraduate Adviser.


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Early wickets, especially Meg Lanning's, were the key, and the Indian pacers did their job masterfully in the World Cup semi-final.
At the pre-departure press conference in Mumbai, Mithali Raj was asked about India being the only team in the ICC Women's World Cup 2017 with three fast bowlers in the squad, even though India's plan has been about putting runs on the board and then allowing the spinners to take control.
Wins against England, West Indies (where it bowled first), Pakistan and Sri Lanka vindicated that approach. South Africa, though, cracked the code and posted 273 for 9 after being asked to bat first. Australia too read the spinners well in the league game and chased down 227 easily, though Rajeshwari Gayakwad's five-wicket haul against New Zealand helped India to a 186-run win and took it to the semi-finals in Derby on Thursday. But, with Australia, which uses its feet against slower bowlers well, the spinners needed support.
In a chase of 227 in the league game against India, Nicole Bolton and Beth Mooney had put on an opening stand of 62 in 15.4 overs. It negated the effect of the new ball before Meg Lanning and Ellyse Perry got down to work. In that game, Deepti Sharma, the off-spinner, had opened the bowling from one end. Raj was not going to commit the same error again.
After Harmanpreet Kaur's 115-ball 171 not out took India to 281 for 4 in a rain-affected, 42-overs-a-side game, Jhulan Goswami and Shikha Pandey were given the mandate to build dot-ball pressure and not allow the openers to get off to a big start.
They stuck to bowling on one side of wicket and with scoreboard pressure very much there, Mooney, lucky to have survived an lbw appeal after India did not review, was the first to fall, bowled off a delivery by Pandey.
The moment of the game, however, came in the fifth over, when Goswami bowled Lanning for a duck. Seeing the ball coming in, Lanning prepared to play it with a slightly closed bat face only for it to move just enough to take off stump – Ian Bishop, on air, called it the ball of the tournament.
It was Lanning's first duck in close to three years, and she remained one short of the 3000-run landmark.
"On this wicket there was hardly any movement, it looked like a very good batting track, for bowlers you had to keep looking at one side of the track, bowling in one good area, I was hitting the ball early and trying to get in good shape and hitting the ball in the right area," said Goswami, who is now India's most successful bowler in World Cups with 33 scalps, having gone past Diana Edulji's 31, when asked about the Lanning dismissal.
"There was a little bit of late movement there so that was our plan, don't give her too much room because she is very good square of the wicket, so I tried to bowl stump-to-stump. That was our plan and it worked so we are happy all the plans worked at the right time."
To understand the significance of that moment, it is important to delve a bit into numbers. Lanning is the only batter with 10 or more centuries in One-Day Internationals, she averages 54.52, and her strike rate is 95.97. Her average in successful chases goes up to 84.04, and no one has scored more runs than her 1765 while batting second in winning games in the history of ODIs. In this tournament, she had scored an unbeaten 152 in a chase of 258 against Sri Lanka.
The value of Lanning's early dismissal became even more evident when Ellyse Perry and Elyse Villani hit 15 fours, mostly off the spinners, in their fourth-wicket stand of 105 runs. With the spinners being expensive, it was the first 32 balls of the innings where Goswami and Pandey did not concede a single boundary that proved decisive.
"We knew that it was important for us to get that initial breakthrough because the openers have always given them the start. For us it was really important to get those two early wickets," agreed Raj afterwards. "Of course, they lost the opener very early as well as Meg Lanning's wicket was the turning point I think because huge runs are scored by openers, Meg Lanning and Perry. Once they were three wickets down, it was always going to be very difficult for them to chase 280.
"Meg Lanning is a world-class player and I would not take any credit away from her. But when you are chasing 280, there is always pressure," continued Raj. "No matter how big a player you are and how many runs you have scored, there is always a pressure of chasing a big total. And it is imperative that the team would be depending more on the openers to get a good start, which they didn't get. So, when she walked in, as a player I could understand that she was under immense pressure. It was important to get her wicket in early stages."
In a game where 526 runs were scored in 82.1 overs, it was Pandey's economy of 2.83 and Goswami's two wickets that proved crucial. While Pandey has been consistent since returning to the team for the South Africa game, Goswami has taken her bowling to new levels in the last two encounters. A Goswami in rhythm is a good sign for India ahead of the final at Lord's on Sunday July 23.
"She has definitely worked on her bowling because from the first game to the Sri Lanka game and New Zealand game she was getting better in the nets," said Raj of her long-time colleague. "It's just a matter of time; you get a couple of good spells and you get the confidence."


