november 1, 2010 — space shuttle discovery is ready to fly its final flight this week, but where it will make its last landing is still up in the air. long thought destined for the smithsonian, nasa ' s oldest flying orbiter may actually end up elsewhere unless the washington, dc institution can find the millions of dollars needed to prepare discovery for delivery and display, collectspace has learned. the first of nasa ' s three remaining space shuttles set to retire after flying its last mission - - sts - 133, scheduled to launch nov. 3 at 3 : 52 p. m. edt - - discovery has been identified by nasa since 2008 as being set aside for the smithsonian. " the national air and space museum has been offered the space shuttle discovery, " nasa spokesman michael curie told collectspace almost two years ago when the agency first announced it would award its three orbiters - - discovery, atlantis and endeavour - - to museums. like the 20 other organizations that applied to nasa for a retired orbiter though, the smithsonian ' s national air and space museum would need to pay the then estimated $ 42 million to prepare and transport discovery to the museum, curie said. the cost, which lowered to $ 28. 8 million in january of this year, is still beyond the smithsonian ' s reach and nasa is not in the position to underwrite the cost, sources close to both the museum and space agency told collectspace. " what if " the smithsonian cannot afford discovery " at this point, we ' re not in a position to go down the ' what if ' road, " said robert jacobs, nasa ' s deputy associate administrator for communications. " there have been discussions between nasa and the smithsonian about the issue, " jacobs said, " but i am not sure they are on - going at this point because the process has been put on hold. " according to jacobs, nasa administrator charles bolden will ultimately make the final decision, but he has tabled all discussion of where discovery or any of the orbiters are going for museum display. " we ' ve had a lot of other things on the agency ' s plate besides where the orbiters are going to go, " said jacobs. " the agency is focused on safely flying out the manifest. " originally, nasa had said it would announce the homes for the shuttles by the end of the summer, but schedule changes - - including the delay of endeavour ' s final flight to february and the possible addition of another flight for atlantis in june 2011 - - resulted in the agency delaying


would announce the homes for the shuttles by the end of the summer, but schedule changes - - including the delay of endeavour ' s final flight to february and the possible addition of another flight for atlantis in june 2011 - - resulted in the agency delaying the news " they were pushing toward a decision, and [ then ] decided not to, " said jacobs. the postponement has led to increased speculation inside and outside of nasa. according to sources internal to the agency, whether discovery still goes to the smithsonian changes on a week - by - week, if not day - by - day basis. inappropriate to comment after initially agreeing to provide interviews in support of this article, the smithsonian refused comment and instead provided a brief written statement. " the national air and space museum appreciates nasa designating the smithsonian ' s national air and space museum as a repository for the shuttle orbiter discovery, " began the statement. " the museum has been involved in discussions with nasa about acquiring discovery and other artifacts from the shuttle program. " " it would be inappropriate to comment on plans, including funding, until arrangements are finalized. " as part of the smithsonian institution, the national air and space museum is funded by federal and private sources, including by endowment, contributions and from the profits realized from retail sales. according to its website, the museum ' s annual budget is approximately $ 28 million - - just about the same amount nasa is requiring to deliver discovery - - which covers the national mall building ; its chantilly, virginia - based annex, the steven f. udvar - hazy center ; and the paul e. garber preservation, restoration and storage facility located in suitland, maryland. according to nasa, the $ 28. 8 million being asked is not a price tag, but rather is the sum of two component costs : $ 8. 3 million to ferry the orbiter atop nasa ' s modified boeing 747 shuttle carrier aircraft, and $ 20. 5 million for " display preparation, " including setting up the crew cabin in flight configuration and installing structural shells and skins in place of hazardous systems that will be removed at nasa ' s expense. as these expenses are not included within nasa ' s 2011 budget, the museums - - including the smithsonian - - must assume their cost to be eligible to receive an orbiter. the smithsonian ' s 2011 budget request to congress does not include a substantial increase to the national air and space museum ' s funding, nor does it include among its planned activities mention of accessioning an orbiter. the budget documents do however, mention the


the smithsonian ' s 2011 budget request to congress does not include a substantial increase to the national air and space museum ' s funding, nor does it include among its planned activities mention of accessioning an orbiter. the budget documents do however, mention the on - going efforts by the institution to raise private funds to complete " phase two " of the udvar - hazy, including the move of the garber facility to a new wing under construction at the virginia annex. ( a congressional mandate prohibits federal funds from being used for construction. ) championing for a champion the smithsonian already owns a space shuttle orbiter - - the prototype enterprise used for glide and landing tests in the late 1970s. should the institution obtain the funding, the plan is to replace enterprise with discovery on display at the udvar - hazy center. why then does the smithsonian desire discovery? other than enterprise having never flown in space, the national air and space museum specifically favors discovery over atlantis and endeavour because it is the fleet leader. " we consider it to be the champion of all the orbiters because when the program ends, it will have flown the most missions, " said curator valerie neal in an august 2010 interview with the radio news show the takeaway. ( collectspace requested to speak to neal for this article but the museum declined ). " it will retire with 39 missions and because it is the oldest of the remaining orbiters, it has the most varied history. it has flown every kind of mission that the shuttle program was designed to fly, " said neal. congress has yet to weigh in specifically about discovery or any other orbiter going to the smithsonian. in a recently passed nasa authorization act though, congress did insert language addressing the shuttles ' retirement and in doing so, implied that the national air and space museum should be considered for a retired flown orbiter. " the smithsonian institution... shall determine any new location for the enterprise, " the bill states. it was signed into law by president obama last month. the astronaut commanding discovery ' s final flight, steven lindsey has said in media interviews that he expects the orbiter to go to the smithsonian. asked by collectspace about the possibility of discovery not going there, lindsey focused his reply on what he hoped exhibiting the orbiter would achieve, regardless of where it was retired. " in terms of it being displayed, i have several criteria and i don ' t think you can meet them all at the same time, " he said. " i would like it to be displayed in a place where the most people can


bicycle safety : new law helps protect cyclist a new maryland legislation that would impose stiffer fines and penalties on negligent drivers in bicycle accidents has once again highlighted the importance of bicycle safety. the recently - passed statute would impose a fine of up to $ 5, 000 and three years in jail. prior to this new legislation, drivers only faced a fine of up to $ 300 and some points on their license. around 20 other states have already adopted similar punishments and fees as the new maryland legislation. however, legislation or not, bicyclists should try to take some simple safety tips to heart. when sharing the road, it is all too easy for accidents to occur, even if both the bicyclist and the driver are being cautious. tip # 1 : some jurisdictions actually allow bicyclists to cycle on sidewalks. of course, you should check your city ' s ordinances first to be absolutely sure. cycling on the sidewalk can help you avoid any unnecessary run - ins with unruly drivers, though it also creates the possibility that you might hit pedestrians, so continue to take extra care. tip # 2 : be informed about dangerous intersections. some streets are just more dangerous than others due to general traffic conditions, or due to blind spots. ask friends who cycle regularly, or do an internet search. san francisco has a bike accident tracker that gives information on collisions and where they often take place. tip # 3 : wear the appropriate gear. helmets won ' t necessary prevent fatal accidents, but they can offer some element of protection. wearing bright colors at night can help distinguish you against the darkness. invest in a headlight or some other light to attach on your bike so that cars can actually see you. tip # 4 : keep track of where your bike is - and where cars are. all too often, drivers may be looking one way to look out for car traffic, but then pull out and hit a bike. some simple tips about what to do in various situations and different intersections can help save you from injury. such as, did you know that a common bike accident occurs when a driver opens their door - and the bicyclist runs into it? being aware of your surroundings can definitely go a long way. while this is in no ways a complete list of bicycle safety tips, it ' s a start to help you get biking in the right direction. - rules of road for bicyclists proposed ( baltimore sun ) - many drivers and cyclists still need some education ( greater greater washington ) - bicycle accidents (


the u. s. consumer product safety commission ( cpsc ) warns residents in the path of hurricane ophelia in north carolina and nearby coastal communities to take special precautions. " based on our experience with hurricane katrina on the gulf coast, people often use portable generators when their power is knocked out, " said cpsc chairman hal stratton. " but if you don ' t use them safely, you risk deadly carbon monoxide poisoning. never use a generator inside the house or attached garage. keep it a safe distance from your home. don ' t take a chance. " unofficial estimates indicate at least 11 deaths and numerous injuries have been attributed to carbon monoxide poisoning stemming from portable generators used in the aftermath of hurricane katrina on the gulf coast. the commission provided these important life - saving tips : - never use a portable generator indoors – including garages, basements, crawlspaces and sheds. opening doors and windows or using fans will not prevent co buildup in the home. - during use, keep portable generators outdoors and far away from open doors, windows and vents, which can allow co to build up indoors. - if you start to feel sick, dizzy or weak while using a generator, get to fresh air right away. the co from generators can readily lead to full incapacitation and death. - keep generators dry and wait for the rain to pass before using a generator. consumer - grade generators are not weatherproof and can pose the risk of electrocution and shock when used in wet conditions. - do not connect the generator directly into your home ' s electrical system through a receptacle outlet – this is an extremely dangerous practice that poses a fire hazard and an electrocution hazard to utility workers and neighbors served by the same transformer. - if using a generator, plug individual appliances into heavy duty, outdoor - rated extension cords and plug cords into the generator. - check that the extension cords have a wire gauge adequate for the appliance loads and have all three prongs, including a grounding pin. - keep charcoal grills outside. never use them indoors. burning charcoal in an enclosed space can produce lethal levels of carbon monoxide poisoning. - check to make sure your smoke alarms and carbon monoxide alarms have batteries and are working. wet carpets and furniture are dangerous to your health - discard water - damaged mattresses, wicker furniture, straw baskets and the like that have been water damaged. these cannot be recovered. - throw out wet room - size carpets, drapes, upholstered


