miércoles, 29 de junio de 2011

PRASUGREL

 

se abre Trial con prasugrel en casimiro en colaboracion con clinica INCA de Dr Mogrovejo

 

Prasugrel

 
Prasugrel
Systematic (IUPAC) name
(RS)-5-[2-cyclopropyl-1-(2-fluorophenyl)-2-oxoethyl]-4,5,6,7-
tetrahydrothieno[3,2-c]pyridin-2-yl acetate
Clinical data
Licence data EMA:LinkUS FDA:link
Pregnancy cat. B(US) B
Legal status POM (UK) -only (US)
Routes Oral
Pharmacokinetic data
Bioavailability ≥79%
Protein binding Active metabolite: ~98%
Metabolism Rapid intestinal and serum metabolism via esterase-mediated hydrolysis to a thiolactone (inactive), which is then converted, via CYP450-mediated (primarily CYP3A4 and CYP2B6) oxidation, to an active metabolite (R-138727)
Half-life ~7 hours (range 2-15 hours)
Excretion Urine (~68% inactive metabolites); feces (27% inactive metabolites)
Identifiers
CAS number 150322-43-3
ATC code B01AC22
PubChem CID 6918456
ChemSpider 5293653 YesY
ChEMBL CHEMBL1201772 N
Chemical data
Formula C20H20FNO3S 
Mol. mass 373.442 g/mol
SMILES eMolecules & PubChem
 N(what is this?)  [1]

Prasugrel (marketing name Effient in the US, Efient in the EU and Prasita in India) is a novel platelet inhibitor developed by Daiichi Sankyo Co. and produced by Ube and currently marketed in the United States in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). Prasugrel was approved for use in Europe in February 2009, and is currently available in the UK. On July 10, 2009, the US Food and Drug Administration approved the use of prasugrel for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndrome who are to be managed with PCI.[1]

[edit] Pharmacology

Prasugrel is a member of the thienopyridine class of ADP receptor inhibitors, like ticlopidine (trade name Ticlid) and clopidogrel (trade name Plavix). These agents reduce the aggregation ("clumping") of platelets by irreversibly binding to P2Y12 receptors. Compared to clopidogrel, "prasugrel(trade name apagrel) inhibits adenosine diphosphate–induced platelet aggregation more rapidly, more consistently, and to a greater extent than do standard and higher doses of clopidogrel in healthy volunteers and in patients with coronary artery disease, including those undergoing PCI".[2] Clopidogrel, unlike prasugrel, was issued a black box warning from the FDA on March 12, 2010, as the estimated 2-14% of the US population that have low levels of the CYP 2C19 liver enzyme needed to activate clopidogrel may not get the full effect. Tests are available to predict if a patient would be susceptible to this problem or not.[3][4] Prasugrel has not been shown to carry those same limitations.

[edit] Pharmacodynamics

Prasugrel produces inhibition of platelet aggregation to 20 μM or 5 μM ADP, as measured by light transmission aggregometry.[5] Following a 60-mg loading dose of Effient, approximately 90% of patients had at least 50% inhibition of platelet aggregation by 1 hour. Maximum platelet inhibition was about 80% (Figure 2). Mean steady-state inhibition of platelet aggregation was about 70% following 3 to 5 days of dosing at 10 mg daily after a 60-mg loading dose of Effient. Platelet aggregation gradually returns to baseline values over 5–9 days after discontinuation of prasugrel, this time course being a reflection of new platelet production rather than pharmacokinetics of prasugrel. Discontinuing clopidogrel 75 mg and initiating prasugrel 10 mg with the next dose resulted in increased inhibition of platelet aggregation, but not greater than that typically produced by a 10 mg maintenance dose of prasugrel alone. It should also be noted that increasing platelet inhibition could increase bleeding risk. The relationship between inhibition of platelet aggregation and clinical activity has not been established. [2]

[edit] Pharmacokinetics

Prasugrel is a prodrug and is rapidly metabolized to a pharmacologically active metabolite and inactive metabolites. The active metabolite has an elimination half-life of about 7 hours (range 2–15 hours). Healthy subjects, patients with stable atherosclerosis, and patients undergoing PCI show similar pharmacokinetics.