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DFT Study on the Interaction of the Smallest Fullerene C20 with Lithium Ions and Atoms
Division of Applied Chemistry, Graduate School of Engineering, Hokkaido University, Sapporo 060-8628, Japan
Author to whom correspondence should be addressed.
Academic Editor: Tomoya Takada
C 2017, 3(2), 15; https://doi.org/10.3390/c3020015
Received: 28 March 2017 / Revised: 26 April 2017 / Accepted: 28 April 2017 / Published: 10 May 2017
(This article belongs to the Special Issue Chemical Bond Formation for Nanocarbon-Based Composites)
The smallest fullerene C20 with positive electron affinity is considered to be a new organic nano-electronic material. The binding structures and electronic states of lithium ions and atoms (Li+ and Li) trapped on the surface of C20 have been investigated by means of density functional theory (DFT) calculation to elucidate the nature of their interaction. It was found that a Li+ can bind to only one site of C20. This is, specifically, on top of the site where Li+ binds to the carbon atom of C20. On the other hand, in the case of a Li atom, two structures were obtained besides the on-top structure. One was pentagonal structure which included a Li atom on a five-membered ring of C20. The other was a triangular structure in which the Li atom bind to the the carbon–carbon bond of C20. Finally, the nature of the interactions between Li ions or atoms and the C20 cluster was discussed on the basis of theoretical results. View Full-Text
Keywords: C20 fullerene; alkali metal; organic electronic materials; binding energy; transition state; diffusion mechanism; density functional theory►▼ Show Figures
Figure 1
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
MDPI and ACS Style
Kawabata, H.; Tachikawa, H. DFT Study on the Interaction of the Smallest Fullerene C20 with Lithium Ions and Atoms. C 2017, 3, 15.
AMA StyleShow more citation formats Show less citations formats
Kawabata H, Tachikawa H. DFT Study on the Interaction of the Smallest Fullerene C20 with Lithium Ions and Atoms. C — Journal of Carbon Research. 2017; 3(2):15.Chicago/Turabian Style
Kawabata, Hiroshi; Tachikawa, Hiroto. 2017. "DFT Study on the Interaction of the Smallest Fullerene C20 with Lithium Ions and Atoms." C 3, no. 2: 15.
Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.
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"K.M.K. Systems" is a Ukrine-Polish company that brings together a group of professionals who work in various areas of computer and telecommunication technologies.
The main areas of specialization of the company K.M.K. Systems is the development and manufacture of specialized equipment and software for automating business needs.
In our work, we value long-term relationships with our customers and their privacy.
We provide following services:
• Development of customized software
• Development of Mobile Applications
• Professional translation, software and websites localization
• Integration of developed software with other customers products
• Support and maintenance of databases (ORACL, MySQL and others.)
• Writing queries and procedures in PL / SQL, optimization of processing plans
• Hosting, Dedicated servers (Ukraine, Germany)
• Solutions (retail, logistics, medicine, distribution, etc.).
• IT Audit
• Technical support and outsourcing
• Sale of specialized equipment
K.M.K. Systems mission:
All complex consists of a simple. We exist to solve complex problems through simple solutions.
K.M.K. Systems strategy:
Cooperation with partners. We work together to achieve the same goal. We are allies, who move together towards success, and not competitors, searching for profit. That is why we follow win-win business strategy, when victory is divided between both partners, thus benefiting everyone!
We wish your business to be successful and prosperous with us!