furniture are dangerous to your health - discard water - damaged mattresses, wicker furniture, straw baskets and the like that have been water damaged. these cannot be recovered. - throw out wet room - size carpets, drapes, upholstered furniture, stuffed toys, ceiling tiles and anything that can ' t be picked up and cleaned by dry cleaning, steam cleaning or put in a washing machine or dryer. - remove and replace wet insulation. - microorganisms may grow in these water - damaged products and may cause allergic reactions and infections. for more information, go to http : / / www. cpsc. gov / cpscpub / pubs / 425. html avoid electrical and gas hazards - look for signs that your appliances have gotten wet. discard electrical or gas appliances that have been wet because they pose electric shock and fire hazards. - before using your appliances, have a professional or your gas or electric company evaluate your home and replace all gas control valves, circuit breakers, and fuses that have been under water. dangers to children - medicines and chemicals should be thrown away. water may have infected the integrity of the medicine. the u. s. department of health and human services offers additional safety tips. for more information, go to fda drug safety site - young children and water don ' t mix. watch children around buckets, tubs and standing water in and around the home. even small amounts of water can be a drowning hazard. the u. s. consumer product safety commission is charged with protecting the public from unreasonable risks of injury or death associated with the use of the thousands of consumer products under the agency ' s jurisdiction. deaths, injuries and property damage from consumer product incidents cost the nation more than $ 900 billion annually. cpsc is committed to protecting consumers and families from products that pose a fire, electrical, chemical or mechanical hazard. cpsc ' s work to ensure the safety of consumer products - such as toys, cribs, power tools, cigarette lighters and household chemicals - contributed to a decline in the rate of deaths and injuries associated with consumer products over the past 30 years. federal law bars any person from selling products subject to a publicly - announced voluntary recall by a manufacturer or a mandatory recall ordered by the commission. to report a dangerous product or a product - related injury go online to www. saferproducts. gov or call cpsc ' s hotline at ( 800 ) 638 - 2772 or teletypewriter at ( 301 ) 595 - 7054


we ' re on the brink of summer, seattle ' s biggest outdoor season. more likely than not, one day in the next few months you ' ll find yourself gazing out at puget sound. the waters will be sparkling, the rugged olympics or cascades will make a spectacular backdrop and overhead — for a couple of days in august — might be, as perry como sang, " the bluest skies you ' ve ever seen.... " if you ' re lucky, you ' ll be out there on a boat, perhaps on one of the innumerable pleasure craft or on a ferry crossing elliott bay. you ' ll point out the visible wonders to your fellow shipmates, and your out - of - town guests will be in awe. but the reality is, you might as well be the little yachtsman in the old bathroom cleanser commercials : the man from ty - d - bol. indeed, he probably sailed on cleaner waters in a freshly scrubbed toilet. the fact is, puget sound is a toxic dump and a sewer. sure, we ' ve heard that puget sound needs to be cleaned up. but even knowing the sound ' s long history of industry around its edges — and that sometimes septic tanks leak into its waters — it looks so damn good. how can anything be wrong? puget sound ' s pollution isn ' t the kind that sets waters on fire, as happened to the old cuyahoga river in cleveland, ohio, once upon a time. it ' s a quiet, almost invisible disaster. the sound is an arm of the sea, and it ' s deep. that ' s what attracted so many settlers, adventurers and city builders : good ports and protected waters. in the last 150 years, humans have swarmed into the puget sound basin, some 4 million of us. the sound is now suffering, but its pain is masked by its pristine surface. the deep waters hide much of the problem : in sediments and throughout the food chain, our presence is being felt. take this shocking figure, reported in the olympian earlier this year. the number - one source of pollution in the sound isn ' t industry, it ' s us. runoff from our roads, sidewalks, driveways, etc. is the biggest single source of pollutants, according to the state department of ecology. every year, 22, 580 metric tons of oil and petroleum flow in just from this source. to put that in perspective, that ' s roughly the equivalent of an exxon valdez - size oil spill every other


to the state department of ecology. every year, 22, 580 metric tons of oil and petroleum flow in just from this source. to put that in perspective, that ' s roughly the equivalent of an exxon valdez - size oil spill every other year. this in a body of water from which oil tankers are banned. can you imagine the outrage if we ' d had 10 exxon valdez spills in the last 20 years? much of the pollution flowing into the sea is more personal. the sound ' s chinook salmon have high levels of flame retardants, the kind of chemicals used to make your upholstery and pajamas fire resistant. every drug we put into our bodies finds its way into the water, mostly through the sewer system ( what goes in, comes out, eventually, and not everything is " treated " at your local sewage treatment plant ). what finds its way into the water eventually gets into the creatures that live there. on the east coast, a study showed that chemicals from the anti - depressant prozac were altering the reproductive cycles of mussels. and our lifestyle is a factor, too. in california, some sea otters have been infected with parasites that can only have come from pet cats, presumably when their poop is flushed down the toilet or washed away by rain. last year, researchers detected elevated levels of vanilla extract and cinnamon in puget sound right around thanksgiving, evidence that traces of our seasonal diet, cookies and all, are reflected in our waste and, therefore, in our waters. the onslaught of christmas fruitcake could have consequences! our impact on the environment is so extensive that we really have to begin rethinking the whole concept of " wilderness. " all that beauty we look at from our decks or high - rise offices is not what it appears to be. a six - year study by the environmental protection agency ' s national health and environmental effects laboratory found that even the most remote parts of our national parks are polluted. it found high levels of mercury in fish in lakes of the olympics and mount rainier. citizens have been trying to mobilize to " save " puget sound for decades. the government is working on the problem with task forces and studies. but a sense of urgency is still lacking. one recent poll asked central puget sound - area residents what the top priority for state government was. only 2 percent named cleaning up puget sound. it ' s hard to take a crisis seriously when it looks so pretty. like what you just read?


commemorating international roma day by dr. angel w. colon - rivera april 8th marks international roma day – a day to remember that europe ’ s largest ethnic minority still faces anti - roma violence, violations of their human rights, discrimination, and systematic marginalization, so that many have difficulty meeting their basic human needs, such as education, housing, health care and, in some cases, even clean water. in a number of osce participating states, roma live in segregated communities, their children attend segregated schools, and they are discriminated against in employment and other areas of public life. in some osce countries, roma are subject to violence or threat of violence on a daily basis. the helsinki commission has long monitored and reported on human rights violations against roma and other ethnic, linguistic and religious minorities. in the early 1990s, the commission issued a series of reports on osce countries making the transition from communism to democracy – almost every report identified the deteriorating situation of roma as a problem. commissioners have addressed violations of roma rights through hearings and briefings, engagement with representatives of the osce participating states, and by encouraging the department of state to ensure that human rights violations of persons belonging to romani communities are appropriately reported in the annual country reports on human rights. last year, the commission hosted two special roundtables in washington for representatives of osce embassies to elevate the discussion of romani human rights concerns : the first, in january, was a conversation with andrzej mirga, the osce senior advisor for romani issues ; the second, in october, was with viktoria mohacsi, who had served as one of two romani mps in the european parliament and was a recipient of the human rights first 2010 award. during the osce review conference in warsaw, the commission also organized a meeting for the u. s. delegation with romani participants, many of whom are now advisors to their governments. the discussion focused on mass expulsions of roma from france and the dangerous rise in anti - roma political rhetoric in much of europe. commissioners have paid particular attention to the escalation of anti - roma violence in the czech republic and hungary, and to comments by public figures in a number of countries associating roma with criminality – discourse that echoes the rhetoric of the nazi period. in september and october of 2011, the osce will hold its annual human dimension implementation meeting, where one of this year ’ s special topics will be “ enhancing implementation of osce commitments regarding roma and sinti. ” the osce chair - in


- our story - in memory caf ' s dr. tanzi on the latest on alzheimer ' s disease genes the four known alzheimer ’ s genes over the past several decades, it has become increasingly clear that inheritance plays a major role in alzheimer ’ s disease. the roughly 25, 000 genes in the human genome are comprised of deoxyribonucleic acid ( dna ) packaged into 24 different chromosomes, 1 - 22, x and y. a gene ’ s job is to either make proteins or control the activity of other genes. over many generations, the dna of a gene can mutate to create a “ variant ”. a very rare dna variant is called a “ mutation ”, while a variant that is common in the population is called a “ polymorphism ”. dna variants allow for all of us to be a little different from each other. there are about 3 million variants that differ between any two individuals. variants in certain genes can directly cause a disease like alzheimer ’ s, can increase susceptibility to disease, or can even confer protection against disease. one ’ s risk for most age - related diseases such as cancer, diabetes, heart disease, stroke, and alzheimer ’ s is strongly influenced by our genes. for all of these age - related diseases, we know of mutations that guarantee onset of these diseases with no need for input from any other genes or environmental factors. and, we know of polymorphisms that can increase ( or decrease ) one ’ s susceptibility to the disease, but without guaranteeing onset of the disease. in this latter case, other genes and environmental factors usually conspire together to determine when and whether one will get disease. any gene which can contain a variant ( s ) that significantly influence one ’ s susceptibility to alzheimer ’ s, whether it be to guarantee the disease or serve to increase ( or decrease ) risk, is called an “ alzheimer ’ s gene ”. it is important to remember that all genes are “ good ” ; it is only the variants in the dna of these genes that can influence one ’ s lifetime risk for a disorder such as alzheimer ’ s disease. in the 1980 ’ s and 90 ’ s, my laboratory co - discovered the three known genes that can carry mutations causing early - onset ( < 60 yrs ) familial alzheimer ’ s disease. these three genes, known as app, psen1 and psen2, can harbor any of over 200 different gene mutations that guarantee onset of alzheimer ’ s at a


