text:
Skip to comments.Ronald Reagan Move Over
Posted on 12/18/2010 11:46:43 AM PST by timesthattrymenssouls
The extension of the Bush tax rates (what the media is now calling Obama's tax cuts) is a victory for Conservatives that should not be squandered. The Obama tax cuts are neither Obama's--they are Bush's--nor are they tax cuts--they are an extension of the current rates that were set to expire on 12/31/10. But the claim of the Democrats that these extensions had to be made because raising taxes on Americans in this economy would be disastrous is a true victory for Conservatives. It is also sound fiscal policy and should be capitalized on.
An editorial in today's Wall Street Journal points out: "As Milton Friedman taught us with his "permanent income hypothesis," consumers base their consumption on their longer-term income expectations, not merely on current income." Temporary tax rates return money to its rightful owner, the earner, but without the certainty of knowing what future tax rates are increased consumption will be muted by the lack of clarity. The Republican majority in the House has a golden opportunity to revisit the tax question while they have the Democrats on their heels and push for further, permanent cuts in 2011.
After passage of the bill Senator Dick Durbin (D) claimed: "The president has a big victory here. It's big because it means there won't be a tax increase at the first of the year, which could have hurt our economy."
Suddenly, though not un-coincidentally (recall the landslide November elections), the Democrats have found lower tax religion. If, as the Senator says higher taxes "hurt" our economy, why has it taken two years for the Democrats to support this extension of the Bush tax rates in an economy they call the worst since the Great Depression? Additionally, why didn't they propose lower and permanent rates to further stimulate demand?
President Obama, too, is a an enthusiastic member of the lower tax club. Only a week ago he was complaining that the House Republicans were holding unemployment benefits hostage to the tax rate extensions, then upon signing the bill declared: "This is real money that's going to make a real difference in people's lives. That's how we're going to spark demand, spur hiring, and strengthen our economy in the new year" (Reuters)
Ronald Reagan move over and meet the new supply-sider in the White House. His claim that "lower taxes spark demand, spur hiring and strengthen our economy" should be rung from every mountain top from now until 2012.
You heard it here folks.
What garbage. Obama was forced into this, he knows he needs an improving economy to have any chance at re-election, so he can then finish America off. This is pure leftist strategy. Obama is the opposite of Reagan, Obama hates America and wants to destroy it and will do so by any means necessary, even if that means is to act conservative.
Exactly. That is what makes it so rich. Let's hope the Republicans leverage it in 2012. I miss Ronnie.
That is not the conservatives' brief against taxes, but the economists' brief. The economic strength of the country is not a government function, the conservative would argue, but a private function, which the private sector will provide for quite bountifully if government will just stay out of the way.
The conservative brief is that government is limited and restricted to certain functions and that taxes should only be assessed to provide for those minimalist functions, those we agreed to in our compact with each other to form a government for the national defense and general welfare. Anything more is a violation of the constitution - a violation of that pact between and among the People - and a theft of private property.
Moreover, the conservative would argue, additional funding to the government means additional bureacrats, additional interference in the lives of its citizens, and not irrelevantly, interference in the ability of individuals to engage in productive enterprise to provide their peronal wealth, which collectively results in the wealth and power of the country.
But a liberal misconstrues the conservative position by attempting to argue, "we are all conservatives now."
They change their political mind as needed to survive honest workable conservative conviction.
By Christmas it will be touted as the Obama tax cuts.
That of which started out as a promotion of giving of the poor peoples money to the EVIL rich by the party of "change".
Eight years of Bush tax cuts destroyed us and NOW Obama is promoting 2 more years of it after stating with conviction that higher taxes is the ONLY way out of the desperate financial situation that we are in presently.
I would hate to be a democrat politician right now....
I called our local newspaper's soundoff this morning with the very same comment.....that until the tax extension passed, it was called Bush's tax cuts but as soon as it was voted on and Obowsalot signed it, all of a sudden it became Obama's tax cuts.....I pointed out that it was an extension of the Bush tax cuts, meaning extension of the current tax rates. Wondered if zer0 will acknowledge that this is one thing that really is Bush's fault - oh wait, that would mean admitting that W knew what he was doing....
This article is pure BS. Move over Jimmy Carter.
Disclaimer: Opinions posted on Free Republic are those of the individual posters and do not necessarily represent the opinion of Free Republic or its management. All materials posted herein are protected by copyright law and the exemption for fair use of copyrighted works.


text:
Fables TP Vol 02 Animal Farm Paperback
by Bill Willingham
Collecting FABLES #6-10, the second story arc of the fan-favorite, critically acclaimed VERTIGO series.
Travel to upstate New York, where the non-human Fable characters have found refuge on a farm, miles from mankind.
But all is not well on the farm - and a conspiracy to free them from the shackles of their perceived imprisonment may lead to a war that could wrest control of the Fables community away from Snow White.
Starring Goldilocks and the Three Bears. Plus, a sketchbook section featuring art by Willingham, Buckingham and Jean.
- Format: Paperback
- Pages: 128 pages
- Publisher: DC Comics
- Publication Date: 01/08/2003
- Category: Modern & contemporary fiction (post c 1945)
Free Home Delivery
on all orders
Pick up orders
from local bookshops
Showing 1 - 5 of 28 reviews.
Previous | Next
Review by bookwormteri
Love this series!!!! love it love it love it. Imagine all your favorite fairy tales all grown up and with human flaws. They have been kicked out of their homelands and now live in New York City and are trying to blend in and keep their community cohesive. In this book the nonhuman looking fables (the three little pigs, the giants, shere khan and the like) who live up at the farm are revolting and have taken Snow White hostage.This series is a fresh look at ancient stories. It is enthralling and quaint all at the same time. To take characters that everyone knows and loves and put recreate them so that they are still recognizable but completely new is just amazing.
Review by abbylibrarian
The saga of Fabletown continues with Volume 2, which collects issues 11-18 of the comic. The non-human members of Fabletown, who are forced to stay on a large farm in upstate New York, decide to collect weapons and plan to invade the homeland. When Snow White stumbles upon their plan she discovers that they will stop at nothing to get their way. What's more, she believes that even with all their weapons, they have no real hope of besting the Adversary. Another gripping installment of a very well-thought-out and innovative story. I've already got the next volume on hold at the library and can't wait to read it. Highly recommended.
Review by tapestry100
The continuing adventures of the inhabitants of Fabletown, Bill Willingham's Fables series continues in the second story arc, Animal Farm. With the more "un"-human occupants of Fabletown not being able to live in NYC with those that can pass as human, they have moved into the Fabletown extension in upstate New York called the Farm. Feeling they are being treated unfairly, they decide to rebel against the rules and regulations of Fabletown to try and make it back to their homelands, until one of their number decides to take things too far.I continue to be impressed with this series. Bill Willingham is able to create ties between seemingly unrelated fairy tales and fables and create one of the most original stories I've seen in comics in a long time.This particular volume I felt fell a little bit from the strong beginning of the first volume, Legends in Exile and the prelude volume 1001 Nights of Snowfall, but I still enjoyed it all the same. Looking forward to continuing reading this series.
Review by ElizaJane
Now having read this second book in the series I am officially a fan and can't wait to get my hands on the next volume. This is very different from the first one which had a classic noir feel to it. This time around Animal is indeed an Orwellian reference. The non-human fables and those unable to to take human form live on a large plot of land that has been enchanted with a spell to keep humans away. This is called "The Farm" and a large amount of the population is unhappy with the rather prison like conditions. Though the place is nice enough and not lacking in any way there is still the fact they can't leave. I loved the thematic cross between Animal Farm and Lord of the Flies. Lots of new characters were introduced while Snow White and Rose Red remained main characters as from the first volume. In this book we meet the three little pigs, Goldilocks and the Three Bears, giants, a dragon, several animals from The Jungle Book including Baghera and Shere Khan plus many others.
Review by -Eva-
Trouble is brewing at The Farm, where the Fables who can't pass for human are confined; led by Goldilocks, the Fables are planning a bloody rebellion and, since Bigby isn't allowed near the place, Snow White must work hard to outwit the leaders, which will prove disastrous for her health. Whereas the first five issues of the series introduced the Fables of Fabletown, these next five introduce those Fables who live at The Farm, and it does an equally good job at that. Although some come across as quite malicious, it is important that the difference between these characters and those fairytale characters they hail from is made absolutely clear; they may already have history in the fairytale world, but they are quite contemporary in their actions and their thinking. Happily Ever After is not a guarantee here - more likely, the exact opposite is to be expected when these characters show their true, non-traditional, colors.
Previous | Next
Also by Bill Willingham | View all

