text:
6th-grader's Marine Corps shirt too much for school
School administrators told a Mississippi sixth-grader whose grunt brother is deployed to Afghanistan to turn his shirt inside-out because they were offended by its depiction of an anatomically correct U.S. Marine Corps bulldog.
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Jordan Griffith, 13, of Ellisville, Miss., received the shirt from his older brother, Lance Cpl. Timothy Swann Jr., a member of 2nd Battalion, 9th Marines out of Camp Lejeune, N.C. Swann gave it to his little brother while he was on leave before deploying.
"Jordan just idolizes Timothy," said their mother, Sandy Griffith. "Timothy gave him the shirt and told him, 'Always remember you're a leader, not a follower.'"
The front of the shirt shows the dog's head and body with the words "If you are not the lead dog." The back shows the dog's rear with the words "The view never changes."
Officials at South Jones Elementary objected to the realistic view of the dogs' genitals and asked the student to turn the shirt inside-out or have his parents bring him a new shirt.
The school's superintendent, Tommy Parker, said the decision had nothing to do with it being a Marine Corps shirt.
"We're very pro-military," Parker said. "We're one of the most conservative places in the United States."
But that may have played a part in upsetting some of the school's teachers, he said, adding "all the details are there" regarding the dog's anatomy. Teachers also didn't want to look at it all day or have younger students see it.
Sandy Griffith, who pulled her son from class instead of bringing him a new shirt, said the picture is no more offensive than the view one has while walking a dog.
"My father made a joke that the woman who told him to turn the shirt inside-out must have been in the Navy," she said.
The shirt's message about leadership is one that kids should think about, she said, especially when men and women are still fighting on behalf of the country.
After leaving the school, Griffith called "The Rush Limbaugh Show," a conservative syndicated radio program. The host seemed surprised to hear this incident had happened in Mississippi.
"Now your kid can't wear a T-shirt given to him by a member of the U.S. military that espouses a positive character trait, leadership?" Limbaugh asked on his show. "People are fed up. They're fed up with being told what they can't eat, and what they can and can't do in their own yards and in their own homes. It's just not America anymore."
Parker, the superintendent, was dismayed to read the show's transcript.
"It's almost absurd that anyone would accuse us here in Mississippi of being anti-military," he said. "We recite the Pledge of Allegiance every morning. This very school has sent cards and letters to our troops overseas."
Posted | Updated


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The Hertz Corporation (Park Ridge, N.J., U.S.A.), a car rental company, last week announced the expansion of its Global Electric Vehicle (EV) initiative to China, marking the first EV rental service to be offered in the country.
Hertz now offers EVs across the U.S. in cities including New York, Washington, D.C., San Francisco, Los Angeles, and in London, United Kingdom and other cities in Europe.
The expansion involves Hertz forming an alliance with GE Industrial Solutions in China to develop a new business model to market EVs. According to the company, Hertz and GE Industrial Solutions will bundle EV leasing and charging facilities as a package, which will be offered to multinational companies and government agencies to promote new energy applications. Both Hertz and GE Industrial Solutions will market the package together as business partners, according to the companies.
Hertz also signed an agreement to participate in the China International EV Pilot City to help develop an EV rental program by building out the infrastructure across the Jiading district of Shanghai. According to Hertz, this will act as the starting point to make EVs accessible to corporations, local government and the general public.
Earlier this year, Shanghai was selected as the electric vehicle international pilot city by the Chinese government and Jiading district of Shanghai as the electric vehicle international demonstration zone, with a goal of increasing public awareness and integration within the industry.
Additionally, Hertz launched a partnership with BYD, the largest Chinese local auto brand, to combine electrical vehicle sales and leasing as a mobility service for MNC and government agencies in metropolitan Chinese cities, according to the company.
"China has committed to rapidly expand electric vehicle travel," said Mark P. Frissora, Hertz chairman and chief executive officer.
Other current partners of the China International EV Pilot City include auto manufactures, energy suppliers, insurance companies and the other EV supply chain participants. According to Hertz, it is the first rental car company to sign a MoU to become a partner of the China (Shanghai) International Electric Vehicle Pilot City. The agreement supports the Twelfth Five-Year Plan objective for the promotion of EVs in China.
Communications 2020
July 18 - 20, 2017
Las Vegas, NV
M2M Zone Pavilion @ MWC Americas 2017
September 12-14, 2017
San Francisco, Calif.

subset: commoncrawl


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Hodgson, Ann and Spours, Ken (2002) Key skills for all? The Key Skills Qualification and Curriculum 2000. Journal of Education Policy, 17 (1). pp. 29-47. ISSN 0268-0939. DOI UNSPECIFIED
PDF (HodgsonSpours2002Key29.pdf)
HodgsonSpours2002Key29.pdf - Other
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It is widely recognised that the Key Skills Qualification, an important component of the Curriculum 2000 advanced level curriculum reforms has experienced extensive problems during its first full year of implementation. This much is not in dispute. What is being keenly debated, however, are the ways in which this experience should be analysed and what lessons should be drawn. Is it a case of understandable 'teething problems' which will be overcome as the qualification 'beds in' or are there deeper and more fundamental problems of the purpose and design of the Key Skills Qualification for advanced level students? In order to address these questions, this article examines the Key Skills Qualification within its historical and policy context as well as bringing together a range of quantitative and qualitative evidence gathered as part of an Institute of Education (IOE)/Nuffield Foundation Research Project. The research suggests that while there is support for the concept of key skills, the Qualification has been met with considerable student and professional resistance due to its narrow skills focus and assessment regime within the context of increased study programmes at advanced level. We conclude that the Government's aim of 'key skills for all' at advanced level is unlikely to be achieved unless it takes a fundamentally different approach to policy in this area.
|Item Type:
|IOE Departments > Departments > Education and International Development
IOE Departments > Departments > Lifelong and Comparative Education
|Depositing User:
|IOE Repository Editor (2)
|Date Deposited:
|11 Mar 2010 12:47
|Last Modified:
|29 Jan 2015 07:48