onset ( < 60 yrs ) familial alzheimer ’ s disease. these three genes, known as app, psen1 and psen2, can harbor any of over 200 different gene mutations that guarantee onset of alzheimer ’ s at a relatively early age with no need for additional input from other genes or environmental factors. these mutations are rare, accounting for only 1 - 2 % of alzheimer ’ s cases. inheritance of one of these mutations from just one parent virtually guarantees onset of alzheimer ’ s, usually by 60 years old. if a parent carries such a mutation, each child has a 50 % chance of inheriting the same mutation and getting early - onset alzheimer ’ s disease with virtual certainty before 60 years old. genetic testing is available for the early - onset alzheimer ’ s gene mutations, but is usually reserved for those who have a family history of early - onset alzheimer ’ s disease. the fourth known alzheimer ’ s gene is apoe. in the early 1990 ’ s, investigators at duke university found that a common gene variant ( polymorphism ) of apoe, called epsilon 4, can increase risk for late - onset ( > 60 yrs ) alzheimer ’ s disease. this variant is present in about 20 % of the general population but this increases to > 50 % in alzheimer ’ s patients. unlike the early - onset ad gene mutations, this variant does not guarantee alzheimer ’ s, but only serves to increase risk. inheriting one copy of the variant ( from one parent ) increases risk by 4 - fold ( versus the general population ) and two copies ( from both parents ), > 10 - fold. importantly, a person can inherit the apoe epsilon 4 gene variant from one or both parents and never get alzheimer ’ s in the span of a normal lifetime. with regard to genetic testing for the common late - onset form of alzheimer ’ s, we are not yet able to do so reliably. this is because the apoe epsilon 4 gene variant is not sufficient on it ’ s own to predict one ’ s risk for alzheimer ’ s reliably. other genes and environmental factors need to combine with the apoe epsilon 4 gene variant to cause alzheimer ’ s. some gene variants can exacerbate while others mitigate the risk for alzheimer ’ s conferred by the apoe epsilon 4 gene variant. and, we do not yet know the full set of gene variants that can increase or decrease risk for alzheimer ’ s when inherited together with the apoe epsilon 4 gene variant. thus, apoe gene testing is


the apoe epsilon 4 gene variant. and, we do not yet know the full set of gene variants that can increase or decrease risk for alzheimer ’ s when inherited together with the apoe epsilon 4 gene variant. thus, apoe gene testing is not recommended as a sole means for predicting alzheimer ’ s risk. the other late - onset alzheimer ’ s genes must first be identified in order to reliably test for risk for late - onset alzheimer ’ s disease. so how many other alzheimer ’ s genes are there? we know that the four known alzheimer ’ s genes, app, psen1, psen2, and apoe account for roughly 30 % of the inheritance of alzheimer ’ s. thus, 70 % of the genetics of alzheimer ’ s remains undefined. we as well as others have been engaged in comprehensive projects to find the other alzheimer ’ s genes. once we have all of the alzheimer ’ s genes in hand, we will be able to more reliably predict one ’ s lifetime risk for the common late - onset form of alzheimer ’ s disease. however, one might ask, “ why bother to test if there is nothing we can currently do to prevent, stop, or reverse it? ” this is certainly a fair question since we still do not have drugs that stop the disease process in alzheimer ’ s. we only have drugs like aricept and namenda that modestly and temporarily alleviate the symptoms of cognitive decline, but without affecting the progress of the disease. we need to do better more effective therapies for alzheimer ’ s, but how do we get there? first we need to identify all of the genes and variants involved in influencing risk for alzheimer ’ s disease. studies of the known alzheimer ’ s disease genes ( the four previously mentioned ) have provided the vast majority of information being used to guide novel drug discovery aimed at preventing, stopping and maybe even reversing alzheimer ’ s disease. every new alzheimer ’ s gene defect we find provides new clues regarding the cause of the disease what we need to do to stop the disease. thus far, all four genes have pointed to a small protein called “ abeta ” as the cause. abeta is normally made in the brain, but is found in excessive amounts in the brains of alzheimer ’ s patients, e. g. in senile plaques that litter the alzheimer ’ s brain around nerve cells. small clumps of abeta can gum up the connections between nerve cells known as synapses. billions of nerve cells in the brain form trillion


, e. g. in senile plaques that litter the alzheimer ’ s brain around nerve cells. small clumps of abeta can gum up the connections between nerve cells known as synapses. billions of nerve cells in the brain form trillions of synapses making up our neural network. the neural network, in all its complexity, is needed for all brain function, including memory and learning. excessive abeta disrupts synaptic communication between nerve cells leading to loss of memory and learning and eventually dementia. dementia is defined as global and catastrophic cognitive failure ; alzheimer ’ s disease is the most common form of dementia in the elderly. beyond the original four alzheimer ’ s genes most drug discovery for alzheimer ’ s today is based on studies of the four original alzheimer ’ s genes. but, we know that there are many more alzheimer ’ s genes yet to be identified. since 2005, the cure alzheimer ’ s fund has supported a project called the alzheimer ’ s genome project ( agp ), carried out in my laboratory at massachusetts general hospital. the goal of this project is to study 5000 families with multiple members who are affected with the common late - onset form of alzheimer ’ s disease in an effort to identify all of the other alzheimer ’ s genes. in addition to the alzheimer ’ s genome project, the international genomics of alzheimer ' s project ( igap a consortium of dozens of research institutions in europe and the u. s., in which we are members ), uses tens of thousands of individual alzheimer ’ s cases from the general population in the u. s. and europe, to find common dna variants that influence risk for alzheimer ’ s. the family - based method of our alzheimer ’ s genome project and the population - based method of igap have identified some of the same alzheimer ’ s genes, but also find different ones with different effects on risk. in the family - based studies of the alzheimer ’ s genome project, we are able to find not only common dna variants that influence one ’ s risk for alzheimer ’ s, but also rare mutations that profoundly affect risk or for the disease or directly cause it. the alzheimer ’ s genome project places a high priority on finding these rare but very potent gene mutations because historically, amongst the four known alzheimer ’ s genes, it has been the rare early - onset familial alzheimer ’ s gene mutations that have been most effectively guiding drug discovery efforts. this is mainly because hard - hitting mutations have clear - cut adverse effects on biological systems, which can be elegant


, it has been the rare early - onset familial alzheimer ’ s gene mutations that have been most effectively guiding drug discovery efforts. this is mainly because hard - hitting mutations have clear - cut adverse effects on biological systems, which can be elegantly recapitulated in animal models. this then allows for more effective drug discovery and development. along these lines, one of the first new alzheimer ’ s genes to be identified in the alzheimer ’ s genome project was adam10. this gene was specifically chosen for testing as a potential alzheimer ’ s gene because like the four original alzheimer ’ s genes, it affects the production of abeta in the brain. we identified two rare mutations in this gene that strongly predispose carriers to alzheimer ’ s disease at around 70 years old. these two mutations were found in only 7 ( of 1000 ad families tested ). thus, they are very rare. we have recently demonstrated these two mutations dramatically impair the activity of adam10. adam10 normally blocks the production of abeta. accordingly, we have found that these two rare mutations greatly enhance alzheimer ’ s amyloid pathology in animal - based models of the disease. with the validation of these mutations to be “ pathogenic ”, or disease causing, the alzheimer ’ s genome project considers adam10 to be the fifth alzheimer ’ s gene. we published the original findings showing adam10 to carry rare mutations causing alzheimer ’ s disease in 2008 in the prestigious scientific journal, human molecular genetics. the publication of the validation data from transgenic mouse models is planned for the coming year in 2011. also beginning in 2005, with cure alzheimer ’ s fund support, as part of the alzheimer ’ s genome project, we carried out the first family - based “ genome - wide association study ” for new alzheimer ’ s genes. this entailed a screen of the entire human genome in patients and their relatives in thousands of alzheimer ’ s families. the first phase of this study was completed in 2008 and led to the identification of over 100 new alzheimer ’ s candidate genes. we reported the top four alzheimer ’ s candidate genes from this study in 2008 ; it was named by time / cnn to be one of the ten top medical research breakthroughs of 2008. the cure alzheimer ’ s fund alzheimer ’ s genome project was the first large - scale study of the human genome performed in the world on the world ’ s largest collection of families affected by alzheimer ’ s disease. it was also the first genome - wide study for alzheimer ’ s in the world to discover novel alzheimer ’ s