subset: commoncrawl


text:
Inflammatory brain disease may damage cerebral vascular endothelium leading to cerebral blood flow dysregulation. The proinflammatory cytokine TNF-α causes oxidative stress and apoptosis in cerebral microvascular endothelial cells (CMVEC) from newborn pigs. We investigated contribution of major cellular sources of reactive oxygen species to endothelial inflammatory response. Nitric oxide synthase and xanthine oxidase inhibitors (Nω-nitro-l-arginine and allopurinol) had no effect, while mitochondrial electron transport inhibitors (CCCP, 2-thenoyltrifluoroacetone, and rotenone) attenuated TNF-α-induced superoxide (O2•−) and apoptosis. NADPH oxidase inhibitors (diphenylene iodonium and apocynin) greatly reduced TNF-α-evoked O2•− generation and apoptosis. TNF-α rapidly increased NADPH oxidase activity in CMVEC. Nox4, the cell-specific catalytic subunit of NADPH oxidase, is highly expressed in CMVEC, contributes to basal O2•− production, and accounts for a burst of oxidative stress in response to TNF-α. Nox4 small interfering RNA, but not Nox2, knockdown prevented oxidative stress and apoptosis caused by TNF-α in CMVEC. Nox4 is colocalized with HO-2, the constitutive isoform of heme oxygenase (HO), which is critical for endothelial protection against TNF-α toxicity. The products of HO activity, bilirubin and carbon monoxide (CO, as a CO-releasing molecule, CORM-A1), inhibited Nox4-generated O2•− and apoptosis caused by TNF-α stimulation. We conclude that Nox4 is the primary source of inflammation- and TNF-α-induced oxidative stress leading to apoptosis in brain endothelial cells. The ability of CO and bilirubin to combat TNF-α-induced oxidative stress by inhibiting Nox4 activity and/or by O2•− scavenging, taken together with close intracellular compartmentalization of HO-2 and Nox4 in cerebral vascular endothelium, may contribute to HO-2 cytoprotection against inflammatory cerebrovascular disease.
- inflammatory brain disease
- brain endothelium
- blood-brain barrier
- cerebral vascular injury
- heme oxygenase isoform-2
- carbon monoxide-releasing molecule-A1
- reduced nicotinamide adenine dinucleotide phosphatase oxidase isoforms 2 and 4
- bilirubin
- antioxidants
inflammation plays an important role in pathogenesis of neonatal brain diseases, including meningitis, septic shock, brain trauma, asphyxia, ischemia, and seizures. Inflammatory brain diseases may damage cerebral vessels and cause cerebral blood flow dysregulation thus adding to a secondary neurological sequelae. Of the various proinflammatory cytokines, tumor necrosis factors-α (TNF-α) plays a pivotal role in inflammatory brain disease (4, 6, 52). Recently, we showed that TNF-α targets cerebral vascular endothelial cells, increases formation of reactive oxygen species (ROS), and causes apoptosis (5) that may lead to inflammatory cerebral vascular dysfunction. Superoxide anion (O2•−) appears to be a primary mediator of TNF-α-induced oxidative stress in cerebral vascular endothelium. ROS production is provided by numerous enzyme complexes, including NADPH oxidase, nitric oxide (NO) synthase, xanthine oxidase, and the mitochondrial respiratory chain. However, the cellular sources generating proapoptotic O2•− in response to TNF-α in cerebral vascular endothelium are not known.
NADPH oxidase (Nox family), which was originally discovered in phagocytes, is a potent cellular source of O2•− in the cardiovascular system (7, 20, 22, 25, 38, 45) and in the brain (2, 19, 26, 27, 33, 50). NADPH oxidase components include flavocytochrome b558, an integral membrane heterodimer composed of the large catalytic Nox1–Nox5 subunits (homologues of phagocytic gp91phox/Nox2) associated with the small anchoring p22phox subunit, and the cytoplasmic regulatory subunits p47phox, p67phox, p40phox, and small GTPase Rac1/2 (7, 17, 22). NADPH oxidase is posttranslationally activated to produce oxidative bursts in response to various stimuli. Posttranslational activation of NADPH oxidase occurs in a cell- and signal-specific manner and may include phosphorylation and spatial relocation of the cytosolic subunits to the catalytic cytochrome to form the active enzyme complex (14, 22, 29).
NADPH oxidase has important functions in cerebral circulation that include regulation of vascular smooth muscle tone and modulation of endothelium-dependent dilator responses (10, 15, 27, 33, 36). NADPH oxidase activation has been also implicated in loss of neuronal coupling to cerebral blood flow (27), disruption of the blood-brain barrier following stroke (26), and in apoptosis (33, 36). Among other catalytic Nox homologues, high expression of Nox4 appears to be a specific characteristic of vascular cells (3, 13, 22, 28, 38, 39, 43, 49, 51), although Nox2 expression also has been reported (9, 43, 49). Nox4 upregulation has been implicated in the development of cardiovascular pathologies (43, 45). Current knowledge on the role of distinct Nox isoforms in cerebral circulation remains very limited. Nox4 in the human brain cortex is upregulated following cerebral ischemia (50). Recent reports indicate the importance of gp91phox/Nox2 and Nox4 in the regulation of cerebral vascular tone (27, 33, 36). However, the functions of Nox4 in cerebral vascular endothelium have not been investigated.
Heme oxygenase (HO), in cooperation with biliverdin reductase, catalyzes the degradation of intracellular heme to carbon monoxide (CO) and bilirubin and functions as an endogenous antioxidant defense system in various cells (1, 37, 40, 41, 48). Inducible HO-1 is important in cytoprotection against sustained oxidative stress caused by inflammatory disease (1, 40, 48), whereas constitutively expressed HO-2 may protect against damage caused by acute oxidative stress (37). In cerebral vascular endothelial cells, HO-2 is critical for immediate cytoprotection against apoptosis caused by TNF-α. Brain endothelial cells from HO-2 knockout mice are more susceptible to TNF-α-induced apoptosis than are wild-type cells (5). Pharmacological inhibition of HO-2 activity in brain endothelial cells from newborn pigs augments apoptosis caused by TNF-α (5). The HO-2-mediated mechanism of cytoprotection against apoptosis caused by inflammation is far from clear. Previously, we reported that the products of HO activity, bilirubin and CO, have antioxidant properties in cerebral vascular endothelium exposed to inflammatory stimulation (5). However, the ROS-producing targets for the antioxidant effects of the HO products in cerebral vascular endothelium have not been identified.
The present study using primary cultures of cerebral vascular endothelial cells addresses the hypotheses that 1) Nox4 NADPH oxidase is the primary source of proapoptotic ROS evoked by TNF-α and 2) CO and bilirubin protect against inflammation-induced apoptosis by inhibiting Nox4-derived O2•− radicals.
Cerebral microvascular endothelial cells.
All protocols and procedures that involve animals were reviewed and approved by the Animal Care and Use Committee of the University of Tennessee, Memphis. Cerebral microvessels (60–300 μm) obtained from the brain cortex of newborn pigs (1–5 days old) were digested by collagenase-dispase, and cerebral microvascular endothelial cells (CMVEC) were separated by density gradient centrifugation as we described elsewhere (5). CMVEC were plated on Matrigel-coated plates or glass coverslips and were cultured for 5–6 days until confluence in Dulbecco's modified Eagle's medium (DMEM) containing 20% fetal bovine serum (FBS), 30 μg/ml endothelial cell growth supplement, 1 U/ml heparin, and antibiotic-antimycotic mixture. CMVEC identified by von Willebrand factor accounted for >90% of the cell population. All experiments were performed on confluent quiescent cells in primary cultures. To achieve quiescence, CMVEC were exposed overnight to 0.1% FBS-DMEM.
Nox small interfering RNA-mediated gene silencing.
CMVEC were transfected with Nox4 small interfering RNA (siRNA), Nox2 siRNA, or nontargeting control siRNA (Dharmacon RNA Technologies, Lafayette, CO) according to standard protocols. Briefly, confluent CMVEC were replated to 12-well plates (3 × 105 cells/ml) and grown in 20% FBS-DMEM without antibiotic for 24 h to 60–70% confluence. To prepare the transfection complex, DharmaFECT-1 transfection reagent (3 μl/well) was incubated with Nox4 siRNA, Nox2 siRNA, or control siRNA (100 pmol/well) in antibiotic- and serum-free medium for 30 min at room temperature. For siRNA transfection, cells were incubated with the siRNA-DharmaFECT-1 complexes in antibiotic- and serum-free medium for 24 h at 37°C. For recovery, the cells were cultured in 20% FBS-DMEM (antibiotic free) for another 72 h. Before the experiment, CMVEC were serum deprived overnight in antibiotic-free 0.1% FBS-DMEM.
Experimental treatments.
CMVEC were untreated or treated with TNF-α (15 ng/ml) for 1–3 h at 37°C in the presence or absence of ROS inhibitors. To inhibit NADPH oxidase, we used diphenyliodonium (DPI, 5–200 μM) and apocynin (0.1–2 mM) (10, 24, 31, 53, 55, 56). To inhibit the Rac1 component of NADPH oxidase, we used the Rac1 inhibitor NSC-23766 (10–100 μM, 16, 42). To inhibit the mitochondrial electron transport chain, we used carbonyl cyanide 3-chlorophenylhydrazone (CCCP; respiratory uncoupling agent, 5–10 μM), 2-thenoyltrifluoroacetone (TTFA; complex II inhibitor, 5–10 μM), and rotenone (complex I inhibitor; 5–10 μM) (53, 55, 56). Nω-nitro-l-arginine (l-NNA; 0.5–2 mM) and allopurinol (50–100 μM) were used to inhibit NO synthase and xanthine oxidase, respectively (53, 56). To block overall O2•− content, we used the cell-permeable superoxide dismutase polyethylene glycol (PEG)-SOD (1,000 units), an O2•− scavenger (5, 10, 55). To select the maximally effective concentrations for our cell system, we conducted preliminary experiments using a wide concentration range of the inhibitor (5- to 50-fold over the Ki value).
Detection of O2•− generation.
Dihydroethidium (DHE) is oxidized by O2•− to ethidium and oxyethidium, intercalates with DNA in the nucleus, and emits red fluorescence. The O2•− production by cultured cells was quantitatively detected by fluorescence spectroscopy as we described previously (5). CMVEC grown on 12-well plates were incubated with 15 ng/ml TNF-α alone or with ROS inhibitors for 1 h at 37°C. DHE (20 μM) was added to the incubation media for an additional 20 min. TNF-α causes an apoptosis-related cell detachment and increases O2•− level in both attached and detached cells (5). To detect overall O2•− generation, we collected attached and floating cells by scraping and aspiration. The pooled cells were pelleted by centrifugation and washed twice with ice-cold Dulbecco's phosphate-buffered saline (DPBS). CMVEC were sonicated in ice-cold DPBS, and the lysates were cleared by centrifugation. Supernatants were transferred to Falcon 96-well black plates, and ethidium fluorescence (excitation/emission maxima, 485/590 nm) was measured by the Synergy HT multi-mode microplate reader (BioTek Instruments, Winooski, VT) and normalized to the protein amount.
Detection of DNA fragmentation.
DNA fragmentation was detected using a cell death detection kit (Roche Applied Science, Indianapolis, IN) by formation of cytoplasmic histone-associated DNA fragments (5). CMVEC were treated with TNF-α (15 ng/ml) for 3 h at 37°C. Detached floating cells were collected by aspiration for counting. Attached cells were lysed with the lysis buffer. Aliquots of the nuclei-free supernatant were placed in streptavidin-coated wells and incubated with anti-histone-biotin antibody and anti-DNA peroxidase-conjugated antibody for 2 h at room temperature. Immunobilized DNA fragments were visualized with 2,2′-azino-di(3-ethylbenzthiazolin-sulfonate), and the absorbance at 405 nm was normalized to the protein amount.
Protein detection.
To detect the amount of protein in samples dissolved in Laemmli sample buffer before Western immunoblotting, we used the amidoblack dot-blot method (5). For all other purposes, cell protein was measured by the bicinchoninic acid method (Pierce, Rockford, IL).
Western immunoblotting.
Proteins (10–20 μg/lane) were separated by 15% sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to polyvinylidene fluoride membranes, and blocked with 5% milk-0.1% Tween 20. Cleaved caspase-3 fragments (17 kDa) were detected by anti-caspase-3-Asp 175 polyclonal antibodies (Cell Signaling, Beverly, MA). Nox4 was detected by anti-Nox4 (N-15) polyclonal antibodies (Santa Cruz Biotechnology, Santa Cruz, CA) or by anti-Nox4 polyclonal antibodies to a COOH-terminal region of the human protein (Novus Biologicals, Littleton, CO). Nox2 was detected using polyclonal antibodies to a human gp91phox peptide (Upstate, Temecula, CA). Peroxidase-conjugated secondary antibodies were from Sigma (St. Louis, MO). The membranes were reprobed for actin as a loading control using monoclonal anti-actin (Roche Molecular Biochemicals, Indianapolis, IN). The immunocomplexes were visualized with the Western lightning chemiluminescence kit (Perkin Elmer Life Sciences, Shelton, CT) and digitally quantified using ImageJ 1.33 software (National Institutes of Health, Bethesda, MD).
Cells were fixed with 3.7% paraformaldehyde (20 min), permeabilized with 0.1% Triton X-100 (20 min), and blocked with 5% bovine serum albumin-DPBS. The cells were incubated with monoclonal antibodies against Nox4 (1:30), p22phox (1:30), or p47phox (1:30) (all from Santa Cruz Biotechnology) for 1 h at 37°C followed by FITC-conjugated secondary antibodies (Vector Laboratories, Burlingame, CA) for 1 h at 37°C. For F-actin staining, cells were additionally incubated with rhodamine-phalloidin (1:100, Molecular Probes, Eugene, OR). To detect colocalization of HO-2 and Nox4, cells were first incubated with anti-Nox4 monoclonal antibodies for 1 h (as above) followed by anti-HO-2 polyclonal antibodies (1:50; StressGen Biotechnologies, Victoria, BC, Canada) for 1 h. Primary antibodies were visualized with FITC- and Cy3-conjugated secondary antibodies (Vector Laboratories) for 1 h at 37°C. Coverslips were mounted using anti-fade mounting medium with a nuclear counterstain, 4′,6-diamidino-2-phenylindole (DAPI; Vector Laboratories). Slides were viewed using Nikon Diaphot fluorescence microscope equipped with an image deconvolution system. Images were deconvolved and processed using IPLab Spectrum software and Adobe Photoshop (Adobe Systems).
NADPH oxidase activity.
NADPH oxidase activity in cell homogenates was measured by O2•− production from NADPH using the lucigenin-enhanced luminescence assay (21). CMVEC were lysed by sonication in 5 ml of ice-cold lysis buffer (20 mM KH2PO4, 1 mM EGTA) containing a protease inhibitor cocktail (Sigma). NADPH oxidase activity was measured in a reaction mixture containing 50 mM KH2PO4 (pH 7.0), 1 mM EGTA, 150 mM sucrose, and protease inhibitors (total volume, 300 μl). Cell homogenates (∼100 μg protein) were incubated with 100 μM NADPH in the absence or presence of TNF-α (15 ng/ml), ROS inhibitors (DPI, apocynin, and SOD), bilirubin, and CO-releasing molecule (CORM)-A1 for 40 min at 37°C. Lucigenin (50 μM) was added to the reaction mixture, and the incubation continued for 20 min. Luminescence indicative of O2•− concentration was measured by a Synergy HT microplate reader (BioTek Instruments) and normalized to the protein amount.
Statistical analysis.
Data are presented as means ± SE of absolute values or percentage of control. Data were analyzed by analysis of variance for repeated measurements, followed by Fisher's test for protected least significant difference to isolate differences between groups. A level of P < 0.05 was considered significant in all statistical tests.
Cell culture reagents were purchased from Life Technologies (Gaithersburg, MD), Hyclone (South Logan, UT), and Amersham Pharmacia Biotech (Piscataway, NJ). Human TNF-α and Matrigel were from BD Biosciences (Bedford, MA). Apocynin and Rac1 inhibitor (NSC-23766) were from Calbiochem (San Diego, CA). Dihydroethidium was from Molecular Probes. CORM-A1 was a generous gift from Hector Knight from Tyco-Mallincrodt Medical (Petten, Holland). All other reagents were from Sigma.
Effects of ROS inhibitors on TNF-α-induced oxidative stress in CMVEC.
TNF-α (15 ng/ml, 1 h) increased O2•− formation two- to threefold above the baseline as detected by hydroethidium spectroscopy (Fig. 1). We investigated the contributions of distinct ROS-generating cellular systems, NADPH oxidase, mitochondria, NO synthase, and xanthine oxidase to TNF-α-induced oxidative stress (Fig. 1). NADPH oxidase inhibitors, DPI (5–100 μM) and apocynin (0.5–2 mM), inhibited TNF-α-induced O2•− production by 50–70%, whereas the inhibitor of the Rac1 component, NSC-23766 (10–100 μM), did not affect the oxidative stress. Mitochondrial electron transport chain inhibitors, CCCP (respiratory uncoupling reagent, 5–10 μM), TTFA (complex II inhibitor, 5–10 μM), and rotenone (complex I inhibitor, 5–10 μM), reduced TNF-α-evoked O2•− generation by 20–40%. The NO synthase inhibitor l-NNA (0.5–2 mM) and xanthine oxidase inhibitor allopurinol (50–100 μM) did not alter TNF-α-induced oxidative stress. Overall, these data suggest that NADPH oxidase, and, to a lesser extent, mitochondrial electron transport chain, are the cellular sources of O2•−generated by CMVEC in response to TNF-α stimulation.
NADPH oxidase inhibitors attenuate apoptosis caused by TNF-α.
