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Tinting Services
Tinting Services are offered here at Nails Glamour. Whether you want darker, fuller eyebrows or eyelashes or simply want to wake up beautiful and save time in your morning routine, tinting will open up your eyes and give you more definition and thickness!
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Tue, 21 Dec 2010
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From disco to dupstep to straight up techno, here's our run down of what's on in Melbourne this New Year's Eve.
Wed, 15 Oct 2008
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The breaks label will release a three CD set in celebration.
Tue, 20 May 2008
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Breaks label Finger Lickin' celebrates ten years in the biz with a tent at this year's Get Loaded in the Park.
Tue, 23 Oct 2007
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Ewan Pearson, Todd Terje and Para One will be suiting up next March for British rave-in-snow Snowbombing.
Fri, 19 Jan 2007
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Prog house DJ Steve Porter crams in fifty seven tracks of breaks, house, techno and trance across two CDs on his latest compilation.
Thu, 18 Jan 2007
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The popular British snowboarding rave Snowbombing is back this April with a lineup featuring Digitalism, Justice and James Zabiela.
Thu, 11 Jan 2007
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It's a quiet one across Blighty this weekend, but a great weekend for London breaks heads with three top nights happening in the capital.
Thu, 24 Aug 2006
Are you banking on a big one? Clubbers in the capital are spoilt for choice this long weekend. RA previews the myriad of options...

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The cost for early educators from a program not enrolled in Learn & Grow or for those not in a DEED grant funded proram is $45 .
Free to early educators from a program which is either participating in Learn & Grow or is DEED grant funded. Please include name of program during registration to assist thread in identifying educators who may take this training at no cost.
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January 7, 2019
Hole Bandits (2011)
Release Year: 2011
Cast: Rock Bottom, Orion Cross, Karsin Knightly, Dani, Gabriel, Keith, Mitch
Genres: Gay, Bareback, Oral/Anal Sex, Humiliation, Muscle Men, Dildos, Toys, Big Dicks, Spitting, Interracial, Rimming, Rough Sex, Straight Men, Tattoos
Video language: English
Gabriel is one of our favorite Hole Bandits. He is a sexy straight stud who can take a cock down his throat and up his ass almost as good as Rock can. We decided it was time for Gabriel to enter into the Satyr boot camp. At Satyr boot camp we take selected guys whom we feel need to be inducted into the ways of Satyr. This of course requires that the ideal candidate is capable of throat fucking hot studs but also capable of taking the biggest toys and ultimately a fist up his ass. Gabriel was finally ready to move up in rank. So we paired him up with the Master, Rock Bottom. No one that we have ever found has been able to match Rock's intensity both as a top and as a bottom.
Format: avi
Duration: 2:46:37
Video: 976x464, XviD, 1657kbps
Audio: 218kbps
File size: 2.2 GB