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A beginner's guide to writing assignments
Academic skills CAN be mastered
Beginners Guide to Writing Assignments
In today's technology driven society, written communication is king. In fact, written communication is often more important and frequent than face-to-face communication. One of the advantages of online education is that the students develop solid written communication skills, probably more so than those on campus. At least this was the case for me. While college writing was not easy for me at first, I learned, and so can you.
- LeAnne Prenovost
The Writing Centre, located within the Language Development Group, is a student-oriented space which aims to provide mediation in the process of academic writing. Students from all disciplinary backgrounds as well as tertiary levels are encouraged to engage in the one-on-one consultancy service offered.
Writing Centre
Level 6, Steve Biko Building
North Lane, Upper Campus, UCT
Tel: +27 21 650 5021
Fax: +27 21 650 5022
Email: email@example.com
Mastering the Art of Writing Essays
Learning how to write an essay can be a maddening, exasperating process, but it doesn't have to be. If you know the steps and understand what to do, writing can be easy and even fun.
Writing in College: A Short Guide to College Writing
This guide is intended to help first and second year students write effective papers in the Humanities Core and Social Sciences Core.
- Jospeh M Williams and Lawrence McEnerney. Chicago University.


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I am glad to recommend Grant Peacock Images to everyone looking for quality video production near Washington, D.C. Mr. Peacock already produced 3 videos (including interviews and b-roll) about show heroes living in the Washington DC area. Each time Grant met our stiff deadlines, and we received great video and quality sound.
Gene Rose, Exec Prod., Marmillion & Co.
Laetitia Ducom, Chargée de Production - Euronews
Our fast-paced, single-camera news department needs crew members who are creative, flexible, & quick-thinking. It is my pleasure to recommend Grant Peacock as a cameraman/editor and because we are very impressed with his work for us, he will be working with us on further assignments .
I am happy to recommend Grant to anyone looking for a diligent and experienced cameraman.
Janice McDonald, J-Mac Productions, Altanta GA
Tim Wilson, Correspondent, TVNZ New Zealand
Grant Peacock is fantastic. While I was the U.S. correspondent for New Zealand's national broadcaster, I worked with him on many stories, including the Virginia Tech massacre, and interviewing Hillary Clinton at the U.S. State Department. Two very different situations, with very different demands. Grant met all the challenges with grace and efficiency. His technical skills only add to his abilities as a cameraman, and he always keeps calm under pressure. He is also unfailingly honest. I have no hesitation whatsoever in recommending him to prospective clients.
Ann Davison, Director, PricewaterhouseCoopers
Rep. Joe Sestak, U.S. Congress 2007-11
Kevin Prange, Nat'l Assoc. Electrical Distributors
Kathleen Foster, Coordinating Producer, New York
Dennis Wholey, Host, 'This is America', PBS
Considering working with Grant Peacock? -- just do it. Grant always put together a full crew -- lighting efficiently and exactly and executing programs -- often two or three on a shoot -- with perfection.
Perfection is the key to Grant's work. He is practical, enthusiastic, cooperative, calm and patient. All important since we interview top journalists, authors, celebrities, Ambassadors, etc.
And the price was always fair and reasonable. Just do it.