TNF-α is a potent inducer of apoptosis in CMVEC as evidenced by caspase-3 activation, DNA fragmentation, and loss of cell contacts (5). We investigated whether NADPH oxidase-derived O2•−anions contribute to TNF-α-evoked apoptosis. NADPH oxidase inhibitors DPI (5 μM) and apocynin (500 μM), but not the Rac1 inhibitor NSC-23766 (50 μM), reduced caspase-3 activation (Fig. 2, A and B), DNA fragmentation (Fig. 3A), and cell detachment (Fig. 3B) caused by TNF-α (15 ng/ml, 3 h). The mitochondrial electron transport chain inhibitors, CCCP (5 μM) and TTFA (5 μM), also partially reduced TNF-α-evoked apoptosis (Fig. 3, A and B). These data suggest that NADPH oxidase-derived O2•− greatly contributes to TNF-α-induced endothelial apoptosis.
Immunofluorescence detection of Nox4 in CMVEC.
CMVEC highly express Nox4, the cell-specific catalytic subunit of NADPH oxidase (Fig. 4A). p22phox, the membrane-bound subunit, and p47phox, the cytosolic regulatory subunit of the enzyme, are also immunodetectable in CMVEC (Fig. 4, B and C). All subunits of NADPH oxidase are localized to the perinuclear compartment of endothelial cells that corresponds to endoplasmic reticulum.
Effect of Nox4 knockdown on TNF-α-induced apoptosis.
To delineate the role of Nox4 in inflammation-induced apoptosis in CMVEC, we downregulated Nox4 protein by posttranscriptional gene silencing using siRNAs. CMVEC transfected with Nox4 siRNA showed a significantly reduced Nox4 expression by immunoblotting (50–60% reduction) and immunofluorescence as compared with control nontransfected or transfected cells (Fig. 5, A–C). Nox2 expression in CMVEC was not reduced by the transfection (Fig. 5A), confirming the specificity of Nox4 siRNA. Nox4 knockdown resulted in 40% reduction in basal production of O2•− (4,950 ± 350 and 2,820 ± 170 fluorescence units/mg protein in control siRNA- and Nox4 siRNA-transfected cells; n = 4, P < 0.05), suggesting that Nox4 is constitutively active in unstimulated CMVEC. Most importantly, in Nox4 knockdown CMVEC, TNF-α completely failed to increase O2•− production, in contrast to nontransfected or control transfected cells (Fig. 6). The key apoptotic responses to TNF-α, including caspase-3 activation and DNA fragmentation, were also greatly reduced in Nox4 knockdown CMVEC (Figs. 7 and 8). Unlike control CMVEC, Nox4 knockdown cells stimulated by TNF-α were largely insensitive to DPI, apocynin, or PEG-SOD (Figs. 7 and 8). Overall, these data suggest that Nox4 is activated by TNF-α and is the major contributor to oxidative stress and apoptosis caused by TNF-α in CMVEC. Because PEG-SOD did not completely block apoptosis in control and Nox4 knockdown cells (Figs. 7 and 8), it appears that ROS-independent component(s) also contribute to TNF-α-induced caspase 3-mediated apoptosis in CMVEC.
Effect of Nox2 knockdown on TNF-α-induced oxidative stress and apoptosis.
gp91phox/Nox2 is also expressed in CMVEC from newborn piglets (Fig. 5). To investigate the role of Nox2 in CMVEC, we downregulated Nox2 expression using the siRNA technique. The transfection with Nox2 siRNA reduced Nox2 expression in CMVEC by 80% (Fig. 5, D and E). Nox4 expression was not altered by the transfection (Fig. 5D), confirming the Nox2 knockdown specificity. Knockdown of Nox2 did not produce any reduction in basal production of O2•− (2,180 ± 230 and 2,830 ± 430 fluorescence units/mg protein in control siRNA- and Nox2 siRNA-transfected cells; n = 3, P > 0.05) and did not alter the oxidative response to TNF-α (Fig. 6). Furthermore, Nox2 knockdown only partially attenuated TNF-α-induced DNA fragmentation, and this effect was greatly enhanced by apocynin (Fig. 8), indicating predominant contributions of other Nox homologues (presumably, Nox4) to inflammation-induced apoptosis. Overall, these data suggest that, in cerebral vascular endothelium, Nox2 is dormant under basal conditions and has only limited contribution to oxidative stress and apoptosis caused by TNF-α.
Colocalization of Nox4 and HO-2 in CMVEC.
HO-2 is the endogenous constitutive anti-oxidant enzyme that is an important component of antiapoptotic protection against TNF-α (36). To establish potential interaction between the prooxidant and antioxidant enzymes, we determined whether Nox4 is colocalized with HO-2 in CMVEC (Fig. 9). Using double immunofluorescence staining, we detected that Nox4 and HO-2 are colocalized in the perinuclear compartment and the nuclear envelope, indicating potential functional interaction between the two enzymes.
Bilirubin and CO prevent TNF-α-induced apoptosis in CMVEC.
We examined the effects of the products of HO-catalyzed heme degradation, bilirubin and CO, on endothelial apoptosis initiated by TNF-α. We used CORM-A1, a CO-releasing molecule that slowly releases gaseous CO in physiological solutions (35, 57). Bilirubin (1 μM) and CORM-A1 (50 μM) blocked DNA fragmentation caused in CMVEC by TNF-α (Fig. 10). CORM-A1 inactivated by overnight exposure to air failed to reduce DNA fragmentation caused by TNF-α (data not shown). These data suggest that bilirubin and CO are cytoprotective against apoptosis caused by TNF-α in cerebral vascular endothelium.
Effects of TNF-α, CO, and bilirubin on endothelial NADPH oxidase activity.
We investigated whether cytoprotective effects of the HO products against inflammation-induced apoptosis involve modulation of endothelial NADPH oxidase activity. NADPH oxidase activity in CMVEC was detected as O2•− production from 100 μM NADPH (21). TNF-α (15 ng/ml) rapidly (within 1 h) increased NADPH oxidase activity two- to threefold (Fig. 11). DPI (5 μM) and apocynin (500 μM) completely blocked the TNF-α-stimulated O2•− production, indicating the specificity of the method for NADPH oxidase activity detection. Given that TNF-α completely failed to elevate O2•− in Nox4 knockdown CMVEC, Nox4 is the catalytic isoform responsible for NADPH oxidase activation by the cytokine. Bilirubin (1 μM) and CORM-A1 (50 μM) completely blocked the NADPH oxidase response to TNF-α stimulation (Fig. 11), indicating that the Nox4 NADPH oxidase enzyme complex and/or NADPH oxidase-derived O2•− are the targets for antioxidant and antiapoptotic effects of the HO products during inflammation.
Cerebral vascular endothelial cells respond to proinflammatory cytokine TNF-α by oxidative stress and apoptosis. Constitutive HO-2 is an important antioxidant enzyme that is cytoprotective against TNF-α-induced damage of brain endothelial cells. We report major novel findings on the mechanism of apoptosis caused by the proinflammatory cytokine in cerebral vascular endothelial cells: 1) O2•− anions are major mediators of TNF-α-induced apoptosis; 2) Nox4 NADPH oxidase is highly expressed, constitutively active, and contributes to basal O2•− production; 3) Nox4 functions as a major source of proapoptotic O2•− that is rapidly activated by TNF-α; 4) Nox4 is colocalized with antioxidant HO-2 in the perinuclear compartment of the cell; and 5) the products of HO-2-catalyzed reaction of heme degradation, CO and bilirubin, block inflammation-induced apoptosis by decreasing the amount of O2•− produced by the Nox4 NADPH oxidase.
The proinflammatory cytokine TNF-α, a mediator of inflammatory brain disease, causes oxidative stress and apoptosis of cerebral vascular endothelial cells from newborn pig and adult mice (5) that may lead to cerebral vascular dysfunction. O2•− anions are primary contributors to TNF-α-induced oxidative stress in cerebral vascular endothelium. Our new data in cerebral vascular endothelial cells show that cell-permeable O2•−-scavenging enzyme PEG-SOD promotes endothelial survival, indicating that oxidative stress is a trigger of TNF-α-induced apoptosis. To determine the cellular sources of O2•− that are activated by TNF-α in cerebral vascular endothelial cells, we used pharmacological and molecular approaches. Inhibitors of NADPH oxidase and, to a lesser extent, complex I and II inhibitors of the mitochondrial electron transport chain reduced TNF-α-evoked O2•− production and inhibited key events of apoptosis (caspase-3 activation, DNA fragmentation, and loss of cell contacts). Conversely, inhibition of two other ROS-generating enzymes, NO synthase and xanthine oxidase, did not affect oxidative stress or apoptosis in TNF-α-stimulated cells. These data indicate that NADPH oxidase is a major source of proapoptotic O2•− produced in brain endothelial cells in response to inflammatory stimulation.
NADPH oxidase, a multisubunit enzymatic complex that generates O2•− from molecular oxygen and NADPH, is represented by distinct membrane-spanning catalytic subunits (large subunits Nox1–Nox5 in conjunction with the small subunit gp22phox) that are activated via spatial interaction with the cytosolic regulatory factors (gp47phox, gp67phox, and small GTPase Rac1/2). NADPH oxidase was originally described in phagocytes (gp91phox/Nox2), where it generates oxidative bursts involved in bacterial killing. Although the mechanism of activation of phagocytic Nox2 NADPH oxidase, dormant during the resting state, is well characterized, much less is known about the expression and regulation of other members of the Nox family (8, 29). We found that in cerebral vascular endothelial cells, Nox4 is highly expressed along with the small anchoring subunit p22phox and the regulatory subunit p47phox. Other investigators also detected Nox4 in cerebral arterioles (33, 36). In confluent cerebral vascular endothelial cells, Nox4, p22phox, and p47phox are localized to the perinuclear compartment of the cell, presumably, in the endoplasmic reticulum. This is in agreement with the observations in human vascular endothelial cells (9, 51). Nox4 localization is independent of F-actin stress fibers that are localized to the periphery of brain endothelial cells. In contrast, Nox4 in differentiated aortic smooth muscle cells is colocalized with actin (11). We did not find Nox4 immunofluorescence in the nuclei of confluent CMVEC in primary cultures, although there are reports on nuclear localization of Nox4 in subcultured human umbilical vein endothelial cells (HUVEC; 28) and in dedifferentiated aortic smooth muscle cells at late passages (11). Little is known on Nox4 functions in endothelial cells. In HUVECs, Nox4 regulates cell-cell adhesion, motility, and proliferation (12, 51).
The functional significance of endothelial Nox4 in cerebrovascular inflammatory disease is not known. Our data, for the first time, show that Nox4 is the major source of evoked O2•− that triggers apoptosis in cerebral vascular endothelial cells exposed to TNF-α. TNF-α rapidly (in ≤1 h) stimulated NADPH oxidase, indicating that new protein synthesis does not account for the enzyme activity. To investigate the functional significance of Nox4 in CMVEC, we downregulated Nox4 protein by gene-specific siRNA. Nox4 knockdown reduced basal NADPH oxidase activity by 40%, indicating that Nox4 is constitutively active during resting conditions in CMVEC. In addition to Nox4, expression of Nox1 and Nox2 in cerebral arteries has been reported by other investigators (27, 33, 36). We found that Nox2 expressed in cerebral vascular endothelium is dormant in unstimulated cells and does not contribute to O2•− production under resting conditions. Importantly, knockdown of Nox4 completely blocked O2•− responses to TNF-α, indicating that Nox4 is the only NADPH oxidase isoform in cerebral vascular endothelium that is activated by the inflammatory stimulation. Conversely, Nox2 knockdown had only limited effect on the burst of oxidative stress evoked by the cytokine. Furthermore, TNF-α did not cause apoptosis in Nox4 siRNA knockdown cells. Overall, these data demonstrate that Nox4 knockdown prevented acute deleterious effects of TNF-α and conferred resistance of brain endothelial cells to inflammation-induced injury. These observations support the concept that Nox4 is activated by TNF-α in cerebral vascular endothelium and functions as the major source of O2•− that causes apoptosis and endothelial injury during inflammatory cerebral vascular disease.
We report that Nox4 is constitutively active in resting brain endothelial cells and is rapidly activated by TNF-α via a posttranslational mechanism. NADPH oxidase activation by a variety of (patho)physiological factors, such as inflammatory cytokines, angiotensin II, histamine, and thrombin, has been described in phagocytes and other cell types (10, 21–24, 29, 31, 39, 49). Mechanisms that regulate activity of phagocytic Nox2-based NADPH oxidase include phosphorylation and translocation of regulatory cytosolic subunits (p47phox and p67phox) to the membrane catalytic complex Nox2-gp22phox and activation of small GTPase Rac1/2 (22, 23, 29). However, little is known on regulation of other members of the Nox family (23, 29, 39). In contrast to Nox2-based NADPH oxidase, Nox4 is constitutively active (32, 39), as supported by our data in brain endothelial cells. NADPH oxidase activation by TNF-α involves interaction of catalytic and regulatory (p47phox) subunits (18, 23, 29, 31). Conversely, Martyn et al. (32) reported that Nox4 activity does not require cytosolic subunits p47phox, p67phox, or Rac1. Our data in brain endothelial cells show that Rac1 inhibitor did not reduce Nox4-mediated apoptosis in response to TNF-α, supporting the notion that Rac1 activity is not essential in the mechanism of the Nox4 activation.
Mitochondrial electron chain complexes I and II also appear to contribute to a burst of proapoptotic O2•− generated by CMVEC exposed to TNF-α. Complex I and II inhibitors, rotenone and TTFA, inhibited O2•− production and apoptosis evoked by the cytokine, whereas CCCP, a respiratory uncoupling agent, had less effect. Surprisingly, CMVEC with knockdown Nox4 did not respond to TNF-α by increasing O2•− formation or apoptosis, demonstrating the absence of mitochondrial involvement. Recent reports indicate a signaling cross talk between NADPH oxidase- and mitochondria-derived ROS (30, 54). These observations support the concept that Nox4 is the primary target for TNF-α in promoting cell death, whereas the ROS responses of the mitochondrial complexes are secondary to Nox4 stimulation by the cytokine in cerebral vascular endothelium.
In cerebral vascular endothelium, constitutive HO-2 is a critical member of the antioxidant cell defense system (37). We have found that deletion of HO-2 gene or inhibition of HO activity aggravates the apoptotic effects of TNF-α in CMVEC (5). Because Nox4 NADPH oxidase is a major source of O2•− in TNF-α-stimulated cells, we investigated its relationships with antioxidant HO-2. We found that HO-2 and Nox4 are colocalized in the perinuclear area of the cytoplasm, thus providing a structural basis for functional association between the two enzymes. We investigated whether the antiapoptotic effects of the HO products CO and/or bilirubin are based on their abilities to block Nox4-derived O2•− anions in cerebral vascular endothelium. For the CO source, we used sodium boranocarbonate (CORM-A1) that provides spontaneous dose-dependent release of gaseous CO into the media (35, 57). In our experiments, TNF-α rapidly increased NADPH oxidase activity in the brain endothelial cells measured as O2•− production from the NADPH substrate. Nox4 appears to be the major isoform that accounts for TNF-α's stimulation of NADPH oxidase activity in cerebral vascular endothelial cells, because Nox4 knockdown completely abolished responses to the cytokine. CORM-A1 and bilirubin in physiologically relevant doses completely blocked Nox4-mediated O2•− responses to TNF-α. Taken together with close subcellular compartmentalization of HO-2 and Nox4, these data suggest that the HO-2 products can attenuate Nox4 activation in response to inflammatory stimulation.
What are the mechanisms by which CO and bilirubin reduce Nox4 NADPH oxidase activity? CO is known for its ability to bind to heme and, therefore, may regulate functions of heme-containing proteins. The large transmembrane Nox subunit contains two heme-binding domains that are critical for the enzyme activity (7, 8, 17). Therefore, we may suggest that NADPH oxidase activation by TNF-α can be reduced by CO binding to the Nox heme and/or decreasing heme availability. HO-1 overexpression reduced NADPH oxidase activity in phagocytes and vascular smooth muscle cells (12, 46). A CO-releasing molecule, CORM-2, inhibited NADPH oxidase activity in human airway smooth muscle (47). Bilirubin, on the other hand, is rapidly oxidized to biliverdin, and is recognized as a potent ROS scavenger (34, 44). The antioxidant potencies of bilirubin are enhanced by biliverdin reductase activity that provides recycling of biliverdin to bilirubin. Our findings may support the notion that CO inhibits Nox4 activation and subsequent ROS formation induced by TNF-α, whereas bilirubin eliminates Nox-derived ROS by scavenging.
In conclusion, we have demonstrated that Nox4 is an important component of the NADPH oxidase complex in porcine cerebral vascular endothelial cells. Furthermore, Nox4 is a major prooxidant that is rapidly activated by TNF-α and accounts for oxidative stress leading to apoptosis in cerebral vascular endothelium under inflammatory conditions. HO-2 is colocalized with Nox4, providing a structural basis for functional interaction between the two enzymes. HO-2, via production of CO and bilirubin, inhibitors of Nox4-derived ROS, provides antioxidant protection of cerebral vascular endothelium against TNF-α-induced apoptosis.
This research was supported by National Institute of Neurological Disorders and Stroke and by National Heart, Lung, and Blood Institute. S. Basuroy is supported by the Beginning-Grant-in-Aid from American Heart Association.
We are deeply grateful to Hector Knight from Tyco-Mallincrodt Medical (Petten, Holland) for the generous gift of CORM-A1. The authors thank Danny Morse for helping with preparation of the figures.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2009 the American Physiological Society