[edit] TRITON-TIMI 38 study

As published in the New England Journal of Medicine's online edition, the TRITON-TIMI 38 study of 13,608 patients with acute coronary syndromes compared prasugrel against clopidogrel, both in combination with aspirin, and found that, as a more potent anti-platelet agent, prasugrel reduced the combined rate of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke (12.1% for clopidogrel vs. 9.9% for prasugrel). This difference in the primary endpoint was mainly driven by the reduction of non-fatal myocardial infarctions. However, an increased rate of serious bleedings (1.4%, vs. 0.9% in the clopidogrel group) and fatal bleedings (0.4% vs. 0.1%) was also observed.[6] Overall mortality did not differ between the two treatment groups.

From the editorial in the NEJM, "In TRITON–TIMI 38, for each death from cardiovascular causes prevented by the use of prasugrel as compared with clopidogrel, approximately one additional episode of fatal bleeding was caused by prasugrel".[7]

In patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI), prasugrel was associated with a significantly lower incidence of ischemic events than clopidogrel, and was particularly effective in specific subgroups of patients, such as those with diabetes mellitus. In this sub-group there is a 30% relative risk reduction (4.2% ARR for unstable angina/NSTEMI and 5% AAR for STEMI) compared to the clopidogrel group without significant increased risk for major bleeding(2.2% vs. 2.3%). However, the efficacy of prasugrel was offset by a higher risk of bleeding than clopidogrel, with patients aged ≥75 years, those weighing <60 kg and those with a history of stroke or transient ischemic attack at the greatest risk. A lower dose of prasugrel in patients aged ≥75 years and those weighing <60 kg may help to minimize the bleeding risk, although more data are needed to establish this; prasugrel is contraindicated in patients with a history of stroke or transient ischemic attack.[8] The estimated number of patients needed to be treated with prasugrel at the dosage studied, as compared with standard-dose clopidogrel, to prevent one primary efficacy end point during a 15-month period was 46. The number of patients who would have to be treated to result in an excess non–CABG-related TIMI major hemorrhage was 167.[9]

Furthermore, data from a pharmacodynamic study suggests that acute coronary syndrome (ACS) patients can be safely switched from clopidogrel to prasugrel and that doing so results in a further reduction in platelet function after one week.[10] When patients receive a loading dose of prasugrel prior to switching from clopidogrel, the reduction in platelet function occurs within two hours.[11]

[edit] Adverse Effects

Cardiovascular: Hypertension (8%), hypotension (4%), atrial fibrillation (3%), bradycardia (3%), noncardiac chest pain (3%), peripheral edema (3%) Central nervous system: Headache (6%), dizziness (4%), fatigue (4%), fever (3%), extremity pain (3%) Dermatologic: Rash (3%) Endocrine & metabolic: Hypercholesterolemia/hyperlipidemia (7%) Gastrointestinal: Nausea (5%), diarrhea (2%), gastrointestinal hemorrhage (2%) Hematologic: Leukopenia (3%), anemia (2%) Neuromuscular & skeletal: Back pain (5%) Respiratory: Epistaxis (6%), dyspnea (5%), cough (4%)

[edit] References

  1. ^ Baker WL, White CM. Role of Prasugrel, a Novel P2Y12 Receptor Antagonist, in the Management of Acute Coronary Syndromes. American Journal of Cardiovascular Drugs Aug 1, 2009; 9 (4): 213-229. Link text
  2. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  3. ^ Food and Drug Administration (United States) (March 12, 2010). "FDA Announces New Boxed Warning on Plavix: Alerts patients, health care professionals to potential for reduced effectiveness". Press release. http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm204253.htm. Retrieved March 13, 2010. 
  4. ^ "FDA Drug Safety Communication: Reduced effectiveness of Plavix (clopidogrel) in patients who are poor metabolizers of the drug". Drug Safety and Availability. Food and Drug Administration (United States). March 12, 2010. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm203888.htm. Retrieved March 13, 2010. 
  5. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function" (in English). http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011. 
  6. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  7. ^ Bhatt DL (2007). "Intensifying Platelet Inhibition — Navigating between Scylla and Charybdis". N Engl J Med 357 (20): 2078–81. doi:10.1056/NEJMe0706859. PMID 17982183. http://content.nejm.org/cgi/content/full/NEJMe0706859?query=TOC. 
  8. ^ Duggan ST, Keating GM. Prasugrel: A Review of its Use in Patients with Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention. Drugs Aug 20, 2009; 69 (12): 1707-26 Link text
  9. ^ Wiviott SD, Braunwald E, McCabe CH, et al. (2007). "Prasugrel versus clopidogrel in patients with acute coronary syndromes". N Engl J Med 357 (20): 2001–15. doi:10.1056/NEJMoa0706482. 
  10. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". 1.Angiolillo DJ, Saucedo JF, DeRaad R, et al. Increased platelet inhibition after switching from maintenance clopidogrel to prasugrel in patients with acute coronary syndromes. J Am Coll Cardiol 2010; 56: 1017-23.. http://www.theheart.org. http://www.theheart.org/article/1123367.do. Retrieved 1 April 2011. 
  11. ^ O'Riordan, Michael. "Switching from clopidogrel to prasugrel further reduces platelet function". http://www.theheart.org. http://www.theheart.org/article/1123367.do#bib_1. Retrieved 1 April 2011. 