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Vacant land for sale in Newcastle. All the vacant land are situated in the suburb of Newcastle 2940. Rates paid up, well maintained and cheap. The reason we are selling is because we want to provide shelter for people seeking to build their dream homes. Call Dr Jamaloodeen on 072 889 2581 email: email@example.com
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Julie is a phenomenal Photographer. She melted into the group and took beautiful shots without us even realizing she was there! On top of that she's just a wonderful person!!!
An amazing experience! I've never had so many great shots to choose from ! She brings out the natural smile and Poses -wow do you get to Pose and feel like a Top Model !! Loved the experience! Having hair and makeup professionally done by Carrie Wilson Make Up just put this experience over the top!
I had an exceptional photo shoot experience with Julie! She has a real gift for bringing out your personality in a beautifully creative way. I appreciated the quality time she took with me to understand my needs and ensure my satisfaction before, during and after the session.
Julie is not only a formidable talent behind the lens but she has an uncanny way of making one feel comfortable and confident in front of the camera. I was floored by the quality, professionalism and the way she captured the vision I had for the lifestyle shoot. I cannot recommend her enough!
I've read the reviews from other clients and DITTO everything everybody wrote. I never thought of myself as a "get headshots" kind of person, but after seeing a few friends' photos, I was SO impressed, I knew I needed my own headshots to help me grow my brand and presence on social media. When I first started with Julie, I told her I felt stupid. After she showed me the first pic she took of me, my mouth dropped open and I was ready to GO FOR IT like a top model. I could NOT believe how easy and effortless it was for her to capture EXACTLY the me that was "me". PLEASE do this for yourself, for your business, for your social media presence, for your WALL, for your hubby (she does that too!). I can not express what an amazing EXPERIENCE this is and THEN you cry when you see the pictures. I promise.. You will CRY at how amazing YOU look!
I couldn't be more thrilled with the results of my photoshoot. It was so fun and comfortable! If you can move as your told, this is easy-breezy and enjoyable!! Julie just knows how pose you, impose great lighting, and let's you bring your ideas too.
Life changing would be an understatement! This was the re-launch I needed for my business and several months later I went back for family photos and anniversary photos. Julie makes you so comfortable and the whole time is a true experience.
Once again I had another wonder photoshoot experience with Julie Ryan! I love getting my photos done by her, not only because the pictures are amazing, but I just love the experience. Julie is caring, fun, professional, and easy going. Blessings to you and your business Julie!!
Just had an amazing mother daughter shoot. Very comfortable environment and super sweet team of people to do this precious shoot with. We love you Julie! Thank you for such an amazing experience!
Julie is an extremely talented photographer, AND someone you can feel very comfortable with as she takes your photos. You can't go wrong with her images.... they'll turn out stunning! Including the hair and make up with the photo shoot is really a stroke of brilliance. Definitely use her services when you need new photos.


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Thank you for Supporting soulfest
SoulFest is sponsored by New Sound Concerts, Inc, a Massachusetts 501c3 non-profit organization. Whether a donation of $1 or $100, we are infinitely grateful for your help in sustaining SoulFest. These funds will help cover the costs of artists, programming, production, marketing and provide affordable tickets to low-income individuals and families. If you've experienced the life-changing and transformative power of live Christian music at one of our events, consider giving back this season - your dollar will continue to fund this cause!
Why donate to SoulFest & New Sound Concerts?
Because of your continued support and patronage, we've been able to produce 22 annual festivals and numerous concerts providing encouraging Christian music to New England. To continue our mission to bring our anthem of music, love, and action to New England and beyond, we need funds to be able to underwrite our festival.Over $300,000 has been given to local and global charities and ministries since SoulFest's inception. Minimally 150 tickets are donated annually for pastors to attend for free, to support church and school fundraisers, and to provide tickets for low income families and those experiencing financial hardship. In the past 8 years, SoulFest has partnered with organizations to impact various needs in the U.S. and abroad, including, but not limited to: The Salvation Army, Compassion International, clean water projects, disaster relief, foster care, the ONE Campaign, and fighting injustices such as sex-trafficking in New England, suicide prevention, opioid addiction, and so much more.


