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Horne: Beauty for ashes
By Dorothy Horne
March 18, 2017 at 4 a.m.
As my husband's Alzheimer's progresses, I find it harder to write about because it is so personal. However, I believe it is a ministry to which God has called me so I will continue to write. It is always my prayer that these writings will encourage those who are dealing with Alzheimer's and other difficult circumstances. My objective is to testify to God's grace and provision in all things, and to raise awareness about Alzheimer's disease and people affected by it. My hope is that one day soon I can stop writing about it because a cure has been found.
These days, Byron seems less aware of his losses and is usually fairly content. The "blessing" of progressive memory loss is you are not aware of the sadness most of the time. But I am — it is a part of me and every caregiver who is watching or has watched their loved one slowly fade away. That is the way Alzheimer's takes its victims.
Sometimes, however, Byron will have a moment of clarity into his current reality and it is heartbreaking. He has always been a talented artist and still enjoys drawing. Recently he drew a picture that consisted of two simple figures. One was smiling and arrayed in vibrant colors; the other was smaller and without color. I asked him to tell me about the picture. He pointed to the bright figure and said, "This one is happy, like a child."
"What about the other one?" I asked.
He looked at it a minute and frowned slightly. "I think that one is just fading away." He was quiet, and I knew then he was aware of what was happening to him.
Sometimes we'll be sitting at the table and I'll notice his eyes welling up. "Are you sad?" I'll ask with a lump in my throat, while silently praying God will give me the right words to say.
"What's wrong with me?" he will ask anxiously. I'll gently remind him he has Alzheimer's disease, and that it is not his fault. I'll assure him when God calls him home he will not have the disease anymore. Sometimes we'll pray or I will read encouraging Bible verses and devotional selections to him. And we'll cry.
Occasionally, Byron will express that he doesn't know what his purpose is _ that he feels useless, that he has ceased to matter. He will ask, "What am I supposed to be doing? I know I'm supposed to be doing something, but I just don't know what." He will tell me, in so many words, what he has told me since he was first diagnosed. "I want to make a difference. I want to help people. I want to be a kind person. I want to be someone who cares."
I'll hold his hand and tell him he is all those things and more, and that he does indeed make a difference. I'll tell him that through his faith and courage, God is encouraging and touching many people. And we'll cry.
But the question he raised recently was the most heartbreaking yet. "Where are all my people? I used to have more people. I haven't seen them in a long time."
I assured him that his family and friends love and care for him and that they do come and see him. I reminded him I am here and will take care of him. We held each other and cried together until there were no more tears. What else can you do?
Maybe the best thing, the only thing to do is just to let go — to allow ourselves to be held, to rest in Christ. To be still and listen, to allow him to take us deeper, to have faith. For what is faith but trusting even when we don't understand? As we let go and trust, we will begin to sense his presence and his arms holding and comforting us. Under the shadow of his wings, we experience "the peace of God, which transcends all understanding" (Philippians 4:7). When we give him praise and thanks, our eyes open to the myriad miracles, both great and small, surrounding us. We rise up and discover he has given us "beauty for ashes."
He has sent me to bind up the brokenhearted,
to proclaim freedom for the captives
and release from darkness for the prisoners,
to proclaim the year of the Lord's favor
and the day of vengeance of our God,
to comfort all who mourn,
and provide for those who grieve in Zion —
to bestow on them a crown of beauty
instead of ashes.
— Isaiah 61:1-3
— Dorothy Horne's book, "Glimpses of Grace: Walking in Hope through Alzheimer's and Ordinary Days," is available in paper back or Kindle at amazon.com. Find her blog, Glimpses of Grace, at news-journal.com and dorothyhorneauthor.com.
— Dorothy Horne's book, "Glimpses of Grace: Walking in Hope through Alzheimer's and Ordinary Days," is available in paper back or Kindle at amazon.com. Find her blog, Glimpses of Grace, at news-journal.com and dorothyhorneauthor.com.


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Modern electric cars make for sensible, efficient transportation, but every car fan knows that classic cars have a certain personality that newer models just can't match. So what do you if you want the style and fun of an old car, but with a modern electric powertrain?
There are actually a few companies that will install electric powertrains in vintage cars. One of them is San Diego-based Zelectric, which specializes in 1950s and 1960s Volkswagens, as detailed in a recent profile by The Verge. The converted cars still look like the originals, but they run a bit quieter.
With its California location, Zelectric seems to have hit a sweet spot between Californians' interest in environmentalism, and their love of VW Beetles and Microbuses. The company converts about 10 vehicles a year, at prices that reflect the demand for classic Volkswagens in the Golden State. Beetle conversions range from $68,000 for a sedan to $88,000 for a convertible, while buses run as much as $130,000.
When it comes to Beetles, Zelectric prefers to work on models built between 1958 and 1966. A typical conversion includes an electric motor making 85 horsepower and 120 pound-feet of torque, meaning an electric Beetle should have substantially better performance than a stock model with the air-cooled flat-four gasoline engine. The company says its electric Beetles average 80 to 100 miles of range, with a top speed of 100 mph.
Unlike most modern electric cars, these Beetles also have multi-speed transmissions. Zelectric retains the factory-stock manual transmission, with the stock gearing. The electric motor's instant torque means relatively little shifting is actually required; the car can move away from a stop in second or third gear, and reach 50 mph in third. The clutch is only used for shifting, not stopping and starting, making negotiating city traffic a lot easier.
With classic styling and the efficiency of modern electric powertrains, Zelectric's electrified Volkswagens seem to be the best of both worlds. If you can afford one, that is.

subset: commoncrawl


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Sunrise Hut: our first climb in the Ruahine Ranges
What do you do when you find yourself with a sudden free weekend before the new school term starts? Climb a mountain of course!
What do you do when you find yourself with a sudden free weekend before the new school term starts? Climb a mountain of course!
Ok – I'm going to be honest right from the start. I have ALWAYS wanted to go to Lapland to see Santa in his homeland. Imagine my excitement when I managed to persuade Ashley to let me blow my first post-career break paycheque on a trip of a lifetime.
I'm pleased to report than on the last day of our Arctic Adventure, we finally managed to track down the Big Man.
After a rather mild and often wet Christmas, the arrival of a really cold spell caused great excitement in our house. When I announced that it was minus 6 degrees and suggested we go out and find some ice, the boys couldn't get out of the house fast enough.
Wow, what a winter we have had and it's still going on! It has snowed again over the last few days and although its not been settling at the house this week, we have had swirling snowflakes coming down and playing in the garden, and it's April!
According to Gavin, our North Pole Guide, if you want to get anything done in Lapland, you need to make friends with Santa's Elves. Luckily, he already knew a few, so first on our to-do list after crossing the Arctic Circle, was to find an Elf and ask them for some Magic Dust to put on our heads, otherwise, we wouldn't be able to see them. Apparently, the forests are full of them, if you know where to look.


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Transplant Legacy Tree
Transplant patients are certainly familiar with the need to face life's challenges with strength and courage. From that courage often springs the desire to help others.
- Would you like to remember or honor a loved one who was a champion along their transplant journey?
- Do you have a desire to reach out and help other patients because you've been where they are now?
- Would you like to honor a living donor or donor family in a meaningful way?
The Transplant Legacy Tree is an opportunity to give back and do something more--raise hope and make a difference in the lives of others. For more information, please e-mail us at firstname.lastname@example.com.
NFT honors the following transplant patients and their families and friends
for raising hope for others.
Their continued support honors their loved ones and helps others receive the gift of life.
- Barbara Davis Memorial Fund: After receiving a heart transplant more than ten years ago, Barbara was a strong supporter of organ donation and extremely grateful for the gift which allowed her additional time with her family and friends.
- Francisco Galdos
- Bob Logue Memorial: The 2013 New England Parking Council golf tournament was in memory of NFT patient, Bob Logue. Everyone at NFT was honored to be a part of this annual tournament.
- James E. "Coach" Pennington Heart Fund: This site was created for friends and family of James Elwood "Coach" Pennington after he and his family had numerous requests from friends and loved ones who asked how they can support the Pennington Family during Coach's transplant process.
- Kenny Scordo Memorial Fund: This was was created in memory of Kenny Scordo, who passed away while awaiting a potentially lifesaving liver transplant. His loved ones hope that Kenny's incredible legacy will live forever in the lives of the people helped by his Legacy Tree fund.
- Ryan Sopko...Forever In Our Hearts: This site was created in memory of Ryan Sopko, who lost his health battle while awaiting a heart transplant in May of 2014. Ryan had a passion for living and brightened everyone's day with his positive energy. Through this legacy tree fund, Ryan's beautiful legacy will prevail and live forever in the lives of the people they help.
- In Memory of Jim Veltman: After he lost his health battle while awaiting a heart transplant, Jim's family created this page as a way to honor his memory. All those whose lives he touched will miss him fervently and constantly.
- Roger Wall Memorial Golf Tournament
- Noa Walsky Small Bowel Fund


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The season for blueberries is slowly arriving, and I absolutely love them. The dusty blue colour on the fresh fruit is beautiful, and the vibrant purple colour they turn when baked is gorgeous- and tasty too. Do any of you grow blueberries? I'm thinking of adding them to the garden, but I've heard they can be tricky to get to fruit.
I'd painted this cheese board with blueberries about 6 years ago, it stays at my Mum's along with most of my porcelain painting. For those of you who've never seen much of porcelain painting or onglaze painting or china painting, it's like watercolour painting in style that is fired onto porcelain or bone china. I will post a little more about my absolute passion for porcelain another time. But, basically porcelain painting uses a technique of building up fine layers of paint which are fired in a kiln, after each layer is painted. The paint is fired at a high temperature so that the lead based paints seep into the layer of porcelain, so that when it cools, it can't be removed. I'll be returning to painting again on china when my studio is finished (that's another story for a big cuppa and piece of cake, and I hope you'll join me then!)
BACK TO CAKE! Blueberries and lemons make a really fresh feel, perfect combination of tart and sweet, with colours resembling spring and sunshine! The most difficult part of baking with fresh bluberries is having enough for the recipe...I really need to stop using the excuse of 'tasting them to make sure they're ripe.'
And yes, the lemon creamer in the picture is one of my handpainted porcelain pieces too, it sits on my kitchen bench next to other object d'Art.
For this cake I used a rich vanilla bundt batter or you could use any butter cake or pound cake basic recipe, to which I added about 1/2 cup lemon juice (start with 1/3 first and adjust the taste as you go, depending on the season, your lemons will vary in flavour and intensity) and 2-3 tablespoons of freshly grated lemon rind, and stirred them at the end of the batter mixing process. Then I carefully folded through about 1 cup of blueberries- fresh if you have them or frozen if they're not in season. Don't stir them through too much or you can break up the fruit too much- particularly if they're frozen.
The frosting was made with a 250g tub of light cream cheese (easier to mix by hand and I don't need to pull out the electric beaters) about 3/4 cup of sifted icing sugar and 1/8-1/4 cup of lemon juice, with a dash of good quality pure vanilla essence. Whisk vigorously until smooth and oozey in consistency, not runny. Spread icing over cake and let set.
Enjoy, and blissful blueberry cake baking!


