text:
United Nations Stabilisation Mission in Haiti
|The factual accuracy of parts of this article (those related to article) may be compromised due to out-of-date information. (May 2011)
Chilean helicopter during the 2006 elections
|MINUSTAH (French: Mission des Nations Unies pour la stabilisation en Haïti)
|1 June 2004
|Peacekeeping Mission
Legal status
|Mariano Fernández Amunátegui (Special Representative of the Secretary-General)
Parent organization
|UN Department of Peacekeeping Operations, United Nations Security Council
|UN Peacekeeping: MINUSTAH, www.minustah.org (French)
The United Nations Stabilisation Mission In Haiti (UNSTAMIH) (French: Mission des Nations Unies pour la stabilisation en Haïti), also known as MINUSTAH, an acronym of the French translation, is a United Nations peacekeeping mission in Haiti that has been in operation since 2004. The mission's military component is led by the Brazilian Army and the force commander is Brazilian. MINUSTAH's mandate was recently extended by United Nations Security Council Resolution 1944 past its October 15, 2010 deadline[1] amid fears of instability.[2] The mission's current mandate runs through October 15, 2012 with the intention of further renewal.[3] The force is composed of 8,940 military personnel and 3,711 police, supported by an international civilian personnel, a local civilian staff and United Nations Volunteers.[4]
Following the 2010 Haiti earthquake, the United Nations reported that the headquarters of the mission in Port-au-Prince had collapsed and that the mission's chief, Hédi Annabi of Tunisia, his deputy Luiz Carlos da Costa of Brazil, and the acting police commissioner, RCMP Supt. Doug Coates of Canada, were confirmed dead.[5][6][7] On 14 January 2010, UN headquarters dispatched the former head of MINUSTAH and current Assistant Secretary-General for Peacekeeping Operations, Edmond Mulet, as the organisation's Acting Special Representative of the Secretary-General and interim head of MINUSTAH.[8] Mulet clarified on January 22 that MINUSTAH will concentrate on assisting the Haitian National Police in providing security within the country after the earthquake, while American and Canadian military forces will distribute humanitarian aid and provide security for aid distribution.[9]
According to its mandate from the UN Security Council, MINUSTAH is required to concentrate the use of its resources, including civilian police, on increasing security and protection during the electoral period and to assist with the restoration and maintenance of the rule of law, public safety and public order in Haiti.[10] MINUSTAH was established by United Nations Security Council Resolution 1542 on 30 April 2004 because the Security Council deemed the situation in Haiti to be a threat to international peace and security in the region.[11] In 2004, UN peacekeepers stormed Cité Soleil in an attempt to gain control of the area and end the anarchy.[12]
In 2004, independent human rights organizations accused MINUSTAH and the Haitian National Police (HNP) of collaborating in numerous atrocities against civilians.[13][14][15] The UN, after repeatedly denying having taken the lives of any civilians, later admitted that civilians may have been killed, but argued that this was not intentional, and that it occurred as a by-product of their crackdown on what they call "gangs". They also said that the UN and MINUSTAH deeply regretted any loss of life during the operation.[16][17]
In early 2005, MINUSTAH force commander Lieutenant-General Augusto Heleno Ribeiro Pereira testified at a congressional commission in Brazil that "we are under extreme pressure from the international community to use violence," citing Canada, France, and the United States.[18] Later in the year, he resigned, and on 1 September 2005, was replaced by General Urano Teixeira da Matta Bacellar as force commander of MINUSTAH. On 7 January 2006, Bacellar was found dead in his hotel room.[19] His interim replacement was Chilean General Eduardo Aldunate Hermann.
On 17 January 2006, it was announced that Brazilian General José Elito Carvalho de Siqueira would be the permanent replacement for Bacellar as the head of the United Nations' Haiti force.[20]
On 14 February 2006, in Security Council Resolution 1658, the United Nations Security Council extended MINUSTAH's mandate until 15 August 2006.[21]
MINUSTAH is also a precedent as the first mission in the region to be led by the Brazilian and Chilean military, and almost entirely composed of, Latin American forces, particularly from Brazil, Argentina, Chile, Bolivia, Ecuador and Uruguay.[22] From 1 September 2007 until his death following the earthquake on 12 January 2010, the mission was led by Tunisian Hédi Annabi.[23]
United Nations reports and resolutions[edit]
On 23 February 2004, the United Nations Security Council was convened at the request of CARICOM for the first time in four years to address the deteriorating situation in Haiti.[24]
On 29 February 2004, the Security Council passed a resolution "taking note of the resignation of Jean-Bertrand Aristide as President of Haiti and the swearing-in of President Boniface Alexandre as the acting President of Haiti in accordance with the Constitution of Haiti" and authorized the immediate deployment of a Multinational Interim Force.[25]
On 30 April 2004, MINUSTAH was established and given its mandate with a military component of up to 6,700 troops.[26]
In July the General Assembly authorized the financing of the mission with $200 million[27] which followed a donors' conference in Washington DC.[28]
The first progress report from MINUSTAH was released at the end of August.[29]
In September the interim president of Haiti, Boniface Alexandre, spoke to the United Nations General Assembly in support of MINUSTAH.[30]
In November there was a second report,[31] and the Security Council mandate for MINUSTAH.[32]
The mandate has most recently been extended by the Security Council until October 2010 "with the intention of further renewal".[33]
Although the United Nations Stabilization Mission (MINUSTAH) has been in Haiti since 2004, as of 2007, it continued to struggle for control over the armed gangs. It maintains an armed checkpoint at the entrance to the shanty town of Cité Soleil and the road is blocked with armed vehicles.[34] In January 2006, two Jordanian peacekeepers were killed in Cité Soleil.[35] In October 2006 a heavily armed group of the Haitian National Police were able to enter Cité Soleil for the first time in three years and were able to remain one hour as armored UN troops patrolled the area. Since this is where the armed gangs take their kidnap victims, the police's ability to penetrate the area even for such a short time was seen as a sign of progress.[36] The situation of continuing violence is similar in Port-au-Prince. Ex-soldiers, supporters of the ex-president, occupied the home of ex-president Jean-Bertrand Aristide against the wishes of the Haitian government.[37] Before Christmas 2006 the UN force announced that it would take a tougher stance against gang members in Port-au-Prince, but since then the atmosphere there has not improved and the armed roadblocks and barbed wire barricades have not been moved. After four people were killed and another six injured in a UN operation exchange of fire with criminals in Cité Soleil in late January 2007, the United States announced that it would contribute $20 million to create jobs in Cité Soleil.[38][39]
In early February 2007, 700 UN troops flooded Cité Soleil resulting in a major gun battle. Although the troops make regular forcible entries into the area, a spokesperson said this one was the largest attempted so far by the UN troops.[40] On 28 July 2007, Edmond Mulet, the UN Special Representative in Haiti and MINUSTAH Mission Chief, warned of a sharp increase in lynchings and other mob attacks in Haiti. He said MINUSTAH, which now has 9,000 troops there, will launch a campaign to remind people lynchings are a crime.[41]
On 2 August 2007, UN Secretary-General Ban Ki Moon arrived in Haiti to assess the role of the UN forces, announcing that he would visit Cité Soleil during his visit. He said that it was Haiti's largest slum and as such was the most important target for U.N. peace keepers in gaining control over the armed gangs. During his visit he announced an extension of the mandate of the UN forces in Haiti.[42] It took MINUSTAH three months and 800 arrests to deal with the gangs and lessen the number of kidnappings on the streets.[43]
President René Préval has expressed ambivalent feelings about the UN security presence, stating "if the Haitian people were asked if they wanted the UN forces to leave they would say yes."[44] Survivors frequently blame the UN peace keepers for deaths of relatives.[45]
In April 2008, Haiti was facing a severe food crisis as well as governmental destabilization to Parliament's failure to ratify the president's choice of a prime minister. There were severe riots and the UN force fired rubber bullets in Port-au-Prince and the riot calmed.[46] The head of MINUSTAH has called for a new government to be chosen as soon as possible. Meanwhile, the UN provided emergency food.[47] Haiti was hit by four consecutive hurricanes between August and September 2008. These storms crippled coastal regions, requiring humanitarian aid for 800,000.[48]
Critics of MINUSTAH's goal of providing security say that the provision of increased police presence is coming with the unfortunate consequence of neglecting the vast socioeconomic problems in the area, the lack of effort in addressing infrastructure improvement, the joblessness and the pervasive poverty. In 2009, with the appointment of former U.S. President Bill Clinton as the UN Special Envoy, there is hope that the international donor community will provide increased aid. MINUSTAH renewed its commitment to Haiti, and $3 billion for projects has been pledged by the international community, much of this for rebuilding after the hurricanes. However, in Cité Soleil, there are signs of a desire for political independence that the international community would rather ignore.[43]
In October 2010, 9 months after the earthquake, the UN extended MINUSTAH's mission. The extension was greeted by unusual anger in Port-au-Prince with demonstrators saying "Down with the occupation" and burning the flag of Brazil, as representative of the largest contingent of MINUSTAH.[49]
2010 Haiti earthquake[edit]
On 12 January 2010, the United Nations reported that headquarters of the United Nations Stabilization Mission in Haiti (MINUSTAH), the Christopher Hotel in Port-au-Prince, collapsed, and several other UN facilities were damaged; a large number of UN personnel were unaccounted for in the aftermath of the 2010 Haiti earthquake.[50] The Mission's Chief, Hédi Annabi, was reported dead on 13 January by President René Préval and French news sources and on 16 January the United Nations confirmed the death after his body was recovered by a search and rescue team from China.[51] Principal Deputy Special Representative Luiz Carlos da Costa was also confirmed dead, as well as the Acting Police Commissioner, Royal Canadian Mounted Police (RCMP) Superintendent Doug Coates, who were meeting with eight Chinese nationals—four peacekeepers and a delegation of four police officers from China—when the earthquake struck.[52] The Chinese search and rescue team recovered the bodies of the ten individuals on 16 January 2010. Jens Kristensen, senior humanitarian officer for the UN was rescued by a Fairfax, Virginia team after five days trapped in the rubble.[53]
Mission composition[edit]
Heads of the United Nations Stabilization Mission in Haiti:
- Juan Gabriel Valdés of Chile, August 2004 to May 2006.[54]
- Edmond Mulet of Guatemala, June 2006 to August 2007.[55]
- Hédi Annabi of Tunisia, September 2007 to January 2010.[56]
- Edmond Mulet of Guatemala, January 2010 to June 2011.[57]
- Mariano Fernández of Chile, June 2011 to present.[58]
Force commanders of the MINUSTAH military component:
- Army General Augusto Heleno Ribeiro Pereira, Brazil, 2004 to August 2005
- Divisional General Urano Teixeira da Matta Bacellar, Brazil, September 2005 to January 2006.[59]
- General Eduardo Aldunate Hermann, Chile, January 2006 (interim appointment).
