text:
my.bionity.com
With an accout for my.bionity.com you can always see everything at a glance – and you can configure your own website and individual newsletter.
My saved topics
Keep logged in
Cookies deactivated
To use all functions of this page, please activate cookies in your browser.
Chernobyl_disaster_effects
Chernobyl disaster effects
The neutrality of this article is disputed.
Please see the discussion on the talk page.(December 2007)
Please do not remove this message until the dispute is resolved.
This article is about the effects of the Chernobyl disaster, for the main article on the disaster see: Chernobyl disaster
The Chernobyl disaster triggered the release of substantial amounts of radiation into the atmosphere in the form of both particle and gaseous radioisotopes, and is the most significant unintentional release of radiation into the environment to date. The International Atomic Energy Agency (IAEA) alleges that, while the Chernobyl disaster released as much as 400 times the radioactive contamination of the Hiroshima bomb, it was 100 to 1,000 times less than the contamination caused by atmospheric nuclear weapons testing in the mid-20th century.[citation needed]
The effects of this release of radioisotopes are the subject of substantial study, and the full effect of the radiation will not be understood for some time. Ukraine, Belarus and Russia were affected by the radioactive contamination due to the radioactive cloud, as were countries of western Europe. Due to the sensitive nature of nuclear-related issues, it has been difficult for the public to appreciate the full extent of the catastrophe. Scientific studies are incomplete in part because of political concerns (for example, in Belarus, Yuri Bandazhevsky, a scientist criticizing the official research being conducted into the Chernobyl disaster was jailed for four years).
Additional recommended knowledge
How to Quickly Check Pipettes?
8 Steps to a Clean Balance – and 5 Solutions to Keep It Clean
How to ensure accurate weighing results every day?
1 Dose to the general public within 30 km of the plant
2 Short-term health effects and immediate results
2.1 Workers and liquidators
2.2 Evacuation
2.3 Civilians
3 Long-term health effects
3.1 Science and politics: the problem of epidemiological studies
3.2 Caesium radioisotopes
3.3 Food restrictions
3.4 Effect on the natural world
3.5 The September 2005 IAEA report and criticisms
4 Controversy over human health effects
4.1 The TORCH report
4.2 Greenpeace
4.3 The April 2006 IPPNW report
4.4 Other studies and claims
4.5 French legal action
5 Comparisons to other radioactivity releases
Dose to the general public within 30 km of the plant
The inhalation dose (internal dose) for the public (during the time between the accident occurring and their evacuation from the area) in what is now the 30 km evacuation zone around the plant has been estimated (based ground deposition of 137Cs) to be between 3 and 150 mSv {between a 1 in 6666.67 and a 1 in 133.33 chance of a fatal cancer assuming the ICRP risk factor of a 5% of a fatal cancer per Sv of exposure} for adults (depending on the distance from the reactor and the day of evacuation) and for one year old children a dose estimate of between 10 and 700 mSv {between a 1 in 2000 and a 1 in 28.57 chance of fatal cancer} has been made.[1] Thyroid doses for adults were between 20 and 1000 mSv, while for the 1 year old infants these were higher at 20 to 6000 mSv. For those who left at an early stage in the accident the internal dose due to inhalation was 8 to 13 times higher than the external dose due to gamma/beta emitters. For those who remained until later (day 10 or later) the inhalation dose was 50 to 70% higher than the dose due to external exposure. The majority of the dose was due to 131I (circa 40%), tellurium and rubidium isotopes (circa 20 to 30% for Rb and Te).[2]
The ingestion doses in this same group of people have also been estimated using the cesium activity per unit of area, isotope ratios, average day of evacuation, intake rate of milk and green vegetables and what is known about the transfer of radioactivity via plants/animals to humans. For adults the dose has been estimated to be between 3 and 180 mSv while for the one year old infants a dose of between 20 and 1300 mSv has been estimated. Again the majority of the dose was due to 131I and the external dose was much smaller than the internal dose due to the radioactivity in the diet.[3]
Short-term health effects and immediate results
The explosion at the power station and subsequent fires inside the remains of the reactor provoked a radioactive cloud which drifted over Russia, Belarus and Ukraine, but also the European part of Turkey, Greece, Moldova, Romania, Lithuania, Finland, Denmark, Norway, Sweden, Austria, Hungary, the Czech Republic and the Slovak Republic, Slovenia, Poland, Switzerland, Germany, Italy, Ireland, France (including Corsica[4]) and the United Kingdom (UK).[5][6] In fact, the initial evidence in other countries that a major exhaust of radioactive material had occurred came not from Soviet sources, but from Sweden, where on April 27 workers at the Forsmark Nuclear Power Plant (approximately 1100 km from the Chernobyl site) were found to have radioactive particles on their clothes. It was Sweden's search for the source of radioactivity, after they had determined there was no leak at the Swedish plant, that led to the first hint of a serious nuclear problem in the Western Soviet Union. In France, the government then claimed that the radioactive cloud had stopped at the Italian border. Therefore, while some kinds of food were prohibited in Italy because of radioactivity (in particular mushrooms), the French authorities didn't take any such measures, in an attempt to appease the population's fears (See below).
Contamination from the Chernobyl disaster was not evenly spread across the surrounding countryside, but scattered irregularly depending on weather conditions. Reports from Soviet and Western scientists indicate that Belarus received about 60% of the contamination that fell on the former Soviet Union. A large area in Russia south of Bryansk was also contaminated, as were parts of northwestern Ukraine.
203 people were hospitalized immediately, of whom 31 died (28 of them died from acute radiation exposure).[citation needed] Most of these were fire and rescue workers trying to bring the disaster under control, who were not fully aware of how dangerous the radiation exposure (from the smoke) was (for a discussion of the more important isotopes in fallout see fission products). 135,000 people were evacuated from the area, including 50,000 from the nearby town of Pripyat, Ukraine. Health officials have predicted that over the next 70 years there will be a 2% increase in cancer rates in much of the population which was exposed to the 5-12 (depending on source) EBq of radioactive contamination released from the reactor. An additional 10 individuals have already died of cancer as a result of the disaster.[citation needed]
Soviet scientists reported that the Chernobyl Unit 4 reactor contained about 180-190 metric tons of uranium dioxide fuel and fission products. Estimates of the amount of this material that escaped range from 5 to 30 percent, but some liquidators, who have actually been inside the sarcophagus and the reactor shell itself — e.g. Mr. Usatenko and Dr. Karpan[citation needed] — state that not more than 5-10% of the fuel remains inside; indeed, photographs of the reactor shell show that it is completely empty. Because of the intense heat of the fire, much of the ejected fuel was lofted high into the atmosphere (with no containment building to stop it), where it spread.
Workers and liquidators
The workers involved in the recovery and cleanup after the disaster, called "liquidators", received high doses of radiation. In most cases, these workers were not equipped with individual dosimeters to measure the amount of radiation received, so experts can only estimate their doses. Even where dosimeters were used, dosimetric procedures varied. Some workers are thought to have been given more accurate estimated doses than others. According to Soviet estimates, between 300,000 and 600,000 people were involved in the cleanup of the 30 km evacuation zone around the reactor, but many of them entered the zone two years after the disaster.[7] Estimates of the number of "liquidators" — workers brought into the area for disaster management and recovery work — vary; the World Health Organization, for example, puts the figure at about 800,000; Russia lists as liquidators some people who did not work in contaminated areas. In the first year after the disaster, the number of cleanup workers in the zone was estimated to be 211,000, and these workers received an estimated average dose of 165 millisieverts (16.5 rem). The plume of radioactive debris has been said to be equal to the contamination of 400 Hiroshima bombs. This is correct, but misleading. The main effect of the bomb was the direct radiation from the gamma blast. Compared to that, the contamination was only a minor addition. Furthermore the comparison to bomb fallout is very misleading, as an atomic bomb has a very different isotope signature to a power reactor. In bomb fallout plenty of the very shortlived isotopes are present while the activity in used power reactor fuel tends have a medium to long halflife. The time required for the dose rate to decline by a factor of 10 in an area covered with fallout from an atomic bomb which has detonated an hour ago is much shorter than the time required for the same reduction in dose rate due to Chernobyl fallout (one hour after the reactor suffered the steam explosion).
Soviet authorities started evacuating people from the area around Chernobyl only on the second day after the disaster (within 36 hours). By May 1986, about a month later, all those living within a 30 km (18 mile) radius of the plant — about 116,000 people — had been relocated. This area is often referred to as the zone of alienation. However, radiation affected the area in a much wider scale than this 30 km radius.
According to reports from Soviet scientists, 28,000 km² (10,800 mi²) were contaminated by caesium-137 to levels greater than 185 kBq/m². Roughly 830,000 people lived in this area. About 10,500 km ² (4,000 mi²) were contaminated by caesium-137 to levels greater than 555 kBq/m². Of this total, roughly 7,000 km² (2,700 mi²) lie in Belarus, 2,000 km² (800 mi²) in the Russian Federation and 1,500 km² (580 mi²) in Ukraine. About 250,000 people lived in this area. These reported data were corroborated by the International Chernobyl Project.
Some children in the contaminated areas were exposed to high radiation doses of up to 50 grays (Gy) because of an intake of radioactive iodine-131, a relatively short-lived isotope with a half-life of 8 days, from contaminated milk produced locally. Several studies have found that the incidence of thyroid cancer among children in Belarus, Ukraine and Russia has risen sharply. The IAEA notes "1800 documented cases of thyroid cancer in children who were between 0 and 14 years of age when the disaster occurred, which is far higher than normal", but fails to note the expected rate. The childhood thyroid cancers that have appeared are of a large and aggressive type but, if detected early, can be treated. Treatment entails surgery followed by iodine-131 therapy for any metastases. To date, such treatment appears to have been successful in the vast majority of cases.
Late in 1995, the World Health Organisation (WHO) linked nearly 700 cases of thyroid cancer among children and adolescents to the Chernobyl disaster, and among these some 10 deaths are attributed to radiation. However, the rapid increase in thyroid cancers detected suggests that some of it at least is an artifact of the screening process. Typical latency time of radiation-induced thyroid cancer is about 10 years, but the increase in childhood thyroid cancers in some regions was observed as early as 1987. Presumably either the increase is unrelated to the disaster or the mechanisms behind it are not well understood.
So far, no increase in leukemia is discernible, but this is expected to be evident in the next few years along with a greater, though not statistically discernible, incidence of other cancers. There has been no substantiated increase attributable to Chernobyl in congenital abnormalities, adverse pregnancy outcomes or any other radiation-induced disease in the general population, either in the contaminated areas or further afield.[citation needed]
This is contradicted by documentary "The Battle of Chernobyl", which relates how much information has either not been gathered, or covered up. Congenital deformities and increased risk of cancer was documented, but difficult to affirm due to the lack of proper research.
Long-term health effects
Science and politics: the problem of epidemiological studies
The issue of long-term effects of Chernobyl disaster on civilians is very controversial. The number of people whose lives were affected by the disaster is enormous. Over 300,000 people were resettled because of the disaster; millions lived and continue to live in the contaminated area. On the other hand, most of those affected received relatively low doses of radiation; there is little evidence of increased mortality, cancers or birth defects among them; and when such evidence is present, existence of a causal link to radioactive contamination is uncertain.
An increased incidence of thyroid cancer among children in areas of Belarus, Ukraine and Russia affected by the Chernobyl disaster has been firmly established as a result of screening programs and, in the case of Belarus, an established cancer registry. The findings of most epidemiological studies must be considered interim, say experts, as analysis of the health effects of the disaster is an ongoing process.
Epidemiological studies have been hampered in the former Soviet Union by a lack of funds, an infrastructure with little or no experience in chronic disease epidemiology, poor communication facilities and an immediate public health problem with many dimensions. Emphasis has been placed on screening rather than on well-designed epidemiological studies. International efforts to organize epidemiological studies have been slowed by some of the same factors, especially the lack of a suitable scientific infrastructure. Furthermore, the political nature of nuclear energy may have affected scientific studies. In Belarus, Yuri Bandazhevsky, a scientist who questioned the official estimates of Chernobyl's consequences and the relevancy of the official maximum limit of 1,000 Bq/kg, was imprisoned from 2001 to 2005. Bandazhevsky and some human rights groups allege his imprisonment was a reprisal for his publication of reports critical of the official research being conducted into the Chernobyl incident.
