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A weekly podcast discussing each episode every episode of the insanely popular 80s cartoon show, Jem.
A weekly podcast discussing each episode every episode of the insanely popular 80s cartoon show, Jem.
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Vancouver, BC
A weekly podcast discussing each episode every episode of the insanely popular 80s cartoon show, Jem.
S3E12: "A Father Should Be…"
In Season 3, episode 12: "'A Father Should Be...,' Jem and The Holograms (with help from Riot and his dad) search for Ba Nee's father. The Holograms travel to different parts of the country using information provided by Riot and speak to three men they think might be Ba Nee's father: Leonard Martin, Andy Martin and Martin O'Carolan.
Duration: 01:09:12
S3E11: "Riot's Hope"
In Season 3, episode 11: "'Riot's Hope,' When Riot's mother collapses from stress, he is revisited by his rejecting strict father and they begin to fight constantly. It's up to Jem to try and mend their relationship."
Duration: 01:06:49
S3E10: "A Change of Heart"
In Season 3, episode 10: "'A Change of Heart,' when Minx has a near-death experience, she decides to change her attitude and become kind and helpful, much to the dismay of Riot and Rapture. She sets out to do all kinds of good deeds for Rio, Jerrica, Jem and the rest of the Holograms to make up for her past bad behavior. Unfortunately, the new Minx turns out to be much more trouble than the old one."
Duration: 00:46:01
S3E9: "Straight from the Heart"
In Season 3, episode 9: "'Straight from the Heart,' A new fashion designer, Regine Cesaire, comes to town and starts working with Jem and The Holograms. When they initially reject her designs, her frustration turns her to the glamour of The Stingers. However, they soon take advantage of her and eventually cast her aside. Repented, she then returns to The Holograms, asking for another opportunity."
Duration: 00:58:42
S3E8: "That Old Houdini Magic"
In Season 3, episode 8: "'That Old Houdini Magic,' Jem and The Holograms are invited to perform at a magic convention with Astral, hosted by the gullible Mrs. Farnsworth, but when Rapture tricks Mrs. Farnsworth into thinking Houdini has possessed her body, it's up to The Holograms and Astral to help her see the truth."
Duration: 01:04:05
S2E24: "Britrock"
In Season 2, episode 24: 'Britrock,' "The Misfits go to England to meet Jetta's supposedly aristocratic family. Jetta's lower-class parents, Bertie and Flo strike up a deal with a Lord of England which ends up badly. Meanwhile, The Holograms come to play a show in London and meet Craig and his band. Both him and Aja renew their romance and help the true Earl, Mason Hawthorne, get back his title, which Pizzazz almost got tricked into buying."
S2E22: "Journey to Shangri-La"
In Season 2, episode 22: 'Journey to Shangri-La,' "The Holograms try to find Shangri-La, the mythological city where all music and art is kept, to add a new twist to their music. When Pizzazz and Roxy end up sick and Shangri-La's music is the only thing that can cure them, it's a race against time to save them."
S2E20: "The Middle of Nowhere"
Synopsis: "Jem and The Holograms visit Ba Nee's pen pal in Alaska. It's up to them to stop The Misfits and Eric Raymond from ruining the trip and destroying a natural seal habitat." Summary: Episode 46 (S2E20) is written by Chris Pelzer. We open with a very busy Harvey Gabor, frantically making phone calls. Pizzazz […]
Duration: 00:36:25
S2E19: "Mardi Gras"
Synopsis: "The Holograms are invited to wear the pirate Jean Lafitte's jewels for the Mardi Gras celebration. But could Lafitte's ghost be after them?" Summary: Episode 45 (S2E19) is written by returning writer, Mary Skrenes. We open on a cruise ship as Jem and the Holograms patiently wait for their mystery contact to divulge what […]
S2E12: "Danse Time"
Synopsis: "Richard Xanthos holds a contest for $250,000 for the group that can make the best music video that personifies friendship and goodwill. Jerrica Benton decides that if Jem and The Holograms win, they will donate all the money to Haven House. Naturally, the only opponents are The Misfits." Summary: Episode 38 (S2E12) is written […]
S2E11: "The Jazz Player"
Synopsis: "Legendary trumpet player, Taps Tucker, is humiliated on the Lin-Z Pierce show when The Misfits crash his interview and harass him. Outraged, Jem and The Holograms visit Taps and offer to help him put his famous Taps Tucker Band back together." Summary: Episode 37 (S2E11) is written by Michael Reaves. We open with legendary […]
S2E10: "Music Is Magic"
Synopsis: "The Holograms are the musical guests at a magic show. When strange things start happening and people start to disappear, the Holograms have to team up with the magicians and the Misfits to solve the mysteries before it's too late." Summary: Episode 36 (S2E10) is written by Paul Dini. We open with Kimber attempting […]
Duration: 00:47:48
S2E9: "Aztec Enchantment"
Synopsis: "A prestigious film contest is coming up and Video is determined to win the competition. She brings Jem, The Holograms and Rio down to Mexico to film their newest video at a top secret location that is sure to give her the first prize." Summary: Episode 35 (S2E9) is written by Misty Stewart-Taggart. We […]
S2E8: "The Treasure Hunt"
Synopsis: "Richard Xanthos sponsors a literature-themed treasure hunt in which the winning team will get a priceless item from the Zanthos collection. Jem chaperones the Starlight Girls team which consists of Ashley, Krissie and Ba Nee, while Pizzazz chaperones three street urchins named Molly, Ellen and Sandra, that Eric paid off." Summary: Episode 34 (S2E8) […]
Duration: 01:02:50
S2E7: "Father's Day"
Synopsis: "Video is having trouble coming up with a Father's Day present, so Jem suggests creating a film featuring video footage of their fathers and an original song. Everyone is excited except for Kimber, who is sad about having no father to celebrate with and refuses to write the song." Summary: Episode 33 (S2E7) is […]
Duration: 01:07:01
S2E6: "The Fan"
Synopsis: "A wealthy young man, Prescott Wentworth, who is completely obsessed with Jem offers a reward to anyone who can tell him her real name. The Misfits convince him to build an exact replica of Starlight Mansion and hire actors to pose as The Holograms." Summary: Episode 32 (S2E6) is written by returning Jem writer, […]
S2E5: "The Bands Break Up"
Synopsis: "Upset with the way their bands treat them and over Jerrica's objections, Kimber and Stormer form a friendship and subsequently decide to form a duo and begin performing together." Summary: Episode 31 (S2E5) is written by Marv Wolfman, and Cherie Wilkerson. We open with Jem and the Holograms debating if the song on the […]
Duration: 01:08:36
S2E4: "One Jem Too Many"
Synopsis: "Jerrica, stressed-out from dealing with tax forms and the usual trouble at home and the office, gets into trouble with a nasty-tempered Jem impersonator, whose outrageous, public meltdowns and temper tantrums threaten to destroy the real Jem's career." Summary: Episode 30 (S2E4) is written by Buzz Dixon. We open with an exhausted looking Jerrica […]
Duration: 00:48:38
S2E3: "Scandal"
Synopsis: "When Jetta finds Kimber's diary the Misfits start a scandal to try to ruin the Holograms." Summary: Episode 29 (S2E3) is written by Mary Skrenes. We open with Jem and the Holograms arriving in beautiful Venice Beach, California. Raya is to make her debut interview appearance with the rest of the Holograms on Harriet […]
28: "The Talent Search: Part 2"
Synopsis: "As the Holograms deliberate over which semi-finalist will be their new drummer, the Misfits try to bribe one of them to reveal Jem's secret identity." Summary: Episode 28 is written by Christy Marx and is the conclusion to two-part episode: "The Talent Search." We open with Jerrica bringing the good news to the Holograms […]
See More


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March 7, 2014
To achieve success, there is a wall in between.
W: W stands for Will. If we have strong Will, anything is possible.
A: A stands for Ability. Though we have strong Will, we should improve ourselves to develop our Ability, either through learning, experience etc.
L: L stands for Liaison. We should develop our networks, should develop the relationships and cooperate with each other so that when we need something, we get help from others.
L: Final L stands for Luck. So, luck comes only at the end. We should not be disappointed that we don't have luck; rather we should concentrate on our Will /desire and to achieve it, we should focus on our Ability.
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Re: network question
Expand Messages
- I just wanted to point out that I have read somewhere that either
inetd or xinetd may be used, but not both. So if you choose xinetd,
you may want to verify that you aren't already using inetd (correct
me if I am wrong on this).
I'm using SuSE and it comes preconfigured with inetd. The default
installation (probably for security reasons) doesn't start telnet,
ftp, and httpd services upon bootup. I may manually start them after
bootup, or configure bootup parameters to start these services.
henry noerdlinger
Blessed are they who convert their neighbour's ox,
For they shall inhibit their girth
- Monty Python, Life of Brian
--- In linux-dell-laptops@y..., Paul <paul@d...> wrote:
> > telnet, ftp etc arent working even though I've given a valid IP
> > DNS, etc. It wont even telnet to the localhost! Could some one
> telnet usually requires xinetd. ftp requires an ftp daemon such as
> wu-ftpd. Instead, try enabling sshd through setup|system services
> use ssh and sftp.