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George de Mohrenschildt relaxes with a dog in this undated photograph. Photos provided
By Thom Smith
"What sort of day was it? A day like all days, filled with those events that alter and illuminate our times … and you were there."
Although the…
Added by Mary Kate Leming on March 31, 2015 at 10:42pm — No Comments
The Plate: Chicken fried chicken
The Place: Tryst, 4 E. Atlantic Ave., Delray Beach; 921-0201 or trystdelray.com
The Price: $15
The Details: Our cardiologist will thank us not to order this again.
But our belly tells us otherwise.
After all, what could be more…
Added by Mary Kate Leming on March 31, 2015 at 10:28pm — No Comments
Delray Beach County Fair, 1913. Delray Beach won many blue ribbons.
Photos courtesy Delray Beach Historical Society
By J.D. Vivian
Ever wonder why the first settlers moved to what is now Delray Beach? Or how the Pineapple Grove district earned its name? Or…
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Added by Mary Kate Leming on March 10, 2015 at 9:00pm — No Comments
After three decades, a death warrant may be near
for Palm Beach County's most notorious killer.
We look back at the case that still haunts our memories.
Why we …Continue
Added by Mary Kate Leming on March 5, 2015 at 1:30pm — 1 Comment
How could you write this story? Why dredge up such horrible memories?
I expect to hear those questions. I anticipate this story may upset many of our readers. I recognize that this is a very different sort of story for The Coastal Star.
Let me explain:
When I saw late last year that Duane Owen had had what seemed to be a final clemency hearing, I felt that his imminent execution should not go unnoted. I wanted to know how a heinous killer could be lingering on death…
Added by Mary Kate Leming on March 5, 2015 at 12:47pm — No Comments
By Dan Moffett
In their federal racketeering lawsuit against Martin O'Boyle and Christopher O'Hare, attorneys for the town of Gulf Stream allege the two men have conspired to use the state's public records laws as weapons to extort legal fees from hundreds of municipalities and contractors across the state.
Added by Mary Kate Leming on March 5, 2015 at 12:36pm — 1 Comment
By Randy Schultz
The debate about whether Duane Owen should live or die is about whether Duane Owen is the person he was or the person he supposedly has become.
Inmate 101660 at Union Correctional Institution in Raiford is serving two death sentences, six life sentences, one 15-year sentence and one five-year…
Added by Mary Kate Leming on March 5, 2015 at 12:30pm — No Comments
The museum building anchors Old School Square, now the cultural hub of Delray Beach. Jerry Lower/The Coastal Star
By Rich Pollack
For three and a half years, Frances Bourque and a small but tireless group worked on an enormous undertaking — which many at the time…
Added by Mary Kate Leming on March 5, 2015 at 12:19pm — No Comments
Andy Bregman (l) with his mentee, Logan. Logan's grades have improved to the point that next year he'll be a freshman at Florida Atlantic University. Tim Stepien/The Coastal Star
By Rich Pollack
A lot has changed in the seven years since Highland Beach resident…
Added by Mary Kate Leming on March 5, 2015 at 12:11pm — No Comments
By Jane Smith
The Boynton Beach Community Redevelopment Agency did not skip a beat when Ken Spillias stepped aside as its attorney.
At its February meeting, Spillias sat in the audience and another law firm colleague, Tara Duhy, took his place on the dais next to the agency's executive director.
"We knew that he (Spillias) was going to retire, it just came more quickly than we thought," said Duhy, a partner with the Lewis, Longman & Walker law firm…
Added by Mary Kate Leming on March 5, 2015 at 11:59am — No Comments
Meet Jacqie, whose karaoke night brings crowds to Manalapan
John Justice Parker, 28, of Royal Palm…Continue
Added by Mary Kate Leming on March 5, 2015 at 11:36am — 1 Comment
March 14: Six women from Palm Beach County who exemplify the national initiatives of the female scouting program and serve as role models for today's girls will be honored at the evening affair. Time is 6 to 10 pm. Cost is $225. Call 427-0190 or visit gssef.org. Photo: (in front) Melissa Patrick, troop leader; Heidi…Continue
Added by Mary Kate Leming on March 4, 2015 at 3:37pm — No Comments
Bachannal backers: (in front)John Frezza, Joanne Mancari, Lisa Vander Ploeg, Mike and Amy Kazma, Al and Joni Goldberg, Robin and Charles Deyo, Joyce and Thom DeVita, Susan Whelchel, Mary Csar (in back), Mark Nichols, Kelly Loudermilk, Cynthia McDonough, Timothy Loudermilk, Ed McDonough, Guy LaFerrera, Suzanne Spinner and Mindy Nichols.…Continue
Added by Mary Kate Leming on March 4, 2015 at 3:32pm — No Comments
Love of Literacy Luncheon committee members (in front) Penny Kosinski, Bettina Young, Chiara Clark, (in back) Gina Brody, Cristy Fimiani, Sylvie Bergeron, Kristin Calder and Megan Mulry. Photo provided
By Amy Woods
The chairwoman of this year's Love of Literacy…
Added by Mary Kate Leming on March 4, 2015 at 1:42pm — No Comments
More than 200 guests attended the season's third conversation, featuring Jonathan Adler and Simon Doonan. Adler is an author, designer and potter, and Doonan has worked in fashion for three decades. Both are part-time Palm Beach residents. ABOVE: Penny and Alan Murphy, with Elaine Meier. Photo provided by Corby Kaye's Studio Palm…Continue
Added by Mary Kate Leming on March 4, 2015 at 1:18pm — No Comments
The American Humane Association honored philanthropist Lois Pope at a special event with the theme 'Lois Pope: Our Light of Compassion.' Pope was recognized for her generosity and leadership in building a more humane world. 'We can think of no humanitarian making a greater difference for children, animals and veterans than Lois Pope,' said…Continue
Added by Mary Kate Leming on March 4, 2015 at 1:12pm — No Comments
Honoree Mary Wong and Grammy Award-winning reggae star Shaggy shined a light on Haiti's housing needs during the 20th-annual fundraiser, where guests pledged enough money to build homes for 40 destitute families in the area surrounding Pon Batay. 'Everyone in this room is a voice for the voiceless,' Food for the Poor President and CEO Robin Mahfood told the crowd of…Continue
Added by Mary Kate Leming on March 4, 2015 at 1:09pm — No Comments
The annual matchup ended in victory for the faculty team, with a final score of 5–3. Competitive spirit aside, this year's game brought the community together to share in the school's 'Live Green, Live Healthy' initiative. 'We really appreciate opportunities where our faculty and students can enjoy a chance to spend time outside the…Continue
Added by Mary Kate Leming on March 4, 2015 at 12:53pm — No Comments
The South County treatment center had a benefit for The Body Positive, a movement aimed at helping clients of all ages overcome challenges and respect their bodies. The HEArt (Healing Through Expressive Arts) Show gave attendees the opportunity to purchase donated artwork, taste culinary creations and listen to live music. More than $7,000 was…Continue
Added by Mary Kate Leming on March 4, 2015 at 12:50pm — No Comments
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The Snf1 protein kinase is essential for the transcription of glucose-repressed genes in Saccharomyces cerevisiae. We identified Nrg2 as a protein that interacts with Snf1 in the two-hybrid system. Nrg2 is a C2H2 zinc-finger protein that is homologous to Nrg1, a repressor of the glucose- and Snf1-regulated STA1 (glucoamylase) gene. Snf1 also interacts with Nrg1 in the two-hybrid system and co-immunoprecipitates with both Nrg1 and Nrg2 from cell extracts. A LexA fusion to Nrg2 represses transcription from a promoter containing LexA binding sites, indicating that Nrg2 also functions as a repressor. An Nrg1 fusion to green fluorescent protein is localized to the nucleus, and this localization is not regulated by carbon source. Finally, we show that VP16 fusions to Nrg1 and Nrg2 allow low-level expression of SUC2 in glucose-grown cells, and we present evidence that Nrg1 and Nrg2 contribute to glucose repression of the DOG2 gene. These results suggest that Nrg1 and Nrg2 are direct or indirect targets of the Snf1 kinase and function in glucose repression of a subset of Snf1-regulated genes.
THE Snf1 protein kinase is highly conserved from yeast to plants to mammals (for reviews, see Gancedo 1998; Hardieet al. 1998). In Saccharomyces cerevisiae, Snf1 is a key component of the glucose signaling pathway and is essential for the transcription of many glucose-repressed genes in response to glucose limitation (Celenza and Carlson 1986). This kinase also has roles in metabolic regulation, glycogen accumulation, stress responses, meiosis and sporulation, invasive growth, life span, and aging (Thompson-Jaegeret al. 1991; Hardyet al. 1994; Honigberg and Lee 1998; Ashrafiet al. 2000; Cullen and Sprague 2000). Its mammalian homolog, AMP-activated protein kinase, regulates metabolism and transcription in response to the cellular energy supply, and the plant homologs are thought to be involved in sugar regulation.
The role of the Snf1 kinase in transcriptional control has been characterized in some detail. The adaptation of yeast cells to growth on nonpreferred carbon sources is accompanied by major changes in transcriptional patterns, and Snf1 appears to act at many control points. Thus far, Snf1 has been shown to regulate the expression and function of both transcriptional repressors and activators in response to glucose availability (for review, see Carlson 1999). Recent evidence also implicates Snf1 in direct regulation of the RNA polymerase II holoenzyme (Kuchinet al. 2000).
One of the major mechanisms by which Snf1 regulates transcription is by regulating the function of the transcriptional repressor Mig1. Mig1 is a zinc-finger protein that binds to sites in the promoters of many glucose-repressed genes and recruits the global corepressor Ssn6(Cyc8)-Tup1 (Nehlin and Ronne 1990; Treitel and Carlson 1995; Tzamarias and Struhl 1995). Several lines of evidence indicate that Snf1 phosphorylates Mig1 in response to glucose limitation and thereby regulates its nuclear localization and inhibits its repressor function (DeVitet al. 1997; Ostling and Ronne 1998; Treitelet al. 1998).
Snf1 also effects transcriptional control by regulating transcriptional activators. Snf1 regulates the phosphorylation and function of the Cys6 zinc-cluster activators Sip4 and Cat8, which bind to the carbon source-responsive elements (CSRE) of gluconeogenic genes (Lesageet al. 1996; Rahner et al. 1996, 1999; Randez-Gilet al. 1997; Vincent and Carlson 1998; Rahneret al. 1999). Snf1 has been shown to interact physically with Sip4 (Lesageet al. 1996; Vincent and Carlson 1998).
The two-hybrid system has been useful in detecting interactions of Snf1 with transcriptional activators and repressors. Sip4 was first identified by its two-hybrid interaction with Snf1 (Yanget al. 1992). Mig1 also interacts with Snf1 in two-hybrid assays (Treitelet al. 1998), and in this case interaction was much stronger with a catalytically defective mutant Snf1 protein, Snf1K84R (Celenza and Carlson 1986), which bears a substitution of arginine for the conserved lysine in the ATP-binding site. Several Srb/mediator proteins associated with the RNA polymerase II holoenzyme have also been shown to interact with Snf1 (Kuchinet al. 2000).
In an effort to identify new downstream targets of the Snf1 kinase, we performed a two-hybrid screen with the catalytically defective Snf1K84R. We recovered Nrg2, a zinc-finger protein that is a close homolog of the DNA-binding repressor protein Nrg1. Nrg1 functions in glucose repression of the STA1 gene, which encodes one of the glucoamylase isozymes responsible for starch degradation in S. cerevisiae var. diastaticus (Parket al. 1999). Furthermore, the Snf1 kinase is known to be required for derepression of STA2 (Kuchinet al. 1993), which is identical to STA1 throughout the promoter and coding region. We therefore examined the relationship of Nrg1 and Nrg2 to the Snf1 kinase. Both proteins interact with Snf1 in the two-hybrid system and both co-immunoprecipitate with Snf1 from cell extracts. We present evidence that Nrg2 functions as a repressor and that the nuclear localization of Nrg1, unlike that of Mig1, is not regulated by carbon source. Finally, we examine the roles of Nrg1 and Nrg2 in repression of Snf1-dependent genes.
Strains and genetic methods: The S. cerevisiae strains used are listed in Table 1. To construct strain MCY4531, we first generated a 2.5-kb DNA fragment using the polymerase chain reaction (PCR) with the template pFA6a-GFP(S65T)-kanMX6 (Longtineet al. 1998) and two primers, one including the 15 codons preceding the termination codon of NRG1 and the other including 45 base pairs following the stop codon. This fragment was used to transform strain MCY2916, with selection on rich medium containing 200 μg/ml G418 (Life Technologies, Gaithersburg, MD), and its integration at the NRG1 locus was verified by PCR. Strain MCY4536 was created in the same way, except that the targeting sequence was for NRG2. To construct the nrg1Δ::kanMX6, nrg2Δ::kanMX6, and nrg2Δ:: His3MX6 mutations, we first amplified kanMX6 or His3MX6 (Longtineet al. 1998) with oligonucleotides containing 45 nucleotides flanking the open reading frame of NRG1 or NRG2. PCR products were used to transform MCY3912 or MCY3913 with selection for the marker, and disruption was verfied by PCR amplification of genomic DNA.
Standard methods for yeast genetic analysis and transformation were used (Roseet al. 1990). Cells were grown in synthetic complete (SC) medium lacking appropriate supplements to maintain selection for plasmids.
Plasmids: Plasmids used in this study are listed in Table 2. pRJ215 contains the BamHI fragment from pRJ80 (Ludinet al. 1998) in the BamHI site of pEG202 (Golemiset al. 1997). pSK106 was created by cloning the BamHI fragment from pRJ215 into the BamHI site of pGBT-9 (Bartelet al. 1993). The coding regions of NRG1 and NRG2 were amplified by PCR from genomic DNA using Vent polymerase (New England Biolabs, Beverly, MA) with oligonucleotides K47 and K48 (Nrg2) and K49 and K50 (Nrg1), each containing a BamHI site. BamHI-digested PCR product was cloned into the BamHI site of plasmids pACTII (Legrainet al. 1994), pVP16 (Vojteket al. 1993), pWS93 (Song and Carlson 1998), pSH2-1 (Hanes and Brent 1989), and pEG202.
Oligonucleotides: Oligonucleotides used as primers in PCR were the following: K47, GCGCGGATCCTAATGTCCATAGG TTACAAAGAC; K48, GCGCGGATCCTCAACTGCTAGCCT CCCTCC; K49, GCGCGGATCCTAATGTTTTACCCATATAA CTATAG; K50, GCGCGGATCCGTCAATTATTGTCCCTTT TTC (BamHI sites are underlined).
Two-hybrid screen: A two-hybrid screen (Fields and Song 1989) for proteins that interact with a Gal4 DNA-binding domain (GBD) fusion to Snf1K84R was carried out in strain HF7C, which contains a chromosomally located GAL1-HIS3 reporter. The strain was transformed with pSK106, which expresses GBD-Snf1K84R, and with a library (gift of S. Elledge, Baylor College of Medicine) of S. cerevisiae cDNAs fused to the Gal4 activating domain (GAD). Transformants were selected on SC-His + 2% glucose plates for a His+ phenotype. Five plasmids conferred a His+ phenotype and gave blue color in CTY10-5d and were subjected to sequence analysis. Besides NRG2, the recovered sequences were SNF4, GPM1, POR1, and TDH1. The others were not analyzed further.
Two-hybrid assays with LexA fusion proteins were carried out in strain CTY10-5d or in strain FY250 transformed with the pSH18-34 reporter, containing LexA binding sites 5′ to a GAL1-lacZ reporter (Estojaket al. 1995; Golemiset al. 1997).
Invertase and β-galactosidase assays: Invertase activity was assayed in whole cells as previously described (Jiang and Carlson 1996). β-Galactosidase activity was assayed in permeabilized cells (Guarente 1983) and expressed in Miller units (Miller 1972). A filter assay in which β-galactosidase activity confers blue color was also used as previously described (Jiang and Carlson 1996).
Co-immunoprecipitation assays: Preparation of protein extracts and immunoprecipitation procedures were essentially as described previously (Celenzaet al. 1989). The extraction buffer was 50 mm HEPES (pH 7.5), 150 mm NaCl, 0.5% Triton X-100, 1 mm dithiothreitol, 10% glycerol, and contained 2 mm phenylmethylsulfonyl fluoride and complete protease inhibitor cocktail (Roche Molecular Biochemical). Proteins were immunoprecipitated with anti(α)-hemagglutinin (HA) monoclonal antibody (Roche Molecular Biochemical) or α-LexA monoclonal antibody (CLONTECH, Palo Alto, CA) in the same buffer, except that it contained 0.25% Triton X-100 for immunoprecipitation with α-HA and 50 mm NaCl and 0.1% Triton X-100 for immunoprecipitation with α-LexA.
Immunoblot analysis: Proteins were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and analyzed by immunoblotting using polyclonal α-Snf1 (Celenza and Carlson 1986), monoclonal α-HA (Roche Molecular Biochemical), or polyclonal α-LexA (Invitrogen, San Diego). Antibodies were detected by chemiluminescence with ECL or ECL Plus reagents (Amersham, Arlington Heights, IL).
Imaging of green flourescent protein fluorescence: Cells were grown to midlog phase in synthetic media containing 5% glucose or 2% glycerol plus 2% ethanol, harvested by centrifugation, and resuspended in nonfluorescent media [0.9 g/liter KH2PO4, 0.23 g/liter K2HPO4, 0.5 g/liter MgSO4, 3.5 g/liter (NH4)2SO4] containing the appropriate carbon source. Nuclei were stained by addition of 0.8 μg/ml of 4′,6-diamidino-2-phenylindole (DAPI) for 5 min. Fluorescence of green fluorescent protein (GFP) fusion proteins was visualized in unfixed cells by using a Nikon Eclipse E800 fluorescent microscope. Images were captured by using a digital camera (Hamamatsu Orca-100, Hamamatsu, Japan) and Openlab software (Improvision) and were converted to Adobe Photoshop 2.5.1 files for processing.
Microarray analysis: Strain MCY3912 carrying pV46 or pVP16 was grown in SC-Leu + 5% glucose. Total yeast RNA was extracted with hot phenol, and poly(A)+ RNA was purified by oligo(dT) chromatography (QIAGEN, Chatsworth, CA). Fluorescently labeled cDNA was prepared, and expression of 5805 yeast open reading frames (ORFs) was analyzed using DNA microarrays as described (DeRisiet al. 1997). Microarrays were produced by the Columbia University Microarray Project.
Identification of Nrg2 in a two-hybrid screen for interaction with Snf1: We carried out a two-hybrid screen for proteins that interact with the catalytically defective Snf1 protein kinase, Snf1K84R. GBD-Snf1K84R was used as a bait to screen a library of cDNAs fused to GAD. We recovered six clones that were His+ in combination with GBD-Snf1K84R (see materials and methods). Five clones also caused blue color in combination with both LexA-Snf1K84R and LexA-Snf1 in strain CTY10-5d.
Sequence analysis showed that one of these clones (pKRIP6) encodes an in-frame fusion of GAD at a position five nucleotides preceding codon 1 of the NRG2 gene (YBR066C). NRG2 encodes a protein of 220 amino acids with a predicted molecular mass of 25 kD and two zinc fingers at the C terminus. The zinc fingers are homologous to those of the transcriptional activators Msn2 and Msn4, which bind stress response elements (Martinez-Pastoret al. 1996), and to those of the repressors Mig1 and Mig2. However, the closest homolog to Nrg2 is Nrg1, which is 44% similar overall and 84% identical in the zinc-finger region (Figure 1).
NRG1 was identified as a multicopy inhibitor of the glucose-repressible STA1 promoter in S. cerevisiae var. diastaticus (Parket al. 1999). In the selection scheme, the STA1 promoter was used to drive expression of TPK2, encoding a catalytic subunit of cyclic AMP-dependent protein kinase, which is toxic to cells at high levels. Multicopy NRG1 restored healthy growth and repressed glucoamylase expression. Nrg1 bound to sites in the STA1 upstream region, and a LexA fusion to Nrg1 repressed transcription of a reporter with LexA sites, dependent on the corepressor Ssn6-Tup1 (Parket al. 1999). Mutation of NRG1 relieved glucose repression of STA1. Release from glucose repression of glucoamylase genes requires the Snf1 protein kinase (Kuchinet al. 1993), and thus these studies suggest a functional connection between Nrg1 and Snf1. We therefore included Nrg1 in subsequent experiments to assess its interaction with Snf1.
The Snf1 kinase comprises a catalytic domain (residues 1-392, designated Snf1KD) and a regulatory domain (residues 392-633, designated Snf1RD), which binds to the kinase domain and inhibits its activity (Jiang and Carlson 1996). We assayed the two-hybrid interaction of GAD-Nrg1 and GAD-Nrg2 with LexA DNA-binding domain (LexA87) fusions to Snf1KD and Snf1RD. Interaction was monitored by assaying β-galactosidase activity in cells grown under glucose-repressing conditions (5% glucose) and after a 3-hr shift to 0.05% glucose. Both GAD-Nrg1 and GAD-Nrg2 interacted with LexA87-Snf1KD but not with LexA87-Snf1RD (Table 3).
Co-immunoprecipitation of the Snf1 kinase with Nrg1 and Nrg2: To confirm that Snf1 interacts with Nrg1 and Nrg2, we tested for co-immunoprecipitation of the kinase with triple HA epitope-tagged proteins. Protein extracts were prepared from snf1Δ cells expressing HA-Nrg1 or HA-Nrg2 and Snf1, Snf1K84R, or no Snf1 protein. Immunoblot analysis showed that levels of both HA-Nrg1 and HA-Nrg2 were severely reduced in cells expressing no Snf1 protein, but levels were normal in cells expressing Snf1K84R and thus defective only for Snf1 catalytic activity (Figure 2A; input panel); these results are consistent with physical interactions in vivo. Proteins were immunoprecipitated with α-HA antibodies, and the precipitates were analyzed by SDS-PAGE and immunoblot analysis with α-Snf1 antibodies. Snf1 and Snf1K84R co-immunoprecipitated with both HA-Nrg1 and HA-Nrg2, but coprecipitation with HA-Nrg2 was more efficient (Figure 2A; CoIP panel). In control experiments, Snf1 did not coprecipitate with the triple HA tag expressed from the vector.
We also tested for co-immunoprecipitation of HA-Nrg1 and HA-Nrg2 with LexA-Snf1 (Figure 2B). Extracts were prepared from wild-type cells expressing LexA-Snf1 or LexA-Snf1K84R and HA-Nrg1 or HA-Nrg2, and LexA proteins were immunoprecipitated with α-LexA antibodies. Immunoblot analysis with α-HA antibody showed that HA-Nrg1 and HA-Nrg2 co-immunoprecipitated with both LexA-Snf1 and LexA-Snf1K84R, but not with LexA alone. Again, HA-Nrg1 was less efficiently recovered than HA-Nrg2.
To examine the possibility that Snf1 phosphorylates Nrg1 or Nrg2, we performed kinase assays with both of the above sets of immunoprecipitates. No Snf1-dependent phosphorylation of Nrg1 or Nrg2 was detected (data not shown). In addition, we examined HA-Nrg1 and HA-Nrg2 for phosphorylation in vivo by immunoblot analysis. No Snf1-dependent differences in the mobility of either protein were detected when wild-type and snf1 mutant cells were grown in 5% glucose or shifted to 0.05% glucose or shifted to 2% glycerol plus 2% ethanol (data not shown). Subsequent analysis of LexA fusion proteins also revealed no Snf1-dependent differences in mobility (Figure 3C).
Repressor function of Nrg1 and Nrg2: Previous studies showed that LexA87-Nrg1 represses expression of a reporter with LexA binding sites in glucose-grown cells (Parket al. 1999). We therefore tested the ability of LexA87-Nrg2 to function as a repressor in this assay. Wild-type strain MCY829 was transformed with plasmids expressing LexA87-Nrg1, LexA87-Nrg2, or LexA87 alone from the ADH1 promoter, and a CYC1-lacZ reporter with either four or zero LexA binding sites 5′ to the upstream activation sites (UAS; Figure 3A). Reporter gene expression was monitored by assaying β-galactosidase activity. LexA87-Nrg1 and LexA87-Nrg2 both repressed transcription about 15-fold in cells grown in 5% glucose (Figure 3B).
We then examined the regulation of transcriptional repression by carbon source. Repression by both LexA87-Nrg1 and LexA87-Nrg2 was maintained after a shift to low glucose (0.05%) or during steady-state growth in raffinose, sucrose, or galactose (data not shown). In accord with these findings, the STA genes are not derepressed under these growth conditions, but only during growth in glycerol plus ethanol (Pretoriuset al. 1986; Kartashevaet al. 1996). No repression of the reporter was observed when cells were grown in 2% glycerol plus 2% ethanol (Figure 3B); however, immunoblot analysis showed that levels of both fusion proteins were very low when cells were grown in glycerol plus ethanol (Figure 3C), which could account for the lack of repression. The low protein levels can probably be attributed to reduced expression from the ADH1 promoter because levels of ADH1 mRNA are 6- to 10-fold lower during growth on ethanol than on glucose (Deniset al. 1983). Moreover, the levels of HA-Nrg1, HA-Nrg2, and LexA87-Sip4, when expressed from this vector, were also very low in glycerol/ethanol-grown cells (data not shown). These data exclude effects specific to the LexA87 tag, and Sip4 is unlikely to be specifically degraded under these conditions as it functions in the activation of gluconeogenic genes. Park et al. (1999) reported that LexA87-Nrg1 does not repress in cells grown in glycerol plus ethanol, but it is likely that the protein was not present because their expression vector was identical to ours.
We attempted to obtain evidence for a role of Snf1 in inhibiting repressor function by examining release from repression in wild-type and snf1 mutant cells after a shift from glucose to glycerol plus ethanol. Unfortunately, in wild-type cells the release occurred too slowly. Cells expressing LexA87-Nrg1 or LexA87-Nrg2 and containing a reporter with LexA sites only doubled their β-galactosidase activity during a 3-hr shift (repression ratios decreased to ∼7; data not shown), and protein levels were already lower by 3 hr (Figure 3C). In snf1-K84R mutant cells, LexA87-Nrg1 and LexA87-Nrg2 repressed transcription ∼15-fold during growth on glucose, and repression was not relieved during the 3-hr shift (repression ratios of ∼20; data not shown); however, protein levels remained high in the mutant cells (Figure 3C).
Nuclear localization of Nrg1: One of the mechanisms by which the Snf1 kinase regulates the function of the Mig1 repressor in response to the glucose signal is by regulating its nuclear localization (DeVitet al. 1997; DeVit and Johnston 1999). To address the possibility that the localization of Nrg1 or Nrg2 is similarly regulated, we constructed strains expressing Nrg1 or Nrg2 fused to GFP from the cognate chromosomal promoters. We did not detect significant fluorescence from Nrg2-GFP. Nrg1-GFP was localized in the nucleus when cells were grown in glucose, consistent with its function as a repressor, but also remained in the nucleus when cells were grown in glycerol plus ethanol (Figure 4). Similarly, no export of Nrg1-GFP was observed when cells were shifted from glucose to glycerol for 15 min (data not shown). Immunoblot analysis confirmed that Nrg1-GFP is a stable protein (data not shown). These findings suggest that the ability of Nrg1 to function as a repressor is not regulated by differential subcellular localization.
Nrg1 and Nrg2 fused to the VP16 activation domain activate low-level SUC2 expression in glucose: The repressor Mig1 has broad roles in glucose repression of many genes, whereas thus far, Nrg1 is known to affect only the glucoamylase genes. NRG1 and NRG2 have not been identified genetically in searches for regulators of other glucose-repressed genes; however, it is possible that their contributions to repression are modest. To test the possibility that Nrg1 and Nrg2 regulate SUC2, another glucose-repressed gene that is controlled by the Snf1 pathway, we fused the viral VP16 activation domain to both Nrg proteins. Our rationale was that the overexpressed VP16-Nrg fusion protein would compete with the native protein for binding to its sites. Similar fusions of VP16 to the repressor Mig1 activate expression of SUC2 in glucose-grown cells (Ostlinget al. 1996).
We first used a SUC2::HIS3 reporter that exhibits glucose-repressible expression of HIS3 (Tu and Carlson 1994). Transformants of strain MCY3912 (his3) bearing SUC2::HIS3 and expressing VP16-Nrg1 or VP16-Nrg2 were His+ on medium containing 2% glucose, whereas transformants expressing VP16 alone were His- (Figure 5A). All transformants were His+ on medium containing 2% sucrose. We also assayed expression of invertase activity from the chromosomal SUC2 locus in cells grown in 5% glucose. VP16-Nrg1 and VP16-Nrg2 both activated SUC2 expression about 10-fold relative to VP16 alone (Figure 5B). However, invertase activity was still about 30-fold lower than the levels typically detected in derepressed wild-type cells. Although it is possible that overexpression of the fusion proteins leads to aberrant binding, these data suggest that the native Nrg1 and Nrg2 proteins have some role in glucose repression of SUC2, which may involve either direct binding to the SUC2 promoter or an indirect mechanism. Consistent with these results, an independent study has demonstrated that an nrg1Δ mutation causes defects in glucose repression of transcription of the SUC2, GAL1, and GAL10 genes (Zhou and Winston 2001).
Mutations in NRG1 and NRG2 affect glucose repression of the DOG2 gene: To identify other Snf1-dependent genes that are targets of repression, we used DNA microarray analysis to identify genes that are upregulated in glucose-grown cells expressing VP16-Nrg1, as compared to cells expressing VP16 alone (data not shown; see materials and methods). Among the genes that were upregulated, we identified one gene, DOG2, that is known to be regulated by glucose repression and by Snf1 (Randez-Gilet al. 1995; Lutfiyyaet al. 1998; Tsujimotoet al. 2000). DOG2 encodes 2-deoxyglucose-6-phosphate phosphatase and confers resistance to 2-deoxyglucose toxicity. DOG2 is regulated by the repressors Mig1 and Mig2 in response to glucose and also by the stress response factors Msn2 and Msn4.
To explore the regulation of DOG2 by Nrg1 and Nrg2, we constructed nrg1Δ and nrg2Δ single and double mutants (see materials and methods) and introduced a plasmid bearing a DOG2 promoter fusion to lacZ, pBM3501 (Lutfiyyaet al. 1998). When transformants were grown in 2% glucose, the mutants showed a two- to threefold elevation in β-galactosidase activity (2.1-3.3 units) relative to wild type (1.1 units); values are averages for 5-15 transformants. Although the defect in glucose repression is small, Nrg1 and Nrg2 are predicted to have only a modest role. Mig1 and Mig2 are largely responsible for glucose repression of DOG2-lacZ, and the residual repression in a mig1Δ mig2Δ double mutant is only twofold (Lutfiyyaet al. 1998). The nrg1Δ and nrg2Δ mutations did not affect derepression as all strains produced similar activity (15-20 units) after a shift to 0.05% glucose for 3 hr.
Previous studies showed that derepression of DOG2 in response to glucose limitation requires the Snf1 kinase (Tsujimotoet al. 2000). To examine the relationship of Snf1 to Nrg1 and Nrg2, we assayed derepression of DOG2-lacZ in strains mutant for snf1Δ in combination with nrg1Δ or nrg2Δ or both. Transformants were grown in 2% glucose, shifted to 0.05% glucose for 3 hr, and assayed for β-galactosidase activity. Both nrg1Δ and nrg2Δ partially suppressed the snf1Δ mutant defect (Figure 6). Again the effect is small, but only partial suppression would be expected because repression by Mig1 is not relieved in a snf1Δ mutant (DeVitet al. 1997; Ostling and Ronne 1998; Treitelet al. 1998). These findings suggest that one of the roles of Snf1 in regulating the DOG2 promoter is to inhibit repression by Nrg1 and Nrg2.
We have identified Nrg2 in a two-hybrid screen for proteins that interact with the Snf1 protein kinase. Nrg2 was of particular interest because its close homolog, Nrg1, functions in glucose repression of the STA1 gene, and release from repression depends on Snf1. We here present evidence that both Nrg1 and Nrg2 interact physically with the Snf1 kinase. Both proteins interact with the catalytic domain of Snf1 in two-hybrid assays and co-immunoprecipitate with Snf1 from cell extracts.
We show that Nrg2, like Nrg1, functions as a transcriptional repressor. LexA87-Nrg2 represses transcription of a reporter containing LexA binding sites in glucose-grown cells, as previously reported for LexA87-Nrg1 (Parket al. 1999). We also examined the regulation of this repression and found that repression was not relieved by a shift from high to low (0.05%) glucose or by steady-state growth in sucrose, raffinose, or galactose. Correspondingly, glucoamylase gene expression is not derepressed by growth in these carbon sources (Pretoriuset al. 1986; Kartashevaet al. 1996). An attempt to assess repression during growth in glycerol plus ethanol, a condition allowing derepression of glucoamylase genes, was inconclusive because the fusion proteins were not expressed well.
The finding that release from repression of STA genes occurs only when the carbon source is glycerol/ethanol is at first glance puzzling because the Snf1 kinase is also active during growth on sucrose, raffinose, and galactose. A plausible explanation comes from recent evidence that the Snf1 catalytic subunit and one of the β-subunits of the kinase, Gal83, are enriched in the nucleus when cells are grown on glycerol/ethanol but not when cells are grown on a fermentable carbon source (Vincentet al. 2001). The nuclear localization of Nrg1-GFP is consistent with the idea that nuclear import of Snf1 is required for inhibition of Nrg1 repressor function.
Together, the evidence suggests that Nrg1 and Nrg2 are either direct or indirect targets of Snf1. Previous studies showed that Nrg1 mediates glucose repression of glucoamylase genes (Parket al. 1999) and that Snf1 is required for release from repression (Kuchinet al. 1993). Here we present genetic evidence that Nrg1 and Nrg2 contribute modestly to glucose repression of DOG2 and that one of the roles of the Snf1 kinase in derepression of this gene is to inhibit repression by Nrg1 and Nrg2. We further show that Nrg1 and Nrg2 interact physically with the Snf1 kinase. Although we did not detect Snf1-dependent phosphorylation of Nrg1 or Nrg2, our data do not exclude the possibility that Snf1 phosphorylates these proteins in vivo. Alternatively, other as yet unidentified components may be involved in the regulatory mechanism; for example, Snf1 may phosphorylate another protein that is bound to and affects the function of Nrg1 and Nrg2.
Repression by Nrg1 and Nrg2 may be regulated at multiple steps. However, regulation of Nrg1 function does not appear to involve nuclear export; Nrg1-GFP was localized to the nucleus whether cells were grown in glucose or glycerol plus ethanol. Some control may be exerted at the RNA level. Park et al. (1999) found that NRG1 RNA levels are 6-fold lower in glycerol/ethanol than in glucose, but it has also been reported that NRG1 RNA is induced 2.7-fold during the diauxic shift (DeRisiet al. 1997). NRG2 RNA is neither significantly induced nor repressed during the diauxic shift (DeRisiet al. 1997).
The targets and physiological roles of Nrg1 and Nrg2 are still largely unknown, and it is possible that the repressor function of Nrg1 or Nrg2 is regulated in response to other signals besides carbon source. Expression of the NRG2 gene is clearly regulated by other signals. DNA microarray analysis of genomic expression patterns showed that NRG2 RNA levels are elevated five-fold in response to zinc limitation, and NRG2 has a potential binding site for the zinc-responsive transcription factor Zap1 (Lyonset al. 2000). NRG2 RNA is also induced by alkaline pH, and induction is partially dependent on the transcription factor Rim101, which is required for expression of various alkaline response genes (Lambet al. 2001). The physiological significance of these findings remains to be clarified.
We thank Robert Townley and Olivier Vincent for help with localization studies, Tony Ferrante for assistance with microarray analysis, and Rong Jiang and Mark Johnston for plasmids. The Columbia University Microarray Project is supported by the Columbia Genome and Naomi Berrie Diabetes Centers. This work was supported by grant GM34095 from the National Institutes of Health (NIH) to M.C. V.K.V. also received support from NIH training grant T32GM08224.
Communicating editor: F. Winston
- Received January 19, 2001.
- Accepted February 26, 2001.
- Copyright © 2001 by the Genetics Society of America