- Divisional General José Elito Carvalho Siqueira, Brazil, January 2006 to January 2007.[60]
- Brigadier General Carlos Alberto dos Santos Cruz, Brazil, January 2007 to April, 2009.[61]
- Brigadier General Floriano Peixoto Vieira Neto, Brazil, April, 2009 to March 2010.
- Brigadier General Luiz Guilherme Paul Cruz, Brazil, March, 2010 to March 2011
- Brigadier General Luiz Eduardo Ramos Baptista Pereira, Brazil, March, 2011 to March 2012
- Brigadier General Fernando Rodrigues Goulart, Brazil, March 2012 to present
Countries contributing military personnel (7,206 in all):
- Argentina (558 including a field hospital ), Bolivia (208), Brazil (2,200), Canada (10), Chile (499), Croatia (3), Ecuador (67), France (2), Indonesia (167), Guatemala (118), Jordan (728), Nepal (1,075), Paraguay (31), Peru (209), the Philippines (157), Sri Lanka (959), United States (4), and Uruguay (1,135).[62][63]
Countries contributing police/civilian personnel (2,031 in all):
- Israel (14), Benin (32), Brazil (4), Burkina Faso (26), Cameroon (8), Canada (94), Central African Republic (7), Chad (3), Chile (15), China (143), Colombia (37).[62][63] Côte D'Ivoire (60), DR Congo (2), Egypt (22), El Salvador (7), France (64), Grenada (3), Guinea (55), India (139), Italy (4), Jamaica (5), Jordan (312), Madagascar (2), Mali (55), Nepal (168), Niger (62), Nigeria (128), Pakistan (248), Philippines (18), Romania (23), Russian Federation (10), Rwanda (14), Senegal (131), Serbia (5), Spain (41), Sri Lanka (7), Togo (5), Turkey (46), United States (48), Uruguay (7), and Yemen (1).[62][63]
Cholera controversy[edit]
In October 2010, a Cholera outbreak was confirmed in Haiti—the first in Haitian modern history. According to the Centers for Disease Control and Prevention (CDC), as of August 4, 2013, 669,396 cases and 8,217 deaths have been reported since the outbreak first began in October 2010.[64] MINUSTAH has been linked with introducing the disease to the country by a variety of independent sources, including the CDC, the American Society for Microbiology, and Yale Law School and the School of Public Health.[65] The cause of the disease was attributed to faulty construction of UN sanitation systems in its base located in the Haitian town of Méyè.[66] Many reports from Méyè stated that people had seen sewage spilling from the UN base into the Artibonite River, the largest river in Haiti that is most often used by residents for drinking, cooking, and bathing.[67]
In December 2010, a study traced the Haitian cholera strain to South Asia. After denying the accusations many times, the UN announced that it would be conducting an independent investigation into the origin of the epidemic at the end of 2010. A panel of independent UN experts was assembled and their collective findings were compiled in a report. The panel determined that the evidence implicating the Nepalese troops was inconclusive. Though they admitted that the cholera strain was most likely from Nepal, it cited a confluence of factors that also contributed to the outbreak and that no one "deliberate action of, a group or individual was to blame".[68] However, in 2013, the committee changed its statement concluding that the UN troops from Nepal "most likely" were the cause of the outbreak.[69]
The Bureau des Avocats Internationaux (BAI), a Haitian coalition of lawyers, and the Institute for Justice & Democracy in Haiti (IJDH), its US-affiliate, filed claims with MINUSTAH on behalf of 5,000 Haitian petitioners in November 2011 . The claims asked for the installation of the water and sanitation infrastructure necessary to control the epidemic, compensation for the victims, and an apology.[70] Fifteen months later, on February 2013, the UN stated that the case was "not receivable," because it involved "review of policy matters", citing the Convention on Privileges and Immunities of the United Nations.[71]
In February 2013, The Haitian government created its National Plan for the Elimination of Cholera, a 10-year plan set to eradicate the disease. Two of the ten years will be devoted as a short-term response to the epidemic. The last eight will be to completely eliminate the disease. The projected budget for the plan is $2 billion.[72] To support the initiative, UN Secretary General, Ban Ki-Moon, pledged $23.5 million to combat cholera. However, following the pledge, there was much discontent with the UN's progress. 19 Members of U.S. Congress urge UN to take responsibility for cholera in Haiti. In two separate occasions, members of the US Congress sent a letter to the US ambassador to the UN, Susan Rice, urging her and the organization to ensure that the cholera initiative was fully funded and implemented quickly.[73] Nineteen US Representatives also wrote to Ban Ki-Moon to express concerns about the seemingly lack of progress in the UN's cholera response.[74] Ban Ki-moon told members of the US Congress that the UN was committed in helping Haiti overcome the epidemic though no financial compensation to the victims would be granted.[75] Since 2010, the UN has spent and/or committed more than $140 million to the epidemic.
On May 9, 2013, the Haitian Senate unanimously voted—save for one abstention—on a policy that would demand the UN to compensate Haitian cholera victims. Senators also proposed to form "a commission of experts in international and penal law to study what legal means, both nationally and internationally, we could use to prove MINUSTAH's responsibility for starting the cholera outbreak."[76]
A number of incidents and the aim of the UN mission itself have led to widespread criticism of its actions and appeal for its departure.
Political bias[edit]
The United Nations Stabilization Mission in Haiti is the only significant military mission of the United Nations dispatched to a country facing an internal conflict without a peace agreement between the parties.[77] Critics have characterized MINUSTAH as an attempt by the United States, Canada and France to oust Haiti's democratically elected populist president Jean-Bertrand Aristide, neutralize the supporters of Fanmi Lavalas,[78] and secure the more pro-Western government of Gérard Latortue. In 2005, a report undertaken by Harvard Law Student Advocates for Human Rights claimed that the UN stabilization force "effectively provided cover for the police to wage a campaign of terror in Port-au-Prince's slums",[79] which constitute "an unflinching bastion of support for Aristide and for Lavalas".[80]
6 July 2005 incident[edit]
On 6 July 2005, MINUSTAH carried out a raid in the Cité Soleil section of Port-au-Prince.[81] MINUSTAH spokespeople claimed that the raid targeted a base of illegally armed rebels led by Dread Wilme. Reports from pro-Lavalas sources, as well as journalists such as Kevin Pina, contend that the raid targeted civilians and was an attempt to destroy the popular support for Haiti's exiled former leader, Aristide, before scheduled upcoming elections. The "totally inappropriate solution for the member-states to tell the UN to take sides in Haiti" has not only been denounced by Westerners but also resented by the local population.
Estimates on the number of fatalities range from five to as high as 80, with the higher numbers being claimed by those reporting that the raid targeted civilians. All sources agree that no MINUSTAH personnel were killed. All sources also agree that Dread Wilme (born "Emmanuel Wilmer") was killed in the raid. MINUSTAH spokespeople called Wilme a "gangster." Other sources, such as the pro-Aristide Haitian Lawyers Leadership Network call Wilme a community leader and a martyr.[82]
The incident became a focal point for groups who oppose the MINUSTAH occupation of Haiti and who support the return of President Aristide.[34] MINUSTAH has also been accused by opponents of standing by and allowing the Haitian National Police to commit atrocities and massacres against Lavalas supporters and Haitian citizens opposed to the current occupation.
On 6 January 2006, UN mission head Juan Gabriel Valdés announced that MINUSTAH forces would launch another raid on Cité Soleil. Dismissing fears by human rights groups that more civilians will be killed, Valdés said, "We are going to intervene in the coming days. I think there'll be collateral damage but we have to impose our force, there is no other way."[83]
Sex scandal[edit]
MINUSTAH has been accused of being involved in a number of sexual assault cases. In 2008, Nepalese UN soldiers were charged with the rape of a Haitian female adolescent.[84] In 2011, four Uruguayan UN marines were accused of gang raping a 19-year-old Haitian boy in Port Salut, Haiti. The alleged rape was recorded with a cell phone by the peacekeepers themselves and leaked to the Internet.[85] The teenager and his family were forced to relocate their house after the video went viral.[86] In March 2012, three Pakistani MINUSTAH officers were found guilty of raping a mentally challenged 14-year-old boy in the Haitian town of Gonaives. Pakistani officials sentenced each officer to one year in Pakistan prison.[87]
In November 2007, 114[88] members of the 950 member Sri Lanka peacekeeping contingent in Haiti were accused of sexual misconduct and abuse.[89][90] 108 members, including 3 officers were sent back after being implicated in alleged misconduct and sexual abuse.[91] UN spokeswoman Michele Montas said: "The United Nations and the Sri Lankan government deeply regret any sexual exploitation and abuse that has occurred."[90] The Sri Lankan Officials claim that there is little tangible evidence on this case.[88] After inquiry into the case the UN Office of Internal Oversight Services (OIOS) has concluded 'acts of sexual exploitation and abuse (against children) were frequent and occurred usually at night, and at virtually every location where the contingent personnel were deployed.' The OIOS is assisting in the pending legal proceedings initiated by the Sri Lankan Government and has said charges should include statutory rape "because it involves children under 18 years of age".[92]
Human Rights Cases[edit]
In 2010, MINUSTAH was accused with the murder of Gérard Jean-Gilles, a 16-year-old Haitian boy who ran miscellaneous errands for the Nepalese soldiers in Cap Haitien. His body was found hanging inside of MINUSTAH's Formed Police Unit base. UN soldiers denied responsibility, claiming that the teen committed suicide. The troops released the body for autopsy seventy-two hours after the death; the examination ruled out suicide as a potential cause of death.[93] Nepalese UN troops were also accused for a variety of other misdeeds. Several days before the Jean-Gilles incident, the local press charged a Nepalese soldier of torturing a minor in a public area in Cap-Haitien. The soldier was said to have forced "his hands into the youth's mouth in an attempt to separate his lower jaw form his upper jaw, tearing the skin of his mouth.[94]"
Many have also expressed discontent with MINUSTAH and its management of political public dissent. Past incidents include November 15, 2010 when Haitian residents protested against MINUSTAH occupation. The protests, which occurred in Cap-Haitien and other areas throughout the country, resulted in at least two civilian deaths and numerous injuries. MINUSTAH released a statement claiming that the protest seemed politically motivated, "aimed at creating a climate of insecurity on the eve of elections." Moreover, it acknowledged the deaths, stating that a UN peacekeeper shot out of self-defense.[95]
On June 18, 2009, Fanmi Lavalas (Haiti's largest political party and grassroots movement) laid Catholic priest Father Gerard Jean-Juste to rest on 18 June accompanied by thousands of mourners. The procession and demonstration were suddenly interrupted by gunfire that could be heard from around the corner. Witnesses report that Brazilian soldiers with the United Nations military mission opened fire after attempting to arrest one of the mourners. The UN has since denied the shooting and claim that the victim had been killed by either a rock thrown by the crowd or a blunt instrument. Eyewitnesses on the scene have countered that the UN is trying to cover-up the incident.[96]
Legal proceedings[edit]
A trial involving the Brazilian contingent of the military forces of the MINUSTAH is currently in progress at the Inter-American Court of Human Rights (IACHR). The case, brought forward by Mario Joseph from the Bureau des Avocats Internationaux (BAI) and Brian Concannon from the Institute for Justice & Democracy in Haiti, concerns Jimmy Charles, a grassroots activist who was arrested by UN troops in 2005, and handed over to the Haitian police. His body was found a few days later in the morgue, filled with bullet holes.[97] The BAI filed a complaint in Haitian courts, to no avail, and in early 2006 it filed a petition with the IACHR. The IACHR accepted the case regarding the State of Haiti, and rejected the complaint against Brazil,[98] showing a legal vacuum in the UN's accountability.