text:
Submit News
Republican Rep. Wants Taxpayers to Pay for Piracy Police (Again)
Jason Mick
July 12, 2012 4:10 PM
Recipient E-mail
Sender E-mail
(Source: Sodahead)
Tax and expand the federal gov't says Texas Rep. Lamar Smith (R)
"When there's copyright infringement / In your neighborhood / Who you gonna call? / The U.S. federal taxpayer funded IP task-force!"
I. SOPA Returns, Renamed and Pared Down
It sounds like a joke, but that's precisely what the
The Intellectual Property Attaché Act
[PDF], hopes to implement. The goal is to fight "global" piracy, but the proposal admittedly acknowledges that the taskforce -- a sub-agency of the
U.S. Department of Commerce
-- could be used in the homeland, as well.
In fact, it seems more than likely that the task-force created by the IP Attaché Act, would operate
in the U.S., given difficulties in sending IP "cops" overseas to quasi-hostile infringement-prone regions like China. (What would they do in China, "arrest" street merchants selling knockoff DVDs?)
Overseas complaints are already well-policed -- or about as well policed as is possible -- by the
World Trade Organization
So the new Commerce Department copyrights cops are essentially redundant, unless their policing happens to primarily focus on the U.S. And you can bet it does.
The bill is essentially a repackaging of the heart and soul of the fortunately deceased
) and the U.S. Senate's Protect Intellectual Property Act (PIPA) (
). In fact, it's authored by the same fellow --
Rep. Lamar Smith
(R- Tex.) -- who wrote SOPA.
Rep. Smith surely was sweating a bit under the collar when SOPA went down in flames. After all, big media wrote him a check for $85,000 USD during the last campaign cycle [source] and lawyers, many of whom represent big media clients, chipped in another $58,000 USD. [
Rep. Lamar Smith feels he's above the laws he's looking to subject his lowly proles to.
[Image Source: Lamar Smith]
Together these contributions gave him about 10 percent of the money he needed to crush Lainey Melnick 69-to-28 percent voting margin (Mr. Melnick only raised $34,000 USD lacking sufficient big media sponsors). To be fair, many of Rep. Smith's colleagues
received similar payouts
from big media.
That kind of money doesn't come for free or cheap. It comes with big favors. In this case the cost of the donations was likely a commitment to tirelessly push "anti-piracy" legislation even if it ignores big media corporations'
own flagrant
copyright theft
, wastes taxpayer money, and likely tramples on civil liberties.
Clearly Rep. Smith doesn't truly take his rhetoric to heart, given the fact that he
ripped off an independent artist's work
for his homepage art, and reportedly initially refused requests from the artist for acknowledgement.
II. Will it Pass?
So does the IP Attaché Act stand any more of a chance of surviving than Rep. Smith's last monstrosity, SOPA?
The largely politically apathetic public burned through
a great deal of energy
killing the last bill
. And this revised version will likely draw
less corporate opposition
in that it appears to remove its provisions for sweeping website takedowns in its draft.
Further, the SOPA v. 2.0 (of sorts) has the support of House Oversight Chairman,
Rep. Darrell Issa
(R-Calif.) -- who initially supported SOPA as well, but later became a critic who helped sink the measure.
has obtained a statement from Rep. Issa's office,
Rep. Issa is set to support the legislation, with small modifications. The Intellectual Property Attaché Act is written to help American individuals and companies that are experiencing intellectual property infringement in certain foreign countries. The legislation will place USPTO trained IP attaches in countries around the world, focusing on areas where American job creators and innovators are experiencing especially high levels of IP-theft. These attaches will work with the foreign governments to help eliminate in-country IP theft that is occurring. This is a net benefit to all Americans both IP holders and consumers. Also, the training and other programs that the attaches may provide can also help local law enforcement to deal with IP-infringement that is occurring. The cost for these attaches will come from collected PTO fees, meaning that the bill is revenue neutral. Additionally, we expect that an amendment will be made to the legislation before it is marked up that will instruct the attaches to promote clear IP exceptions like fair use – already codified in U.S. Law.
The biggest hope for killing the measure perhaps lies in its likely substantial costs and sweeping expansion of the federal government. Ballooning federal government and burdening taxpayers with the expense of large new federal programs certainly sounds outside the line of traditional fiscal conservative rhetoric that's in vogue these days.
SOPA v. 2.0 has crawled back onto the scene, but might be killed yet.
[Image Source: DeviantArt;~k1ow3]
Some Republicans may balk at essentially voting for "a tax" in order to scratch the back of big media. Although, the fact that big media donated generously to a great many members of Congress may allow them to look past their own political beasts and shove this copyright debt on the shoulders of the masses.
At least overseas there are signs of a break in the storm of big media trolling. Denmark has
turned off
its warning letters program. And Canada has implemented strong protections/permissions for user-generated content (e.g. montages) and
capped non-commercial infringement
at $5,000 USD.
In other words, the U.S. is one of the last places where big media can hope to sue individual citizens for millions of dollars for pirating a few songs. It also looks to become one of the few nations to install a special redundant "copyright police" agency at the federal level, financed by its citizens' tax burden.
House of Representatives [PDF]
"We don't know how to make a $500 computer that's not a piece of junk." -- Apple CEO Steve Jobs
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text:
This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
The major virulence factors of
CDI is a toxin-mediated disease. Two exotoxins, toxin A (TcdA) and toxin B (TcdB), are the most extensively studied major virulence factors, supported by reports demonstrating that
TcdA and TcdB possess a wide spectrum of biological activities, which may contribute to the range of symptoms associated with CDI. Toxin-induced disruption of the cytoskeleton leads to cytopathic effects in cultured cells within hours of intoxication, and this effect has been suggested to be mediated through Rac1 inactivation [
Asymptomatic carriage of
In animal models, an unusual observation with
Studies in animal models have contributed greatly to our understanding of the pathogenicity of TcdA and TcdB. It was speculated that TcdA was the most important component in disease production because it elicits extensive tissue damage and fluid accumulation in several animal models [
Why TcdB does not show enterotoxicity in ileal loops of animal models, while TcdA−TcdB+
TcdA (308 kDa) and TcdB (269 kDa) belong to the Clostridial glucosylating toxins family, and share high amino acid sequence identity [
Structure of TcdA and TcdB. TcdA and TcdB consist of four domains: an
The most striking feature of the RBDs of TcdA and TcdB is the presence of CROPs of 21-, 30-, or 50-amino acid residues. Different approaches to analyzing the sequence of CROPS of TcdA reveal that this region contains between 30 and 38 contiguous repeats, whereas in TcdB those appear to be between 19 and 24 residues [
The putative TMD makes up more than 50% of the total size of the toxins and contains a hydrophobic region which is most probably responsible for membrane insertion. To date, little is known about exact functions of the TMD. However, recently it was suggested that the Asp-Xaa-Gly (DXG) motif of TcdB possesses aspartate protease activity, which could be involved in toxin cleavage [
The newly identified CPD domain is located between the GT and TMD domains, starting from residue 543 to residue 767 in TcdB. The CPD domain contains a conserved catalytic triad (Asp587-His653-Cys698) of a cysteine protease and mediates toxin autocleavage. Interaction between the RBD and the host cell receptors is believed to initiate receptor-mediated endocytosis [
The common features of small GTPases include their small molecular mass (18–28 kDa), their
Once in the cytosol, the GT effector domain of the toxins mono-O glucosylates low molecular weight GTPases of the Rho family, including RhoA, Rac1, and CDC42 [
In addition to TcdA and TcdB, some
The clinical appearance of CDI is highly variable, ranging from mild self-limited diarrhea to severe pseudomembraneous colitis. The disease starts in the large bowel and shows distinguishing "volcanic eruption" characteristics of the pseudomembranous lesion observed in severe colitis. Diarrhea and colitis are two major clinic manifestations of CDI. In severe cases of CDI, patients present with systemic inflammatory syndromes that include abdominal pain, fever, hypotension, tachypnea, and leukocytosis. Most of these clinical presentations can be ascribed to direct intestine tissue damage and inflammation mediated by TcdA and TcdB. This section describes how TcdA and TcdB can induce such intestinal damage and inflammation. The proinflammatory mediators involved in the enterotoxicity of TcdA and TcdB are summarized in
Proinflammatory mediators involved in the enterotoxicity of TcdA and TcdB.
|Proinflammatory mediators
|Sources (cells or tissue)
|Known or proposed functions
|Intestinal epithelia, macrophages, peripheral blood monocytes
|Neutrophil recruitment
|GRO-α (growth-related oncogene)
|Intestinal epithelia
|Neutrophil recruitment
|MIP-1 (macrophage inflammatory protein-1)
|Intestinal epithelia, macrophages
|Neutrophil recruitment
|MIP-2 (macrophage inflammatory protein-2)
|Intestinal epithelia, macrophages
|Neutrophil recruitment
|ENA-78 (epithelial neutrophil-activating peptide-78)
|Intestinal epithelia
|Neutrophil recruitment
|MCP-1 (monocytes-chemotactic protein-1)
|Intestinal epithelia
|Neutrophil recruitment
|ICAM-1 (intercellular adhesion molecule-1)
|Endothelial cells, neutrophils, epithelia
|Neutrophil adhesion to endothelial cells
|Macrophages, dendritic cells,
|Neutrophil recruitment, enhancing IL-8 production,
|Monocytes, dendritic cells
|not specified
|Macrophages, monocytes
|Neutrophil recruitment
|Enhancing chemokine and ICAM-1 expression expression
|LB4 (Leukotriene B4)
|Macrophages, mast cells
|Neutrophil recruitment, activation of transient receptor potential vailloid (TRPV1) and SP release
|LC4 (Leukotriene C4)
|Mast cells
|Stimulation of fluid secretion by intestinal epithelia
|RMCP II (rat mast cell protease II)
|Mast cells
|Indicator of mast cell activation
|SP (substance P)
|Intestinal neurons
|Activation of mast cells and macrophages
|CGRP (calcitonin gene-related peptide)
|Intestinal neurons
|Activation of mast cells and macrophages
|NT (neurotensin)
|Intestinal neurons
|Activation of mast cells
|VIP (vasoactive intestinal polypeptide)
|Colonic submucosal neurons
|Activated partially via an IL-1β-dependent pathway ( its role in the intestine is to increase motility
|PAR2 (protease activated receptor 2)
|Enterocytes, neurons, endothelial cells, neutrophils
|Intestinal inflammation
|IL-1β production
|Melanin-concentrating hormone (MCH)
|Intestinal tissue
|Upregulation of IL-8 transcription
|Reactive oxygen species (ROS)
|Direct damage of proteins and lipids, induction of IL-8 and ICAM-1
|Cyclooxygenase-2 (COX-2)
|Human colonocyte, human intestinal xenograft
|Formation of PGE2
|Prostaglandin E2 (PGE2)
|Human colonocyte, human intestinal xenograft
|Intestinal inflammation
|Phospholipase A2
|Rabbit ileal tissue, human T-84 cells
|Synthesis of inflammatory lipid mediators
|Platelet-activating factor (PAF)
|Rabbit ileal tissue
|Stimulation of fluid secretion by intestinal epithelial cells
|Na+/H+ exchanger (NHE)
|Intestinal epithelial cells
|Involvement in Na+ absorption and fluid homeostasis
|Angiotensin II (ANGII)
|Rabbit ileal tissues
|Regulation of intestinal secretion and absorption
|Epidermal growth factor receptor (EGFR)
|Human colonic epithelial cells
|Activation of IL-8
The direct target tissue of the
The apoptogenic properties of TcdA and TcdB are well known, and they may contribute to the inflammatory process induced by these toxins. Treatment of intestinal epithelial cell lines with either TcdA or TcdB results in their apoptosis [
Brito and his colleagues reported that TcdA-induced apoptosis of T84 cells is completely inhibited by blocking toxin enzymatic activity on Rho GTPases with uridine 5'-diphosphate-2',3'-dialdehyde, and is partially inhibited by caspase-1, -3, -6, -8, and -9 inhibitors [
Glucosyltransferase-independent apoptosis was reported as well. Matarrese and colleagues demonstrated that TcdB causes apoptosis in human epithelial HEp-2 cells by directly acting on mitochondria, which does not require the
In addition to apoptosis, necrosis is also likely to contribute to mucosal damage. For instance, TcdA has been shown to induce cell necrosis [
The roles of transcription factors in
An intense inflammatory response with a marked neutrophil accumulation is a key characteristic of the clinical pathophysiology of CDI [
In addition to chemokines, release of proinflammatory cytokines or other mediators from immune cells seems to be a critical activation event in TcdA-mediated inflammation [
Neutrophil-derived proinflammatory mediators act on epithelial cells, causing destruction and necrosis of enterocytes and colonocytes [
Intestinal mast cells are critically involved in neutrophil activation in TcdA-mediated inflammation. Increased mucosal and circulating levels of the specific mucosal mast cell enzyme, rat mast cell protease II (RMCP II), and degranulation of mucosal mast cells are observed within 15–30 min after TcdA exposure [
Dendritic cells (DCs) are antigen-presenting cells that play important roles in innate and adaptive immune responses [
Macrophages play an important role in the pathogenesis of
There is clear evidence that primary sensory neurons are also involved in
Melanin-concentrating hormone (MCH) is a hypothalamic orexigenic neuropeptide that regulates energy balance. Pothoulakis and colleagues found that TcdA induced upregulation of MCH and its receptor MCHR1 in the human intestinal xenograft model and of MCHR1 in colonocytes. Treatment of colonocytes with MCH upregulates the transcription of IL-8. Moreover, MCH-deficient mice develop an attenuated TcdA-mediated intestinal inflammation and secretion [
Neurotensin (NT) is another neuropeptide mediator in TcdA-induced enteritis [
Further support for a neuronal involvement in CDI is provided by a study demonstrating the involvements of protease-activated receptor 2 (PAR2) in TcdA-induced enteropathy [
Another potential mediator of neuronal-mediated enteropathy in response to TcdA is leukotriene B4 (LTB4). Using rat ileal loops, McVey and Vigna showed that TcdA induces LTB4 secretion, a mediator that can cause a similar ileitis as TcdA [
The acute intestinal inflammatory response to TcdA in animal models (mostly demonstrated in ileal loops of mice, rats, and rabbits), have demonstrated a clear role for TcdA in modulating inflammatory events. This inflammation is also implicated in the intestinal hyper-secretion and tissue damage. In addition to the mediators described above, several other classes of signaling molecules have been implicated in CDI.
Qiu and colleagues reported that ROS participates in TcdA-induced enteritis in rats [
Lipid inflammatory mediators are also implicated in the initiation and perpetuation of TcdA-induced inflammation. Alcantara
The Na+/H+ exchanger (NHE) family consists of eight identified members (NHE1-8), all of which are integral membrane proteins that catalyze electro-neutral exchange of alkali cations for H+. NHE3 is expressed in the apical membrane and in subapical endosomes of polarized epithelial cells. In intestine, NHE3 is thought to play a critical role in Na+ absorption and fluid homeostasis [
The renin-angiotensin system (RAS) is a multi-organ system of proteins and receptors that is regulated by hormones and cytokines to control a number of mechanisms associated with fluid balance and vasoconstriction. Angiotensin II (Ang II) is the main active peptide in the renin-angiotensin system. It was known that Ang II was vasoactive, capable of stimulating vascular smooth muscle cells. AngII binding to the type 1 receptor (AT1) results in vasoconstriction, and its binding to the type 2 receptor (AT2) results in vasorelaxation. Both AT1 and AT2 are known to play a major role in the cardiovascular and renovascular systems that mediate inflammation, cell growth, and fibrosis. There has been considerable interest in the presence of a local angiotensin system in the gastrointestinal tract. Alcantara and colleagues investigated the role of Ang II in a rabbit ileal loop model of CDI [
Even though
Our understanding of the enterotoxicity of TcdA and TcdB and their mechanisms of action has been expanded based on many exciting developments in this field. We can only highlight several pioneering work defining our views on
Mechanisms of TcdA- and TcdB-mediated enterotoxicity. TcdA and TcdB cause intestinal damage and inflammation by direct actions on intestinal epithelial cells, leading to chemokine release, cell rounding and apoptosis or necrosis. Alternatively, the toxins may target immune cells and neurons once the intestinal epithelial barrier is disrupted. The toxins may also act indirectly by stimulating cells to produce chemokine, proinflammatory cytokine, neuropeptides, and other mediators. IL-8: interleukin-8; MIP-2: macrophage inflammatory protein-2; SP: substance P; CGRP: calcitonin gene-related peptide; NT: neurotensin; PAF: Platelet-activating factor; LC4: Leukotriene C4; ROS: Reactive oxygen species.
Despite the progress that we have made in understanding the molecular mode of action of the two toxins, many fundamental questions remain unanswered. Are there specific receptors for TcdA and TcdB? And if so, what are they? Why do TcdA and TcdB differ considerably with respect to their biological activities while they share high sequences homology and similar domain structures, and act in a similar molecular mode? What are the respective roles of these two toxins in the host inflammatory response and pathogenesis? Given the increasing importance of CDI in public health, significant more research is necessary to fill these gaps in our knowledge in order to better tackle the disease.