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Georgia Department of Early Care and Learning
A large number of young children in Georgia are cared for outside their homes each day. It is important that these settings be safe, healthy, and nurturing, as
well as offer quality early learning experiences to support and promote the healthy growth and development of young children.
In Georgia there are approximately 3000 child care learning centers, 3100 family child care learning homes and approximately 2000 informal care
providers. The Child Care Services division of Bright from the Start monitors and licenses these child care programs. Responsibilities include:
On the Child Care Services page you will find information on how to open a child care facility, resources for child care programs and parents, licensing reports
for child care programs, and other helpful information on subjects such as developmentally appropriate practices for infants, toddlers and preschoolers, best
inclusion practices and much more. We hope this information will be useful to you. If you need information not found on this website please contact us at 404-657-5562.


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We previously identified that autoreactive B cells from BXD2 mice can be targeted by IL-17, leading to upregulation of the expression of regulators of G-protein signaling (Rgs) genes that facilitated the development of spontaneous germinal centers. Little is known about the signaling pathway used by IL-17 to upregulate RGS. In the current study, we found that IL-17 rapidly activates the canonical NF-κB signaling pathway and that BXD2 B cells exhibit higher basal and activated phosphorylated p65 levels than B6 or BXD2-Il17ra−/− B cells. Inhibition of p65 phosphorylation down-regulated RGS16 expression and abrogated the IL-17-induced chemotactic arrest of B cells in response to CXCL12. Knockdown of TNFR-associated factor 6 or NF-κB activator 1 in 70Z/3 pre-B cells led to decreased Rgs16 expression, indicating that both of these two genes are involved in IL-17-mediated activation of NF-κB signaling in B cells. These findings identify the signaling pathway regulated by IL-17 to contribute to the development of spontaneous germinal centers in autoimmune BXD2 mice.
Interleukin-17 has been shown to play a major role, especially in enhancing chemotaxis as related to the innate immune response. Chemokines upregulated by IL-17 include CXCL1, CXCL2 (1), CXCL5(2), CXCL8 (IL-8) (3), CXCL9, CXCL10 (4), CCL2, and CCL20 (5). IL-17 upregulates additional pro-inflammatory mediators, including IL-6, TNF-α, G-CSF, GM-CSF, C-reactive protein, matrix metalloproteases, and anti-microbial proteins, and is especially potent in expansion and recruitment of neutrophils (6).
The importance of IL-17 regulation on B cells has been shown recently to be associated with the development of spontaneous germinal centers (GCs) in autoimmune BXD2 mice (7). The BXD2 recombinant inbred mouse strain was generated by inbreeding the intercross progeny of C57BL/6J and DBA/2J mice for more than 20 generations (8, 9). These mice develop high titers of pathogenic autoantibodies and a spontaneous erosive arthritis that progresses as the mice age. BXD2 mice also exhibit spontaneous development of GCs in the spleen, and we have established that this formation of GCs plays a critical role in the production of pathogenic autoantibodies (7).
IL-17 signaling has been shown to be mediated through NF-κB activator 1 (ACT1) nd TNFR-associated factor 6 (TRAF6) (10, 11). The IL-17R family cytoplasmic tails have been shown to have homology with IL-1/TLR/IL-1R domain now referred to as the SEFIR. The SEFIR domain in IL-17RA is essential for IL-17 signaling (10, 12, 13). The IL-1/TLR domain contains a protein-protein interaction motif found in TLRs (IL-1Rs) and also is found in ACT1, an activator of NF-κB that had been linked to the B cell activation factor from the TNF family (BAFF) and CD40L signaling (11, 14). ACT1 also contains a TRAF6 binding motif and IL-17 activation of the NF-κB and MAPK pathways requires TRAF6 to induce IL-6 (10).
The chemokine receptors CXCR4 and CXCR5 and their respective ligands CXCL12 and CXCL13 facilitate recruitment of lymphocytes in lymphoid follicles to create GCs (15). The high levels of IL-17 that are characteristic of the BXD2 mice (7) are associated with the upregulation in the expression of the regulators of G-protein signaling (Rgs) 16 and Rgs13 genes in B cells. This increased expression of the Rgs16 and Rgs13 genes reduces the B cell chemotactic responses to the CXCL12 and CXCL13 chemokines, thereby promoting the retention of the B cells within the GCs and providing an optimal microenvironment for the generation of pathogenic autoantibodies (7). The associated reduction in the B cell chemotactic responses are absent in BXD2-Il17ra−/− mice, suggesting that one important IL-17/IL-17RA signaling function in B cells is to mediate the upregulation of Rgs genes.
It has been shown that NF-κB is involved in the mediation of IL-17 downstream signaling in various mammalian cell types, such as myofibroblasts (16), intestinal epithelia cells (17), and articular chondrocytes (18). IL-17 has been shown to use the NF-κB pathway to promote the survival and differentiation of B cells from human lupus patients (19). It is not known whether the IL-17-mediated RGS response also is dependent on the NF-κB signaling pathway. In this study, we show that in autoimmune B cells of BXD2 mice, the IL-17-mediated upregulation in RGS16 expression was associated with rapid phosphorylation and degradation of IκBα as well as phosphorylation of p65 (P-p65) and its translocation to the nucleus. Inhibition of phosphorylation of Ser276 on p65 with a specific membrane-permeable peptide inhibitor blocked IL-17-induced upregulation of RGS16 expression, and thus the IL-17-induced inhibition of chemotaxis of B cells in responses to CXCL12. In 70Z/3 pre-B cells, knockdown of Traf6 or TNFR-associated factor 3 interacting protein 2 (Traf3ip2), the gene encoding ACT1, by small interfering RNA (siRNA) also blocked the increase in P-p65 and Rgs16 expression levels by IL-17 signaling. Together, this finding extends our previously described model in which IL-17 can inhibit B cell chemotactic responses to CXCL12 (7) via its activation of the SEFIR and NF-κB signaling pathway, leading to upregulation of RGS16.
C57BL/6 and BXD2 recombinant inbred mice were obtained from The Jackson Laboratory (Bar Harbor, ME). B6-Il17ra−/− mice, obtained from Amgen (Thousand Oaks, CA), were backcrossed with the BXD2 mice for seven generations (7). All of the mice were cared for according to the Institutional Animal Care and Use Committee guidelines.
B cells were enriched from single-cell suspensions of spleens from 8- to 12-wk-old mice using magnetic anti-CD19 microbeads and an AutoMACS magnetic cell sorter (Miltenyi Biotech, Auburn, CA). The B cell preparations were 98% pure as confirmed by FACS.
The 70Z/3 cell line was obtained from the American Type Culture Collection (Manassas, VA). Abs against p65 (C22B4), P-p65 (93H1), transcription factor RelB (C1E4), IκBα (44D4), phospho-IκBα (14D4), phospho-p38 MAPK (28B10), phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (197G2) rabbit mAb, phospho-C/EBPβ (Thr235) (Cell Signaling Technology, Beverly, MA), p50 (H119), p52 (K27), SP1 transcription factor (1C6), C/EBPβ (C-19), C/EBPδ (C-22) (Santa Cruz Biotechnology, Santa Cruz, CA), RGS16 (Prosci, Poway, CA), and GAPDH (R&D Systems, Minneapolis, MN) were used to detect their respective Ags.
RNA was isolated by TRIzol reagent (Invitrogen, Carlsbad, CA) and converted to cDNA by a First Strand cDNA Synthesis kit (Fermentas, Burlington, Ontario, Canada). Real-time PCR reactions were performed in triplicate using the SYBR Green PCR Master Mix (Bio-Rad, Hercules, CA) in an iQ™5 Multicolor Real-Time PCR Detection System (Bio-Rad) with the following primers: Il17ra, GGTGGCGGTTTTCCTTCAG (F), GTGGTTTGGGTCCCCATCA (R); Il17rc, GCGGTATTTGACTGTTTCG (F), TGCTCCTCAGAGACATCC (R); Rgs16, GGTACTTGCTACTCGCTTTTCC (F), CAGCCGCGTCTTGAACTCT (R); Rgs13, TGCAGAGATGAATCTAAGAGGCT (F), GGTTTCACATGCCATCCAGAAT (R); Rgs1, TTTTCTGCTAGCCCAAAGGA (F), TGGTTGGCAAGGAGTTTTTC (R); Traf6, GCGAGAGATTCTTTCCCTGAC (F), TGTATTAACCTGGCACTTCTGG (R); Traf3ip, TTTAGAAGGCACCCTGAAC (F), CCGTAAGTGTGAACCGATG (R); Gapdh, AGGTCGGTGTGAACGGATTTG (F), TGTAGACCATGTAGTTGAGGTCA (R).
The cytoplasmic and nuclear extracts from B cells were prepared with NE-PER® Nuclear and Cytoplasmic Extraction Reagents (Pierce, Rockford, IL). Equal amounts of protein extracts were electrophoresed on 8–10% SDS polyacrylamide gels, and transferred onto polyvinylidene difluoride membranes. Anti-rabbit HRP-conjugated Ab (Cell Signaling Technology) was used at a 1:3000 dilution, and anti-mouse HRP-conjugated Ab (Santa Cruz Biotechnology) was used at a 1:5000 dilution. HRP Abs were detected using the chemiluminescence reagent (Pierce). The scanned figures were visualized and quantified using ImageJ software.
Cytospin preparations of splenic B cells were fixed and permeabilized with BD Cytofix/Cytoperm™ solution (BD Biosciences, San Jose, CA), then sequentially stained with 1:100 dilution of P-p65 rabbit mAb (93H1, Cell Signaling Technology) and 1:200 dilution of FITC-conjugated donkey anti-rabbit Ab (BD Biosciences). The slides were viewed with a DM IRBE inverted Nomarski/epifluorescence microscope (Leica Microsystems, Deerfield, IL) outfitted with TCS NT laser confocal optics (Leica Microsystems).
Whole spleen cells from B6, BXD2 and BXD2-Il17ra−/− mice were stained with biotin-peanut agglutinin (PNA) (Vector Laboratory, Burlingame, CA), CD19-Alexa Fluor 700 (eBioscience, San Diego, CA) and IL17RA-PE (eBioscience). PNA+ cells were revealed by a secondary allophycocyanin-streptavidin conjugate. The purified splenic B cells from B6 and BXD2 mice were stained in the cold with biotin-PNA (Vector Laboratory) and PE-anti-Fas (Biolegend, San Diego, CA). The B cells were quickly warmed to 37°C and stimulated with IL-17 (30 ng/ml) for 5 min. The B cells then were cooled quickly, fixed and permeabilized with BD Cytofix/Cytoperm™ solution (BD Biosciences), then sequentially stained with 1:100 dilution of P-p65 rabbit mAb (93H1, Cell Signaling Technology) and 1:200 dilution of FITC-conjugated donkey anti-rabbit Ab (BD Biosciences). An isotype control rabbit IgG was used for gating of P-p65-positive cells. The stained whole spleen cells or purified B cells were analyzed on a LSRII FACS analyzer (BD Biosciences).
The NF-κB p65 (Ser276) inhibitory peptide (DRQIKIWFQNRRMKWK-KQLRRPSDRELSE) contains a protein transduction (PTD) sequence (DRQIKIWFQNRRMKWKK) derived from antennapedia and a Ser276 site (boldface) that is phosphorylated during NF-κB activation thereby blocking p65-Ser276 phosphorylation (IMGENEX, San Diego, CA). The control peptide consists of the PTD sequence (IMGENEX).
The purified spleen B cells from BXD2 mice or 70Z/3 pre-B cells were loaded into the upper well insert of a Transwell system (Costar, Cambridge, MA), and the chemokine CXCL12 (100 ng/ml) was added to the bottom chamber. After incubation for 2 h, the cells that remained in the inserts or that had migrated to the lower chamber were counted. The chemotaxis index was calculated by dividing the number of cells that migrated in response to the chemokine by the number of cells that migrated in the absence of chemokine (7).
siRNAs for Traf3ip2 (AAAGCAUUAGGUAAACUUGGGUCUG, Invitrogen), Traf6 (AAAGUUCACAAAUUUCACCACCUCC, Invitrogen) and control scrambled siRNAs (Invitrogen) were transfected into 70Z/3 cells at a final concentration of 100 nM using BLOCK-iT™ Transfection Kit (Invitrogen). The transfection efficiency in 70Z/3 is >80%, as determined by the BLOCK-iT™ Fluorescent Oligo. After transfection for 24 h, cells were stimulated with IL-17 (30 ng/ml) for 4h, and harvested for quantitative real-time PCR or for cell migration analysis as described earlier.
NF-κB is the best known mediator of IL-17-associated cellular responses (16–18). It is constitutively activated in many autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus and type1 diabetes (20). We found that the B cells from the spleens of autoimmune BXD2 mice exhibited significantly higher levels of basal P-p65 as compared with those of the B cells from the spleens of the parental B6 mice (Fig. 1A, Supplemental Fig 1), and that the levels of P-p65 in the B cells from the spleens of these mice were enhanced by stimulation with IL-17 (30 ng/ml, Fig. 1A, Supplemental Fig 1). The levels of P-p65 in the spleens of the BXD2-Il17ra−/− mice were markedly lower and were not responsive to IL-17 treatment (Fig. 1A, Supplemental Fig 1).
BXD2 mice display high levels of serum IL-17 and IL-17 expression in the splenic CD4 T cells (7), which may account for higher levels of IL-17 signaling. To determine whether B cells of B6 mice could exhibit an equivalent response to IL-17 at higher levels of IL-17 or at longer incubation times, B cells from BXD2 and B6 mice were analyzed after incubation with IL-17 (150 ng/ml) for 5 min or after 15 and 30 min with 30 ng/ml IL17 (Fig. 1B). Higher levels of IL-17 were not able to significantly elevate P-p65 in B cells of B6 mice compared with those of the control with no IL-17. There was a markedly lower P-p65 induction by IL-17 in B6 B cells at 15 and 30 min with 30 ng/ml IL17 compared with that of BXD2 B cells (Fig. 1B).
There is an ~5-fold increase in the Il17ra mRNA in total spleen B cells of BXD2 mice compared with those of B6 mice (7). B cells from BXD2 contain a dramatically increased population of Fas+PNA+ GC B cells compared with those of B cells from B6 mice (21). We therefore asked whether increased IL-17R and IL-17 stimulation of P-p65 in B cells from BXD2 mice was limited to GC B cells, or all of the B cells exhibited higher responses to IL-17. Responses of B cell subpopulations were analyzed by intracellular staining and FACS analysis of IL-17-stimulated B cells (Fig. 1C, 1D). There were increased P-p65 levels in response to IL-17 in both GC and non-GC B cells of BXD2 mice compared with those of the corresponding B cells from B6 mice. Consistent with this result, both non-GC (Fas−PNA−) and GC (Fas+PNA+) B cells exhibited higher levels of Il17ra expression (Fig. 1E). Increased expression of IL-17RA on the surfaces of B cells from BXD2 mice also was confirmed by FACS analysis (Fig. 1F). B cells from BXD2 mice also exhibited higher levels of Il-17rc (Supplemental Fig 2). There are also higher levels of Il17rc in BXD2-Il17ra−/− mice. Together, these results suggest that higher levels of Il17ra expression and higher IL-17-stimulated P-p65 are intrinsic properties of B cells from BXD2 mice.
The addition of IL-17 not only upregulated the levels of P-p65 in the B cells from the spleens of BXD2 mice, but also promoted its translocation to the nucleus. In the absence of IL-17 stimulation, the levels of P-p65 in the cytoplasm were considerably higher in BXD2 B cells than in B6 B cells (Fig. 2, upper panels). Within 5 minutes after addition of IL-17, the levels of P-p65 in the cytoplasm of BXD2 B cells were increased in most of these cells (Fig. 2A, middle panels), compared those of similarly treated B cells from the B6 control mice (Fig. 2B, middle panels). There was a dramatic reduction of the levels of P-p65 in the nuclei of B cells from BXD2 mice at 15 minutes after the addition of the IL-17, but high levels of P-p65 persisted in the cytoplasm (Fig. 2A, lower panels). The upregulation of P-p65 observed in almost all B cells of BXD2 mice further supports that this increased response to IL-17 is not due to an increased population of GC B cells compared with that of normal B6 mice.
Consistent with the results described above, within 5 min after addition of IL-17, the levels of P-p65 in total and cytoplasmic extracts of BXD2 B cells increased (Fig. 3A–3D). There was also a dramatic increase in the levels of P-p65 in nuclear extract (Fig. 3E, 3F). The levels of P-p65 in the B cell nuclear extract from BXD2 mice returned to baseline levels at 15 min after the addition of IL-17 (Fig. 3E, 3F), but high levels of P-p65 persisted in the cytoplasmic extract (Fig. 3C, 3D).