[edit] External links

lunes, 27 de junio de 2011

Feocromocitoma

Cuadros Chavez posted in cibermedicos.Maximo Cuadros Chavez10:07am Jun 26

Feocromocitoma
http://www.facebook.com/l/338ffmF_D4jZcTuKUtQ1Hnnl8Eg/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13125936&pident_usuario=0&pident_revista=62&fichero=62v10n15a13125936pdf001.pdf&ty=147&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Medicine. 2008;10:997-1005.

PUNTOS CLAVE:
Concepto. El feocromocitoma es un tumor poco frecuente, pero su malignidad funcional y su 10% de malignidad histológica obligan a pensar en él. Debemos tener en cuenta que el 15-20% es de localización extraadrenal.

Clínica. La clínica está marcada por la hipertensión arterial, frecuentemente paroxística, en la que puede haber graves complicaciones: infarto de miocardio, accidente vascular cerebral, etc. ¿ Es imprescindible establecer el tratamiento quirúrgico lo antes posible.

Preparación preoperatoria. El paciente debe llegar a la cirugía con bloqueo alfa-adrenérgico. ¿ El anestesista debe conocer el manejo de estos tumores, tanto para la inducción de la anestesia como para solventar los problemas que surjan en el acto quirúrgico.

Feocromocitoma: actualización diagnóstica y terapéutica
http://www.facebook.com/l/338ffgVppqwxv9qOUEFcGQ-GJYw/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_revista=12&fichero=12v55n05a13120617pdf001.pdf&ty=129&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Endocrinol Nutr. 2008;55:202-16.
http://www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_
apps.elsevier.es

---------- Mensaje reenviado ----------
De: Maximo Cuadros Chavez <notification+yfo6tzj9@facebookmail.com>
Fecha: 26 de junio de 2011 10:07
Asunto: [cibermedicos] Feocromocitoma
Para: cibermedicos <internetymedicos@groups.facebook.com>


Maximo Cuadros Chavez posted in cibermedicos.
Feocromocitoma http://www.facebook.com/l/338ffmF_D4jZcTuKUtQ1Hnnl8Eg/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13125936&pident_usuario=0&pident_revista=62&fichero=62v10n15a13125936pdf001.pdf&ty=147&accion=L&origen=medicine&web=www.medicineonline.es&lan=es Medicine. 2008;10:997-1005.  PUNTOS CLAVE: Concepto. El feocromocitoma es un tumor poco frecuente, pero su malignidad funcional y su 10% de malignidad histológica obligan a pensar en él. Debemos tener en cuenta que el 15-20% es de localización extraadrenal.  Clínica. La clínica está marcada por la hipertensión arterial, frecuentemente paroxística, en la que puede haber graves complicaciones: infarto de miocardio, accidente vascular cerebral, etc. ¿ Es imprescindible establecer el tratamiento quirúrgico lo antes posible.  Preparación preoperatoria. El paciente debe llegar a la cirugía con bloqueo alfa-adrenérgico. ¿ El anestesista debe conocer el manejo de estos tumores, tanto para la inducción de la anestesia como para solventar los problemas que surjan en el acto quirúrgico.  Feocromocitoma: actualización diagnóstica y terapéutica http://www.facebook.com/l/338ffgVppqwxv9qOUEFcGQ-GJYw/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_revista=12&fichero=12v55n05a13120617pdf001.pdf&ty=129&accion=L&origen=medicine&web=www.medicineonline.es&lan=es Endocrinol Nutr. 2008;55:202-16.
Maximo Cuadros Chavez 10:07am Jun 26
Feocromocitoma
http://www.facebook.com/l/338ffmF_D4jZcTuKUtQ1Hnnl8Eg/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13125936&pident_usuario=0&pident_revista=62&fichero=62v10n15a13125936pdf001.pdf&ty=147&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Medicine. 2008;10:997-1005.

