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Hot Shoe Records
The Best In Jazz From The Best Contemporary Artists
JOE GRANSDEN & RUSSELL GUNN
ALBUM SPECIAL:
CD for $11.99
Download album for 9.99 or
Download individual tracks for $1.00 each
(Click on track below to download)
A great trumpeter who emerged from the classic bebop era of the mid-1940s, Kenny Dorham (1924-72) was a major musical force throughout the 1950s and '60s. A very lyrical and thoughtful trumpeter who was also a skilled composer (his "Blue Bossa" has been a standard for decades), Dorham fit comfortably into both bop and hard bop settings.
The Atlanta-based trumpeters Russell Gunn and Joe Gransden are longtime friends who decided that a Kenny Dorham tribute was long overdue, particularly since the Dorham family lives in Atlanta. Russell and Joe present here some of their favorite Kenny Dorham songs.
The two trumpeters are joined by three of the top players in Atlanta: pianist Louis Heriveaux , bassist Kevin Smith and drummer Clay Hulet who has worked with Gransden for 12 years. The trio's timeless playing would have fit in perfectly on a vintage Blue Note album yet sounds fresh and original within the style.
Joe Gransden (trumpet, vocals)
Russell Gunn (trumpet)
Louis Heriveaux (piano)
Kevin Smith (bass)
Clay Hulet (drums)
© 2018-2022 by Hot Shoe Records, LLC.

redpajama_set_name: RedPajamaCommonCrawl


Premium, all nautral mustache wax. Smells like honey. Resist the urge to taste. No perfume.
Ridiculously strong hold, tested for durance in snow, rain, blizzards, and bloody awful weather, just a tad south of the Arctic Circle.


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Caribbean Monk Seal Habitat
By Judith Willson
NA/AbleStock.com/Getty Images
The Caribbean monk seal (Monachus tropicalis) is another example of a marine mammal that is no longer with us. The species was exterminated in the first half of the 20th century, with the last confirmed sighting being in 1952. Habitat destruction might have played a part in their demise, although the main reason appears to have been uncontrolled hunting.
The Caribbean monk seal used to be plentiful in the warm waters of the Gulf of Mexico, the western Atlantic and, as the name suggests, the Caribbean Sea. Their range extended from the coasts of Georgia and South Carolina right down to the north east side of South America. The events leading to their eventual extinction began with the arrival of the first Europeans in the area at the end of the 15th century.
The Habitat
Caribbean monk seals inhabited temperate to tropical waters. Although they were not creatures of the open ocean, they didn't often venture onto the mainland, preferring isolated islands when they needed to come out of the water. This might have been an adaptation to avoid large land predators but it didn't help the species avoid humans.
Human hunters killed the seals in huge numbers for their pelts and oil. Later, they were also persecuted as a perceived threat to fish stocks. A significant number of seals were killed and stuffed for exhibition in museums or caught alive for zoos. At the same time as the seals were being slaughtered in their thousands, their habitat was being degraded and polluted by the developments springing up along the coast. According to Animal Diversity Web, loss of suitable habitat was the last straw.
Last Sightings
The last sightings occurred in the first years of the 1950s. By the 1960s, it was suspected the species was extinct. In 2008, it was officially confirmed with the removal of Caribbean monk seals from the US Endangered Species Act. Occasional reports of sightings still occur, but these are almost certainly misidentification of other seal species, such as the hooded seal. Exhaustive scientific surveys have found no trace of Caribbean monk seals in their former habitat.
Monk Seal Distribution Today
The Caribbean monk seal has gone but two relatives remain. Both are critically endangered and may end up going the same way if current population trends continue. The survivors of the genus Monachus are the Mediterranean monk seal and the Hawaiian monk seal. Their range is now restricted to small areas of, respectively, the Mediterranean (and North Atlantic) and around the islands of Hawaii. The major threats to both species are overfishing, habitat destruction and disturbance, death as bycatch in fishing nets, pollution and deliberate persecution. The International Union for the Conservation of Natures notes that Hawaiian monk seals are also threatened by military activities in the area and may be vulnerable to diseases carried by domestic pets.
NOAA Fisheries -- Office of Protected Resources: Caribbean Monk Seal
International Union for the Conservation of Nature: Monachus tropicalis
Animal Diversity Web: Monachus tropicalis
International Union for the Conservation of Nature: Monachus monachus
International Union for the Conservation of Nature: Monachus schauinslandi
Judith Willson has been writing since 2009, specializing in environmental and scientific topics. She has written content for school websites and worked for a Glasgow newspaper. Willson has a Master of Arts in English from the University of Aberdeen, Scotland.
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Endangered Species in Germany
Are River Otters Endangered?
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Endangered Animals From the Democratic Republic of Congo
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Animals of the Brazos River
How Fast Can an Elephant Seal Move on Land?
Marine Otters Habitat
What Do Seals Eat?


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Mike The Gun Guy™
A Magazine With News and Notes From Both Sides About Guns.
Do Campus Guns Prevent Campus Rape? They Do And They Don't.
Posted on February 20, 2015 by mikethegunguy
Now that the gun lobby has succeeded in getting all 50 states to issue some form of concealed-carry license, the next battle which they want to fight is over gun-free zones. And while states have passed laws liberalizing the possession of concealed weapons in establishments serving liquor, houses of worship and other locations traditionally considered pistole verboten, the locations where pro-gun heat is being turned up are the nation's college campuses which tend, by and large, to have fairly restrictive policies on students and faculty walking around with guns.
Currently only a handful of states have fairly liberal gun policies in effect, seventeen states forbid guns altogether and the remainder leave it up to individual school option, but in most such places a no-gun policy tends to be the rule. You would think, incidentally, that states with blanket prohibitions against guns would be located in the Northeast and other parts of the country that both lean liberal and don't have high percentages of residents who own guns. In fact, more than half of the strongest, no-guns-on-campus states are located in the South, where gun laws in general tend to be the least strict. Even Florida, known as the "gunshine" state, forbids guns on all college campuses; ditto Georgia which last year opened up all sorts of public locations to concealed carry of guns.
The campaign to allow guns on campus recently hit the national news when state legislators in Florida and Nevada introduced pro-gun campus bills and linked the necessity for ending gun-free college zones to what continues to be a complicated and hot-button issue; namely, the question of campus rape. The sponsor of the Nevada bill, Michele Fiore (R-Las Vegas) may have stuck her foot a little too far into her mouth when she referred to the "hot little girls on campus" who needed to protect themselves, and in case you're still wondering, her reference to heat had nothing to do with staying outside in the sun.
The issue of campus rape keeps bubbling back and forth between those who claim that the numbers don't justify all the recent concern, as opposed to those who declare with equal certainty that the numbers are meaningless because young women, particularly on campuses with large residential populations, are afraid to come forward and report a rape. Much campus sexual assaults occur during 'animal house'-style parties, and while collage administrations are on notice to be more diligent in monitoring dangerous behavior, no educational institution wants to be considered just a party school whose lack of campus security puts students at risk.
One group that has used the campus rape issue to increase its visibility and perhaps its membership is a group called Students for Concealed Carry, which claims to have more than 40,000 members which is pretty close to the number of 'likes' on their Facebook page. The group gets lots of promotional help from the NRA (gee – what a surprise) and while they tend to promote their demand for campus gun rights as part of a loosely-defined libertarianism, their website motto states explicitly that guns are "an effective means of self defense."
I really don't know anything about sexual assault so I'll let other experts explain the ins and outs as well as the various theories for the prevention of same. But I do know something about guns and I also know a lot about whether guns represent, a la the SCC website, an "effective" means of defense. And the truth is that guns do represent an effective means of defense against assaults, but they are no more effective than other methods, such as running away or calling for help. And this isn't my opinion, it's research published by the pro-gun criminologist Gary Kleck. And the good news about calling for help is that a droid can't do much damage if it falls into the wrong hands. Can anyone say that about guns?
Available on Amazon.
This entry was posted in Blogs and tagged CCW, Concealed carry, NRA, rape. guns on campus, SCC by mikethegunguy. Bookmark the permalink.


In describing the basic essentials for fire, many talk about the fire tetrahedron. In other words, aside from the original fire triangle of fuel, heat and air, they add the fourth essential of chemical reaction. Fire starts use all four! It is necessary for us to understand the part each of these works in producing fire in order that we can put it to use in either lighting our fire pit and preventing or extinguishing excess fires. For example , to put out a grease fire at the stove, turn off the stove (removing the heat) and cover with a lid (removing the oxygen that bottles the fire). This will likewise benefit those contemplating buying a fireplace pit, helping them to decide which fire pits are best for these people.
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Enter News, Quotes, Companies or Videos
https://www.wsj.com/articles/when-the-levee-breaks-brazilian-town-on-alert-for-imminent-disaster-11558517405
Maria Rodrigues's bar, which lies on the edge of Barão de Cocais' evacuated area, has been empty since February. Victor Moriyama for The Wall Street Journal
Imminent Vale Dam Disaster Bears Down on Brazilian Town
Vale has warned authorities that one of its major dams could collapse at any moment, likely burying a nearby town
Samantha Pearson
samantha.pearson@wsj.com
May 22, 2019 5:30 am ET
BARÃO DE COCAIS, Brazil—In this once-thriving town at the heart of Brazil's mining region, there is one question on everybody's minds: Will a nearby dam burst and obliterate their community by the week's end?