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A Frontier Airlines plane sits on the tarmac at the Pittsburgh International Airport July 9, 2008 in Pittsburgh, Pennsylvania.
Frontier Airlines is adding a fee for carry-on bags, and plans to start charging $2 for soda and coffee.
The new carry-on fee announced Wednesday will be $25 if paid in advance, and $100 if paid at the gate. It applies to bags in the overhead bin, so small bags under the seat will still be free.
Passengers who buy their tickets on the airline's website won't have to pay.
Frontier says the new fee will take effect this summer, and it will announce a specific date later.
The new drink fee begins July 1. Water will still be free.
Spirit Airlines Inc. began charging a carry-on fee three years ago.
Frontier's parent, Republic Airways Holdings Inc., is trying to fix Frontier's finances and sell it.


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At St. John's our desire is to provide Christ-centered pastoral care to our congregation. If you have a need for pastoral care, such as prayer before an upcoming surgery, a desire for a counseling appointment, or you would just like to connect with one of our pastors, please fill out the form below.
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End of the World fondue
Vintage staffer Shari's "End of the World" fondue is sure to be a hit.
End of the World Fondue
2 cups aged white cheddar (I used one that was aged 4 years but any old white cheddar will work)
2 cups gouda
Grate cheese and toss with 2 tbsp corn starch, ½ tsp fresh ground black pepper and ½ tsp mustard powder. Set aside.
Next, you'll make some roasted garlic. Take 1 whole head of garlic and chop the very top off, to expose the cloves. Pour some olive oil on it, getting it into the cloves, and wrap tightly with tin foil. Bake for 45 minutes in a 400F oven.
Once roasted, squeeze the cloves out of their paper and mash into a paste.
Small onion, finely diced
1 clove of garlic, finely diced
Sauté onion and garlic in a mix of olive oil and butter, over medium heat. When translucent, add roasted garlic paste and heat through.
Add 1 ¼ cup of lager or light ale (I used La Fin Du Monde) and bring to a boil over medium high heat. Once boiling, reduce heat to medium and let mix, simmer for 3 minutes.
Decrease heat to medium-low and sprinkle 1 handful of cheese into pot. Stir until fully incorporated and smooth. When ready, add another handful of cheese. Repeat this process until all cheese is incorporated and mixture is silky smooth.
When all cheese is added, if the mix is too thick, add more beer (a small amount at a time), until proper consistency has been reached.
Taste and season with salt & pepper, if necessary. Pour the fondue in a fondue pot and serve immediately with dippers.
Fondue Dippers
When we made this fondue at home, I served it with the following dippers:
Roasted mushrooms, potatoes & asparagus
Blanched broccoli
Cherry tomatoes
Granny Smith apples
Spicy chorizo sausage
Multigrain baguette
Homemade garlic cayenne croutons
*Be sure to prepare all dippers before making the fondue. They take more time than the cheese mixture does.
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Martin luther book of revelation
Olaf College and has written many books andarticles on Martin Luther.(more about Edwards)Luther had many messages. When Luther wrote, he wrote about specific issues orproblems. But he had one over-arching message. And that one message, he putin his pamphlets, he put in his longer treatises, he put in his hymns. Andthat was: Christ died for you. If you can believe and have faith, you aresaved. In fact, evenbelieving is a gift of the Holy Spirit. While the Lutheran Confessions specifically did not define a canon, it is widely regarded as the canon of the Lutheran Church. These books are considered to be canonical in modern Lutheran churches, with the caveat that they are not quite on the same level as the other books as complete expressions of evangelical truth, and should be used with care.Luther himself took the liberty of criticizing some of these books in a polemical manner which few Lutherans today would find completely acceptable.
He had a low view About this Book of the Revelation of John, I leave everyone free to hold his own opinions. I would not have anyone bound to my opinion or judgment. I say what I feel. I miss more than one thing in this book, and it makes me consider it to be neither apostolic nor prophetic.First and foremost, the apostles do not deal with visions, but prophesy in clear and plain words, as do Peter and Paul, and Christ in the gospel. For it befits sample introduction essay apostolic office to speak clearly of Christ and his deeds, without images and visions.
Moreover there martin luther book of revelation no prophet in the Old Testament, to say nothing of the New, who deals so exclusively with visions and images. Frontispiece, Book of Revelation, Bible of San Paolo fuori le Mura, 9th centuryThe Book of Revelation, often called the Revelation to John, the Apocalypse of John, The Revelation, or simply Revelation or Apocalypse, is a book of the New Testament that occupies a central place in Christian eschatology. He attributes this to Martin Luther. McGrath drawn the distinction between the notion of revelation from God and a revelation of God.
This distinction is best illustrated by how Christian and Islam regard their holy book. The basic Islamic understanding is that the book is an authoritative revelation in the form of a book, not a person. Martin luther book of revelation difference between this and the Christian view is brought out clearly by Martin Luther. Christ is the offspring promised to AbrahamThe following link popped up a few weeks ago: Martin Luther- The Bare Martin luther book of revelation Unfolded. The hosting website is Shoebat.com, and, as far as I can tell, is some sort of Anti-Islam pro-Roman Catholic website.
From time to time they put up articles blaming Luther for the evils of the world (see the Beggars All archives). This article is similar to their previous offerings. In fact, as a fellow Christian, I wish to extend my sympathies to such. A sampling of books written by Mother Angelica.Fruits of His LoveHis Pain Like MineIn His SandalsJesus Needs MeLiving the Way Of The CrossMarriageMy Life In The RosarySpiritual HangoversThe Promised Woman.
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The singular effects and interplay of cAMP- and cGMP-dependent protein kinase (PKA and PKG) on Ca2+ mobilization were examined in dispersed smooth muscle cells. In permeabilized muscle cells, exogenous cAMP and cGMP inhibited inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release and muscle contraction via PKA and PKG, respectively. A combination of cAMP and cGMP caused synergistic inhibition that was exclusively mediated by PKG and attenuated by PKA. In intact muscle cells, low concentrations (10 nM) of isoproterenol and sodium nitroprusside (SNP) inhibited agonist-induced, IP3-dependent Ca2+ release and muscle contraction via PKA and PKG, respectively. A combination of isoproterenol and SNP increased PKA and PKG activities: the increase in PKA activity reflected inhibition of phosphodiesterase 3 activity by cGMP, whereas the increase in PKG activity reflected activation of cGMP-primed PKG by cAMP. Inhibition of Ca2+ release and muscle contraction by the combination of isoproterenol and SNP was preferentially mediated by PKG. In light of studies showing that PKG phosphorylates the IP3 receptor in intact and permeabilized muscle cells, whereas PKA phosphorylates the receptor in permeabilized cells only, the results imply that inhibition of IP3-induced Ca2+ release is mediated exclusively by PKG. The effect of PKA on agonist-induced Ca2+ release probably reflects inhibition of IP3 formation.
- smooth muscle
- relaxation
- protein kinase
- 1,4,5-trisphosphate
the main relaxant neuropeptides in the gut, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP), stimulate cAMP and cGMP in smooth muscle cells and activate both cAMP-dependent protein kinase (PKA) and cGMP-dependent protein kinase (PKG) (23). The neuropeptides interact with VIP-PACAP (VPAC)2 receptors to activate adenylyl cyclase and with the natriuretic peptide clearance receptors (NPR-C) to activate sequentially nitric oxide synthase and soluble guanylyl cyclase (28). The resultant generation of cAMP and cGMP leads to a complex interplay of cyclases and cyclic nucleotide-dependent kinases and phosphodiesterases (PDE3, PDE4, and PDE5) that alter the levels of cAMP and cGMP and their relative affinities for PKA and PKG (7, 8). cAMP is formed in much greater abundance than cGMP (∼10-fold) and can cross-activate PKG at high concentrations (7, 13, 14, 19, 22, 23). In the presence of cGMP, the affinity of cAMP for PKG and its ability to cross-activate this kinase are greatly enhanced, endowing PKG with the major role in cellular responses (2, 7, 11, 17).
PKG can act on various targets to regulate Ca2+mobilization and induce relaxation in vascular or visceral smooth muscle (1, 7, 20). Evidence exists that PKG 1) inhibits the formation of the Ca2+-mobilizing messenger inositol 1,4,5-trisphosphate (IP3) by phosphorylating various isoforms of phospholipase C (PLC)-β (44);2) inhibits IP3-dependent Ca2+release by phosphorylating the IP3receptor/Ca2+ channel (15, 16); 3) stimulates plasmalemmal and sarcoplasmic Ca2+-ATPase pumps, thereby increasing Ca2+ uptake into the stores and stimulating Ca2+ efflux from the cells (3); and 4) inhibits Ca2+ channel activity and stimulates K+ channel activity, causing membrane hyperpolarization and a reduction of Ca2+ influx into the cell via voltage-dependent Ca2+ channels (32,39).