text:
PCS and Unison joint statement
PCS and Unison are committed to working together to fight cuts and promote public services. This will involve campaigning, co-ordinating and, where possible, taking action in unity and support of each other.
The attack launched by this government on public services and the welfare state is unprecedented and unjustified. In freezing pay, slashing jobs and attacking pensions the government is seeking to make public service workers, and everyone who relies on the services they provide, pay for the deficit caused by the financial sector – whose benefits, bonuses and tax concessions remain largely unchanged.
There is an alternative
The cuts to welfare entitlements and public services will be detrimental to the vulnerable, to the quality of service and to the economy.
There is an alternative, as set out in UNISON's 'Alternative Budget' and the 'The PCS alternative to cuts':
- Protect and create jobs to secure the economic recovery
- Tax the banks, big business and the super-rich, with a crackdown on evasion and avoidance
- End wasteful spending on Trident, consultants, agency staff and the costs of privatisation
- Involve staff, unions, service-users and communities in developing an alternative agenda for a sustainable economy and fairer society.
What we will do together
At national level PCS and UNISON will establish a Liaison group to promote joint activity and co-ordinate our joint campaign. This liaison group will co-ordinate a joint approach to TUC public sector campaign activity. The liaison group will also promote, build and co-ordinate public sector alliances across central and local government, and co-operation in terms of communications and media strategy, including press releases, leaflets and sharing resources.
To highlight the alternative to the government's budget cuts and promote public services, PCS and UNISON will jointly organise a "There is an Alternative" event in later 2010 or early 2011. This will bring together trade unionists, politicians, academics, voluntary and community groups. The aim will be to raise awareness that there is an alternative economic strategy to the cuts and develop a broad coalition to fight the cuts and promote public services.
At regional level the unions develop practical ways of supporting joint campaigns. This will include twinning officers and organisers, developing regional campaign teams, regional events and road shows, and developing links with voluntary and groups. The aim will be to build and support regional public sector alliances across central and local government.
At local level we will develop and support links between members and activists. This will include joint workplace meetings, joint public leafleting, locally organised town meetings and joint community activities.
United we stand
The government's cuts agenda will devastate public services and undermine the fabric of the welfare state.
Working together over 1.5 million union members will be united to fight the cuts to public services. Working together we can present our economic alternative to the coalition cuts agenda to the public.