text:
For Sale By Owner
1907 Victorian
Pine Farm
Scroll down for more information
|Full Baths
|Heated Sq. Ft.
|Unheated Sq. Ft.
- 1st Floor Bath
- 1st Floor Bedroom
- 1st Floor Laundry Room
- Attic
- Basement
- Bonus Room
- Den
- Dining room
- Entry Hall
- Exercise Room
- Foyer
- Galley Kitchen
- Laundry Room
- Living room
- Music Room
- Reader's Loft
- Study
- Unfinished Basement
- Walk out Basement
- Walk-Up Attic
- Master bedroom upstairs
- 1 Car Garage
- 2 Car Garage
- Automatic outside lights
- Barn
- Casement windows
- Driveway - Dirt
- Fresh paint
- Garden
- Patio
- Porch
- Storage Building
- Storm Windows
- Garage Workshop
- 2nd Staircase
- Ceiling Fans
- Ceramic Tile
- High Ceilings
- Original wood windows
- Walk-In Closets
- Wood floors
- Shingle Roof: Asphalt shingle
- Central air
- Range
- Refrigerator
- Septic Tank
- Water Heater - Electric
- Butler's Pantry
- 9-foot Ceilings
- Claw-foot Tub(s)
- Hand-hewn Beams
- Plaster Walls
- Pocket Doors
- Servant's Staircase
- Transoms
- Widow's Walk
- Wrap Around Porch
- 2-Story Indoor Silo
- 3 Connected Pastures
- Antique hardware
- Douglas Fir Trim
- Etched glass windows
- New Loft - Party Barn
- Original farm sink
- Panoramic Country Views
- Pocket Doors
- Water/Electricity to Barn
- Wrought Iron Fence & Gate
Like This Listing?
Seller Contact Information
Please leave message if no answer for additional information or to schedule showing.
Cathy Hombs
Phone: email@example.com
Mobile: 815-288-4585
Tell 'em you saw it on OldHouses.com!
Best of all worlds: Charm, character and convenience
Want charm and solid architecture of a Victorian home built by turn-of-the-century craftsman with trim, flooring materials and woodworking skills that cannot be duplicated today? How about a home with a separate, private foyer entrance that can be used for a home office visitors without living area exposure or could function as a 5th bedroom including a walk-in closet on the first floor? Desire a full bathroom on the first floor, a large, formal dining room, extra living room to tailor to your needs or first floor laundry? With open staircase in front and servant's staircase into the kitchen in back, the 1st and 2nd floors offer 2,236 sq ft of living space.
Require the convenience of a full walk-out, clean basement with high ceilings, workshop, laundry sink and 2nd washer and dryer for "farm fresh" laundry? Wishing for a full walk-up 3rd-story attic with fantastic gable views on all sides that can be used for over 1,100 sq ft of additional storage, a bonus room or converted to a master bedroom suite?
The restored, not re-"muddled", home is located on beautiful, historic Lincoln Highway - a peaceful, paved state road. Drink your coffee or relax on the porch swing on the beautiful wrap-around porch, take a nap on the tree hammock, cookout on the private patio or read a book while enjoying the rolling hills from the barn loft. The peace and flexibility of use of the country but access to the conveniences of the city are all here. Please call for more information or to schedule a showing.
Location, location, location - history, history, history
Location important? Want it placed high in the country with rolling hill, countryside views on a manageable 5 acres that is Zoned Ag-1 with no close neighbors behind or beside the property. Want it with 3 enclosed, connected pastures that can be rotated or used for gardening? Need it close to recreation? Dixon offers a beautiful parks with public boat access to the Rock River. Various state parks are within an hour's drive. Also, within a few minutes is a marina with grill, the Midway Drive-In Theater (one of the last in the country), and big box stores and a mall. Only 15 minutes to I-88, 1 hour drive to Quad Cities, Rockford, and DeKalb and only 2 hours to Chicago.
So much history and Victorian architecture in this home including 100-year old mural; functioning pocket doors; transoms; etched-glass windows; carriage step; antique hardware; rainwater, gravity-fed tanks and pump; gas light fixtures and more. See the image of the barn tour guide that lists the historic circa 1891 barn features.
Land and good outbuildings galore
Want a property with multiple (3) enclosed, connected pastures that can be rotated or used for gardening? Do you need more than 3 car stalls that the 2 detached garages provide? Well, all of the outbuildings are in great condition, include new steel siding and roofs and are very functional. The dairy barn's space, which was featured in a century barn tour this year, has been tastefully opened up to allow for 7 more vehicles but still can be used for other storage/horses/hobbies. Just installed a new full staircase to the hay mow - perfect for barn dances and parties - and built a 3rd-story loft with patio door and amazing views for relaxation or workout area. Water is accessible in the milk house that also has mancave/motorcycle shed space which could be converted to chicken coop.
The 800 sq. foot corn crib has been gutted and enclosed with steel siding and roofing to make useful for equipment storage and/or year- round hobby workshop when using the wood burning stove. The open machine shed faces east and also shelters 4 boats, trailers etc.
Recent Improvements
Want the character of an older home but don't want to replace plumbing; insulation; porches; mechanicals; and electrical, siding and roofs on home and most outbuildings? We've already taken care of that for you!!! (update details available upon request)
This home has it all!!! If you appreciate the architecture of yesteryear, and are not persuaded by HGTV's push for open concept living space, then you will love the current owner's period-friendly updates, decor and antiques as well as the original footprint of the home.
Comments & Feedback
All information deemed reliable but not guaranteed and should be independently verified. All properties are subject to prior sale, change or withdrawal. OldHouses.com is not responsible for any typographical errors, misinformation, misprints and shall be held totally harmless.