Vale SA has warned Brazilian authorities that one of its dams about 8 miles away could collapse at any moment, likely burying the town of Barão de Cocais in mining waste just months after the rupture of the company's dam in Brumadinho killed 270 people.
"It's the uncertainty that is pushing people over the edge," said José Apolinário, deacon of a local church. Some men tell him they are so afraid of not hearing the mine's warning sirens they stay awake at night to keep watch over their families. "This town is no longer the same—the dam is the only thing people talk about."
The 280-foot-high Sul Superior dam here in southeastern Brazil is one of Vale's nine remaining dams built via the cheaper "upstream" method, a model that has come under intense global scrutiny after the collapse of the similarly built Brumadinho dam on Jan. 25.
Engineers now believe the dam here to be so fragile that any small vibration could cause it to come crashing down. They have watched with horror over recent weeks as ever-larger cracks appear in an adjacent disused mine pit in Vale's Gongo Soco mine.
© 2021 Dow Jones & Company, Inc. All Rights Reserved.


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Finance Act 1996
1996 c. 8
Changes over time for: Section 154
There are outstanding changes not yet made by the legislation.gov.uk editorial team to Finance Act 1996. Any changes that have already been made by the team appear in the content and are referenced with annotations.
Changes and effects yet to be applied to Section 154:
s. 154(2) repealed by 2009 c. 4 Sch. 1 para. 438 Sch. 3 Pt. 1
s. 154(2) words inserted by 2005 c. 5 Sch. 1 para. 488(2)(b)
s. 154(2) words substituted by 2005 c. 5 Sch. 1 para. 488(2)(a)
s. 154(4) repealed by 2005 c. 5 Sch. 1 para. 488(3) Sch. 3
s. 154(6) words repealed by 2005 c. 5 Sch. 1 para. 488(4) Sch. 3
Act amendment to earlier affecting provision S.I. 2006/964, reg. 95 by S.I. 2008/1463 reg. 2
Act modified by S.I. 2006/964 reg. 95 (This SI is amended by SI 2009/2036 reg. 30)
Act modified by S.I. 2009/317 art. 3 Sch.
Blanket amendment words substituted by S.I. 2011/1043 art. 3 4
s. 40(4) inserted by 2018 c. 3 Sch. 12 para. 2(3)
s. 40A inserted by 2018 c. 3 Sch. 12 para. 3
s. 41(3)-(8) inserted by 2018 c. 3 Sch. 12 para. 4(3)
s. 42(3A)(3B) inserted by 2015 c. 11 Sch. 15 para. 2(3)
s. 42(4)-(6) substituted for s. 42(4) by 2010 c. 33 s. 24(1)
s. 42(4)(a) words inserted by 2015 c. 11 Sch. 15 para. 2(4)
s. 42(6) words inserted by 2015 c. 11 Sch. 15 para. 2(5)
s. 43(5) inserted by S.I. 2007/2909 art. 2
s. 43(5) words inserted by 2018 c. 3 Sch. 12 para. 5
s. 43C(3)(d) inserted by S.I. 2005/725 art. 3
s. 46(2)(za) inserted by 2018 c. 3 Sch. 12 para. 8
s. 47(3A) inserted by 2018 c. 3 Sch. 12 para. 17(3)
s. 47(5A)(5B) inserted by 2018 c. 3 Sch. 12 para. 17(4)
s. 47(9)-(9B) substituted for s. 47(9) by 2018 c. 3 Sch. 12 para. 17(6)
s. 50A inserted by 2018 c. 3 Sch. 12 para. 23
s. 53(4)(ca) inserted by 2007 c. 11 s. 24(1)
s. 54(1)(ca) inserted by 2008 c. 9 s. 151(3)
s. 54(2)(b) and word inserted by 2018 c. 3 Sch. 12 para. 24(b)
s. 54A-54G inserted by S.I. 2009/56 Sch. 1 para. 235
s. 54G(4) substituted by S.I. 2014/1264 art. 5
s. 55(3A)(3B) inserted by S.I. 2009/56 Sch. 1 para. 236(6)
s. 56(5A) inserted by S.I. 2009/56 Sch. 1 para. 237(7)
s. 63(4A) inserted by 2015 c. 11 Sch. 15 para. 3
s. 63A inserted by 2015 c. 11 Sch. 15 para. 4
s. 71(7)(cza) inserted by 2015 c. 11 Sch. 15 para. 6(3)
s. 71(7)(aa) inserted by 2015 c. 11 Sch. 15 para. 6(2)
s. 71(7)(ca)(cb) inserted by 2009 c. 10 Sch. 60 para. 3
s. 71(7)(ca)(cb) omitted by 2018 c. 3 Sch. 12 para. 15(b)
s. 71(7)(za) inserted by 2018 c. 3 Sch. 12 para. 15(a)
s. 81(2)(c) and words inserted by 2006 c. 25 Sch. 6 para. 10(2)(b)
s. 85A repealed by 2009 c. 4 Sch. 1 para. 409 Sch. 3 Pt. 1
s. 85A(1) words inserted by 2006 c. 25 Sch. 6 para. 11(2)
s. 85B repealed by 2009 c. 4 Sch. 1 para. 410 Sch. 3 Pt. 1
s. 85B(1) modified by S.I. 2005/3422 reg. 9(5)
s. 85B(1)(a) words inserted by 2005 c. 7 Sch. 4 para. 26(2)
s. 85B(2) substituted by 2005 c. 7 Sch. 4 para. 26(3)
s. 85B(3)(a) words inserted by 2005 c. 7 Sch. 4 para. 26(4)(a)
s. 85B(3)(b) words substituted by 2005 c. 7 Sch. 4 para. 26(4)(b)
s. 85B(4) words inserted by 2005 c. 7 Sch. 4 para. 26(5)
s. 85B(6) repealed by 2005 c. 22 Sch. 11 Pt. 2(6)
s. 85C inserted by 2006 c. 25 Sch. 6 para. 12(1)
s. 85C repealed by 2009 c. 4 Sch. 1 para. 411 Sch. 3 Pt. 1
s. 85C(1)(c) words substituted by 2007 c. 11 Sch. 5 para. 11(2)(a)
s. 85C(1)(d)(e) words substituted by 2007 c. 11 Sch. 5 para. 11(2)(b)
s. 85C(2) words substituted by 2007 c. 11 Sch. 5 para. 11(3)(a)
s. 85C(2) words substituted by 2007 c. 11 Sch. 5 para. 11(3)(b)
s. 91A and cross-heading inserted by 2005 c. 22 Sch. 7 para. 10(1)(2)
s. 91A(1) words substituted by 2006 c. 25 Sch. 6 para. 13(2)
s. 91A(2)(b) words omitted by 2008 c. 9 Sch. 22 para. 6(1)(a)
s. 91A(2A) inserted by 2008 c. 9 Sch. 22 para. 7(2)
s. 91A(3) words omitted by 2008 c. 9 Sch. 22 para. 7(3)
s. 91A(5)(a) words inserted by 2006 c. 25 Sch. 6 para. 13(4)(a)
s. 91A(5)(b) words inserted by 2006 c. 25 Sch. 6 para. 13(4)(b)
s. 91A(5A) inserted by 2006 c. 25 Sch. 6 para. 13(5)
s. 91A(7) words substituted by 2008 c. 9 Sch. 22 para. 10(2)
s. 91A(7)(a) words omitted by 2008 c. 9 Sch. 22 para. 19(2)(a)
s. 91A(8)(b) words inserted by 2008 c. 9 Sch. 22 para. 10(3)
s. 91A(11) inserted by 2007 c. 11 Sch. 5 para. 12(3)
s. 91B inserted by 2005 c. 22 Sch. 7 para. 10(3)
s. 91B(1) words substituted by 2006 c. 25 Sch. 6 para. 14(2)(a)
s. 91B(1) words substituted by 2006 c. 25 Sch. 6 para. 14(2)(b)
s. 91B(2) words inserted by 2006 c. 25 Sch. 6 para. 14(3)
s. 91B(2)(b) words omitted by 2008 c. 9 Sch. 22 para. 6(1)(b)
s. 91B(2A) inserted by 2008 c. 9 Sch. 22 para. 8(2)
s. 91B(3) words omitted by 2008 c. 9 Sch. 22 para. 8(3)
s. 91B(4) words substituted by 2007 c. 11 Sch. 5 para. 13(2)
s. 91B(5)(a) words omitted by 2008 c. 9 Sch. 22 para. 13(1)
s. 91B(8) inserted by 2007 c. 11 Sch. 5 para. 13(3)
s. 91C-91E inserted by 2005 c. 22 Sch. 7 para. 10(4)
s. 91C(1) words substituted by 2008 c. 9 Sch. 22 para. 11(2)
s. 91C(3)(c) substituted by 2008 c. 9 Sch. 22 para. 14(1)
s. 91C(3)(f) substituted by 2007 c. 11 Sch. 14 para. 15
s. 91D repealed by 2009 c. 4 Sch. 1 para. 420 Sch. 3 Pt. 1
s. 91D(2) substituted by 2006 c. 25 Sch. 6 para. 15(2)
s. 91D(2)(a) word omitted by 2008 c. 9 Sch. 22 para. 15(1)
s. 91D(2)(c) and word inserted by 2008 c. 9 Sch. 22 para. 15(1)