In most cell types, NF-κB is retained usually in the cytoplasm of the unstimulated cells by IκB family proteins. Upon stimulation, the IκB kinase (IKK) complex is activated, resulting in the phosphorylation of IκBs (22, 23). The phosphorylated IκBs are ubiquitinated and subsequently degraded, which will release transcription factor NF-κB (22, 23). In this study, we also found that IL-17 stimulation was associated with a significant increase in the levels of phosphorylated IκBα in the cytoplasm at the 5 min time point. Consistent with this, the total levels of IκBα in the cytoplasm decreased at the 5 min time point (Fig 3C, 3D). The levels of p50, a product of p105, were not elevated in the nuclear extracts of the BXD2 B cells with IL-17 stimulation (Fig. 3A, 3E).
Activation of p38 MAP kinase (MAPK), p44/42 MAPK (Erk1/2), and C/EBPβ also has been shown as a downstream signaling pathway of IL-17 (10, 12, 24). There was significantly increased induction of phospho-p38 MAPK and phospho-p44/42 MAPK (Erk1/2) in BXD2 B cells up to 30 min after IL-17 stimulation (Fig. 3A, 3B), but we did not find the increased induction of phospho-C/EBPβ (Fig. 3A, 3B) or increased nuclear levels of C/EBPβ or C/EBPδ (Supplemental Fig. 3). We also did not find any increase in the formation of p52, the noncanonical NF-κB subunit, or translocation of p52 or transcription factor RelB to the nucleus (Supplemental Fig. 3). Taken together, IL-17 strongly activates the canonical NF-κB signaling pathway in autoimmune BXD2 B cells.
We have found previously that after 4 h of culture with IL-17, there was equivalent upregulation of Rgs16 and Rgs13 in B cells from the spleens of BXD2 and B6 mice (7). Consistent with these previously published data, we found that treatment of the B cells from BXD2 mice with IL-17 resulted in a significant increase in the expression of Rgs16 mRNA, as determined by quantitative real-time PCR, within 2 h of IL-17 treatment (p < 0.01) (Fig. 4A). Similarly, treatment of B6 B cells with IL-17 enhanced the levels of Rgs16 mRNA, but the magnitude of the response was lower and the response was delayed in that it peaked at 4 h after addition of IL-17 (Fig. 4A, left panel). It has been reported that Rgs1 (25) and Rgs13 (26, 27) are highly expressed in GC B cells and some B cell lines. Although we found that Rgs13 expression was upregulated significantly in the IL-17-treated B cells (p < 0.05) (Fig. 4B), the relative magnitude of the response was lower than that observed for Rgs16. However, consistent with the results of Rgs16, the peak response occurred more rapidly in BXD2 B cells than in B6 B cells. Rgs1 was not upregulated in B cells after IL-17 stimulation (Fig. 4C), which is consistent with the previously published data (7).
To determine whether IL-17 signaling through the canonical NF-κB pathway is required for upregulation of RGS16 at the protein level, the BXD2 B cells were preincubated with a membrane-permeable inhibitory peptide that specifically blocks the phosphorylation of Ser276 of p65 during NF-κB activation (28). We found that pretreatment with this inhibitor blocked the IL-17-induced RGS16 in the B cells of BXD2 mice (Fig. 5A, 5B). To further determine whether the down-regulation of RGS16 induced by this peptide inhibitor affected the IL-17-induced migration toward the CXCL12 chemokine, the BXD2 B cells were pretreated with the NF-κB p65-Ser276 inhibitory peptide (inhibitor) or control peptide PTD prior to culture for 4 hours in the presence or absence of IL-17. Analysis of the migration toward CXCL12 using a chemotaxis chamber confirmed our previous finding that IL-17 treatment resulted in a significant reduction in the migration activity of BXD2 B cells in response to CXCL12 (p < 0.05) (Fig. 5C) (7). Furthermore, pre-incubation of the BXD2 B cells with the NF-κB p65-Ser276 inhibitory peptide prevented the inhibitory effect of IL-17 on the chemotactic response of the BXD2 splenic B cells to CXCL12 (p < 0.01) (Fig. 5C). Our data indicate that in the B cells of autoimmune BXD2 mice, IL-17 activates the canonical NF-κB signaling pathway, and that the activation of the canonical NF-κB signaling pathway is associated with the upregulation of RGS16 expression and the physiologically important response of these B cells to the CXCL12 chemokine.
TRAF6 and ACT1 have been reported to be involved in upstream signaling of IL-17 in many cell types (13, 29). Both of them are expressed at equivalent levels in B cells from BXD2 mice compared with those in B6 and BXD2 Il17ra−/− B cells (Supplemental Fig 4). To determine whether TRAF6 or ACT1 was required for IL-17R signaling in B cells, we used siRNA for Traf6 or Traf3ip2, the gene encoding ACT1, to knock down these genes in the 70Z/3 pre-B cell line. Comparison between the 70Z/3 pre-B cell line and B cells from the spleens of BXD2 mice indicated that 70Z/3 cells would be an appropriate model for BXD2 B cells. 70Z/3 cells exhibited comparable expression levels of Il17ra (data not shown).
Treatment of 70Z/3 cells with IL-17 resulted in increased levels of P-p65 from 5–60 min after IL-17 stimulation, although the peak time of induction differed somewhat from that for BXD2 B cells (Fig. 6A, 6B). Consistent with the results from BXD2 B cells, treatment of 70Z/3 B cells with IL-17 also led to significantly increased expression of RGS16 from 1–10 h following stimulation (Fig. 6C, 6D). We also confirmed that upregulation of RGS16 in the 70Z/3 cells was dependent upon P-p65 as determined by pretreatment with the NF-κB p65-Ser276 inhibitory peptide (Fig. 6E, 6F). These results are consistent with the report by Li et al. (30) that after LPS stimulation, the expression of Rgs16 is dependent on the canonical NF-κB pathway in the 70Z/3 pre-B cell line.
Treatment of 70Z/3 cells with siRNA for Traf6 or Traf3ip2 resulted in ~67% and 66% reductions in the respective mRNA levels at 24 h after transfection compared with those for the scrambled siRNA results, respectively (Fig. 7A). Treatment of 70Z/3 cells with siRNA for Traf6 or Traf3ip2 also resulted in a significant decrease in the P-p65 activation level (Fig. 7B, 7C).
On treatment of the 70Z/3 cells with IL-17 (30 ng/ml) for 4 h after siRNA transfection, we found that pre-treatment with siRNA for Traf6 resulted in ~57% reduction in expression of Rgs16 (p < 0.05) and that pre-treatment with siRNA for Traf3ip2 resulted in an ~60% reduction in expression of Rgs16 (p < 0.05) (Fig. 7D), compared with that for the scrambled siRNA. That is to say, a block in expression of either of these two genes resulted in a dramatic reduction in the IL-17-stimulated expression of Rgs16. Chemotaxis of B cells in response to CXCL12 was reduced significantly in 70Z/3 cells pretreated with scrambled siRNA after culture with IL-17. This decreased chemotaxis was strongly reversed by treatment with Traf6 siRNA (Fig. 7E) and was restored partially by treatment with Traf3ip2 siRNA (Fig. 7E). These results indicate that IL-17/IL-17RA signaling in B cells requires both TRAF6 and ACT1 and signals through the canonical NF-κB pathway to upregulate RGS16 expression, which inhibits chemotaxis in response to CXCL12.
An understanding of the signaling pathways associated with stimulation of IL-17R in B cells should shed light on the circumstances that promote B cell retention in the GCs and the subsequent development of pathogenic autoantibodies. We previously showed that IL-17 (20 ng/ml) stimulation of purified B cells from B6 or BXD2 mice resulted in ~10-fold upregulation of Rgs16 and a lesser increase in Rgs13 levels at 4 h after stimulation. There was equivalent upregulation of Rgs16 levels in BXD2 compared with those in B6 mice (7). In the present experiment, we found that Rgs16 is the major RGS that is upregulated in BXD2 B cells compared with those in B6 B cells. We also found that the kinetics of upregulation Rgs mRNA is faster in BXD2 B cells compared with that in B6 B cells. Upregulation of Rgs16 levels in BXD2 B cells peaks at 2 h and is higher than the upregulation of Rgs16 levels in B6 B cells, which peaks at 4 h. IL-17-induced upregulation of Rgs13 also peaked at 2 h in BXD2 B cells and 4 h in B6 B cells. The present study therefore clearly showed that there was more rapid and greater upregulation of both Rgs13 and Rgs16 levels in BXD2 compared with those in B6 B cells.
A question is whether IL-17 acts on a small population of B cells, such as GC B cells in BXD2 mice, or on a larger population of B cells in B6 and BXD2 mice. The present experiments show that Il17ra expression is greatly increased on all B cells of BXD2 mice compared with that of B6 B cells. The level of stimulation indicated by P-p65 is upregulated significantly on all B cells of BXD2 mice compared with that off B cells from B6 mice. There is no significant greater increase in P-p65 signaling in GC B cells in BXD2 mice compared with that of non-GC B cells. These results indicate that IL-17RA expression and signaling, although higher on B cells of BXD2 mice, are features of all of the B cells and are not restricted to a subpopulation of B cells. However, because the majority of IL-17 producing CD4 T cells locate in the vicinity of a GC (7), this may be one factor that promotes the migration arrest of B cells in the GC area in the spleen of BXD2 mice in vivo.
IL-17R signaling occurs through homodimers or heterodimers of IL-17A and IL-17F, which interact through heterodimers of IL-17RA and IL-17RC, usually at a 2:1 ratio. Downstream signaling pathways have been characterized to use the NF-κB, MAPK and C/EBP pathways. IL-17 was shown to induce NF-κB signaling in mouse fibroblasts and human macrophages (31, 32). IL-17 also was shown to activate the NF-κB subunits p50 and p65 in intestinal epithelial cells (17). This activation appears to require TRAF6 and IκBα kinase, IKKα. IL-17 induced signal transduction resulted in regulation of three different families of MAPKs in IEC-6 cells (17). These can be linked to the NF-κB activation pathways. TRAF proteins also can activate JNK and NF-κB. Therefore, activation of ERK, JNK/stress-activated protein kinase, and p38 MAPKs by IL-17 in IEC-6 cells may be linked to the NF-κB activation pathway. Because the NF-κB pathway appeared to be most critical, it was studied in B cells in the current study.
Our results show that there is rapid upregulation of the P-p65 canonical pathway in B cells of B6 and BXD2 mice. Upregulation of P-p65 is increased greatly in B cells of BXD2 mice compared with those of B6 mice, which may be in part due to increased expression of Il17ra on the surfaces of both GC and non-GC B cells of BXD2 mice. Cytoplasmic and nuclear staining also demonstrates that almost all off the B cells in BXD2 mice exhibit upregulation of P-p65 first in the cytoplasm and then in the nucleus at 5 min after IL-17 stimulation. There was nearly complete downregulation of P-p65 and NF-κB in the nuclei of BXD2 B cells at 15 min, but P-p65 levels remained high in the cytoplasm and in cytoplasmic extracts from BXD2 mice. B cells from B6 mice exhibited a lesser degree of upregulation of P-p65 in both the cytoplasm and the nucleus in response to IL-17 stimulation. Also, at 5 min after IL-17 stimulation, P-IκBα levels increased in the cytoplasm. Activation of P-p65 was associated with induction of p38 MAPK and p44/42 MAPK (Erk1/2) as has been reported previously in other cells (17), but C/EBPβ was not upregulated in B cells. Similar to cytoplasmic levels of P-p65, which persists for 1 h after IL-17 stimulation, P-p38 MAPK and P-p44/42 MAPK (Erk1/2) remained high in total lysate for 30–60 min after IL-17 stimulation. However, levels of P-p65 in the nucleus were rapidly regulated at 5 min and were down-regulated at 15 min as confirmed by confocal microscopy and analysis of nuclear extract. These results suggest that NF-κB target genes are quickly modulated after IL-17 activation in B cells of BXD2 mice.
NF-κB is essential for upregulation of RGS16. B cells incubated with a specific decoy peptide inhibitor of P-p65 that contained a PTD and could permeate into primary B cells of BXD2 mice resulted in nearly complete block of upregulation of RGS16 levels after IL-17 treatment. Treatment of primary B cells from BXD2 mice with IL-17 exhibited a decreased response to CXCL12. Treatment of primary B cells with the P-p65 decoy peptide was highly effective in blocking this IL-17-induced inhibition of chemotaxis to CXCL12. Together, these results indicate that IL-17 specifically signals through the classical NF-κB P-p65 pathway to induce expression of RGS16.
To determine whether TRAF6 and ACT1 are required for IL-17R signaling in B cells, we used a 70Z/3 pre-B cell line. This cell line expresses IL-17R and also signals upregulation of RGS16 to the canonical NF-κB pathway, because pretreatment with the P-p65 peptide inhibitor blocked IL-17 upregulation of RGS16. 70Z/3 B cells transfected with siRNA for Traf6 or Traf3ip2 exhibited significant inhibition of P-p65 signaling. siRNA for Traf6 or Traf3ip2 also significantly blocked IL-17 induction of RGS16. Correspondingly, there was normalization of the chemotactic response to CXCL12 after IL-17 treatment in B cells transfected with siRNA for either Traf6 or Traf3ip2. These results indicate that IL-17 signaling in B cells is similar to mechanisms in previously described in non-B cells and require TRAF6 and ACT1 to signal NF-κB (13, 29).
Finally, the results show that IL-17 induces a relatively larger increase in Rgs16 level (10 fold) compared with that for Rgs13 (2- to 3- fold). This is consistent with previous findings that NF-κB is a known transcription factor for RGS16 (30). However, RGS13 levels are constitutively higher in B cells and IL-17 leads to a larger absolute increase in the RGS13 level compared with that in untreated B cells. We propose that although RGS13 and RGS16 both regulate B cell chemotaxis and GC formation in response to IL-17, RGS16 upregulation, compared with that for RGS13, may provide a more finely tuned response to IL-17 to regulate the spontaneous GC response in BXD2 mice.
This work was supported by grants from the American College of Rheumatology Research and Education Foundation Within Our Reach: Finding a Cure for Rheumatoid Arthritis campaign (to J.D.M.), Alliance for Lupus Research Target Identification in Lupus program (to J.D.M.), Veterans Administration Merit Review (1I01BX000600–01 to J.D.M.), Daiichi-Sankyo (to J.D.M.), National Institutes of Health (1AI 071110–01A1 and ARRA 3RO1AI71110–02S1 to J.D.M. and RR-020136 and AI 083539Z to L.E.S.), Arthritis Foundation, and Lupus Research Institute (to H.-C.H.). Imaging of the translocation of NF-κB signaling was carried out by the Molecular Pathology and Human Cell/Tissue Core, Mucosal HIV and Immunobiology Center, University of Alabama at Birmingham, which is supported by Grant DK 064400 (to L.E.S.).
We thank Enid Keyser of the Arthritis and Musculoskeletal Disease Center Analytic and Preparative Cytometry Facility for operating theFACS instrument. We thank Dr. Fiona Hunterfor expert review of the manuscript and Carol Humber for excellentsecretarial assistance. We thank Dr. Sarah L. Gaffen for critical discussion and technical assistance for the analysis of C/EBP by western blot. Il17ra−/− mouse is a generous gift from Amgen Inc.
Publisher's Disclaimer: This is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (AAI), publisher of The JI, holds the copyright to this manuscript. This version of the manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the U.S. National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Heavy rain, T-storm watch until 9 p.m.
Hub commuters tonight should expect to be a little more cautious on the roads as thunderstorms and heavy rain hit the Boston area, officials said.
Most of Massachusetts is under a severe thunderstorm watch until 9 p.m., said National Weather Service Meteorologist Alan Dunham, with the exception of Cape Cod, Nantucket and Martha's Vineyard.
"Be prepared for suddenly reduced visibility and heavy rain," Dunham said, as the downpour hits the Boston area around 5:30 p.m. Or later. "Basically, just slow down."
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B Novak
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Lovely. Tastes like the Relais de Venice red. — 3 years ago
Nice flavours. Good with lighter meals or by itself. — 4 years ago
Soft but crisp. Nice with subtle flavours or on its own. — 4 years ago
Love the berry flavours! — 4 years ago
Nice and light but not too sweet. — 4 years ago
Nice and crisp. Very light. Good for lighter foods and on its own. — 4 years ago