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Video Conference
Video conferencing has been around for sometime, and is now gaining in popularity. The demand for a national integrated videoconferencing and streaming network infrastructure for the Higher Education in Egypt is highlighted. In the spirit of the continuous development of the services offered to the Higher Education Community and after the successful implementation of the EUN WAN Infrastructure network which connects all the Universities together and to the Internet through a high bandwidth and robust network. EUN is in the process of implementing a Video Conference and Streaming Solution for the Egyptian Universities Network and the 17 governmental Universities in addition to the Azhar University. The Video Conference System will include: Endpoints, Video Conference Infrastructure, and Streaming Solution with the Central management to be located at EUN
Among the main functions of this department is:
- Provide a Value Added Services for the Universities.
- EUN Video Conference Department will be responsible for the smooth operation and the management of the Video Conference Network for the Egyptian Universities.
- Provide end-to-end video conference facility for any planned and required conferences for the Higher Education Community.
- Provide a Video Conference facility to be an effective technological tool in Education.
- Stream/Record Video Conferences.
- Provide a Video on Demand (VoD) facilities.
- Manage the secured Video Conference Network with the main focal point to be at EUN NOC.
- Provide a tool for extensive training at the Egyptian Universities.
- Provide a cheaper way of communication between endpoints through the high bandwidth EUN IP network.


