Publications by authors named "Christian Doutremepuich"

18 Publications

  • Page 1 of 1

Effects of Ultra-Low-Dose Aspirin in Thrombosis and Haemorrhage.

Homeopathy 2019 08 20;108(3):158-168. Epub 2019 Apr 20.

Laboratoire d'Hématologie, UFR des Sciences Pharmaceutiques, Université de Bordeaux, Bordeaux, France.

Background: Aspirin is the oldest and possibly the most widely used pharmacologically active substance still used in allopathic medicine. Its effect on fever and inflammation has paved the way to its anti-thrombotic effect. Dilutions of aspirin have been tested for many years in the University of Bordeaux, in humans as well as in animal models.

Methods: This article is a review of the totality of articles published by the Laboratory of Hematology of the Faculty of Pharmacy of the University of Bordeaux, reporting different doses and dilutions of aspirin, different kinds of inhibitors, transgenic mice and animal models of disease such as portal hypertension and cirrhosis.

Results: Homeopathic dilutions of aspirin, notably 15 cH, have shown a pro-thrombotic effect in humans and in in-vivo animal studies. Longitudinal studies in rats have also shown an initial anti-thrombotic effect followed by a pro-thrombotic effect of aspirin several days after a single high-dose administration. This pro-thrombotic effect seems to act by inhibiting the cyclooxygenase (COX)-2 pathway in studies performed with COX selective inhibitors and in knock-out mice without COX-1 or COX-2. This effect may explain the thrombo-embolic complications described after aspirin withdrawal for the purposes of surgery or after non-compliance with anti-platelet therapy, and it may be beneficial in normalising primary haemostasis and decreasing haemorrhage in animal models of portal hypertension and cirrhosis.

Conclusions: Aspirin 15 cH acts through the inhibition of the COX-2 pathway producing a clear pro-thrombotic effect. Further studies should clarify if the pro-thrombotic effect of aspirin withdrawal and the effect of aspirin 15 cH are related, as secondary effects of the same drug. Clarifying this last outcome may be of great significance to public health.
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http://dx.doi.org/10.1055/s-0038-1677495DOI Listing
August 2019

Aspirin discontinuation syndromes: clinical implications of basic research studies.

Am J Cardiovasc Drugs 2013 Dec;13(6):377-84

Laboratoire d'Hématologie, Université Bordeaux Segalen, 146 rue Leo Saignat, 33076, Bordeaux Cedex, France,

Abrupt discontinuation of many drugs used in medicine causes withdrawal syndromes, some of which can be fatal. Discontinuation of a number of cardiovascular drugs can increase the risk of cardiovascular events. Whereas aspirin administration is known to decrease the risk of vascular ischemic problems, aspirin withdrawal may temporarily increase the risk of thrombotic events. Indeed, aspirin withdrawal has been associated with an increased risk of thrombosis both in clinical and fundamental research studies. Such complications occur within the first month after interrupting aspirin therapy and their mechanism remains unexplained. We have previously demonstrated that aspirin, when injected as a single high dose (100 mg/kg), induces a prothrombotic state in the rat, similar to that described above, 8 and 10 days after administration. This effect in the rat may be reproduced 1 hour after a single injection of ultra-low-dose aspirin. Caution is therefore required regarding the possibility of drug discontinuation effects within the framework of drug safety evaluation.
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http://dx.doi.org/10.1007/s40256-013-0044-1DOI Listing
December 2013

[Legal implication of DNA profiling].

Bull Acad Natl Med 2012 Jun;196(6):1117-29; discussion 1130

Laboratoire d'hématologie médico-légale, 43 avenue de la République-- 33073 Bordeaux cedex, et Université Victor Segalen Bordeaux II.

In recent years, DNA profiling has been used regularly by the justice system, and has seen a number of improvements, with the need for fewer cells, more efficient DNA extraction and purification, and more rapid genotyping. These methods can now identify an individual more rapidly, from a corpse, blood stain, sperm or epithelial cells, by comparison with familial profiles. In France, DNA profiling can only be ordered by a judge.
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June 2012

Thrombosis and aspirin: clinical aspect, aspirin in cardiology, aspirin in neurology, and pharmacology of aspirin.

Thrombosis 2012 21;2012:626289. Epub 2012 Oct 21.

Laboratoire d'Hématologie, Université Victor Segalen Bordeaux 2, 146 Rue LéoSaignat, 33076 Bordeaux Cedex, France.

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http://dx.doi.org/10.1155/2012/626289DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485536PMC
November 2012

Paradoxical effect of aspirin.

Thrombosis 2012 15;2012:676237. Epub 2012 Jan 15.

Laboratoire d'Hématologie, Université Bordeaux Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France.

Low-dose aspirin is an important therapeutic option in the secondary prevention of myocardial infarction (MI) and ischemic stroke, basedon its unique cost-effectiveness and widespread availability. In addition, based on the results of a number of large studies, aspirin is also widely used in the primary prevention of MI. This paper provides an update of the available data to offer greater clarity regarding the risks of aspirin with respect to hemorrhagic stroke. In the secondary prevention of cardiovascular, cerebrovascular, and ischemic events, the evidence supports that the benefits of aspirin treatment significantly outweigh the risk of a major hemorrhage. When considering whether aspirin is appropriate, the absolute therapeutic cardiovascular benefits of aspirin must be balanced with the possible risks associated with its use, being hemorrhagic stroke. Regarding these clinical facts, normal, COX 1 -/-, and COX 2 -/- mice were treated with a wide range of doses of aspirin and studied by induced hemorrhagic time. The results outlined three major conclusions: high doses of aspirin induce hemorrhage, while low doses of aspirin do not. In the absence of COX 1, ultra low doses of aspirin produce an antihemorrhagic effect not observed with intermediate doses. The absence of COX 2 induced a hemorrhagic effect that needs further research, probably originated in compensatory phenomena.
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http://dx.doi.org/10.1155/2012/676237DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3265119PMC
August 2012

Thrombotic events associated to aspirin therapy.