See also[edit]
- United Nations Mission in Haiti
- List of UN peacekeeping missions
- List of countries where United Nations peacekeepers are currently deployed
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- ^ Rosalyn Chan, Tassity Johnson, Charanya Krishnaswami, Samuel Oliker-Friedland, & Celso Perez Carballo. "Peacekeeping Without Accountability". Yale Law School. Retrieved 9 September 2013.
- ^ "Haiti cholera: UN peacekeepers to blame, report says". bbc.co.uk. BBC News. 8 December 2010. Retrieved 25 July 2013.
- ^ Sontag, Deborah (31 March 2012). "In Haiti, Global Failures on a Cholera Epidemic". NY Times. Retrieved 25 July 2013.
- ^ "UN's Own Independent Experts Now Say MINUSTAH Troops "Most Likely" Caused Cholera Epidemic". Center for Economic and Policy Research. Retrieved 9 September 2013.
- ^ "The Cholera Accountability Project". Institute for Justice and Democracy in Haiti. Retrieved 25 July 2013.
- ^ "Haiti's Cholera Outbreak Tied To Nepalese U.N. Peacekeepers". NPR. Retrieved 9 September 2013.
- ^ Watts, Jonathan. "Haiti seeks $2bn for cholera epidemic 'introduced by UN peacekeepers'". Guardian News and Media Limited. Retrieved 9 September 2013.
- ^ "Members of U.S. Congress urge U.S. government to support UN cholera initiative". Canada Haiti Action Network.
- ^ Waters, Maxine. "19 Members of U.S. Congress urge UN to take responsibility for cholera in Haiti". The Defend Haiti.
- ^ Lederer, Edith. "UN chief assures US Congress of commitment to help Haiti overcome cholera epidemic".
- ^ Ives, Kim. "Cholera Legal Suit Against the UN Takes Shape: Lawyers Seek Haitian Claimants in New York". Haiti Analysis.
- ^ Lindsay, Reed. "Peace despite the Peacekeepers in Haiti." NACLA Report on the Americas 39:6 (May 2006):31-6, p. 34.
- ^ Evens Sanon, and Jonathan Katz (2009-12-24). "US lawmaker criticizes Haiti election exclusions". Taiwan News. Retrieved 23 January 2010.
- ^ Harvard Law Student Advocates for Human Rights and Centro de Justica Global. Keeping the Peace in Haiti? An Assessment of the UN Stabilization Mission In Haiti, March 2005.
- ^ Hallward, Peter. Damming the Flood: Haiti, Aristide and the Politics of Containment, p. 280. Verso 2007.
- ^ Klein, Naomi (July 21–28, 2005). "My date with Aristide Ousted Haitian prez reveals he was tossed because he refused to privatize". Now (magazine). Retrieved 2009-04-20.
- ^ "Haitian Lawyers Leadership Network". Retrieved 2007-08-15.
- ^ "Half-Hour for Haiti: Stop "Collateral Damage" in Cite Soleil". Institute for Justice & Democracy in Haiti. Retrieved 2007-08-15.
- ^ "What Happened to Gerald Jean Gilles?". Center for Economic and Policy Research. 21 September 2010. Retrieved 11 September 2013.
- ^ Weisbrot, Mark (3 September 2011). "Is this Minustah's 'Abu Ghraib moment' in Haiti?". Guardian News and Media Limited. Retrieved 11 September 2013.
- ^ Klarreich, Kathie (13 June 2012). "Will the United Nations' legacy in Haiti be all about scandal?". The Christian Science Monitor. Retrieved 10 September 2013.
- ^ "Human Rights Watch: Haiti". 2013. Retrieved 12 September 2013.
- ^ a b "Haiti: Over 100 Sri Lankan blue helmets repatriated on disciplinary grounds – UN". United Nations. 2007-11-02. Retrieved 2007-11-04.
- ^ Williams, Carol J. (2007-12-15). "U.N. confronts another sex scandal". Los Angeles Times. Retrieved 2008-11-07.
- ^ a b "Sri Lanka to probe UN sex claims". BBC. 2007-11-03. Retrieved 2007-11-05.
- ^ Reddy, B. Muralidhar (2007-11-05). "Part of Sri Lankan contingent in Haiti to be sent back". The Hindu. Retrieved 2007-11-05.
- ^ "UN confirms sex charges". Sundaytimes. 2008-03-30. Retrieved 2008-03-30.
- ^ "MINUSTAH: Keeping the peace, or conspiring against it?". Harvard University. Retrieved 9 September 2013.
- ^ "What Happened to Gerald Jean Gilles?". Center for Policy and Economic Research. Retrieved 12 September 2013.
- ^ "In Response to Protests, MINUSTAH Disregards Legitimate Grievances". Center for Policy and Economic Research. Retrieved 12 September 2013.
- ^ Pena, Kevin (June 20, 2009). "A funeral and a boycott: 'The struggle continues' in Haiti". San Francisco Bay View. Retrieved 2010-01-14.
- ^ "Photo of Jimmy Charles in morgue". Institute for Justice and Democracy in Haiti. Retrieved 2009-06-26.
- ^ "Admissibility Jimmy Charles v. Haiti, Case 81-06, Report No. 65/06, Inter-Am. C.H.R., OEA/Ser.L/V/II.127 Doc. 4 rev. 1 (2007)". .umn.edu. Retrieved 2012-05-02.
External links[edit]
|Wikimedia Commons has media related to United Nations Stabilization Mission in Haiti (MINUSTAH).
- Official website (French)
- Official website
- MINUSTAH Background
- MINUSTAH Historique (French)
- U.S. State Department Bureau of International Affairs' Fact Sheet
- Documentation of Nepal's contribution to MINUSTAH
- Documentation of Argentine Army's contribution to MINUSTAH
- Documentation of Argentine Air Force's contribution to MINUSTAH
- Documentation of Argentine Navy's contribution to MINUSTAH
- Documentation of Japan's contribution to MINUSTAH
- Sri Lanka's contribution to MINUSTAH
- MINUSTAH Photos in Haiti
- MINUSTAH Videos in Haiti
- MINUSTAH FM RADIO Streaming iTunes
- MINUSTAH FM RADIO Streaming Windows Media Player
- Institute for Justice and Democracy in Haiti


text:
Subsequent Neoplasms
Therapy-Related Leukemia
Therapy-Related Solid Neoplasms
Subsequent Neoplasms and Genetic Susceptibility
Drug-metabolizing enzymes and DNA repair polymorphisms
Screening and Follow-up for Subsequent Neoplasms
Subsequent neoplasms (SNs), which may be benign or malignant, are defined as histologically distinct neoplasms developing at least 2 months after completion of treatment for the primary malignancy. Childhood cancer survivors have an increased risk of developing SNs that varies by host factors (e.g., genetics, immune function, hormone status), primary cancer therapy, environmental exposures, and lifestyle factors. The Childhood Cancer Survivor Study (CCSS) reported a 30-year cumulative incidence of 20.5% (95% confidence interval [CI], 19.1%–21.8%) for all SNs, 7.9% (95% CI, 7.2%–8.5%) for SNs with malignant histologies (excluding nonmelanoma skin cancer [NMSC]), 9.1% (95% CI, 8.1%–10.1%) for NMSC, and 3.1% (95% CI, 2.5%–3.8%) for meningioma.[1] This represents a sixfold increased risk of SNs among cancer survivors, compared with the general population.[1] SNs are the leading cause of nonrelapse late mortality (standardized mortality ratio = 15.2; 95% CI, 13.9–16.6).[2] The risk of SNs remains elevated for more than 30 years from diagnosis of the primary cancer. Moreover, prolonged follow-up has established that multiple SNs are common among aging childhood cancer survivors.[3]
The development of an SN is likely multifactorial in etiology and results from combinations of influences including gene-environment and gene-gene interactions. Outcome after the diagnosis of an SN is variable as treatment for some histological subtypes may be compromised if childhood cancer therapy included cumulative doses of agents and modalities at the threshold of tissue tolerance.[4] The incidence and type of SNs differ with the primary cancer diagnosis, type of therapy received, and presence of genetic conditions. Unique associations with specific therapeutic exposures have resulted in the classification of SNs into the following two distinct groups:
- Chemotherapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML).
- Radiation-related solid SNs.