text:
Current address: Laboratory of Respiratory and Special Pathogens, Division of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892, USA
This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
Systemic anthrax disease is characterized by vascular leakage pathologies. We previously reported that anthrax lethal toxin (LT) induces human endothelial barrier dysfunction in a cell death-independent manner with actin stress fiber formation and disruption of adherens junctions (AJs). In the present study, we further characterize the molecular changes in the AJ complex and investigate whether AJ structure and barrier function can be preserved by modulating key cytoskeletal signaling pathways. Here, we show that LT reduces total VE-cadherin protein and gene expression but the expression of the key linker protein beta-catenin remained unchanged. The changes in VE-cadherin expression correlated temporally with the appearance of actin stress fibers and a two-fold increase in phosphorylation of the stress fiber-associated protein myosin light chain (p-MLC) and cleavage of Rho-associated kinase-1 (ROCK-1). Co-treatment with ROCK inhibitors (H-1152 and Y27632), but not an inhibitor of MLC kinase (ML-7), blocked LT-induced p-MLC enhancement and stress fiber formation. This was accompanied by the restoration of VE-cadherin expression and membrane localization, and attenuation of the LT-induced increase in monolayer permeability to albumin. Together, these findings suggest the ROCK pathway may be a relevant target for countering LT-mediated endothelial barrier dysfunction.
Inhalational anthrax is a disease caused by inhaling spores of the gram-positive bacterium
Systemic anthrax infection is often accompanied by profound vascular pathologies including edema, hemorrhage, pleural effusion, and vasculitis in animals and humans [
Consistent with the vascular pathologies of anthrax, we previously reported that LT induces cell death-independent barrier dysfunction in primary human lung microvascular endothelial cell culture characterized by actin stress fiber formation and altered adherens junction (AJ) structure [
Phosphate-buffered saline (PBS) and Hank's balanced salt solution with calcium and magnesium (HBSS) were obtained from Invitrogen (Carlsbad, CA, USA). The MLC kinase (MLCK) inhibitor ML-7, the ROCK inhibitors H-1152 (Rki) and Y-27632 (Y27) were purchased from EMD Chemicals (Gibbstown, NJ, USA). LF, PA, and inactive mutant LFE687C were kindly provided by Dr. Stephen H. Leppla (National Institutes of Health, Bethesda, MD) [
Goat polyclonal antibodies to VE-cadherin (catalog #sc-6458) and ROCK-1 (C-19) (catalog #sc-6055), and rabbit polyclonal antibodies to ROCK-1 (H-85) (catalog #sc-5560), ROCK-2 (catalog #sc-5561), beta-catenin (catalog #sc-7199) and tubulin (catalog #sc-9104) were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Rabbit polyclonal antibody to p-MLC (Thr18/Ser19) (catalog #3674) was purchased from Cell Signaling Technology (Danvers, MA, USA). Rabbit polyclonal antibody to MEK1 (catalog #07-641) was obtained from Millipore (Billerica, MA, USA).
Primary human lung microvascular endothelial cells were obtained from Lonza (Walkersville, MD, USA) and cultured as described previously [
Cells grown to confluence on porous membrane inserts (12 mm diameter, 0.4 µm pore size) were treated as described above. After 72 h, 50 µL of culture medium from the upper chamber was replaced with an equal amount of medium containing 5 mg/mL FITC-HSA (final concentration 500 µg/mL). After 2 h, 20 µL samples were drawn from the lower chamber and diluted 10-fold. Data were collected from duplicate inserts per treatment in each experiment. Fluorescence measurements were obtained using a microplate reader (Genios™, Tecan, Research Triangle Park, NC, USA) with excitation and emission filters of 485 and 535 nm, respectively. FITC-HSA concentrations were calculated using a FITC-HSA standard curve. To quantify the trans-membrane flux (μg/h/cm2), the FITC-HSA concentration was multiplied by the volume of the lower chamber and divided by the membrane area and the FITC-HSA incubation time.
Cells were grown to confluence in 24-well dishes, and treated with LT in the presence or absence of inhibitors as indicated. Monolayers were fixed with 3.7% paraformaldehyde, washed, and blocked in HBSS containing 10% goat serum. Monolayers were incubated with anti-phospho-MLC (1:100) and anti-VE-cadherin (1:200) for 1 h at room temperature. Immunofluorescence analysis using Alexa Fluor 555-labeled secondary antibodies (1:800 dilution) and Alexa Fluor 488-labeled phalloidin (1:100 dilution) to stain filamentous actin (Invitrogen) was performed as described previously [
RNA extraction and gene expression procedures were described previously [
Whole cell extracts were prepared as described previously using ice cold RIPA lysis buffer (50 mM Tris, 150 mM NaCl, 1% IgePal-630, 1 mM EDTA, 0.25% sodium deoxycholate) containing protease inhibitors (Cocktail Set III, Calbiochem, CA) and the phosphatase inhibitors NaF (1 mM), sodium orthovanadate (1 mM), sodium pyrophosphate (2.5 mM), and beta glycerophosphate (1 mM) [
Reduced samples were run on NuPAGE 4-12% gradient Bis-Tris gels in MOPS SDS running buffer. Proteins were transferred to PVDF membranes and detected as described previously [
Data are represented as means ± SE for replicate experiments. Statistical analysis was performed by ANOVA with
We previously reported that LT disrupts AJ integrity in endothelial cells [
Lethal toxin (LT) reduces expression of VE-cadherin but not beta-catenin. Cells were treated with medium (-) or LT for indicated time points. Whole cell lysates were analyzed by Western blot for VE-cadherin (
We previously showed that LT-induced changes in AJs were accompanied by actin stress fibers [
MLC phosphorylation is primarily catalyzed by myosin light chain kinase (MLCK) and ROCK [
To further delineate the contribution of ROCK, we analyzed the expression of the two main isoforms, ROCK-1 and ROCK-2. Total expression of both isoforms, each identified as a main band at 160 kDa, was similar in LT-treated cells compared to non-treated cells at 24 and 72 h (Figure 2C). At 72 h, a cleavage band was detected in LT-treated cells when using an antibody raised against an internal sequence of ROCK-1 (H-85). This cleavage fragment was not observed in non-treated cells or mutant LT-treated cells. Proteolytic cleavage of the inhibitory
LT enhancement of myosin light chain (MLC) phosphorylation is attenuated by Rho-associated kinase (ROCK) inhibition. Cells were treated with medium, lethal factor (LF) (100 ng/mL), protective antigen (PA) (500 ng/mL), LT (100 ng/mL LF + 500 ng/mL PA), or inactive mutant LT (LTm; 100 ng/mL LFE687C + 500 ng/mL PA). Where indicated, cells were pretreated with the MLCK inhibitor ML-7 (5 µM), or the ROCK inhibitors Rki (1 µM) or Y27 (5 µM) for 30 min. (
We hypothesized that modulating the formation of actin stress fibers could preserve VE-cadherin contacts. To test this hypothesis, we examined the effect of ROCK and MLCK inhibitors on VE-cadherin localization and expression. In non-treated cells, VE-cadherin localized to intercellular junctions exhibiting a continuous and intense cortical staining pattern (
LT-induced VE-cadherin changes are attenuated by ROCK inhibition. Cells were treated with medium or LT. Where indicated, cells were pretreated with the MLCK inhibitor ML-7 (5 µM), or the ROCK inhibitors Rki (1 µM) or Y27 (5 µM) for 30 min. (
In separate experiments, we investigated whether LT-induced AJ disruption could be ameliorated by inhibiting ROCK activity after LT exposure. Cells were treated with LT for 24 h prior to the addition of Y27. Similar to the inhibitor pretreatment experiments, Y27 prevented morphological changes and rescued VE-cadherin localization after 72 h (data not shown). The protective effect of ROCK inhibition on endothelial morphology and VE-cadherin contacts was particularly evident at time intervals beyond 72 h. After 120 h, LT-treated monolayers and VE-cadherin contacts were mostly disintegrated (
ROCK inhibition prevents long-term effects of LT on cellular architecture and VE-cadherin contacts. Cells were treated with medium or LT. Where indicated, cells were pretreated with the MLCK inhibitor ML-7 (5 µM), or the ROCK inhibitors Rki (1 µM) or Y27 (5 µM) for 30 min. After 120 h, monolayers were stained with Hoechst 33342 (blue, nuclei), phalloidin (green, actin), and a VE-cadherin antibody (red) as described in Materials and Methods. Representative fields are shown for each treatment by phase contrast and corresponding immunofluorescence images (400 × magnification).
We next examined whether the preservation of AJ integrity by ROCK inhibition translates to attenuation of barrier dysfunction. LT produced a two-fold increase in monolayer permeability to albumin. LF, PA, or mutant LTm had no effect on albumin flux. Rki and Y27, but not ML-7, significantly inhibited the LT-mediated increase in monolayer permeability to albumin (
LT-induced barrier dysfunction is partially prevented by ROCK inhibition. Cells grown on porous membrane inserts were treated with medium or LT. Where indicated, cells were pretreated with the MLCK inhibitor ML-7 (5 µM), or the ROCK inhibitors Rki (1 µM) or Y27 (5 µM) for 30 min. After 72 h, albumin flux was measured as described in Materials and Methods. Means ± SE for three separate experiments are shown. *
Vascular leakage pathologies such as pleural effusion, edema, and hemorrhage are hallmarks of anthrax pathogenesis [
Endothelial AJs play a major role in regulating barrier function [
Due to the dynamic and selectively permeable nature of the endothelial barrier, several intrinsic signaling pathways function to modulate the barrier in cases where controlled passage of proteins and leukocytes is beneficial. Infectious and/or inflammatory agents often trigger these same mechanisms to induce pathological barrier dysfunction. One of these mechanisms involves rearrangement of the actin cytoskeleton from barrier-protective cortical actin to stress fibers, a common consequence of bacterial cytotoxins [
While the present findings suggest a role for ROCK in LT-mediated endothelial dysfunction, the precise mechanisms have yet to be defined. An important experimental limitation in our study was that the ROCK inhibitors alone produced profound effects on the actin cytoskeleton. Moreover, under certain conditions, these inhibitors may nonspecifically inhibit other protein kinases such as PKA and PKC [
The ROCK family consists of two closely related serine/threonine kinases, ROCK-1 and ROCK-2, both of which are highly expressed in the endothelium [
Rolando and colleagues showed that LT does not activate the small GTPases RhoA, Rac and Cdc42 [
Antibiotic therapy is currently the primary option to treat anthrax. However, antibiotics are not effective in treating the later stages of an infection due to substantial toxemia [
Vascular leakage pathologies such as pleural effusion, edema, and hemorrhage are hallmarks of anthrax pathogenesis. Emerging evidence points to the endothelial lining of blood vessels as a critical pathogenic target. Anthrax LT, the major virulence factor of anthrax, triggers human endothelial barrier dysfunction
We thank S. H. Leppla for kindly providing the anthrax toxin proteins. This project was supported in part by an appointment of J. M. Warfel to the National Institutes of Health-Georgetown University Graduate Partnership Program and the Research Fellowship Program for the Center for Biologics Evaluation and Research administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the US Department of Energy and the US Food and Drug Administration.
The authors declare no conflict of interest.