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HBO is diving into the world of comic books.
Its upcoming TV show, "Watchmen," is inspired by the 1986 graphic novel of the same name by writer Alan Moore and artist Dave Gibbons, which is considered a classic deconstruction of the superhero genre.
But if you ask the show's creator, Damon Lindelof, his series isn't so much a deconstruction because "nobody has superpowers."
READ MORE: We looked back at the long history of failed 'Watchmen' adaptations, as HBO sets an October release date for its own star-studded TV series
In his first in-depth interview for the series with Entertainment Weekly, Lindelof — who also cocreated "Lost" and HBO's "The Leftovers" — was asked how he plans to "break new ground on super anti-heroes" when other movies or TV shows like "Deadpool" and Amazon's "The Boys" have recently tackled the idea.
"I started to think that for 'Watchmen' maybe the more interesting point is to think about masking and authority and policing as an adjunct to superheroes," Lindelof told EW. "In 'Watchmen,' nobody has superpowers — the only super-powered individual is Dr. Manhattan and he's not currently on the planet."
He added, "In 'The Boys,' you have superpowered individuals in capes that can shoot lasers out of their eyes and fly around and have feats of strength and turn invisible. Nobody on 'Watchmen' can do that."
In "The Boys," a group of government operatives keep corrupt superheroes in check, from the Superman-like Homelander to the Flash-esque A-Train.
READ MORE: How 'The Boys' comic book survived cancellation and inspired Amazon's new hit superhero TV series
The "Watchmen" graphic novel follows a group of costumed vigilantes who uncover a vast conspiracy after one of their own is murdered. In Lindelof's "Watchmen" show, which takes place nearly 30 years after the events of the novel, vigilantes are outlawed and police officers wear masks.
"I felt like we wouldn't be deconstructing the superhero myth because all the characters in Watchmen are just humans who play dress up," Lindelof continued. "It would be more interesting to ask psychological questions about why do people dress up, why is hiding their identity a good idea, and there are interesting themes to explore here when your mask both hides you and shows you at the same time — because your mask is actually a reflection in yourself."
"Watchmen" premieres on HBO on October 20.