large - scale study of the human genome performed in the world on the world ’ s largest collection of families affected by alzheimer ’ s disease. it was also the first genome - wide study for alzheimer ’ s in the world to discover novel alzheimer ’ s gene candidates with statistically significant results and confirmation in thousands of subject from families with a high incidence of alzheimer ’ s disease. the four new alzheimer ’ s genes reported by the alzheimer ’ s genome project in 2008 in the american journal of human genetics included : atxn1, cd33, gwa14q34, and dlgap1. atxn1 is known to carry mutations that cause another neurodegenerative disease called spinal cerebellar ataxia, a movement disorder. we found that when this gene is inactive, abeta levels increase dramatically leading to cognitive decline in mouse models. another gene, cd33, is perhaps the most interesting since it controls the brain ’ s innate immune system and inflammation in the brain. in a related study funded by the cure alzheimer ’ s fund, abeta was found to play a role in the brain ’ s innate immunity system. cd33 regulates the brain ’ s immune system and concurrently, levels of abeta. we are now developing cd33 as a drug target for alzheimer ’ s based on the genetic findings of the alzheimer ’ s genome project. it should be emphasized that without the cure alzheimer ’ s fund alzheimer ’ s genome project we would probably have never guessed that genes like atxn1 and cd33 might be involved with alzheimer ’ s. as part of the current activities of the alzheimer ’ s genome project, we are now testing these as well as over one hundred other new alzheimer ’ s candidate genes, coming out of our genome screen, to identify all of the dna variants and mutations that influence risk for alzheimer ’ s in the five thousand alzheimer ’ s families under study in the alzheimer ’ s genome project. we are specifically searching for dna mutations and variants in these genes that very strongly affect risk for onset of alzheimer ’ s. as new defects are found in these genes, we will not only increase our ability to reliably predict risk for alzheimer ’ s, but more importantly, garner new clues regarding the causes of alzheimer ’ s, and in doing so, gather new ideas and biological targets for novel drug discovery aimed at preventing, stopping and reversing alzheimer ’ s disease. in the parallel screen for new alzheimer ’ s genes conducted by the igap, the dna from tens of thousands of individual alzheimer ’


new ideas and biological targets for novel drug discovery aimed at preventing, stopping and reversing alzheimer ’ s disease. in the parallel screen for new alzheimer ’ s genes conducted by the igap, the dna from tens of thousands of individual alzheimer ’ s patients was compared to the dna of elderly subjects without alzheimer ’ s to find common variants that influence risk for alzheimer ’ s. in 2009, this led to the identification of four new alzheimer ’ s gene candidates called picalm, clu, cr1, and bin1. more recently in april 2011, igap found four more alzheimer ’ s genes called cd2ap, ms4a, epha1, and abca7. in addition, they found alzheimer ’ s risk to be influenced by the gene cd33, which was first reported by our alzheimer ’ s genome project in 2008. it should be noted for the sake of clarity that the igap had stated in their reports and press releases that they had increased the number of known late - onset genes from “ five to ten ”. however, these numbers only pertained to studies of individual alzheimer ’ s patients in the general population screened in igap, and not the family - based alzheimer ’ s genes reported by the alzheimer ’ s genome project. the igap considered the original five late - onset alzheimer ’ s genes to be apoe ( discovered as mentioned earlier at duke u. in the early 1990 ’ s ), picalm, clu, cr1, and bin1. they then considered the next five to be cd2ap, ms4a, epha1, abca7, and cd33. however, as mentioned above, cd33 had been already identified earlier in our alzheimer ’ s genome project in 2008, which was reported in the major scientific journal, the american journal of human genetics. in the igap announcement, they also overlooked the other three late onset genes, which had been discovered three years earlier in our alzheimer ’ s genome project. so, in fact, with the 8 new genes reported by igap and the 5 new genes reported by the agp, there have been 13 new late onset alzheimer ’ s genes discovered in the last 5 years, which, when added to the discovery of apoe yields 14 total late onset genes now reported in the scientific literature. to that total would be added the 3 early onset genes co - discovered by dr. tanzi and colleagues to reach a total of alzheimer ’ s genes discovered of 17. in addition, dr


14 total late onset genes now reported in the scientific literature. to that total would be added the 3 early onset genes co - discovered by dr. tanzi and colleagues to reach a total of alzheimer ’ s genes discovered of 17. in addition, dr. tanzi and agp have also identified over 100 unpublished alzheimer ’ s candidate genes that are currently being confirmed and validated for publication over the coming year. with regard to effects on risk, all of the new alzheimer ’ s gene candidates reported by the igap carry common dna variants that confer only tiny effects on risk. specifically, according to igap, the new genes contain common dna variants that are present in a large proportion ( 30 - 70 % ) of the general population, but only increase or decrease risk for a given individual by a mere 10 - 20 %. in contrast, the epsilon 4 variant in apoe, which is present in 20 % of the population, increases risk by 400 – 1200 %! and the adam gene just discovered by the agp increases risk for the individuals who have it by about 500 % with regard to the cd33 gene, which was identified as an alzheimer ’ s gene in both our alzheimer ’ s genome project in 2008 and the igap in 2011, each project actually discovered different alzheimer ’ s - associated dna variants in this gene. in our family - based alzheimer ’ s gene study, we originally reported a relatively uncommon variant in cd33 that increases risk for alzheimer ’ s in a subset ( < 100 ) of the 5000 alzheimer ’ s families we studied. in contrast, the igap discovered a very common variant in cd33, present in about 50 % of the population that conferred only marginal protection against alzheimer ’ s ( decreasing risk by only 11 % ). the fact that we now know of two different alzheimer ’ s - associated dna variants in the cd33 gene from multiple alzheimer ’ s samples increases the odds that cd33, is a bona fide alzheimer ’ s gene. as with all of the new genes found in the genome - wide association screens of the alzheimer ’ s genome project and igap, the next critical step is to identify all of the dna variants and mutations in these genes that increase or decrease risk for late - onset alzheimer ’ s disease. the cure alzheimer ’ s fund continues to support these efforts. we are currently screening over a 100 new alzheimer ’ s candidate genes found in the alzheimer ’ s genome project along with those found in the igap, to identify the all of dna variants and mutations in


’ s fund continues to support these efforts. we are currently screening over a 100 new alzheimer ’ s candidate genes found in the alzheimer ’ s genome project along with those found in the igap, to identify the all of dna variants and mutations in these genes that influence risk for alzheimer ’ s disease. elucidating the full deck of alzheimer ’ s - associated gene variants and mutations and understanding the interrelationships among them is is necessary to fully understand all of the biological processes that are affected in alzheimer ’ s disease. this will give us the best odds of reliably predicting the disease early in life ( with appropriate counseling and legal protection ). but, most importantly, the full set of alzheimer ’ s genes and the knowledge of how they biologically influence risk for disease will continue to provide the most critical information needed to guide the development of new and effective therapies aimed at preventing, stopping or reversing alzheimer ’ s disease. finally, it should be noted that whether a dna mutation in an alzheimer ’ s gene is rare and restricted to a small subset of families or more broadly observed in the general population, most believe that new drugs or therapies for alzheimer ’ s based on what is learned from that mutation will be useful in preventing and treating all cases of alzheimer ’ s. as noted above, in the alzheimer ’ s genome project, we place a high priority on family - based gene studies of alzheimer ’ s since there we have the highest odds of finding dna mutations with very strong effects on risk for alzheimer ’ s, akin to those of the early - onset familial alzheimer ’ s disease gene mutations discussed above. these mutations are most useful for driving successful drug discovery since their biological effects on the disease process are of much greater impact and more clear - cut in terms of mechanism by which they cause disease. they also lend themselves to more useful animal models for drug testing. ultimately, the full list of alzheimer ’ s genes emerging from the family - based genetic studies of the alzheimer ’ s genome project and the population - based studies of igap getting us closer and closer to someday being able to eradicate alzheimer ’ s disease using a strategy of early prediction and early intervention. alzheimer ’ s genes identified to date ( total of 17 ) : early - onset familial alzheimer ’ s disease genes ( onset < age 60 ) : late onset genes ( onset > age 60 ) : adam 10 ( 2008 ) * * * co - discovered in tanzi laboratory * * discovered by the cure alzheimer ’ fund alzheimer


##milial alzheimer ’ s disease genes ( onset < age 60 ) : late onset genes ( onset > age 60 ) : adam 10 ( 2008 ) * * * co - discovered in tanzi laboratory * * discovered by the cure alzheimer ’ fund alzheimer ’ s genome project in alzheimer ’ s families - these genes are expected to contain dna variants that significantly increase risk for alzheimer ’ s. * * * discovered by the igap - these genes are expected to contain dna variants that are common in the general population but which have only tiny effects on risk for alzheimer ’ s. n. b. the alzheimer ’ s genome project has also discovered over 100 additional alzheimer ’ s candidate genes that are in the process of being confirmed and validated. in addition, the cure alzheimer ’ fund supports a website called alzgene http : / / alzgene. org, in which we are tracking all of the alzheimer ’ s candidate genes reported in the scientific literature, including their ongoing testing for confirmation as bona fide alzheimer ’ s disease genes. with regard to functional effects, the above list of 17 alzheimer ’ s genes can be divided into four major categories based on their known or predicted biological effects on alzheimer ’ s risk : 1. the production and clearance of abeta, the major protein in beta - amyloid deposits in the brains of alzheimer ’ s patients ( app, psen1, psen2, apoe, adam10, atxn1, cd33, clu ) 2. cholesterol metabolism ( apoe, clu, abca7 ) 3. the innate immune system and inflammation ( apoe, cd33, clu, cr1 ) 4. cell signaling and protein trafficking ( picalm, bin1, epha1, cd2ap )


salaam and greetings of peace : “ i was a hidden treasure and wanted to be known. ” this is the beginning of probably the most famous hadith qudsi, or extra - qur ’ anic word of god, hadits - e kanz - e makf. its more correct translation might be as follows : “ i was a treasure unknown then i desired to be known so i created a creation to which i made myself known ; then they knew me. ” tradition says that it is the divine response to the prophet david ’ s query, when he asked about the purpose of creation. these are not the words of the prophet muhammad ( saw ), and no chain of transmission is known for this hadith, whether sound or weak, as ibn taymiyya and others state. but the meaning is true and is inferred from q51 : 56 : “ i created the jinn and humankind only that they may worship me! ” meaning “ that they may know me ” as the prophet ’ s ( saw ) cousin ibn abbas explained it. since human beings were created in his image ( as self - aware consciousnesses evolved in a physical body ), all human beings are also hidden treasures to each other. and all have this deep desire to be known. so, all of us create our own little worlds, each according to his or her capabilities of love, talents, and gifts. of course it is a limited and ephemeral world, not comparable with almighty allah ’ s creation, but part of our nature nonetheless : ) - edited and adapted from a post on br. fahad ’ s freelance blog.