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Toy Watch Unisex FLD09PS Disco Plasteramic Watch Feature
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Lookupuk.com - Scotland Genealogy Board
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Board Name: Scotland Genealogy
Tom Taggart
Athens, OH US
Nov 19, 2000
Looking for information on ancestors & siblings of John Taggart, b. 12/Aug/1756 Co. Antrim, d. 23/Aug/1830 Belmont Co. Ohio, M. Sarah McCartney, 15/Oct/1777. Believed family orig. Scotland, cleared in early 1700's
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Well summer 2014 is about to start soon and I am ready for the Sun in the N.W.
As I start to write this newsletter, we are down at Seventh Feathers RV Resort south of Roseburg, Oregon and it is raining fairly heavy. As my granddaughter Addison would say at 6 years old it is raining dogs and cats, plus buckets of water with snails. Yes snails, when it is warm and we have heavy rains it brings the snails out in groves.
2014 has started out with a bang on RV Sales throughout the country and here at B Young RV the increases from 2013 are tremendous, thanks to all the referrals that we get. Seems all categories of RV's are selling at B Young RV and other dealers around the country. Guess the Baby Boomers want to hit the road and those that are still working with families are finding that spending time in the outdoor environment with the whole family to be an adventurer! It is interesting though how many people are selling their homes and with some of the equity hitting the roads in an RV for a while, then settle in a tax friendly state. I find it is like being off the Grid a bit and not having to take care of your yard anymore, pay property taxes, plus you can leave at any time to a new playground in your RV.
While down at Seventh Feathers RV Resort (p.s. I don't gamble) I have had the privilege to play golf a couple of times out at the Myrtle Creek Golf Course. The first time I only had a couple of old Walter Hagen 6 & 8 irons (probably about 75 years old, given to me by my grandfather in 1967) in the back of the motorhome with a putter. I was able to borrow a driver with trust that I would return it after play. What a great time, I have now learned that I need to carry my regular clubs with me at all times. What amazed me was the amount of Turkeys and Deer running around on the challenging course. It was before Turkey season started in Oregon and the Toms were out strutting everywhere on the course!
Yes! They stopped play as I had to take a video of the birds working the green:
LINK: Tom's on the Green
The second time down at Seventh Feathers RV Resort I had my clubs and played well in the wind, rain, sun and hail at Myrtle Creek Golf Course. The course held up great and was a blast to play and being able to work the Par 3's with more than one ball. I had the course to myself into the late afternoon! The Course GM and the Course PGA Pro are really great guys and the atmosphere is very homely and open. The Marshall was a hoot and warned me I should go up a club on the Elevated Tee box Par 3 13th Hole, as the wind will catch the ball. Two times I did it my way and put the ball into the sand trap (2' apart) at the edge of the green, the next shot I took his advice and put it on the green. "I told you so" Ok! Enough Golf, go and have fun there though.
You can even get a great hot dog or hamburger at the diner!
Made a trip into California this spring also and found a really nice campground to stay in with friendly staff along the Northern California Coastline at Benbow KOA! It was great to find that particular campground late into the evening. Checked out other campgrounds, but felt uncomfortable, seems many of the old campgrounds in the Redwoods have lived on from the old days (60's and 70's) with little upkeep. There is a great deal of remoteness in the area and sometimes I think I had gone back in time to when I was a kid… Maybe a some paint and trimming of trees would have help change the atmosphere of RV Parks in the Redwoods!
A couple of our Tiffin Customers Russ and Pam will be heading to RED BAY, Alabama to see their Tiffin being built in July after the holidays. The welcome mat has been put out for them to have a memorable experience! Russ will be sending me a series of pictures on the build and I can't wait to see how it is done from the customer's view. Russ I think will be assisting in the production… I have a couple of restaurants down in Bandon,that everyone that heads down the way might enjoy to eat. Always 1st cabin food and I have given you pictures so you can remember the buildings along the wharf in Bandon.
There is plenty of parking and time to enjoy either of the restaurants on the Wharf at Bandon, Oregon
A new addition to B Young RV inventory is the Rubicon, a pull behind Toy Hauler, a great looking Toy Hauler at a great value. Now is the time to get great deals on all Toy Haulers at B Young RV. The "B" in the Young has order more inventory and we need to move the 2014's out!
As we say at B YOUNG RV:


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Fritz Stephey-, Delaware, US
Through my own funding, I run a weekly podcast called FritzCast, available via iTunes, SoundCloud, Google Play, and Stitcher Radio. In that podcast, I cover content relevant to current mainstream news stories, offer commentary on the Political landscape throughout the United States and the world. Most recently I have enjoyed analyzing the 2016 Presidential Election from the beginning of Primary season.
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While I have not worked in any official, professional capacity, I have freelanced for websites such as We Want Insanity, and have hosted over 40 episodes of my weekly podcast, which is still being continued on a weekly basis. I have also submitted work in various contests for voice over opportunities.
I graduated from Cab Calloway School of the Arts High School in June of 2007, and attended there from Middle School grade 6. During my tenure, my art focus was Communications, especially focused on technical and creative writing, web, film making, and photography. I also was a member of the school newsletter team, consulting in layout design and contributed as a writer.
I have attended Colorado State University through their online Global Campus program and am slated to graduate in May 2017 with a Bachelors in Communications. I have been awarded certificates from Colorado State in the areas of: 1.) Effective Communication In The 21st Century; 2.)Applying Leadership & Communication Strategies For The Global Marketplace.
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Heh heh...yeah right.He isn't coming back, furthermore like everything in "that book" it's all non-literal and simply a book of stories by which people should emulate to live "good lives".
No HE isn't coming back....SHE is--as with anything that is dual both sides will have a chance and then we will all become one with everything.........no division from anyone or anything like there is today.
Think about it!
Everyone has a chance right now LG.
From Galatians 3
Thumbs Up!!
People on the earth have a decision to make: either believe Jesus Christ and accept him as Lord and Savior and go to heaven with other believers when they die, or don't do anything and be damned to hell when they die where they will be tormented for all of eternity.
I assume you are just looking for a fight here. And thanks, but I declined your invitation to be friends on facebook. One look at your other freinds was enough to persuade me.
Did Jesus teach you how to make money through facebook?
Dude I'm a Christian too, and that is NOT the way to go about proclaiming God's message. It feels like you are jamming it down people's throat when you put it like that. You may want to try another approach next time.
Regardless if it is the Truth or not people resist forceful persuasion.
By the way, im the one who wrote that. Not Mark. Mark is an aethist. You are correct, but this is important stuff and needs to be heard.
What needs to be heard is already within you--in everyone. Jesus said that. Did you hear him or read those words? Jesus told his followers to go tell of his miracles and the good news that they can do the same and much more.......he didn't say shove it down anyone's throats, nor go to war against them nor kill tem if they didn't believe nor tell them they are going to hell if they don't believe nor convert anyone to anything. I believe Paul said those things when forcing his views on others brought him down. He wasn't the Foundation for the Church---it was Peter that Jesus told to be the foundation...............We should be edifying the teachings that Peter got from Jesus and not Paul's.. What do you say on those?
Look, I'm not trying to shove it down people throats. I guess the way I wrote it sounded kinda wrong. I want people to know the God I know. I don't want anyone to be damned to hell.
Yet you believe it will happen. You believe in a god with lower moral standards than your own, because he apparently does want people tortured for eternity even though you don't Why don't you stand up to him and tell him he's evil??
"People on the earth have a decision to make: either believe Jesus Christ and accept him as Lord and Savior and go to heaven with other believers when they die, or don't do anything and be damned to hell when they die where they will be tormented for all of eternity."
Is this fascism?
Jesus said in His word, that he came unto His own and His own received Him not. But as many as do receive Him become the children of God. You can not serve two masters. We either serve God or Satan. If we are saved and received salvation then great will be our reward for serving the Lord Jesus Christ. If we follow after Satan then we are sentenced to death and the punishment will be hell. God said, it is not His will that anyone would perish. Everyone is given a choice and He doesn't force anyone against their will. But, God loves every body. We make the choice for how we live our life. God is a just and merciful God and He will give people chance after chance to repent and turn from the ways of this world and live for Him.
1 John 5:13 These things have I written unto you that believe on the name of the Son of God; that you may know that you have eternal life, and that you may believe on the name of the Son of God.
Romans 6:23 For the wages of sin is death, but the gift of God is eternal life through Jesus Christ our Lord.
John 3:36 He that believes in Him is not condemned: but he that believes not is condemned already, because he has not believed in the name of the only begotten Son of God.
Revelation 1:3 Blessed is he that reads, and they that hear the words of this prophecy, and keep those things which are written therein: for the time is at hand.
OK - here's a simple exercise for you based on your statements:
1. I serve God and not Satan
2. I serve Satan and not God
3. I serve both God and Satan
4. I serve Neither God nor Satan
You allow for options 1 or 2
You disallow option 3
You totally ignore option 4 !
What's your take on option 4 - that vast class of people who do not serve God or Satan?
Paraglider- You are too logical and at the same time a very smart teacher.
Hi CW - I just get a little tired of being told what I must or can't do especialy from a perspective that doesn't even stand up to entry level logic
The reason I said "too" is now proved by your statement "entry level". I personally feel different people are at different levels as far as logical thinking goes(especially with respect to certain touchy subjects). And what may seem "entry level" to you may not be entry level for all. I guess what I am saying is that it is relative. Anyway have a good day
Well, please tell me what statement I made that required higher than entry level logic?
I really admire you for the ability to frame those 4 alternatives to explain (hence I used the word teacher earlier). It may seem basic entry level logic but then those who have taken a leap of faith then logic itself may not be sufficient to get the point across to them. Even if there is a acceptance of "GOD"(which you don't accept) those who belong to religion A may think of religion B's beliefs as "illogical" and vice versa. It may make perfect sense to somebody who has strict scientific standards of assessment (like yourself) but for others it may not seem so. Anyway it is 1 am and my husband has finished watching his movie. Time to say Good Night. It was nice talking to you
Jesus said the everything him his love, his laws, his Kingdom is all in one place and it is for everyone and thre was no discrimination of anyone or any race, color, creed, bleife or thereof/ He said it is all WITHIN us. Now that that is said there is not justification to tell others they are going to hell or that becasue they believe differently then your do that they are believing in Satan or are following that myth.
So you really think that Bible has not been tampered with--try reading the verses before and after those you posted here and see if you get a different meaning to the whle thing. How much histroy do you believe in and how about Bilology and Phsychology and the workings of minds and those who like to control others so that they have --what--moreglory and are closer to God??
No one is closer to God then anyone else--anywhere or anyone--it is all within them.
Gosh LG, go easy on her. She hasn't done anything but relay what is already in the bible. It isn't her fault, plus she never gives any explanation of meanings or history so it doesn't seem fair that you say such things to her to justify your own. Doing so is not right either.
I do agree though, there is no justification for telling people they will go to hell however we all will go to hell, we all go to the place of death, there isn't any suffering in death just not a promise of another life in perfection with God.
The bible says that everyone has a lot in life, those who have riches, wealth, success, etc.. have received their lot or reward in life under the sun but at death it all leaves. There is no hoping, longing, thinking, sadness, happiness etc. No one hangs out in purgatory, no one goes right to Heaven, no one burns "alive" in a lake of fire.
When your done, your done. We all go down the same way. The day you die there is nothing, their is no praising God on your way down either because a dead person is conscious of nothing. http://thanksgod.org/?page_id=31
God does not burn alive living souls for all eternity in agony. God may burn dead one.... so think about it for a while, but once it is dead, it feels nothing and thinks nothing.
But you are wrong in one thing. Some people are definitely closer to God then other. God says that God is "closest" to those with a broken heart. Also, how do intend to back up a claim like that when I can only wonder how a person can be closer to God then you or me or DeanMac if they honestly in all their hearts do not believe in God?
Well, there we go. DeaneMc believes that some are saved and some are fried. LG believes we are all one with God. Sandra believes we all die but still believes in God. Hey - you can't all be right, you know. Would anyone like to explain why belief (in anything unknowable) is a good thing? I can't see it
Beats me.
I mean - Sandra even knows what god says...."God says that God is "closest" to those with a broken heart."
Which has to be worth something..................... Seeing as how it is God and all. And God must be pretty broken hearted about ........... whateva.
Does it make you mad that God is close to people with a broken heart?
No, it makes me laugh out loud.
I do find it entertaining that you have adopted the "well, you must be mad at god." approach though.
It makes you laugh that God is there for people with a broken heart?
No - it makes me laugh that you think there is a god that shows a preference and you know what god says.
Got to admit it is rather funny.
I am sending you a pm.
Certainly but at least we all agree that there is a God.
Somewhere in the Bible it say "blessed is he who believe, and haven't seen." I like so many other, believed only because of fear of not believing. but not any more. different ways has brought us to the truth. but the good thing is once your here, you will never go back. Not like the unbeliever who continue to wander.
That's not necessarily true either. I was brought up to believe, and did, until I didn't. But looking back, that was a step forwards, not backwards. What you call wandering, some call thinking. It's good. And far far better than contemplating hell fire and everlasting worms for unbelievers
Exactly! I was a beleiver and still am, but not in the way that those with doctrine and blind want or expect me to be. How I see it is that everyone who disagrees with a "believer" automatically is JUDGED and put into the cetegory of "un-believer" That is a wrong assumption on their parts and totally unfair to those who are categorized as un-believers.
There is no "coming to him", when he says that he is already within you. How is it possible to come to anything that is already there---you can't.
I also see little need for most of the confrontation. It usually arises when people, sometimes accidentally, say things that exclude or degrade others who simply think differently. Hence my new thread - thanks for joining it
You always get me to think--and that is a very good thing because we were given brains to think with. If everyone was supposed to be like the "BORG" then we would all be like them, but we are not. If we were not supposed to think, then we wouldn't have brains to think ith. What a horrible existence. What would be the use of the flowers, trees, oceans, clouds, animals, insects and all the other beauty that is here to see and think about and enjoy.
I read all that has been posted and i understand that many feel that the warning is to harsh!
Many in the days of the prophets felt this way too! I don't believe that the warning was trying to make any one do any thing. Take it as it is written. A warning to the lost! may sound hard, but time is short! Its your choice!
He will return! As in the days of Noah many will scoff and say were is he! He isn't coming! Your own words are in the bible! It took Noah some time to finish the ark, but when he was finished God closed the door and the floods came. Less standards! I think NOT! He is warning and has warned! I believe that is above standard! But than that is something I understand and many just refuse to see and hear. Your choice!
Myself are the one that wrote the warning will not or can not make you choose to receive this warning! No! Not even God will make you, He and yes I say He wants you to come to Him on your own! That's called free will!
Your choice!
My choice indeed. And here's another anomaly. Some very devout believers are adamant about free will while others insist on predestination. People who can't agree with each other expect the rest of us to take notice and obey. And the best reason they can offer is fear of damnation. I think there are bigger issues to work on than the afterlife or the second coming.
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When a person says this:" Disbelievers will be given Hell & suffering for eternity. Have fear. "in a Question thread, yet says this: "Love to share! Sharing is caring!!"in his/her profile, can...
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Logical thinking. Quick note about John In Revelations 22:10, Don't seal the prophetic words of this book, because the time is near. Let the unrightous go on in unrightousness; let the filthy go on being made...
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Justin is an American guitarist/singer who specialises in stripped back organic sounding original music and covers.
With over twenty years experience playing Justin has become adept at many different styles including classical, flamenco, bluegrass and gypsy jazz. Through this study of instrumental music he has also developed a very melodic approach to his instrument and arrangements. He has performed in numerous original and cover bands both here in Perth and in the states. Recent projects include original rock/indi bands "Atticus Finch", "Half tree road", "Van Houten", "Sycamore" and currently in the gypsy jazz tribute "Belleville".
The Beatles, Radiohead, Seal, Ben Harper, Boards of Canada, Jimi Hendrix, Led Zeppelin, DJ Shadow, Van Morrison, Django Reinhardt, The Doors, Coldplay, Brian Jonestown Massacre.
Justin is available for special occassions, cocktail functions, venue bookings, corporate events and private parties etc...
Everything was awesome. Justin sounded great. I have spoken to him and he said the generator drop off and delivery was all easy and worked well.
Thanks so much! We are very happy that we found you guys.