text:
The Courage to Love Trailer (2000)
"In a world of tradition, they dared to break the rules." 24 January 2000 Drama, History, Romance 87 mins
In 19th century New Orleans creole Henriette must choose between love and devotion to the church. Neither choice is going to be easy, as there is great opposition to her ideas of breaking traditions.
Watch the official The Courage to Love 2000 trailer in HD below or find more The Courage to Love videos on Vidimovie.


text:
The Ancient Tree Hunt team were invited to work with Autumnwatch as they will be raising awareness about ancient trees as a part of the programme in 2007. Go behind the scenes to see how Autumnwatch is made...
The ATH team start the day at Martin Sands at 8.30am, helping the Autumnwatch team decide on content for the day and preparing for Kate & Bill's arrival
Meet the director. Mark Jones is a popular director who before coming onto Autumnwatch worked on such prestigious shows as Antiques Roadshow and DIY SOS – which is why he is so in demand!
The team spend over 2 hours setting up the camera's to be able to film Autumnwatch prior to Kate & Bill's arrival, carrying heavy camera equipment deep into the forest….
Autumnwatch is infamous for its beautiful and intricate camera work that showcases wildlife at its best. See the team in action capturing those magical images. You can also see more on the bbc website
Our stars of the Autumnwatch screen. Kate & Bill start to walk and talk through how they will help us tell the nation about the ancient tree hunt in the up and coming series
After a long days filming every one went off to enjoy a few sandwiches and then the Ancient Tree Hunt team headed back to Grantham while Kate and Bill prepared for another series of wildlife watching and woodland frolics
find out more....


text:
Cardamom, (also known as amomum cardamomum, bai dou kou, great cardamom and large cardamom), is an herb often used to treat stomach and intestinal problems such as upset stomach, intestinal spasms, heartburn, irritable bowel syndrome and constipation. Cardamom is also sometimes used as an alternative medicine to treat cold and flu symptoms, urinary problems, gallbladder problems (other than gallstones) and liver disorders, according to WebMD.
Gallstone Pain
Gallstones are hard deposits of cholesterol and other bile components that form in the gallbladder, according to WebMD. Most people with the condition do not experience symptoms. Some gallstone sufferers do experience stomach pain. According to the Web site, people with gallstones should not take Cardamom, as it may increase gallstone pain and the risk of gallstone complications such as bleeding or infection.
Drug Interaction
Cardamom may interact with blood-thinning drugs such as aspirin, anticoagulants and anti-platelet drugs. This interaction may increase the risk of bleeding, according to HealthLine. The herb may also interfere with the process of certain liver medications, HIV drugs and antidepressants.
Allergic Reaction
Some people may experience cardamom allergy, according to HealthLine. Although few adverse affects have been reported, according to the Web site, the most likely adverse response is allergic contact dermatitis (hives or an itchy rash). Other allergic responses include shortness of breath, chest or throat tightness and chest pain. Respiratory allergic reactions require emergency medical attention.
Fetal and Infant Complications
The effects of cardamom on developing fetuses are unknown, so WebMD advises that pregnant women avoid cardamom (other than that found in food). There is limited scientific evidence as to whether cardamom has negative effects on babies, so women who are breast-feeding should avoid large amounts of the herb as well.


text:
Beijing: Pakistan has welcomed the idea of expanding the Asian Infrastructure Investment Bank (AIIB) and has hoped that this would lead to boosting infrastructure network for common development in regional countries. The Pakistan Embassy said that China's led bank has given strong support to member countries to improve the living conditions of the people.
Pakistan is one of the founding members of the bank and has supported China's stance on cooperative partnership in the banking sector. AIIB would be reviewing 30 membership applications beginning in September and the bank would have 90 members by the start of 2017 which would be outstripping the members of US and Japan led development banks.
Jin Liqun said that, "China-initiated AIIB to absorb the experience of current multilateral banks. However, we don't want to clone them, but rather innovate and expand on them." AIIB is initiating cooperation with private capital on pension and commercial insurance which would foster the role of private sector in public affairs. The banking is also developing new financial instruments to build a flexible and efficient investment system. Jin added that, "AIIB upholds its universal procurement procedures and gives players from all countries a fair appraisal when bidding for contracts."
The institution plans to start projects in many fields which includes communication, logistics, energy, electricity and transport. New projects and intelligent upgrades would also be considered by the bank said Jin. AIIB approved 165 million dollars in June on loads for a project in Bangladesh which are the first batch of loans the county got from the China led development bank.
AIIB was launched in December 2015 which aims to support construction of infrastructure in the Asia-Pacific region. There are 57 founding members of the bank which includes the BRICS countries (China, Russia, India, Brazil and South Africa), four Group of Seven countries (Britain, Germany, France and Italy) and also Egypt, Australia and New Zealand. USA and Japan have not joined as members so far.