Characteristics of t-MDS/AML include a short latency (<10 years from primary cancer diagnosis) and association with alkylating agents and/or topoisomerase II inhibitors.[5,6] Although the long-term risk of subsequent leukemia more than 15 years from primary diagnosis remains significantly elevated (standardized incidence ratio [SIR] = 3.5; 95% CI, 1.9–6.0), these events are relatively rare with an absolute excess risk of 0.02 cases per 1000 person-years.[7] Solid SNs have a strong and well-defined association with radiation and are characterized by a latency that exceeds 10 years.[5] Furthermore, the risk of solid SNs continues to climb with increasing follow-up, whereas the risk of t-MDS/AML plateaus after 10 to 15 years.[8]Therapy-Related Leukemia
Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/AML) has been reported after treatment of Hodgkin lymphoma (HL), acute lymphoblastic leukemia (ALL), and sarcomas, with the cumulative incidence approaching 2% at 15 years after therapy.[8-11] Some cases of late recurrence among childhood acute lymphoblastic leukemia have been shown to represent cases of new primary leukemia based on TCR gene rearrangement.[12,13] t-MDS/AML is a clonal disorder characterized by distinct chromosomal changes. The following two types are recognized by the World Health Organization classification:[10]
- Alkylating agent-related type: Alkylating agents associated with t-MDS/AML include cyclophosphamide, ifosfamide, mechlorethamine, melphalan, busulfan, nitrosoureas, chlorambucil, and dacarbazine.[14] The risk of alkylating agent–related t-MDS/AML is dose dependent, with a latency of 3 to 5 years after exposure; it is associated with abnormalities involving chromosomes 5 (-5/del[5q]) and 7 (-7/del[7q]).[14]
- Topoisomerase II inhibitor-related type: Most of the translocations observed in patients exposed to topoisomerase II inhibitors disrupt a breakpoint cluster region between exons 5 and 11 of the band 11q23 and fuse mixed lineage leukemia with a partner gene.[14] Topoisomerase II inhibitor-related t-AML presents as overt leukemia after a latency of 6 months to 3 years and is associated with balanced translocations involving chromosome bands 11q23 or 21q22.[15]
Therapy-related solid SNs represent 80% of all SNs and demonstrate a strong relationship with ionizing radiation. The histological subtypes of solid SNs encompass a neoplastic spectrum ranging from benign and low-grade malignant lesions (e.g., NMSC, meningiomas) to high-grade malignancies (e.g., breast cancers, glioblastomas).[1,11,16-19] SN solid tumors in childhood cancer survivors most commonly involve the breast, thyroid, central nervous system (CNS), bones, and soft tissues.[1,8,11,17,20] With more prolonged follow-up of cohorts of adults surviving childhood cancer, epithelial neoplasms involving the gastrointestinal tract and lung have emerged.[1,8,16] Benign and low-grade SNs, including NMSCs and meningiomas, have also been observed with increasing prevalence in survivors treated with radiation for childhood cancer.[1,17,18]
The risk of solid SNs is highest when the exposure occurs at a younger age, increases with the total dose of radiation, and with increasing follow-up after radiation.[1] In recipients of a hematopoietic cell transplant conditioned with high-dose busulfan and cyclophosphamide (Bu-Cy), the cumulative incidence of new solid cancers appears to be similar regardless of exposure to radiation. In a registry-based, retrospective, cohort study, Bu-Cy conditioning without total-body irradiation (TBI) was associated with higher risks of solid SNs than in the general population. Chronic graft-versus-host disease increased the risk of SN, especially those involving the oral cavity.[21] Some of the well-established radiation-related solid SNs include the following:[5]
- Skin cancer: NMSCs represent one of the most common SNs among childhood cancer survivors and exhibit a strong association with radiation. Compared with participants who did not receive radiation, CCSS participants treated with radiation had a 6.3-fold increase in risk (95% CI, 3.5–11.3) of reporting a NMSC. Ninety percent of tumors occurred within the radiation field. A CCSS case-control study of the same cohort reported on subsequent basal cell carcinoma. Children who received 35 Gy or more to the skin site had an almost 40-fold excess risk of developing basal cell cancer (odds ratio [OR], 39.8; 95% CI, 8.6–185), compared with those who did not receive radiation; results were consistent with a linear dose-response relationship, with an excess OR per Gy of 1.09 (95% CI, 0.49–2.64).[22] These data underscore the importance of counseling survivors about sun protection behaviors to reduce ultraviolet radiation exposure that may exacerbate this risk.[18] The occurrence of a NMSC as the first SN has been reported to identify a population at high risk for a future invasive malignant SN.[3] CCSS investigators observed a cumulative incidence of a malignant neoplasm of 20.3% (95% CI, 13.0%–27.6%) at 15 years among radiation-exposed survivors who developed NMSC as a first SN compared with 10.7% (95% CI, 7.2%–14.2%) whose first SN was an invasive malignancy.
Malignant melanoma has also been reported as a SN in childhood cancer survivor cohorts, although at a much lower incidence than NMSCs. A systematic review including data from 19 original studies (total N = 151,575 survivors; median follow-up of 13 years) observed an incidence of 10.8 cases of malignant melanoma per 100,000 childhood cancer survivors per year. Risk factors for malignant melanoma identified among these studies included radiation therapy or the combination of alkylating agents and antimitotic drugs. Melanomas most frequently developed in survivors of Hodgkin lymphoma, hereditary retinoblastoma, soft tissue sarcoma, and gonadal tumors, but the relatively small number of survivors represented in the relevant studies preclude assessment of melanoma risk among other types of childhood cancer.[23] CCSS investigators observed an approximate 2.5-fold increased risk (SIR, 2.42; 95% CI, 1.77–3.23) of melanoma among members of their cohort (median time to development, 21.0 years). The cumulative incidence of first subsequent melanoma at 35 years from initial cancer diagnosis was 0.55% (95% CI, 0.37–0.73), and absolute excess risk was 0.10 per 1,000 person-years (95% CI, 0.05–0.15). Family history of cancer, demographic, or treatment-related factors did not predict risk of melanoma.[24]
- Breast cancer: Breast cancer is the most common therapy-related solid SN after HL, largely because of the high-dose chest radiation used to treat HL (SIR of subsequent breast cancer = 25 to 55).[8,25] Excess risk has been reported in female survivors treated with high-dose, extended-volume radiation at age 30 years or younger.[26] Treatment with higher cumulative doses of alkylating agents and ovarian radiation greater than or equal to 5 Gy (exposures predisposing to premature menopause) have been correlated with reductions in breast cancer risk, underscoring the potential contribution of hormonal stimulation on breast carcinogenesis.[27,28] Emerging data indicate that females treated with low-dose, involved-field radiation also exhibit excess breast cancer risk.[29] For female HL patients treated with chest radiation before age 16 years, the cumulative incidence of breast cancer approaches 20% by age 45 years.[8] The latency period after chest radiation ranges from 8 to 10 years, and the risk of subsequent breast cancer increases in a linear fashion with radiation dose (P for trend < .001).[30] Radiation-induced breast cancer has been reported to have more adverse clinicopathological features than breast cancer in age-matched population controls.[31] Although currently available evidence is insufficient to demonstrate a survival benefit from the initiation of breast cancer surveillance in women treated with chest radiation for childhood cancer, interventions to promote detection of small and early-stage tumors may improve prognosis, particularly for those who may have more limited treatment options because of prior exposure to radiation or anthracyclines.
- Thyroid cancer: Thyroid cancer is observed after neck radiation for HL, ALL, and brain tumors; after iodine I 131 metaiodobenzylguanidine (131I-mIBG) treatment for neuroblastoma; and after TBI for hematopoietic stem cell transplantation.[1,8,32] The risk of thyroid cancer has been reported to be 18-fold that of the general population.[33] Radiation therapy at a young age is the major risk factor for the development of subsequent thyroid cancers. A linear dose-response relationship between thyroid cancer and radiation is observed up to 29 Gy, with a decline in the OR at higher doses, especially in children younger than 10 years at treatment, demonstrating evidence for a cell kill effect.[34,35] Female gender, younger age at exposure, and longer time since exposure are significant modifiers of the radiation-related risk of thyroid cancer.[35]
- Brain tumors: Brain tumors develop after cranial radiation for histologically distinct brain tumors [17] or for management of disease among ALL or non-Hodgkin lymphoma patients.[5,36,37] Standardized incidence ratios reported for subsequent CNS neoplasms after treatment for childhood cancer range from 8.1 to 52.3 across studies.[38] The risk for subsequent brain tumors also demonstrates a linear relationship with radiation dose.[1,17,37] The risk of meningioma after radiation not only increases with radiation dose but also with increased dose of intrathecal methotrexate.[39] Cavernomas have also been reported with considerable frequency after CNS radiation but have been speculated to result from angiogenic processes as opposed to true tumorigenesis.[40-42] Despite the well-established increased risk of subsequent CNS neoplasms among childhood cancer survivors treated with cranial irradiation, the current literature is insufficient to evaluate the potential harms and benefits of routine screening for these lesions.[38]
- Bone tumors: The risk of subsequent bone tumors has been reported to be 133-fold that of the general population, with an estimated 20-year cumulative risk of 2.8%.[43] Survivors of hereditary retinoblastoma, Ewing sarcoma, and other malignant bone tumors are at a particularly increased risk.[44] Radiation therapy is associated with a linear dose-response relationship.[44,45] After adjustment for radiation therapy, treatment with alkylating agents has also been linked to bone cancer, with the risk increasing with cumulative drug exposure.[44] These data from earlier studies concur with those observed by the CCSS. In this cohort, an increased risk of subsequent sarcoma was associated with radiation therapy, a primary diagnosis of sarcoma), a history of other SNs, and treatment with higher doses of anthracyclines or alkylating agents.[46] The 30-year cumulative incidence of subsequent sarcoma in CCSS participants was 1.08% for survivors who received radiation and 0.5% for survivors who did not receive radiation.
- Sarcomas: Subsequent sarcomas are uncommon SNs and can be of various histologic subtypes, including nonrhabdomyosarcoma soft tissue sarcomas, rhabdomyosarcoma, malignant peripheral nerve sheath tumors, Ewing/primitive neuroectodermal tumors, and other rare types. The CCSS reported on 105 cases and 422 matched controls in a nested case-control study of 14,372 childhood cancer survivors. Sarcomas occurred at a median of 11.8 years (range, 5.3–31.3 years) from original diagnoses. Any exposure to radiation was associated with increased risk (OR, 4.1; 95% CI, 1.8–9.5), which demonstrated a linear dose-response relationship. Anthracycline exposure was associated with sarcoma risk (OR, 3.5; 95% CI, 1.6–7.7), independent of radiation dose.[47]
- Lung cancer: Among pediatric childhood cancer survivor cohorts, lung cancer represents a relatively uncommon SN; the 30-year cumulative incidence of lung cancer among CCSS participants was 0.1% (95% CI, 0.0%–0.2%).[1] Lung cancer has been reported after chest irradiation for HL. The risk increases in association with longer elapsed time from diagnosis. Smoking has been linked with the occurrence of lung cancer developing after radiation for HL. The increase in risk of lung cancer with increasing radiation dose is greater among patients who smoke after exposure to radiation than among those who refrain from smoking (P = .04).[48]
- Gastrointestinal (GI) cancer: There is emerging evidence that childhood cancer survivors develop GI malignancies more frequently and at a younger age than the general population. The Late Effects Study Group reported a 63.9-fold increased risk of gastric cancers and 36.4-fold increased risk of colorectal cancers in adult survivors of childhood HL.[8] In addition to previous radiation therapy, younger age (0–5 years) at the time of the primary cancer therapy significantly increased risk.