PUNTOS CLAVE:
Concepto. El feocromocitoma es un tumor poco frecuente, pero su malignidad funcional y su 10% de malignidad histológica obligan a pensar en él. Debemos tener en cuenta que el 15-20% es de localización extraadrenal.

Clínica. La clínica está marcada por la hipertensión arterial, frecuentemente paroxística, en la que puede haber graves complicaciones: infarto de miocardio, accidente vascular cerebral, etc. ¿ Es imprescindible establecer el tratamiento quirúrgico lo antes posible.

Preparación preoperatoria. El paciente debe llegar a la cirugía con bloqueo alfa-adrenérgico. ¿ El anestesista debe conocer el manejo de estos tumores, tanto para la inducción de la anestesia como para solventar los problemas que surjan en el acto quirúrgico.

Feocromocitoma: actualización diagnóstica y terapéutica
http://www.facebook.com/l/338ffgVppqwxv9qOUEFcGQ-GJYw/www.elsevier.es/watermark/ctl_servlet?_f=10&pident_articulo=13120617&pident_usuario=0&pident_revista=12&fichero=12v55n05a13120617pdf001.pdf&ty=129&accion=L&origen=medicine&web=www.medicineonline.es&lan=es
Endocrinol Nutr. 2008;55:202-16.

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carta de labetall y enoxiparina ALTEPLASE

De Claudio Guido Mori Gonzales
Medico asistente del Departamento de Medicina
Cardiologo Internista Intensivista
 
a
 
Dr Marcos Martinez
Jefe de Departamento de Medicina
 
MOTIVO: compra de labetatol  enoxiparina alteplase clopidogrel atorvastatina 40 mg carvedilol, tirofiban ampollas
 
Me dirigo a usted para comunicarle que en el Petitorio Nacional de Medicamentos esta la enoxiparina heparina de bajo peso molecular
cuyo costo en el Hospital Loayza es de 19 soles la ampolla prellenada de 80 mg.
Le solicito por favor que disponga lo necesario para que el hospital la adquiera.
Los Ensayos clinico o triales de SICA se han hecho con enoxiparina no con dalteparene y las  heparinas de bajo peso molecular no son intercambiables farmacologicamente. Ademas la enoxiparina cuesta menos y la presentacion de dalteparene de que dispone el hospital es para uso profilactivo (ampollas de 5000 U) NO TERAPEUTICO. Todos los infartos tienen que ser anticoagulados 8 dias con enoxiparina en dosis de 1mg por kg cada 12 horas
Asimismo los hospitales del Minsa como San Bartolome  Loayca etc ya cuentan con labetatol un antihipertensivo EN AMPOLLAS QUE SE USA EN BOLOS  para emergencias hipertensivas que cuentan con trials que demuestrasn su superioridad sobre el nitroprusiato que dicho sea de paso esta dicontinuado o el hospital no lo compra.
No contamos con ALTEPLASE un trombolitico superior a la estreptoquinasa en infartos exten sos que tambien consta en el PETITORIO NACIONAL
Tampoco tenemos carvedolol un betabloqueador util en insuficiencia cardiaca y en infartos con FE baja. Esta tambien el petitorio.
No tenemos tampoco una cefalosporina de tercera generacion oral. En el mercado existe la cefpodoxima de 200 mg que se usa cada 12 horas. Util en infecciones cuando se quiere pasar los antibioticos a via oral y se estan usando cefalosporinas de tercera generacion.
No tenemos tirofiban (AGRASTAT) un farmaco que ya esta en los protocolos de SICA y que otros hospitales del MINSA si tienen.Y QUE ES UTIL EN LIS SICAS QUE no se trombolizan o en aquellos que van a angioplastia.
Necesitamos una atorvastatina de 40 u 80 mg. Las dosis de atorva en sica son de 80 mg
T
atte
 
Claudio Mori Gonzales
CARDIOLOGO INTERNISTA INTENSIVISTA
CMP 18700
DNI 07963726
CMP 18700 RNE 13969 13626
 