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Career Counselor
Joyce Colburn, LCSW
Licensed Clinical Social Worker
225 Main St., Westport, Connecticut
My approach to clients undergoing career issues begins with an assessment to determine the type of problem, including lack of direction, negative performance reviews, workload anxiety, lack of advancement, or the need for a transition. Once we've established the priority, treatment includes setting goals together and developing a therapeutic relationship, including coaching, to support and maintain the client's progress.
Career Counselor
Kevin Fleming Ph.D.
Coach/Change Agent/Consultant
Weston, Connecticut
While most career counselors love to give you capacity based profiles of what your talents and interests are for your best bet career choices, Grey Matters international believes that most people make predictably irrational decisions and then after making them learn way to make them fit into their identities using various types of rationalizations and strategies. We are able to assist folks in career counseling type settings by giving a deeper look at their decision making profile so they can better understand where the core frustration or desire is coming from in the world of work. Contact email@example.com or 877-606-6161.
Career Counselor
Linda Palmieri, MFT
prelicensed Marriage and Family Therapist
755 Main street,Building 2,Suite1, Monroe, Connecticut
I will assist you on your journey in choosing your path. Together we can examine your desires and options. We will look at how others in your life, including your family, are playing apart in your process of making a decision in your life. Lets figure out what your passion in life is, what lights you up and that will make you happy, after all you are the most important person in your search for what adds meaning to your life.
06601 is a zip code located in Fairfield County and part of Bridgeport, Connecticut.


text: Rawalpindi- Federal Police has decided to conduct basic investigation courses for making the investigation process better in which lectures will be delivered to all the investigation officers of all Police stations about investigation and interrogation matters. Taking a strict notice of capacity problems of investigation officers IG directed to conduct courses for investigation officers of all Police stations for increasing their capacity building and for making the investigation circle more effective and better. Senior officers of Islamabad Police, Police College Sahala and Lawyers will deliver lectures. Investigation officers will learn about registration of a comprehensive FIR, responsibilities of a person who reached a crime scene at first, physical investigation, to present an accused before the court and method of application for physical remand, interrogation, geo fencing and search of crimes through mobile Sims.


text:
Anti-establishment candidate Bruno Boccara has won the by-election for a place on the Paris Bar Council ahead of Willkie Farr & Gallagher partner Dominique Mondolini, who had been hoping to exploit international firms' discontent with what they perceive as the bar's isolationist attitude.
The Paris Bar is now faced with a maverick councillor and a disgruntled and under-represented international contingent.
"I'm very satisfied that the international firms mobilised 204 votes for this particular election," Mondolini told The Lawyer.
This was the bar's first contested election, held after the previous councillor retired mid-term. Full elections for councillors and the presidency will be held in November, with the added bonus of an internet election saving voters from trudging down to the courts.
Mondolini will discuss with his partners whether he will stand again.
He added: "I look forward to the November elections. The reasons that motivated my candidacy in this election still stand."
The main reason is that lawyers from international firms feel under-represented with just three seats on the 36-member council.
A recent letter to a French newsletter by former bar president Paul-Albert Iweins provoked fury among international firms when Iweins revealed that he had discussed favouring French firms with French president Jacques Chirac.
Iweins has since apologised, saying that his views were misinterpreted.
Boccara won the second ballot against criminal lawyer Dominique Tricaud and sole practitioner Michel Cervoni.
Boccara believes that the Bar Council is a closed club for former presidents and stands for reform.


text:
Safety On The Slopes
02/27/12 12:00PM By Jane Lindholm
| Download MP3
Skiing and snowboarding are popular sports, but as this winter has proven, they can be dangerous. And this winter's erratic weather has made them even more challenging.
Stratton Snow Sports School Manager Alison Cummings, Neil Van Dyke of Stowe Mountain Rescue and Dr. Robert Williams discuss slope conditions, choosing the right trail level, skiing back country and wearing the proper equipment.Also in the program, a legislative update from Concord. John Gregg, political editor of the Valley News, discusses a few key health care and social issues before the New Hampshire Legislature, as lawmakers near the half-way point of the session.


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Celebrating 15 years
The Sticker Factory is 15 years old! We are very happy that the news was featured in our local paper today, the Suffolk Free Press. Click on the link and take a look at the press clipping: 10.05.12 TSF press… Continue reading
Press release: Reward good behaviour in style
A press release for you that was written about our 'Stickers at Home' launch:
The Sticker Factory's array of uniquely designed products are now available for parents.
Parents of young children, from toddlers to pre-teens, can now reward… Continue reading