In a French and British cohort-nested, case-control study of childhood solid cancer survivors diagnosed before age 17 years, the risk of developing a SN in the digestive organs varied with therapy. The SNs most often involved the colon/rectum (42%), liver (24%), and stomach (19%). The risk was 9.7-fold higher than in population controls and exhibited a strong radiation dose-response relationship, with an OR of 5.2 (95% CI, 1.7–16.0) for local radiation doses between 10 Gy and 29 Gy and 9.6 (95% CI, 2.6–35.2) for doses of 30 Gy and above, compared with the dose response in survivors who had not received radiation therapy. Chemotherapy alone and combined-modality therapy were associated with a significantly increased risk of developing a GI SN (SIR, 9.1; 95% CI, 2.3–23.6; SIR 29.0; 95% CI, 20.5–39.8).[49]
CCSS investigators reported a 4.6-fold higher risk for GI SNs among their study participants than in the general population (95% CI, 3.4–6.1). The most prevalent GI SN histology was adenocarcinoma (56%). The SNs most often involved the colon (39%), rectum/anus (16%), liver (18%), and stomach (13%). The highest risk for GI SNs was associated with abdominal radiation (SIR, 11.2; CI, 7.6–16.4), but survivors not exposed to radiation also had a significantly increased risk (SIR, 2.4; CI, 1.4–3.9). High-dose procarbazine (relative risk [RR], 3.2; CI 1.1–9.4) and platinum drugs (RR, 7.6; CI, 2.3–25.5) independently increased the risk for GI SNs. The SIR for colorectal cancer was 4.2 (CI, 2.8–6.3).[50]
St. Jude Children's Research Hospital investigators observed that the incidence of a subsequent colorectal carcinoma increased steeply with advancing age, with a 40-year cumulative incidence of 1.4% ± 0.53% among the entire cohort (N = 13,048) and 2.3% ± 0.83% for 5-year survivors. The SIR for subsequent colorectal carcinoma was 10.9 (95% CI, 6.6–17.0) compared with U.S. population controls. Colorectal carcinoma risk increased by 70% with each 10 Gy increase in radiation dose and increasing radiation volume also increased risk. Treatment with alkylating agent chemotherapy was also associated with an 8.8-fold excess risk of subsequent colorectal carcinoma. Collectively, these studies support the need for initiation of colorectal carcinoma surveillance at a young age among survivors receiving high-risk exposures.[51]
- Renal carcinoma: Consistent with reports among survivors of adult-onset cancer, CCSS investigators reported a significant excess of subsequent renal carcinoma among 14,358 5-year survivors in the cohort (SIR, 8.0; 95% CI, 5.2–11.7) compared with the general population. The reported overall absolute excess risk of 8.4 per 105 person-years indicates that these cases are relatively rare. Highest risk was observed among neuroblastoma survivors (SIR, 85.8; 95% CI, 38.4–175.2) and among those treated with renal-directed radiation therapy of 5 Gy or greater (RR, 3.8; 95% CI, 1.6–9.3) and platinum-based chemotherapy (RR, 3.5; 95% CI, 1.0–11.2).[52]
Radiation has been hypothesized to predispose to renal carcinoma among children with high-risk neuroblastoma.[53] Cases of secondary renal carcinoma associated with Xp11.2 translocations and TFE3 gene fusions have also been reported and suggest that cytotoxic chemotherapy may contribute to renal carcinogenesis.[54,55] Underlying genetic predisposition may also play a role because rare cases of renal carcinoma have been observed in children with tuberous sclerosis.[52]
Literature clearly supports the role of chemotherapy and radiation in the development of SNs. However, interindividual variability exists, suggesting that genetic variation has a role in susceptibility to genotoxic exposures, or that genetic susceptibility syndrome confers an increased risk of cancer, such as Li-Fraumeni syndrome. Previous studies have demonstrated that childhood cancer survivors with either a family history of cancer, but more so, presence of Li-Fraumeni syndrome, carry an increased risk of developing an SN.[56,57] The risk of SNs could potentially be modified by mutations in high-penetrance genes that lead to these serious genetic diseases (e.g., Li-Fraumeni syndrome).[57] However, the attributable risk is expected to be very small because of the extremely low prevalence of mutations in high-penetrance genes. Table 1 below summarizes the spectrum of neoplasms, affected genes, and Mendelian mode of inheritance of selected syndromes of inherited cancer predisposition.Table 1. Selected Syndromes of Inherited Cancer Predispositiona
|Major Tumor Types
|Affected Gene
|Mode of Inheritance
|Adenomatous polyposis of the colon
|Colon, hepatoblastoma, intestinal cancers, stomach, thyroid cancer
|Leukemia, lymphoma
|Beckwith-Wiedemann syndrome
|Adrenal carcinoma, hepatoblastoma, rhabdomyosarcoma, Wilms tumor
|Bloom syndrome
|Leukemia, lymphoma, skin cancer
|Fanconi anemia
|Gynecological tumors, leukemia, squamous cell carcinoma
|Juvenile polyposis syndrome
|Gastrointestinal tumors
|Li-Fraumeni syndrome
|Adrenocortical carcinoma, brain tumor, breast carcinoma, leukemia, osteosarcoma, soft tissue sarcoma
|Multiple endocrine neoplasia 1
|Pancreatic islet cell tumor, parathyroid adenoma, pituitary adenoma
|Multiple endocrine neoplasia 2
|Medullary thyroid carcinoma, pheochromocytoma
|Neurofibromatosis type 1
|Neurofibroma, optic pathway glioma, peripheral nerve sheath tumor
|Neurofibromatosis type 2
|Vestibular schwannoma
|Nevoid basal cell carcinoma syndrome
|Basal cell carcinoma, medulloblastoma
|Peutz-Jeghers syndrome
|Intestinal cancers, ovarian carcinoma, pancreatic carcinoma
|Osteosarcoma, retinoblastoma
|Tuberous sclerosis
|Hamartoma, renal angiomyolipoma, renal cell carcinoma
|von Hippel-Lindau syndrome
|Hemangioblastoma, pheochromocytoma, renal cell carcinoma, retinal and central nervous tumors
|WAGR syndrome
|Gonadoblastoma, Wilms tumor
|Wilms tumor syndrome
|Wilms tumor
|Xeroderma pigmentosum
|Leukemia, melanoma
|WAGR = Wilms tumor, aniridia, genitourinary anomalies, mental retardation.
|aAdapted from Strahm et al.[58]
Drug-metabolizing enzymes and DNA repair polymorphisms
The interindividual variability in risk of SNs is more likely related to common polymorphisms in low-penetrance genes that regulate the availability of active drug metabolites or are responsible for DNA repair. Gene-environment interactions may magnify subtle functional differences resulting from genetic variations.Drug-metabolizing enzymes
Metabolism of genotoxic agents occurs in two phases. Phase I involves activation of substrates into highly reactive electrophilic intermediates that can damage DNA, a reaction principally performed by the cytochrome p450 (CYP) family of enzymes. Phase II enzymes (conjugation) function to inactivate genotoxic substrates. The phase II proteins comprise the glutathione S-transferase (GST), NAD(P)H:quinone oxidoreductase-1 (NQO1), and others. The balance between the two sets of enzymes is critical to the cellular response to xenobiotics; for example, high activity of a phase I enzyme and low activity of a phase II enzyme can result in DNA damage.DNA repair polymorphisms
DNA repair mechanisms protect somatic cells from mutations in tumor suppressor genes and oncogenes that can lead to cancer initiation and progression. An individual's DNA repair capacity appears to be genetically determined.[59] A number of DNA repair genes contain polymorphic variants, resulting in large interindividual variations in DNA repair capacity.[59] Evaluation of the contribution of polymorphisms influencing DNA repair to the risk of SN represents an active area of research.Screening and Follow-up for Subsequent Neoplasms
Vigilant screening is important for those at risk.[60] Because of the relatively small size of the pediatric cancer survivor population and the prevalence and time to onset of therapy-related complications, undertaking clinical studies to assess the impact of screening recommendations on the morbidity and mortality associated with the late effect is not feasible. However, well-conducted studies on large populations of childhood cancer survivors have provided compelling evidence linking specific therapeutic exposures and late effects. This evidence has been used by several national and international cooperative groups (Scottish Collegiate Guidelines Network, Children's Cancer and Leukaemia Group, Children's Oncology Group [COG]) to develop consensus-based clinical practice guidelines to increase awareness and standardize the immediate care needs of medically vulnerable childhood cancer survivors. The COG Guidelines employ a hybrid approach that is both evidence-based (utilizing established associations between therapeutic exposures and late effects to identify high-risk categories) and grounded in the collective clinical experience of experts (matching the magnitude of the risk with the intensity of the screening recommendations). The screening recommendations in these guidelines represent a statement of consensus from a panel of experts in the late effects of pediatric cancer treatment.[60]
In regard to screening for malignant SNs recommended by the COG Guidelines, certain high-risk populations of childhood cancer survivors merit heightened surveillance due to predisposing host, behavioral, or therapeutic factors.
- Screening for leukemia: t-MDS/AML usually manifests within 10 years after exposure. Recommendations include monitoring with annual complete blood count for 10 years after exposure to alkylating agents or topoisomerase II inhibitors.
- Screening after radiation exposure: Most other SNs are associated with radiation exposure. Screening recommendations include careful annual physical examination of the skin and underlying tissues in the radiation field. Specific comments about screening for more common radiation-associated SNs follow:
- Screening for early-onset skin cancer: Annual dermatological exam should focus on skin lesions and pigmented nevi in the radiation field. Survivors should be counseled about their increased risk of skin cancer, the potential exacerbation of risk through tanning, and the benefits of adhering to behaviors to protect the skin from excessive ultraviolet radiation exposure.
- Screening for early-onset breast cancer: Since outcome after breast cancer is directly linked to stage at diagnosis, close surveillance resulting in early diagnosis should confer survival advantage.[61] Mammography, the most widely accepted screening tool for breast cancer in the general population, may not be the ideal screening tool by itself for radiation-related breast cancers occurring in relatively young women with dense breasts; hence, the American Cancer Society recommends including adjunct screening with magnetic resonance imaging (MRI).[62] Many clinicians are concerned about potential harms related to radiation exposure associated with annual mammography in these young women. In this regard, it is important to consider that the estimated mean breast dose with contemporary standard two-view screening mammograms is about 3.85 mGy to 4.5 mGy.[63-65] Thus, 15 additional surveillance mammograms from age 25 to 39 years would increase the total radiation exposure in a woman treated with 20 Gy of chest radiation to 20.05775 Gy. The benefits of detection of early breast cancer lesions in high-risk women must be balanced by the risk predisposed by a 0.3% additional radiation exposure. To keep young women engaged in breast health surveillance, the COG Guideline recommendations for females who received radiation with potential impact to the breast (i.e., radiation doses of 20 Gy or higher to the mantle, mediastinal, whole lung, and axillary fields) include monthly breast self-examination beginning at puberty; annual clinical breast examinations beginning at puberty until age 25 years; and a clinical breast examination every 6 months, with annual mammograms and MRIs beginning 8 years after radiation or at age 25 years (whichever occurs later).