cc Direccion ejecutiva
Farmacia
Comite Farmacologico
 

domingo, 26 de junio de 2011

Criminal genes


The Nutshell
Criminal genes
Experts come together to revisit the controversial field of genetics and criminology
By Cristina Luiggi | June 22, 2011
 1 Comment
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madamepsychosis | Flickr
How genes influence a person's risk for committing crimes has always been controversy-laden subject for experts, particularly criminologists and sociologists, who find it hard to disentangle it from notions of discrimination, racism, and eugenics. Yet as the general field of behavioral genetics gains momentum due to the recent explosion of genomic information, researchers are taking a hard, objective look at how inherited traits predispose people to violence and aggression.
This week for example, the National Institute of Justice's annual conference devoted its opening session to the creation of databases of newly discovered forensic genetic markers, The New York Times reports. Such genetic markers include the serotonin-controlling monoamine oxidase A enzyme (MAO), certain variants of which have been linked to increased impulsivity and aggression. But experts are quick to stress that these genes merely predispose an individual to such behaviors and that additional environmental factors—such as stress, socio-economic background, and even marital status—are usually required for the negative manners to manifest. Therefore, the challenge going forward is not only to produce a list of genetic markers associated with criminal behavior, but to also identify the environmental factors with which they interact.
http://the-scientist.com/2011/06/22/criminal-genes/
http://www.cvent.com/events/nij-conference-2011/agenda-1352e477d83a4ddcbefc9bc4a59c9acd.aspx
Plenary Sessions

Translating the Science of Community to Criminal Justice Practice (and Back)
Research shows that healthy communities share basic values, neighbors look out for one another, and social connections are strong. A groundbreaking study from one of the largest  research projects funded by the National Institute of Justice—the Project on Human Development in Chicago Neighborhoods—produced important understandings about community well-being and the relationship between neighborhoods and crime. The panelists on this plenary session are deeply committed to improved civic life and lower violence. They will discuss the research and its implications for thinking about community capacity and crime and draw on their own experiences to describe how the research affects their own diverse and changing communities.
 
• Edward F. Davis, Police Commissioner, Boston Police Department
• Michael A. Davis, Chief of Police, Brooklyn Park Police Department
• Robert J. Sampson, Henry Ford II Professor of the Social Sciences, Harvard University