The activities undertaken by Belarus and Ukraine in response to the disaster — remediation of the environment, evacuation and resettlement, development of uncontaminated food sources and food distribution channels, and public health measures — have overburdened the governments of those countries. International agencies and foreign governments have provided extensive logistic and humanitarian assistance. In addition, the work of the European Commission and World Health Organization in strengthening the epidemiological research infrastructure in Russia, Ukraine and Belarus is laying the basis for major advances in these countries' ability to carry out epidemiological studies of all kinds.
Caesium radioisotopes
Further information: Fission products
Immediately after the disaster, the main health concern involved radioactive iodine, with a half-life of eight days. Today, there is concern about contamination of the soil with strontium-90 and caesium-137, which have half-lives of about 30 years. The highest levels of caesium-137 are found in the surface layers of the soil where they are absorbed by plants, insects and mushrooms, entering the local food supply. Some scientists fear that radioactivity will affect the local population for the next several generations. Note that cesium is not mobile in most soils because it binds to the clay minerals.[1][2][3] Recent tests (ca. 1997) have shown that caesium-137 levels in trees of the area are continuing to rise. There is some evidence that contamination is migrating into underground aquifers and closed bodies of water such as lakes and ponds (2001, Germenchuk). The main source of elimination is predicted to be natural decay of caesium-137 to stable barium-137, since runoff by rain and groundwater has been demonstrated to be negligible.
Food restrictions
Twenty years after the catastrophe, restriction orders remain in place in the production, transportation and consumption of food contaminated by Chernobyl fallout. In the UK, they remain in place on 374 farms covering 750 km² and 200,000 sheep. In parts of Sweden and Finland, restrictions are in place on stock animals, including reindeer, in natural and near-natural environments. "In certain regions of Germany, Austria, Italy, Sweden, Finland, Lithuania and Poland, wild game (including boar and deer), wild mushrooms, berries and carnivorous fish from lakes reach levels of several thousand Bq per kg of caesium-137", while "in Germany, caesium-137 levels in wild boar muscle reached 40,000 Bq/kg. The average level is 6,800 Bq/kg, more than ten times the EU limit of 600 Bq/kg", according to the TORCH 2006 report. The European Commission has stated that "The restrictions on certain foodstuffs from certain Member States must therefore continue to be maintained for many years to come".[5]
As of 2006, sheep farmed in some areas of the UK are still subject to inspection which may lead to them being prohibited from entering the human food chain because of contamination arising from the accident:
"Some of this radioactivity, predominantly radiocaesium-137, was deposited on certain upland areas of the UK, where sheep-farming is the primary land-use. Due to the particular chemical and physical properties of the peaty soil types present in these upland areas, the radiocaesium is still able to pass easily from soil to grass and hence accumulate in sheep. A maximum limit of 1,000 becquerels per kilogramme (Bq/kg) of radiocaesium is applied to sheep meat affected by the accident to protect consumers. This limit was introduced in the UK in 1986, based on advice from the European Commission's Article 31 group of experts. Under power provided under the Food and Environment Protection Act 1985 (FEPA), Emergency Orders have been used since 1986 to impose restrictions on the movement and sale of sheep exceeding the limit in certain parts of Cumbria, North Wales, Scotland and Northern Ireland... When the Emergency Orders were introduced in 1986, the Restricted Areas were large, covering almost 9,000 farms, and over 4 million sheep. Since 1986, the areas covered by restrictions have dramatically decreased and now cover 374 farms, or part farms, and around 200,000 sheep. This represents a reduction of over 95% since 1986, with only limited areas of Cumbria, South Western Scotland and North Wales, covered by restrictions.[8]
In Norway, the Sami people were affected by contaminated food (the reindeer had been contaminated by eating lichen, which are very sensitive to radioactivity).[9]
Effect on the natural world
According to reports from Soviet scientists at the First International Conference on the Biological and Radiological Aspects of the Chernobyl Accident (September 1990), fallout levels in the 10 km zone around the plant were as high as 4.81 GBq/m². The so-called "Red Forest" of pine trees [4][5], previously known as Worm Wood Forest and located immediately behind the reactor complex, lay within the 10 km zone and was killed off by heavy radioactive fallout. The forest is so named because in the days following the disaster the trees appeared to have a deep red hue as they died due to extremely heavy radioactive fallout. In the post-disaster cleanup operations, a majority of the 4 km² forest was bulldozed and buried. The site of the Red Forest remains one of the most contaminated areas in the world.
In recent years there have been many anecdotal reports suggesting the zone may be a fertile habitat for wildlife.[10] For example in the 1996 BBC Horizon documentary 'Inside Chernobyl's Sarcophagus', birds are seen flying in and out of large holes in the structure itself. Other casual observations suggest biodiversity around the massive radiation spill has increased due to the removal of human influence (see the first hand account of the wildlife preserve). Storks, wolves, beavers, and eagles have been reported in the area.[10] However none of these reports are scientific studies.[10] The first controlled scientific study was by biologist Timothy A. Mousseau of the University of South Carolina in 2007 on the subject of birds[11]. Wearing a protective suit, Dr. Moller conducted simple bird counts throughout the zone. He found both the number of species and abundance of individual birds declined with increasing radiation levels. For example, the most contaminated sites had about two-thirds fewer birds than those with normal levels of radiation.[10] Chernobyl is far from a wildlife paradise, at least for birds, the contamination appears to have had a major effect, "This was a big surprise to us," Dr. Mousseau said. "We had no idea of the impact."[10]
It is unknown whether fallout contamination will have any long-term adverse effect on the flora and fauna of the region, as plants and animals have significantly different and varying radiologic tolerance compared with humans. Some birds are reported with stunted tail feathers (which interferes with breeding). There are reports of mutations in some plants in the area, leading to unsubstantiated tales of a "forest of wonders" containing many strangely mutated plants. Specifically, some trees have weirdly twisted branches that do not reach for the sky.[12]
The September 2005 IAEA report and criticisms
In September 2005, a controversial report by the Chernobyl Forum, comprising a number of agencies including the International Atomic Energy Agency (IAEA), the World Health Organization (WHO), United Nations bodies and the Governments of Belarus, the Russian Federation and Ukraine, put the total predicted number of deaths due to the disaster at 4,000 (of which 2,200 deaths are expected to be in the ranks of 200,000 liquidators). This predicted death toll includes the 47 workers who died of acute radiation syndrome as a direct result of radiation from the disaster, nine children who died from thyroid cancer and an estimated 3,940 people who could die from cancer as a result of exposure to radiation. The report also stated that, apart from a 30 kilometre area around the site and a few restricted lakes and forests, radiation levels had returned to acceptable levels.[13][14]
The methodology of the Chernobyl Forum report has been disputed by Greenpeace, the International Physicians for Prevention of Nuclear Warfare (IPPNW), Elisabeth Cardis of the International Agency for Research on Cancer[15], Dr. Michel Fernex, retired medical doctor from the WHO and Dr. Christopher Busby (Green Audit). The main criticism has been with regard to the restriction of the Forum's study to Belarus, Ukraine and Russia. Furthermore, it only studied the case of 200,000 people involved in the cleanup, and the 400,000 most directly affected by the released radiation. German Green Party Member of the European Parliament Rebecca Harms, commissioned a report on Chernobyl in 2006 (TORCH ,The Other Report on Chernobyl). The 2006 TORCH report claimed that:
"In terms of their surface areas, Belarus (22% of its land area) and Austria (13%) were most affected by higher levels of contamination. Other countries were seriously affected; for example, more than 5% of Ukraine, Finland and Sweden were contaminated to high levels (> 40,000 Bq/m² caesium-137). More than 80% of Moldova, the European part of Turkey, Slovenia, Switzerland, Austria and the Slovak Republic were contaminated to lower levels (> 4,000 Bq/m² caesium-137). And 44% of Germany and 34% of the UK were similarly affected." (See map of radioactive distribution of Caesium-137 in Europe)[5]
While the IAEA/WHO and UNSCEAR considered areas with exposure greater than 40,000 Bq/m², the TORCH report also included areas contaminated with more than 4,000 Bq/m² of Cs-137.
The TORCH 2006 report "estimated that more than half the iodine-131 from Chernobyl [which increases the risk of thyroid cancer] was deposited outside the former Soviet Union. Possible increases in thyroid cancer have been reported in the Czech Republic and the UK, but more research is needed to evaluate thyroid cancer incidences in Western Europe". It predicted about 30,000 to 60,000 excess cancer deaths, 7 to 15 Times greater than the figure of 4,000 in the IAEA press release; warned that predictions of excess cancer deaths strongly depend on the risk factor used; and predicted excess cases of thyroid cancer range between 18,000 and 66,000 in Belarus alone depending on the risk projection model.[16]
Another study claims possible heightened mortality in Sweden.[17]
Greenpeace quoted a 1998 WHO study, which counted 212 dead from only 72,000 liquidators. The environmental NGO estimated a total death toll of 93,000 but cite in their report that "The most recently published figures indicate that in Belarus, Russia and the Ukraine alone the disaster could have resulted in an estimated 200,000 additional deaths in the period between 1990 and 2004." In its report, Greenpeace suggested there will be 270,000 cases of cancer alone attributable to Chernobyl fallout, and that 93,000 of these will probably be fatal (compare with the IAEA 2005 report which claimed that "99% of thyroid cancers wouldn't be lethal". Blake Lee-Harwood, campaigns director at Greenpeace, declared that cancer was likely to be the cause of less than half of the final fatalities; "intestinal problems, heart and circulation problems, respiratory problems, endocrine problems, and particularly effects on the immune system," are also concerns. Lee-Harwood alleged that the nuclear industry had a "vested interest in playing down Chernobyl because it's an embarrassment to them". Responding to these criticisms, the WHO spokesman Gregory Hartl explained that "the Greenpeace report is looking at all of Europe, whereas our report looks at only the most affected areas of the three most affected countries,".[18] Though it should be noted that Greenpeace is decidedly anti-nuclear power in its stance. [6]
According to the Union Chernobyl, the main organization of liquidators, 10% of the 600,000 liquidators are now dead, and 165,000 disabled.[19]
According to a April 2006 report by the International Physicians for Prevention of Nuclear Warfare (IPPNW), entitled "Chernobyl's consequences on health", more than 10,000 people are today affected by thyroid cancer and 50,000 cases are expected. In Europe, the IPPNW claims that 10,000 deformities have been observed in newborns because of Chernobyl's radioactive discharge, with 5,000 deaths among newborn children. They also claim that several hundreds of thousands of the people who worked on the site after the disaster are now sick because of radiation, and tens of thousands are dead.[19]
Controversy over human health effects
The majority of premature deaths caused by Chernobyl are expected to be the result of cancers and other diseases induced by radiation in the decades after the event. This will be the result of a large population (some studies have considered the entire population of Europe) exposed to relatively low doses of radiation increasing the risk of cancer across that population. It will be impossible to attribute specific deaths to Chernobyl, and many estimates indicate that the rate of excess deaths will be so small as to be statistically undetectable, even if the ultimate number of extra premature deaths is large. Furthermore, interpretations of the current health state of exposed populations vary. Therefore, estimates of the ultimate human impact of the disaster have relied on numerical models of the effects of radiation on health. Furthermore, the effects of low-level radiation on human health are not well understood, and so the models used, notably the linear no threshold model, are open to question.
Given these factors, several different studies of Chernobyl's health effects have come up with substantially different conclusions and are the subject of considerable scientific and political controversy. The following section presents some of the major studies on this topic. The Chernobyl Forum report