Some but not all of these properties are shared by PKA. Thus PKA inhibits agonist-stimulated IP3 formation mediated by PLC-β but does not inhibit voltage-dependent Ca2+ channel activity or stimulate Ca2+ uptake into the stores (5,21, 26, 27). PKA inhibits agonist-stimulated Ca2+release in intact smooth muscle cells, but whether this effect represents inhibition of IP3 formation only or also inhibition of IP3-dependent Ca2+ release is uncertain. PKA, like PKG, can inhibit IP3-dependent Ca2+ release in permeabilized smooth muscle cells, but its effect in intact smooth muscle cells has not been determined. Our recent studies (25) indicate that PKG can phosphorylate the IP3 receptor in both intact and permeabilized smooth muscle cells, whereas PKA phosphorylates the IP3 receptor in permeabilized smooth muscle cells only. Thus inhibition of agonist-stimulated Ca2+ release in intact smooth muscle cells by PKA could reflect inhibition of IP3 formation (and/or stimulation of IP3 inactivation) rather than inhibition of IP3-dependent Ca2+ release (26).
PKA and PKG can also induce relaxation by acting on targets downstream of Ca2+ mobilization. Both protein kinases can decrease myosin light chain (MLC) phosphorylation during the initial phase of contraction by inhibiting Ca2+/calmodulin-dependent activation of MLC kinase and/or by activating MLC phosphatase via telokin (18, 22, 35, 37). During the sustained (tonic) phase of contraction, which is Ca2+ independent, both kinases decrease MLC phosphorylation by inhibiting the activity of the monomeric G protein RhoA (30, 33).
In the present study, we sought to examine the singular effects and the interplay of PKA and PKG on IP3-dependent Ca2+release and smooth muscle contraction. The effects of exogenous cAMP and cGMP, alone and in combination, on Ca2+ release and smooth muscle contraction induced by exogenous IP3 were determined in permeabilized, dispersed smooth muscle cells. In parallel experiments, the effects of isoproterenol and sodium nitroprusside (SNP), alone and in combination, on agonist (cholecystokinin octapeptide; CCK-8)-stimulated, IP3-dependent Ca2+ release and muscle contraction were determined in intact smooth muscle cells. When used alone at low concentrations (10 nM), isoproterenol selectively stimulates cAMP and activates PKA, whereas SNP selectively stimulates cGMP and activates PKG (23). The results show that when used separately, isoproterenol and exogenous cAMP inhibited Ca2+ release and muscle contraction (i.e., induced relaxation) via PKA, whereas SNP and exogenous cGMP elicited the same effects via PKG. When isoproterenol and SNP were used in combination, both PKA and PKG activities increased but inhibition of Ca2+ release and muscle contraction was preferentially mediated by PKG. When exogenous cAMP and cGMP were used in combination, inhibition of Ca2+ release and muscle contraction was preferentially mediated by PKG and attenuated by PKA.
Preparation of dispersed muscle cells.
Muscle cells were dispersed from the circular muscle layer of the rabbit stomach as described previously (23, 28). Briefly, muscle strips were incubated for 30 min at 31°C in a HEPES medium containing 0.1% collagenase (type II) and 0.1% soybean trypsin inhibitor. The medium consisted of (in mM) 115 NaCl, 5.8 KCl, 2.1 KH2PO4, 2 CaCl2, 0.6 MgCl2, and 25 glucose as well as 2.1% essential amino acid mixture (pH 7.4). The partly digested tissues were washed with 50 ml of enzyme-free medium, and the muscle cells were allowed to disperse spontaneously for 30 min. The cells were harvested by filtration through 500-μm Nitex and centrifuged to eliminate broken cells and organelles.
Dispersed muscle cells were permeabilized by incubation for 10 min with 35 μg/ml of saponin in a medium containing (in mM) 20 NaCl, 100 KCl, 5 MgSO4, 1 NaH2PO4, 25 NaHCO3, 0.34 CaCl2, and 1 EGTA with 1% bovine serum albumin (23,27). The cells were centrifuged at 350 g for 5 min, washed free of saponin, and resuspended in the same medium with 1.5 mM ATP and ATP-regenerating system (5 mM creatine phosphate and 10 U/ml creatine phosphokinase).
cAMP- and cGMP-dependent protein kinase assay.
PKA and PKG activities were measured by the method of Jiang et al. (13) as described previously (23). PKA activity was measured in a volume of 60 μl containing 50 mM Tris, 10 mM MgCl2, 100 μM [γ-32P]ATP, 50 μM kemptide (Leu-Arg-Arg-Ala-Ser-Leu-Gly), and 0.25 mg/ml of bovine serum albumin. The assay was done in the presence or absence of 10 μM cAMP and was initiated by the addition of 20 μl of cell supernatants to the reaction mixture. The measurements were corrected for cAMP-independent kinase activity by separate measurements in samples containing 2 μM PKA inhibitor protein kinase inhibitor(6–22) amide [PKI(6–22) amide]. Protein kinase activity was calculated as picomoles of phosphate transferred into kemptide per minute per microgram of protein and expressed as the ratio of activity in the presence or absence of 10 μM cAMP (−cAMP/+cAMP). A similar procedure was followed for the assay of PKG activity, and the synthetic heptapeptide histone H2B [Arg-Lys-Arg-Ser-Arg-Ala-Glu (RKRSRAE)] was used as phosphate-accepting substrate. The assay was performed in the presence of PKI(6–22) amide and in the presence or absence of 10 μM cGMP. Enzyme activity was calculated as picomoles per milligram of protein and expressed as the ratio of activity in the presence or absence of 10 μM cGMP (−cGMP/+cGMP).
Radioimmunoassay for cAMP.
cAMP levels were measured by radioimmunoassay as described previously (23, 26, 28). Dispersed muscle cells (3 × 106 cells) were stimulated for 1 min with 10 nM isoproterenol alone or in combination with trequinsin or SNP, and the reaction was terminated with 10% trichloroacetic acid. The samples were centrifuged, and the supernatant was extracted with diethyl ether and then lyophilized. For assay, lyophilized samples were acetylated with triethylamine-acetic anhydride (2:1) for 30 min. cAMP was measured in duplicate using 100-μl aliquots, and the results were expressed as picomoles per milligram of protein.
Measurement of Ca2+ release in dispersed muscle cells.
Ca2+ release was measured in intact and permeabilized muscle cells by an adaptation of the method of Poggioli and Putney (31) as described previously (23, 27). The cells were incubated with 45Ca2+ (10 μCi/ml), and Ca2+ uptake was measured at intervals for 90 min when a steady state was attained. After 90 min, IP3 was added and the reaction was terminated after 15 s. Cyclic nucleotides or relaxant agents were added 60 s before IP3. The decrease in 45Ca2+ content, representing net Ca2+ efflux, was expressed as nanomoles per 106cells.
Measurement of relaxation in dispersed muscle cells.
Relaxation was measured in intact muscle cells contracted with CCK-8 (1 nM) or in permeabilized muscle cells contracted with IP3 (1 μM) (23, 27). Intact cells were treated for 60 s with isoproterenol and/or SNP followed by CCK-8 for 30 s. Permeabilized muscle cells were treated for 60 s with cAMP and/or cGMP followed by addition of IP3 for 15 s. The reaction was terminated with 1% acrolein. The length of 50 cells treated with CCK-8 or IP3 was measured in sequential microscopic fields by scanning micrometry, and the contractile response was expressed as the decrease (in μm) in mean cell length from control. Relaxation was expressed as percent increase in the length of cells contracted with CCK-8 or IP3.
[γ-32P]ATP was from NEN Life Science Products (Boston, MA); collagenase type II from Worthington (Freehold, NJ); IP3, trequinsin, and PKI(6–22) amide from Calbiochem (San Diego, CA); kemptide and RKRSRAE from Peninsula Laboratories (Belmont, CA); KT5823 from Kamiya Biomedical, (Thousand Oaks, CA); myristoylated PKI(14–22) amide from Biomol (Plymouth Meeting, PA); and cAMP, cGMP, and all other chemicals from Sigma (St. Louis, MO).
Synergistic inhibition of IP3-induced muscle contraction by combinations of cAMP and cGMP in permeabilized smooth muscle.