http://www.nytimes.com/2011/06/20/arts/genetics-and-crime-at-institute-of-justice-conference.html?pagewanted=2&_r=3&adxnnl=1&adxnnlx=1309124960-4KQzoO1LamZqOQU3zQaifg
Genetic Basis for Crime: A New Look
By PATRICIA COHEN
Published: June 19, 2011
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It was less than 20 years ago that the National Institutes of Health abruptly withdrew funds for a conference on genetics and crime after outraged complaints that the idea smacked of eugenics. The president of the Association of Black Psychologists at the time declared that such research was in itself  "a blatant form of stereotyping and racism."
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The tainted history of using biology to explain criminal behavior has pushed criminologists to reject or ignore genetics and concentrate on social causes: miserable poverty, corrosive addictions, guns. Now that the human genome has been sequenced, and scientists are studying the genetics of areas as varied as alcoholism and party affiliation, criminologists are cautiously returning to the subject. A small cadre of experts is exploring how genes might heighten the risk of committing a crime and whether such a trait can be inherited.    
The turnabout will be evident on Monday at the annual National Institute of Justice conference in Arlington, Va. On the opening day criminologists from around the country can attend a panel on creating databases for information about DNA and "new genetic markers" that forensic scientists are discovering.
"Throughout the past 30 or 40 years most criminologists couldn't say the word 'genetics' without spitting," Terrie E. Moffitt, a behavioral scientist at Duke University, said. "Today the most compelling modern theories of crime and violence weave social and biological themes together."  
Researchers estimate that at least 100 studies have shown that genes play a role in crimes. "Very good methodological advances have meant that a wide range of genetic work is being done," said John H. Laub, the director of the justice institute, who won the Stockholm Prize in Criminology last week. He and others take pains to emphasize, however, that genes are ruled by the environment, which can either mute or aggravate violent impulses. Many people with the same genetic tendency for aggressiveness will never throw a punch, while others without it could be career criminals.
The subject still raises thorny ethical and policy questions. Should a genetic predisposition influence sentencing? Could genetic tests be used to tailor rehabilitation programs to individual criminals? Should adults or children with a biological marker for violence be identified?
Everyone in the field agrees there is no "crime gene." What most researchers are looking for are inherited traits that are linked to aggression and antisocial behaviors, which may in turn lead to violent crime. Don't expect anyone to discover how someone's DNA might identify the next Bernard L. Madoff.  
And that is precisely the problem, said Troy Duster, a professor of sociology and bioethics at New York University, who argues that studies examine not the remorseless and rapacious behavior of the rich and powerful, but the behavior of disadvantaged minorities. "Every era believes that the technology and the methodology have improved," he said, "but the science itself is problematic." 
One gene that has been linked to violence regulates the production of the monoamine oxidase A enzyme, which controls the amount of serotonin in the brain. People with a version of the gene that produces less of the enzyme tend to be significantly more impulsive and aggressive, but, as Ms. Moffitt and her colleague (and husband) Avshalom Caspi discovered, the effect of the gene is triggered by stressful experiences. 
Steven Pinker, a professor of psychology at Harvard whose forthcoming book, "The Better Angels of Our Nature," argues that humans have become less violent over the millenniums, suggests that the way to think about genetics and crime is to start with human nature and then look at what causes the switch for a particular trait to be flipped on or off.
"It is not a claim about how John and Bill differ, but about how every male is the same," he said. Understanding the genetics of violence can "tell you what aspect of the environment you should look at." 
He mentioned one of the biggest risk factors leading to crime: remaining single instead of getting married, a link uncovered by Mr. Laub and Robert J. Sampson, a Harvard sociologist who was a co-winner of the Stockholm Prize. Marriage may serve as a switch that directs male energies toward investing in a family rather than competing with other males, Mr. Pinker said.
Kevin Beaver, an associate professor at Florida State University's College of Criminology and Criminal Justice, said genetics may account for, say, half of a person's aggressive behavior, but that 50 percent comprises hundreds or thousands of genes that express themselves differently depending on the environment.
He has tried to measure which circumstances — having delinquent friends, living in a disadvantaged neighborhood — influence whether a predisposition to violence surfaces. After studying twins and siblings, he came up with an astonishing result: In boys not exposed to the risk factors, genetics played no role in any of their violent behavior. The positive environment had prevented the genetic switches — to use Mr. Pinker's word — that affect aggression from being turned on. In boys with eight or more risk factors, however, genes explained 80 percent of their violence. Their switches had been flipped.
A rash of new research has focused on self-control as well as callousness and a lack of empathy, traits regularly implicated in the decision to commit a crime. Like other personality traits, these are believed to have environmental and genetic components, although the degree of heritability is debated. 
In findings from a long-term study of 1,000 babies born in 1972 in a New Zealand town, Ms. Moffitt and her colleagues recently reported that the less self-control a child displayed at 3 years of age, the more likely he or she was to commit a crime more than 30 years later. Forty-three percent of the children who scored in the lowest fifth on self-control were later convicted of a crime, she said, versus 13 percent of those who scored in the highest fifth.  
But a predisposition is not destiny. "Knowing something is inherited does not IN ANY WAY tell us anything about whether changing the environment will improve it," Ms. Moffitt wrote in an e-mail. "For example, self-control is a lot like height, it varies widely in the human population, and it is highly heritable, but if an effective intervention such as better nutrition is applied to the whole population, then everyone gets taller than the last generation."
Criminologists and sociologists have been much more skittish about genetic causes of crime than psychologists.  In 2008 a survey conducted by John Paul Wright, who heads graduate programs at the University of Cincinnati's School of Criminal Justice, discovered that "not a single study on the biology-crime link has been published in dissertation form in the last 20 years" from a criminal justice Ph.D. program, aside from two dissertations he had personally overseen (one of which was Mr. Beaver's). He also noted that the top four journals in the field had scarcely published any biological research in the past two decades.
Mr. Wright said he now thinks "in criminology the tide is turning, especially among younger scholars."
But recent work has tended to air outside the main criminology forums. Mr. Beaver, for example, published a paper in Biological Psychiatry in February that concluded that adoptees whose biological parents had broken the law "were significantly more likely to be arrested, sentenced to probation, incarcerated, and arrested multiple times when compared with adoptees whose biological parents had not been arrested."
At the American Association for the Advancement of Science's meeting in February, Adrian Raine, chairman of the criminology department at the University of Pennsylvania and a pioneer in the field, presented a paper showing how variations in the parts of a toddler's brain that regulate emotions — believed to be a product of genes and environment — turned out to be a good predictor of criminal behavior later in life.
Mr. Sampson, who planned to attend the opening day of the justice institute conference, said that "sociology has nothing to fear from genetic research," but he maintained that the most interesting questions about crime, like why some communities have a higher crime rate than others, are not traceable at all to genetics. "The more sophisticated the genetic research, the more it will show the importance of social context," he said.

--

 

 
   Gloria Maria Anicama Orcon.
 