- Screening for early-onset colorectal cancer: Screening of those at risk of early-onset colorectal cancer (i.e., radiation doses of 30 Gy or higher to the abdomen, pelvis, or spine) should include colonoscopy every 5 years beginning at age 35 years or 10 years after radiation (whichever occurs later).
- Friedman DL, Whitton J, Leisenring W, et al.: Subsequent neoplasms in 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. J Natl Cancer Inst 102 (14): 1083-95, 2010. [PUBMED Abstract]
- Mertens AC, Liu Q, Neglia JP, et al.: Cause-specific late mortality among 5-year survivors of childhood cancer: the Childhood Cancer Survivor Study. J Natl Cancer Inst 100 (19): 1368-79, 2008. [PUBMED Abstract]
- Armstrong GT, Liu W, Leisenring W, et al.: Occurrence of multiple subsequent neoplasms in long-term survivors of childhood cancer: a report from the childhood cancer survivor study. J Clin Oncol 29 (22): 3056-64, 2011. [PUBMED Abstract]
- Travis LB, Rabkin CS, Brown LM, et al.: Cancer survivorship--genetic susceptibility and second primary cancers: research strategies and recommendations. J Natl Cancer Inst 98 (1): 15-25, 2006. [PUBMED Abstract]
- Bhatia S, Sklar C: Second cancers in survivors of childhood cancer. Nat Rev Cancer 2 (2): 124-32, 2002. [PUBMED Abstract]
- Berger C, Trombert-Paviot B, Casagranda L, et al.: Second malignant neoplasms following childhood cancer: a study of a recent cohort (1987-2004) from the childhood cancer registry of the Rhône-Alpes region (ARCERRA) in France. Pediatr Hematol Oncol 28 (5): 364-79, 2011. [PUBMED Abstract]
- Nottage K, Lanctot J, Li Z, et al.: Long-term risk for subsequent leukemia after treatment for childhood cancer: a report from the Childhood Cancer Survivor Study. Blood 117 (23): 6315-8, 2011. [PUBMED Abstract]
- Bhatia S, Yasui Y, Robison LL, et al.: High risk of subsequent neoplasms continues with extended follow-up of childhood Hodgkin's disease: report from the Late Effects Study Group. J Clin Oncol 21 (23): 4386-94, 2003. [PUBMED Abstract]
- Bhatia S, Sather HN, Pabustan OB, et al.: Low incidence of second neoplasms among children diagnosed with acute lymphoblastic leukemia after 1983. Blood 99 (12): 4257-64, 2002. [PUBMED Abstract]
- Vardiman JW, Harris NL, Brunning RD: The World Health Organization (WHO) classification of the myeloid neoplasms. Blood 100 (7): 2292-302, 2002. [PUBMED Abstract]
- Hijiya N, Hudson MM, Lensing S, et al.: Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia. JAMA 297 (11): 1207-15, 2007. [PUBMED Abstract]
- Hijiya N, Ness KK, Ribeiro RC, et al.: Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer 115 (1): 23-35, 2009. [PUBMED Abstract]
- Szczepanski T, van der Velden VH, Waanders E, et al.: Late recurrence of childhood T-cell acute lymphoblastic leukemia frequently represents a second leukemia rather than a relapse: first evidence for genetic predisposition. J Clin Oncol 29 (12): 1643-9, 2011. [PUBMED Abstract]
- Thirman MJ, Larson RA: Therapy-related myeloid leukemia. Hematol Oncol Clin North Am 10 (2): 293-320, 1996. [PUBMED Abstract]
- Pedersen-Bjergaard J, Philip P: Balanced translocations involving chromosome bands 11q23 and 21q22 are highly characteristic of myelodysplasia and leukemia following therapy with cytostatic agents targeting at DNA-topoisomerase II. Blood 78 (4): 1147-8, 1991. [PUBMED Abstract]
- Bassal M, Mertens AC, Taylor L, et al.: Risk of selected subsequent carcinomas in survivors of childhood cancer: a report from the Childhood Cancer Survivor Study. J Clin Oncol 24 (3): 476-83, 2006. [PUBMED Abstract]
- Neglia JP, Robison LL, Stovall M, et al.: New primary neoplasms of the central nervous system in survivors of childhood cancer: a report from the Childhood Cancer Survivor Study. J Natl Cancer Inst 98 (21): 1528-37, 2006. [PUBMED Abstract]
- Perkins JL, Liu Y, Mitby PA, et al.: Nonmelanoma skin cancer in survivors of childhood and adolescent cancer: a report from the childhood cancer survivor study. J Clin Oncol 23 (16): 3733-41, 2005. [PUBMED Abstract]
- Boukheris H, Stovall M, Gilbert ES, et al.: Risk of salivary gland cancer after childhood cancer: a report from the Childhood Cancer Survivor Study. Int J Radiat Oncol Biol Phys 85 (3): 776-83, 2013. [PUBMED Abstract]
- Ronckers CM, Sigurdson AJ, Stovall M, et al.: Thyroid cancer in childhood cancer survivors: a detailed evaluation of radiation dose response and its modifiers. Radiat Res 166 (4): 618-28, 2006. [PUBMED Abstract]
- Majhail NS, Brazauskas R, Rizzo JD, et al.: Secondary solid cancers after allogeneic hematopoietic cell transplantation using busulfan-cyclophosphamide conditioning. Blood 117 (1): 316-22, 2011. [PUBMED Abstract]
- Watt TC, Inskip PD, Stratton K, et al.: Radiation-related risk of basal cell carcinoma: a report from the Childhood Cancer Survivor Study. J Natl Cancer Inst 104 (16): 1240-50, 2012. [PUBMED Abstract]
- Braam KI, Overbeek A, Kaspers GJ, et al.: Malignant melanoma as second malignant neoplasm in long-term childhood cancer survivors: a systematic review. Pediatr Blood Cancer 58 (5): 665-74, 2012. [PUBMED Abstract]
- Pappo AS, Armstrong GT, Liu W, et al.: Melanoma as a subsequent neoplasm in adult survivors of childhood cancer: a report from the childhood cancer survivor study. Pediatr Blood Cancer 60 (3): 461-6, 2013. [PUBMED Abstract]
- Kenney LB, Yasui Y, Inskip PD, et al.: Breast cancer after childhood cancer: a report from the Childhood Cancer Survivor Study. Ann Intern Med 141 (8): 590-7, 2004. [PUBMED Abstract]
- Travis LB, Hill D, Dores GM, et al.: Cumulative absolute breast cancer risk for young women treated for Hodgkin lymphoma. J Natl Cancer Inst 97 (19): 1428-37, 2005. [PUBMED Abstract]
- Travis LB, Hill DA, Dores GM, et al.: Breast cancer following radiotherapy and chemotherapy among young women with Hodgkin disease. JAMA 290 (4): 465-75, 2003. [PUBMED Abstract]
- van Leeuwen FE, Klokman WJ, Stovall M, et al.: Roles of radiation dose, chemotherapy, and hormonal factors in breast cancer following Hodgkin's disease. J Natl Cancer Inst 95 (13): 971-80, 2003. [PUBMED Abstract]
- O'Brien MM, Donaldson SS, Balise RR, et al.: Second malignant neoplasms in survivors of pediatric Hodgkin's lymphoma treated with low-dose radiation and chemotherapy. J Clin Oncol 28 (7): 1232-9, 2010. [PUBMED Abstract]
- Inskip PD, Robison LL, Stovall M, et al.: Radiation dose and breast cancer risk in the childhood cancer survivor study. J Clin Oncol 27 (24): 3901-7, 2009. [PUBMED Abstract]
- Dores GM, Anderson WF, Beane Freeman LE, et al.: Risk of breast cancer according to clinicopathologic features among long-term survivors of Hodgkin's lymphoma treated with radiotherapy. Br J Cancer 103 (7): 1081-4, 2010. [PUBMED Abstract]
- van Santen HM, Tytgat GA, van de Wetering MD, et al.: Differentiated thyroid carcinoma after 131I-MIBG treatment for neuroblastoma during childhood: description of the first two cases. Thyroid 22 (6): 643-6, 2012. [PUBMED Abstract]
- Sklar C, Whitton J, Mertens A, et al.: Abnormalities of the thyroid in survivors of Hodgkin's disease: data from the Childhood Cancer Survivor Study. J Clin Endocrinol Metab 85 (9): 3227-32, 2000. [PUBMED Abstract]
- Sigurdson AJ, Ronckers CM, Mertens AC, et al.: Primary thyroid cancer after a first tumour in childhood (the Childhood Cancer Survivor Study): a nested case-control study. Lancet 365 (9476): 2014-23, 2005 Jun 11-17. [PUBMED Abstract]
- Bhatti P, Veiga LH, Ronckers CM, et al.: Risk of second primary thyroid cancer after radiotherapy for a childhood cancer in a large cohort study: an update from the childhood cancer survivor study. Radiat Res 174 (6): 741-52, 2010. [PUBMED Abstract]
- Neglia JP, Friedman DL, Yasui Y, et al.: Second malignant neoplasms in five-year survivors of childhood cancer: childhood cancer survivor study. J Natl Cancer Inst 93 (8): 618-29, 2001. [PUBMED Abstract]
- Neglia JP, Meadows AT, Robison LL, et al.: Second neoplasms after acute lymphoblastic leukemia in childhood. N Engl J Med 325 (19): 1330-6, 1991. [PUBMED Abstract]
- Bowers DC, Nathan PC, Constine L, et al.: Subsequent neoplasms of the CNS among survivors of childhood cancer: a systematic review. Lancet Oncol 14 (8): e321-8, 2013. [PUBMED Abstract]
- Taylor AJ, Little MP, Winter DL, et al.: Population-based risks of CNS tumors in survivors of childhood cancer: the British Childhood Cancer Survivor Study. J Clin Oncol 28 (36): 5287-93, 2010. [PUBMED Abstract]
- Faraci M, Morana G, Bagnasco F, et al.: Magnetic resonance imaging in childhood leukemia survivors treated with cranial radiotherapy: a cross sectional, single center study. Pediatr Blood Cancer 57 (2): 240-6, 2011. [PUBMED Abstract]
- Vinchon M, Leblond P, Caron S, et al.: Radiation-induced tumors in children irradiated for brain tumor: a longitudinal study. Childs Nerv Syst 27 (3): 445-53, 2011. [PUBMED Abstract]
- Koike T, Yanagimachi N, Ishiguro H, et al.: High incidence of radiation-induced cavernous hemangioma in long-term survivors who underwent hematopoietic stem cell transplantation with radiation therapy during childhood or adolescence. Biol Blood Marrow Transplant 18 (7): 1090-8, 2012. [PUBMED Abstract]
- Tucker MA, D'Angio GJ, Boice JD Jr, et al.: Bone sarcomas linked to radiotherapy and chemotherapy in children. N Engl J Med 317 (10): 588-93, 1987. [PUBMED Abstract]
- Hawkins MM, Wilson LM, Burton HS, et al.: Radiotherapy, alkylating agents, and risk of bone cancer after childhood cancer. J Natl Cancer Inst 88 (5): 270-8, 1996. [PUBMED Abstract]
- Le Vu B, de Vathaire F, Shamsaldin A, et al.: Radiation dose, chemotherapy and risk of osteosarcoma after solid tumours during childhood. Int J Cancer 77 (3): 370-7, 1998. [PUBMED Abstract]