you can view the current or previous issues of diabetes health online, in their entirety, anytime you want. click here to view latest bariatric surgery articles popular bariatric surgery articles highly recommended bariatric surgery articles send a link to this page to your friends and colleagues. this press release is an announcement submitted by monash university centre for obesity research and education, and was not written by diabetes health. a new world - first study by monash university researchers has found gastric banding surgery has a profound impact on one of society ' s biggest health issues - diabetes. the study, published today in journal of the american medical association ( jama ), found obese patients with type 2 diabetes who underwent gastric banding were five times more likely to have their diabetes go into long term remission, compared with patients who engaged in conventional weight loss therapies, such as a controlled calorie diet and exercise. the four - year study, which was led by drs john dixon and paul o ' brien from monash university ' s centre for obesity research and education ( core ), monitored 60 volunteers for two years who underwent significant weight loss of more than 10 per cent of their body weight. dr dixon said of those who underwent gastric banding surgery, 73 per cent achieved remission for type 2 diabetes, compared to just 13 percent of the people who underwent conventional therapy. " our study presents strong evidence that obese patients with a body mass index greater than 30 with type 2 diabetes need to lose a significant amount of weight to improve their overall health and glycemic management, " dr dixon said. " our study shows that gastric banding surgery can assist those patients to achieve this - and with sustained results. " professor o ' brien said obesity and type 2 diabetes were strongly linked and combine to present one of the greatest public health problems facing our community. " we found that the amount of weight loss was a key determinant of effectiveness. most of those losing ten per cent of their total weight had remission of the diabetes. few who lost less did so. " dr dixon said the study also found patients who lost substantial weight could not only dramatically reduce their diabetes medications, but also those for controlling blood pressure and lowering blood fats. " we found that after two years, the surgical group when compared to the conventional therapy group displayed a four times greater reduction in glycated haemoglobin, which can be an indicator of poorly controlled diabetes, " dr dixon said. gastric banding is


word origin & history c. 1300, from o. fr. as " one at dice, " from l. as ( gen. assis ) " a unit, " from the name of a small roman coin, perhaps originally etruscan and related to gk. eis " one. " it meant the side of the die with only one mark before it meant the playing card. since this was the lowest roll at dice, ace was used metaphorically in m. e. for " bad luck ; " but as the ace is often the highest playing card, the extended senses based on " excellence, good quality " arose 18c. as card - playing became popular. meaning " outstanding pilot " dates from 1917 ( technically, in wwi aviators ' jargon, one who has brought down 10 enemy planes, though originally in ref. to 5 shot down ), from fr. l ' ace ( 1915 ), which, according to bruce robertson ( ed. ) " air aces of the 1914 - 1918 war " was used in prewar fr. sporting publications for " top of the deck " boxers, cyclists, etc. sports meaning of " point scored " ( 1819 ) led to that of " unreturnable serve " ( 1889 ). the verb meaning " to score " ( in sports ) is first attested 1923, and led to the extended student slang sense of " get high marks " ( 1959 ). ace in the hole " concealed advantage " is attested from 1915.


the most common biomechanical explanation for the chin is that it acts as a buttress against masticatory stress. however, recent evidence suggests that this hypothesis is unlikely [... ] more recently ichim et al. ( 2007 ) have suggested that speech production is associated with mechanical stresses acting on the mandibular symphysis due to tongue and orofacial muscle activity. thus, they argue that the chin is an adaptive response to resist stresses caused by oblique contractions of the genioglossus muscles during speech. computer simulations provide results that are consistent with the orofacial stress hypothesis ( ichim et al., 2007 ), but this hypothesis has yet to be fully tested. a less well - established adaptive hypothesis, but one worth considering, is that chin shape variation is a consequence of sexual selection ( e. g., hershkovitz, 1970 ). psychological studies of facial attractiveness suggest that a ‘ ‘ broad chin ’ ’ in males is correlated with social dominance, which some females may prefer in a potential mate our study provides the first quantitative evidence of sexual dimorphism in chin shape among a geographically diverse sample of modern humans. the presence of sexual dimorphism appears to refute mechanical explanations of the chin that preclude sexual dimorphism, such as the masticatory and orofacial stress hypotheses ( e. g. daegling, 1993 ; ichim et al., 2007 ). while the presence of sexual dimorphism is consistent with the hypothesis that sexual selection influences variation in chin shape, the degree of overlap between males and females requires further explanation. it is safe to say that the male chin pales in comparison to the more exaggerated ornaments found in other animals, such as the large and colorful tail of the peacock ( pavo cristatus ) ( petrie, 1991 ). the modest contrasts in male and female chin shape indicated by our data ( see fig. 4 ) do not seem to fit a runaway process of selection driven by female choice ( fisher, 1958 ). we suggest there are at least two possible explanations for this pattern. one hypothesis for why male chin shape is not more exaggerated is that some females may avoid mating with extremely aggressive males second, the large amount of overlap in male and female chin shape may be due to regional differences inchin shape dimorphism ( see fig. 6 ). regional differencesin the level of dimorphism would tend to inflate within - sex variance in the


of overlap in male and female chin shape may be due to regional differences inchin shape dimorphism ( see fig. 6 ). regional differencesin the level of dimorphism would tend to inflate within - sex variance in the pooled human sample, thereby reducingthe probability of finding between - sex differences. sexual dimorphism in chin shape : implications for adaptive hypotheses zaneta m. thayer, seth d. dobson the chin, or mentum osseum, is one of the most distinctive anatomical traits of modern humans. a variety of hypotheses for the adaptive value of the chin have been proposed, ranging from mechanical stress resistance to sexual selection via mate choice. while the sexual selection hypothesis predicts dimorphism in chin shape, most biomechanical hypotheses preclude it. therefore determining the presence or absence of significant sexual dimorphism in chin shape provides a useful method for differentiating between various adaptive hypotheses ; however, this has yet to be done due to a lack of quantitative data on chin shape. the goals of this study are therefore : ( 1 ) to introduce a new method for quantifying chin shape and ( 2 ) to determine the presence or absence of sexual dimorphism in chin shape in a diverse sample of modern humans. samples were drawn from recent human skeletal collections representing nine geographic regions. outlines of mentum osseum contours were quantified using elliptical fourier function analysis ( effa ). fourier coefficients were analyzed using principal components analysis ( pca ). sexual dimorphism in chin shape was assessed using pc loadings in the pooled geographic sample, and statistically significant differences were found. these findings provide the first quantitative, morphologically based evidence in support of adaptive hypotheses that predict dimorphism in chin shape, including the sexual selection hypothesis.


watchable wildlife sites fish slough is a lush oasis amid an otherwise arid landscape - with less than six inches of rain, and summer temperatures of 100 degrees fahrenheit. the unusual surface water supply provides for varied plant and animal life, from unique and sensitive species such as owens pupfish and owens tui chub, to resident and migrating birds, and small mammals. haiwee deer winter range this area on the edge of the owens valley in the eastern sierra nevada mountains was designated as a watchable wildlife site because it offers outstanding opportunities to view a portion of the east monache mule deer herd. as winter moves in, deer move down from the mountains to the valley bottom, at about 4, 000 feet above sea level. here they can forage on diverse grasses and forbs and find water in hidden springs. desert tortoise natural area for three million years, the desert tortoise survived and adapted to changing climates in what is now the california desert. but in recent years, their numbers have been greatly reduced. this public land in the northwestern mojave desert in northeastern kern county, is managed to protect a unique habitat in its natural state. most of harper lake is a dry lake bed that lies under the flight area of edwards air force base. but in its southwest corner, water runoff from nearby farms has created what is probably the largest marsh in the mojave desert. this oasis attracts resident wildlife and thousands of migratory waterfowl, shorebirds and wading birds, making this a prime birdwatching spot. one of the only places where the mojave river flows above ground all year round. this unusually reliable mojave desert water source provides bounty for many animals. more than 180 species of birds have been spotted, and bighorn sheep can now find water here, thanks to habitat restoration efforts. the area also hosts various turtles and lizards, and desert tortoises. big morongo canyon preserve big morongo creek rises to the surface for just three miles between the mojave and colorado deserts, before it disappears underground again. the resulting canyon oasis has gained a national reputation among birdwatchers as " a usual spot to see the unusual. " at least 235 species of birds have been observed here - including several rare species - along with desert bighorn sheep, mule deer and smaller mammals, lizards and more. southeastern great basin and mojave desert 1 - fish slough 2 - haiwee deer winter range 3 - desert tortoise natural area 4 - harper lake 5 - afton


date of this version nebraska public power district ( nppd ) has monitored water quality since 1989 and fish populations since 1993 on the niobrara river in nebraska in the vicinity of spencer hydro during " flushing " or " sluicing " activities. these sluicing activities alter water quality in the river downstream, which can negatively impact fish populations. higher numbers offish were sampled in 1995 when compared to 1993 and 1994. of the 6, 187 fish and 22 total species sampled above and below the hydro, six species comprised approximately 93 percent of the total sample. the most common species sampled were sand shiner, notropis ludibundus ( 35. 4 % ), red shiner, cyprinella lutrensis ( 22. 9 % ), flathead chub, hybopsis gracilis ( 14. 4 % ), carpsucker spp., carpoides sp. ( 10. 9 % ), bigmouth shiner, hybopsis dorsalis ( 5. 1 % ), and channel catfish, lctalurus punctatus ( 4. 0 % ). operational modifications instituted since 1989, such as opening the flood gates slower and dropping the pond at a slower rate, have reduced sluicing impacts and the hydro structure may not be limiting species diversity to the extent originally thought.