"El Perú carece de memoria. Y la memoria no es la inteligencia de los brutos sino la arquitectura del aprendizaje".
Cesar Hildebrant
 

---------- Forwarded message ----------
From: Gloria Anicama gloria.vcbj@gmail.com
 

Criminal genes

Experts come together to revisit the controversial field of genetics and criminology

By Cristina Luiggi | June 22, 2011

Link thisStumbleTweet this
madamepsychosis | Flickr
madamepsychosis | Flickr

How genes influence a person's risk for committing crimes has always been controversy-laden subject for experts, particularly criminologists and sociologists, who find it hard to disentangle it from notions of discrimination, racism, and eugenics. Yet as the general field of behavioral genetics gains momentum due to the recent explosion of genomic information, researchers are taking a hard, objective look at how inherited traits predispose people to violence and aggression.

This week for example, the National Institute of Justice's annual conference devoted its opening session to the creation of databases of newly discovered forensic genetic markers, The New York Times reports. Such genetic markers include the serotonin-controlling monoamine oxidase A enzyme (MAO), certain variants of which have been linked to increased impulsivity and aggression. But experts are quick to stress that these genes merely predispose an individual to such behaviors and that additional environmental factors—such as stress, socio-economic background, and even marital status—are usually required for the negative manners to manifest. Therefore, the challenge going forward is not only to produce a list of genetic markers associated with criminal behavior, but to also identify the environmental factors with which they interact.

http://the-scientist.com/2011/06/22/criminal-genes/

http://www.cvent.com/events/nij-conference-2011/agenda-1352e477d83a4ddcbefc9bc4a59c9acd.aspx

Plenary Sessions

Translating the Science of Community to Criminal Justice Practice (and Back)
Research shows that healthy communities share basic values, neighbors look out for one another, and social connections are strong. A groundbreaking study from one of the largest  research projects funded by the National Institute of Justice—the Project on Human Development in Chicago Neighborhoods—produced important understandings about community well-being and the relationship between neighborhoods and crime. The panelists on this plenary session are deeply committed to improved civic life and lower violence. They will discuss the research and its implications for thinking about community capacity and crime and draw on their own experiences to describe how the research affects their own diverse and changing communities.
 
• Edward F. Davis, Police Commissioner, Boston Police Department
• Michael A. Davis, Chief of Police, Brooklyn Park Police Department
 Robert J. Sampson, Henry Ford II Professor of the Social Sciences, Harvard University
Genetic Basis for Crime: A New Look
By
Published: June 19, 2011

It was less than 20 years ago that the National Institutes of Health abruptly withdrew funds for a conference on genetics and crime after outraged complaints that the idea smacked of eugenics. The president of the Association of Black Psychologists at the time declared that such research was in itself  "a blatant form of stereotyping and racism."

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The tainted history of using biology to explain criminal behavior has pushed criminologists to reject or ignore genetics and concentrate on social causes: miserable poverty, corrosive addictions, guns. Now that the human genome has been sequenced, and scientists are studying the genetics of areas as varied as alcoholism and party affiliation, criminologists are cautiously returning to the subject. A small cadre of experts is exploring how genes might heighten the risk of committing a crime and whether such a trait can be inherited.    

The turnabout will be evident on Monday at the annual National Institute of Justice conference in Arlington, Va. On the opening day criminologists from around the country can attend a panel on creating databases for information about DNA and "new genetic markers" that forensic scientists are discovering.

"Throughout the past 30 or 40 years most criminologists couldn't say the word 'genetics' without spitting," Terrie E. Moffitt, a behavioral scientist at Duke University, said. "Today the most compelling modern theories of crime and violence weave social and biological themes together."  

Researchers estimate that at least 100 studies have shown that genes play a role in crimes. "Very good methodological advances have meant that a wide range of genetic work is being done," said John H. Laub, the director of the justice institute, who won the Stockholm Prize in Criminology last week. He and others take pains to emphasize, however, that genes are ruled by the environment, which can either mute or aggravate violent impulses. Many people with the same genetic tendency for aggressiveness will never throw a punch, while others without it could be career criminals.

The subject still raises thorny ethical and policy questions. Should a genetic predisposition influence sentencing? Could genetic tests be used to tailor rehabilitation programs to individual criminals? Should adults or children with a biological marker for violence be identified?

Everyone in the field agrees there is no "crime gene." What most researchers are looking for are inherited traits that are linked to aggression and antisocial behaviors, which may in turn lead to violent crime. Don't expect anyone to discover how someone's DNA might identify the next Bernard L. Madoff.  

And that is precisely the problem, said Troy Duster, a professor of sociology and bioethics at New York University, who argues that studies examine not the remorseless and rapacious behavior of the rich and powerful, but the behavior of disadvantaged minorities. "Every era believes that the technology and the methodology have improved," he said, "but the science itself is problematic." 