s. 91D(2A) inserted by 2006 c. 25 Sch. 6 para. 15(3)
s. 91D(7) words substituted by 2006 c. 25 Sch. 6 para. 15(4)
s. 91D(11) words substituted by 2007 c. 3 Sch. 1 para. 373
s. 91E repealed by 2009 c. 4 Sch. 1 para. 421 Sch. 3 Pt. 1
s. 91E(1) words inserted by 2008 c. 9 Sch. 22 para. 16(2)(a)
s. 91E(1) words inserted by 2008 c. 9 Sch. 22 para. 16(2)(b)
s. 91E(3) words inserted by 2008 c. 9 Sch. 22 para. 16(3)
s. 91F inserted by 2005 c. 22 Sch. 7 para. 10(5)
s. 91F repealed by 2009 c. 4 Sch. 1 para. 422 Sch. 3 Pt. 1
s. 91G inserted by 2005 c. 22 Sch. 7 para. 10(6)
s. 91G repealed by 2009 c. 4 Sch. 1 para. 423 Sch. 3 Pt. 1
s. 91H 91I and cross-heading inserted by 2008 c. 9 Sch. 22 para. 17(1)
s. 91H repealed by 2009 c. 4 Sch. 1 para. 424 Sch. 3 Pt. 1
s. 91I repealed by 2009 c. 4 Sch. 1 para. 425 Sch. 3 Pt. 1
s. 94A(1) words substituted by 2005 c. 7 Sch. 4 para. 28(2)
s. 94B inserted by 2008 c. 9 Sch. 22 para. 18(1)
s. 97(2A) inserted by 2005 c. 22 Sch. 7 para. 11(3)
s. 97(4B) inserted by 2007 c. 11 Sch. 14 para. 16(3)
s. 100(1)(c)(iii) and word inserted by 2005 c. 7 Sch. 4 para. 9(3)
s. 100(1)(c)(iv) and word inserted by 2005 c. 22 Sch. 7 para. 12(2)
s. 100(1A) inserted by 2005 c. 22 Sch. 7 para. 12(3)
s. 100(1A)(e) substituted by 2006 c. 25 Sch. 6 para. 17(2)
s. 100(1B) inserted by 2006 c. 25 Sch. 6 para. 17(3)
s. 100(2A) repealed by 2007 c. 11 Sch. 14 para. 17 Sch. 27 Pt. 2(14)
s. 100(2ZA)(2ZB) inserted by 2005 c. 22 Sch. 7 para. 12(5)
s. 100(3A)(3B) inserted by 2005 c. 22 Sch. 7 para. 12(6)
s. 100(14) added by 2005 c. 7 Sch. 4 para. 9(5)
s. 103(1AA) inserted by 2005 c. 7 Sch. 4 para. 29
s. 103(1AA) substituted by 2005 c. 22 Sch. 6 para. 10
s. 103(3)(c) and word inserted by 2007 c. 11 Sch. 10 para. 6(2)
s. 103(3A) omitted by 2008 c. 9 Sch. 22 para. 19(1)
s. 103(3B) omitted by 2008 c. 9 Sch. 22 para. 19(1)
s. 103(3B) words substituted by 2007 c. 3 Sch. 1 para. 375(3)
s. 148(6A) inserted by 2004 c. 12 Sch. 35 para. 44
Sch. 9. para. 12E(4) modified (temp.) by S.I. 2008/1579 reg. 6(1) Sch. 4 para. 3(d)
Sch. 5 para. 23A inserted by 2007 c. 15 Sch. 13 para. 123
Sch. 5 para. 33(1A) inserted by 2009 c. 10 Sch. 51 para. 40(3)
Sch. 5 para. 1A and cross-heading inserted by 2009 c. 10 Sch. 60 para. 7
Sch. 5 para. 1B inserted by 2009 c. 10 Sch. 60 para. 11
Sch. 5 para. 1C and cross-heading inserted by 2018 c. 3 Sch. 12 para. 16(3)
Sch. 5 para. 2A(1)(b) and word inserted by 2018 c. 3 Sch. 12 para. 16(4)(c)
Sch. 5 para. 27(8A)(8B) inserted by 2018 c. 3 Sch. 12 para. 25(2)(a)
Sch. 5 para. 33(1A)(aa) inserted by 2018 c. 3 Sch. 12 para. 25(3)(b)
Sch. 5 para. 36(2A) inserted by 2018 c. 3 Sch. 12 para. 25(4)(b)
Sch. 5 para. 35(1)(ba) inserted by S.I. 2013/755 Sch. 2 para. 390
Sch. 5 para. 23A omitted by 2008 c. 9 Sch. 43 para. 5
Sch. 5 para. 1B omitted by 2018 c. 3 Sch. 12 para. 16(2)
Sch. 5 para. 33(4)(4A) substituted for Sch. 5 para. 33(4) by 2009 c. 10 Sch. 51 para. 40(5)
Sch. 5 para. 33(1A)(a) word omitted by 2018 c. 3 Sch. 12 para. 25(3)(b)
Sch. 5 para. 2B 2C and cross-headings words inserted by 2015 c. 11 Sch. 15 para. 7(3)
Sch. 5 para. 10(1A) words inserted by 2015 c. 11 Sch. 15 para. 7(4)
Sch. 5 para. 2A heading words inserted by 2018 c. 3 Sch. 12 para. 16(4)(a)
Sch. 5 para. 2A(1) words substituted by 2018 c. 3 Sch. 12 para. 16(4)(b)
Sch. 9 para. 19A applied by 2005 c. 22 Sch. 6 para. 7(6)
Sch. 9 para. 2(1E)-(1G) inserted by 2005 c. 22 Sch. 8 para. 2(3)
Sch. 9 para. 10A(1A) inserted by 2005 c. 22 Sch. 7 para. 15(2)
Sch. 9 para. 12A and cross-heading inserted by 2005 c. 22 Sch. 7 para. 18(1)
Sch. 9 para. 12B and cross-heading inserted by 2005 c. 22 s. 54(1)
Sch. 9 para. 18(1B)(1C) inserted by 2005 c. 22 Sch. 8 para. 3(6)
Sch. 9 para. 18(1ZA) inserted by 2005 c. 22 Sch. 8 para. 3(4)
Sch. 9 para. 19A(4BA) inserted by 2005 c. 22 Sch. 6 para. 6(1)
Sch. 9 para. 4A and cross-heading inserted by 2005 c. 7 Sch. 4 para. 10
Sch. 9 para. 5(8) inserted by 2005 c. 7 Sch. 4 para. 11(6)
Sch. 9 para. 5ZA and cross-heading inserted by 2005 c. 7 Sch. 4 para. 12
Sch. 9 para. 6D and cross-heading inserted by 2005 c. 7 Sch. 4 para. 16
Sch. 9 para. 14A and cross-heading inserted by 2005 c. 7 Sch. 4 para. 30
Sch. 9 para. 19A(4A)-(4D) inserted by 2005 c. 7 Sch. 4 para. 31(3)
Sch. 9 para. 12(2B) inserted by 2006 c. 25 Sch. 6 para. 19(3)
Sch. 9 para. 12(2C) inserted by 2006 c. 25 Sch. 6 para. 19(4)
Sch. 9 para. 11A(7)-(10) inserted by 2007 c. 11 Sch. 5 para. 15(1)
Sch. 9 para. 1(1A) inserted by 2008 c. 9 Sch. 22 para. 3(1)
Sch. 9 para. 11B and cross-heading inserted by 2008 c. 9 Sch. 22 para. 4(1)
Sch. 9 para. 12(2D)-(2F) inserted by 2008 c. 9 Sch. 22 para. 5(1)
Sch. 9 para. 12A(5A) inserted by S.I. 2007/3186 Sch. 1 para. 17(a) (This SI is amended by SI 2008/1579 reg. 4(1))
Sch. 9 para. 12D-12G and cross-heading inserted by S.I. 2007/3186 Sch. 1 para. 16 (This SI is amended by SI 2008/1579 reg. 4(1))
Sch. 9 para. 12H-12J and cross-heading inserted by S.I. 2007/3186 Sch. 3 para. 2 (This SI is amended by SI 2008/1579 reg. 4(2))
Sch. 9 para. 12B(2)(e) and word inserted by S.I. 2008/1579 Sch. 2 para. 3(2)(b)
Sch. 9 para. 12C(2)(f) and word inserted by S.I. 2008/1579 Sch. 2 para. 4(b)
Sch. 9 para. 12A(5A) modification to earlier affecting provision SI 2007/3186 reg. 3(1) by S.I. 2008/1579 reg. 4(1)
Sch. 9 para. 12A(8) modification to earlier affecting provision SI 2007/3186 reg. 3(1) by S.I. 2008/1579 reg. 4(1)
Sch. 9 para. 12D-12G modification to earlier affecting provision SI 2007/3186 reg. 3(1) by S.I. 2008/1579 reg. 4(1)
Sch. 9 para. 12H-12J modification to earlier affecting provision SI 2007/3186 reg. 3(3) by S.I. 2008/1579 reg. 4(2)
Sch. 9 para. 12B(2)(d) modified (temp.) by S.I. 2008/1579 reg. 6(1) Sch. 4 para. 3(a)
Sch. 9 para. 12C(2)(e) modified (temp.) by S.I. 2008/1579 reg. 6(1) Sch. 4 para. 3(b)
Sch. 9 para. 12D(4) modified (temp.) by S.I. 2008/1579 reg. 6(1) Sch. 4 para. 3(c)
Sch. 9 para. 12B(5) omitted by S.I. 2008/1579 Sch. 2 para. 3(4)
Sch. 9 para. 12B(9)(d) omitted by S.I. 2008/1579 Sch. 2 para. 3(5)
Sch. 9 para. 12D(5) omitted by S.I. 2008/1579 Sch. 2 para. 5(4)
Sch. 9 para. 18(1)(aa) repealed by 2005 c. 22 Sch. 8 para. 3(2) Sch. 11 Pt. 2(9)
Sch. 9 para. 19A(6) repealed by 2005 c. 7 Sch. 4 para. 31(5) Sch. 11 Pt. 2(7)
Sch. 9 para. 4A and cross-heading substituted by 2005 c. 22 Sch. 6 para. 5(1)
Sch. 9 para. 12(2A)(aa) substituted by 2005 c. 22 Sch. 7 para. 17(3)
Sch. 9 para. 12(2A)(aa) substituted by 2006 c. 25 Sch. 6 para. 19(2)(b)