text:
The handsome American singer Moby's net worth is $32 million today. He own a house and earn around $1.5 million dollar as annual salary & had a girlfriend. He is also a DJ, and photographer is an inspiration to many. orn in New York City in Harlen on September 11, 1965, his original name is Richard Melville Hall. Famous as the king or face of techno, Mody rose from the pack of anonymous DJ's to get a fan following matching that of a rock star! His music is a symphonic and almost hypnotic combination of disco beats, anthemic lyrics as well as punk-rock speed which appeals to all. His nickname was given to him by his parents after his great, great uncle, author Herman Melville's legendary novel, 'Moby Dick'.
|Richard Melville Hall
|Net Worth
|$32 Million
|Source of Income
|Annual Salary
|$1.5 Million
|Monthly Income
|Weekly Income
|Daily Income
|Album List
|Innocents (Deluxe Edition)
|Destroyed Remixed
|Destroyed (Deluxe Edition)
|Wait for Me Remixes
|Birth Date
|September 11, 1965
|English and Scots-Irish
|1.71 m / 5.7 feet
|69 kg
|Kelly Tisdale (2001-2004)
He was born when his parents were very young and lost his father in a car accident at the age of two. Post it, her then 23 year old mother, Elizabeth McBride Warner Hall moved to Darien Connecticut where he was raised by his maternal grandfather. Often left to his own devices, he got interested in music early. His interest was nurtured by his mother who was a fantastic pianist and avid record collector. He dropped his study of philosophy from Connecticut early to seek serious success in the field of music. Starting from working in a record store and playing in various local bands, he got his first taste of success as DJ when his gigs were much appreciated in several nightclubs.
Moby's House
In 1989 he stepped into New York City and signed a contract with Instinct Records. His first solo, 'Mobility' was released in 1990 but his second single 'Go' paved the way of his success and made him a public celebrity. His rise to success started with number of notable releases but his album 'Play' released in 1999, got him unparalleled success. Of all musical instruments, guitar is what defines this charismatic man.
Apart from music, he is recognized as a man with deep Christian faith. A dedicated vegan, he is an aggressive supporter of animal rights. He is also actively involved with numerous charities and causes for children, Human Rights or even Aids. In 2004, he was awarded with IMNF's Music Has Power Award for his endeavors towards music therapy.


text:
Results 1 to 3 of 3
Thread: sql server 2000 database
10-19-08, 22:22 #1Registered User
- Join Date
- Oct 2008
- Posts
- 1
Unanswered: sql server 2000 database
We have a website hosted on the intranet of our company . Now we have to host on the internet . The database is sql server on the intranet and will still be sql server when it is hosted on the internet . Any suggested ideas how this can be accomplished. I have been asked to use DTS packages . Can any tell me the process of accomplishing this process . Can I use replication at any stage of this process ?
Responses are appreciated !!!
10-20-08, 04:52 #2King of Understatement
- Join Date
- Feb 2004
- Location
- One Flump in One Place
- Posts
- 14,912
You want to move the database from one SQL Server 2000 instance to another? If so just backup your internal database, ftp it to the hosted server and restore it there.
Replication is for maintaining two copies of a database simultaneously. DTS is for ETLing data, not moving a database in its entirety.Testimonial:
pootle flump
ur codings are working excelent.
10-20-08, 16:49 #3Registered User
- Join Date
- Jun 2004
- Location
- Long Island
- Posts
- 696
Don't forget to bring over logins, and fix them following the DB restore.
look at:


text:
Find your tourSearch term(s):Location - Please Select - Amsterdam Gouda Haarlem Hoek van Holland Keukenhof Kinderdijk Leiden Rotterdam The Hague Price Show tours Reset filter
Exploring the Westland regionDutch landscapes - Greenhouses - Coastal management
Read more »»
Exploring the bulb flower region and Dutch coastTulips - Windmills - Sea
Visit the famous windmills of KinderdijkClassic polders - Windmills - Cheese
Visit the Keukenhof, world's largest spring flower gardenTulip fields - Flower villages - Pick your own tulips
Discover the 750-year-old town of OudewaterWater - Witch Weighing
Looking for a special route through Rotterdam with family, friends or your company? We would be happy to tailor your bike tour exactly to your wishes.
Taste deli Dutch foodLocal - Traditional - Exotic - Sweet & savory
Experience the harbour from up close Containerships - Nature - High Tech - Cranes
Get to know the real Rotterdam Architecture - History - Culture - Landmarks
Explore the raw RotterdamStreet art - Off track - Local - Design - Culture
Not found what you're looking for?See all guided tours »» orAdjust the filter to find your guided tour »»
We'd love to hear what you have to say. Please leave a message in our guest book.
Copyright © 2013-2017 Holland-Cycling.com | About Us | Contact | Join us on Facebook and Twitter


text:
Computer Vision Projects
An international project focused on building the best embedded computer vision platform ever. EoT is an Innovation Action funded under the European Union's H2020 Framework Programme that is going to unfold for three years starting in January 2015.Eyes of Things
Its not complete yet, its only tracking points and it hasnt got a memory yet.
Theres a few more videos on my youtube about it. rouncer81 channel.
CANDELOR is a computer vision library for 3D scene interpretation. It sports high performance object localization algorithms that are robust and simple to use.CANDELOR
The rotation between the camera and the environment is found from the directions of edgels extracted from the image. Any camera model / projection can be used. This example is an equirectangular image, from Google StreetView.Corisco - camera orientation from infinitesimal segments by constrained optimization
The goal of this project is to land a UAV on a runway using computer vision. The UAV has no sensors other than a forward-looking video camera. The video is transmitted in real time to a ground-station that uses image registration to detect and determine the orientation of the runway in each frame. The ground-station sends radio commands back to the UAV to guide it to the runway.Landing a UAV on a Runway Using Image Registration
A team of University of Notre Dame biometrics experts is developing a crime-fighting tool that can help law enforcement and military officials identify suspicious individuals at crime scenes.Questionable Observer Detector Biometrics System
The goal of this project was to elaborate a computer vision based method for the automatic tracking of golf clubs. It can provide additional information to the users such as club trajectory, speed and acceleration.Robust Visual Golf Club Tracking
Tracking multiple people from standard cameras is challenging, mostly due to the occlusions that occur as soon as several people are involved. We tackle this problem by using several cameras, observing the scene with different points of views. We developed a people detection algorithm called POM that uses a generative model of background subtraction to estimate the positions of people in an individual time frame.Tracking People using Multiple Cameras
Detecting and reading text from natural images is a hard computer vision task that is central to a variety of emerging applications. Related problems like document character recognition have been widely studied by computer vision and machine learning researchers and are virtually solved for practical applications like reading handwritten digits. Reliably recognizing characters in more complex scenes like photographs, however, is far more difficult: the best existing methods lag well behind human performance on the same tasks. In this paper we attack the problem of recognizing digits in a real application using unsupervised feature learning methods: reading house numbers from street level photos.Reading Digits in Natural Images with Unsupervised Feature Learning
This paper presents a system for performance-based character animation that enables any user to control the facial expressions of a digital avatar in realtime. The user is recorded in a natural environment using a non-intrusive, commercially available 3D sensor. The simplicity of this acquisition device comes at the cost of high noise levels in the acquired data. To effectively map low-quality 2D images and 3D depth maps to realistic facial expressions, we introduce a novel face tracking algorithm that combines geometry and texture registration with pre-recorded animation priors in a single optimization.Realtime Performance-Based Facial Animation (SIGGRAPH 2011)
Panoramic photography creates fascinating images. Very wide angle images are closer to the human field of view than conventional pictures. If seen through a panoramic viewer they let us experience a location as if we were there. Panoramic image stitching can create panoramas from pictures taken one after another. Unfortunately, acquiring the images takes a lot of time and moving objects may cause ghosting. It is also difficult to obtain a full spherical panorama, because the downward picture cannot be captured while the camera is mounted on the tripod.Throwable Panoramic Ball Camera
Weakly supervised discovery of correspondence among a set of complex, cluttered images is one of the key problems in recognition. We address this problem using deformable part-based models (DPM's) with latent SVM training. This method has originally been developed for fully supervised training of object detectors, but we demonstrate that it is also capable of more open-ended discovery of latent common structure for tasks such as scene recognition and weakly-supervised object localization.Scene Recognition and Weakly Supervised Object Localization with Deformable Part-Based Models
The goal of this work is to find visually similar images even if they appear quite different at the raw pixel level. This task is particularly important for matching images across visual domains, such as photos taken over different seasons or lighting conditions, paintings, hand-drawn sketches, etc. We propose a surprisingly simple method that estimates the relative importance of different features in a query image based on the notion of "data-driven uniqueness".Data-driven Visual Similarity for Cross-domain Image Matching


text:
Looking at Act II of Women's Lives: Thriving & Striving from 45 On
The AARP Foundation's Women's Leadership Circle Study
To guide its Women's Leadership Circle in developing programs, information and services for midlife and older women, the AARP Foundation commissioned Roper Public Affairs, part of GfK, to conduct a research study exploring the attitudes and experiences of American women age 45 and older.
Many of those interviewed for this study say growing older is not only better than expected, but can be a positive time of life with new rewards. They report being happier now, experiencing freedom to be themselves, pursue dreams and do things they have always wanted to do.
Although 92 percent have a network of friends and family that they can rely on, particularly in a time of crisis, many worry about what might happen to them as they age If they were alone, 39 percent say they would find the idea of sharing a home with women friends appealing.
Some exhibited possibly false assurance about their future financial and health situations even when they had not taken steps to adequately prepare themselves. While 61 percent feel confident that they will have enough money to enjoy life in their later years, 62 percent (55 percent of whom are age 60+) do not have a long-term spending plan for when they retire.
While 81 percent consider their health to be "good" and 56 percent call it "very good" or "excellent"...
- 28 percent say having to care for other people leaves them with too little time for taking care of their own health
- 32 percent feel the cost of healthcare or prescription drugs sometimes prevents them from seeing a doctor or getting treatment when they need it
Between August 17th and November 14th, 2005, 1,200 age 45+ women were surveyed by telephone, with additional over-samples of 500 African Americans, 500 Hispanics, and 500 Asian/Pacific Islanders. (94 pages).
Join the Discussion0 | Add Yours
Please leave your comment below.
You must be logged in to leave a comment.
Next ArticleRead This


text:
- Not Fee assured
- Verified this account
Specialises in
- Ankle
- Foot
About me
Mr Mark Davies took up a place to read medicine at Oxford University in 1981 and undertook his clinical training at St Mary's Hospital, London. Mr Davies carried out his post-graduate training in and around London on the North West Thames circuit, gaining the FRCS (Orth) accreditation in 1996. In 1997 he worked for a year with the world-renowned foot and ankle surgeon, Mr Terence Saxby, in Brisbane, and completed his training on his return at The Royal National Orthopaedic Hospital.
Mr Davies was appointed as a Consultant Orthopaedic Surgeon, specialising in foot and ankle disorders, at Guy's & St Thomas' Hospitals in 1999. He has re-written chapters for Gray's Anatomy and the New Aird's Companion in Surgical Studies on foot and ankle conditions. He was one of the authors of the most recent edition of Bailey & Love's "Short practice of surgery" and has published extensively within his field.
Mr Davies founded the London Foot and Ankle Centre (LFAC) in 2002 and is Clinical Director of the LFAC. He now works full time at the LFAC, accepting referrals from all over the UK and abroad.
Areas of interest
Ankle surgery; Foot surgery
Medical secretaries
- Gill McCloy
- The Lister Hospital Chelsea Bridge Road London SW1W 8RH
- 020 7881 2008
- 020 7881 2009
- email@example.com
- The Hospital Of St John & St Elizabeth 60 Grove End Road London NW8 9NH
- 020 7078 3800
- 020 7078 3801
- firstname.lastname@example.com
Anaesthetists worked with (Bupa members, please ask your consultant whether your anaesthetist is fee-assured)
Research interests
please refer to our website