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Cerebral Aneurysms
An aneurysm occurs when a weakness in the wall of an artery leads to the swelling, or "ballooning" of that artery. It is estimated that up to 5 million Americans have cerebral aneurysms, although most do not experience any symptoms.1 Aneurysms likely occur at a higher rate in women than men, and about 20% of people who have had an aneurysm will have at least one more develop at some point in their lives.
Most brain aneurysms —up to 85%—typically occur in the anterior or front part of the brain's blood vessel system, whereas approximately 15% occur in the posterior or back section of the brain's blood vessel network. Most aneurysms occur along vessels that comprise the "circle of Willis" or the set of collateral blood vessels that link right to left and front to back.
Certain genetic conditions that lead to familial aneurysm formation include fibromuscular dysplasia and polycystic kidney disease.
Risk factors for aneurysm development include smoking, obesity and hypertension. Some people may also be born with a predisposition to experience an aneurysm, although most people develop them after the age of 40. Certain genetic conditions that lead to familial aneurysm formation include fibromuscular dysplasia and polycystic kidney disease. Aneurysms can also occur due to infections, drug abuse, or head trauma.
When aneurysms develop along the arteries in the brain, they can rupture into the fluid spaces (subarachnoid space) that surround the brain with devastating results. This subarachnoid hemorrhage may cause stroke and, ultimately, death in a high percentage of patients if not treated expeditiously at expert treatment centers. Aneurysms may also press against the nearby brain tissues or cranial nerves causing neurological symptoms or even seizures. New neurological changes due to an aneurysm can be an ominous sign that the aneurysm is suddenly expanding and may rupture causing hemorrhage. Patients with new neurological deficits due to aneurysm should receive urgent medical attention in most cases.
Warning signs
The majority of people with aneurysms do not experience warning signs that they are at risk of having aneurysmal hemorrhage. About 40% of patients with aneurysms, however, may experience the following symptoms:
- Nausea or vomiting
- Pain above and behind the eye
- Numbness or weakness
- Neck pain
- Headache confined to a specific area
- Visual difficulties
- Apeech difficulties
- Memory problems
- Seizures
When these symptoms are present, assessment procedures should include a computed tomography scan (CT) or magnetic resonance imaging (MRI). These techniques can help to identify aneurysms before they rupture. A more accurate diagnosis, however, is still typically made using catheter cerebral cerebral angiography. This involves the injection of dye into the blood vessels through a catheter or tube. These images define the anatomy and location of an aneurysm with great detail and form the basis on which treatment planning using either can be performed. Treatment using either open surgery with craniotomy and surgical clipping of the aneurysm or endovascular surgery with internal occlusion of the aneurysm can then be undertaken. There are benefits and risks to either approach and the treatment team must comprise members with expertise in both types of procedures in order to achieve optimal patient outcomes.
Descriptions of aneurysms
There are 3 different shapes of aneurysms:
- Berry – the most common type of aneurysm, these are small and shaped like a blister, balloon, sac or even a little red "berry" appearance at the time of craniotomy and direct surgical exposure. These aneurysms most often arise at a blood vessel branch point or bifurcation where a relatively weak point is subject to high stress factors from the flowing blood.
- Fusiform – this type of aneurysm is elongated and shaped like a spindle. I often liken the appearance to a snake that swallowed a rat. Rather than a balloon or bulge from one side of the blood vessel wall, the entire circumference of the blood vessel has become involved in the formation of a fusiform aneurysm.
- Dissecting – this type of aneurysm occurs when blood passes through a tear in the inner layer of the blood vessel wall that causes the wall to split weakening its ability to contain the flow of blood. The result can be aneurysmal dilatation of the blood vessel, narrowing of the main flow channel for blood to reach the brain causing stroke, or even rupture through the weakened blood vessel wall causing subarachnoid hemorrhage.
Aneurysms are further characterized by size. A small aneurysm is considered to be less than 7-10 millimeters. An aneurysm between 10 and 25 millimeters is classified as large, and a giant aneurysm is greater than 25 millimeters.
Rupture of aneurysms
The rupture of aneurysms, also known as aneurysmal bleed or subarachnoid hemorrhage (SAH), is believed to occur at a rate of 1-2% per year and the risk is cumulative over time. The hemorrhage rate is the subject of ongoing debate based upon the available epidemiological data, but most physicians still agree on this range for hemorrhage risk. Various factors influence whether an aneurysm is at risk of rupture, including its size, type, location, and previous history of rupture. Common warning signs of a subarachnoid bleed include an extremely painful headache, drowsiness, and nausea or vomiting. We do not yet fully understand what causes aneurysms to form, grow, and rupture. Conditions over which we have control in an effort to prevent aneurysmal hemorrhage include strict control of high blood pressure and strict abstinence from all tobacco use or exposure.
When a rupture of a brain aneurysm does occur, the blood typically seeps into the fluid space closely surrounding the brain called the subarachnoid space. The subarachnoid space is filled with cerebrospinal fluid and is mostly one continuous area although filamentous bands of fibrous tissue may compartmentalize certain parts of the subarachnoid space and limit flow from one part to another. Blood may also travel directly into the brain substance, although this is less common. In more severe hemorrhages, blood may back up into the ventricles or caverns deep within the brain where the spinal fluid is originally produced.
It cannot be overstated that the rupture of a brain aneurysm is a true medical emergency and warrants immediate medical attention; it is estimated that 25% of patients with this condition will die before arrival in the emergency room, and that 45% of patients will die within 30 days of the bleed.2 Furthermore, once an aneurysm has ruptured, it is at greater risk for additional bleeding in the first minutes, to hours, and days following the initial hemorrhage. In hindsight, some patients who experience subarachnoid hemorrhage will recall a back headache days to weeks before the big hemorrhage. This is often referred to as a "sentinel" headache and is thought to represent an early small hemorrhage that went unrecognized.
A CT scan can usually diagnosis bleeding in the brain and subarachnoid area. If necessary, a lumbar puncture, commonly referred to as a spinal tap, may also be conducted to examine if blood is present in fluid around the brain. In this procedure, a thin needle is inserted into the lower part of the spinal column to obtain a small fluid specimen to examine for evidence of bleeding not apparent on the CT scan. Lumbar puncture is required in the vast minority of patients who have experienced acute subarachnoid hemorrhage.
Treatment of aneurysm
In the past, treatment of brain aneurysm has entailed a surgical procedure.. First, a small opening in the skull called a craniotomy is made so that the surgeon can dissect away the tissues surrounding the aneurysm and apply a clip to the aneurysm. A clip looks somewhat like a tiny clothes pin that pinches the walls of the blood vessel together at the base of the aneurysm and prevents flowing blood from access to the aneurysm. If the flowing blood cannot get into the aneurysm, then it also cannot leak out. Although this procedure can be effective, it is invasive, requiring exposure and retraction of the brain. Newer methods of treating aneurysm are always in development. One relatively newer method of treatment is known as endovascular embolization or occlusion of the aneurysm from within the blood vessel. In the same way that the surgical clip pinches closed an aneurysm preventing flowing blood from access to the aneurysm, tiny platinum coils can be placed into the aneurysm that also prevent flowing blood from access to the aneurysm and allow aneurysm healing.
Endovascular aneurysm treatment from start to finish
Prior to undergoing an endovascular surgery, patients are expected to sign a consent form and will have the opportunity to have any questions answered. The anesthesiologist will administer medications and fluids through the use of an intravenous line (IV) into a vein in the hand or arm. Usually, endovascular procedures are also performed under general anesthesia not so much for pain control but rather so that the patient will be completely still for the entire procedure. Aneurysms are very small and measured in millimeters. The treatment coils are also small, delicate, and measured in millimeters. Precision is very important for the success of the endovascular procedure, and general anesthesia facilitates this success. Otherwise, the procedure is essentially painless.
Blood pressure can be monitored through the catheters used to perform the aneurysm treatment. An electrocardiogram (EKG) will monitor heart rate and rhythm and a pulse oxymeter monitors oxygen levels. A specific type of catheter known as a Foley catheter will be placed through the urethra into the bladder to allow urine to drain. Anesthesiologists often monitor urine output as a simple indicator that the body's major systems are functioning well.
Very simply, endovascular treatment of a cerebral aneurysm is an extension of the diagnostic arteriogram used to diagnose the aneurysm. Special training is required to perform this type of treatment procedures, however. For the diagnostic arteriogram, the catheter is passed into the arteries that lead to the brain, but the catheter is usually positioned within the blood vessel around the level of the collar bones or voice box. The x-ray contrast material is injected through the catheter into the blood vessels in the neck, and x-ray images are obtained over the head as blood flows through brain arteries.
Endovascular treatment requires passage of a tiny, "hair-like" catheter through a supporting catheter positioned within the blood vessels in the neck. The tiny catheter is then navigated through the brain blood vessels on high resolution "road-map" images. These images obtained from two different directions allow the physician to monitor the progress of the catheter toward the aneurysm and control its ever movement. Finally, the tiny catheter is positioned in the orifice or hole leading into the aneurysm.
Again, under high resolution road-map imaging, the physician carefully passes delicate detachable platinum-base coils into the aneurysm. For a number of years, there was only one type and one vendor of cerebral aneurysm coils: Guglielmi Detachable Coils (GDC) by Target Therapeutics, Inc. Now, there are an increasing variety of coils with unique properties suited to aneurysm treatment. Each coil is carefully sized to the specific aneurysm under treatment based upon three-dimensional computer reconstructions of the aneurysm. Once placed into the aneurysm, each coil is carefully detached from its delivery device, and the aneurysm is progressively filled with a succession of smaller coils until it is completely occluded. When the coils are inserted, the aneurysm becomes tightly packed to prevent blood from flowing into it, with the ultimate goal of preventing the aneurysm from rupturing. The newest coils approved by the FDA for aneurysm treatment even appear to promote aneurysm healing for durable and long-lasting results.
Some aneurysms have relatively wide apertures or holes leading into the aneurysm. These present a challenge to coil placement because it can be difficult to place the coils within the aneurysm without blocking the blood vessel from which the aneurysm arises. To facilitate endovascular treatment of these aneurysms, adjunctive tools and techniques have been developed. In some cases, a small balloon is used to create a temporary buttress to help hold the coils in the aneurysm during their deployment. In these cases, the coils develop a stable configuration that does not require any further support following occlusion of the aneurysm. In a small number of cases, the aneurysm orifice is too broad even for balloon remodeling. In these cases, the FDA approved a specialize brain stent that allows placement of a tiny stent in the brain artery that acts as a permanent scaffolding to hold the artery open while the aneurysm is occlude with coils outside the confines of the stent.
Once the procedure is complete, the patient will be transferred from the operating room to either the Neurological Intensive Care Unit (NICU) or the Post-Anesthesia Care Unit (PACU). In the intensive care setting, patients are carefully monitored for any neurological changes that might require urgent medical attention. For patients who underwent treatment of a ruptured aneurysm, their stay in the NICU often lasts for up to two weeks as they recover from their hemorrhage. For patients who undergo treatment of an unruptured or incidental aneurysm, the hospitalization is often as short as one day. Some patients can even be discharged home right from the intensive care unit on the morning after endovascular surgery.
Follow-up procedures may include an x-ray, MRI, or angiogram to assess the effectiveness of the procedure. Although there is no absolute concensus, arteriographic surveillance is usually performed for two main reasons. 1.) Surveillance arteriography allows the treating physician to confirm durable occlusion of the aneurysm or plan further treatment if necessary. Over time in a small minority of aneurysms, the coil mass can compact itself so that a portion of the aneurysm reopens. A brain aneurysm is a very delicate structure and so are the coils used to occlude the aneurysm. The treating physician can only push so many coils into an aneurysm before the risk of rupturing the aneurysm increases dramatically. After treatment, however, continuous blood flow and beating of the heart and pack or compress the coils into a smaller bundle than at the time of the original treatment procedure. In these cases additional coils can be added to refill the aneurysm. If retreatment is required, a few extra coils is all that is necessary to permanently block the aneurysm. The newest coils that promote aneurysm healing are meant to preclude this problem by encouraging scar formation in the aneurysm and permanently sealing off the aneurysm orifice or hole. 2.) We have said that up to 20% of patients will develop a second or multiple aneurysms during the course of their lives. This is another way of saying that whatever conditions caused the development of an aneurysm at one location, these same conditions exist at many other branch points in the blood vessel network. Surveillance arteriography also allows the treating physician to evaluate for development of other aneurysms that could pose a risk to the patient and may require treatment or periodic observation. Medication may also be prescribed in the form of aspirin or other blood thinner after treatment.
Once at home, certain activities such as heavy lifting and driving must be avoided until the physician provides approval. Most patients, however, can begin resuming normal activity after a relatively brief period.
Although the GDC method was once only used to treat high-risk aneurysms only, its high success rate has led to its recent approval for use in treating all types of brain aneurysms. It is also linked to a reduction in the incidence of future episodes of bleeding.3 Age is believed to be a factor that influences the outcome of treatment. The younger the patient, the more likely surgical treatment is to be successful.2 Smaller aneurysms are also associated with better outcomes. If aneurysmal bleeding has occurred, recovery is most closely tied to the degree of injury caused by the hemorrhage or any further bleeding episodes.
The International Subarachnoid Aneurysm Trial (ISAT) was a multinational study comparing surgical clipping with endovascular aneurysm occlusion in patients with subarachnoid hemorrhage. In summary, ISAT found that patients who underwent endovascular treatment of their aneurysms recovered far better (up to 25% better in the first year) than patients who underwent surgical clipping of comparable aneurysms. In fact, the safety monitoring committee prematurely terminated the study because the primary endpoint (neurological outcome) was reached before the required number of patients were enrolled in the study.4 As time continues since the end of the difference in outcomes between the surgical and endovascular groups continues to increase. Similar differences have been suggested by other smaller trials for both ruptured and unruptured aneurysms. This is not to say that all aneurysms should be or can be treated by endovascular methods. The decision to treat an aneurysm and the method by which treatment will be performed requires the recommendation of neurosurgeons skilled at skull base and cerebrovascular surgery and endovascular surgeons skilled at endovascular procedures performed under x-ray fluoroscopic guidance.