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Welcome to my shiny idea.
My name is Carmen and SLVR Linings is not just a new chapter for me, but a whole new book.
My Roots
My passion for Airstreams developed in the mid-1990s. In 2003 my husband and I finally acquired our first, a 1966 Overlander Land Yacht. Together, Pete and I renovated "Bertie," an homage to the original owner, into an updated space we both loved.
In 2008 we found our 1962 Bambi, a treasured diamond in the rough and my heart's desire, which we gutted for a rebuild and complete renovation. It was my dream to one day rent both out for others to have opportunity to have the Airstream experience.
My silver lining
In the years that followed, life shifted, our focus shifted, and the Bambi project was put on hold. In 2016 Pete passed away, and my partner in life, love, and Airstreams were gone. Since then my life has been one of transitions, trials and tribulations. I shed many possessions but kept the beloved silver trailers. After the clouds cleared a little, I made a decision; the time had come to get that Airstream dream rolling again.
This is my Silver Lining story in progress.
It is my greatest thrill to be working toward creating an experience to share.
Thanks for coming along on this journey with me.
I can't wait to share this journey with you— from inspired spaces for photo and film backdrops, to pop-up boutiques and party venues, but especially camping adventures where one can come away with their own campfire tales.


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How did you get started with your craft/art?
I wanted a cell phone charm for my phone and could not find anything in purple...lol!!!! I also wanted a pretty dangle charm for my purse but there did not seem to be anything out there at the time.
What prompted you to set up a home-based business?
I went to a local bead shop and picked out purple beads and a sun charm to make my own cell phone charm!! The lady at the shop was telling us of Etsy and how we could sell handmade items there. She really liked my cell charm.
What part of your craft is your favorite?
I guess you could say my favorite part is "seeing" my design come to life after piecing it all together!!! Of course when it sells is a great high too....lol!!!!
I have learned a lot of new ways to create my pieces. Wire wrapping, clusters. Trying to get better pictures in my shop!! I am always trying to find new ways to improve everything. Some day I hope to actually take classes.
What is the most challenging aspect of running your business?
I would have to say trying to market and sell my product!! Everyone says you need to find your target group, however, with the economy the way it is I think my target group is in hiding....lol!!!
How did you come up with your shop name?
My last name is Dean so it just sorta came together. Not that original but I like it.
Where do you see yourself in five years? Where do you see your business?
I hope to see my business grow! I would love everyone to have a Purskey on a purse, key chain, backpack, diaper bag, or wearing any of my charm bracelets. It would be wonderful to be a household name.......
How do you keep a balance between home and business responsibilities?
I wait for inspiration and money to work on my designs. In between I work on the house...lol. My husband helps out with marketing and sales. It is a team effort.
What is the funniest/craziest/most touching thing that has happened while having a business?
Customer Satisfaction all the way!! I am always thrilled, humbled, and honored when a customer says they are amazed at the craftsmanship.
If you could give one piece of advice to others who are just getting started with their businesses, what would it be?
Take your time. Make something YOU like. If you have an online store, try to make the pictures as pretty as possible. Show the item as it is intended to be used. Customers can not touch the product so do all you can to make them feel like they are.
Can you give us some links to be able to follow you?
My Etsy shop http://deancustomdesigns.etsy.com/
Twitter http://twitter.com/DeanDesigns
Facebook http://www.facebook.com/DeanDesigns
BLOG http://homeofthepurskey.blogspot.com/


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Fort Hood Area Habitat for Humanity
- Non Profit Organizations
Fort Hood Area Habitat for Humanity
2601 Atkinson Ave.
Killeen, TX 76543
(254) 680-4007
Office: Tues.- Fri. 9 - 5 pm
ReStore: Tues. - Fri. 9am- 5 pm, Sat.10am -5 pm
ReStore: Tues. - Fri. 9am- 5 pm, Sat.10am -5 pm
Seeking to put God's love into action, Habitat brings people together to build homes, communities & hope. By building homes with volunteer labor we are able to sell the homes to qualified families.
Atkinson Ave runs between W.S. Young and 38th Street, parallel to Rancier. We are at the corner of Liberty and Atkinson (by Billy Bob's Burgers).