In September 2005, a draft summary report by the Chernobyl Forum, comprising a number of UN agencies including the International Atomic Energy Agency (IAEA), the World Health Organization (WHO), the United Nations Development Programme (UNDP), other UN bodies and the Governments of Belarus, the Russian Federation and Ukraine, put the total predicted number of deaths due to the accident at 4000.[20] This death toll predicted by the WHO included the 47 workers who died of acute radiation syndrome as a direct result of radiation from the disaster and nine children who died from thyroid cancer, in the estimated 4000 excess cancer deaths expected among the 600,000 with the highest levels of exposure.[21] The full version of the WHO health effects report adopted by the UN, published in April 2006, included the prediction of 5000 additional fatalities from significantly contaminated areas in Belarus, Russia and Ukraine and predicted that, in total, 9000 will die from cancer among the 6.9 million most-exposed Soviet citizens.[15] This report is not free of controversy, and has been accused of trying to minimize the consequences of the accident.[22]
The TORCH report
Main article: TORCH report
In 2006 German Green Party Member of the European Parliament Rebecca Harms, commissioned two UK scientists for an alternate report (TORCH, The Other Report on CHernobyl) in response to the UN report. The report included areas not covered by the Chernobyl forum report, and also lower radiation doses. It predicted about 30,000 to 60,000 excess cancer deaths and warned that predictions of excess cancer deaths strongly depend on the risk factor used, and urged more research stating that large uncertainties made it difficult to properly assess the full scale of the disaster.[5]
Greenpeace claimed contradictions in the Chernobyl Forum reports, quoting a 1998 WHO study referenced in the 2005 report, which projected 212 dead from 72,000 liquidators.[23] In its report, Greenpeace suggested there will be 270,000 cases of cancer attributable to Chernobyl fallout, and that 93,000 of these will probably be fatal, but state in their report that "The most recently published figures indicate that in Belarus, Russia and Ukraine alone the accident could have resulted in an estimated 200,000 additional deaths in the period between 1990 and 2004." Blake Lee-Harwood, campaigns director at Greenpeace, believes that cancer was likely to be the cause of less than half of the final fatalities and that "intestinal problems, heart and circulation problems, respiratory problems, endocrine problems, and particularly effects on the immune system," will also cause fatalities. However, concern has been expressed about the methods used in compiling the Greenpeace report.[24][22]
The April 2006 IPPNW report
According to an April 2006 report by the German affiliate of the International Physicians for Prevention of Nuclear Warfare (IPPNW), entitled "Health Effects of Chernobyl", more than 10,000 people are today affected by thyroid cancer and 50,000 cases are expected. The report projected tens of thousands dead among the liquidators. In Europe, it alleges that 10,000 deformities have been observed in newborns because of Chernobyl's radioactive discharge, with 5000 deaths among newborn children. They also claimed that several hundreds of thousands of the people who worked on the site after the accident are now sick because of radiation, and tens of thousands are dead.[25]
Other studies and claims
The Ukrainian Health Minister claimed in 2006 that more than 2.4 million Ukrainians, including 428,000 children, suffer from health problems related to the catastrophe.[4] Psychological after-effects, as the 2006 UN report pointed out, have also had adverse effects on internally displaced persons.
Another study alleged heightened mortality in Sweden.[26][27]
One study reports increased levels of birth defects in Germany and Finland in the wake of the accident.[28]
A change in the human sex ratio at birth in several European countries has been linked to Chernobyl fallout.[29]
In the Czech Republic, thyroid cancer has increased significantly after Chernobyl.[30]
A report from the European Committee on Radiation Risk (a body sponsored by the European Green Party) claims that the World Health Organization, together with most other international and national health bodies, has marginalized or ignored, perhaps purposely, the terrible consequences of the Chernobyl fallout to protect the vested interests of the nuclear industry.[31]
The Abstract of the April 2006 International Agency for Research on Cancer report Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident stated "It is unlikely that the cancer burden from the largest radiological accident to date could be detected by monitoring national cancer statistics. Indeed, results of analyses of time trends in cancer incidence and mortality in Europe do not, at present, indicate any increase in cancer rates – other than of thyroid cancer in the most contaminated regions – that can be clearly attributed to radiation from the Chernobyl accident."[32][33] However, while undetectable, they estimate, based on the linear no threshold model of cancer effects, that 16,000 excess cancer deaths could be expected from the effects of the Chernobyl accident up to 2065. Their estimates have very wide 95% confidence intervals from 6,700 deaths to 38,000.[34]
The application of the linear no threshold model to predict deaths from low levels of exposure to radiation was disputed in a BBC (British Broadcasting Corporation) Horizon documentary, broadcast on 13 July 2006. It offered statistical evidence to suggest that there is an exposure threshold of about 200 millisieverts, below which there is no increase in radiation-induced disease. Indeed it went further, reporting research from Professor Ron Chesser of Texas Tech University, which suggests that low exposures to radiation can have a protective effect. The program interviewed scientists who believe that the increase in thyroid cancer in the immediate area of the explosion had been over-recorded, and predicted that the estimates for widespread deaths in the long term would be proved wrong. It noted the view of the World Health Organization scientist Dr Mike Rapacholi that, while most cancers can take decades to manifest, leukemia manifests within a decade or so: none of the previously expected peak of leukemia deaths has been found, and none is now expected. Identifying the need to balance the "fear response" in the public's reaction to radiation, the program quoted Dr Peter Boyle, director of the IARC: "Tobacco smoking will cause several thousand times more cancers in the [European] population."[35]
Professor Wade Allison of Oxford University (a lecturer in medical physics and particle physics) gave a talk on ionising radiation 24 Nov 2006 in which he gave an approximate figure of 81 cancer deaths from Chernobyl (excluding 28 cases from acute radiation exposure and the thyroid cancer deaths which he regards as "avoidable"). In a closely reasoned argument using statistics from therapeutic radiation, exposure to elevated natural radiation (the presence of radon gas in homes) and the diseases of Hiroshima and Nagasaki survivors he demonstrated that the linear no-threshold model should not be applied to low-level exposure in humans, as it ignores the well-known natural repair mechanisms of the body.[36][37]
French legal action
Since March 2001 400 lawsuits have been filed in France against "X" by the French Association of Thyroid-affected People, including 200 in April 2006. These persons are affected by thyroid cancer or goitres, and have filed lawsuits alleging that the French government, at the time led by Prime Minister Jacques Chirac, had not adequately informed the population of the risks linked to the Chernobyl radioactive fallout. The complaint contrasts the health protection measures put in place in nearby countries (warning against consumption of green vegetables or milk by children and pregnant women) with the relatively high contamination suffered by the east of France and Corsica. Although the 2006 study by the French Institute of Radioprotection and Nuclear Safety said that no clear link could be found between Chernobyl and the increase of thyroid cancers in France, it also stated that papillary thyroid cancer had tripled in the following years.[38]
Comparisons to other radioactivity releases
Main article: Chernobyl compared to other radioactivity releases
^ mSv (milisievert) is a unit of radiation effect in living things, the dose in terms of energy alone is in Gy (Grays) but after a quaility factor is applied (different forms of radiation have different abilities to cause harm to living things) the dose in Sv is calculated. Sv is the modern SI unit which is a replacement of the cgs system unit rem. 1000 mSv is equal to 1 Sv which is equal to 100 rem. It is commonly thought that a 1 Sv whole body dose of radiation has a 5% chance of causing cancer
^ K. Muck, G. Prohl, I. Likhtarev, L. Kovgan, V. Golikov and J. Zeger, Health Physics, 2002, 82(2), 157-172
^ a b (French) "Tchernobyl, 20 ans après", RFI, April 24, 2006. Retrieved on April 24, 2006.
^ a b c d TORCH report executive summary. European Greens and UK scientists Ian Fairlie PhD and David Sumner (April 2006). Retrieved on April 21, 2006. (page 3)
^ (French) Map of radioactive cloud with flash animation, French IRSN (official Institut de Radioprotection et de Sûreté Nucléaire — Institute of Radioprotection and Nuclear Safety) Les leçons de Tchernobyl. IRSN. Retrieved on 2006-12-16.
^ Chapter IV: Dose estimates, Nuclear Energy Agency, 2002
^ Post-Chernobyl Monitoring and Controls Survey Report. UK Food Standards Agency. Retrieved on April 19, 2006.
^ "Chernobyl fallout: internal doses to the Norwegian population and the effect of dietary advice", Strand P, Selnaes TD, Boe E, Harbitz O, Andersson-Sorlie A., National Institute of Radiation Hygiene, Osteras, Norway
^ a b c d e "Did Chernobyl Leave an Eden for Wildlife?", by Henry Fountain, New York Times, August 28, 2007
^ "Elevated frequency of abnormalities in barn swallows from Chernobyl", in Biology Letters, Volume 3, Number 4 / August 22, 2007
^ "Wildlife defies Chernobyl radiation", BBC News, April 20, 2006.
^ IAEA Report. In Focus: Chernobyl. Retrieved on 2006-03-29.
^ For full coverage see the IAEA Focus Page and joint IAEA/WHO/UNDP press release Chernobyl: The True Scale of the Accident, IAEA/WHO/UNDP, September 5, 2005 (pdf file)
^ a b . "Special Report: Counting the dead", Nature, April 19, 2006. Retrieved on April 21, 2006.
^ TORCH report executive summary, op.cit., p.4
^ Chernobyl 'caused Sweden cancers', BBC News, November 20, 2004
^ "Greenpeace rejects Chernobyl toll", BBC News, April 18, 2006.
^ a b c (French) "Selon un rapport indépendant, les chiffres de l'ONU sur les victimes de Tchernobyl ont été sous-estimés (According to an independent report, UN numbers on Chernobyl's victims has been underestimated)", Le Monde, April 7, 2006. and see also "'On n'a pas fini d'entendre parler de Tchernobyl', interview with Angelika Claussen, head of the German section of the IPPNW", Arte, April 13, 2006.
^ For full coverage see the IAEA Focus Page (op.cit.) and joint IAEA/WHO/UNDP September 5, 2005 press release Chernobyl: The True Scale of the Accident
^ a b Spiegel, The Chernobyl body count controversy. In Focus: Chernobyl. Retrieved on 2006-08-25.
^ WHO Chernobyl report 2006 pdf
^ Wall Street Journal, 27 April 2006
^ 20 years after Chernobyl – The ongoing health effects. IPPNW (April , 2006). Retrieved on 2006-04-24.
^ Increase of regional total cancer incidence in north Sweden due to the Chernobyl accident?
^ Scherb, Hagen; Weigelt, Eveline. Congenital Malformation and Stillbirth in Germany and Europe Before and After the Chernobyl Nuclear Power Plant Accident (PDF).
^ Scherb, Hagen; Voigt, Kristina. Trends in the human sex odds at birth in Europe and the Chernobyl Nuclear Power Plant accident (HTML).
^ Murbeth, S; Rousarova M, Scherb H, Lengfelder E. Thyroid cancer has increased in the adult populations of countries moderately affected by Chernobyl fallout (PDF).
^ Eds Busby, C C and Yablokov, A V (2006): Chernobyl: 20 Years On. Green Audit Press, Aberystwyth, UK. ISBN 1-897761-25-2
^ Abstract of April 2006 IARC report 'Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident'
^ IARC Press release on the report 'Estimates of the cancer burden in Europe from radioactive fallout from the Chernobyl accident'
^ Briefing document: Cancer burden in Europe following Chernobyl
^ "Inside Chernobyl's Sarcophagus" (13 July 1996), Horizon, BBC.
^ Allison, Wade (24 November 2006). How dangerous is ionising radiation?.
^ Allison, Wade (2006). "The safety of nuclear radiation; a careful re-examination for a world facing climate change". Physics Department of Oxford University. Retrieved on 2007-07-30.
^ (French) "Nouvelles plaintes de malades français après Tchernobyl", RFI, 2006-04-26. Retrieved on 2006-04-26. (includes Audio files, with an interview with Chantal Loire, president of the French Association of Thyroid-Affected People, as well as interviews with member of the CRIIRAD
Yuri Bandazhevsky, a Belarusian scientist imprisoned from 2001 to 2005 after his publication of a report critical of the official investigation on the consequences of the Chernobyl disaster
Acute radiation syndrome
Fission products, a more complete description of the radioactive byproducts of nuclear reactors
Bellesrad
Red Forest
Three Mile Island accident
Chernobyl2020
Chernobyl compared to other radioactivity releases
Chernobyl Heart
Chernobyl in the popular consciousness
Chernobyl Shelter Fund
Liquidator (Chernobyl)
Chernobyl Children's Project International
List of Chernobyl-related articles
Category: Radiation health effects
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Chernobyl_disaster_effects". A list of authors is available in Wikipedia.
About bionity.com
Read what you need to know about our industry portal bionity.com.
About LUMITOS
Find out more about the company LUMITOS and our team.
Advertise with LUMITOS
Find out how LUMITOS supports you with online marketing.
The LUMITOS industry portals
https://www.bionity.com/en/encyclopedia/Chernobyl_disaster_effects.html
© 1997-2019 LUMITOS AG
Determination of 4 product properties in less than 20 sec
COMPANIES & INSTITUTIONS
Place your Job Ad
Your browser is not current. Microsoft Internet Explorer 6.0 does not support some functions on Chemie.DE
Your browser does not support JavaScript. To use all the functions on Chemie.DE please activate JavaScript.