Sch. 9 para. 12D(1)(d) substituted by S.I. 2008/1579 Sch. 2 para. 5(2)
Sch. 9 para. 12G substituted by S.I. 2008/1579 Sch. 2 para. 8
Sch. 9 para 12B 12C and cross-heading substituted for Sch. 9 para. 12B by S.I. 2007/3186 Sch. 2 para. 8
Sch. 9 para. 2(1B)(c)(d) substituted for Sch. 9 para. 2(1B)(c) by 2005 c. 22 Sch. 8 para. 2(2)(d)
Sch. 9 para. 6(3)(a)(b) substituted for Sch. 9 para. 6(3)(a)-(c) by 2005 c. 7 Sch. 4 para. 13(3)
Sch. 9 para. 19A(4B)(g) word inserted by 2005 c. 22 Sch. 6 para. 4(2)
Sch. 9 para. 12B(3) word inserted by S.I. 2008/1579 Sch. 2 para. 3(3)
Sch. 9 para. 12D(6) word inserted by S.I. 2008/1579 Sch. 2 para. 5(5)
Sch. 9 para. 12B(2)(c) word omitted by S.I. 2008/1579 Sch. 2 para. 3(2)(a)
Sch. 9 para. 12C(2)(d) word omitted by S.I. 2008/1579 Sch. 2 para. 4(a)
Sch. 9 para. 10A(2) word substituted by 2005 c. 22 Sch. 7 para. 15(3)
Sch. 9 para. 12H(2)(b) word substituted by S.I. 2008/1579 Sch. 2 para. 9(3)(b)
Sch. 9 para. 12I(2)(b) word substituted by S.I. 2008/1579 Sch. 2 para. 10(3)(b)
Sch. 9 para. 5(5) words added by 2005 c. 7 Sch. 4 para. 11(5)
Sch. 9 para. 19A(4) words inserted by 2005 c. 7 Sch. 4 para. 31(2)
Sch. 9 para. 15(2)(b) words inserted by 2006 c. 25 Sch. 6 para. 20(2)
Sch. 9 para. 12A(8) words inserted by S.I. 2007/3186 Sch. 1 para. 17(b) (This SI is amended by SI 2008/1579 reg. 4(1))
Sch. 9 para. 12A(5A) words inserted by S.I. 2008/1579 Sch. 2 para. 2
Sch. 9 para. 12D(3) words inserted by S.I. 2008/1579 Sch. 2 para. 5(3)
Sch. 9 para. 12H(4) words inserted by S.I. 2008/1579 Sch. 2 para. 9(4)
Sch. 9 para. 12H(5)(a) words inserted by S.I. 2008/1579 Sch. 2 para. 9(5)
Sch. 9 para. 12I(4) words inserted by S.I. 2008/1579 Sch. 2 para. 10(4)
Sch. 9 para. 12I(5)(a) words inserted by S.I. 2008/1579 Sch. 2 para. 10(5)
Sch. 9 para. 12J(1) words inserted by S.I. 2008/1579 Sch. 2 para. 11(2)(a)
Sch. 9 para. 19A(4B)(g) words inserted by S.I. 2008/1579 Sch. 2 para. 12
Sch. 9 para. 12J(1)(b) words omitted by S.I. 2008/1579 Sch. 2 para. 11(2)(b)
Sch. 9 para. 12J(2) words omitted by S.I. 2008/1579 Sch. 2 para. 11(3)
Sch. 9 para. 5(4) words substituted by 2005 c. 7 Sch. 4 para. 11(4)
Sch. 9 para. 12E(5) words substituted by S.I. 2008/1579 Sch. 2 para. 6
Sch. 9 para. 12F(3) words substituted by S.I. 2008/1579 Sch. 2 para. 7
Sch. 9 para. 12H(1)(a) words substituted by S.I. 2008/1579 Sch. 2 para. 9(2)(a)
Sch. 9 para. 12H(1)(a) words substituted by S.I. 2008/1579 Sch. 2 para. 9(2)(b)
Sch. 9 para. 12I(1)(a) words substituted by S.I. 2008/1579 Sch. 2 para. 10(2)
Sch. 9 para. 12I(2)(a) words substituted by S.I. 2008/1579 Sch. 2 para. 10(3)(a)
Sch. 10 para. 4(5)(6) inserted by 2007 c. 11 Sch. 5 para. 16(3)
Sch. 10 para. 8(7G)-(7I) inserted by S.I. 2006/981 art. 5
Sch. 10 para. 8(2)(e)-(h) substituted for Sch. 10 para. 8(2)(e)(f) by S.I. 2006/981 art. 3
Sch. 11 para. 1(1C) inserted by 2005 c. 22 Sch. 7 para. 20(2)
Sch. 11 para. 3A(2A)(2B) inserted by 2008 c. 9 Sch. 17 para. 9(1)
Sch. 11 para. 2(2A) omitted by 2008 c. 9 Sch. 17 para. 3(a)
Sch. 11 para. 1(1A)-(1C) repealed by 2007 c. 11 Sch. 10 para. 6(4) Sch. 27 Pt. 2(10)
Sch. 13 para. 13A-13D and cross-heading inserted by 2005 c. 22 Sch. 7 para. 21(5)
Sch. 20 para. 47(b)(c) repealed by 2011 c. 11 Sch. 9 para. 5(a)
Sch. 26 para. 16 repealed by 2005 c. 22 Sch. 6 para. 9(1)(b) Sch. 11 Pt. 2(6)
Commencement Orders yet to be applied to the Finance Act 1996
Commencement Orders bringing legislation that affects this Act into force:
S.I. 2005/950 art. 2-4 commences (2003 c. 44)
S.I. 2005/1126 art. 2 commences (2005 c. 11)
S.I. 2006/982 art. 2 commences (2005 c. 22)
S.I. 2007/2483 art. 2-5 commences (2007 c. 11)
S.I. 2008/2358 art. 2 3 commences (2008 c. 17)
S.I. 2009/402 art. 2 commences (2008 c. 9)
S.I. 2009/571 art. 2-5 commences (2008 c. 9)
S.I. 2009/803 art. 2-10 commences (2008 c. 17)
S.I. 2010/862 art. 2 3 commences (2008 c. 17)
S.R. 2006/21 art. 2 commences (S.I. 2005/1455 (N.I.))
S.R. 2006/22 art. 2-7 commences (S.I. 2005/1455 (N.I.))
154 FOTRA securities.U.K.
(1)The modifications which, under section 60 of the M1Finance Act 1940, may be made for the purposes of any issue of securities to the conditions about tax exemption specified in section 22 of the M2Finance (No. 2) Act 1931 shall include a modification by virtue of which the tax exemption contained in any condition of the issue applies, as respects capital, irrespective of where the person with the beneficial ownership of the securities is domiciled.
(2)Subject to subsections (3) to (5) below, nothing in the Tax Acts shall impose any charge to tax on any person in respect of so much of any profits or gains arising from a FOTRA security, or from any loan relationship represented by a FOTRA security, as is expressed to be exempt from tax in the tax exemption condition applying to that security.
(3)Exemption from tax shall not be conferred by virtue of subsection (2) above in relation to any security unless the requirements imposed as respects that exemption by the conditions with which the security is issued (including any requirement as to the making of a claim) are complied with.
(4)The tax exemption condition of a FOTRA security shall not be taken to confer any exemption from any charge to tax imposed by virtue of the provisions of Chapter IA of Part XV or Chapter III of Part XVII of the Taxes Act 1988 (anti-avoidance provisions for residents etc.)
(5)Nothing in this section shall entitle any person to any repayment of tax which he has not claimed within the time limit which would be applicable under the Tax Acts (apart from this section) to a claim for the repayment of that tax.
(6)A person with the beneficial ownership of a FOTRA security who would, by virtue of this section, be exempt from tax in respect of some or all of the profits and gains arising from that security, or from any loan relationship represented by it, shall not be entitled for the purposes of income tax or corporation tax to bring into account any amount—
(a)in respect of changes in the value of that security;
(b)as expenses or disbursements incurred in, or in connection with, the holding of the security or any transaction relating to the security; or
(c)as a debit given, in respect of any loan relationship represented by that security, by any provision of Chapter II of this Part of this Act in respect of such a relationship.
(7)Schedule 28 to this Act (which contains amendments consequential on the provisions of this section) shall have effect.