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Robert O'Dowd's article was entirely appropriate for a journal devoted to "clandestine activities"
by Jim Fetzer
Inside a closed Walmart in California Something is wrong right here at Veterans Today. A former Marine, who has published many articles here, was slammed by Gordon Duff and by Jim Dean for perpetrating "a hoax" by raising concerns about this mysterious "training op" called JADE HELM. I admire VT and like Gordon personally, although from time to time we have a divergence in our point of view. I have never felt as positive about Jim Dean because, as an old-time reporter and editor, he has come across to me as having an anti-academic prejudice, which I as a former professor have sensed from our initial encounters.
But that doesn't mean he's wrong. Robert O'Dowd But let's consider the case of this article and its author, Robert O'Dowd. Although I had not read any of his work at VT before, I thought it was raising a perfectly appropriate issue as to whether or not JADE HELM, which is an operation that covers at least seven states (and now seems to have expanded to five or six more) could possibly be the cover for imposing martial law under the pretext of conducting operations in urban settings, which are meant to train personnel "for foreign operations", where nothing about this has struck me as right from the beginning. As a consequence, I was glad to see he had published about it: O'Dowd's article with Editor's Note
But I could hardly believe the response from Gordon and Jim. Not only did they "tag team" Robert and imply that he had been played for a sap but asserted that, "We have checked our sources who would be in a position to know if something like this were going on, and it categorically is not." The problem with this approach is that we ordinary readers are not in the position to verify "their sources". This is a classic appeal to authority, where we are supposed to take their word for it. And while I might be disposed to accept those assurances on routine matters, in this instance, the case of JADE HELM is anything but "routine".
Jim Dean piles onIt further astonished me that Jim Dean would reiterate his and Gordon's position in both the facebook and ordinary comments sections on O'Dowd's article, which you can easily confirm for yourself. This left some readers, such as Bonny Amey, at a loss as to exactly what was going on. And, indeed, others expressed concern, even in the ordinary comments section, where O'Dowd (in my view, with complete justification) submitted his resignation as a journalist for VT on facebook, explaining that he did not appreciate being used as a whipping boy for having published "a bogus story", especially when the facts are still in doubt:
If Gordon had not looked into the situation "deeply enough", however, then it makes no sense for him to have attacked Robert's article and assailed him as a dupe who was pushing "a bogus story". I was troubled enough by all of this that I brought together a group of four guests, including Terri from Nebraska (who had sent me many links), Robert O'Dowd himself (as the one who had raised this issue on VT), Preston James (whom I regard as one of the most astute intellects I have ever known), and last but not least (as a late arrival), Dennis Cimino (with whom I have co-authored multiple articles here) to try to sort all this out:
While I think we made progress in sorting this out, none of our considerations supported the idea that this was "a bogus story" and that no one should be concerned. It came as news to me when my producer, Chance, observed that a parallel operation is taking place in Canada under the name of "Maple Resolve", which includes closing some 133 Target Stores, not merely for the two months the operation is officially supposed to run but for nine months at the cost of some 17,000 jobs, where their former employees are even being encouraged to find other lines of work. In my opinion, this alters the equation and leaves no doubt:
What conclusion should we draw?
Several features of "the big picture" strike me as enormously important. Walmart and Target are stores with mass appeal for the middle and lower class of both Canadian and American society. That some 15 Walmarts should be taken over in the United States alone and now another 133 Targets in Canada is alarming! There is nothing "bogus" about this story. And other sources, such as David Hodges' "Common Sense Show" have made equally telling observations about the redistribution of resources for a purported "training op" when it entails the dismissal of 17,000 employees, who no doubt are being left in desperate straits:
So what conclusions do I draw from my investigations to this date? Gordon Duff and Jim Dean were wrong to censor Robert O'Dowd, whose article was entirely appropriate for a journal devoted to "clandestine activities". JADE DOWD is not a "training op" but something far more serious. When you calculate the profits per store to Walmart and to Target, they are taking an enormous hit, which can only be for some transcendent purpose that override "the conduct of business as usual". (We are talking about billions of dollars in lost profits, not to mention the loss of highly qualified, experienced personnel to stock products, to resupply those facilities and to process check outs and deliveries.) As an investigative journalist for Veterans Today, I am committed to doing my best to expose the truth, even when it conflicts with the views of Gordon Duff and Jim Dean, who are at liberty to deal with me as severely as they dealt with Robert O'Dowd. I am committed to serve my nation and its best interests, which I do, come what may.