Inhibition of IP3-induced contraction (i.e., relaxation) was measured in permeabilized smooth muscle cells in response to various concentrations of cAMP or cGMP, alone and in combination. Concentration responses for cAMP and cGMP alone and in various combinations are shown in Figs. 1 and2. No relaxation was observed with 0.01 or 0.1 μM cAMP or cGMP alone. However, a combination of 0.1 μM cAMP with either 0.01 μM or 0.1 μM cGMP elicited significant responses of 10 ± 2% (P < 0.01) and 19 ± 3% (P < 0.01), respectively (Fig. 1). A similar synergistic effect was observed when 0.1 μM cGMP was combined with either 0.01 μM or 0.1 μM cAMP (8 ± 3% and 16 ± 2%, respectively; Fig. 2). Synergistic effects were also observed at higher concentrations: the response to a combination of 1 μM cGMP and 1 μM cAMP (39 ± 2%) or 10 μM cAMP and 10 μM cGMP (86 ± 4%) was significantly greater than the corresponding additive response (17 ± 4% and 49 ± 5%, respectively; Figs. 1 and 2). In permeabilized muscle cells exposed to steady-state levels of cyclic nucleotides in the medium, the synergistic effect could not be attributed to an increase in the levels of cAMP resulting from inhibition of cAMP-specific PDE3 by cGMP.
Selective inhibitors were used to determine whether synergistic relaxation reflected cross-activation of PKA or PKG. Relaxation induced by 1 μM cAMP alone was inhibited by PKI(6–22) amide, a selective inhibitor of PKA, but was not affected by KT5823, a selective inhibitor of PKG (Fig. 3). Conversely, relaxation induced by 1 μM cGMP was inhibited by KT5823 but not by PKI (Fig. 3). The synergistic response to a combination of 1 μM cAMP and 1 μM cGMP, however, was augmented by PKI(6–22) amide and abolished by KT5823. The results implied that in the presence of cGMP relaxant effects induced by cAMP were mediated by PKG, consistent with increase in the affinity of PKG for cAMP in the presence of cGMP (7, 11,17). The increase in relaxation induced by inhibition of PKA suggested the existence of a competitive interaction between PKA and PKG on a common cellular target.
Synergistic inhibition of IP3-induced Ca2+ release by combinations of exogenous cAMP and cGMP in permeabilized smooth muscle.
The synergistic effect of combinations of cAMP and cGMP on relaxation (i.e., inhibition of IP3-induced contraction) was reflected in the inhibition of IP3-induced Ca2+ release. Ca2+ release, measured as the decrease in steady-state45Ca2+ cell content during the first minute of stimulation with IP3, was 0.72 ± 0.04 nmol/106 cells. cAMP (1 μM) and cGMP (1 μM) inhibited IP3-induced Ca2+ release by 10 ± 2% and 13 ± 2%, respectively (P < 0.01). Inhibition of Ca2+ release by cAMP was blocked by PKI(6–22) amide but not by KT5823, whereas inhibition of Ca2+ release by cGMP was blocked by KT5823 but not by PKI(6–22) amide (Fig.4). Inhibition of Ca2+release by a combination of 1 μM cAMP and 1 μM cGMP (29 ± 4%) was significantly increased by PKI(6–22) amide (42 ± 5%, P < 0.05) but was abolished by KT5823 (Fig. 4). The results suggest that in permeabilized muscle cells, the IP3 receptor is a target for inhibitory phosphorylation by either PKG or PKA (15, 25). In the presence of cGMP, however, phosphorylation induced by cAMP or cGMP is mediated by PKG only. The increase in the inhibition of Ca2+ release induced by PKI(6–22) amide suggests that, when present with PKG, PKA attenuates the interaction of PKG with the IP3 receptor.
Inhibition of agonist-induced Ca2+release and muscle contraction by combinations of cAMP- and cGMP-stimulating agents in intact smooth muscle.
Experiments were done in intact, nonpermeabilized muscle cells to determine the effects and interplay of PKA and PKG when activated by endogenous cAMP and cGMP. The muscle cells were treated with isoproterenol (10 nM) or SNP (10 nM), alone or in combination. As shown previously, at these concentrations, isoproterenol selectively stimulates cAMP formation and activates PKA, whereas SNP selectively stimulates cGMP formation and activates PKG (23). Isoproterenol (10 nM) and SNP (10 nM) inhibited CCK-stimulated contraction (i.e., induced relaxation) in nonpermeabilized muscle cells by 22 ± 2% and 26 ± 4% (P < 0.01), respectively. Relaxation induced by isoproterenol was abolished by myristoylated PKI(14–22) amide but was not affected by KT5823, whereas relaxation induced by SNP was abolished by KT5823 but was not affected by myristoylated PKI(14–22) amide (Fig. 5). Relaxation induced by a combination of isoproterenol and SNP (59 ± 6%) was not affected by myristoylated PKI(14–22) amide (59 ± 4%) but was abolished by KT5823 (Fig. 5).
Similar results were obtained for inhibition of CCK-stimulated, IP3-dependent Ca2+ release. Ca2+release measured during the first minute after stimulation with 1 nM CCK-8 was similar to that elicited by exogenous IP3(0.68 ± 0.05 nmol/106 cells) (23, 27). Isoproterenol and SNP inhibited CCK-stimulated Ca2+ release by 15 ± 3% and 15 ± 2%, respectively (P< 0.01). Inhibition of Ca2+ release by isoproterenol was blocked by myristoylated PKI(14–22) amide but not by KT5823, whereas inhibition of Ca2+ release by SNP was blocked by KT5823 but not by myristoylated PKI(14–22) amide (Fig. 6). Inhibition of Ca2+ release by a combination of isoproterenol and SNP (47 ± 9%) was not affected by myristoylated PKI(14–22) amide (44 ± 5%) but was abolished by KT5823 (Fig. 6). In nonpermeabilized muscle cells, a greater inhibition of Ca2+ release or muscle contraction by a combination of isoproterenol and SNP could be partly attributed to increase in cAMP levels resulting from inhibition of cAMP-specific PDE3 by SNP-stimulated cGMP (29). As shown in Fig.7, isoproterenol-stimulated cAMP levels were augmented in the presence of SNP to the same extent as in the presence of the selective PDE3 inhibitor trequinsin. Nevertheless, the effects of endogenous cAMP or cGMP when stimulated concurrently were mediated exclusively by PKG.
Preferential activation of PKG by cAMP in presence of cGMP.
Conclusions based on the use of selective PKA and PKG inhibitors were corroborated by direct measurements of PKA and PKG. Isoproterenol (10 nM) increased PKA activity by 38 ± 3% above basal level (P < 0.01); the increase was selectively inhibited by myristoylated PKI(14–22) amide (Fig.8). A smaller increase (19 ± 4%) in basal PKA activity elicited by SNP was also selectively inhibited by myristoylated PKI(14–22) amide (Fig. 8). A combination of 10 nM isoproterenol with 10 nM SNP increased PKA activity by 95 ± 4%, which is more than double the increase in PKA activity elicited by isoproterenol alone; the PKA activity was selectively inhibited by myristoylated PKI(14–22) amide. The large increase in isoproterenol-stimulated PKA activity was attributed to increase in cAMP levels resulting from inhibition of PDE3 activity by SNP-stimulated cGMP (Fig. 7; Refs. 4,29).
Isoproterenol had no effect on basal PKG activity, whereas SNP increased PKG activity by 101 ± 5% above basal level (P < 0.01; Fig. 9). In the presence of isoproterenol, SNP increased PKG activity by 190 ± 12%, which is more than the increase elicited by SNP alone (P < 0.01 for difference between response to SNP alone vs. SNP + isoproterenol; Fig. 9). PKG activity stimulated by SNP alone or in the presence of isoproterenol was selectively inhibited by KT5823 (Fig. 9).
The present study focused on the singular effects and interplay of PKA and PKG on IP3-dependent Ca2+ mobilization because of its crucial importance in initiating contraction in smooth muscle. Direct measurements and selective inhibitors of PKA and PKG activities were used to evaluate the role of each kinase in inhibiting IP3-dependent Ca2+ release. Activation of PKA and/or PKG was elicited by exogenous cAMP and cGMP in permeabilized smooth muscle or by isoproterenol and SNP in intact smooth muscle. The PKA inhibitors PKI(6–22) amide and myristoylated PKI(14–22) amide and the PKG inhibitor KT5823 were used at concentrations at which they selectively inhibited PKA and PKG, respectively (23, 24).
In previous studies (23), we showed that low concentrations of SNP stimulated cGMP and activated PKG in gastric smooth muscle cells, whereas equally low concentrations of isoproterenol (<1 μM) stimulated cAMP and activated PKA without cross-activating PKG. The present study confirmed preferential activation of PKA and PKG by low concentrations (10 nM) of isoproterenol and SNP, respectively, but also showed that treatment of smooth muscle cells with a combination of SNP and isoproterenol increased both PKA and PKG activities. The increase in PKA activity probably reflected an increase in cAMP resulting from inhibition of cAMP-specific PDE3 by SNP-stimulated cGMP (Fig. 7; Refs.4, 8, 29). The increase in PKG activity, however, reflected an increase in the affinity of cAMP for PKG, resulting in greater activation of this kinase (7, 11,17). The two main isoforms of PKG I expressed in gastrointestinal smooth muscle (70% PKG Iα and 30% PKG Iβ) undergo autophosphorylation and preferentially bind cGMP; autophosphorylation and the binding of cGMP enhance the affinity of cAMP for PKG by up to 10-fold (2, 7, 12). cAMP, which is generated in ∼10 times greater abundance than cGMP, becomes the major activator of PKG when the two cyclic nucleotides are present together (7, 11, 13, 17, 23).