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It's here! It's here! All the local news headlines you need to know about, delivered straight to your e-mail box and from there to your little grey brain.
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The Tribune Co.-owned broadcast TV station formerly known as KTZZ is holding an all-day Looney Tunes Marathon today, and another (with a whole different set of cartoons) this Sunday.
So far, the only commercials in it are for the station's new brand identity, "Joe.TV." You may have seen the many billboards and street posters for it. No more MyNetwork TV. Instead, its evening schedule relies on reruns of The Simpsons, South Park, Family Guy, King of the Hill, Entourage, and Curb Your Enthusiasm, plus the existing 9 p.m. newscast produced by sister station KCPQ. The rest of the station's schedule will be mostly forgettable judge shows and infomercials.
And, no, classic Warner Bros. cartoons will not be on the station after the second marathon on Sunday.
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We promise to help make your story a great one; however, the staff of the Texas State Aquarium, including keepers, curators and veterinarians, as well as the Communications department, may occasionally set guidelines and limitations to ensure the safety of our animals and Aquarium guests.
All interviews with Aquarium employees will be arranged through the Communications department.
Here's practical information to help you plan a press trip or your story about the Aquarium:
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We'll assist with story development and logistics, even help with suggestions and access to resources if you're covering other aspects of the story in the Corpus Christi area. We can also provide high-resolution images for use with your story. Contact the Communications department.
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We offer complimentary admission to working journalists on assignment. Contact our Communications department in advance of your visit to make arrangements.
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All Aquarium visitors can take photos and video for their private, personal use only. For safety reasons, use of tripods or monopods is prohibited. Taking photos or video, including for stock images and other commercial purposes, is prohibited unless authorized in advance by the Public Relations department. For media, there are also some restrictions on use of tripods and supplemental lighting. If you're planning a photo or video shoot as part of a story about the Aquarium, please review our Photo and Video Guidelines, and contact the Communications department in advance to make arrangements.
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text:
Flames NewsFlames Home > Lacrosse Home > News
Familiar Women's Lacrosse Opponent to Join Big South
The Big South Conference has added Davidson College as an associate member in women's lacrosse, it was announced Thursday by Big South Commissioner Kyle B. Kallander. Davidson will begin competing in the Big South in the 2013 season, as part of the conference's inaugural women's lacrosse campaign.
The Big South first announced the addition of women's lacrosse as the conference's 19th championship sport on June 8, and the addition of Davidson will give the Big South seven Division I women's lacrosse members. The Wildcats will join current Big South members Campbell, Coastal Carolina, High Point, Liberty, Presbyterian College and Winthrop on the field in 2013.
Liberty, along with High Point and Presbyterian College, is already familiar with Davidson's women's lacrosse program, having competed in the National Lacrosse Conference (NLC) with the Wildcats the last two seasons. While the Lady Flames dropped a tough contest against Davidson in their 2010 inaugural season, 21-4, the gap was closed considerably this past season with four and five-goal defeats, 12-8 and 11-6.
Davidson will bring a longstanding women's lacrosse program into the Big South. The Wildcats will play their 19th season in 2012, after the program began in 1994. It remained independent until joining the American Lacrosse Conference (ALC) in 2002. The program then competed independently again from 2005-2009 before joining the NLC in 2010. During the same season, the program achieved its 100th victory.
"Davidson will be a great addition for women's lacrosse in the Big South. Adding a program that has nearly 20 years of experience will only make the conference stronger as we move forward. We've faced them three times already in NLC play and look forward to competing against them as a Big South member in the future," commented Liberty Head Coach Regan Denham.


text:
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Is Arthur's Grave at Glastonbury Genuine?
The medieval historian, Gerald of Wales, tells us that sometime before he died in 1189, King Henry II sent a
message to the abbot of Glastonbury Abbey regarding the location of the grave of King Arthur. An unnamed Welsh bard had
allegedly given this information to Henry and he had kept it to himself until the time was right to divulge it.
In 1190, the Glastonbury monks, presumably acting on this information, uncovered a hollowed-out log
containing two bodies, while digging between two stone pyramids standing together in the abbey cemetery. The log coffin
had been buried quite deep, at around 16 feet down. A stone slab cover had been found at the seven foot level. Attached to the
underside of the slab was an oddly shaped cross with a Latin inscription on it, naming the occupants of the coffin as the renowned
King Arthur and his queen, Guinevere.
Beside Gerald's account, there were several current versions of the discovery of the grave and cross. Each
account was different from the others and included or omitted details which the others did not. There were, at least, five
reported versions of the inscription on the cross. This inconsistency in the details of the story has led some to think that a hoax
was being perpetrated by the monks for the purpose of generating pilgrim traffic to the abbey.
After all, hadn't their magnificent abbey church, the most glorious in all England, possibly in all of
Christendom, been destroyed by fire in 1184, just six years before? And hadn't their greatest pilgrim attraction, the
"Old Church", the ancient cradle of British Christianity been burned up with it? Also, since their chief benefactor,
the recently departed Henry II, was no longer in a position to finance their efforts to rebuild, it would not take a great leap of
imagination to expect that some other scheme to raise funds would have to be developed.
There are certain difficulties with the hoax theory, though, one of which was that the abbey never really went
to great lengths to publicize the discovery. Another is that the abbey enjoyed and benefited from a reputation for integrity and
uprightness. Also, if the abbey had been willing to sacrifice its reputation for this deception, then wouldn't it have made
sure that all aspects of the story were consistent and that everyone involved was using the same story?
The timing of the "discovery" seemed fortuitous for the abbey, but, surprisingly, nothing is heard
of the grave or the bodies of Arthur and Guinevere until about forty years later when there is a report of them being moved to
another vault. The bodies remained in storage until the year 1278, when Edward I came to Glastonbury to preside over
their re-interment in a new marble coffin, underneath the high altar, in the newly rebuilt abbey church. It seems that if a
hoax were being perpetrated, it would've been monumental stupidity to allow your main attraction, your meal ticket,
your passport to untold riches to sit in cold storage, losing 88 years of pilgrim dollars.
The final disposition of their bodies is unknown, but they probably didn't survive the Dissolution of the
abbey by Henry VIII and his zealots in 1539. The burial cross, though, did. It was seen by John Leland in 1533 and illustrated
for a book, "Britannia", by William Camden in the early seventeenth century. It was last reported in the possession
of one William Hughes, an official of Wells Cathedral, sometime in the early eighteenth century.
Below are collected most of the historical details relevant to the Burial Cross of King Arthur:
A cross was found during the excavation of a grave site next to the Lady Chapel at Glastonbury Abbey in 1190.
The cross was said to be "leaden".
The cross was fastened to the underside of a stone slab located seven feet down (the actual bones were found at
the 16 foot level), and the inscription was turned in toward the stone slab.
Gerald of Wales' account states that the inscription was on one side of the cross.
There are two more or less contemporary accounts of the dig; one by Gerald of Wales (Giraldus Cambrensis or
Gerald de Barri) and the other in the Margam Abbey Chronicle (thought to be copied from a monastic "newsletter"
sent out by Glastonbury Abbey, reporting the discovery).
The Margam account stated that the grave site was discovered by accident, that there were three separate
coffins (one each for Arthur, Guinevere and Mordred) and that the wording on the cross did not mention Guinevere.
Gerald of Wales' account, penned later, said that the grave site location was given to the monks by none
other than Henry II, after it had been revealed to the great monarch by a Welsh bard. It stated also that there was only one
coffin (actually a hollowed-out log, split into two sections, one each for Arthur and his queen) and that the cross specifically
mentioned her by name (see version two, below).
Ralph of Coggeshall in 1193 supported the version told by the Margam Chronicle. This should not be viewed
as unqualified support for Margam since Gerald of Wales didn't write up his eyewitness account until 1195. Until then,
Margam was the only game in town.
Adam of Domerham, writing in 1290, and John of Glastonbury, around 1350, tell us that there were two
tombs and adds the interesting detail that while the digging was being done, the grave site was surrounded by white
draperies or curtains.
There are five different versions of how the cross was actually inscribed:
"Here lies the famous King Arthur, buried in the isle of Avalon"
"Here lies buried the famous King Arthur with Guinevere his second wife in the isle of Avalon"
"Here lies interred in the isle of Avalon the renowned King Arthur"
"Here lies Arthur, the famous King, in the isle of Avalon"
"Here lies buried the famous King Arthur with Guinevere his fortunate wife in the isle of Avalon"
The letterforms used in the inscription are not consistent with any known fifth or sixth century script.
The only unifying elements in all five versions are King Arthur, death and Avalon. With that established, the
following argument could then be constructed: Arthur's last resting place is the isle of Avalon, Arthur lies in Glastonbury,
therefore Glastonbury is the isle of Avalon.
The only drawings of the cross (that we know of) were done by one William Camden for the 1607 and 1608
editions of his historical work, Britannia. There was some variation in the shapes of the letters between the two editions.
The usually reliable John Leland, writing in 1533, actually held the cross in his hands and said that it measured
nearly a foot in length and that it bore the words written in the Margam Chronicle (see version one, above).
The cross was attached to the marble coffin in which "Arthur's" bones were reinterred in 1278
by Edward I, and remained there until the Dissolution of the Monasteries in 1539, after which it spent the next hundred years
or so in the Revestry of the parish church of St. John Baptist, Glastonbury (according to the late seventeenth century document
Bodleian Rawlinson B.416A, folio 10v ), after which it disappeared from view and wound up in the early eighteenth century in
the possession of a certain Mr. William Hughes, Chancellor of Wells.
The story of the cross doesn't end there, though; it continues even to the present day. There have been several
reports in this century that the cross has been found, but in each case, the reports have proven to be false. Those erroneous
reports don't mean that the cross does not exist, only that it hasn't been found.
The Exhumation of Arthur's Body at Glastonbury by Giraldus Cambrensis
Gordd Cymru for
other great Websites
Copyright © 2000 Gordd Cymru. All Rights Reserved.


text: May 16, 2012 - I am not a HUGE fan of spray gels because I do not feel that it gives my curls enough hold. I bought this as a way to add more hold after my hair is drying as a form of "hairspray". I found that this works wonders for me when I use it for my second day hair. The night before I will spray a lavender water mixture I made on my hair then add some Kinky Curly Knot Today and Curl Keeper to my hair then spray with some of this gel and plop over night. When I wake up and unwrap my hair I have FULL beautiful soft curls. I have to say right now I LOVE my second day curls much better than my first day! So bottom line, I would buy this again to keep up with my second day curls, but not good for my applying it as a gel for first day curls.