text:
Baker Hughes Collaborates with C3 AI, Accenture, and Microsoft on Industrial Asset Management Solutions
HOUSTON, Tex. and REDWOOD CITY, Calif. — March 22, 2022 — Energy technology company Baker Hughes (NASDAQ: BKR) is collaborating with C3 AI (NYSE: AI), Accenture (NYSE: ACN) and Microsoft on industrial asset management (IAM) solutions for clients in the energy and industrial sectors.
The collaboration will focus on creating and deploying Baker Hughes IAM solutions that use digital technologies to help improve the safety, efficiency, and emissions profile of industrial machines, field equipment, and other physical assets. Applying their individual strengths, the four companies will collaborate on Baker Hughes IAM capabilities that help optimize plant equipment, operational processes, and business operations through improved uptime, increased operational flexibility, capital planning, and energy efficiency management.
The solutions will be designed for industries including oil and gas; renewable energy and thermal power generation; metals and mining; chemicals; and pulp and paper.
Baker Hughes, C3 AI, Accenture and Microsoft will also explore collaborating on solutions that help achieve net-zero carbon emissions and decarbonize energy and industrial sectors, including emissions management.
"This collaboration accelerates our growth strategy to provide differentiated IAM solutions that enhance our customer's industrial operations by optimizing the performance of industrial equipment and processes," said Lorenzo Simonelli, Baker Hughes chairman and CEO. "IAM connects industrial data to domain-specific insights for improved efficiencies and lowered energy use and emissions. We see this as an important step to support the industry's net-zero targets."
Baker Hughes, C3 AI, Accenture and Microsoft have a history of strategic collaboration, and each company brings specific expertise to accelerate IAM solution development for energy and industrial applications. Baker Hughes will provide domain-specific digital expertise and technology for industrial customers, including leading condition-monitoring software for mission critical machinery, industrial asset strategy advisors, proven machine and equipment edge sensor and related controls capabilities, enterprise AI capabilities from the BakerHughesC3.ai alliance for oil and gas and industrial applications, and proprietary original equipment manufacturer (OEM) analytics. Baker Hughes' IAM portfolio also includes the recent acquisition of ARMS Reliability and a strategic alliance with Augury.
C3 AI will provide a flexible artificial intelligence (AI) application development platform that complements Baker Hughes technologies as well as extensive experience developing and deploying applications at scale for a wide range of equipment used across industries.
Accenture will help drive product innovation, design and development and provide strategic support and systems integration at scale, drawing on its experience to transform asset management across industries to help improve profitability and reduce risk.
Microsoft will provide secure cloud infrastructure for big data, advanced Microsoft Azure services including AI, Internet of Things (IoT), high performance computing (HPC) as well as modern work and business applications.
"This is an important effort, and we're excited to participate in providing the core Enterprise AI technology," said C3 AI Chairman and CEO Thomas M. Siebel. "Enterprise AI software is critical for increasing performance and ROI from industrial assets management solutions."
"Through this unique collaboration, we are helping companies embed intelligence across their operations to increase performance and safety, advance decarbonization goals, and drive greater innovation and competitiveness," said Julie Sweet, chair and CEO of Accenture.
"Together, we have a tremendous opportunity to deliver cloud-based technologies across customers' industrial operations that enable them to reduce costs and increase efficiencies while advancing their net zero goals," said Judson Althoff, Microsoft's executive vice president and Chief Commercial Officer.
About Baker Hughes
Baker Hughes (NYSE: BKR) is an energy technology company that provides solutions to energy and industrial customers worldwide. Built on a century of experience and with operations in over 120 countries, our innovative technologies and services are taking energy forward – making it safer, cleaner, and more efficient for people and the planet. Visit us at bakerhughes.com.
Baker Hughes Media Relations
Ashley Nelson
Ashley.Nelson1@bakerhughes.com
Jud Bailey
investor.relations@bakerhughes.com
About C3.ai, Inc.
C3 AI is the Enterprise AI application software company. C3 AI delivers a family of fully integrated products including the C3 AI Suite, an end-to-end platform for developing, deploying, and operating enterprise AI applications and C3 AI Applications, a portfolio of industry-specific SaaS enterprise AI applications that enable the digital transformation of organizations globally.
C3 AI Public Relations
Lisa Kennedy
pr@c3.ai
ir@c3.ai
Accenture is a global professional services company with leading capabilities in digital, cloud and security. Combining unmatched experience and specialized skills across more than 40 industries, we offer Strategy and Consulting, Interactive, Technology and Operations services — all powered by the world's largest network of Advanced Technology and Intelligent Operations centers. Our 674,000 people deliver on the promise of technology and human ingenuity every day, serving clients in more than 120 countries. We embrace the power of change to create value and shared success for our clients, people, shareholders, partners and communities. Visit us at accenture.com
Accenture Media Relations
Guy Cantwell
guy.cantwell@accenture.com
C3 AI CEO Tom Siebel says precision health to be the largest commercial application of AI
Without AI, we won't meet ESG goals and address climate change
Royal Marines General Sir Gordon Messenger Joins C3 AI Advisory Board