(8)References in this section to a FOTRA security are references to—
(a)any security issued with such a condition about exemption from taxation as is authorised in relation to its issue by virtue of section 22 of the M3Finance (No. 2) Act 1931; or
(b)any 3½% War Loan 1952 Or After which was issued with a condition authorised by virtue of section 47 of the M4Finance (No. 2) Act 1915;
and references, in relation to such a security, to the tax exemption condition shall be construed accordingly.
(9)This section and Schedule 28 to this Act shall have effect—
(a)for the purposes of income tax, for the year 1996-97 and subsequent years of assessment; and
(b)for the purposes of corporation tax, for accounting periods ending after 31st March 1996.
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text:
> Sheet Music>Digital Sheet Music>Symphonic music>Symphonic Orchestra>Orchestra with soloist
Orchestra with soloist There are 17 products.
Auris Concertum
Author: Civilotti, Alejandro
The play Auris Concertum by Alejandro Civilotti is a hymn about return to the world of sounds.
Concert per a percussió i orquestra
Author: Puértolas, Pere J.
The Concert for Percussion and Orchestra by Pere J. Puértolas is a concert with a classical bent in three movements: Allegro, Andante moderato and Allegro con fuoco, and the brilliance of the soloist and, indeed, the whole orchestra is evident from the first few bars.
Concerto for saxophone and orchestra
Author: Benejam, Lluís
Concerto for Saxophone and Orchestra stems from the orchestration that made Lluís Benejam of one of his compositions, the Sonata for Saxophone and Piano, one of the most brilliant works of the author.
Concert per a tuba i orquestra
Concerto for Violin & Orchestra
Author: Bozzo, David
First and last movements of this Concerto by David Bozzo are made with the same thematic material and with a similar formal structure, like a house from where one leaves and where one returns.
Concerto núm. 2 per Clarinetto e Orchestra
Author: Rodríguez Picó, Jesús
There is a certain degree of continuity between the Concerto Nr. 1 for clarinet and orchestra (1989) and the Concerto Nr. 2 (1990), and they in fact have many similarities, such as the relationship that is established between the orchestra and the solo clarinet, the use of expressive clarinet passages of great technical complexity, and also thematic...
Author: Lamote de Grignon, Ricard
The structure of this Divertimento for orchestra of symphonic jazz is as follows: The 1st movement is an Allegro, with a joyful Fox rhythm; The 2nd movement, Moderato, has a Waltz time; The 3rd movement has a Slow tempo; Finally, the last movement is an Allegro molto, with a Ragtime rhythm.
Fantasia Concertante 1968
The piece Fantasia Concertante, which is structured as a single movement, fits perfectly into the fantasia genre: a free discourse from the solo instrument which, in spite of being based on an initial theme, includes various themes by way of improvisation.
La rosa dels vents
Author: Larios, Oscar
La Rosa dels Vents by Oscar Larios is a music tale for symphonic orchestral ensemble of elementary grade and narrator. The work has been composed and arranged to be played by musicians at least attending the third or fourth elementary grade. This edition has been revised and orchestrated to ensure maximum adaptability of the orchestration available to...
Suite per a viola i orquestra
Author: Borgunyó, Agustí
La Suite per viola i orquestra is imbued with the air of Hispanic festivity and Andalusian folklore which was so fashionable in the mid-20th century and is so appreciated by audiences around the world. Agustí Borgunyó displays a total mastery of orchestration as well as an exquisite taste for approaching the various themes without ever giving into the...
Variacions per a orquestra i piano
Author: Serra, Joaquim
Variations for orchestra and piano op. 38 belongs to the symphony/concerto genre, with a brilliant piano part that weaves a continuous discourse through a series of virtuosic sections. It is presented and organised as a theme and five variations that make up an organic whole.
Variacions simfòniques s. tema d'H. Eccles...
Author: Bertran, Moisès
The Symphonic Variations on a theme by Henry Eccles, comprise one Theme, six Variations, one Cadence and a reprise of the theme. These small sections follow one anotherwithout any interruption, with the aim of creating a work with a single stroke within a structure is discontinuous in places.


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American Lung Association gives R.I. failing grades for smog
Alex Kuffner Journal Staff Writer kuffneralex
Apr 21, 2020 at 11:01 AM Apr 21, 2020 at 11:32 AM
PROVIDENCE — The economic shutdown caused by the coronavirus pandemic has led to widespread reductions in air pollution, but Rhode Island still has a long way to go to make longer-lasting improvements in air quality.
The American Lung Association gave counties in Rhode Island failing grades for ozone pollution — also known as smog — in its 2020 State of the Air report, with Providence and Kent counties recording more unhealthy days than in last year's report.
And while they and Washington — the three counties that report data in the state — all recorded drops in short-term spikes of particle pollution, or soot, Kent saw a small increase in year-round soot levels.
TO OUR READERS: This content is being provided for free as a public service during the coronavirus outbreak. Sign up for our daily or breaking newsletters to stay informed. Please support local journalism by subscribing to The Providence Journal.
The report, released Tuesday, tracks exposure to ozone and particle pollution, the two most widespread outdoor air pollutants, over a three-year period. Although the report doesn't cover air quality during the recent COVID-19 crisis, it does shed light on the extent of pollution that harms lung health and has put people at greater risk from the virus, according to the American Lung Association.
"For many Americans, the COVID-19 pandemic has illustrated just how important lung health really is," said Dr. Terrance Healey, director of thoracic radiology at Rhode Island Hospital. "We must do more to protect our lungs from anything that puts our ability to breathe at risk, be it a virus, tobacco smoke or air pollution."
A recent report from researchers at Harvard University found that people who live in areas with high levels of air pollution are more likely to die from the coronavirus than people who live in less-polluted areas.
Despite that study and other research, the U.S. Environmental Protection Agency is declining to move forward with more stringent air-pollution standards. The agency has rejected recommendations from staff scientists to tighten standards and is instead proposing that they remain unchanged.
In a letter to EPA administrator Andrew Wheeler, U.S. Senators Jack Reed and Sheldon Whitehouse, both of Rhode Island, and 16 other Democrats in the Senate raised concerns about the proposal.
"The Environmental Protection Agency should be taking actions that will further protect health during this crisis, not put more Americans at risk," they wrote.
The 2020 State of the Air report covers 2016, 2017 and 2018, the years with the most recent available data and three of the five hottest years on record. Ozone pollution is exacerbated by higher temperatures.
"Rhode Island residents are breathing more unhealthy air driven by extreme heat as a result of climate change, placing our health and lives at risk," said Jennifer Wall, director of advocacy for the American Lung Association in Rhode Island.
All three reporting counties in Rhode Island got F grades for ozone, A grades for short-term particle pollution and passing grades for long-term particle pollution.
akuffner@providencejournal.com
On Twitter: @KuffnerAlex


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text:
Nottingham theatre stages hit children's TV show
Published: 8 July 2012
Reporter: Steve Orme
The CBeebies television hit Grandpa in my Pocket will be making its stage debut at Nottingham Playhouse from this week.
This new stage show called Teamwork! taps into themes at the heart of the TV series, such as the playful cross-generational relationship between grandparent and grandchild.
Nottingham Playhouse is producing the show which has an ensemble storytelling technique with song, dance, physicality, puppetry and interaction with the audience.
Teamwork! is directed by Rosamunde Hutt and designed by Nettie Scriven. Kate Edgar is musical director and Matt Dilley music arranger. Roman Stefanski is puppetry consultant.
Mellie Buse and Jan Page, co-founders of Adastra Creative, writers and producers of Grandpa in my Pocket, said, "Nottingham Playhouse has embraced all the core elements of the television series that have made it so popular, and are totally in tune with the brand.
"We have an incredibly accomplished team working to bring the show to life on the stage and believe this will offer a different experience of Grandpa, without losing any of its special magic and charm."
Nottingham Playhouse artistic director Giles Croft and chief executive Stephanie Sirr said, "Everyone at Nottingham Playhouse is thrilled to be creating this first stage interpretation of such a well-loved children's television show.
"We've assembled an outstanding creative team to bring Jason, his grandpa and their friends to the stage; we're confident that this new story, magically brought to life with inspired design, songs, puppetry and an exceptional cast, will delight all fans of Grandpa in my Pocket and also introduce a new audience to the magic of live theatre."
Grandpa in my Pocket runs at Nottingham Playhouse from Friday (13 July) until Saturday, 11 August.


I fumbled in the dark, searching for the source of the chirping sound. Eventually I flipped open my phone, too incoherent from pain to be pissed at the person interrupting my midday nap.
"Hello, is this Jennette?" a female voice asked.
"Yeah," I replied. I hadn't felt like myself for a long time now, but technically I was still me.
"Dr. Reiner?" I spoke the name with a question mark at the end. Who was Dr. Reiner? He wasn't my general practitioner. He wasn't my neurologist. He wasn't my other neurologist. He wasn't my allergist. He wasn't my acupuncturist. He wasn't my chiropractor. He wasn't my ophthalmologist. Who was Dr. Reiner and where was he going to stick a needle in me?
"Um, what does Dr. Reiner do exactly?" I asked, knowing there was no way to phrase the question without sounding stupid.
"Oh! Dr. Rheinberg," I exclaimed in realization. I hadn't heard the name correctly over the phone. Dr. Carson was my dentist, but he worked for Dr. Rheinberg 's practice. So the answer to the question of where he'd be sticking a needle was: my gums.