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"All the adversity I've had in my life,
all my troubles and obstacles,
have strengthened me…
You may not realize it when it happens,
but a kick in the teeth
may be the best thing in the world for you."
-Walt Disney
all my troubles and obstacles,
have strengthened me…
You may not realize it when it happens,
but a kick in the teeth
may be the best thing in the world for you."
-Walt Disney
I am back from my trip to California and finally getting organized! Does anyone feel like it takes forever to get organized and back to a normal schedule after a trip?! Ugh! So much work, cleaning and life to catch up on. Since today's outfit post was photographed in Disneyland, I'll be doing a little bit of a different content post and talking about about some hidden park food gems for you to try on your next trip there!
{On Me} | Dress: c/o Stella B | Hat: Forever21 (almost exact) | Sunglasses: B.P. Nordstrom | Clutch: old (similar) | Slip: Daisy Shop (similar) | Sandals: 6pm (almost exact) | Earrings: sold out (similar) |
{On Him} | Watch: c/o Chic Timepieces | Tee: H&M | Jeans: sold out (similar) | Sunglasses: Lucky | Shoes: Nordstrom Rack |
Theme park food is not always amazing, but Disney is an exception if you know where to eat
One of my best friends works in food management at Disneyland, so over the past six years she has shown me where all the best food is. Since not everyone can be as lucky as I am to have a best friend with this knowledge, I thought I'd share some gems with you so you can branch out from the typically chicken fingers and pizza you might gravitate toward.
Sit Down Restaurants
I recommend doing a sit down meal for lunch because lunch prices are less expensive and it's usually hot and crowded in the middle of the day anyway. A sit down lunch is the perfect way to take a break.
1. Blue Bayou-Located INSIDE Pirates of the Caribbean. Great setting, lunch prices are affordable and the food is actually GOOD. Make a reservation before you go though, it can get super booked.
2. Big Thunder Ranch-All you can eat BBQ…enough said! If you need more convincing think ribs, chicken and awesome side dishes!
3. Carthay Circle (California Adventure)-Steaks, risotto, creme brûlée and so much more. It's great if you are at the park with family or friends that enjoy spending time visiting and having a nice dinner.
4. Cove Bar (California Adventure)-My favorite there were the lobster nachos, it also has a great view of World of Color. Tip: if you go during world of color, go early. There is a long line to be seated (1-2 hours) if you go right before World of Color. Plan to go ahead and eat a nice slow meal and then get dessert during the show.
5. Cafe Orleans-The Monte Cristo there is amazing!
Fast Food
Fast food is great to maximize park time, but that doesn't mean you can't have great food!
1. Harbour Galley-The stuffed baked potatoes are a great quick meal.
2. Churros-Any churro stand in the park has pretty dang good churros.
3. Tiki Juice Bar-Dole pineapple whip. So good on a hot day, and if the line is long go inside and watch the show. There is not much of a line for pineapple whip on the show side and watching the show gives you a place to sit and enjoy your treat out of the hot sun.
4. Fruit Cart (right next to Jungle Cruise)-Great place for a healthy snack. Enjoy pineapple spears, papayas with lime, etc. Something healthy to munch on while you're waiting in the Indiana Jones line!
Hope you enjoyed these recommendations and have fun on your next trip there!