text:
On May 11, 2014—Mother's Day—Governor Mark Dayton signed into law the Women's Economic Security Act ("WESA"). WESA is a major piece of legislation designed to improve working conditions for women through a variety of new protections for employees and new requirements for Minnesota employers. This legislation is a combination of different bills, and will have a significant impact on Minnesota businesses. Some of the key aspects of WESA are described below.
Parental and Pregnancy Leave
WESA amends Minnesota statute § 181.941, which applies to employers with at least 21 employees, to provide up to twelve weeks of unpaid leave for: (1) a biological or adoptive parent in conjunction with the birth or adoption of a child, or (2) a female employee for prenatal care, or incapacity due to pregnancy, childbirth or related health conditions. This section previously provided employees with six weeks of unpaid leave for the birth or adoption of a child, and did not contain a provisions providing for leave due to pregnancy-related conditions. The amendments take effect on July 1, 2014.1
Reasonable Accommodation Requirements for Pregnancy and Childbirth
WESA includes a new statute—Minnesota statute § 181.9414—establishing reasonable accommodation requirements for health conditions related to pregnancy or childbirth for employers with at least 21 employees. If an employee requests an accommodation upon the advice of her licensed healthcare provider or certified doula, the employer must provide a reasonable accommodation unless the employer can demonstrate that the accommodation would impose an undue hardship on the operation of the employer's business. A pregnant employee is not, however, required to obtain the advice of her licensed health care provider or certified doula, nor can an employer claim undue hardship, for the following accommodations: (1) more frequent restroom, food, and water breaks; (2) seating; and (3) limits on lifting over 20 pounds. Upon a request for a reasonable accommodation, the employer and the employee must engage in an interactive process to determine the reasonable accommodation. Reasonable accommodations may include, but are not limited to, temporary transfer to a less strenuous or hazardous position, seating, frequent restroom breaks, and limits to heavy lifting. Employers are prohibited from retaliating against an employee for requesting or obtaining an accommodation. The reasonable accommodation requirements relating to pregnancy are effective immediately.
Nursing Mothers
Minnesota Statute § 181.939 requires employers to provide nursing mothers with reasonable unpaid break time in order to express breast milk and to make reasonable efforts to provide a private area for nursing mothers. The amendments to this section now require employers to provide a private room, other than a bathroom or a toilet stall, that is "shielded from view and free from intrusion from coworkers and the public and that includes access to an electrical outlet." Perhaps most significantly, the amended statute now explicitly prohibits retaliation against an employee for asserting rights under § 181.939. An employee may now bring a civil action to recover damages, including costs and attorney's fees, based on a claim that the employer violated § 181.939 or retaliated against an employee for exercising rights under this section. The amendments to the Nursing Mothers statute take effect July 1, 2014.
Discrimination Based on Familial Status
Effective immediately, WESA expands the list of protected classes under the Minnesota Human Rights Act to include "familial status." WESA defines "familial status" as "the condition of one or more minors being domiciled with (1) their parent or parents or the minor's legal guardian or (2) the designee of the parent or parents or guardian with the written permission of the parent or parents or guardian." The protections afforded against discrimination on the basis of family status also apply to any person who is pregnant or is in the process of securing legal custody of a minor.
Except when based on a bona fide occupational qualification an employer may not refuse to hire, discharge, or otherwise discriminate against a person with respect to the terms and conditions of employment based on that person's familial status.
Wage Disclosure Protection
Effective July 1, 2014, WESA creates a new Minnesota Statute § 181.172 that prohibits an employer from: (1) preventing an employee from disclosing his or her wages as a condition of employment; (2) requiring an employee to sign a waiver or other document which purports to deny an employee the right to disclose the employee's wages; and (3) from taking any adverse employment action against an employee for disclosing or discussing the employee's own wages or another employee's wages that have been disclosed voluntarily. The statute also prohibits retaliation and creates a private right of action for employees to sue. If the employer has an employee handbook, the handbook must include a notice to employees regarding their rights and remedies under this new statute.
Expansion of Sick Leave and Leave for Care of Relatives
WESA further expands the law allowing employees to use their personal sick leave benefits for the benefit of various family members. Specifically, the law now permits employees to use sick leave benefits to care for an ill or injured mother-in-law, father-in-law, or grandchild. Employees may also now use earned sick leave for "safety" leave, which includes providing or receiving assistance because of sexual assault, domestic abuse, or stalking. The amendments to Minnesota Statute § 181.9413 take effect July 1, 2014.
Equal Pay Certificates
The new law, Minnesota Statute § 363A.44, generally requires employers with 40 or more full-time employees to obtain an equal pay certificate from the state if the employer seeks a state contract in excess of $500,000. To obtain an equal pay certificate, the employer must pay a $150 filing fee and submit an equal pay compliance statement to the Commissioner of Human Rights certifying the following:
(1) that the business is in compliance with Title VII of the Civil Rights Act of 1964;
(2) that the average compensation for its female employees is not consistently below the average compensation for its male employees within each of the major job categories in the EEO-1 employee information report for which an employee is expected to perform work under the contract, taking into account factors such as length of service, requirements of specific jobs, experience, skill, effort, responsibility, working conditions of the job, or other mitigating factors;
(3) that the business does not restrict employees of one sex to certain job classifications and makes retention and promotion decisions without regard to sex;
(4) that wage and benefit disparities are corrected when identified to ensure with the laws cited in clause (1) and with clause (2); and
(5) how often wages and benefits are evaluated to ensure compliance with the laws cited in clause (1) and with clause (2).
The equal pay compliance statement must also indicate whether the business, in setting compensation and benefits, utilizes: (1) a market pricing approach; (2) state prevailing wage or union contract requirements; (3) a performance pay system; (4) an internal analysis; or (5) an alternative approach to determine what level of wages and benefits to pay employees. If the business uses an alternative approach, the business must provide a description of its approach. This law takes effect August 1, 2014.
Unemployment Benefits
Effective October 5, 2014, WESA expands eligibility for unemployment benefits to victims of stalking and sexual assault.
What Should Employers Do to Company with the Women's Economic Security Act?
Minnesota employers should do the following to comply with WESA:
Please contact Marnie DeWall or the Lindquist & Vennum employment attorney with whom you regularly work with any questions about the sweeping effects of the Women's Economic Security Act or other workplace policies.
1 Since Governor Dayton signed WESA into law, there have been questions regarding the effective date of certain sections—specifically the sections regarding parenting/pregnancy leave, sick leave, nursing mother breaks, and wage disclosure protection, all of which are silent as to effective date. Pursuant to Minnesota Statute § 645.02, when an act does not specify an effective date, the act generally takes effect on August 1, with the exception of bills containing an item of appropriation, which take effect July 1. Because some sections of WESA contain certain appropriations, Lindquist & Vennum recommends that employers presume the sections that are silent as to effective date become effective July 1, 2014, and act accordingly.
You may use the wildcard symbol (*) as a root expander. A search for "anti*" will find not only "anti", but also "anti-trust", "antique", etc.
Entering two terms together in a search field will behave as though an "OR" is being used. For example, entering "Antique Motorcars" as a Client Name search will find results with either word in the Client Name.
AND and OR may be used in a search. Note: they must be capitalized, e.g., "Project AND Finance."
The + and - sign operators may be used. The + sign indicates that the term immediately following is required, while the - sign indicates to omit results that contain that term. E.g., "+real -estate" says results must have "real" but not "estate".
To perform an exact phrase search, surround your search phrase with quotation marks. For example, "Project Finance".
Searches are not case sensitive.


text:
Humble Pie Trailer (2007)
01 January 2007 Comedy 94 mins
At nearly 400 pounds, Tracy Orbison is a wide target. When he sets out to pursue his dream of acting, the grocery clerk finds an assortment of people waiting to dash his dreams. Through it all, Tracy remains irrepressibly upbeat, convinced he's destined for something big.
Watch the official Humble Pie 2007 trailer in HD below or find more Humble Pie videos on Vidimovie.


text:
& This adorable and huggable graduation bear in his cap and gown comes with a jelly bean Jelly Belly champagne bottle and a box of hand dipped chocolates. ;
Contains: 1 Graduation Bear, 1 Jelly Belly Champagne Bottle, 1 Box of Chocolate
Under the strict kosher supervision of any one of the following kosher certification agencies: OU, OK, Kaf-K, Star-K, CRC, COR, MK (Montreal Kosher), Edah HaChareidis Badatz.
Chalav Yisrael option is available upon request. Please specify in the order comments, or call us.


text: Hi guys im trying to add a custom flash recovery to my rogers 2.1 htc magic which is already rooted following xda dev. tuts. and im having trobules with ABD i just skiped the first abd install by regularly installing a apk instead of abd install when ever i do "cd\ cd\android-sdk-windows\tools abd devices" it says " "Abd" is not an internal or an external command *something something* batch"


text:
My Trackers
my Nutrition
my Fitness
my Weight
Other Goals
my SparkPoints
Community Home
Community Feed
Message Boards
Challenge Central
Member Blogs
What's New
Health & Wellness
Weight Loss
Stuff We Love
Healthy Family
Pregnancy & Postpartum
Instant Inspiration
Food Database
Lifestyle Centers
The SparkPeople Blog
Stream hundreds of free workout videos and track them in one click. Get fit at home, at work or wherever you are!
Today's Featured Video:
Visit SparkPeople.TV
Access hundreds of thousands of recipes that are healthy and easy to make. Get full nutrition info for every recipe and track with one click!
Today's Featured Recipe:
Layered Mexican Dip with Baked Lime Chips
Visit SparkRecipes.com
Six Months
Friday, June 28, 2013
It was six months ago today that I lost my friend Ali after a 2+ year battle with cancer. Obviously I'm a little emotional today, but I'm trying not to let it affect my decision making. I had a healthy breakfast, sushi for lunch, and yes I did have some chocolate covered almonds but just a few and I'm not binging or letting my emotional state drive me to stupidity. That's about all I can hope for on a day like today when I keep looking at Facebook, seeing Ali's face, and bursting into tears. (Which is totally my own fault since I changed my profile picture to one of her and me.) I miss her. :(
Anyway, after lunch I went to the grocery store since I was out of food and got healthy things. I'm leaving Wednesday so I didn't need a ton of food, but I want to stay healthy this week.
Yesterday's food was OK too.
Breakfast: I had the rest of the cantaloupe at home, but then stopped by Whole Foods for a vegan scone since I was still hungry.
Lunch: Leftover Gardein Chick'n and roasted broccoli.
Afternoon snack: Honeydew from the farmbox in the office kitchen. SO good!
Dinner: We had a late kickball game so I got to go to Whole Foods for a salad instead of grabbing a protein bar at Trader Joe's. I opted for guacamole instead of salad dressing, but the guacamole was stupidly spicy for me so I ended up eating around that and leaving a bunch of the salad behind.
Snack: (snack? Whatever.) I had a beer at the bar.
On the upside, we're now 2-0 and I got to play catcher and didn't screw it all up. Go me!
Share This Post With Others
Report Inappropriate Blog
Member Comments About This Blog Post
Report Inappropriate Comment
My SparkPage
1605 days ago
Report Inappropriate Comment
My SparkPage
I'm sorry. It's so hard to lose people we love, and hard to make good choices when we are used to being comforted by food.
1605 days ago
Report Inappropriate Comment
My SparkPage
My heart sympathizes with you. I lost my baby sister to cancer and 6 months later my beloved father to a heart attack. But well done on keeping it together....you know that's what they would tell you if they could. Your food blogs are fabulous and give me ideas when I'm blank.
1606 days ago
Report Inappropriate Comment
My SparkPage
You are doing the best you can and it's totally ok to be emotional. I'm always impressed at how much love comes across when you talk about Ali. You are a really, really good friend.
I'm glad you were able to still make good decisions food-wise.
1606 days ago
Add Your Comment to the Blog Post
Log in to post a comment
Disclaimer: Weight loss results will vary from person to person. No individual result should be seen as a typical result of following the SparkPeople program.
Get An Email Alert Each Time
MUFFIY831 Posts
See Today's Featured Member Blog Posts
More Blogs by MUFFIY831
Going Off the Rails On a Crazy Train ...
- 10/16/2017
- 10/11/2017
250 Day Streak - A Self Pep Talk
- 10/4/2017
The Backslide ... IS POSTPONED (And Meal Planning!)
- 9/25/2017
View All ›
close ×