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In November, General Motors Co (NYSE: GM) emerged from bankruptcy and raised over $20 billion re-entering the stock market at $33 a share. But there haven't been a lot of fireworks since then – almost six months later, the stock price is largely unchanged.
But there was good news today for investors looking for growth and consumers worried about their favorite brands like the iconic Corvette. The company just reported great sales for first quarter of 2011, marking the fifth-consecutive quarterly profit and a nearly 4x jump in income compared with last year.
So what does this mean for General Motors cars, customers and investors? Well, unfortunately … the news may not be as good as you think.
Yes, first-quarter net income surged over the first three months of the prior year — $3.6 billion in 2011, compared with $900 million in 2010. But take that with a grain of salt, since we are comparing current sales one of the darkest periods in the history of General Motors. At the beginning of 2010, GM was still a bankrupt organization and struggling to return to profitability. A year makes a lot of difference.
Yes, the company was bleeding billions of dollars each quarter in 2008 so these developments are very good for the automaker. However, it's important to acknowledge how low the bar was that GM just stepped over this time.
Another impressive statistic in the recent GM earnings report involves strong sales increases at home and abroad. Specifically, worldwide sales climbed 12% and domestic sales surged 25% over 2010. This is indeed encouraging. But General Motors is only recovering slightly faster than competitors as the auto market in general rebounds, and again, we are measuring growth based on previous historic lows for GM.
Consider that competitor Ford (NYSE: F) saw U.S. sales rise 16% — not as much as GM, but still impressive and a sign that GM isn't alone in its positive performance. What's more, Ford outsold General Motors in April for only the second time in 13 years thanks to gains in market share during the last few years as a GM suffered.
In short, GM's growth involves making up a lot of lost ground – not necessarily a return to dominance.
Last but not least, we can't overlook "one-time" benefits that juiced GM's numbers. Consider that the recent $1.6 billion sale of its stake in auto parts division Delphi accounts for nearly half of General Motor's quarterly income of $3.6 billion. Those are real profits that the company can put to use, but obviously GM can't just sell off divisions every few months to make money – it needs to develop a sustainable way to get bigger profits.
So while there are many reasons to be optimistic about the future of General Motors and the solvency of this American manufacturing icon, let's not declare the Detroit automaker back in top form just yet. There are many reasons that shares of GM stock have been flat since the mammoth GM IPO six months ago – and more importantly, a reason that GM shares are trading down today despite these seemingly impressive numbers.
The reality is that this kind of growth is nice, but General Motors has a long way to go.
Jeff Reeves is editor of InvestorPlace.com. As of this writing, he did not own a position in any of the stocks or funds named here. Follow him on Twitter via @JeffReevesIP and become a fan of InvestorPlace on Facebook.