text: Analysis of the Bispectral Index During Natural Sleep in ChildrenSection Editor(s): Davis, Peter J.Benini, Franca MD; Trapanotto, Manuela MD; Sartori, Stefano MD; Capretta, Anna MD; Gobber, Daniela MD; Boniver, Clementina MD; Zacchello, Franco PhD, MDAnesthesia & Analgesia: September 2005 - Volume 101 - Issue 3 - p 641-644 doi: 10.1213/01.ANE.0000157566.41739.2C Pediatric Anesthesia: Research Report Abstract In Brief Author Information Article Outline The Bispectral Index (BIS) is a system used to measure sedation levels. Some investigators recently analyzed changes in the BIS during natural sleep in adults and found that the BIS diminished considerably as sleep became deeper. No such studies have been undertaken to investigate changes in the BIS in sleeping children. The aim of this work was to assess the trend of the BIS in the various stages of sleep in a group of children, performing a descriptive analysis on a limited number of cases. We evaluated 15 children with negative clinical findings and a normal electroencephalogram (EEG) as part of their follow-up for prior episodes of epilepsy, recording the BIS and EEG in a waking state, in the various stages of sleep and on reawaking. For each stage, the mean value, the standard deviation, and the range of BIS values were calculated. The results showed that the BIS decreased progressively as sleep became deeper. The correlation between the stage of sleep and the BIS was significant. On reawaking, a slow increase was apparent in the BIS. IMPLICATIONS: Some studies in adults found that the Bispectral Index (BIS) decreased as sleep became deeper, providing a nonspecific measure of the subject's level of consciousness. This study investigated the changes of BIS during natural sleep in healthy children. Department of Pediatrics, University of Padova, Padova, Italy Accepted for publication January 12, 2005. Address correspondence and reprint requests to Franca Benini, Department of Pediatrics, University of Padova, Padova, Italy. Address e-mail to firstname.lastname@example.com. Abstract Methods Results Discussion References The Bispectral Index (BIS) system uses an integrated analysis of the electroencephalogram trace (EEG), obtained with 2 frontal leads (F7, F8), to enable an assessment of the level of sedation and anesthesia (1). The BIS records the continuous EEG signal, breaking it down and eliminating artifacts, then it compares the EEG pattern acquired instant-by-instant with EEG traces saved in its database to provide a single number on a scale of 0 to 100 that correlates with the subject's level of sedation (2). Some studies have analyzed changes in the BIS during sleep in adults. Sleigh et al. (3) found that the BIS decreased as sleep became deeper in much the same way as under sedation, thereby demonstrating that this index provides a nonspecific measure of the subject's level of consciousness. Other authors emphasized that the BIS cannot be used conventionally to differentiate between the different stages of sleep because of the overlap in the values recorded by the index at the moment of the shift from one state to the next (4). Moreover, Tung et al. (5) demonstrated that the BIS is able to detect only the beginning of sleep in adults. However, the BIS variables were constructed based on EEG in sedated and anesthetized adults, not during natural sleep. Although several studies have considered the applicability of BIS to evaluate sedation and anesthesia in pediatric patients (6–8), none has investigated its changes during natural sleep in children. The aims of the present study were (a) to evaluate the trend of the BIS in the various stages of sleep in a group of children by means of a descriptive analysis on a limited series of cases; (b) to obtain information on the BIS trend in natural or endogenous situations in order to develop baseline data useful for future research in clinical settings such as sedation. Back to Top | Article Outline Methods After obtaining the informed consent of their parents, and institutional committee approval from our Department, EEG and BIS were recorded during natural sleep in 15 children aged between 1.2 and 16.5 yr (mean age 8.2 yr; 8 boys and 7 girls), who were being followed for prior episodes of epilepsy and at the time of this evaluation were seizure-free for 2 yr. They had negative clinical findings and an EEG (waking and sleeping) with no significant anomalies, and they were receiving no neuroactive pharmacological treatment. The study was performed at the Neurophysiology Service of the University of Padova Pediatrics Department. Before the assessment, the children were deprived of sleep (from 11 pm to 3 am on the previous night). When they arrived at the Department, they were accompanied to a soundproofed room (some of them asked to have a parent with them in the room). Electrodes were applied to record the EEG (Galileo Planet 300 Plus Basic) and the BIS (Aspect A-2000). A conventional EEG polysomnograph was recorded using a 16-channel computerized system. The electrodes for the BIS were applied according to the standard layout, i.e., with 2 bilateral frontal electrodes coinciding with the right and left prefrontal cortex (F7 and F8) to provide a bipolar bifrontal signal and 1 earthing electrode between the corner of the eye and the hairline. The low- and high-frequency filters were set respectively at 0.5 and 30.0 Hz. The quality of the signal was expressed by SQI (signal quality index) that provides a score from 0% to 100%. We only considered BIS values with an SQI >50%. None of the data were eliminated because of electromyograph artifacts. Changes were simultaneously recorded, continuously for the EEG and at 1-min intervals for the BIS, in the following stages of sleep: while falling asleep, during the 4 stages of sleep, and on subsequent reawaking. We differentiated each stage of sleep according to the classification of Rechtschaffer and Kales (9). EEG and BIS recordings were obtained for at least one sleep cycle in each child, though it was not always complete with all sleep stages according to conventional EEG staging. A descriptive analysis was performed on the resulting data. Back to Top | Article Outline Results For each stage considered (waking, sleeping stages I–IV, reawaking), we calculated the mean values, standard deviation and range (minimum and maximum), and the duration of the recording obtained in minutes (Table 1). The total recording time for the BIS was 621 min. Some of the first few minutes of the waking stage were not recorded in four subjects because of recording artifacts. Three subjects woke up (for 1–2 min) and then fell asleep again during the course of the recording. The average latency period between waking and light sleeping (stage I) was 16.22 min (range, 2–59). All the children reached stage II sleep; 3 children reached stage III and 1 reached stage IV (Fig. 1). Data analysis revealed considerable variations in the BIS during the various stages of sleep: these changes reflect the classic description of sleep architecture. As the stage of sleep became deeper, the BIS values progressively decreased (Table 1). On reawaking, the BIS gradually increased again to a mean of 87.67. Table 1 Figure 1 A correlation analysis performed on the data recorded by the BIS in the various stages of sleep was found significant (r = −0.713; P < 0.05): as sleep became deeper (from stage I to IV), there was a concomitant decrease in the BIS (Fig. 2). Figure 2 To analyze the trend of the BIS in the reawaking stage, a comparison was drawn with the EEG values coinciding with wakefulness. It emerged that the BIS reaches the values >90 typical of a wakeful condition with a mean latency of 2.5 min (sd 1.6; range, 0–5) with respect to the EEG recording. Back to Top | Article Outline Discussion Although it was conducted on a limited number of subjects, our study nonetheless shows that the BIS is sensitive in reflecting the changes on the EEG trace that accompany the various stages of natural sleep. To be more specific, the BIS values decrease progressively as the stage of sleep becomes deeper. There are very few studies on this topic in the literature and they were all performed on very small samples (from 5 to 10) of adults (3–5). Sleigh et al. (3) found BIS values between 75 and 90 for sleep stages I and II and between 20 and 70 for stages III and IV. In addition to the limited number of subjects considered, an important drawback of this study was that the authors did not subdivide the sleep stages into four, but rather into the coarser gradation of light sleep and slow-wave sleep. Nieuwenhuijs et al. (4) found lower mean values for the BIS than Sleigh et al. in a similar study. Both these studies drew a distinction only between light and deep sleep. Similar to the method adopted more recently in the adult (5), our study distinguished each single stage of sleep. It is worth noting that the BIS values recorded in deep sleep are comparable with those observed under deep sedation, a finding that confirms the nonspecificity of the BIS. This tool does not enable a distinction between the cause of the change in level of consciousness and the ability to wake up again (3). It is consequently impossible to use BIS values to distinguish "natural or endogenous" from "exogenous or pharmacological" sedation; such a discrimination has to be based on known clinical variables (reaction to touch or voice, eye movement, etc.) to avoid the risk of misinterpreting the subject's real condition. A child's reaction to a painful stimulus or surgical incision would be very different in the two above-mentioned situations, despite similar BIS values being recorded in the two cases. The same applies when a child's degree of wakefulness needs to be assessed after a procedure conducted under sedation-analgesia; a low BIS may not necessarily indicate a persistent sedative effect of the medication administered, it might simply be a state of deep sleep resulting from the cessation of a stressful condition. Finally, when children are woken, their BIS gradually increases until it reaches values similar to those recorded before they fell asleep. Observations in adults (4) have shown a gap, during the reawaking stage, between the subjects' behavior and their slower gradual return to normal BIS values (4). This gap was also identifiable in our study, between the EEG values corresponding to a waking condition and the BIS values recorded, the latter demonstrating a prolonged latency. There are two main hypotheses to explain this: either this prolonged latency is caused by the BIS recording method (which averages the values recorded at intervals ranging between 5 seconds and 1 minute) or the slow change in the BIS values derives from a differential reactivation of the various cortical sites as the subject wakes up. One of the drawbacks of our study is undeniably the limited number of subjects analyzed. For this reason, we were unable to evaluate the BIS differences according to children' ages. Publications in the literature on adults are also of an exploratory nature, however, and have analyzed even smaller samples. Another shortcoming is that no data were recorded for the REM stage of sleep, so we are unable to say what changes the BIS may be able to record during this stage. The few works available in the literature on adults report BIS values very similar to those recorded in our study during the waking stage (3,4). In conclusion, as in adults, the BIS recorded in children decreases considerably with deeper stages of natural sleep, in much the same way as in deep sedation and irrespective of the reason for the altered state of consciousness.Back to Top | Article Outline References1. Vernon JM, Long E, Sebel PS, Manberg P. Prediction of movement using bispectral electroencephalographic analysis during propofol/alfentanil or isoflurane/alfentanil anesthesia. Anesth Analg 1995;80:780–5. Cited Here... 2. Sigl JC, Chamoun NC. An introduction to bispectral analysis for the electroencephalogram. J Clin Monit 1994;10:392–404. Cited Here... | PubMed 3. Sleigh JW, Andrzejowski J, Steyn-Ross A, Steyn-Ross M. The bispectral index: a measure of depth of sleep? Anesth Analg 1999;88:659–61. Cited Here... 4. Nieuwenhuijs D, Coleman EL, Douglas NJ, et al. Bispectral index values and spectral edge frequency at different stages of physiologic sleep. Anesth Analg 2002;94:125–9. Cited Here... 5. Tung A, Lynch JP, Roizen MF. Use of the BIS monitor to detect onset of naturally occurring sleep. J Clin Monit 2002;17:37–42. Cited Here... 6. Denaman WT, Swanson EL, Rosow D, et al. Pediatric evaluation of the bispectral index (BIS) monitor and correlation of BIS with end-tidal sevoflurane concentration in infants and children. Anesth Analg 2000;90:872–7. Cited Here... 7. Bannister CF, Brosius KK, Sigi JC, Meyer BJ. The effect of BIS monitoring on anesthetic use and recovery in children anesthetized with sevoflurane in nitrous oxide. Anesth Analg 2001;92:877–81. Cited Here... 8. Berkenbosch JW, Fichter CR, Tobias JD. The correlation of the bispectral index monitor with clinical sedation score during mechanical ventilation in the pediatric intensive care unit. Anesth Analg 2002;94:506–11. Cited Here... 9. Rechtschaffer A, Kales A, eds. A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects (NIM publication no. 204). Washington, DC: US Government Printing Office, 1968. Cited Here... © 2005 International Anesthesia Research Society Article Outline Abstract Methods Results Discussion References Source Analysis of the Bispectral Index During Natural Sleep in Children Anesthesia & Analgesia101(3):641-644, September 2005. 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text: School starts back tomorrow. This means a shower tonight for a kid that's shower/bath resistant (can you say MELTDOWN?) and 5am mornings again for someone who is decidedly not a morning person. Soooo not looking forward to school starting back up. Oy. She had a nice meltdown last night over who-knows-what (never did get quite to the bottom of that one) and was up until almost midnight.