economics research institute study paper utah state university department of economics careful studies of the distribution of income in nineteenth - century united states have been hampered by a paucity of available data. this study undertakes the analysis of factors influencing the distribution of personal income in communities in the great basin region of the western united states for the years 1860 - 61 and 1870. the study utilizes estimates of full income by individual based on information contained in the general economic records of the church of jesus christ of latter - day saints, demographic and economic data from the manuscript censuses of 1860 and 1870, and other relevant data from contemporary sources. mean income and gini ratios are calculated for nearly all great basin communities, and econometric analysis is undertaken to identify the impact on income distribution of changes in mean income, community size, crop destruction by grasshoppers, and the percentage of the population born in non - english speaking countries. the econometric results are compared to the results of an earlier study that looked at factors influencing income inequality for the great basin as a whole over the period 1855 - 1900. of particular interest is the impact of ethnic mix on relative income inequality. while the earlier study found that gini ratios for the great basin region rose as the fraction of the population born in non - english speaking countries increased, the current study finds that gini ratios first rose, then fell as the percentage of the community born in non - english speaking countries rose. at the territorial level, grasshopper infestation increased relative inequality, but at the community level it decreased inequality. the completion of the transcontinental railroad allowed a few individuals in urban communities to earn large incomes in capital - intensive activities, increasing community income inequality, ceteris paribus, but community access to the railroad had a leveling effect on labor income and product prices, reducing community income inequality. israelsen, karl e. and israelsen, l. dwight, " nativity and income distribution in frontier utah communities " ( 2000 ). economic research institute study papers. paper 179.


| skip navigation links | | exit print view | | trusted extensions user ' s guide oracle solaris 11 information library | in contrast to traditional unix systems, superuser ( the root user ) is not used to administer trusted extensions. rather, administrative roles with discrete capabilities administer the system. in this way, no single user can compromise a system ' s security. a role is a special user account that provides access to certain applications with the rights that are necessary for performing the specific tasks. rights include labels, authorizations, privileges, and effective uids / gids. the following security practices are enforced on a system that is configured with trusted extensions : you are granted access to applications and authorizations on a need - to - use basis. you can perform functions that override security policy only if you are granted special authorizations or special privileges by administrators. system administration duties are divided among multiple roles. in trusted extensions, you can access only those programs that you need to do your job. as in the oracle solaris os, an administrator provides access by assigning one or more rights profiles to your account. a rights profile is a special collection of programs and security attributes. these security attributes enable successful use of the program that is in the rights profile. the oracle solaris os provides security attributes such as privileges and authorizations. trusted extensions provides labels. any of these attributes, if missing, can prevent use of the program or parts of the program. for example, a rights profile might include an authorization that enables you to read a database. a rights profile with different security attributes might be required for you to modify the database or read information that is classified as confidential. the use of rights profiles that contain programs with associated security attributes helps prevent users from misusing programs and from damaging data on the system. if you need to perform tasks that override the security policy, the administrator can assign to you a rights profile that contains the necessary security attributes. if you are prevented from running a certain task, check with your administrator. you might be missing required security attributes. in addition, the administrator might assign you a profile shell as your login shell. a profile shell is a special version of a common shell that provides access to a particular set of applications and capabilities. profile shells are a feature of the oracle solaris os. for details, see the pfexec ( 1 ) man page. note - if you try to run a program and receive a not found error message or if you try to run a command and receive a not in profile error message


06 feb 2012 : report in fast - track technology, hope for a second green revolution with advances in a technique known as fast - track breeding, researchers are developing crops that can produce more and healthier food and can adapt and thrive as the climate shifts. in zambia during the current planting season, a corn crop will go into the fields that begins the process of rapidly boosting vitamin a content by as much ten - fold — helping to address a nutritional deficiency that causes 250, 000 - 500, 000 children to go blind annually, most of them in africa and asia. in china, kenya, and madagascar, also this planting season, farmers will put out a crop of artemisia annua that yields 20 to 30 percent more of the chemical compound artemisinin, the basis for what is now the world ’ s standard treatment for malaria. both improvements are happening because of fast - track breeding technology that promises to produce a 21st - century green revolution. it is already putting more food on tables — though it ’ s unclear whether it can add enough food to keep pace as the world ’ s human population booms to 9 billion people by 2050. fast - track breeding is also giving agronomists a remarkable tool for quickly adapting crops to climate change and the increasing challenges of drought, flooding, emerging diseases, and shifting agricultural zones. and it can help save lives : in the absence of prevention, half those victims of vitamin a deficiency now die shortly after going blind, according to the world health fast - track breeding is a faster and more efficient way of doing what nature and farmers have always done. organization ; and in 2010, lack of adequate treatment — meaning artemisinin — contributed to the deaths of 655, 000 children from malaria. the fast - track technology, called marker - assisted selection ( mas ), or molecular breeding, takes advantage of rapid improvements in genetic sequencing, but avoids all the regulatory and political baggage of genetic engineering. bill freese, a science policy analyst with the center for food safety, a nonprofit advocacy group, calls it “ a perfectly acceptable tool. i don ’ t see any food safety issue. it can be a very useful technique if it ’ s used by breeders who are working in the public interest. ” molecular breeding isn ’ t genetic engineering, a technology that has long alarmed critics on two counts. its methods seem outlandish — taking genes from spiders and putting them in goats, or borrowing insect resistance from soil bacteria and transferring it into corn — and it has also seemed to benefit a handful of agri


has long alarmed critics on two counts. its methods seem outlandish — taking genes from spiders and putting them in goats, or borrowing insect resistance from soil bacteria and transferring it into corn — and it has also seemed to benefit a handful of agribusiness giants armed with patents, at the expense of public interest. by contrast, molecular breeding is merely a much faster and more efficient way of doing what nature and farmers have always done, by natural selection and artificial selection respectively : it takes existing genes that happen to be advantageous in a given situation and increases their frequency in a population. in the past, farmers and breeders did it by walking around their fields and looking at individual plants or animals that seemed to have desirable traits, like greater productivity, or resistance to a particular disease. then they went to work cross - breeding to see if they could tease out that trait and get it to appear reliably in subsequent generations. it could take decades, and success at breeding in one trait often meant bringing along some deleterious fellow traveler, or inadvertently breeding out some other essential trait. cornell university photography photo / lindsay france. a cornell researcher bags rice plant panicles to prevent cross pollination. molecular breeding enables growers to get the improvements they want far more precisely, by zeroing in on the genes responsible for a given trait. if genetic engineering is a tool for “ bludgeoning the genome, ” as cornell university researcher susan mccouch puts it, what molecular breeding does instead is to “ open a window ” into how the genome works, enabling researchers to collaborate with it. sequencing the entire genome of a species is the first step, and this process, which cost millions of dollars a decade ago, is down now to the low thousands. next, researchers sort out which genes are responsible for a given function, the bottleneck in the process so far, though mccouch says it becomes faster and cheaper with each new species that gets sequenced, because nature tends to employ the same mechanisms from one species to another. finally, researchers map out markers — bits of genetic material that are linked to those genes, to flag whether or not the desired genes are present in a given individual. “ it ’ s not uncommon for a company to want to combine 10 or 20 traits in a variety, ” says harry klee, a specialist in tomato breeding at the university of florida in gainesville. in the past, to get the perfect combination of traits using conventional methods, “ you would have to put out millions of plants in the field. ”


” says harry klee, a specialist in tomato breeding at the university of florida in gainesville. in the past, to get the perfect combination of traits using conventional methods, “ you would have to put out millions of plants in the field. ” instead, breeders typically simplified, narrowing down their wish list to a few key traits. with tomatoes, for instance, as many as 30 or 40 different genes influence taste — too many variables to juggle. so shelf life and appearance inevitably trumped taste. “ but this is where molecular breeding really pays off, ” says klee. breeders now use genetic markers to automatically screen one - inch - tall seedlings and immediately weed out the 99 percent they don ’ t want, cutting years off the breeding timetable. that makes it easier to get to desirable cross - breed quickly — and also stack up a complex array of traits in a single strain. as a result, says klee, even mass - produced supermarket tomatoes should actually taste good five years from now. in the two decades since researchers first proposed molecular breeding in 1989, high costs and the difficult work of discovery have largely confined the technology to big companies working in commodity crops like corn and these methods have the potential to make breeding aim at enhancing biological and agricultural diversity. soybeans. but as costs fall even faster than moore ’ s law would predict and genetic methods become routine, researchers are now also applying them to the so - called orphan crops on which much of the developing world depends. molecular breeding is not as effective so far for crops that propagate clonally, including such tropical staples as cassava, sweet potato, yams, bananas and plantains. but for rice and many other crops, it enables breeders to quickly tailor a plant to a particular environment or taste. “ every village has its own favorite rice, ” says ian graham, director of the university of york ’ s centre for novel agricultural products. “ the challenge is if you come up with a great trait, how on earth do you put that trait into all these local varieties easily, economically, and quickly? sequencing gives you the tool to do it. that ’ s the secret of really making molecular breeding work for the developing world. ” there are still economic barriers, he says, but equipment to set up a basic laboratory in a developing country “ is on the order of $ 100, 000 instead of millions. ” thus genetic methods have the potential to make breeding more local, more democratic, and aimed at enhancing biological and agricultural diversity, instead of stripping it away.