Despite the increase in both PKA and PKG activities induced by a combination of isoproterenol and SNP, the inhibition of agonist-induced, IP3-dependent Ca2+ release and muscle cell contraction (i.e., relaxation) in intact muscle cells was exclusively mediated by PKG (abolished by KT5823). Similarly, inhibition of IP3-induced Ca2+ release and muscle contraction in permeabilized muscle cells by a combination of exogenous cAMP and cGMP was exclusively mediated by PKG. The inhibitory effects of combinations of cAMP and cGMP on Ca2+ release and contraction were synergistic, eliciting responses that were more than additive. The synergism could not be attributed to increase in the levels of cAMP resulting from inhibition of cAMP-specific PDE3 by cGMP, because the permeabilized smooth muscle cells were exposed to steady-state levels of exogenous cyclic nucleotides.
In permeabilized muscle cells, PKA stimulated by exogenous cAMP alone, or PKG stimulated by exogenous cGMP alone, was capable of inhibiting Ca2+ release induced by exogenous IP3. Their singular effects were blocked by the corresponding selective kinase inhibitor, implying that each kinase was independently capable of phosphorylating and thus inhibiting IP3 receptor activity. However, the inhibitory effects during concurrent activation of PKA and PKG by a combination of exogenous cAMP and cGMP were exclusively mediated by PKG (abolished by KT5823) and attenuated by PKA [augmented by PKI(6–22) amide]. The pattern suggested that PKG and PKA act competitively in phosphorylating the IP3receptor in permeabilized muscle cells.
In different tissues (9, 15, 16), PKA and PKG phosphorylate serine 1756 and/or serine 1589 of the type I IP3 receptor. Komalavilas and Lincoln (15, 16) showed that, in aortic smooth muscle, PKG preferentially phosphorylates serine 1756 in vitro and in vivo, whereas PKA phosphorylates both serine residues in vitro only. Selective activators of PKG but not PKA elicited IP3 receptor phosphorylation. Phosphorylation of the IP3 receptor by forskolin resulted from cross-activation of PKG by high concentrations of cAMP and was blocked by a PKG inhibitor.
Our recent studies (25) on gastric smooth muscle cells using selective activators and inhibitors of PKA and PKG confirmed that PKG phosphorylates the IP3 receptor in both intact and permeabilized smooth muscle cells, whereas PKA phosphorylates the IP3 receptor in permeabilized smooth muscle cells only. The results suggest that PKA can gain access to the IP3receptor in permeabilized but not intact smooth muscle cells. These results, together with the earlier results of Komalavilas and Lincoln (15, 16), have an important bearing on interpretation of the effects of relaxant neurotransmitters and other agents in intact, nonpermeabilized smooth muscle cells.
In light of these results, the inhibition of agonist-stimulated, IP3-dependent Ca2+ release in intact gastric smooth muscle cells by low concentrations of isoproterenol probably resulted from inhibition of agonist-stimulated IP3formation by PKA rather than inhibition of IP3-dependent Ca2+ release. PKA can be targeted to the plasma membrane by specific anchoring proteins that enable it to phosphorylate membrane-bound PLC-β activity (6, 10) but may not be targeted to the sarcoplasmic membrane to phosphorylate the IP3 receptor. The results suggest that permeabilization facilitates access of PKA to the IP3 receptor spanning the sarcoplasmic membrane, thus enabling PKA to phosphorylate the IP3 receptor in vitro. This would explain why inhibition of IP3-induced Ca2+ release and contraction by exogenous cAMP in permeabilized smooth muscle cells was selectively mediated by PKA. It would also explain the competitive interaction between PKG and PKA in permeabilized muscle cells, in which the same serine residue on the IP3 receptor is phosphorylated by both kinases, albeit with greater affinity by PKG. The inhibition of agonist-stimulated, IP3-dependent Ca2+ release by SNP or by a combination of SNP and isoproterenol in intact muscle cells was mediated by PKG and could result from inhibition of both IP3 formation and IP3-dependent Ca2+ release. A model summarizing the results of this study and illustrating the crucial role of PKG in the inhibition of IP3-dependent Ca2+ release is shown in Fig.10.
It is worth noting that many earlier studies in various types of smooth muscle showed that an increase in cAMP inhibits agonist-stimulated IP3 formation and increase in cytosolic Ca2+levels (5, 36). However, the high levels of cAMP induced by micromolar concentrations of isoproterenol or forskolin, the agents of choice in many studies, can activate PKA and cross-activate PKG, obscuring the ability of PKA to inhibit IP3 formation (13, 14, 23). The inhibition of IP3 formation and/or Ca2+ mobilization by PKA was unmasked in other studies by selective PKA inhibitors (23, 27).
Although a close parallelism exists between inhibition of Ca2+ release and inhibition of muscle contraction (i.e., relaxation), other downstream processes besides inhibition of Ca2+ release could contribute to PKA- or PKG-mediated relaxation, including inhibition of MLC kinase and stimulation of MLC phosphatase activities (18, 22, 35, 37). Sustained (tonic) contraction, which follows the initial Ca2+-dependent contractile transient, is Ca2+ independent and mediated by RhoA-dependent inhibition of MLC phosphatase (34). Our recent studies (30) suggest that relaxation of sustained muscle contraction results from inhibition of RhoA activity by both PKA and PKG, leading eventually to increase of MLC phosphatase activity and inhibition of MLC phosphorylation (30).
This work was supported by National Institute of Diabetes and Digestive and Kidney Diseases Grant DK-28300.
Address for reprint requests and other correspondence: K. S. Murthy, PO Box 980711, Medical College of Virginia, Virginia Commonwealth Univ., Richmond, VA 23298-0711 (E-mail:skarnam{at}hsc.vcu.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2001 the American Physiological Society


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1979 -2016
Expertise in the intersection of entertainment, technology and business.
Skills achieved in the film & digital for feature film, commercials, documentaries and music videos.
Consultant for post-production systems, quotes, reservations, sheets, managing director and general manager.
Camera assistant and photographer.
Film editor assistant, film editor, post-production management, technical director, project manager, post-production supervisor, DI supervisor, VFX coordinator, VFX supervisor, VFX producer, VFX executive producer, on set supervisor, director for commercials, art director, CGI/VFX director and creative director.
- Knowledge of editing and management of the post-production in feature films, advertisings, documentaries and music videos.
- Analogical film process skills and forerunner of the digital process.
- Creative and technical skills.
- Management of a VFX projects , form the idea to the execution.
- Management of the technical-artistic staff .
- Excellent communication and staff management skills.
- Ability to guide and lead a team getting the best result.
- Deep understanding of all aspects of film theory.
- Great aesthetic sense
- Precise prevision of the time and costs associated with a project.
- Problem solving
- Management of the the bidding and negotiation processes.
- Post-production pipeline, techniques and software.
- Development of story and storyboard.
- Consulting to the Art Director in the conception phase of the commercial.
- Consulting to the director and DOP about the shooting with VFX.
- Animatic, pre-visualization
- Set extensions and matte painting
- Blue-screening
- Digital animation
- Visual effects
- 2D/3D Tracking, Compositing
- 3D stereo
1992 – Today
ROLE: general manager, senior editor & editing supervisor, post-production supervisor, post-production & DI supervisor, creative executive producer, VFX executive producer, VFX supervisor and VFX creative director.
TASKS: management and supervision on the creative and technical execution of the advertising and film projects, from the idea to the production (editing, color correction, 3D stereo, CGI and VFX).
- Restoration in 4k of the film "Juliet of the Spirits" by Federico Fellini – Film Restoration Supervisor (2015)
- Restoration in 4k of the film "The Terrace" by Ettore Scola – Film Restoration Supervisor (2015)
- Nomination at the David Donatello for Best Digital Effects "Greenery will bloom again" (2015)
- Post-production executive producer and DI supervisor – "Our host Planet" by Ermanno Olmi (2015)
- Post-production executive producer and DI supervisor of Maccio Capatonda's first film "The average Italian" (2015)
- first Italian film fully realized in 4K from 35mm negative ("greenery will bloom again" by Ermanno Olmi – 2014)
- Restoration in 4k of the film "Soap thieves" by Maurizio Nichetti - Film Restoration Supervisor (2012)
- first feature film in 3D stereo in Italy (Ligabue "Campovolo" – 2011)
- unique in Italy to have a Barco 2K projector (2011)
- first to work with Raw files with Nucoda Fuse (2011)
- first short film in 3D stereo (Il Volo – 2009)
- creation of a pipeline in 2K/HD DPX/LOG (2009)
- first San in Italy (DVS – 2009)
- nomination at HPA Hollywood for outstanding color grading television (4 single fathers - 2009)
- first color grading system NLE in Italy (Da Vinci Resolve – 2009)
- first film scanner in Italy (Arriscan – 2008)
- operations partner to launch the All music channel (2006)
- first to create a Volkswagen auto in CGI (VW Polo – 2006)
- operations Sky partner to launch Sky Sport and Sky Cinema channels (2003)
- first HD feature film (Scacco Pazzo – 2003)
- nomination at the David Donatello for the Best Editing (Honolulu baby - 2000)
- first digital intermediate film in Italy (Honolulu baby – 2000)
- first commercial created in live action/CGI (Loacker - 2000)
- collaborates with MTV Italy creating the figure of the "designer" for television (1999)
- collaborates with Discreet Logic to develop Flint and Flame software for the compositing (1992)
2014 – 2016:
Collaborates with the Experimental Cinematography Centre in Milan as Professor of visual effects, teaching production, editing, color grading and post-production.