One gene that has been linked to violence regulates the production of the monoamine oxidase A enzyme, which controls the amount of serotonin in the brain. People with a version of the gene that produces less of the enzyme tend to be significantly more impulsive and aggressive, but, as Ms. Moffitt and her colleague (and husband) Avshalom Caspi discovered, the effect of the gene is triggered by stressful experiences. 

Steven Pinker, a professor of psychology at Harvard whose forthcoming book, "The Better Angels of Our Nature," argues that humans have become less violent over the millenniums, suggests that the way to think about genetics and crime is to start with human nature and then look at what causes the switch for a particular trait to be flipped on or off.

"It is not a claim about how John and Bill differ, but about how every male is the same," he said. Understanding the genetics of violence can "tell you what aspect of the environment you should look at." 

He mentioned one of the biggest risk factors leading to crime: remaining single instead of getting married, a link uncovered by Mr. Laub and Robert J. Sampson, a Harvard sociologist who was a co-winner of the Stockholm Prize. Marriage may serve as a switch that directs male energies toward investing in a family rather than competing with other males, Mr. Pinker said.

Kevin Beaver, an associate professor at Florida State University's College of Criminology and Criminal Justice, said genetics may account for, say, half of a person's aggressive behavior, but that 50 percent comprises hundreds or thousands of genes that express themselves differently depending on the environment.

He has tried to measure which circumstances — having delinquent friends, living in a disadvantaged neighborhood — influence whether a predisposition to violence surfaces. After studying twins and siblings, he came up with an astonishing result: In boys not exposed to the risk factors, genetics played no role in any of their violent behavior. The positive environment had prevented the genetic switches — to use Mr. Pinker's word — that affect aggression from being turned on. In boys with eight or more risk factors, however, genes explained 80 percent of their violence. Their switches had been flipped.

A rash of new research has focused on self-control as well as callousness and a lack of empathy, traits regularly implicated in the decision to commit a crime. Like other personality traits, these are believed to have environmental and genetic components, although the degree of heritability is debated. 

In findings from a long-term study of 1,000 babies born in 1972 in a New Zealand town, Ms. Moffitt and her colleagues recently reported that the less self-control a child displayed at 3 years of age, the more likely he or she was to commit a crime more than 30 years later. Forty-three percent of the children who scored in the lowest fifth on self-control were later convicted of a crime, she said, versus 13 percent of those who scored in the highest fifth.  

But a predisposition is not destiny. "Knowing something is inherited does not IN ANY WAY tell us anything about whether changing the environment will improve it," Ms. Moffitt wrote in an e-mail. "For example, self-control is a lot like height, it varies widely in the human population, and it is highly heritable, but if an effective intervention such as better nutrition is applied to the whole population, then everyone gets taller than the last generation."

Criminologists and sociologists have been much more skittish about genetic causes of crime than psychologists.  In 2008 a survey conducted by John Paul Wright, who heads graduate programs at the University of Cincinnati's School of Criminal Justice, discovered that "not a single study on the biology-crime link has been published in dissertation form in the last 20 years" from a criminal justice Ph.D. program, aside from two dissertations he had personally overseen (one of which was Mr. Beaver's). He also noted that the top four journals in the field had scarcely published any biological research in the past two decades.

Mr. Wright said he now thinks "in criminology the tide is turning, especially among younger scholars."

But recent work has tended to air outside the main criminology forums. Mr. Beaver, for example, published a paper in Biological Psychiatry in February that concluded that adoptees whose biological parents had broken the law "were significantly more likely to be arrested, sentenced to probation, incarcerated, and arrested multiple times when compared with adoptees whose biological parents had not been arrested."

At the American Association for the Advancement of Science's meeting in February, Adrian Raine, chairman of the criminology department at the University of Pennsylvania and a pioneer in the field, presented a paper showing how variations in the parts of a toddler's brain that regulate emotions — believed to be a product of genes and environment — turned out to be a good predictor of criminal behavior later in life.

Mr. Sampson, who planned to attend the opening day of the justice institute conference, said that "sociology has nothing to fear from genetic research," but he maintained that the most interesting questions about crime, like why some communities have a higher crime rate than others, are not traceable at all to genetics. "The more sophisticated the genetic research, the more it will show the importance of social context," he said.


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   Gloria Maria Anicama Orcon.
 
"El Perú carece de memoria. Y la memoria no es la inteligencia de los brutos sino la arquitectura del aprendizaje".
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