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Our She Said, He Said, She Said feature returns with an Olympics-themed installment!
2 articles Tag Homophobia
Happy Pride!
Continue reading →
Yesterday was Pride Day in Winnipeg, when members of our city's LGBT community and their allies come out (heh) to celebrate with a rally at the Manitoba Legislative Building, a march through downtown and an afternoon festival at The Forks. Mother Nature graced this year's event with some beautiful weather — a welcome treat after a week of rain — and a fun time was had by all.


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Travelling to Budapest
If you are travelling to Budapest you may well be interested in knowing what to expect from your visit to this magical city. Each year thousands of people travel to the magical city of Budapest.
There is nothing more frustrating the wandering around a foreign city, hoping to enjoy some local delights, but being unable to find a good bar or a restaurant to enjoy them in.
Help is at hand as we are happy to present to you some of our favourite Budapest pubs, bars, restaurants and clubs.
Flights to Budapest
Details of airlines and websites offering cheap flights to Budapest.
Trains to Budapest
Details about trains to and from Budapest to other European cities.
Coaches to Budapest
Information about coaches to Budapest and companies providing coaches to Budapest.
Weather in Budapest
Forecasts for the weather in Budapest, descriptions of the weather to expect in Budapest by month.
If you would like a member of our team to assist you with planning your trip to Budapest we would be happy to help. We can advise you on the most suitable accommodation in Budapest so your holiday in Budapest is a delight.


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Category: Books
The Paris Wife: Book Review
May 1, 2014
I recently finished the audio version of The Paris Wife and LOVED it. I am fascinated by the stories of writers and also historical stories from the point of view of a supporting character. I admit I knew nothing about this book when I decided to listen to it. All I know is I am […]
Amazon Kindle Deal For Select Customers – I Got It & Donated the Kindle
April 27, 2014
My friend posted this offer for an Amazon Kindle Only $19 after seeing it on Budget Savvy Diva. It's only available to some people, so you have just try it. I did get the deal (not sure if it's because I'm a Prime member or don't already have a Kindle). What to do: Click this […]
I've Got Your Number by Sophie Kinsella: Book Review
February 13, 2014
I've Got Your Number by Sophie Kinsella is a romantic comedy novel that is perfect for a commuting woman. I really like I've Got Your Number audio book because it is easy to listen to and the speaker was British so that was kind of fun. Throughout the day (after listening to it in the morning) […]


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MillionYoung gets a physical release of his debut album Replicants on February 15th via Old Flame. You can listen to a recent in-studio performance on KEXP. Check out the new Snoretex remix of "Perfect Eyes" below. Snoretex is the new project from Sam Willis of Walls.
MillionYoung-Perfect Eyes (Snoretex Remix) by Old Flame Records


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My mom liked Angelina and Alexandria. They almost named me Elizabeth but didn't because my uncle's wife (we call her yuck lol) said they could call me Erp, which would've been my initials.
They ended up naming me Natasha Rae, after my grandma Norma Rae.
I like that I'm named after my grandma but don't care too much for my name. 9 times outta 10 I'm asked if I'm Russian, which I'm not. A LOT of people mispronounce my name and after correcting them they still mispronounce it. Instead of Nuh-Tahhhh-shuh they say nut-ASH-uh. Never in my life have I EVER heard it said that way. I don't mind telling people how to spell it but some people argue with me and tell me I'm spelling my name wrong.


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Supplier Directory
KAVA Farms was established in 2013 by the KAAPA Aqua Ventures Alliance (KAVA), and still retains some of the original shrimp farmers. Built in 1982, the farm itself is the longest continuously operating shrimp farm in the United States. The 850 acres hosts 25 shrimp ponds, as well as a hatchery where the larvae grow. The ponds are supplied by high salinity seawater from the bay, which is circulated through the system then back into the bay. With several processing facilities in the area, the shrimp can be processed and packed in almost any form. Traditionally, KAVA Farms has packed in 10/5 block or IQF 40# bulk, 20# bulk, 5# bag or 2# bag. They can also deliver fresh never frozen during harvest season - July through October. The vision of KAVA Farms is to be an innovative and progressive aquaculture venture, sustainably producing consumer-preferred seafood without any added antibiotics, hormones, or other chemicals.
Call for delivery options. Harlingen Farms will work with your needs to set up distribution.
|Seafood Products
|Seafood Origin(s)
|Harvest Method(s)
|Sustainability Ratings/Scores
|Seafood Cert.
|Min. Order
Whiteleg Shrimp
Texas, USA
|0 lbs


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Fact: a number of those seemingly perfect #nofilter selfies have a little help from a re-touching app—and thankfully, Tyra Banks is here to show us the secrets.
On Wednesday's episode of FABLife, the 41-year-old former supermodel asked the audience to confess whether they've every posted a pic with the hashtag #nofilter when in reality, the image has been retouched.
"I have a confession to make," the television host told the crowd. "I don't lie when I say #nofilter. However, I do like to touch it up just a little bit, some of my pictures."
Never one to shy away from candidly speaking about her personal life, the Top Model admitted, "I have insecurities, nobody's perfect" before revealing she likes to touch up her "skinny calves."


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