- Henderson TO, Whitton J, Stovall M, et al.: Secondary sarcomas in childhood cancer survivors: a report from the Childhood Cancer Survivor Study. J Natl Cancer Inst 99 (4): 300-8, 2007. [PUBMED Abstract]
- Henderson TO, Rajaraman P, Stovall M, et al.: Risk factors associated with secondary sarcomas in childhood cancer survivors: a report from the childhood cancer survivor study. Int J Radiat Oncol Biol Phys 84 (1): 224-30, 2012. [PUBMED Abstract]
- van Leeuwen FE, Klokman WJ, Stovall M, et al.: Roles of radiotherapy and smoking in lung cancer following Hodgkin's disease. J Natl Cancer Inst 87 (20): 1530-7, 1995. [PUBMED Abstract]
- Tukenova M, Diallo I, Anderson H, et al.: Second malignant neoplasms in digestive organs after childhood cancer: a cohort-nested case-control study. Int J Radiat Oncol Biol Phys 82 (3): e383-90, 2012. [PUBMED Abstract]
- Henderson TO, Oeffinger KC, Whitton J, et al.: Secondary gastrointestinal cancer in childhood cancer survivors: a cohort study. Ann Intern Med 156 (11): 757-66, W-260, 2012. [PUBMED Abstract]
- Nottage K, McFarlane J, Krasin MJ, et al.: Secondary colorectal carcinoma after childhood cancer. J Clin Oncol 30 (20): 2552-8, 2012. [PUBMED Abstract]
- Wilson CL, Ness KK, Neglia JP, et al.: Renal carcinoma after childhood cancer: a report from the childhood cancer survivor study. J Natl Cancer Inst 105 (7): 504-8, 2013. [PUBMED Abstract]
- Fleitz JM, Wootton-Gorges SL, Wyatt-Ashmead J, et al.: Renal cell carcinoma in long-term survivors of advanced stage neuroblastoma in early childhood. Pediatr Radiol 33 (8): 540-5, 2003. [PUBMED Abstract]
- Hedgepeth RC, Zhou M, Ross J: Rapid development of metastatic Xp11 translocation renal cell carcinoma in a girl treated for neuroblastoma. J Pediatr Hematol Oncol 31 (8): 602-4, 2009. [PUBMED Abstract]
- Argani P, Laé M, Ballard ET, et al.: Translocation carcinomas of the kidney after chemotherapy in childhood. J Clin Oncol 24 (10): 1529-34, 2006. [PUBMED Abstract]
- Andersson A, Enblad G, Tavelin B, et al.: Family history of cancer as a risk factor for second malignancies after Hodgkin's lymphoma. Br J Cancer 98 (5): 1001-5, 2008. [PUBMED Abstract]
- Hisada M, Garber JE, Fung CY, et al.: Multiple primary cancers in families with Li-Fraumeni syndrome. J Natl Cancer Inst 90 (8): 606-11, 1998. [PUBMED Abstract]
- Strahm B, Malkin D: Hereditary cancer predisposition in children: genetic basis and clinical implications. Int J Cancer 119 (9): 2001-6, 2006. [PUBMED Abstract]
- Collins A, Harrington V: Repair of oxidative DNA damage: assessing its contribution to cancer prevention. Mutagenesis 17 (6): 489-93, 2002. [PUBMED Abstract]
- Landier W, Bhatia S, Eshelman DA, et al.: Development of risk-based guidelines for pediatric cancer survivors: the Children's Oncology Group Long-Term Follow-Up Guidelines from the Children's Oncology Group Late Effects Committee and Nursing Discipline. J Clin Oncol 22 (24): 4979-90, 2004. [PUBMED Abstract]
- Diller L, Medeiros Nancarrow C, Shaffer K, et al.: Breast cancer screening in women previously treated for Hodgkin's disease: a prospective cohort study. J Clin Oncol 20 (8): 2085-91, 2002. [PUBMED Abstract]
- Saslow D, Boetes C, Burke W, et al.: American Cancer Society guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin 57 (2): 75-89, 2007 Mar-Apr. [PUBMED Abstract]
- Berrington de Gonzalez A, Berg CD, Visvanathan K, et al.: Estimated risk of radiation-induced breast cancer from mammographic screening for young BRCA mutation carriers. J Natl Cancer Inst 101 (3): 205-9, 2009. [PUBMED Abstract]
- Young KC, Burch A, Oduko JM: Radiation doses received in the UK Breast Screening Programme in 2001 and 2002. Br J Radiol 78 (927): 207-18, 2005. [PUBMED Abstract]
- Spelic DC: Updated Trends in Mammography Dose and Image Quality. Silver Spring, Md: U.S. Food and Drug Administration, 2006. Available online. Last accessed April 04, 2014.

subset: commoncrawl


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Manning was one of the first soldiers to learn of the fiasco, having been ordered to investigate the "bad guys" after the raid. "It turned out they had printed a benign political critique titled 'Where Did the Money Go?' following a corruption trial within the prime minister's cabinet," he said. Shocked, Manning "immediately took that information and ran to the officer [in charge] to explain what was going on." The officer told him to "shut up," he said. "He didn't want to hear any of it."
Manning knew the 15 Iraqis were doomed. The Iraqi police were known to torture their prisoners, while the U.S. military looked the other way. Manning couldn't. "That was a point where I was actively involved in something that I was completely against," he said. "And completely helpless." From then on, "everything started slipping. I saw things differently."
According to the government's charges, Manning made his first contact with WikiLeaks in November 2009, either just before or not long after the detainee incident. He would ultimately say he made direct contact with the "crazy white-haired Aussie" otherwise known as Julian Assange, though whether he spoke directly to Assange is unknown. "I've talked to Julian many times, but I've also talked to other guys too who were also 'Julian,'" says one hacker who's worked with WikiLeaks. "You can never be sure who is who."
Among the first things Manning leaked was a 17-minute video, which was titled "Collateral Murder." The video, taken in 2007, depicts Apache helicopters firing on unarmed civilians who appear to be mingling with insurgents in the street. The wounded crawl away and are shot dead. A van appears to retrieve the bodies; there are kids inside. They are shot, too. The crew banters back and forth as if they're playing Call of Duty. "Look at those dead bastards," one says. "Well," remarks another, "it's their fault for bringing their kids into a battle."
Manning had watched the video in the SCIF – these kinds of films played routinely and were watched by dozens of people. "At first glance, it was just a bunch of guys getting shot up by a helicopter . . . . No big deal," he said. "But something struck me as odd with the van thing . And also the fact that it was being stored in a JAG officer's directory." So Manning dug deeper, eventually tracking down the date of the incident and the GPS coordinates, and coming up with a story from The New York Times discussing the death of two Iraqi journalists among 16 killed in a clash with "Shiite militias." "It was unreal," Manning said. "It humanized the whole thing. I just couldn't let these things stay inside my head."
"Collateral Murder" was released on April 5th, 2010, at a WikiLeaks press conference at the National Press Club in Washington, D.C. Within days, it had gone viral – a graphic snapshot of 21st-century soldiering run amok – and was held up by media organizations worldwide as documentation of a war crime.
Manning, meanwhile, had the surreal experience of watching the reaction to his leak from the confines of his base. He was amazed when several of the perpetrators of the attack issued mea culpas, and he friended a few on Facebook without them having any idea who he was. But the crushing routine of the FOB, made worse by his isolation and gender-identity crisis, weighed on Manning. Between December 2009 and May 2010, the period Manning was allegedly in contact with WikiLeaks, superiors noticed a drop-off in both his performance and his mental state, culminating with an incident on May 7th, 2010, when he was found curled up on the floor of the SCIF in a fetal position, having carved the words I WANT into a chair. A few hours later, Manning punched a superior in the face. "I'm tired of this!" he said, as his target, Spc. Jihrleah Showman, pinned him to the ground.
The following day, Manning was demoted back to private first class, removed from his job as an analyst and assigned to the supply room as a clerk. Already miserable, he was now as marginalized as he'd ever been. For Manning, it seemed as if the "only safe place," as he put it, was the Internet.
One lonely night, looking for connection and having reached out to strangers online before, he e-mailed a 29-year-old security consultant named Adrian Lamo. A once-handsome Colombian-American with a prescription-drug habit, Lamo had become famous in the early 2000s as the "homeless hacker," a digital savant who, having dropped out of high school in San Francisco, traveled the country on a Greyhound, sleeping on friends' couches or in abandoned buildings, downing handfuls of amphetamines and using his battered Toshiba laptop to troll through the databases of corporate behemoths like Yahoo, AOL and MCI WorldCom – after which he'd helpfully explain to the companies' system administrators how to plug the holes he'd found.
Lamo's career as a "security do-gooder" ended abruptly in 2002, after he, then 21, hacked The New York Times and notified the company to point out its security flaws. The Times was not amused. In 2004, after a lengthy FBI investigation, Lamo pleaded guilty to computer crimes, for which he was given a sentence of six months under house arrest.
Other hackers regarded Lamo with a mix of curiosity and distrust. "No one can really pinpoint anything particular that he'd done, at least since he'd stopped actively hacking," says Griffin Boyce, a Web developer who knows Lamo. "He took otherwise-secret activities and was fairly open about them; that made people nervous. It's incredibly foolish to speak to the media about doing something illegal." Within many circles, the consensus was that Lamo, desperate for recognition, might do virtually anything for publicity.