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Bayleys news & articles
Tags: Commercial
Augusta Funds Management Ltd is breaking new ground with its latest syndication of Mercury's new head office building in Newmarket while it is still under construction.
Augusta Funds Management Ltd is breaking new ground with its latest syndication of Mercury's new head office building in Newmarket while it is still under construction. "This signals a key strategic step for Augusta as we move from not just being a buyer of quality completed buildings but into the funding and development of those assets as well," says Augusta managing director Mark Francis.
The NZX listed company has unconditionally agreed to purchase the 3,090 sq m site at 33 Broadway on which the two-building complex is being developed by Mansons Broadway Ltd for $141,611,878.
Augusta Funds Management Ltd is to raise $83.5 million of investors' equity to facilitate the acquisition through the offering of 1670 $50,000 interests in the 33 Broadway Trust that will own the property. Mike Houlker, Samara Phillips and Sarah Prebble, of Bayleys Investment Products and Syndications division, are the sole selling agents for the offering.
The trust is forecast to provide investors with an initial forecast 7% pre-tax return until March 2020, paid from settlement of the sale which will occur when earthworks and piling have been completed - expected to be by the end of June 2017. Earthworks began last September on the development which is scheduled for completion by the end of 2018 with tenants moving in in the first quarter of 2019.
Mike Houlker says during this development phase Mansons Broadway Ltd will pay interest on investors' equity as well as covering the trust's bank interest costs. "The developer will effectively fund initial investor returns until building completion when the rental income from the property's long-term tenancies will kick in. All of the leases will have built in rental growth of three per cent per annum."
The property will have 13,103 sq m of net lettable space over six levels located in two adjoining buildings (east and west) separated by a large enclosed central atrium. The majority Government owned energy company Mercury NZ Ltd, also listed on the New Zealand and Australian stock exchanges, intends to consolidate its four Auckland offices into the 5-Green star complex over which it has naming rights.
It will occupy level 2 of the east building and levels 3, 4 and 5 of both the west and east buildings, encompassing a net rentable area of 7845 sq m, on a 12-year lease with two six-year rights of renewal.
The other office tenant so far signed is New Zealand's largest poultry producer Tegel Foods Limited which will lease Level 1 of the east and west buildings encompassing 2,283 sq m of office space on a 10-year lease.
Houlker says these two tenants will occupy 77 per cent of the property's lettable area. Mansons Broadway will provide a nine-year rental underwrite, backed by a bank bond, on any space that remains unleased at practical completion of the development. Both Mercury and Tegel have options to lease further space prior to completion.
"If completion of the development is not achieved by certain dates, Mercury and Tegel do have the option to cancel their leases," says Houlker. "However, in this case, Mansons Broadway will underwrite that additional vacant space also. The current progress of development will see the likely start date of leases as February 2019, providing a buffer which is currently 12 months before the cancellation options can be actioned."
Samara Phillips says the complex is being benchmarked to Mansons' mostly recently completed office complex, the BDO Centre in central Auckland which won the Supreme Award for the best new development in the Property Council New Zealand Rider Levett Bucknall Property Industry Awards for 2016.
Phillips says Mansons are obligated to design and complete the complex so that it has 5 Green Star 'Design' and 'Built' ratings, with this being one of a number of conditions required to be satisfied for release of a final retention payment to the developer. She says Mansons have built more certified green star buildings than any other developer in New Zealand. The family business was founded in the 1970s with developments totalling $1.16 billion completed since 1999.
Houlker says Mansons will at its own cost, carry out a subdivision of 33 Broadway to enable separate titles to be issued for each building (east and west) with an associated proportionate share in the common areas such as the atrium. This will provide future liquidity options to sell one of the titles.
Mark Francis says Augusta recognises the investment offering is different from previous syndications in that it involves a property that is under development rather than already built and occupied.
"We are conservative in our approach and committed to only offering high quality properties to our investors. With assets of this calibre difficult to find in the current market, our business model has evolved to be a part of the creation of these assets as well.
"The development agreement between Augusta and Mansons has been set up to mitigate risk to investors. It contains guarantees from Mansons' Equity Limited, along with structured retentions and buy back clauses. Mansons also stands behind its work and provides a 10-year expenditure and defects warranty which means it will generally be responsible for repairing any building defects."
Augusta Funds Management is a wholly-owned subsidiary of NZX listed Augusta Capital Limited and has in excess of NZ$1.6 billion of assets under management on behalf of more than 4000 investors, encompassing over 150 commercial and industrial premises in New Zealand and Australia.
Applications for one or more of the $50,000 units in the 33 Broadway Trust can only be made via a Product Disclosure Statement available from Bayleys or by visiting the website www.33broadway.co.nz. Details on how the forecast pre-tax return is calculated and the risks associated with the investment can also be found in the Product Disclosure Statement.
Related articles


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Michael Jackson has invented a new soft drink: wine-flavored Coke. According to an article in the March Vanity Fair, the newly crowned King of Soda Pop routinely drinks wine out of Coke cans so nobody knows he's drinking. The mag also says Jackson gave the young boy he's accused of molesting wine in Coke cans on a flight from Florida in February 2003. No comment from Jacko's camp.
(Disclosure: TV Guide is owned by CBS Interactive, a division of ViacomCBS.)


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Nigerian actress Dorcas Shola Fapson has revealed that the Taxify driver she accused of abducting and attempting to rape her has been arrested.
The actress disclosed this on her Instagram page after weeks of decorum on the case which brought her to the spotlight.
She wrote: "I remain a Fighter. Not a crier. I'd like to thank everyone that's supported me, publicly and privately during this difficult time.. We can leave the social media war now & let the law take its rightful course.
Peace & love,"
In January 2018, Fapson took to her Snapchat page to recount how she nearly got raped by a Taxify driver, identified as Henry Nnaemeka .
When the driver stated his own side of the story, fans were divided on who to believe.
While some took to supporting the actress, others used her video evidences against her.
Henry through his solicitors filed a
lawsuit against the actress, with a ransom of N5 million.
On Tuesday, February 20, the actress shared a photo on Instagram, revealing that the driver had been on the run.
UBA Launches New Online Entertainment Platform, 'RED Radio', Opening With Exclusive Wizkid Interview
Pan- African financial institution, United Bank for Africa, (UBA Plc), continues to lead in innovation with the launch of its dynamic and creative Online Radio channel – RED Radio.
RED Radio, powered by UBA is a lifestyle web platform that has been set up to inform, educate, entertain, and to bring to the fore, the best of Africa. Much like its sister platform, REDTV, RED Radio is expected to showcase the best in lifestyle, entertainment, music, news, comedy, and fashion.
Speaking on the launch of RED Radio, Group Chairman of UBA, Tony O. Elumelu applauded the creative initiative, emphasizing that UBA is a financial institution always ready to support creativity and entrepreneurship. The 2020 Time 100 most influential person in the world who has committed USD100 million to empower young entrepreneurs across Africa said about RED Radio, "Creativity and innovation are a powerful combination and every detail in an art piece is important and meaningful. This applies to growing businesses and budding entrepreneurs. You will encounter challenges like I did, but each experience is a lesson that brings you closer to your goal. That is the beauty of creativity."
Continuing, Elumelu remarked, "There are many ways to make something beautiful, to make a sound interesting, or to bring a story to life. You can define your expression, and today, as UBA's RED Radio launches, I wish Bola Atta and her enterprising team many successes through this beautiful medium of expression."
In appreciation of the support of UBA Group Chairman for the exciting creative initiative, UBA's Group Head, Corporate Communications, Bola Atta, said 'just like, REDTV which is Africa's leading online entertainment network, RED Radio is positioned to fast become the foremost online radio platform in Africa'.
Also expressing his delight, UBA's Brand Ambassador and star boy, Wizkid, said, "I am never too busy for my UBA family as he granted an exclusive interview on one of the station's flagship shows 'On the Street' where he spoke extensively about his upcoming album and what his fans should expect from him in the coming weeks.
RED Radio promises to bring rich and engaging content that will keep its audience coming back constantly for vibrant and robust entertainment. Listeners can tune in to www.itsredio.com 24/7.
Omotola Jalade-Ekeinde In A Happy Mood As She, Children Recover From COVID-19
Prominent Nollywood actress, Omotola Jalade-Ekeinde, is excited about her recovery and those of her children from COVID-19.
A few weeks ago, the actress revealed that she contracted coronavirus and infected her children.
However, the actress took to her Instagram page on Sunday to express her joy as she and her children are now COVID-19 free.
She wrote: "I am grateful to God Almighty the Lord of lords for all He has done for my family and I. He is truly a dependable Friend if you trust in Him.
"I'll also like to thank you all for your love, prayers, calls, messages, posts, and thoughts. All truly appreciated.
"My kids and I are fine and COVID free now, and I do not take the experience for granted at all.
"If you still don't believe that this virus is real, I pray you don't experience it to believe.
"If you ever feel ill during this pandemic, pls know there's nothing to fear or be ashamed of…you're not alone.
"Pls get TESTED immediately, it could save your life. Many have had COVID and treated it as fever, malaria, etc and luckily they've been fine….( note that symptoms are different and viral loads vary). However, a problem with that is they have probably gone on to infect others since they were not monitored or guided. The average span for a COVID infection if not severe is 2 weeks (14 days ) when you should totally isolate so as not to infect others.
"Make sure to use vitamins – VitC (1000ml), vitamin D, and Zinc daily, and please WEAR A MASK. Please maintain physical distancing, wear a mask properly, and wash your hands regularly.
"I'll also like to thank the amazing lead Dr who treated me Dr Folarin Opawoye; and finally, my husband whose Love and Faith nursed us back to health. To God Alone be all the Glory. Thank you all."
Afro-Heritage Broadcasting And Entertainment Awards (AHBEA) Felicitates With Oba Yisa Olusola Adeniyi Olaniyan
The executive committee of Afro-Heritage Broadcasting And Entertainment Awards …. (AHBEA) wishes to congratulate and felicitate with its executive producer, Mr Yisa Sola Olaniyan, – who is also the executive director of afro heritage entertainment promotions, a USA based entertainment company – on his enthronement as the 46th Oba of Ipokia Kingdom in Ogun State.
Oba Yisa Sola Olaniyan's fervent belief in the promotion of African arts and culture to the rest of the world gave birth to the idea of AHBEA. His unflinching support and logistics have sustained and maintained AHBEA's consistency for five uninterrupted years even in the face of so many financial constraints.
Many times, we had thought of canceling AHBEA because of finances but he muscles his way to coughing out funds just to make each year a success.
We, undoubtedly, believe that where he is today is Olodumare's doing. Your love for people, irrespective of background, race or colour, most especially the people of Ipokia kingdom has eventually paid off.
May your reign usher in more progress in human and material form for Ipokia. May your years be long on the throne of your forefathers. May Olodumare and the ancestors continue to guard and guide you to the right path, Kabiyesi.
Yomi Fash-Lanso
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For many people, Impressionism is about as Modern a school of art as they can stand, even though at the time it first appeared in the later half of the 19th century it was a wildly controversial style. Today, it's hard to see what all of the fuss was about, living as we do in a deeply silly, stupid time, in which art critics debate over whether someone's appearance on a television show is, in fact, a work of art. Fortunately however, there are always interesting news stories from the art world involving the Impressionists, and so we turn to them for this week's art news roundup.
Missing Monet
After many years, there's a happy ending to a minor, but interesting art mystery. Like many of the Impressionists, Claude Monet (1840-1926) was fascinated by and collected Japanese art and decorative objects. During Monet's lifetime a small, Japanese ceramic cat sat on a pillow in the dining room at the artist's famous country house in Giverny, but after his death it passed into the collection of his younger son, Michel. Unknown to almost everyone, Michel had a daughter by his mistress, and when he died he left dozens of works of art and Monet family items to his daughter. When she herself died in 2008 her existence became known, and her descendants decided to sell off many of the Monet items, including the cat. It was bought at auction by a Japanese art dealer last fall, who has now returned the sleeping kitty to the Monet Foundation, which has put it back on its cushion in the dining room at Giverny.
Recovered Renoir
The stylish Italian Carabinieri, well-known for press conferences in which they pose stoically before looted or stolen antiquities and works of art that they have recovered, now have a major new feather in their cap. "Girls on the Lawn" by French Impressionist Pierre-Auguste Renoir (1841-1919) and "The Holy Family" by Dutch Old Master Peter Paul Rubens (1577-1640) were stolen by a gang of conmen in the city of Monza, who duped the gallery that owned the paintings into turning them over via an elaborate ruse. The works were recovered as part of a sting organized by the Carabinieri's Cultural Heritage Protection Unit, which to me sounds like a great subject for the next iteration of Law and Order, should Dick Wolf ever decide to come out of retirement. The paintings are currently being examined by experts for any damage and to verify that they are, indeed, the stolen works, before the local prosecutor gets to work on the case against the eight people who have been rounded up and charged with the crime.
Rediscovering Russell
If you've ever heard of Australian Impressionist John Peter Russell (1858-1930) before today, then you're one up on me, and probably a lot of other people as well: fortunately, now his home town is doing something to change that. Russell studied in London and Paris in the 1880's, and spent a great deal of time living and working in France, where he was both a popular, well-liked figure, and friendly with Matisse, Monet, Renoir, Rodin, Toulouse-Lautrec, etc. He was happily married to an Italian model who had posed for Rodin, and they had many children together. When she died in 1908 he became heartbroken, and destroyed over 400 of his own paintings, which may be one reason he is not as well-known as he might otherwise have been. He eventually returned home to Australia and died there, forgotten and ignored.
If you happen to find yourself in Sydney over the next few months then, I highly recommend that you check out a major retrospective of his work at the Art Gallery of New South Wales, which opened this week and runs through November 11th. As lovely as his landscapes are, to me the most striking work of Russell's that I've seen to date is the magnificent portrait he painted in 1886 of his friend and contemporary, Vincent Van Gogh (1853-1890), which is on loan to the exhibition from the Van Gogh Museum in Amsterdam. With great sensitivity, Russell captures the haunted, hunted spirit of his friend in a way that differs from, and yet clearly relates to, Van Gogh's own self-portraits.