"Yeah, sure," I said now that I knew where I was supposed to go and who I would be seeing. Then I flipped the phone closed and stared at the ceiling.
It was official. I had more doctors than I could keep track of.
If I couldn't remember every doctor I'd given money to, there didn't seem to be much harm in adding more physicians to my payroll. What good was health insurance if I didn't max out the deductible and test the out-of-pocket limit?
My neurologist had mentioned a headache clinic in an adjoining state before my last appointment with him. I hadn't been aware such places existed, but upon further research I learned there were several clinics that specialized in head pain. I'd put off going to one directly because they were expensive and over 200 miles away. Now that I'd hit up all the cheaper, local practitioners, I was desperate enough to cross state lines and spend serious money in search of relief.
I'd read about people's experiences at these institutes on the headache forums online. I'd been surprised that people in that much pain had been able to set up and maintain online forums, but there they were. I was a lurker on the forums and never posted or interacted with others. I wasn't sure why I'd never struck up a conversation with my fellow pain sufferers. It was just easier to lurk, read up on the information I needed, and then log off without getting too involved in the misery of others. When I'd blogged about my weight loss, I didn't start commenting on other weight-loss blogs until I'd lost almost 100 pounds. I wasn't sure how long I'd have to have my headache before I felt comfortable enough to raise my hand in front of the class and talk about it. Despite all the suffering I'd endured over the past year, I couldn't quite accept that I was a part of this community. I could still get better, right?
It was on these forums that I discovered there were foundations and advocacy groups for headache suffers. They even petitioned Congress for more research grants to investigate migraine disease. Headaches sucked a huge amount of productivity from the American workforce, as I had been exemplifying by researching headache clinics at work. The National Headache Foundation estimated that $17 billion dollars was lost each year due to headaches that led to absenteeism, lost productivity and medical expenses.
After days of reading about people's experiences on the forums, I concluded that every clinic was run by both arrogant sadists who would make my current suffering feel like a visit to a spa, and empathetic caretakers who would listen to my problems and miraculously heal me of all pain. I suspected the truth lay somewhere in between.
I had narrowed down my choice to the three clinics in adjoining states. A friend of a friend was a doctor who worked at the hospital associated with the first clinic, but the second clinic was closest, and the third clinic was in the smallest city, which meant it would be much easier to find parking there. I was anxious making this choice because I worried that one clinic would provide relief faster than another, or that one clinic would have a nicer staff who would provide a better overall experience than another. I wanted to make the best choice. I didn't want to have to start over at another clinic several months later if I wasn't happy with my first choice.
I researched the clinics online so I could make a more informed decision. I found out that the expert in the type of headache I was suffering from practiced at a clinic I will refer to as The Clinic, located in The City. I picked up the phone and made an appointment. Decision made.
Jennette Fulda has had New Daily Persistent Headache since February 17, 2008, but at least she got a book deal out of it. She is the author of Chocolate & Vicodin: My Quest for Relief from the Headache that Wouldn't Go Away and Half-Assed: A Weight-Loss Memoir. You can catch up with her on her blog JenFul and on Twitter @jennettefulda If you want to send her chocolate and Vicodin, that's cool too.
Hi, Miss Kim. You can read the official definition of New Daily Persistent Headache here: http://ihs-classification.org/en/02_klassifikation/02_teil1/04.08.00_other.html NDPH is constant, 24/7 headache. Migraine attacks typically come and go.
Sorry to hear about all the struggles you've been through. I wish you luck as you continue to battle your pain, and I hope you enjoy the book!
I went to one of those spa-like clinics, with an empathetic staff and a doctor who even is a fellow sufferer. Everyone listened and empathized real well. No new strategies or suggestions though. My experience ended up being a huge waste of time and insurance co-pays. I actually find more helpful suggestions (especially non-pharm) on web forums like this. Of course, I'm not suggesting anyone ditch their doctor and self – diagnose yourself from a web forum. It's just I've had no breakthrough or improvement since Zomig was invented and it can be very frustrating when you feel no one has anything new for you to try. They've run all the tests and they seem tired of you after awhile. I can tell they are frustrated, I am too!
I enjoy reading books from fellow headache/migraine sufferers so I guess I'll head over to Amazon and see if I can find your book to read the rest of your story. Congrats on the "book deal". It's impressive how productive some of us can be – even though we have to work through the pain and brain fog.
I certainly understand your frustration, janenez. I wish there were cures for all of us. Until then, I hope you enjoy the book!
gave you any relief. I have tried literally dozens of other medications, from Cymbalta to Namenda(all useless), Botox to the head (useless), had three radiofrequency ablations of my C2, 3 and 4, lidocaine to the head and NOTHING works but the abortives, ie, the triptans. Can you comment on the abortives?
Jenette, I am delighted that Lamictal helped you. I tried it and it did nothing for me, but increase my insomnia. Probably due to the etiology of the migraine vs. New Persistent Daily Headache.
Hey, Marlene. I haven't had any success with triptans, probably because I have New Persistent Daily Headache. That means my headache has been constant 24/7 for the past four and a half years. I've been doing pretty well on Lamictal lately which keeps the intensity of the headache down. I sometimes take Anaprox when the headache is pretty bad, but I don't know how it well it really works.


I'm trying to resolve some problems with my server 'thing' (this server of course isn't really mine, it's shared ) and I'm a little suprised with some parameters listed by program top. For example my server has only about 100 MB memory free and average load is over 70%.
Could you please post output from 'top' just for compare and maby some discuss? My listing is below.
What scripts are you running, and what customisations have you implemented?
OsCommerce based shop, 4images based photoforum, joomla based news agregator (news acquiring temporary disabled).
I was trying 'wget' from shell and sometimes looks ok, but very often 'connecting to [my.site.adress]' takes 20 seconds and more !
Could you run 'top' on your server and post program output? As you can see my processes use <1% of memory and up to 5% of CPU (for a very short time), but server looks quite busy. I suppose that some other user(s) utilize most of resources, but I'm not sure about that.
Unfortunately my server stats aren't going to help you. Suffice to say they are (of course) nowhere near as high as what you are witnessing on your server.
The server load is what's causing your issues. Those values don't represent a "70% load", they're indicating a demand 70x above what is available. This is an indication that a script has gone berserk and you'll need to contact Support to have them track it down and kill it with extreme prejudice.
Those values don't represent a "70% load", they're indicating a demand 70x above what is available.


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gastrulation-defective: Biological Overview | Regulation | Developmental Biology | Effects of Mutation | References
Gene name - gastrulation-defective
Cytological map position - 11A1--3
Function - protease
Keywords - dorsal/ventral polarity, Toll cascade
Symbol - gd
Genetic map position - 1-36.8
Classification - serine-type endopeptidase
gd orthologs: Biolitmine
In the process of establishing dorsoventral polarity in the Drosophila embryo, cell fates along the dorsoventral axis are determined by a gradient of the extracellular morphogen Spätzle, which activates the receptor Toll. Spätzle, which conveys a 'ventralizing' signal necessary for ventral and lateral development, is activated by proteolytic processing, a reaction that apparently occurs shortly after fertilization and only on the ventral side of the embryo. This crucial processing event requires four serine proteases -- Nudel, Gastrulation defective (Gd), Snake, and Easter -- and a ventrally restricted factor provided during oogenesis by the pipe gene. An important question asks how do these components function to process Spätzle at the right time and place in order to establish embryonic dorsoventral polarity (LeMosy, 2001 and references therein)?
Genetic and molecular studies have suggested that the proteases in the Toll signaling pathway function sequentially in a proteolytic cascade, as seen for mammalian blood clotting. In such a cascade, the proteases exist as zymogens that become activated by cleavage at a defined site between a prodomain and the catalytic domain, and one protease activates the next downstream protease in the cascade. By genetic criteria, Nudel is the most upstream protease in the Toll signaling pathway, followed by Gd, then Snake, and finally Easter, the protease that can process Spätzle to a biologically active form. The zymogen forms of Snake and Easter, as well as the Spätzle protein, appear to be freely diffusible in the extracellular perivitelline space surrounding the embryo. Thus, the activities of these proteases must be ventrally restricted to confine Toll ligand production to the ventral side of the embryo. Spatial control of the blood-clotting proteases, which are also diffusible as zymogens, is partly achieved through dependence of the first and all subsequent zymogen-activation steps on membrane-bound cofactors that are localized to the site of blood-vessel injury. By analogy, it has been proposed that the ventrally restricted factor provided by the pipe gene functions as a cofactor necessary for activation of the proteolytic cascade that produces the Toll ligand (LeMosy, 2001 and references therein).
As the earliest acting protease in the Toll signaling pathway, Nudel would be expected to play an important role in triggering Toll ligand production. The Nudel protease is autoactivated without requiring the activities of the other proteases at the beginning of embryogenesis, which is consistent with its proposed role as the initiator of a protease cascade in which it activates the next downstream protease, presumably Gd. However, Nudel protease activation does not seem to be ventrally restricted or regulated by pipe. The Nudel protease is also required for modification of the extracellular matrix, raising the possibility that Nudel acts indirectly in dorsoventral patterning (LeMosy, 2001 and references therein).