redpajama_set_name: RedPajamaCommonCrawl


The second ground-breaking Power to the Pixel took place at the heart of the Times BFI 52nd London Film Festival.
Power to the Pixel brought together the leading innovators, filmmakers and entrepreneurs who are changing the way film and media is financed, created and reaches audiences.
London 2008 kicked off with a cutting-edge conference which was webcast live to an additional 10,000 'virtual' audience members worldwide.
The workshop labs and meetings with the experts SOLD OUT weeks in advance.
Four leading international filmmakers presented their cross-media film projects to representatives from companies including Babelgum, Sony Computer Entertainment, BBC, Arts Council England, UK Film Council, MySpace, Amazon at the Project Forum launch, a pre-cursor to 2009's new marketplace, The Pixel Pitch.
In all, 32 leading international experts shared their knowledge and expertise with Power to the Pixel's delegates over a jam-packed two days. You can watch the videos online.


The exciting photo on top, is section of Multi-Functional Treadmill Desk IKEA piece of writing which is arranged within Home Decoration, mini treadmill, nordic treadmill, small treadmill and posted at June 6th, 2018 02:14:03 AM by Ignazio. We always effort to show a picture with HD resolution or at least with perfect images. Thank you for visiting.
Treadmill desk IKEAcould be bought from different IKEA stores in the furniture section. This is one of the most innovative breakthroughs especially it would provide you with an exercise space while you would be able to do your work on your laptop in front of you with the desk that is attached to it. Most people when they work, sometime they forget to stop and take time for their exercise routine. This particular type of mixture between a treadmill and a desk would provide you with both at the same time. There are many models and designs that you could choose from, but before you are thinking of buying one, you would want to prepare the sufficient place to place it at.
Treadmill desk IKEA would be able to help you in becoming healthier without having to leave your work in doing so. It is definitely not good for you to always be sitting down while you are doing your work especially when you are doing it for hours every single day without doing much movement and could make your body susceptible to diseases. The table is the perfect solution for people that are too busy doing their job and forgetting other important things in life such as sports. Other than this table can assist you with completing the work that you need to do, it could also help you to be more relaxed while doing your exercise because you could watch some video or TV shows from the monitor that could be placed on the desk too.
Treadmill desk IKEA is just the perfect tool for people that are always busy with their daily routines of work and more work. This way they could still exercise and move around without having to stay at one place and not moving for hours, while still managing to not abandon their work in the process. The shape of the design could also be customized with what you want and need. Choose some simpler model for easier use inside your home and office space.


The play is bathed into the work of Lewis Caroll, Alice's Adventures in Wonderland and Through the Looking Glass. The play challenges the concept of identity itself and tackles issues such as obsessing over time, the rules of logic, and the absurd. The rules of the game unveil alongside the main narrative: the audience understands progressively that they are Alice, and that they must, just like Lewis Caroll's heroine, engage with the characters they meet. The journey becomes a rite of passage, bound to lead to a final crowning.
Alice, The Virtual Reality Play is a complete VR experience which immerses the audience into a virtual scenery and allows them to interact physically in real time with characters and objects. It follows the lead of the immersive theatre, and it takes the status of the spectator to another level: the audience is brought to the stage and they become actors, whose decisions and actions participate in building the narrative and the visual universe of the play.
Showcased in the Cannes Film Festival in May 2017, the experience is now touring international festivals and events.


text:
Sofia Richie got close to Kylie Jenner after Jordyn Woods drama
International / 30 July 2019, 12:30pm / Bang Showbiz
Sofia Richie and Kylie Jenner. Picture: Instagram
Sofia Richie helped Kylie Jenner cope after her feud with Jordyn Woods, and the pair now have an "irreplaceable bond".
The 21-year-old lip kit mogul fell out with her former best friend after she kissed Tristan Thompson at a party in February, while he was still in a relationship with Kylie's half-sister Khloe Kardashian, with whom he has 15-month-old daughter True.
And now, sources say Kylie new friendship with Sofia - who is dating Scott Disick, the ex-boyfriend of Kourtney Kardashian - was forged after the 20-year-old model helped her through the "emotional rollercoaster" that followed Jordyn and Tristan's scandal.
One insider said: "Sofia really helped Kylie through the emotional roller coaster during the Jordyn situation. She was really there for her and took her side through everything. The situation with Jordyn made them closer."
The "Keeping Up with the Kardashians" star is also said to "trust" Sofia around her 17-month-old daughter Stormi, which has created an "irreplaceable bond" between the two pals.
The source added: "Kylie also trusts Sofia around Stormi, which is very important to her. Sofia has been around since Stormi was born and Kylie feels comfortable with having her around her child after getting to know her better. They have now formed an irreplaceable bond."
Now, Kylie and Sofia hang out whenever they can, and the source insists they love having "girls' nights" at home or on the town.
They said: "Kylie loves how fun Sofia is and has been inviting her over to her house more often to hang just the two of them. They love staying home and watching movies and cooking together while hanging with Stormi. Kylie knows whenever she wants a girls' night out on the town, she can always count on Sofia for a good time."
The new friendship is even a hit with Kourtney - who has Mason, nine, Penelope, seven, and Reign, four, with Scott - as she too is on good terms with Sofia.
Speaking to E! News, the source said: "Kourtney is thrilled that Kylie has found a bond with Sofia. She thinks it's great for Kylie and loves that everyone can get along and spend time together. She has seen firsthand how much of a support system Sofia has been for Kylie, and it makes Kourtney feel even better about her dynamic with Sofia as well. There is no more awkwardness or tension like there was a year ago."
Scott Disick happy about Sofia Richie and Kylie Jenner's friendship
Kylie Jenner and Sofia Richie are 'closer than ever'
Kylie Jenner keeping her friends 'very close' after Jordyn Woods fallout


text:
Home Opinion 4th of July: ...
4th of July: Are we the land of the free, land of the brave?
BY ELPIDIO R. ESTIOKO
The Catholic Church somehow had its Bible readings lately coinciding with the 4th of July.
Last Sunday's 2nd reading from the Holy Scriptures according to the Galatians, talks of being free: "When Christ freed us, he meant us to remain free. Stand firm, therefore, and do not submit again to the yoke of slavery…"
Last Sunday was my first official act as a Lector for the St. Elizabeth Catholic Church in Milpitas. Thanks to mass coordinator Tess Santos who officially scheduled me to be one of the lectors of the church's Sunday 6:00 p.m. mass. Fr. Andy, who just came back for a 6-month sabbatical leave and one-month stay in the Philippines, officiated the Sunday mass.
Was this a coincidence? Whatever it is, it was likened to the original 13 US colonies from Great Britain setting themselves free from the British regime. In their Declaration of Independence, it was high time for them to oppose the oppressive rule of the British and set themselves free!
July 4 is Independence Day of the United States which was also referred to as the 4th of July. It is a federal holiday commemorating the adoption of the Declaration of Independence on July 4, 1776, by the Continental Congress declaring that the 13 American colonies regarded themselves as a free nation — the United States of America (USA) – and no longer part of the British Empire… "And were now united, free, and independent states."
The 13 colonies' vision to be free should make the present United States of America (USA) free, united and independent country as the leader of the world. The framers of the Declaration of Independence and the Catholic Church hierarchy's 2nd reading from the Galatians setting us free, should remind us of our declaration to be "the land of the free and the land of the brave." They both complement each other in reminding us of our obligation as citizens of the United States.
Of course, the nation celebrated it with a bang! It is actually associated with fireworks, parade, meet and greet, barbecue, carnivals, fairs picnics, playing golf, concerts, baseball games, family reunions, and political speeches and ceremonies, in addition to various other public and private events celebrating the history, government, and traditions of the United States.
On July 4, the Philippines used to celebrate it too as its Independence Day, which date was later moved to its original Independence Day declaration of June 12, approved by the Philippine government on August 4, 1964. The 4th of July became US-Philippine Friendship Day.
Milpitas celebrated the 4th of July Independence Day 2019 with its annual pool party, concert and fireworks show with a theme: "Waving the Red, White & Blue." The Pool Party was from 1-4 pm, then celebrated it with an evening concert and fireworks show "Red White & Boom" Concert and Fireworks Show. The fireworks were opened to the public and held at Milpitas Sports Center at 1325 E. Calaveras Blvd.
Ruby General, the city's marketing assistant, said "On average, the city of Milpitas hosts 15,000 people at the July 4th celebration." The city's day-long celebration began with a pool party and ended with fireworks.
Meanwhile, several Milpitas streets were modified and closed to control traffic during and after the event to accommodate the crowds. Additional police officers were fielded that assisted with the traffic that increased on surrounding streets that extended up to 11 p.m. in neighborhoods surrounding the sports center.
In San Jose, members of the Boy Scout Troop 390 carried a large flag during the Rose, White and Blue Parade which started at 10 a.m. with marching bands and Rotary-sponsored Centennial Fireworks and co-host San Jose Giants.
In school, we asked our students to do arts & crafts, made greeting cards, and engaged them in drawings in connection with the 4th of July. Other students did crossword puzzles, surfed the net, and made Power Point presentations. The students became creative and innovative and they were happy about their creations. It was an interactive activity that kept them engaged and busy while learning the facts and figures about the 4th of July.
Well, at home, my wife Delia prepared food on the table to celebrate the 4th of July with our Jacksonville, Florida granddaughter-visitors Kayla and Bibay (daughters of my son Jojo and wife Alvi). They are on their summer break from school joining our daughter Tweety and her husband Jonathan from Hawaii who are also vacationing with us here with their siblings May, Jayson and Paul. Our daughter May surprised us by picking them up in Florida and bringing them here for their summer vacation. It was a surprise for us considering that my daughter told us she will be attending a two-day conference in Napa Valley when in fact she flew to Florida to pick up the two. Later at the end of July, Jojo and Alvi will be joining us for a two-week roadside trip to Las Vegas, Los Angeles, Disneyland, Hertz Castle, Six Flags Marine World, and other tourist spots in adjoining cities as part of the family's summer escapade.
So, are we the land of the free? The land of the brave? Let's not be dictated and overwhelmed by the latest developments going on presently in all areas around us. Let's remain to be free, as the 4th of July framers envisioned us to be! Let's remain to be free as the Galatians envisioned us to exercise our freedom to "stand firm… and do not submit again to the yoke of slavery!"
If we are… let's: "Remain free! Stay firm! If you go snapping at each other and tearing each other to pieces, you had better watch or you will destroy the whole community," the word of the Lord according to the Galatians!
(Elpidio R. Estioko was a veteran journalist in the Philippines and an award-winning journalist here in the US. For feedbacks, comments… please email author at estiokoelpidio@gmail.com).
Previous articleThe President, Sara say they will not support Paolo Duterte's run for speaker even as landslide win expected
Next articleThe fox investigates raid on the chicken coop
Watermelon month, anyone?