But Bradley Manning knew none of this. All he knew was that Lamo, who was openly bisexual, had starred in a 2003 documentary, Hackers Wanted, which focused on Lamo's travails with law enforcement; he also knew, from Lamo's tweets, that he supported WikiLeaks. Hackers Wanted had never been released, but in May 2010 it leaked online. Shortly afterward, Lamo received a message from a stranger.
"Hi," wrote aperson named "bradass87." "How are you? I'm an Army intelligence analyst, deployed to eastern Baghdad, pending discharge for 'adjustment disorder.'. . . I'm sure you're pretty busy . . . [but] if you had unprecedented access to classified networks 14 hours a day, 7 days a week for 8-plus months, what would you do?"
Lamo notified the authorities, and over the course of the next several days, he surreptitiously logged their chats. Manning, believing he was speaking confidentially, let loose. He explained the WikiLeaks submission process and said he'd talked with Assange numerous times. He went into depth about lack of security at his FOB and how easy it was to steal information. "The culture bred opportunities," he said. He referred to himself as a "mess," and spoke of his disillusionment – "I don't believe in good guys versus bad guys anymore only [in] a plethora of states acting in self interest." He often seemed like he was having a nervous breakdown.
Lamo would later say that he was afraid Manning's leaking could put American lives at risk. "Brad was detailing his last-ditch vision of an effort to save the world from itself," Lamo says. "I was seeing my own worst-case scenario of long ago play out: the arbitrary scattering of data that was at best hopelessly subjective and at worst prone to misuse. Truth is an elusive, personal thing," he adds. "Brad confused facts with truth. You can't convince people of a truth they don't want to see."
On May 25th, Lamo met with government agents at a Starbucks near his house in Carmichael, California, and handed over the logs of his chats, providing investigators with the crux of their evidence against Manning. Two days later, a week after initiating contact with Lamo, Manning was stopped by Army CID agents while at work in the supply room at FOB Hammer, escorted into a conference room and handed a piece of paper explaining his legal rights. After a brief hearing before an Army magistrate in Baghdad, he was remanded into the custody of the United States military, pending trial. The agony of Manning's Army career was at an end. But the real torture was yet to come.
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---- — PLATTSBURGH — A Potsdam woman was charged Sunday with felony driving while intoxicated with a prior conviction.
At 9:50 p.m. Feb. 16, Plattsburgh City Police received a call reporting that a red passenger car was traveling the wrong way on Oak Street, said Plattsburgh City Police Lt. Scott Beebie.
Officers initially did not find the vehicle but eventually stopped a red Dodge Neon on Court Street, Beebie said.
Officers saw the driver, Felecia Weller, 29, attempt to scoot from the driver's seat to the passenger's seat so it would appear that she had not been driving the vehicle, Beebie said.
Roadside sobriety tests were administered and Weller was found to be impaired, Beebie said.
Her driving history showed a prior driving while intoxicated conviction, he said.
Weller was arrested just before 1:30 a.m. Feb. 17 and was charged with driving while intoxicated with a prior designated offense within the past 10 years, a felony, and three traffic violations: having an expired or no vehicle inspection certificate, refusal to submit to a pre-screen test and having an open container of alcohol in the vehicle.
Weller was arraigned in Plattsburgh City Court, Beebie said.
— By Staff Writer Felicia Krieg


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the best reviews
their picks
what to buy
DVD recorders are home-theater components that can record TV shows (and other programs) onto DVDs, replicating the functions of a VCR. DVD recorders also function as regular DVD players and can play audio CDs, but not high-def Blu-ray Discs. While Blu-ray Disc burners for computers have become commonplace, stand-alone consumer Blu-ray recorders are not available.
Be aware that if you don't need to record to discs, a DVR is a better option. Reviewers say TiVo has the best interface. However, almost all cable and satellite companies also offer a DVR for a monthly fee -- or in some cases free with a qualifying programming package. Critics say these are catching up to TiVo recorders and even surpassing them in some respects. DVRs allow you to record programs to a hard drive for later playback, and many allow you to record in high definition, but you can't record directly to a disc. Most will let you record one show while watching another and introduce useful features, such as the ability to pause live programming, skip backwards to watch something you missed or skip ahead while watching recorded or buffered programs -- sometimes at intervals conveniently timed to coincide with an average TV commercial. See our report on DVRs for more information.
As a category, DVD recorders are among the most maligned of
consumer-electronics products. Common complaints include failure to record
programs (either through user or player error), hard-to-understand instructions
and confusion over recordable-disc formats. Broadcasters and
cable-casters add to the frustrations of DVD-recorder owners -- and makers as well -- by introducing restrictions on what programs can be copied to what devices; see What to Look For to learn more.
DVD recorders with hard-disk drives, though more expensive and harder to find, fare somewhat better: If the process of recording to a disc fails, you still have a copy on the hard drive so you can try again. DVD recorders that include a hard-disk drive have some DVR-like features -- such as instant replay or the ability to watch a previously recorded program while recording another -- but generally can't completely keep up with DVRs when it comes to features and functions. They also have a much more primitive user interface.
Basic DVD recorders are the least expensive and least versatile DVD recorders you can buy. These recorders are thin on features, often lacking elements like an IR blaster, which is helpful for timed satellite or cable TV recording (though many cable and satellite TV boxes now have their own timers). Editing is limited and often difficult, with capabilities largely dictated by the DVD format you use (see our What to Look For section). Some units lack built-in tuners. While these DVD recorders are fine for use with cable TV or satellite TV boxes, they are a poor choice for those who get some or all of their programming the old-fashioned way, via TV antenna.
Once plentiful, relatively few DVD recorders are still in production. Among current basic DVD recorders, the Toshiba DR430 (*Est. $95) gets the most feedback. Not all of it is positive, but complaints reflect the frustrations that DVD recorders typically elicit. Otherwise, most owners seem pleased enough. There's no tuner, but a handful of convenience features are present, such as the ability to begin watching a program before it has finished recording and to skip ahead over commercials. A satellite link feature turns the recorder on if it detects a video signal at a specific input, which can simplify making unattended recordings for cable TV/satellite TV subscribers -- assuming that their converter box has its own timer feature (most do). File support for digital files is pretty skimpy -- just MP3 music files and JPEG photo files -- but a USB input is provided for playing those back from a USB flash drive.
Toshiba DR430 can only play back DVDs recorded in standard definition, but can
upconvert them to 1080p resolution over its HDMI link for display on an HDTV.
If you only have a
standard-definition TV, or if your HDTV does a good job of upconverting standard-def programming on its own, the Magnavox ZC320MW8B (*Est. $100) might be worth considering. Features are otherwise similar, though file support is slimmer still (just MP3 files) and there's no USB input. Feedback is more limited than for the Toshiba DR430, but most users seem happy. That said, since prices are in the same ballpark, the Toshiba DR430 is a better deal at present.
For those who need a DVD recorder with its own tuner, or want something that's more feature-rich/easier to use than a basic model, the only choice is a major step up to a DVD recorder with a built-in hard drive. The cost is really the only downside, as most reviews say that using this type of DVD recorder is a much more pleasant experience. That's why it is so disappointing that virtually every manufacturer has stopped offering them in the U.S. Funai is the sole exception, offering hard-disk drive (HDD) DVD recorders under its Magnavox brand. The good news is that while experts have been slow to report, there's more than enough user feedback that these HDD DVD recorders are capable performers.
The Magnavox MDR515H/F7 ( *Est. $330) features a 500 GB hard-disk drive. That gives you enough capacity for 620 hours of video in the lowest-quality mode or 103 hours of the highest-quality video. Unlike the better recorders of the past, or most current DVRs, the Magnavox MDR515H/F7 lacks its own programming guide, but it can use the one sent by over-the-air digital stations as part of the digital broadcasting standard. Unfortunately, you can't use that guide to select programs to record; users have to resort to the old-fashioned system of entering channels and recording times manually, much like a VCR.
While the Magnavox MDR515H/F7 can't really replace a digital video recorder, it does include some DVR features, such as the ability to pause and resume live TV. DVD recording is generally much easier than with a more basic machine, plus you have the advantage of having your program archived on the hard disk should something go wrong. A one-hour power backup for timers in case of a power failure is another helpful plus. There aren't any professional reviews of the Magnavox MDR515H/F7, but more than 600 owners have weighed in at Walmart.com.
Magnavox also offers the step-down MDR513H/F7 (*Est. $400), but it has become very hard to find at retail so pricing has skewed upwards, making it a very questionable value at the time of this report. The Magnavox MDR513H/F7 has a smaller 320 GB hard drive that can store 387 hours of programming at the lowest-quality setting and 64 hours at the highest-quality setting. It also lacks some features, such as the power backup for the recorder's timers, and the remote is not as well liked. However, performance and overall functionality are similar to the MDR515/F7. User reviews have been equally strong as well.
Most professional reviewers have abandoned coverage of DVD recorders, but About.com covers one current model in a brief report. (Note: ConsumerSearch is owned by About.com, but the two don't share an editorial affiliation.) However, we found lots and lots of user reviews at retailer sites such as Amazon.com, Walmart.com and others. AVSForum.com is an audio and video enthusiast community with a forum dedicated to DVD recorders.
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text:
Founded in 1853 by Jens Wilhelm Hansen. Hansen's two sons Jonas (1850-1919) and Alfred (1854-1923) joined the firm in 1874, the year before acquisition of the Copenhagen publisher C. E. Horneman. Works by Danish composers like Niels Gade and J. P. E. Hartmann plus the Norwegian Christian Sinding were added in this period of expansion, which also saw the acquisition of publishers Lose, Horneman & Erslev, Carl Warmuth (Oslo, 1908) and Nordisk (1910). Notable Scandinavian composers added in the 20th century include Jean Sibelius, Carl Nielsen, Emil Hartmann, Wilhelm Stenhammar, and Selim Palmgren. Hansen opened branches in Leipzig (1887-1940), New York (ca.1974) and subsidiaries included Norsk (Oslo, from 1908), Nordiska (Stockholm, from 1915), Wilhelmiana (Frankfurt, from 1951), and J. & W. Chester (London, from 1957). The Hansen group was absorbed by Music Sales in late 1980s.
Plate Numbers
- Rapoport, Paul. The Compositions of Vagn Holmboe. Hansen, 1996. ISBN 87 598 0813 6. (Contains - unusually - along with an attempt at a complete-up-to-1996 worklist, publishers, plate numbers and edition numbers for the first publications where known of each composition.)
- Hofmeister-Verlag. Hofmeisters Monatsberichte.
- Worldcat.org (to a point...)
Authority control
- VIAF (Edition Wilhelm Hansen AS)