text:
- Home
- Government
- Departments A-F
- City-County Planning
- Current Topics
- Angier-Driver Planning and Zoning Study
Angier-Driver Planning and Zoning Study
For information, contact:
Hannah Jacobson, 919-560-4137, ext. 28247
Public Workshop Materials
The Planning Department hosted a public workshop on June 29 to receive input on the direction of the Angier-Driver Planning and Zoning Study. Materials from the meeting can be found in the links below.
Public Workshop Presentation
Introducing the Angier-Driver Land Use and Zoning Study
What We've Heard So Far…
Sub-Area Boundaries
Sub-Area A
Sub-Area B
Sub-Area C
Sub-Area D
Share Your Comments!
Survey: What is your vision for the business district?
Survey: After reviewing the meeting materials, how do you feel about moving forward with the planning process?
Next Steps
The Planning Department will continue to gather input over the summer. A public workshop to discuss next steps will be scheduled for the fall (date TBD).
Reviving the Angier-Driver business district is a goal shared by community members and the City. In 2014, a public works project to give the "streetscape" a fresh facelift was completed. In beautifying the blocks leading to the intersection of Angier Avenue and Driver Street with new trees, benches, sidewalks and crosswalks, the goal was to make the shops more accessible and pleasant to visit. While the streetscape project has been successful in many ways, there are less obvious factors that pose challenges to reviving the commercial district. One challenge is that current zoning (the rules about how properties can be used and developed) can make it difficult for businesses to re-use the existing commercial buildings.
The Planning Department would like to explore these zoning issues by engaging residents and business owners, and people in the neighborhoods who would frequent the Angier-Driver businesses district to work, shop, or dine. What types of businesses and services are most needed in the community? What zoning rules stand in the way of locating those businesses and services in the Angier-Driver business district?
Revitalization of the Angier-Driver business district will not happen overnight, and it cannot be achieved by zoning changes alone. Therefore, partnerships are vital. We will work in tandem with groups like the City's Small Business Advisory Council, who provide resources and counseling to small and minority owned businesses, to make sure there is awareness among the community of the opportunities in the Angier-Driver business district. It is important that existing residents have a place and have a voice in the success of the Angier-Driver business district now and into the future.


text:
Giveaway type:
Giveaway – Giveaways have winners selected at random.
Entry method:
Find out more about this giveaway:
Giveaway closing date:
Overview of prizes on offer:
– 1 LiLash tube of 3ml
– Premium holder
– Mirror decal
There will be 2 winners to the giveaway on my blog and 1 winner on my Instagram. For a bigger chance, you can enter on both places
Locational eligibility:
Further locational eligibility:
The competition is open internationally and will run until 24 December 2016
If you would like to get involved with Bloggers Required, we're always happy to hear from prospective advertisers, newsletter sponsors and partners, just give us a shout at [email protected]
Blogging assignments/giveaways
Bloggers Required does not write or imply any association with, nor endorsement by or of, the product/service/brand/business/blogger named in this blogging assignment/giveaway or similar, and is not responsible for the assignment/giveaway or similar contents or their authenticity. Please read our T&Cs, blogger FAQ and ethical blogging guide before applying to blogging assignments UK – US.
Receive EXCLUSIVE blogging assignments via our weekly email newsletter
Join over 16,500 bloggers and subscribe to our mailing list to receive NEW and EXCLUSIVE blogging assignments, giveaways and news.
Thank you for subscribing. Your weekly email blogging assignment email will be delivered every Monday.
Something went wrong.


text:
Queen Elizabeth II paves way for Theresa May to begin Brexit talks, signs Bill into law
LONDON, U.K. - Queen Elizabeth II has officially given the Royal Assent to the government's European Union (Notification of Withdrawal) Bill, after the House of Commons and the House of Lords approved it earlier this week.
The Queen signed the Bill into law, paving the way for Prime Minister Theresa May to start the official process to bring the U.K. out of the European Union.
The Royal Assent is now an Act of Parliament after it was presented to both House by their speakers.
Further, it also comes a day after Brexit Secretary David Davis admitted that there has not been an assessment of how the U.K. may suffer if it fails to reach a deal with the EU.
The Treasury meanwhile has warned that crashing the U.K. out of the EU without a bargain could lead to economic collapse.
Davis told the House of Commons that "it's not as frightening as some people think, but it's not as simple as some people think."
May meanwhile has said that "no deal is better than a bad deal."
May has said that she will trigger the process by the end of the month and will now notify Brussels that the U.K. is leaving the EU.
This will then lead to a two year process of exit negotiations.
Reports have noted that May will not trigger the official process next week, to avoid a clash with an informal summit of EU countries.
The meeting will reportedly mark the 60th anniversary of the Treaties of Rome that saw the foundation of the European Economic Area, leading to the European Union.
May would not be attending the meeting on March 25.
Davis has confirmed, "By the end of the month we will invoke Article 50, allowing us start our negotiations to build a positive new partnership with our friends and neighbours in the European Union, as well as taking a step out into the world as a truly Global Britain."
Further, Mayor of London Sadiq Khan called for a new visa process to help EU nationals legally in the U.K. to apply for permanent residency.
He even said that the current system involved a "tsunami" of paperwork and was not fit for the purpose.
Khan has urged the Government to provide an "immediate" cast iron guarantee to the 3.3 million EU citizens living here.


text:
Maynard, MA (PressExposure) June 25, 2014 -- Longwood Software, Inc., developer of the RevBase® software-as-a-service (SaaS) marketing asset management system http://www.revbase.com, has announced a new White Paper entitled, "It's Time for Marketing Asset Management," now available on a complimentary basis to marketers at http://www.revbase.com/whitepapers.html.
This paper covers the ten most important reasons marketers swamped with the demands of their jobs should consider implementing a Marketing Asset Management (MAM) solution:
1. Complaints by sales that it is difficult to find the materials they need.
2. The need to update multiple locations and sites with the same items - over and over.
3. Too much time responding to requests from the field.
4. Limited visibility into which materials are actually being used, and which aren't.
5. Inconsistent presentation of products and programs across sales channels.
6. Duplication of efforts and wasted time across marketing operations.
7. Security concerns regarding sensitive marketing assets and sales tools.
8. Poor traceability and accessibility of previously-created marketing assets.
9. Inability to provide updated sets of materials to mobile applications and other systems.
10. Salespeople frustrated with outdated, irrelevant content.
"Marketers pressured with all the demands of their jobs and lean staffs will learn how leading Marketing Asset Management systems are designed specifically to help marketers. The paper explains the ways these systems support their unique needs, as well as those of salespeople and sales channels," said Scott Richardson, president and CEO of Longwood Software. "The best MAM systems manage, control, track and distribute a company's brand assets, marketing materials, sales tools and creative materials via a customized online portal. Such systems lift many burdens off of marketers' shoulders, as well as serving a company's multiple audiences more professionally and effectively."
Software's Marketing Asset Management system, RevBase®, offers electronic and print fulfillment capabilities, including a searchable database for marketing assets; a visual shopping cart for collecting items for distribution; multiple email delivery modes; and click-through tracking of electronically-fulfilled assets. Users can customize marketing materials with RevBase; schedule automatic reports; and set up item expiration alerts so administrators know when items are becoming outdated. RevBase is mobile-enabled and is designed for "out of the box" use. It requires no technical training, IT support, or custom development.
About Longwood Software, Inc.
Longwood Software, Inc., (Maynard, MA) is a leading provider of software-as-a-service (SaaS) solutions for marketing and sales teams in manufacturing, technology, and business services. The company's products are the RevBase® marketing asset management system and the ForFile® large file transfer service. The company's customers include American Greetings, BBB Industries, Beiersdorf, Corning Life Sciences, Dunkin' Brands, Kronos, Pfizer Consumer Healthcare, Quincy Compressor, Save the Children Federation, The MathWorks, and Thermo Fisher Scientific. For more information visit http://www.revbase.com or http://www.forfile.com.
# # #
ForFile, Longwood Software, and RevBase are registered trademarks of Longwood Software. All other trademarks and registered trademarks mentioned herein are the property of their respective owners.


text:
Best TeamLava GamesJaysTop10List You know when you get the urge to text a new person. Well today I'm going to show you the top 10 of best Teamlava Games that you could text in.
The Top Ten
What I love about these games, is that you can design and decorate your place, however you want. And you can message other players too. - cosmo
There's more cooler people in that game and plus it's all about delicious food. - JaysTop10List
I love this game, but it got old after 2 months and I deleted it. - funnyuser
Too much vulgar language and people in the game but still makes it #2. - JaysTop10List
It's not really the best game to talk to people in but give it a try I guess. - JaysTop10List
It's kinda boring to play but still makes it to #4. - JaysTop10List
How about home design story?
Hm... Well it's fun but not that fun. - JaysTop10List
My favorite TeamLava game. Been playing it for over a year and still do. Its actually really fun! I also play Restaurant and Fashion Story. If you play and want to add me here is my game id: BakeryStoryGirl15 - cosmo
Not really fun but it's food but desserts. - JaysTop10ListV 1 Comment
It's fun taking care of the animals. - JaysTop10List
A remake of Bakery Story but about Halloween. - JaysTop10List
Another remake to Pet Story. - JaysTop10List
The Contenders
Recommended Lists
Related ListsTop Ten MMORPG Games Best Call of Duty Games Best Video Games of All Time Best Pokemon Games Best Video Games of 2013
List Stats
3 years, 237 days old
Top Remixes
2. Nightclub Story
3. Farm Story