text:
Hull FC coach Lee Radford full of praise for 'awesome' support as area to improve highlighted
The Hull coach says the backing of the fans in the defeat to St Helens was brilliant
Hull FC's Scott Taylor scores against St Helens
Lee Radford believes Hull FC players did themselves proud defensively on their final game of the season, despite falling to a 22-6 defeat to St Helens.
The Black and Whites were ultimately denied the chance to advance into the top five, with Castleford Tigers sealing the last spot in the play-offs, but they put on a rousing performance against the League Leaders' Shield winners.
The damage was done in the first half, with a hat-trick from Tommy Makinson taking the game away from FC, despite a Scott Taylor try.
But, in the second half, Mark Percival and Regan Grace sealed what was ultimately a comfortable night for the visitors, and while Radford was proud of his side's efforts on the night in defence, he claims the game highlighted a number of areas to improve on.
"Defensively, I'm really really pleased. Offensively this last month has shown us some areas of improvements and give us some real focus for the off-season." he said.
"Obviously losing Danny Houghton (calf) was a real blow for us but it shouldn't have impacted us like it did. The fluency wasn't there, but this last month has obviously shown us where we need to improve on."
Hull FC season over as St Helens deny departing players a play-off finish
Hull FC's Mark Minichiello against St Helens
The result means Hull finish sixth, missing out on the play-offs through points difference alone, but that didn't stop the fans from cheering their side on throughout the game and Radford reserved special praise for the crowd.
"I thought it was awesome," he added. "Honestly I've had some real flak this last month and rightly so with some of the performances you expect that as a head coach.
"But I can't thank them enough for getting behind the team, the noise they made in certain periods of the game. You don't realise the impact it has on the side and I've been there and played in front of that crowd so I know you can find the extra little effort when they're as vocal as that.
"The chairman spoke about building relationships and that's something we're going to really work on."
Hull FC vs St Helens live reaction as FC's season over following defeat
Hull Live has launched a WhatsApp service dedicated to keeping you up to date with the latest Hull FC news! Click here to join and follow the instructions on your phone. Your number won't be shared with anyone else in the group. If you want more information on signing up, or if the link doesn't work, click here.
Click here for more sports news
Follow Hull FC on Facebook - Like our Facebook page to get the latest news in your feed and join in the lively discussions in the comments. Click here to give it a like!
Follow us on Twitter - For breaking Hull FC news and the latest stories, click here to follow Hull FC News on Twitter!


text:
Police: 65 George Floyd protesters arrested after curfew at Minnesota State Capitol Monday night
George Floyd protest at Minnesota State Capitol ends in arrests
Authorities made 65 arrests Monday night after protesters remained at the Minnesota State Capitol after curfew.
ST. PAUL, Minn. (FOX 9) - Dozens of people protesting the death of George Floyd were arrested at the Minnesota State Capitol Monday night.
Monday's protest started at the Governor's Mansion where thousands of people flooded Summit Avenue before the group eventually marched to the state Capitol.
The start time of St. Paul's curfew was pushed back to 10 p.m., but some demonstrators at the Capitol decided not to obey orders to go home, leading to arrests.
However, even as the demonstrators sat with their hands bound, under arrest, they chanted, "What's his name? George Floyd!" and remained mostly peaceful.
Protesters arrested at Capitol in St. Paul for curfew violation
A group of protesters were arrested at the Capitol in St. Paul Monday night for violating curfew.
The St. Paul Police Department reported at total of 65 people were arrested.
Police also said a "protester support vehicle" was towed from the Capitol grounds. It was marked as a "medic vehicle", but police said when they looked inside, they found helmets and a baseball bat wrapped in barbed wire.
Police towed a "protester support vehicle" from the Capitol grounds Monday night. It was marked as a "medic vehicle", but police said when they looked inside, they found helmets and a baseball bat wrapped in barbed wire.
From: FOX 9
Earlier in the day, a member of the Minnesota National Guard spoke to protesters at the Capitol, saying they support the group's efforts and would stay out of sight as long as things remained peaceful.
National Guardsman gives message of understanding to State Capitol protesters
State Capitol protesters were greeted by a National Guardsman who leveled with them and said he was with them as they protested the death of George Floyd.
"We're here to allow you to exercise your first amendement rights peacefully," Lt. Col. Sam Andrews told the crowd. "We'll remain on scene, but we assure that we'll hear you. To the men and women and children that came out last night to have their voices heard, we heard it. We heard it and we're going to stay back, invisible, so you can't see us."
Minnesota National Guard members at State Capitol Tuesday, June 2.
The Capitol remained surrounded by National Guard troops Tuesday morning.
On Tuesday, state lawmakers plan to talk about what they can do in the wake of the riots following Floyd's death. They have scheduled an 11 a.m. news conference to share their response.
COVID-19 in Minnesota
Minnesota reports 1,237 more COVID-19 cases, 34 deaths Wednesday
All 6,000 vaccine slots this week for Minnesotans ages 65+ filled
Minneapolis School Board moves forward with in-person learning for pre-K through fifth grade
Minnesota's COVID-19 vaccine online appointment portal overloaded on 1st day
State calls for Floyd trials to be rejoined, held this summer amid COVID-19 concerns
'He saved my life': Family fights to keep K-9 with retired Corcoran police officer
Twin Cities has yet to see a subzero temperature in January