Is Gd the localized determinant responsible for the spatially restricted pattern of Toll activation? Probably not. The level of Gd determines the strength of the ventralizing signal, presumably by controlling the activation of the downstream proteases Snake and Easter. Gd at high levels can ectopically induce the ventralizing signal in the absence of nudel or pipe function. The Gd zymogen is not prelocalized to a ventral site, and Gd zymogen cleavage, although requiring the Nudel protease, does not depend on pipe. Surprisingly, these results suggest that the protease cascade producing the ventralizing signal is initiated by a spatially uniform cleavage of the Gd zymogen, with spatial regulation of a downstream step determining where signaling is to occur. If cleavage of Nudel and Gd, necessary to trigger the proteolytic cascade leading to the Toll ligand, is not ventrally localized, then how could Toll ligand production be restricted to the ventral side of the embryo? The last step in the cascade, processing of Spätzle to the active Toll ligand, is controlled by pipe (Morisato, 1994). Thus, spatial regulation could occur at an intermediate step, perhaps involving the proteolytic activation of Snake or Easter. For example, the Gd protease, although broadly activated, may activate Snake only when its substrate is associated with the ventral factor provided by pipe (LeMosy, 2001 and references therein).
Prevailing models based largely on genetic data have suggested that Gd, Snake, and Easter function in a cascade of sequential zymogen activation, like the mammalian proteases involved in blood clotting. The in vitro experiments provide biochemical evidence in support of this idea. Although the data strongly imply that Gd directly activates Snake and that Snake directly activates Easter, experiments with purified proteins will be necessary to obtain proof of an enzyme-substrate relationship between these proteases (LeMosy, 2001).
A surprising finding is that the cascade of Gd, Snake, and Easter is activated when all three proteases are coexpressed as zymogens. One possible explanation is that high concentrations of these proteases generated by overexpression in S2 cells promote protein-protein interactions that are important for cascade activation in vivo. For example, the proteases may normally be activated after being brought together in zymogen-activation complexes, as is the case for the proteases involved in blood clotting (LeMosy, 2001).
Gd is cleaved when it triggers the activation of Snake and Easter in vitro. It is thought that cleavage is important for activation of Gd's proteolytic activity. This conclusion is supported by the findings that a cleaved form of Gd, but not the zymogen, reacts with active-site inhibitors specific for active serine proteases (Han, 2000), and that two truncated forms of Gd are more active than the zymogen in processing Snake. Because Gd lacks a typical zymogen-activation site, as in Snake or Easter, it is unclear where Gd is cleaved (Konrad, 1998). The ability to generate more active forms of Gd by truncation at two different sites may indicate that Gd does not normally require cleavage at a single specific site to become activated (LeMosy, 2001).
Although present as a zymogen during oogenesis, Gd apparently is cleaved during early embryogenesis to a smaller polypeptide similar in size to the 46-kDa form generated during the activation of Snake and Easter in vitro. This cleavage must be significant for Gd function in vivo, since it relies on the activity of the Nudel protease which acts genetically upstream of Gd in the Toll signaling pathway. Additionally, the cleaved form of Gd is detectable throughout the first 3 h of embryonic development when the Toll ligand is produced: this is consistent with it being the functional Gd form that activates the downstream proteases. Although further studies are required to definitively demonstrate enzymatic activity, these findings strongly suggest that the smaller form of Gd present during early embryogenesis represents activation of the Gd zymogen (LeMosy, 2001).
How is the Gd zymogen normally cleaved? In using the coexpression assay, it was observed that the Nudel protease and preactivated forms of Gd and Snake are capable of inducing the cleavage of Gd to the 46-kDa form. However, only the Nudel protease seems to be essential for this cleavage in vivo, because mutagenesis of Gd's catalytic serine or a mutation in the snake gene does not block the appearance of the 46-kDa Gd polypeptide in the early embryo. A model consistent with all of the data is one in which the Nudel protease, detectable during the first 2 h of embryogenesis, directly cleaves the Gd zymogen. Once activated, Gd and perhaps even the downstream proteases could promote further Gd-zymogen cleavage through a positive feedback loop. In the coexpression experiments carried out in the absence of the Nudel protease, a protease normally present in the S2 cells may have cleaved a small amount of Gd sufficient to trigger the subsequent activation of Snake and Easter. This explanation is compatible with the idea that Gd can be activated by the cleavage of an unusually labile region rather than at a specific site in its primary structure (LeMosy, 2001).
Gd activity seems to be restricted to the ventral side of the embryo. One possible explanation is that Gd is prelocalized to a ventral site. On the contrary, the Gd zymogen is uniformly distributed at the oocyte surface, similar to Nudel. Alternatively, Gd could be proteolytically activated only on the ventral side of the embryo. Current results argue against this possibility, because Gd-zymogen cleavage is not regulated by pipe, the key gene that ventrally restricts Toll ligand production. Activation of the Nudel protease, required for Gd cleavage, is also not regulated by pipe (LeMosy, 2001).
Thus the observation that the processing of Spätzle to the active Toll ligand (the last step in the cascade) is controlled by pipe, appears to explain the localized activation of the Toll pathway. Spatial regulation could occur at an intermediate step, perhaps involving the proteolytic activation of Snake or Easter. For example, the Gd protease, although broadly activated, may activate Snake only when its substrate is associated with the ventral factor provided by pipe (LeMosy, 2001).
The mammalian blood-clotting cascade normally generates a blood clot only at the site of tissue injury and thus is a signaling pathway that transmits spatial information. In contrast, these studies suggest the protease cascade involved in dorsoventral patterning initially transmits not spatial but temporal information, which is, perhaps, a cue that embryogenesis has begun. Spatial information in the form of the ventral cue is then integrated at a distinct downstream step in the cascade. As a consequence, the ventralizing signal is generated at the right time and place to pattern the embryo (LeMosy, 2001).
Feedback control also seems to be important for defining the temporal and spatial dimensions of signaling by the dorsoventral cascade, as has been shown for other signaling pathways involved in creating complex developmental patterns. Earlier studies have suggested that a negative feedback loop involving the most downstream component in the Toll signaling pathway inhibits activation of the Easter protease (Misra, 1998). The data also raise the possibility that both positive and negative feedback loops modulate the activation of proteases upstream of Easter. Such feedback could amplify a subtle asymmetry in protease activation level not detectable by the current methods. The integration of positive and negative feedback loops, and of temporal and spatial cues as outlined above, likely provides the precise control of signaling necessary to establish embryonic dorsoventral polarity (LeMosy, 2001).
Independence of chromatin conformation and gene regulation during Drosophila dorsoventral patterning
The relationship between chromatin organization and gene regulation remains unclear. While disruption of chromatin domains and domain boundaries can lead to misexpression of developmental genes, acute depletion of regulators of genome organization has a relatively small effect on gene expression. It is therefore uncertain whether gene expression and chromatin state drive chromatin organization or whether changes in chromatin organization facilitate cell-type-specific activation of gene expression. In this study, using the dorsoventral patterning of the Drosophila melanogaster embryo as a model system, evidence is provided for the independence of chromatin organization and dorsoventral gene expression. Tissue-specific enhancers are defined and linked to expression patterns using single-cell RNA-seq. Surprisingly, despite tissue-specific chromatin states and gene expression, chromatin organization is largely maintained across tissues. The results indicate that tissue-specific chromatin conformation is not necessary for tissue-specific gene expression but rather acts as a scaffold facilitating gene expression when enhancers become active (Ing-Simmons, 2021).
Previous studies produced conflicting results regarding the relationship between gene expression, chromatin state and 3D chromatin organization. This study set out to understand this relationship in the context of embryonic development in Drosophila. Using the well-studied dorsoventral patterning system, it was shown that, despite significant differences in chromatin state and gene expression between tissues along the dorsoventral axis of the embryo, chromatin conformation is largely maintained across tissues. This suggests that cell-type-specific gene regulation does not require cell-type-specific chromatin organization in this context. Nevertheless, developmentally regulated genes and enhancers are organized into chromatin domains. It is suggested that this organization plays a permissive role to facilitate the precise regulation of developmental genes (Ing-Simmons, 2021).
Use was made of maternal effect mutations in the Toll signaling pathway, which lead to embryos that lack the usual patterning of the dorsoventral axis and have long been used as a system to study the specification of mesoderm (Toll10B), neuroectoderm (Tollrm9/rm10) and dorsal ectoderm (gd7) cell fates as well as the regulation of tissue-specific gene expression. However, these embryos are still under the influence of anterior-posterior patterning signals and do not show completely uniform cell identities. This study sought to investigate heterogeneity of cell identity at the single-cell level by using single-cell gene expression profiling. This revealed that certain cell types are indeed maintained in all three Toll pathway mutants, including pole cells and other terminal region cell identities, hemocytes and trachea precursor cells. However, heterogeneity of gene expression is reduced in the mutants, as shown by the loss of cells assigned to mesoderm clusters in gd7 and Toll10B embryos and the depletion of ectoderm subsets in each of the mutants. These datasets showcase the advantages of measuring cellular heterogeneity at the single-cell level and provide a useful resource for further characterization of these embryos and investigation of the regulation of dorsoventral patterning (Ing-Simmons, 2021).