1989 – 1992
ROLE: editing consultant, demo artist and trainer.
TASKS: evaluation systems, software development & fixing bugs, exhibitions NAB & IBC , IBTS.
NLE OFFLINE SOFTWARE: Avid, EditDroid, EMC2, Montage, FilmLight
NLE ONLINE SOFTWARE: Discreet Flame, Softimage DS, Quantel Harry, Henry, Matrox Studio
3D SOFTWARE: Microsoft Softimage, Alias, Wavefront.
PAINTING/COMPOSITING SOFTWARE: Softimage Eddie, Discreet Flint, Parallax Advance/Matador.
MAIN CUSTOMERS: Techexport, Avid technology
1983 – 1992:
ROLE: Art director
TASKS: Conception of advertising campaigns and director.
MAIN ADVERTISING: Golia "Orchestra leader", Sangemini, Viva la vita, Boario, Selvaggia Shoes and Parmalat Mister Day.
AGENCIES: Michele Rizzi&Associates
FILM PRODUCTIONS: Primo Piano
1983 – 1992:
ROLE: editing in Moviola 35MM–16MM– VID MC (1989)
TASKS: post-production management, bookings, quotations and final balances.
EDITING - 35/16MM FLAT TABLE, AVID MC: editing video, ADR/dialogue editor and sound FX editing.
EDITING FILM LAB: offline for negative cut, Truka data sheet, color correction in film grading, visioning standard copies in projection and color correction in Telecinema.
AUDIO: voice casting, sound design and sync audio, dubbing director and mix supervisor.
FILM PRODUCTIONS: Primo Piano, Filmmaster, Brw, Multifilm , Cooper Group and FH.
KEY FACTOR: first Avid editor in Italy (1989)
1979 -1980:
COMPANY: Advision
ROLE: assistant editor in Moviola 35MM–16MM
TASKS: cleaning Moviola, sync audio and second assistant editor.
1979 – 1982:
COMPANY: Green Movie
ROLE: assistant film editor/film editor in Moviola 35MM – 16MM
TASKS: post-production management, supervising, quotes, reservations, cost estimation and sheet.
EDITING: editing video, ADR/dialogue editor and sound FX editing.
FILM LAB: offline for negative cut, Truka data sheet, color correction in film grading, visioning standard copies in projection and color correction in Telecinema.
AUDIO: voice casting and management, sound design and sync audio, dubbing director and mix supervisor.
FILM PRODUCTIONS: Film'77
1978 -1979:
COMPANY: Studio 2B
ROLE: Assistant photographer in studio and camera assistant at the newsreel camera.
TASKS: case holder and camera assistant.


text:
By Babajide Komolafe
The Bank Directors Association of Nigeria (BDAN) has offered to work with the Central Bank of Nigeria (CBN) and Nigeria Deposit Insurance Corporation in a strategic partnership for the implementation of reforms in the banking sector.
BDAN is the umbrella body of non-executive directors of banks established to provide a forum for improving the knowledge and the competence of Bank Directors, thereby promoting honorable practice within the Banking Industry in Nigeria.
The Association affirmed its commitment to effective implementation of reforms in the sector, when its Governing Council visited the CBN Governor, Mallam Lamido Sanusi Lamido and the Managing Director/Chief Executive, NDIC, Alhaji Umar Ibrahim.
The Council commended both regulatory bodies for the various reforms initiatives in the banking industry, as well indicated readiness to contribute to the achievement of the goal of a stable and healthy banking industry. The Council also presented the report of the Survey on Directors' Compensation recently conducted by the Financial Institutions Training Centre (FITC) for the Association and BDAN's first official newsletter.
Speaking at the visit to the CBN Governor, President of the Association, and Chairman, Ecobank, Olor'ogun Dr. Sonny Kuku said, " BDAN can be the needed catalyst to ensure the implementation of the proffered solutions to the challenges of the sector", BDAN"s President, Olor'ogun Sonny Kuku said during the visit to the CBN Governor.
"We at BDAN recognize and align with the various reforms which have been introduced by the CBN. However, implementation is thought to be the greatest challenge. It is in the areas of implementation of the well thought out solutions to FSS challenges and its improvement that BDAN can be a strategic partner since BDAN is made up of representatives of the owners of the business of the FSS in Nigeria," he said.
Specifically, he said BDAN is ready to collaborate with the regulatory bodies in the area of training and recruitment of banks' staff, including continuous training of Bank directors, effective functioning of credit bureaus and compliance with Customer Due Diligence, and creation of specialized courts.
In response, the CBN Governor, commended the Association for its role in the industry especially the recently conducted survey on directors' compensation and its readiness to partner with regulatory bodies in the industry. He said, "If directors are well compensated, they would devote time to do the work well." He added that honest feedback from directors/BDAN on CBN initiatives will go a long way to help the industry.
Receiving the BDAN Council at the NDIC headquarters, Alhaji Umir Ibrahim congratulated the Council for the first edition of the BDAN Newsletter. He stated that the remuneration report is quite timely because compensation in the industry is a very peculiar issue.
He noted that affordability and sustenance are key factors that should be considered when discussing remuneration. He was of the view that payment of directors of banks peanuts should be a thing of the past and it should follow the banks' policies.


text:
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text:
It was like watching a rerun of ''All in the Family.''
After several days of extremely neurotic behavior, the city's leading Democrats decided late last week that fratricide was not a reasonable option. They united behind the mayoral candidacy of Mark Green.
On Friday afternoon -- in a tableau that one observer described as ''a nightmare for Bloomberg'' -- a throng of big-time Democrats, including Senators Charles Schumer and Hillary Rodham Clinton and the Democratic national chairman, Terry McAuliffe, gathered at a midtown hotel to say nice things about Mr. Green and his primary opponent, Fernando Ferrer.
Earlier in the week, some supporters of Mr. Ferrer were threatening to challenge Mr. Green's primary victory in the courts, and others were making sultry eye contact with Michael Bloomberg, the Republican mayoral candidate.
But by Friday afternoon, the Archies and the Meatheads had calmed down, the advances of the wealthy Republican had been rejected, and the Rev. Al Sharpton -- who has gleefully elbowed his way into the power circles of the establishment -- was preparing for his planned trip this week to Israel.
''I'm being briefed on Monday afternoon by Kissinger,'' he said.
Mr. Ferrer looked downcast at the unity gathering, but he said all the right things, and over the weekend he campaigned side by side with Mr. Green. Mr. Ferrer may have lost the primary, but the surprising strength of his campaign, and in particular the healthy turnout among Hispanic voters, ensures that the low-keyed and previously lightly regarded politician from the Bronx will remain a major force in city politics.Continue reading the main story
As a friend of Mr. Green's commented yesterday, ''Everybody understands that you have to deal with Freddy now.''
One of the biggest losers in the election was Roberto Ramirez, the Bronx Democratic chairman and a key Ferrer ally. Mr. Ramirez appeared to be the most bitter and least gracious of the defeated Ferrer forces. Unlike Mr. Ferrer, he has refused to endorse Mr. Green.
A top Ferrer campaign official, who would speak only if assured his name would not be used, said: ''Roberto is angry supposedly because of all the race-baiting and so forth. But you have to understand, he's the boss of the Bronx and he thought he had this thing [the mayor's race] won. He really thought Freddy was going to be the mayor, which to Roberto would mean that his -- Roberto's -- fiefdom would extend to all five boroughs. Can you imagine the jobs he was ready to parcel out? All that's out the window now, and that's the real reason he's angry. It's the loss of power that's making him crazy.''
The rupture between the Green and Ferrer forces began to close Thursday night when Mr. Green held separate private meetings with Mr. Ferrer and Mr. Sharpton. And if the meetings didn't end with expressions of deep and abiding friendships, they did produce agreements to move forward in ways that would not prove destructive to a city weakened by a series of devastating blows.
It's too bad Mr. Bloomberg wasn't at one of those meetings. Even as the Democrats were trying to pull themselves out of the slough of racial politics, Mr. Bloomberg was finding new and creative ways to crawl in. He somehow managed to produce a racially charged television ad for a campaign that, last time I looked, was between two white guys -- Mr. Bloomberg and Mr. Green.