text:
June 2015, Vol 4, No 3
The RET Oncogene in Non–Small Cell Lung Cancer: Review of the Current Literature and Directions for the Future
Rebecca A. Shatsky, MD; Lyudmila Bazhenova, MD
Despite recent advances, lung cancer remains the leading cause of cancer-related death worldwide.1 In the past decade, the treatment of non–small cell lung cancer (NSCLC), which was once a disease with exceedingly few treatment options and historically poor outcomes, has begun to transform. The discovery of targetable cancer-driving mutations has added a promising new dimension to the field, which was once confined to the use of cytotoxic agents that often induced minimal responses that were frequently short-lived. The discovery of the EML4 fusion gene and the success of the ALK mutant–targeting tyrosine kinase inhibitor (TKI) crizotinib has proved that these mutations can have serious clinical impact, and that design of new drugs targeting the mutations can potentially save many lives.2
Importantly, the oncogenic driver mutations in lung adenocarcinoma are generally mutually exclusive, so the discovery of each new oncogenic driver mutation may be helpful to a population of patients who previously were not eligible for available targeted lung cancer therapies.3-6 The list of identifiable drug targetable genetic mutations in lung cancer is growing fast, and one of the newer targets that is just beginning to be explored in human clinical trials is the RET proto-oncogene.
Biology of the Native RET Oncogene
The RET oncogene, located in the pericentromeric region of chromosome 10q11.2, was first identified and mapped in 1985 using cells transfected with human lymphoma DNA.7 RET was first identified as a receptor for the glial cell–derived neurotropic factor family of ligands, which are important for neuron signaling.8,9 RET is expressed at its highest levels during embryogenesis and has been implicated in the process of nephrogenesis, neural crest migration, as well as the maintenance of normal neuron function. RET expression decreases to much lower levels in healthy adult tissues but is still routinely expressed in neurons, parasympathetic ganglia, thyroid C cells, urogenital tract cells, and testis germ cells.10-14
Like many oncogenes, RET encodes a receptor tyrosine kinase (RTK). The RET RTK transmembrane receptor consists of 4 cadherin-like domains in its extracellular region, a calcium binding site, a transmembrane region, and an intracellular region containing the active tyrosine kinase domain.15,16 Upon binding of its ligand and coreceptor, RET autophosphorylates and in turn activates multiple downstream targets, including the RAS-MAPK-ERK1/2 and the PI3K/AKT signaling pathway.17 This leads to activation of multiple essential cell cycle activities, including signaling to induce proliferation and to promote cell survival.18
Oncogenic RET Gene
There have been multiple previously identified mutations to the RET gene implicated in cancer development. For example, germline gain-of-function mutations in RET have long been implicated in the development of multiple endocrine neoplasia, which consists of medullary thyroid cancer, pheochromocytoma, and hyperparathyroidism.19 In addition, many irradiation-induced papillary thyroid cancers contain RET gene rearrangements.20 It is estimated that RET mutations can be found in 30% to 50% of both medullary and papillary thyroid cancers.21,22 Further, germline loss-of-function mutations are now known to be responsible for Hirschsprung disease, a congenital abnormality in which neuroblasts in the developing gut fail to migrate and neural cells do not mature in the gastrointestinal tract, resulting in chronic constipation.23,24
In lung cancer, in a mechanism very similar to that of ALK gene rearrangements, or ROS1, a somatic gain-of-function mutation in RET is responsible for creating a chimeric fusion oncogene, which can then lead to malignant transformation. When the intracellular kinase encoding domain of RET is fused to one of several recently identified gene partners, a fusion gene is created that encodes a constitutively active RTK. In 2011, Ju et al reported the first identified case of adenocarcinoma of the lung containing the RET fusion RTK, RET-KIF5B, in a 33-year-old nonsmoking patient.25 In 2012, several groups independently corroborated these results, identifying multiple different RET gene rearrangements and RET fusion proteins that are expressed at high levels in certain lung adenocarcinomas.6,25-28 The most frequent rearrangement is the fusion of RET to kinesin family member 5B (KIF5B), which is created by a pericentric inversion of chromosome 10.26 This particular gene fusion appears to be unique to adenocarcinoma of the lung. However, to date, 5 fusion partners of RET have been identified in NSCLC, including KIF5B-RET, CCDC6-RET, NCO4-RET, TRIM33-RET, and, most recently, RUFY2-RET.6,25-27,29 The function of these fusion transcripts appears to be similar to ALK gene fusions in that a coiled-coil domain of the N-terminal of the fusion partner is bound to the kinase domain of RET, which allows RET to dimerize and remain constitutively activated independent of ligand binding.26,30
Rearrangements in RET are reported to be found in approximately 1% to 2% of all adenocarcinomas of the lung, but these mutations may contribute to 6% to 19% of lung adenocarcinomas in never-smokers who are "pan-negative" for other similar oncogenic driver mutations, such as EML4-ALK and ROS1.3,30,31 RET mutations are found with higher frequency in light and never-smokers, younger patients, and in patients of European and Asian descent. The histology of lung cancers harboring RET rearrangements are most commonly moderately to well-differentiated adenocarcinomas; however, there are now rare examples of cancers with adenosquamous histology positive for these mutations as well.31
Preclinical Activity of RET Inhibitors
There are currently no drugs available that selectively inhibit only the RET tyrosine kinase. However, several small-molecule multikinase inhibitors that have already been developed for other targets have been found to have preclinical RET RTK inhibitory activity; this is true for sorafenib and sunitinib, the well-studied vascular endothelial growth factor (VEGF) inhibitors that are commonly used to treat renal cell carcinoma and hepatocellular carcinoma.32,33
Several drugs already approved for use in RET-mutated medullary thyroid cancer are currently being examined for their efficacy in RET-mutated NSCLC. Vandetanib is a potent multikinase inhibitor that was approved by the FDA for the treatment of patients with medullary thyroid carcinoma in 2011.34 In 2012, vandetanib was tested by Matsubara et al in preclinical trials using a patient-derived, RET-mutated lung adenocarcinoma cell line, LC-2/ad, which contained the CCDC6-RET fusion gene. Results from this experiment were the first of its kind to reveal specifically that lung cancer cells with RET mutations were sensitive to inhibition by vandetanib and insensitive to the epidermal growth factor receptor inhibitor gefitinib.35 Suzuki et al were able to corroborate these data in vivo using xenograft models with the same LC-2/ad cell line.36 Finally, Saito et al, using xenograft mice models harboring the most common RET fusion gene in NSCLC, KIF5B-RET, were recently able to prove that vandetanib was effective in significantly reducing tumor burden.37 A second drug with RET inhibitory activity, cabozantinib, was approved for the treatment of medullary thyroid carcinoma in 2012 and is just now beginning to be examined in the setting of NSCLC.38,39
Lenvatinib is an oral multi-TKI that targets VEGF receptors 1-3, fibroblast growth factor receptors 1-3, RET, mast/stem cell growth factor receptor, and platelet-derived growth factor beta. Cell-free kinase assays suggest that lenvatinib inhibits RET kinase-expressing cell lines. A recent preclinical study by Okamoto et al using LC-2/ad lung cancer cells revealed that in vitro lenvatinib inhibited cell growth with an inhibitory concentration of 50% of 48 nM. Lenvatinib was also found to decrease the percentage of cells in S phase, suggesting that the inhibition of signaling led to arrest of the growth phase.40
Finally ponatinib, a drug currently approved for the treatment of Philadelphia chromosome–positive leukemia, has been shown in vitro by Mologni et al to inhibit signaling of both wild-type and mutant forms of RET, with inhibition of RET signaling into the low nanomolar range in cell lines harboring RET-mutated thyroid cancer cells.41,42 At the 2013 Annual Meeting of the American Association for Cancer Research, Gozgit et al presented their data comparing the potency of ponatinib at inhibiting RET in the Ba/F3 cell line engineered to express the most common NSCLC RET fusion gene KIF5B-RET with 4 other TKIs known to inhibit RET. These data are presented in Table 1.43
Clinical Activity of RET Inhibitors in Lung Cancer In Vivo
The data surrounding use of the previously described RET inhibitors in patients with NSCLC positive for RET mutations are still extremely limited. Although several drugs with multikinase-inhibiting activity including RET are now in phase 2 clinical trials (Table 2), the majority of these trials are still enrolling patients, so formal reports of results are still very sparse. There are only 2 published reports describing the outcome of patients with NSCLC with RET mutations after treatment with one of the previously described RET-inhibiting drugs. The first, by Drilon et al, is a report of the first 3 patients in their trial testing the drug cabozantinib in patients with RET mutation–positive, advanced NSCLC. The first patient described was a 41-year-old female with a novel TRIM33-RET fusion. This patient had a durable partial response, with a 66% decrease in disease burden as measured by RECIST and was still on the trial with no reported dose reductions at 20 weeks. The second patient, who was significantly older than the first (75-year-old female) also had a confirmed partial response (33% disease reduction). However, this patient suffered several dose-limiting toxicities, including grade 3 fatigue and grade 3 proteinuria, which required 2 dose reductions. Despite dose reductions, she remained progression free and continued on the trial at 16 weeks. The third patient was a 68-year-old female who suffered from grade 3 hypertension requiring dose reduction, but she ultimately had disease stabilization with progression-free survival at 8 months.44 In 2013, Gautschi et al published a report of a 58-year-old male with RET-mutated NSCLC refractory to previous chemotherapy who responded to treatment with vandetanib at a dose of 300 mg per day.45
The field of thoracic oncology has enjoyed considerable growth during the past 5 years since the discovery of oncogenic driver mutations. For the first time in history, a subset of patients with NSCLC that once had a dismal prognosis are being afforded extended survival and improved quality of life on treatment because of the discovery of new "druggable" driver mutations that allow treatment with targeted therapies such as erlotinib or crizotinib, which have fewer toxicities than standard chemotherapy. The success of these therapies has proved that for patients who harbor one of these driver mutations or fusion proteins, treatment with cytotoxic chemotherapy may not be the safest or most effective option for treatment. Previously published trials examining drugs with RET inhibitory activity (sorafenib, sunitinib, and vandetanib) in patients with NSCLC were not performed in populations selected for RET mutations. So although these drugs were previously thought to have little activity in lung cancer, it is possible they were not being tested in the right subset of patients. Whereas it is true that RET mutations are only found in a small percentage of patients with NSCLC, the benefits that RET-inhibiting drugs may have in the right patient population could be, like crizotinib in ALK-mutated patients, fairly dramatic. The results from the various phase 2 clinical trials that are limited to patients predetermined to have RET mutations appear promising and will likely be extremely informative as to whether RET will be another useful drug target to help patients with NSCLC survive longer and with a better quality of life on therapy. What is clear is that the similarities between the RET oncogene and the ALK and ROS1 oncogenes are undeniable, and given the potential benefits to a patient population with too few treatment options, it would be a logical next step to add RET to the list of mutations examined in all new NSCLC cases.
World Health Organization. Cancer fact sheets. 2015. www.who.int/mediacentre/factsheets/fs297/en/. Accessed October 28, 2014.
Kwak EL, Bong YJ, Camidge DR, et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med. 2010;363:1693-1703.
Suehara Y, Arcila M, Wang L, et al. Identification of KIF5B-RET and GOPC-ROS1 fusions in lung adenocarcinomas through a comprehensive mRNA-based screen for tyrosine kinase fusions. Clin Cancer Res. 2012;18:6599-6608.
Kris MG, Johnson BE, Berry LD, et al. Using multiplexed assays of oncogenic drivers in lung cancers to select targeted drugs. JAMA. 2014;311:1998-2006.
Pao W, Girard N. New driver mutations in non-small-cell lung cancer. Lancet Oncol. 2011;12:175-180.
Lipson D, Capelletti M, Yelensky R, et al. Identification of new ALK and RET gene fusions from colorectal and lung cancer biopsies. Nat Med. 2012;18:382-384.
Ishizaka Y, Itoh F, Tahira T, et al. Human ret proto-oncogene mapped to chromosome 10q11.2. Oncogene. 1989;4:1519-1521.
Airaksinen MS, Titievsky A, Saarma M. GDNF family neurotrophic factor signaling: four masters, one servant? Mol Cellular Neurosci. 1999;13:313-325.
Esseghir S, Todd SK, Hunt T, et al. A role for glial cell derived neurotrophic factor induced expression by inflammatory cytokines and RET/GFR alpha 1 receptor up-regulation in breast cancer. Cancer Res. 2007;67:11732-11741.
Mulligan LM. RET revisited: expanding the oncogenic portfolio. Nat Rev Cancer. 2014;14:173-186.
Tahira T, Ishizaka Y, Itoh F, et al. Characterization of ret proto-oncogene mRNAs encoding two isoforms of the protein product in a human neuroblastoma cell line. Oncogene. 1990;5:97-102.
Pachnis V, Mankoo B, Costantini F. Expression of the c-ret proto-oncogene during mouse embryogenesis. Development. 1993;119:1005-1017.
Tsuzuki T, Takahashi M, Asai N, et al. Spatial and temporal expression of the ret proto-oncogene product in embryonic, infant and adult rat tissues. Oncogene. 1995;10:191-198.
Avantaggiato V, Dathan NA, Grieco M, et al. Developmental expression of the RET protooncogene. Cell Growth Differ. 1994;5:305-311.
Takahashi M, Buma Y, Iwamoto T, et al. Cloning and expression of the ret proto-oncogene encoding a tyrosine kinase with two potential transmembrane domains. Oncogene. 1988;3:571-578.
Anders J, Kjær S, Ibáñez CF. Molecular modeling of the extracellular domain of the RET receptor tyrosine kinase reveals multiple cadherin-like domains and a calcium-binding site. J Biol Chem. 2001;276:35808-35817.
Plaza-Menacho I, van der Sluis T, Hollema H, et al. Ras/ERK1/2-mediated STAT3 Ser727 phosphorylation by familial medullary thyroid carcinoma-associated RET mutants induces full activation of STAT3 and is required for c-fos promoter activation, cell mitogenicity, and transformation. J Biol Chem. 2007;282:6415-6424.
Arighi E, Borrello MG, Sariola H. RET tyrosine kinase signaling in development and cancer. Cytokine Growth Factor Rev. 2005;16:441-467.
Mulligan LM, Kwok JB, Healey CS, et al. Germ-line mutations of the RET proto-oncogene in multiple endocrine neoplasia type 2A. Nature. 1993;363:458-460.
Donis-Keller H, Dou S, Chi D, et al. Mutations in the RET proto-oncogene are associated with MEN 2A and FMTC. Hum Mol Genet. 1993;2:851-856.
Romei C, Elisei R. RET/PTC translocations and clinico-pathological features in human papillary thyroid carcinoma. Front Endocrinol (Lausanne). 2012;3:54.
Romei C, Fugazzola L, Puxeddu E, et al. Modifications in the papillary thyroid cancer gene profile over the last 15 years. J Clin Endocrinol Metab. 2012;97:E1758-E1765.
Emison ES, McCallion AS, Kashuk CS, et al. A common sex-dependent mutation in a RET enhancer underlies Hirschsprung disease risk. Nature. 2005;434:857-863.
Seri M, Yin L, Barone V, et al. Frequency of RET mutations in long- and short-segment Hirschsprung disease. Hum Mutat. 1997;9:243-249.
Ju YS, Lee WC, Shin JY, et al. A transforming KIF5B and RET gene fusion in lung adenocarcinoma revealed from whole-genome and transcriptome sequencing. Genome Res. 2012;22:436-445.
Kohno T, Ichikawa H, Totoki Y, et al. KIF5B-RET fusions in lung adenocarcinoma. Nat Med. 2012;18:375-377.
Takeuchi K, Soda M, Togashi Y, et al. RET, ROS1 and ALK fusions in lung cancer. Nat Med. 2012;18:378-381.
Li F, Feng Y, Fang R, et al. Identification of RET gene fusion by exon array analyses in "pan-negative" lung cancer from never smokers. Cell Res. 2012;22:928-931.
Zheng Z, Liebers M, Zhelyazkova B, et al. Anchored multiplex PCR for targeted next-generation sequencing. Nat Med. 2014;20:1479-1484.
Kohno T, Tsuta K, Tsuchihara K, et al. RET fusion gene: translation to personalized lung cancer therapy. Cancer Sci. 2013;104:1396-1400.
Wang R, Hu H, Pan Y, et al. RET fusions define a unique molecular and clinicopathologic subtype of non-small-cell lung cancer. J Clin Oncol. 2012;30:4352-4359.
Kim DW, Jo YS, Jung HS, et al. An orally administered multitarget tyrosine kinase inhibitor, SU11248, is a novel potent inhibitor of thyroid oncogenic RET/papillary thyroid cancer kinases. J Clin Endocrinol Metab. 2006;91:4070-4076.
Plaza-Menacho I, Mologni L, Sala E, et al. Sorafenib functions to potently suppress RET tyrosine kinase activity by direct enzymatic inhibition and promoting RET lysosomal degradation independent of proteasomal targeting. J Biol Chem. 2007;282:29230-29240.
Wells SA Jr, Robinson BG, Gagel RF, et al. Vandetanib in patients with locally advanced or metastatic medullary thyroid cancer: a randomized, double-blind phase III trial. J Clin Oncol. 2012;30:134-141.
Matsubara D, Kanai Y, Ishikawa S, et al. Identification of CCDC6-RET fusion in the human lung adenocarcinoma cell line, LC-2/ad. J Thorac Oncol. 2012;7:1872-1876.
Suzuki M, Makinoshima H, Matsumoto S, et al. Identification of a lung adenocarcinoma cell line with CCDC6-RET fusion gene and the effect of RET inhibitors in vitro and in vivo. Cancer Sci. 2013;104:896-903.
Saito M, Ishigame T, Tsuta K, et al. A mouse model of KIF5B-RET fusion-dependent lung tumorigenesis. Carcinogenesis. 2014;35:2452-2456.
Elisei R, Schlumberger MJ, Müller SP, et al. Cabozantinib in progressive medullary thyroid cancer. J Clin Oncol. 2013;31:3639-3646.
Kurzrock R, Sherman SI, Ball DW, et al. Activity of XL184 (cabozantinib), an oral tyrosine kinase inhibitor, in patients with medullary thyroid cancer. J Clin Oncol. 2011;29:2660-2666.
Okamoto K, Kodama K, Takase K, et al. Antitumor activities of the targeted multi-tyrosine kinase inhibitor lenvatinib (E7080) against RET gene fusion-driven tumor models. Cancer Lett. 2013;340:97-103.
Mologni L, Redaelli S, Morandi A, et al. Ponatinib is a potent inhibitor of wild-type and drug-resistant gatekeeper mutant RET kinase. Mol Cell Endocrinol. 2013;377:1-6.
De Falco V, Buonocore P, Muthu M, et al. Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer. J Clin Endocrinol Metab. 2013;98:E811-E819.
Gozgit JM, Chen T, Clackson T, et al. Ponatinib is a highly potent inhibitor of activated variants of RET found in MTC and NSCLC. Paper presented at: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; April 6-10, 2013; Washington, DC. Abstract 2084.
Drilon A, Wang L, Hasanovic A, et al. Response to cabozantinib in patients with RET fusion-positive lung adenocarcinomas. Cancer Discov. 2013;3:630-635.
Gautschi O, Zander T, Keller FA, et al. A patient with lung adenocarcinoma and RET fusion treated with vandetanib. J Thorac Oncol. 2013;8:e43-e44.
Dr Shatsky is an Oncology Fellow in the Division of Hematology/Oncology, Department of Medicine at the University of California, San Diego (UCSD).
Dr Bazhenova is Associate Clinical Professor of Medicine in the Division of Hematology/Oncology and is Medical Director of the UCSD Moores Cancer Center Infusion Center. Her clinical practice and research concentrate on lung cancer, particularly as it relates to females and nonsmokers. She actively participates in cooperative group trials and takes an active role in designing and implementing clinical investigations, including phase 2 studies and correlative science projects with several UCSD investigators.
PMO Live - June 15, 2015
Case: Former Smoker with Well-Differentiated Adenocarcinoma of the Lung
Genetic tumor profiling, immune profiling, and immunohistocompatibility expression profiling are performed routinely at Yale Cancer Center for patients diagnosed with cancer. The results are presented to the multidisciplinary Molecular Tumor Board, which meets weekly to make treatment decisions. The following case exemplifies a personalized medicine approach and was presented by [ Read More ]
Case Studies: Incorporating Molecular Biomarkers into Therapy for Breast Cancer Is Fraught with Difficulty
Many therapeutic agents target HER2-positive breast cancer. Unfortunately, patient selection for these agents has not been refined, so all HER2-positive patients receive them. In estrogen receptor (ER)-positive disease, new agents improve the response to hormone-targeted therapies, but again, the appropriate patients for targeted agents have not been defined. "Because many [ Read More ]