laboratory in a developing country “ is on the order of $ 100, 000 instead of millions. ” thus genetic methods have the potential to make breeding more local, more democratic, and aimed at enhancing biological and agricultural diversity, instead of stripping it away. the green revolution of the 1960s largely achieved its huge leap in productivity by streamlining plants and farming methods to work across hundreds of millions of hectares, regardless of local tastes or environments. it re - designed plants for high - input industrial agriculture, so they could respond to an intensive regimen of fertilizers, water, and pesticides, regardless of the environment. but the molecular green revolution will work, says mccouch, by fine - tuning crops to perform in a particular environment, minus additional input. farmers are backing off growing rice in water, for instance, “ because they can ’ t afford the water, there isn ’ t enough water in the world. ” molecular breeding will also build crops, mccouch says, to “ respond constructively to changes in the environment that we cannot predict, ” like flooding and drought. “ a really big challenge in discovery genetics right now, ” she says, “ is to understand how plants sense environments : how do they count number of days? how do they count the number hours of daylight? how do they know when to grow and when to hold their breath if they ’ re underwater? once we make the discovery of which genes allow the more from yale e360 can ‘ climate - smart ’ agriculture help africa and the planet? an idea promoted at the recent durban talks is “ climate - smart agriculture, ” which could make crops less vulnerable to heat and drought and turn depleted soils into carbon sinks. the world bank and african leaders back this approach, fred pearce writes, but some critics are skeptical that it will benefit small - scale african farmers. read more plants to sense these things, then we can do marker - assisted selection ” and move those genes into local varieties that already have the other traits farmers want. the potential for molecular breeding to help farmers adapt to a rapidly changing world became evident last month when nature biotechnology published an article about rice breeding in japan. geneticists at the iwate biotechnology research center 130 miles north of fukushima were already using molecular breeding to improve the cold - tolerant rice variety preferred by farmers there, when last year ’ s earthquake hit. the subsequent tsunami left a huge swath of rice paddies — 58, 000 acres, representing almost a fifth of the nation ’ s rice supply — contaminated with too much salt


the number of hurricanes occurring annually on a global basis varies widely from ocean to ocean. globally, about 80 tropical cyclones occur annually, one - third of which achieve hurricane status. the most active area is the western pacific ocean, which contains a wide expanse of warm ocean water. in contrast, the atlantic ocean averages about ten storms annually, of which six reach hurricane status. compared to the pacific ocean, the atlantic is a much smaller area, and therefore supports a smaller expanse of warm ocean water to fuel storms. the pacific waters also tend to be warmer, and the layer of warm surface waters tends to be deeper than in the atlantic. the frequency and intensity of hurricanes varies significantly from year to year, and scientists haven ’ t yet figured out all the reasons for the variability. hurricanes and el nino scientists continue to investigate the interactions between hurricane frequency and el nino. el nino is a phenomenon where ocean surface temperatures become warmer than normal in the equatorial east pacific ocean. in general, el nino events are characterized by an increase in hurricane activity in the eastern pacific and a decrease in activity in the atlantic, gulf of mexico, and the caribbean sea. during el nino years, the wind patterns are aligned in such a way that there is an increase in vertical wind shear ( upper level winds ) over the caribbean and atlantic. the increased wind shear helps to prevent tropical disturbances from developing into hurricanes. oppositely, in the eastern pacific, el nino alters wind patterns in a way that reduces wind shear, contributing to more storms. hurricanes and global warming since warm ocean waters and warm, moist air fuel storms, theory predicts that global warming should increase the number and intensity of tropical cyclones. as the oceans soak up extra heat from the atmosphere, ocean surface temperatures rise, increasing the extent of warm water that can support a hurricane. not only should this mean that more hurricanes can form, but increased ocean surface temperatures could also increase a storm ’ s maximum potential intensity, the strongest a storm can get in ideal conditions. models based on scientists ’ current understanding of hurricanes suggest that if ocean temperatures increased by 2 - 2. 5 degrees, the average intensity of hurricanes would increase by 6 to 10 percent. since 1970, the average ocean temperature has warmed about half a degree, which means that theoretically, storms could be one to three percent stronger. such an increase translates to a few knots in wind speed, too small a change to accurately measure. hurricane wind speeds have historically been measured in increments of five knots, so any increase in intensity that has already occurred as a result


percent stronger. such an increase translates to a few knots in wind speed, too small a change to accurately measure. hurricane wind speeds have historically been measured in increments of five knots, so any increase in intensity that has already occurred as a result of global warming would, in theory, be too small to detect yet. however, in 2005 and 2006, several studies suggested that global warming may be impacting hurricanes more than theory predicts. in an analysis of the historical record, there appeared to be an increase in the number of intense ( category 4 and 5 ) storms in recent years. another analysis charted sea surface temperatures and the number of tropical cyclones. it revealed that as sea surface temperatures went up, the number of cyclones went up. was the increase in sea surface temperatures responsible for the increased number of storms or did some outside factor drive both? the studies triggered many questions. both theory and the studies suggested that there should be a link between global warming and hurricanes, but the studies showed a much greater increase in storm frequency and intensity than theory predicted. what caused the discrepancy? is humanity ’ s current understanding of hurricanes flawed? can the theory be adjusted to explain why hurricanes would have a stronger reaction to warming than previously predicted? one theory put forth to explain the recent increase in storm intensity and frequency in the atlantic basin is the multi - decadal oscillation. storms in the atlantic may go through a natural cycle of 20 - 30 years of increased activity followed by a quieter period. the record seems to show such a cycle, with more intense hurricanes in the 1950s and 1960s followed by two decades of relative quiet, and then increased intensity from the mid - 1990s to the present. some scientists argue that this natural cycle may actually be a product of global warming and atmospheric aerosols. in the 1970s and 1980s, aerosol pollution may have “ shaded ” the earth, keeping temperatures cooler than they had been in previous decades. this cooling would have suppressed hurricane formation. in the 1990s, global warming may have increased enough to overcome aerosol cooling and allowed hurricane intensity and frequency to climb again. other scientists argued that the flaw isn ’ t necessarily in the theory, but in the historical records. satellite data used to estimate hurricane intensity only goes back to the 1970s for the atlantic basin, and other basins have a shorter record. a thirty - year record may not be long enough to coax out real trends. further, satellite technology and the methods used to estimate a storm ’ s intensity have improved, so a storm that may have been


and other basins have a shorter record. a thirty - year record may not be long enough to coax out real trends. further, satellite technology and the methods used to estimate a storm ’ s intensity have improved, so a storm that may have been classified a category 1 or 2 in the 1970s through the mid - 1980s would be classified as a much stronger storm today. the change in intensity - predicting methods could skew the record to show fewer intense storms in the 1970s and 1980s than there are today. from the 1940s to the 1970s, hurricane intensity estimates were based on aircraft and ship data. this means that fewer storms were recorded than probably actually occurred. the intensity records may also be skewed because the early flights did not go directly over the eye of the hurricane, but measured winds in safer flying areas farther from the center of the storm. from those measurements, wind speeds at the center of the storm and thus the storm ’ s intensity were estimated. as a result, many storms may have been stronger than they were estimated to have been. before the 1940s, intensity estimates were made based on surviving ship ’ s records. it is likely that any ship at the center of a category 4 or 5 storm didn ’ t survive, so the record probably contains fewer big storms than actually occurred. from changes in the methods used to estimate hurricane intensity to spotty ship records, the historical record may well be skewed towards weaker storms, argue many scientists. if all these factors were accounted for, the trend toward greater hurricane frequency and intensity could disappear. regardless of their position, scientists need a longer and more accurate data record to fully understand the connection between global warming and other factors that may influence hurricane intensity and frequency. a longer, more accurate record will help improve theory and models, and it will amplify or flatten the currently observed trends.


federal environment officials investigating drinking water contamination near the ranching town of pavillion, wyo., have found that at least three water wells contain a chemical used in the natural gas drilling process of hydraulic fracturing. scientists also found traces of other contaminants, including oil, gas or metals, in 11 of 39 wells tested there since march. the study, which is being conducted under the environmental protection agency ’ s superfund program, is the first time the epa has undertaken its own water analysis in response to complaints of contamination in drilling areas, and it could be pivotal in the national debate over the role of natural gas in america ’ s energy policy. abundant gas reserves are being aggressively developed in 31 states, including new york and pennsylvania. congress is mulling a bill that aims to protect those water resources from hydraulic fracturing, the process in which fluids and sand are injected under high pressure to break up rock and release gas. but the industry says environmental regulation is unnecessary because it is impossible for fracturing fluids to reach underground water supplies and no such case has ever been proven. scientists in wyoming will continue testing this fall to determine the level of chemicals in the water and exactly where they came from. if they find that the contamination did result from drilling, the placid plains arching up to the wind river range would become the first site where fracturing fluids have been scientifically linked to groundwater contamination. in interviews with propublica and at a public meeting this month in pavillion ’ s community hall, officials spoke cautiously about their preliminary findings. they were careful to say they ’ re investigating a broad array of sources for the contamination, including agricultural activity. they said the contaminant causing the most concern – a compound called 2 - butoxyethanol, known as 2 - be – can be found in some common household cleaners, not just in fracturing fluids. but those same epa officials also said they had found no pesticides – a signature of agricultural contamination – and no indication that any industry or activity besides drilling could be to blame. other than farming, there is no industry in the immediate area. in pavillion, a town of about 160 people in the heart of the wind river indian reservation, the gas wells are crowded close together in an ecologically vivid area packed with large wetlands and home to 10 threatened or endangered species. beneath the ground, according to the u. s. geological survey, the earth is a complex system of folded crusts containing at least 30 water - bearing aquifer