Mr. Bloomberg, who is spending tens of millions of dollars of his own money to lip-sync the lyrics of politics, launched the ad on Friday. It features racial and ethnic minorities complaining about Mr. Green. A Hispanic woman in the ad says, ''I feel that Mark Green has been dividing the people with his negative campaigning.'' A black man says, ''Mark Green has flip-flopped on the issues.'' And so on.
Mr. Bloomberg is described in the tag line as ''a leader, not a politician.''
What the ad shows is that Mr. Bloomberg is as opportunistic and hypocritical as any professional pol. For example, it was only after he decided to run for mayor that he relinquished his membership in several private clubs that resisted the inclusion of minorities.
And after running this blatantly racially exploitive ad, he stood before reporters over the weekend and solemnly proclaimed, ''Nobody should be discussing race whatsoever.''Continue reading the main story


text:
|Job Title
|Volunteer Deputy Launching Authority - Walton and Frinton - EXPIRED
|Contract Type
|Temporary / Interim
|Job Published
|14 Jun 2017
|Contact Name
|Volunteers Team
|Contact Email
The RNLI is the charity that saves lives at sea. We provide, on call, a 24 hour lifeboat search and rescue service around the UK and Ireland, and a seasonal lifeguard service. With our lifeboats, lifeguards, safety messages and flood rescue we are committed to saving more lives.
The RNLI's Lifeboat Station in Walton and Frinton is looking for a volunteer to lead the existing team in the role of Lifeboat Operations Manager.
There has been a lifeboat station at Walton and Frinton for over 130 years. The lifesaving achievements of crew members have been recognised by the RNLI 75 times. Today's crew operate a Tamar class all- weather lifeboat.
The role of DLA is to authorise launch of the lifeboats, provide leadership in the absence of the Lifeboat Operations Manager or as delegated and ensure that all operational activities are carried out to maintain the lifeboats and all associated equipment in a constant state of readiness for launching on service.
This is a good opportunity to join a motivated and enthusiastic local team and have the satisfaction of contributing to saving lives at sea.
If you are a team player with leadership skills and local maritime knowledge this could be the role for you. You must live or work within 3 miles of the station and be between 17 and 70 years of age.
To apply for the role, please visit https://volunteering.rnli.org/vacancy/deputy-launching-authority-walton-and-frinton-317509.html
We value diversity at TPP and welcome applications from all sections of the community.


text:
Welcome! I'm a postdoctoral researcher at the Max Planck Institute for Intelligent Systems. My current research focus is on computational inference for social and economic decision making.
- To get a quick overview over my qualifications and experience, please have a look at my CV as PDF.
- If you are interested in my research and related material, you can find publications, slides, blog and software to which I contributed on this web site.
The remainder of this (so far rather small) web page can be navigated by the menu above.
My contact information can be found on my institute web site. You can also find me on Google Scholar.
PhD completed:
In June, I passed the final exam of my PhD. The final version of my thesis "Causal models for decision making via integrative inference" is available for download.
[Posted on 2017-08-29. Updated on 2017-10-08.]
Causal models for cloud computing:
We are investigating how causal models can help for debugging, control and economical challenges in cloud computing. Check out our preprint!
[Posted on 2016-06-03.]


text:
When you need help with your Gulf Coast Spa, please call
Spa Shopper at
or visit our website at SpaShopper.com.
Corporate Address
Spa Parts, Accessories and Services,
11636 54th St. No., Clearwater, Fl 33760
If you order a spa part before 2 p.m. Eastern Standard Time, it ships that day. If you order after 2 p.m., your spa part will ship next day. We can even overnight parts when you need to get your spa working again ASAP.
Returns Address
*Please contact our Customer Service Dept. at 1-866-829-3660 to setup a Return or Exchange and receive an RGA# along with the correct Warehouse address your Return will need to be sent back to.
Normal business hours:
Monday – Saturday 8:00am 8:00pm EST
Home | Contact Us | Site Map | SpaShopper.com
Quality products from Spa Parts, Accessories and Services, 11636 54th St. No., Clearwater, Fl 33760
Copyright © 2009 SpaShopper. All rights reserved


text:
Filter Results:
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Journals and Conferences
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- S M Audenaert, C L Montgomery, B Stone, R E Akins, R L Lock
- Anesthesia and analgesia
- 1991
- S M Audenaert, Y Wagner, +5 authors N W Pedigo
- Anesthesia and analgesia
- 1995
Cardiovascular and respiratory effects of pediatric preanesthetic premedication have received only minimal attention, probably because most children tolerate such drugs without apparent ill effect. In children with congenital heart disease or other serious illness, there is often reluctance to use premedication. We sought to determine whether different… (More)
- R L Lock, H B Triplett, G Rose
- Nurse anesthesia
- 1991
A patient had a subclavian vein catheter placed under general endotracheal anesthesia with positive pressure ventilation. During placement, the superior vena cava, pleura, and pulmonary tissue were punctured, resulting in a tension pneumo/hemothorax, the detection of which was complicated by its slow onset and unusual location. The lesion required an… (More)
- S M Audenaert, R L Lock, G L Johnson, N W Pedigo
- Journal of clinical anesthesia
- 1992
STUDY OBJECTIVE To define the cardiovascular effects of rectal methohexital in children with normal cardiac function. DESIGN Cardiovascular evaluation of each patient was performed before and after medication. Each patient's predrug results were used as control measurements for comparison with measurements made after methohexital administration. SETTING… (More)
- Richard Lock
- Craniomaxillofacial trauma & reconstruction
- 2010
Securing the airway in the patient with craniomaxillofacial trauma can be an extremely difficult challenge for health care practitioners. This article provides several approaches to airway management. Presented here are several options for securing the airway under a variety of conditions and scenarios.
- Jay S Grider, Joseph E Van Sickels, Richard L Lock
- Journal of clinical anesthesia
- 2009
- R Vassilopoulou-Sellin, R L Lock, C O Oyedeji, N A Samaan
- Metabolism: clinical and experimental
- 1987
We studied the effect of high MW cartilage sulfation (somatomedin) inhibitors from rat liver on cartilage growth in vitro. Pelvic rudiments from 11-day-old chicken embryos (5.70 mg average weight) were incubated in an organ-culture system with defined tissue-culture medium; after two days (T0-2), media were changed and incubation continued for another three… (More)
- R L Lock, S M Audenaert, C H Richardson, R C Haydon
- The Laryngoscope
- 1994
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- 1
- ›


text:
Business Investment Awards Boost South Coast Fishing Industry
RDI's Executive Director Heidi Khokhar and Rural Economic Vitality Consultant Amy Hause visited Mach-1 Industries, SeaCoast Compost, and Watson's Live Seafood on Oregon's south coast this week. The businesses were recently awarded WealthWorks grants to purchase equipment and expand operations, which will also benefit the south coast fishing industry more widely.
Mach-1 Industries is a commercial diving company based out of Port Orford, which is currently expanding their business into the production and sales of dulse, a nutrient-rich seafood that tastes like bacon. The grant will enable the company to purchase equipment to increase dulse production.
SeaCoast Compost is a business located in Charleston that transforms highly nutritive waste products from local sources, including timber, cow manure, and fish waste, into biodynamic compost. Funding support will allow them to scale up production of their compost product.
Watson's Live Seafood is a seafood market located in Old Town Bandon that provides fresh, locally caught seafood to the local market. This funding will allow them to purchase equipment for a live tank system to keep live fish.
The investments will result in increased sales for all three businesses, along with five to six new employees in the short term and potentially double the amount in the long term. The funding would also increase income for at least 12 small boat owners and their crews, as well as contribute to non-financial benefits that include the reduction of fish waste, increased availability of local seafood to local markets, and the establishment of a small industry of dulse which is a new product for the Oregon coast.
The WealthWorks grants were awarded by RDI in partnership with NeighborWorks Umpqua and the Southwestern Oregon Food System Collaborative. In 2014, NeighborWorks Umpqua was awarded a grant from RDI to pilot a WealthWorks Northwest project with the goal of connecting community assets to meet market demands while still building livelihoods that last. Food is an enormous asset in Oregon's southwest region, and the Southwestern Oregon Food System Collaborative was formed, with a focus on seafood, as part of the WealthWorks coaching. The collaborative includes a group of diverse organizations, agencies, and businesses, and the goal of the seafood project is to increase access to fresh, local fish in South Coast communities, and to increase income for local fishermen. Click here to read an article in the World for more information.
RDI is a partner in the growing national community of practice that is using the WealthWorks framework, led by Yellow Wood Associates and other national partners, to achieve measureable results on the ground. This integrative economic development approach seeks to leverage existing, or emerging, community assets and economic sectors to connect people, resources, and markets to generate community wealth in rural regions. The model is grounded on the premise that a value chain can generate investments across all eight forms of capital—built, cultural, financial, individual, intellectual, natural, political, and social—and each form of capital is working to reinforce rather than undermine the others to create lasting rural livelihoods and communities.