"Our goal in 2015 is to continue to provide high quality services to our clients and help them and our people, unlock their potential for growth. We are doing this in all areas of the services that we provide from audit to business risk services to business consulting. We enjoy the challenges of helping businesses grow their potential for success."


If You Could Be One Gourmet Food, What Would You Be?
Question 1 : How do you perceive fine dining?
Question 2: Come pay day, what's the first purchase you're most likely to spend on?
Question 3: What's your idea of the 'good life'?
Question 4: What is your favourite beverage to start a meal with?
Question 5: What is a suitable genre of music to accompany your meal?
Question 6: When you're unsure about what wine to go with your meal, what's your strategy?
Pick the next best thing instead – beer!
Question 7: When you have company over for dinner, how do you prepare?
Get my friends involved – makes everything more fun!
Question 8: How do you dress for a fancy dinner date?
This delicate sliver of meat can be someone's gold on their palate, while others turn their noses away instantly. But that's what sets you apart from the lot; you can appreciate the refined life, with a good punch of flavour! For a foie gras dish with an Asian twist, you'll find yourself in for a delightful surprise at Nouvelle Fusion & Bar with their Miso Foie Gras with blinis and pistachios. Defying the stereotype that this sublime meat can only be prepared one of a handful of ways, this dish is done sweet, umami and crunchy.
Who hasn't had something-truffle in their dishes these days? It's everywhere; you can almost smell it in the air! But that doesn't bother you – you wish it were in everything. Make truffle everyone's new BFF by bringing your crew to Fourplay Kitchen & Bar and have a taste of their intense offering of their Creamy Shrooms Truffle Pasta with spaghetti tossed in creamy truffle sauce with sautéed mushrooms and topped with shaved black truffles. Truffle on truffle, now that's how you roll!
You like to get your hands dirty, and know that you have to get into the nitty gritty to reap the benefits of the good stuff (like succulent morsels of lobster meat!). Take your pick of getting your seafood the way you like it at No Signboard Seafood, where they cook up mean Asian sea fare in a multitude of ways like their Salted Egg Pumpkin White Crab and Crispy Cereal King Prawn.
You value your worth and aren't afraid to let the world know it. These tiny bubbles of goodness are also known as roe, and are one of those ingredients you either love or hate. It's potent, fishy and salty. And for something you can only enjoy so little at a time, they can cost a fortune. One of the most expensive caviar on the market today – from the Iranian Beluga fish – can fetch a heart-stopping steady price of $40,000 per kilo!
Liking sashimi just as much as we do is one thing. A whole other bar that's been set is your impeccable standards for only the finest! Popularly seen as a food item that's not only rare, but also risky, you're a daredevil at heart and love a challenge – even when it comes to dining.


The most recent support group & info session run by Dr. Cataland at the James Cancer Hospital was held on Tuesday April 26, 2011. Sydney Kodatsky, Executive Director of Answering TTP Foundation, was in attendance to share and learn from the group.
It was an exciting session discussing TTP, HUS and the potential predictive value of the ADAMTS13 enzyme for assessing risk of relapse for some TTP patients.
The 2nd Toronto TTP Support Group and Information Session held on April 20, 2011 was a great success! We filled the room, Rotman generously donated for the evening, with close to 40 guests including patients, supporters, nurses and doctors. Over 90% of guests who filled out the feedback survey hope to attend the next session within 6 months.
Answering TTP initiatives to raise awareness for blood in our communities has resulted in a feature story in Pulse magazine. Sydney Kodatsky's story is used to personalize the need for blood in our communities. The story raises awareness for TTP by providing a brief overview of the condition and the requirement for blood in the treatment of TTP. Read the full story.
The 1st Vancouver TTP Support Group and Information Session held on March 5, 2011. We had 6 patients, 4 supporters and two doctors in attendance. Dr. Yenson gave an overview of TTP which set the stage for participants to asked questions furthering the knowledge of all in attendance.
But we still have a long way to go!
Answering T.T.P. founding volunteer, Sydney Kodatsky and her brother Andrew Bryant, helped Canadian Blood Services launch Toronto's Bloodmobile on September 14, 2010.
Apheresis Unit to aid in the treatment of T.T.P.
The next thing I knew, I was hospitalized and undergoing apheresis, popping prednisone and dodging suggestions of chemotherapy and spleenectomy (just talk at the time)… and wondering about my future.


Allstate agency has a available immediately for a licensed Property & Casualty (P&C) Sales Producer.
The Allstate Corporation is the largest publicly held personal lines property and casualty insurer in America. Allstate was founded in 1931 and became a publicly traded company in 1993.
Allstate has an exceptional career opportunity for a Represented Casualty Adjuster in Elkridge, MD!. .... * Volunteer opportunities * You can view all Allstate benefits @ .
Work experience at Allstate, State Farm and similar experience is a plus We hire star performers not backgrounds if you have what it takes Apply Now!


text:
Державний народний театр — український театр, який діяв у Києві 1918—1922 років під керівництвом Панаса Саксаганського.

Загальні відомості
У серпні 1918 року при Українській Державі з'явився «Законопроєкт про заснування в місті Києві Державного народного театру (в Троїцькому Народному Домі)». Театр фінансувався з держбюджету і користувався правом безмитного одержання всіх необхідних закордонних матеріалів, приладів, знарядь.

До трупи театру, очолюваного корифеєм української сцени Панасом Саксаганським, увійшли відомі українські театральні діячі — Л. П. Ліницька, Ф. В. Левицький, І. Е. Замичковський, Г. П. Затиркевич-Карпинська, О. І. Корольчук, С. Ф. Паньківський, Р. Л. Чичорський, О. Л. Жулинський та інші.

Художник — С. Худяков.

Діяльність театру припинилася навесні 1922 року.

Його спадкоємцем став Театр ім. М. К. Заньковецької (нині — Національний академічний український драматичний театр імені Марії Заньковецької), до якого увійшло основне акторське ядро Державного народного театру.

Репертуар
українська класика
 «Наталка Полтавка» І. Котляревського
 «Запорожець за Дунаєм» С. Гулака-Артемовського
 «Назар Стодоля» Т. Шевченка
 «Дай серцю волю, заведе в неволю»
 «По ревізії» М. Кропивницького
 «Сава Чалий», «Суєта», «Наймичка», «Безталанна», «Мартин Боруля» І. Карпенка-Карого
твори зарубіжних авторів
 «Розбійники» Ф. Шіллера
 «Урієль Акоста» К. Гуцкова.

У виставі «Розбійники» роль Франца Моора виконував Панас Саксаганський, роль Карла Моора — Б. В. Романицький.

Примітки

Посилання

  djvu, pdf частина 1
 Саксаганський П. К. — Сторінки творчості librarychl.kr.ua

Колишні театри Києва
Театри, засновані 1918
Засновані в Україні 1918

redpajama_set_name: RedPajamaWikipedia


Bookie is a Python web application written using the Pyramid web framework.
Bookie's git repository is managed using a tool/process called git flow. It basically sets standards for how the git repository is set up. You'll find the most up to date working code in the develop branch. Individual features that are being worked on are in branches prefixed by feature/ . As these features get to a workable state they might get merged into the develop branch.
The master branch is only for releases and we're a long away from that. So when you check out Bookie, make sure to start out using the develop branch.