were drilled and assumed liability for them, is either supplying fresh drinking water to the residents or has purchased the land. in the third case, a drilling company bought by encana, tom brown inc., had previously reached an out - of - court settlement to provide water filtering. though the drilling companies have repeatedly compensated residents with the worst cases of contamination, they have not acknowledged any fault in causing the pollution. an encana spokesman, doug hock, told propublica the company wants " to better understand the science and the source of the compounds " found in the water near pavillion before he would speculate on whether the company was responsible. precise details about the nature and cause of the contamination, as well as the extent of the plume running in the aquifer beneath this region 150 miles east of jackson hole, have been difficult for scientists to collect. that ’ s in part because the identity of the chemicals used by the gas industry for drilling and fracturing are protected as trade secrets, and because the epa, based on an exemption passed under the 2005 energy policy act, does not have authority to investigate the fracturing process under the safe drinking water act. using the superfund program gave the agency extra authority to investigate the pavillion reports, including the right to subpoena the secret information if it needs to. it also unlocked funding to pay for the research. epa officials have repeatedly said that disclosure of the fluids used in fracking – something that would be required if the bill being debated in congress were passed – would enable them to investigate contamination incidents faster, more conclusively and for less money. the current study, which is expected to end next spring, has already cost $ 130, 000. about 65 people, many in jeans, boots and 10 - gallon hats, filled pavillion ’ s community hall on aug. 11 to hear the epa ’ s findings. they were told that a range of contaminants, including arsenic, copper, vanadium and methane gas were found in the water. many of these substances are found in various fluids used at drilling sites. of particular concern were compounds called adamantanes, a natural hydrocarbon found in gas that can be used to fingerprint its origin, and 2 - be, listed as a common fracturing fluid in the epa ’ s 2004 research report on hydraulic fracturing. that compound, which epa scientists in wyoming said they identified with 97 percent certainty, was suspected by some environmental groups in a 2004 drilling - related contamination case in colorado, also involving


gladstone ’ s library was founded by victorian statesman, william ewart gladstone ( 1809 - 1898 ), arguably britain ’ s greatest prime minister, and the most significant anglican lay person of the last two centuries. four times liberal prime minister, four times chancellor of the exchequer and a parliamentarian for 63 years, few politicians have achieved as many lasting reforms as gladstone. he even came within a hair ’ s breadth of bringing peace to ireland with his sadly ill - fated home rule bill. gladstone was a pragmatic political leader with an insatiable interest in history, literature, the classical world and theological dispute ; a voracious reader who read 20, 000 books. britain at this time was the most powerful nation on earth, at the height of queen victoria ’ s imperialism. i find it hard to reconcile gladstone ’ s clear christian conviction with the hypocrisy and barbarity of empire. yet he was solidly at the heart of it. was he compromised by this or did he provide the conscience against even greater excesses? ‘ we look forward to the time when the power of love will replace the love of power. then will our world know the blessings of peace … nothing that is morally wrong can be politically right ’. w. e gladstone. gladstone, a millionaire, lived in the castle in the village of hawarden, north wales, just a few miles from chester. this is the site of st deiniol ’ s library which gladstone founded. he bought the land in 1889 and the library opened in 1894. the present grade 1 listed building was opened in 1902 as the national memorial to gladstone. it is the only prime ministerial library in the uk and is unique in being a residential library with 26 study bedrooms, some now fully refurbished and en - suite. it ’ s a fascinating victorian building ; with the double - tier library occupying one entire wing and the residential areas including the dining room, kitchen and chapel the other. the bedrooms and offices are spread across the whole of the first floor. you quickly get to find your way around as the building is not actually that large. i decided, after my week, that this is a rather special and unusual place. gladstone ’ s influence pervades the entire place. there is a huge granite statue in the grounds gazing out over the village! there are pictures, busts and other statues of the gom ( grand old man ) everywhere including a photo collage detailing the main aspects of his life in the main corridor leading to the dining room. the library was created


out over the village! there are pictures, busts and other statues of the gom ( grand old man ) everywhere including a photo collage detailing the main aspects of his life in the main corridor leading to the dining room. the library was created around gladstone ’ s original donation of 32, 000 books. it houses a world renowned collection of theology and nineteenth century studies. the collection boasts more than 250, 000 items. gladstone wanted his library to be a country house “ for the pursuit of divine learning ”, offering ‘ insight and refreshment ’ to visiting scholars and users. the library is galleried with access to the second floor up some very narrow, winding and rickety stairs with rope handholds! here you go back in time. this is an old - style ‘ quiet ’ library ; individual study tables with desk lamps and old comfy leather chairs. it ’ s extremely conducive to study and thought, which of course is the usp of the place. it ’ s why it works so well. you come here specifically to think, write, study, reflect and retreat. it ’ s open in the evening until 10pm which i found to be a real boon. the book collection covers mainly theology and history with the emphasis on publications from the late victorian period. the gladcat computer system makes finding books within the library very easy indeed. there ’ s a thrilling touch of serendipity to come across books with gladstone ’ s own pencilled annotations! the property has a mixture of older and the newer refurbished bedrooms. i had one of the older rooms ( room 7, no view ) which was very spacious, with the bathroom directly opposite. there are no tv ’ s in any of the bedrooms which i think is good! broadband is fast, free and available throughout the building although one guest said it didn ’ t work in some of the bedrooms. i had no problems. one bug - bear however was the horrible noise late at night and early in the morning caused by the expansion of the hot water pipes! i found that in a very short time, the place draws you into its own daily rhythm. you feel very much apart from the day - to - day. there ’ s a lovely modern chapel on the ground floor. communion takes place each weekday morning at 8am, following the church of wales anglican liturgy. the ‘ food for thought ’ coffee shop replaces the dining room during the day and provides snacks and drinks. i found the food overall – both in quantity and quality – adequate but


the no child left behind act of 2001 recognizes that improved student achievement occurs when communities implement programs and strategies scientifically proven to be effective. the 21st century community learning centers ( cclc ) program is an essential part of this initiative. the no child left behind act of 2001 recognizes that improved student achievement occurs when communities implement programs and strategies scientifically proven to be effective. the 21st century community learning centers ( cclc ) program is an essential part of this initiative. many communities across the commonwealth are working together with new energy and inspiration to create a more positive future for their children and youth. their focus is on constructive learning activities during non - school hours. with caring adult guidance, school and community - based academic and youth development programs result in greater achievement and social outcomes for children and youth. the intent of the funds is to enable communities to design and implement effective out - of - school programs that will result in improved student achievement, and be sustained through community partnerships at the conclusion of the grant funds. specifically, the purposes of the no child left behind act of 2001 as authorized under title iv, part b ( 21st cclc ) are to : 1 ) provide opportunities for academic enrichment, including providing tutorial services to help students meet state and local student performance standards in core academic subjects such as reading and mathematics ; 2 ) offer students a broad array of additional services, programs, and activities, such as youth development activities, drug and violence prevention programs, counseling programs, art, music, fitness, and recreation programs, technology education programs, and character education programs, that are designed to reinforce and complement the regular academic program of participating students ; and 3 ) offer families of students served by community learning centers opportunities for literacy and related educational development. 21st cclc grantee documents kentucky ' s current 21st century community learning centers grantees list and other documents. this memorandum contains an overview of the regulatory requirement that religiously affiliated ( or " faith - based " ) organizations be able to compete on an equal footing with other organizations for funding by the u. s. department of education ( the " department " ) in programs in which they are eligible, including state - administered programs such as 21st century community learning centers ( 21st cclc ) program. - the afterschool alliance is a nonprofit organization dedicated to raising awareness of the importance of afterschool programs and advocating for quality, affordable programs for all children. it is supported by a group of public, private and nonprofit organizations that share the alliance ' s vision of ensuring that all children have access to afterschool programs by 2010


of afterschool programs and advocating for quality, affordable programs for all children. it is supported by a group of public, private and nonprofit organizations that share the alliance ' s vision of ensuring that all children have access to afterschool programs by 2010. benton foundation kids campaign - it is the future goal of connect for kids that health, safety, education, and financial security of children be a priority. this website provides best use of communications technologies, specially the internet, to give adults - parents, grandparents, guardians, educators, advocates, policymakers, elected officials and others - the tools and information they need to work on behalf of children, youth and families. c. s. mott foundation - the charles stewart mott foundation is a partner with the u. s. dept. of education which provides tools and funds toward the 21st cclc program. the finance project - under " information resource center " you fill find in this website, " out - of - school - time clearinghouse topics " that provide after school programs information on finding funding resources to sustain their programs. harvard family research project - this project will provide your program with insights on past and new research to evaluate, improve and sustain your program. national institute for out - of - school time - providing information by part of the wellesley centers for women at wellesley college regarding high end programs and activities for children in after school programs. northwest regional educational laboratory - this organization provides research and development assistance for adults, youth and children. they have an online catalog, newsletters, special resources and training / workshop opportunities. u. s. dept. of education - at this location, you will get the current information on purpose, eligibility, applicant info, awards, performance, funding status, laws / regs / guidance, resources, faqs and who to contact regarding the 21st century community learning centers ( 21st cclc ).