text: Hi Marc, The green check-mark is not turned on and snapshots are not being created. I have no idea why this is happening. I looked at every log file to try to find a reason, but I I could not find an error related to this. As explained, the IAM user I am using in Scalr have appropriate permissions, I can trigger a manual snapshot and it works, I can view snapshots, I can view volumes. I have 4 other environments configured exactly the same and everything is working fine. The only difference I could find is that this is the only volume hosted in region us-east1b, others in other environments are in different sub-region, like us-east1a or 1c. I have also tried to create a volume from Scalr and enable auto-snapshot on it, but same behaviour and auto-snapshot stays disabled. Here's some screen capture: <https://lh3.googleusercontent.com/-8D3Bbugln4I/WEDIK-dpnSI/AAAAAAAACNw/PQ7pnOVN7wcTH84-mukWD9iLvYEjSVS2QCLcB/s1600/scalr%2B1.PNG> <https://lh3.googleusercontent.com/-yf-e46VItjE/WEDIRHdkISI/AAAAAAAACN0/Fn_nKN74veYcvuOuWyARs6MMXOwqbSYegCLcB/s1600/scalr%2B2.PNG> <https://lh3.googleusercontent.com/-gGG_q84V-4o/WEDIT7C_n6I/AAAAAAAACN4/1SKLRiiTOMcT1BQdZOMZXjFc4usrB5LWgCLcB/s1600/scalr%2B3.PNG> Le mercredi 30 novembre 2016 13:32:37 UTC-5, Marc O'Brien a écrit : > > Hi Bernard, > > Can you please provide additional details about this behavior. When you > attempt to enable Auto Snapshots and receive the success message, do you > then see the green Check-mark next to Auto-Snaps to indicate that the > setting is turned on? If this does occur, are the snapshots not being > created according to the configured schedule? What is the behavior that > you are seeing that is not allowing you to enable auto snapshots? > > Many thanks, > Wm. Marc O'Brien > Scalr Technical Support > > > > <https://lh3.googleusercontent.com/-jJA8VrPJWYs/WD8bGtIslEI/AAAAAAAAAFI/rqH_lafPOkg7J9SJ4hGtsxTOwPUXu_l8QCLcB/s1600/EBS_Volumes_-_Scalr_CMP.png> > -- You received this message because you are subscribed to the Google Groups "scalr-discuss" group. To unsubscribe from this group and stop receiving emails from it, send an email to scalr-discuss+unsubscr...@googlegroups.com. For more options, visit https://groups.google.com/d/optout.


text:
|14 Mar 2012
Oh yeah anw is there anyway to increase the mousepad speed?
|My System Specs
|14 Mar 2012
Hey boohbah its alright my problem is solved already. Thanks anw!
|My System Specs
|14 Mar 2012
Oh and is there anyway to recover my 'My Music' file. I think i accidentally deleted or may have shifted it to another location and its not in the recycle bin.
|My System Specs
|14 Mar 2012
Microsoft Windows 7 Home Premium 64-bit 7600
you would be better off creating a new thread for each of your new questions, when you say deleted your my music folder do you mean from the library or is it gone completely from your pc?
|My System Specs
|Thread Tools
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Outlook 2010 cannot change my mail view back to normal from list view
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text:
|Student Expectations
|How Will I Meet This Expectation?
|How Did I Meet This Expectation?
|Demonstrate ability to evaluate sources of biology information on the internet
|Demonstrate an ability to read and understand current biology news
|Demonstrate proper use of online resources
|Publish work that is available for peer-review
|Discuss published work with a practicing biologist in that particular field
|Provide constructive peer-review to classmates
|Discuss in-class assignments
|Apply creativity to work
We all remember last spring when we first heard of the terrifying Swine Flu (H1N1). The news came in March and the media loved it. They spoke of how this could cause death on a scale not seen since the 1918 influenza epidemic. Since then there have been 1567 laboratory confirmed deaths from H1N1 in the U.S., little compared to 20 to 100 million people who died from the 1918 flu epidemic.
Although commonly referred to as Swine Flu, the H1N1 virus is a mix of Swine Flu, Avian Flu, and Human Flu. It is called Swine Flu because early studies showed that it was similar to an influenza in pigs. In fact it is made from flu genes from pigs in Europe and Asia, birds, and humans. On October 24 2009 President Obama declared the H1N1 virus a national emergency.
|Chanchoche by jpcolasso.
H1N1 affects almost the same population as the seasonal flu; the very old, the very young, the pregnant, and the sick. But H1N1 is more prone to infect teenagers, young adults and pregnant women than is the seasonal flu, possibly because these younger groups do not have immunity as they were not exposed to previous influenza outbreaks. The H1N1 virus spreads the same way as the seasonal flu, through coughing, sneezing, or touching an area with the virus then touching one's mouth or nose. Once someone is infected with the H1N1 virus he or she is unlikely to contract it again (Although someone with a weak immune system may not be able to become completely immune to the virus).
The symptoms of the H1N1 virus are fever, cough, sore throat, vomiting, diarrhea, runny or stuffy nose, body aches, headache, chills, fatigue and respiratory problems. People can spread the virus from a day before one gets sick to 5-7 days after getting sick.
The CDC says if someone is exhibiting the following symptoms he or she needs medical care immediately.
In children:
- Fast breathing or trouble breathing
- Bluish skin color
- Not drinking enough fluids
- Not waking up or not interacting
- Being so irritable that the child does not want to be held
- Flu-like symptoms improve but then return with fever and worse cough
- Fever with a rash
- Difficulty breathing or shortness of breath
- Pain or pressure in the chest or abdomen
- Sudden dizziness
- Confusion
- Severe or persistent vomiting
The following video can also be found at http://www.cdc.gov/CDCTV/IR_WarningSigns/index.html
The following video can also be found at http://www.cdc.gov/CDCTV/IR_Take3/index.html#. Dr. Bresee talks of ways to protect yourself including the H1N1 vaccine, hygiene, and antivirals if already sick.
To stay healthy and safe people should follow these everyday guidelines. Cover your nose and your mouth when you sneeze or cough with a tissue, after it is used throw it away. Always wash your hands with soap, water or an alcohol based hand-cleaner. Do not touch your nose, mouth, or eyes. Avoid contact with sick people.
The H1N1 vaccination has probably caused the most controversy around Swine Flu. Many fear that the vaccination is unsafe and worry that it won't work. Three recent studies have proven that the vaccination is safe and protective. The studies are shown below.
(Greenberg ME, Lai MH, Hartel GF et al. Response to a monovalent 2009 influenza A (H1N1) vaccine. New Engl J of Med, 2009; 361: 2405-13; Zhu FC, Wang H, Fang HH, et al. A novel influenza A (H1N1) vaccine in various age groups. New Engl J of Med, 2009; 361: 2414-23; Clark TW, Pareek M, Hoschler K et al. Trial of 2009 influenza A (H1N1) monovalent MF59-adjuvanted vaccine. New Engl J Med, 2009; 361: 2424-35.).
Getting the swine flu vaccination is the best way to protect yourself. The harm swine flu could cause is much greater than the harm that the vaccine could.
Contrary to popular belief you cannot get swine flu from eating properly prepared pork, but you can get it from contact with pigs infected with H1N1. Pigs do carry the H1N1 virus, even a pig at the Minnesota state fair was infected with the H1N1 virus.
1. Will the current H1N1 vaccine be effective against next year's flu virus?
2. Are their medications you can take if you already have the H1N1 virus?
3. Is the threat of the pandemic over, or can the H1N1 virus continue to infect the population?
Hello my name is Vincent. I am in 9th grade biology taught by Miss Baker. That's My dog.
My Favorite Bands; The Beach Boys, The Beatles, The Who
God Only Knows By The Beach Boys
Lady Madonna By The Beatles
I also like the Yankees


text:
The Abbey Court Notting Hill
The Abbey Court Hotel is located in a quiet area of London in close proximity to Olympia Exhibition Centre, Hyde Park and West End. The hotel opened in 1850 and remains an example of Victorian architecture in London ever since.
Overlooking Hyde Park Kensington Gardens the property boasts central location in Westminster of London. London city center is 5 km away.
Shoppers will appreciate shops, boutiques and markets at a short distance from the hotel.
This grand hotel provides elegant rooms equipped with a writing desk, a minibar, an iron with ironing board, a laptop safe and satellite TV. All bathrooms are appointed with dressing gowns, a shower and a hairdryer.
A sumptuous full English breakfast is served in the dining room. Guests can enjoy light meals of local cuisine at the hotel's restaurant. Guests can dine in Sun In Splendour and The Fish House of Notting Hill located within a 5-minute walk of the property.
Guests will find themselves a 5-minute stroll from Notting Hill Gate subway station. The Abbey Court Hotel is about 20 minutes' drive towards London City airport.
There are car rentals available on site.
The on-site spa facilities include a spa lounge and a Jacuzzi.