Although the gd7, Toll10B and Toll10B embryos still have heterogeneous gene expression profiles, nevertheless, there are clear differences in chromatin state and overall gene expression between these embryos. This study expanded on previous studies by identifying putative enhancers specific to neuroectoderm in addition to dorsal ectoderm and mesoderm. This allowed the identification of tissue-specific putative enhancer-gene pairs, which correspond well with known dorsoventral patterning enhancers and genes that are differentially expressed (DE across the dorsoventral axis. These regulatory elements and their target genes are located inside chromatin domains, distinct from the enrichment of housekeeping genes at domain boundaries. This is in line with previous results that suggest that 3D chromatin domains act as regulatory domains (Ing-Simmons, 2021).
This domain organization is maintained across tissues, even in cases in which there are significant changes in the local chromatin state and gene expression. This is consistent with earlier results from Hi-C experiments carried out in anterior and posterior embryo halves, which also showed no differences, and with previous studies in Drosophila cell lines and other systems, which suggested that domains are widely conserved across different tissues and even different species. To explain this maintenance of organization across cell lines, it was proposed that active chromatin, especially at broadly expressed genes, is responsible for partitioning the genome into domains. It has been proposed that compartmentalization of active and inactive chromatin, at the level of individual genes, underlies the formation of insulated chromatin domains. This model predicts that, when a developmentally regulated gene is active, its domain would merge with or have increased interactions with neighboring domains containing active genes, such as broadly expressed housekeeping genes. The results do not support this model, as this study found no evidence that differences in domain structure are driven by changes in chromatin state or by active expression of developmentally regulated genes. By contrast, this supports the idea that, similar to mammalian domain architecture, additional factors, such as insulator proteins, modulate domain organization in Drosophila. Therefore, based on current data, it is not believed that active transcription is the key determinant of 3D chromatin organization in this system (Ing-Simmons, 2021).
While overall and locus-specific chromatin organization are maintained across tissues, Hi-C and Micro-C analyses identify a small number of examples of regions that do have changes in organization. However, at these loci, there is no clear relationship between changes in organization and changes in chromatin state or expression, and the vast majority of developmentally regulated loci in this system do not have changes. It will be important for future studies to further investigate these loci to understand what drives these rare changes (Ing-Simmons, 2021).
This study also investigated chromatin organization at the level of enhancer-promoter interactions. Previous studies produced conflicting results about whether these interactions are correlated with tissue-specific activation of gene expression. No evidence was found for widespread enrichment of interactions between enhancers and their target promoters, including in tissues where they are active. This is in contrast with previous studies using 3C approaches that have found evidence of enriched enhancer-promoter interactions, which may precede or correlate with transcriptional activation. Notably, Ghavi-Helm (2019) found that a subset of Drosophila long-range enhancer-promoter pairs do form stable interactions that are enriched above local background19. While these loops are visible in the dataset presented in this study, the results suggest that such loops are not likely to be the primary mechanism of promoter regulation during Drosophila development, perhaps because most enhancers are close to their target promoters. Many stable loops in the Drosophila genome are instead associated with polycomb-mediated repression (Ing-Simmons, 2021).
Hi-C provides information about the average conformation across a population of hundreds of thousands of nuclei, which contain dynamic ensembles of different 3D conformations. While the scRNA-seq results indicate that the mutant embryos contain a range of different cell types, it is believed that the results indicate that the 3D chromatin structures in these cell types are drawn from the same population of possible conformations. This is supported by results from a recent study analyzing the structure of the Doc and sna loci in Drosophila embryos using Hi-M, a high-resolution single-cell imaging approach. Strikingly, this orthogonal technique also reveals chromatin organization that is consistent across different tissues in the embryo, despite differential expression of these genes. Imaging-based approaches directly measure spatial proximity between genomic loci, whereas Hi-C and Micro-C rely on cross-linking to detect chromatin interactions. Therefore, care must be taken when comparing these approaches. Nevertheless, both approaches indicate that genome organization is maintained across different tissues in this system (Ing-Simmons, 2021).
The results are consistent with several recent studies in mammals as well as in Drosophila, which provide evidence that stable enhancer-promoter contacts are not always required for gene activation. This is in line with models in which transient or indirect contacts with a regulatory element are sufficient to activate transcription, such as through the formation of nuclear microenvironments or phase-separated condensates (Ing-Simmons, 2021).
Together, the results indicate that differential chromatin organization is not a necessary feature of cell-type-specific gene expression. It is proposed that chromatin organization into domains instead provides a scaffold or framework for the regulation of developmental genes during and after the activation of zygotic gene expression. This may help render developmental enhancers 'poised' for timely regulation of target genes upon receipt of appropriate cellular signals. Other mechanisms of priming have been described, including paused polymerase (Pol) II at promoters and pioneer factors bound to poised enhancers. Feedback effects, such as downstream modification of chromatin state and additional mechanisms, including looping between polycomb-bound elements and segregation of active and inactive chromatin, may then act as layers on top of the initially established domain structure (Ing-Simmons, 2021).
The cDNA sequence reveals a single long ORF beginning with the first ATG in the sequence. The cDNA contains 30 bp of 5' untranslated sequence that is located 241 bp downstream from the poly(A) site of the tsg gene. The ORF is followed by 247 bp of 3' untranslated sequence containing multiple stop codons in all frames and terminates in a poly(A) tail. The only consensus poly(A) addition signal (AATAAA) in the region is located 37 bp before the end of the gd cDNA. Two AACAAA motifs are located further downstream at bp 2626 and 3218, but there is no evidence from RNA blots that either of these is used as a polyadenylation site. Comparison of the cDNA and the genomic sequence reveals the presence of four introns. No evidence was found for alternative splicing (Konrad, 1998).
Bases in 5' UTR - 62
The gd cDNA sequence predicts a 59-kDa polypeptide. This was confirmed by in vitro translation of transcripts from the cDNA clone, which yielded a protein of ~60 kDa with a pI of 6.94 as determined by two dimensional PAGE. The amino-terminal residues are hydrophobic, suggesting a secretory leader sequence that would be cleaved after amino acid. Because Gd activity is not freely diffusible in the PV fluid, the Gd protein sequence was examined for potential anchoring sites. Two hydrophobic domains are notable, one near the middle of the protein that could represent a membrane spanning region, and the second, a hydrophobic tail, that could act as a membrane anchor. However, each of these domains contains charged amino acid residues. The protein contains three putative N-linked glycosylation sites (NXS/T). There are no RGD amino acid sequences that might interact with extracellular components nor any WIID or LDL repeats, as seen in the NDL protein (Konrad, 1998).
A BLAST search has suggested that Gd is related to the family of serine proteases. The most closely related proteins are factor IX of the mammalian clotting cascade, two crab coagulation factors, and a urokinase-type plasminogen activator. Sequence alignment of Gd with these proteins and chymotrypsin shows that Gd shares the 3 amino acids of the catalytic triad (H, D, S) and all but one of the cysteine bridges. In addition, several other structural features that identify serine proteases are present. However, Gd also has some features that are atypical of the basic serine protease family but that are seen in other related proteins. For example, it contains a putative activating cleavage site that is not typical, and the conserved D adjacent to the active site S is replaced by I and a short insert of amino acids immediately adjacent. There is a small acidic region N-terminal to the catalytic site, which is a feature shared by Snk but not Easter (Konrad, 1998).
The Gd protein possesses the catalytic triad (H, D, S) characteristic of serine proteases. Although the homology to serine proteases suggests a proteolytic role, several significant differences between the sequence of Gd and other members of the chymotrypsin family of serine proteases suggest that Gd may behave atypically. Most eukaryotic serine proteases undergo an activation process after zymogen cleavage in which the alpha amino group of the catalytic domain forms a salt bridge to an aspartate residue (D) located adjacent to the active site serine. In Gd, this aspartic acid residue is replaced by isoleucine, making it unlikely that the protease could be activated via the classical mechanism. However, several bacterial members of the alpha-lytic endopeptidase family (e.g., subtilisin) contain residues other than D (e.g., T) adjacent to the active serine, and complement component C2 contains E instead of D. Typically, activation involves cleavage after a positively charged amino acid (R or K) followed by two branch chain amino acids and a highly conserved G. The N-terminal residue is most commonly I but may be L, V, or M. One putative cleavage site for Gd based on position relative to conserved motifs (e.g., G-WPW and CGGTSLV) is S ITRG. Although this putative site has S instead of R or K and has G in the 4th position rather than the 3rd, cleavage at this site would produce a peptide of 30.5 kDa that could possibly correspond to the 30-kDa species observed on the Western blots. The extensive heteroallelic complementation exhibited by gd is consistent with the possibility that the Gd protein may function as a multimer perhaps during an activation process (Konrad, 1998).
The predicted protein encoded by gd was compared with members of the serine protease superfamily: it lacks sequence conservation within the activation peptide cleavage site. Examination of the protein data bank has revealed two serine proteases, which also deviate from the concensus within the activation peptide region. The complement factors C2 and B are activated by cleavage between an arginine and lysine residue and ~12 amino acids after the cleavage site in factor C2 and B, a type A von Willebrand repeat motif is found. The Gd amino acid sequence was compared with factors C2 and B, and an alignment revealed that Gd possesses an arginine lysine pair as well as a type A von Willebrand motif in a conserved geometry. These features suggest that gd encodes a serine protease zymogen, which is structurally similar to factors C2 and B, and is therefore activated by cleavage between Arg128 and Lys129. Site-directed mutagenesis studies and the analysis of interallelic complementation at gd are consistent with this model (DeLotto, 2001 and references therein).
gastrulation-defective: Regulation | Developmental Biology | Effects of Mutation | References
date revised: 5 August 2021