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hi there,
DH and I are struggling with our insurance company to obtain the coverage of a homebirth for our second child due in March 2013.
A long but sucessful fight for our first baby resulted in a full coverage of the free standing birthing center we wanted.
This time I'm going for homebirth and am ready to fight again!
Anyone out there in the same situation? Let's discuss, exchange tips and support each other. It is a difficult process but it is worthwile and we are lucky enough to have the law behind us in NY State.
Interested to hear from you if you are in another state too but keep in mind that the legislation is different in every state and that it can change a lot in your fight with the insurance company.
looking forward to hearing from you
I am just starting to look into health insurance coverage for a homebirth and I'm also in NYS. I have no idea how complicated and time consuming this process may be! I'm happy to learn that NYS is ahead of the curve in supporting us. Good luck!
hi there,
It will depend on your insurance but I think it is a complicated process in 95% of the cases.
Let keep in touch, good luck to you too
I have Oxford Freedom - a high deductible plan accompanied by a Health Savings Account. I just called customer service and my deductible is $4,000 for an In-Network midwife, homebirth, or hospital birth. If I can prove that none of the providers offer what I need (home birth) they will cover an out of network person at In-Network rates, but of course I still need to pay my deductible. I'm not sure how much HB costs, but this doesn't sound terrible ...
Hi there. I'm in NYS and planning a homebirth in January. It doesn't always have to be a fight, and so far for me it's seeming much easier than I expected. When we started with my midwife we had United Healthcare Choice Plus. My midwife said they usually had no problem with them. Her billing person applied for gap coverage to treat her as in-network and it was granted two weeks later, so all costs would be covered, no deductible or copay.
Then, a few weeks ago we suddenly get notice that our insurance will be switched to Aetna 2 weeks before my due date. That threw me into a brief panic, but my midwife says Aetna is usually no problem either, it's just a matter of applying for gap coverage again.
If you have a deductible even for in-network providers, or are unable to get your midwife treated as in-network, most midwives will sort of over bill your insurance and then not bill you for your deductible by the way. Several midwives I interviewed offered to do this for us if the gap coverage was rejected.
I'm very happy that I chose a midwife with a billing person though. I hate dealing with insurance companies.
Hey Ladyk;
good for you but based on my experience for my first birth it is not always easy to prove that none of their providers offers a homebirth. My insurance company (Cigna) sent me a 16 pages list of people that are suppose to be midwives. These contacts are either outdated/wrong numbers or hospitals / medical center who have no idea why they are in a midwives list. It takes time to call all of them and prepare a convincing document to send to your insurance.
Good luck with that!
hi homebrewer,
great to hear a more postivie experience.
I've heard that my insurance (Cigna) is especially bad with homebirth and heard good things about Aetna.
My request for in network exception was rejected so I sent letter to appeal to that decision. Next step, attorney general...
So happy to find this forum. I am pregnant with baby #4 due in May. My first 2 were induced and I had horrible birthing experiences. My last one came on her own time and was an unplanned homebirth but I loved every minute of it. I would love to have #4 at home. I can only convince hubby though if I can get our insurance company to pay for it. If I have baby at hospital we only have $500 deductible, compared to $5000+ for homebirth.
We have excellus blue cross blue shield. Does anyone know what is the best way to first go about finding out how to get the insurance company to cover it? We also have the option of putting myself on medicaid. Does anyone know anything about medicaid and HB's? I'm guessing since its state run they wouldn't cover it. I've tried researching it and have found no information out. Thanks!
I don't know anything about medicaid or BC/BS from personal experience, but what I would do is contact a couple of midwives that will do the billing for you and ask them what their experience is with BC/BS and with medicaid. Midwives have a lot of experience getting reimbursed for their services and may be able to reduce/eliminate your deductible with BC/BS, or to recommend ways to work around it. My midwife has a billing person who handles all the insurance details and it's great not to have to think about it. They were able to tell me at the interview appointment how billing would work, their experience with my company, and how much I would likely need to spend out of pocket (in the end, only the cost of birth kit, pool rental and doula). They may even be able to tell you over the phone or via email.
For what it's worth I googled "NY medicaid homebirth" just now and found 2 women who left comments on another bulletin board saying that they had their homebirths covered 100% through HIP, which I guess is one of the NY medicaid options?
In NY you have the law on your side since insurance companies are legally obliged to cover it. It doesn't mean it will be easy getting it done or that there will be no deducible, but it's doable.
Good luck!
you do realize thats fraud, right?
What are you referring to? Overbilling is fraud. But gap coverage and getting a home birth covered is not.
I had good luck with BCBS in NYC though that was over 5 years ago. There was a fair amount of paperwork and approval, but it was all fine and the midwife's billing person took care of all that. They were also very good about my son's hospitalization stay when he was a few weeks old. It was unrelated to birth, but it was in the gap between his birth and getting birth certificate and him added to insurance, etc. Another paperwork hassle.
HIP is NYC insurance that many city employees have. I used to have that. They were good, but no home birth experience. They probably have a medicaid version as well.
Book loving, editor mom to 2
Could you explain what you mean?
In that debate one thing is very clear: it is against NY State Insurance law to deny in -network exception to a homebirth midwife when there is a network deficiency as it is often the case. Insurance companies constanly violates law when they give us a hard time to chose the birth we want
As mentionned eartier I heard Medicaid HIP gives good homebirth coverahe. That is one of the provider with whom my midwife had good experiences.
i would follow homebrew advice: contact a few midwives in your area and try to get an idea of your chances with your current insurance.
Good luck!
hi there,
When I started this threat I was up for a fight with my insurance in NYS...
After months and months of phone calls, letters and wait it turned out that my insurance company considers me as being "sitused" in DC (because the main office of my employer is located there).
The law is different in DC and does not mandate coverage of a homebirth. This final argument that was never mentionned to me or my midwife's office after more than 9 months of contacts seems to be very definitive.
Even the Attorney General office can't do anything.
I wish I had better news to share to encourage all of you but here's my advice for the ones who are still fighting:
- start early
- take notes of everything
- prefer written contact to phone calls
- use all the appeals you can
- if you have been denied the last appeal or do not receive answers quick enough: contact the Attorney General office. They did a great job for this and my first birth (first birth in a birthing center was paid entirely thanks to them), were very responsive and quick.
- if you are in NY State (first check that your plan is not sitused in another state): the insurance law is with you so you can be confident. Here is a quote from the letter sent by my insurance company to the AG office: (...) the NY insurance Law 4303 c (1); that mandates the coverage of Certified Nurse Midwives and home births for New York HMO plans " It is not common to see that law clearly quoted especially concerning homebirth and especially coming from an insurance company so please use this quote, this is your most definite argument!
For the future:
I'm more than ready to help others - let's keep in touch!
I wish there was an organisation that was fighting with/for us. In the meantime we can help each other and try to advocate our rights.
There are many opportunities to attend event about natural birth, choices of a different experience etc... and many books available but if the insurance companies are working against us all these nice discussions are useless.
Choices in childbirth is not just a philosophical questions, it needs to be a possible choice financially!
I'm wondering if Obamacare will change anything about that. I've read an article about chiropractor lobbying in certains states to obtain coverage - anyone knows if midwives are involved in that kind of lobbying? It's really a state by state thing but New York has the advantage of the law (as i painfully discovered some States are in much worst situation)
I'm due at the end of March, will keep you updated on my uncovered homebirth...
All the best to all of you
Thank you so much for all of your excellent advice. We also have Cigna and when I called I got the same list of dozens of midwives that I quickly realized were hospital midwives after specifically asking for HB midwives. Thats when I realized exactly how much of an uphill battle this is going to be.
My wife's aunt is a HB midwife in NYC and even with her experience in dealing with insurance companies, Im expecting it to be a long arduous process. But Id prefer to deal withthe stress of dealing with insurance companies when Im not giving birth than to deal with the stress of being in a hospital while I am giving birth.
Off topic but Im curious as to what your emergency transfer plan is, if you feel comfortable sharing. Im finding that is also an issue because since St Vincent's closed and hospitals require a dr to basically "sponsor" HB MWs now. We are looking into Maimondes in Brooklyn since it seems to be more HB friendly. It seems that most midwives are using Woodhull as their emergency plan but Im not comfortable with that hospital at all. My wife is totally supportive of the HB as long as we can get the insurance sorted and we have a solid and realistic emergency plan. I agree with her completely even if the chances of us having to use it are small.
Thanks again for your fantastic information.
I am holding off on getting pregnant until the insurance company agrees to cover a home birth. I am in Staten Island NY. I have Aetna EPO. When I first called they outright told me no. I called again and luckily reached a woman who is willing to research this more. There is some legal jargon stating they cannot rule out home births so she is trying to see exactly what this means.
hi pissyrabbit,
Good luck for your fight with Cigna. As indicated in my post #14, they know very well that they are suppose to cover for your homebirth in NY State (" (...) the NY insurance Law 4303 c (1); that mandates the coverage of Certified Nurse Midwives and home births for New York HMO plans") so if they don't manage to find a complex reason not to cover you like they did with me you have very good chances.
As for the back up plan, if I needed to be transfered to a hospital I guess it would be a real emergency situation and in that case I will not be picky. I'm one block away from SUNY Downstate and Kings County so I guess it would be one of them. In that case the insurance would cover it without a problem (and if in the meantime they accepted to cover your homebirth there will be a complex administrative procedure to see how much they would pay the midwife, but that's the job of your midwife staff)
I hope this help.
Don't hesitate to PM me if you want more details, I can also send you some example of letters I sent to the insurance
Good luck!
hi Kathleen78,
Check out my post #14 with the quote by my insurance - that is the law you should indicate to the insurance.
I hope this helps!
Best of luck
Thats what the agent read to me exactly what you said. So now i await a call from her later to get a definitive decision.
good luck Kathleen!
Turns out my Insurance is not NYS mandated so that clause won't apply to me. They are trying to go to the employer to see if they will make an exception in this case but I won't hear anything until next week...
same here, I found out my insurance plan is sitused in DC - hope they will make an exception for you.
Good luck!
I am planning a home birth and due in September 2013. I just had my first prenatal appointment (12 weeks) with my midwife and she said that insurance coverage shouldn't be a problem and that her insurance person will contact me. A couple days later I heard from her insurance person and there seems to be a problem.
Apparently I have Blue Cross/Blue Shield OF MASSACHUSETTS even though I live in NYS. My insurance is through my husband's job and although he works in NYC, his company's HQ is in Boston. I never even knew that I had BC/BS of MA. Apparently Mass. doesn't cover home births. I was so excited after my first prenatal appt and now I am so upset :( The insurance person told me that I need to file a grievance and ask them to look at my case with individual consideration since I live in NYS and NYS has the mandate for home births to be covered.
Cjeanjot- this sounds similar to your problem. Did you file a grievance with your insurance company? Has anyone else been in the same boat as me? I am just hoping there is some way they will cover it!!
Why does it have to be so difficult to give birth the way we want to ?!?!?
Sorry to hear this.
It does sounds a lot like my case.
I hope your insurance company will be a bit more flexible. It all depend on very specific aspects of your plan but in the end the insurance could just decide to make an exception.
Mine would not and they are apparently well known for being unflexible for homebirth.
In your case like in mine the NYState Attorney General office will probably not be able to help but it does not mean you are figthing alone. These questions are very technical and I felt overwhelmed by the jargon. I found it helpful to put the insurance person of my midwife in touch with the insurance broker of my employer. The broker was very nice and really tried to help convince the insurance and I think it was helpful for her to discuss the case with the insurance person of the midwife who is dealing with these specific cases all the time. If your husband's employer is ready to help and put some pressure on the insurance it might help too.
It is really one of those "in between" cases in which a nice person ready to help out might make the difference.
It is definitly crazy that we can not have the birth we want, especially since it is so much cheaper than any hospital option.
As I said before I think we should find a way to join our efforts and share our stories to help other, not just throguh this forum.
In any case let us know how it worked for you!
Good luck,
New news, my husbands employer has self funded Insurance (Aetna). They dont agree wit home birth. I am going to call HR and work my way up and try to fight
Good luck Kathleen!
The odds are you will get nowhere. Sorry to tell you this.
The NY mandate does not apply if companies are self insured. Aetna has a medical policy denying coverage of home birth UNLESS mandated by law. They won't pay if it's not. This is the official Aetna policy statement on home births:
Hi, Has anyone here had any recent experience with getting a home birth covered by Empire Blue Cross Blue Shield or Anthem Blue Cross Blue Shield recently, in the last year? We have been told we are covered out of network but only 50% of the mysterious allowable amount, which they will not tell you until after the birth. A gentleman at my insurance did provide a website where you can look up the common "allowable amounts" for your zip code. In case this helps anyone the website is fairhealth.org. Not encouraging. We want to fight this and get the birth fully covered with a "homebirth exception". I've heard this was easier in the past but they changed the rules and it is harder now.
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