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Har Shakh Pe Ullu Baitha Hai 24th April 2018 Written Episode, Written Update on TellyUpdates.com
The Episode starts with Dolly coming home to deliver the clothes. She slaps the party man and taunts him. She goes. Chaitu complains about the dirty water of the tanker supply. He couldn't bath by it. Imli jokes on him. Chaitu asks them to get mineral water for his bath, he has to stay healthy so that govt stays healthy. People run in queue to get water. Janta says I m first, stop.
Janta stops the tanker and argues with the man for taking the tanker to minister's house instead public. They beat the tanker driver and loot the water. Janta hides in the chaos. Khoji gives the news of people looting the tanker. Chaitu arranges mineral water for bath. Everyone gets ready to have bath with mineral water. Malai says I m dry cleaned and came. Jha asks Chaitu to hurry up, he has to
give buckets to everyone. Khoji shows the miracle as some taps got water today.
Janta gives the news byte to Khoji. He tells how he found a tap flowing down water. He says we forgot to fill water in excitement. Khoji says I heard CM is coming to give a bucket of water to everyone. Janta says we are waiting for him. Genda says its all a plan of Chaitu. Uncle asks her to collect all the water in a storage, they will attend Chaitu's rally and get all the buckets. Genda says then public won't get anything. Chaitu comes for the rally. Genda and her uncle join the rally in disguise. Chaitu acts great and donates a bucket to everyone. The people get shocked that the bucket is empty, it doesn't have any water. Jha asks them to collect the buckets. Genda says this is cheat. Janta asks where is water. Chaitu says I fulfilled my promise and got the water buckets. Genda argues with Chaitu. They call Chaitu liar.
Chaitu manages to leave from there. Khoji says CM showed the opposition a thumb. Chaitu comes home and says I had to flee for my life, public has turned into goons. Monica asks Chaitu to deliver some water to people. Chaitu calls Pahelwan home and asks him to end the tanker strike. He asks him to deliver water to the people. Tanker driver refuses as the public beats badly. Chaitu says go and sell water, higher the rate. Pahelwan says provide security for tankers. Jha asks how can Chaitu do this. Chaitu says provide security to them, people shouldn't die by water thirst. Khoji says no one can rob tankers now, the tankers have security now, tankers will loot people now.
Genda says Chaitu has ended the strike. Uncle says its hard to tell who has hurt whom in riots, we will instigate the public against Chaitu. Janta says we are already angry, our wives have troubled us a lot. He cries his miseries. Tanker comes to the locality. The driver sells the water. He asks them to come one by one. Janta says water is our right, we will take it for free. Public gets the sticks and beats tanker driver and police. Chaitu gets gifts for the kids. He tells them that they are getting 700 crores, he has made all arrangements, they will get gifts, Imli will own a house in London, Bahumath twill get an imported car. Everyone claps. Khoji tells about the people dying by the water scarcity.
Rajneeti says I m a good singer. She takes music classes. She sings so bad.
Update Credit to: Amena


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I've been going to Kinabalu National Park a lot ever since my transfer. I was aiming to get a glimpse of the Green Magpie. However, my attention quickly turned to the Eyebrowed Jungle-Flycatcher when I was introduced to it by my friends...sigh
For some unknown reason, I became obsessed with it. When compared to the other birds in the park, the Jungle Flycatcher is just one unattractive brown bird with a huge prominent eyebrow!
I'm lucky that I finally got a reasonably good shot of it as you can see in my previous post. I was so relieved to finally have the opportunity to get on with my life!
Moreover, to be able to record these shots;-
Never get tired of the Indigos...This time, with a totally different perspective.
Personally, this image must have a good title to complement the photo. Unfortunately, nothing came across my mind...
A great opportunity came merely seconds after this shot. A better angle...when a tourist came and approached me to ask some questions... I responded accordingly and eventually lose the chance! But never mind, I'll get them next time...
An endemic with a meal. If it had gotten closer, I would have been cursed by my gang...
A black beauty...my next assignment.
The Yellow-Breasted Warbler is a tiny and hyper-active bird! I am thrilled to have captured these shots. At frame filling size, I could not ask for more...I love it! hehehe forgive me!
Anyway, as I said-the Thrush is my next goal... Stay tuned and find out if I could reach my goal. (Wish me luck!)


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Get Involved
Nothing about us without us!
This was the theme of the United Nations Assembly to ratify the Convention on the Rights of People with Disability. IAT works on the same principle – we are run by, and for, people with disability. This ensures that the agency is driven by people with a lived experience of disability and how societal values around disability impact on people's lives. We are therefore able to remain relevant and focussed.
Organisations like IAT can only survive with the involvement of community. We know there are many people with skills and experience that would be an asset to our organisation.
Ambassadors for Independent Advocacy in the Tropics Inc.
Richard Cordukes, Inaugral Ambassador
Qualifications: Ambassador and Life Member of Wheelchair Sports NSW; World Record Holding Paralympian; volunteer member of a number of local community groups and Qld Sporting Wheelies
Richard's 40yrs of Self-Advocacy experience commenced in 1976 when he became a quadriplegic.
The following year he took up wheelchair sports. His first representative experience was in 1979 when he was selected as a member of the NSW Team to compete at the National Wheelchair Games in Perth.
Richard then went on to compete in the Stoke Mandeville Games in the UK on 4 occasions 1981, 1983, 1985 and 1987. These were the unofficial World Championships at the time. As well Richard competed in a FESPIC Games in Hong Kong in 1982 and the Paralympic Games in Seoul in 1988.
In January 1986 at the Australian National Wheelchair Games in Adelaide, Richard set a World Record for his classification in the 100m. He broke his World Record in Melbourne later that year. Richard held this record until the Seoul Paralympics.
Another significant achievement for Richard was the introduction of Wheelchair Rugby to Australia. This came about after playing in the very first Wheelchair Rugby competition in Stoke Mandeville in 1981.
Richard served on the Board of Wheelchair Sports NSW for a total of 23 years and he was President in 1989 when the Board approved the first Oz Day 10K race. He competed in this event and made a return 10 years later in 1999 and again 10 years after that in 2009.


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Let's see what I got for you all Today! Designer Showcase, Evil Bunny's Productions TWE12VE, SWANK, and eBento! Be aware, these are all Monthly Events, and are all ending by the end of this week, or the 31st! If you want to get the Exclusive discounts from these Events, get there this Week!
Those are the Events I am previewing, how about the Designers? My Designers for Today are 1 Hundred, Grumble, Glitter Poses, Truth, 7 Deadly s{K}ins, Bodycult Tattoo, Eclectica, Avada, .lovelysweet., *KATE* and StunnerOriginals! Original Blog Post .:HERE:.


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I finished the game (getting Yveltal and beating Elite4), but I went to places where mega scizor and mega garchomp stones, but they are not there. Anyone help?
Did you beat your rival in Kiloude city yet? If you haven't, that's why. After you beat your rival, they will give you a mega stone and tell you to go to anistar city. When you get there, you should see professor sycamore. After you talk to him, every day at 8-9 pm the giant crystal in anistar city will give off a light, enabling you to get the rest of the mega stones. The light will die down after 9pm. The mega stones look like little stars on the ground, instead of regular pokeballs.
Hope I helped!
Source: Experience
Have you upgraded your Mega Ring yet? If you haven't, that's the reason.
To upgrade your Mega Ring you need to need to get to Kiloude City (If you don't know how to get there look here.) You then need to battle your rival. (Serena/Calem) Once you battle your rival, go to Anistar City and talk to Prof. Sycamore. He should upgrade your Mega Ring, which allows you to get the Mega Stones. Also note that it has to be between the times 20:00 (8:00 PM) and 21:00 (9:00 PM).
Hope this helps!


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1.9 Chinese 14k Yellow Gold Green & White Jadeite Jade Pendant With Crane Birds
Chinese 14K Yellow Gold Green & White JADEITE Jade Pendant w/ Crane Birds. Out of a Local Estate.
This is a Carved Opaque Mottled Green & White Jadeite Double Sided Pendant. This color of Jadeite is called " Moss in Snow ". Depicting a Flying Crane Bird on & Sun or Moon among Ruyi Shaped Clouds. Mounted in 14K Yellow Gold (not marked but tested).
Total weight of 21 grams. Total length of 1.9 Jadeite only approx. 1.7" (43mm) long x 1.425" (37mm) wide x. Good overall condition with minor wear & dirt. I do not know what grade of Jadeite this is or if it has been treated.
Please view my other lots. Please contact me for international rates.
The seller is "silverpaw" and is located in Santa Cruz, California. This item can be shipped to United States.
- Style: Pendant
- Metal: Yellow Gold
- Metal Purity: 14k
- Main Stone Color: Green & White
- Main Stone Treatment: Unknown
- Length (inches): 1.9"
- Main Stone: Jade Jadeite


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In Linux computers that run Apache, this is the directory where any logs that apache generates go. The main one is usually called, access.log. There is also error.log, agent.log and referer.log, as well as zipped versions of older logs.
Grepping the access log for your username is a simple way to see who has been viewing your webpage.
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