Thrombosis 2012 24;2012:247363. Epub 2011 Nov 24.

Laboratoire d'Hématologie, Université Bordeaux 2, 146 Rue Léo Saignat, 33076 Bordeaux Cedex, France.

Acetyl salicylic acid (ASA) is widely used in clinical practice. Previous studies done in rats showed unexpected thrombotic potencies of this drug used at ultra-low doses. This review is the first report in which the effects of a wide range of ASA concentration on a microvessel model of laser-induced thrombus formation and Induced Hemorrhagic Time in animals were largely studied.
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http://dx.doi.org/10.1155/2012/247363DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3236366PMC
August 2012

Paradoxical thrombotic effects of aspirin: experimental study on 1000 animals.

Cardiovasc Hematol Disord Drug Targets 2010 Jun;10(2):103-10

Laboratoire d'Hématologie, Université Victor Segalen, Bordeaux 2, Bordeaux, France.

Unlabelled: Aspirin administration decreases the risk of vascular ischemic problems. However, aspirin withdrawal may temporarily increase this risk. Previous studies reported that high dilutions of aspirin might cause a pro-thrombotic effect. This paper studies the effect of the lower end of the aspirin dose-response curve, its possible mechanism and clinical implications.

Protocol: Wistar rats were distributed into 100 groups of 10 rats each. Aspirin was injected at 100 mg/kg, 1 mg/kg and at several different aspirin dilutions along with cyclooxygenase (COX) 1 (SC-560), COX 2 (NS-398) or both selective inhibitors simultaneously using a laser-induced thrombosis model.

Results: The higher doses of aspirin decreased thrombosis. An opposite trend was observed with the lowest doses. SC-560 produced an anti-thrombotic effect antagonized by the highest aspirin dilutions. NS-398 created a pro-thrombotic effect that was antagonized by aspirin at higher doses. Simultaneous inhibition of COX 1 and 2 produced changes similar to COX 1 inhibition.

Conclusion: COX 2 inhibition induced a pro-thrombotic effect that was antagonized by aspirin at 1 mg/kg or 100 mg/kg. The administration of the lowest aspirin doses induced a pro-thrombotic effect stronger than the antithrombotic effect of COX 1 selective inhibition. The mechanism of this last pro-thrombotic effect is induced by residual aspirin and is independent of COX 1 inhibition. This study may explain the cause of the paradoxical thrombo-embolic complications observed after aspirin discontinuation, an effect of residual aspirin rather than a rebound effect, and highlights the importance of low doses of substances as a barely studied source of side-effects.
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http://dx.doi.org/10.2174/187152910791292510DOI Listing
June 2010

Aspirin therapy: an attempt to explain the events of prothrombotic complications after treatment discontinuation.

Thromb Haemost 2010 Jan 13;103(1):171-80. Epub 2009 Nov 13.

Laboratoire d'Hématologie, Université Victor Segalen, Bordeaux 2, 146 Rue Leo Saignat, 33.076 Bordeaux Cedex, France.

Aspirin remains the most widely used drug for prevention of vascular events. Recent observational epidemiological evidence has raised the concern that aspirin withdrawal for treatment non-compliance, surgery or side effects can carry an increased thrombotic risk. The delay to the thrombotic event was between 7 to 30 days in most reports and most frequently 7 to 10 days. The mechanism underlying this effect remains poorly understood. Using an in vivo model of laser-induced thrombosis, aspirin injected in one single dose of 100 mg/kg bw has also shown a prothrombotic activity in the rat 8 to 10 days after injection in the normal rat. The hypothesis was made that minimal concentrations of aspirin or ultra-low dose aspirin (ULDA) could induce this effect. ULDA showed prothrombotic properties in the same model of induced thrombosis that were very similar to those described after aspirin withdrawal, but the effect was observed only one hour after aspirin administration. This prothrombotic effect of ULDA is very similar to the effect observed after COX 2 selective inhibition with NS 398. The administration of both the selective COX 2 inhibitor and ULDA did not produce further changes. High-dose ASA counterbalances the lack of COX 2 with an antithrombotic effect. No effect of residual ASA was observed in COX 2 -/- mice, thus confirming the existence of a COX 2 inhibition pathway. COX 2 inhibition produced by residual ASA is the probable cause of ischaemic accidents and drug-eluting stents thrombosis a few days after ASA withdrawal.
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http://dx.doi.org/10.1160/TH09-07-0506DOI Listing
January 2010

Forensic analysis of dog (Canis lupus familiaris) mitochondrial DNA sequences: an inter-laboratory study of the GEP-ISFG working group.

Forensic Sci Int Genet 2009 Dec 20;4(1):49-54. Epub 2009 May 20.

Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), Rua Dr. Roberto Frias s/n, 4200-465 Porto, Portugal.

A voluntary collaborative exercise aiming at the mitochondrial analysis of canine biological samples was carried out in 2006-2008 by the Non-Human Forensic Genetics Commission of the Spanish and Portuguese Working Group (GEP) of the International Society for Forensic Genetics (ISFG). The participating laboratories were asked to sequence two dog samples (one bloodstain and one hair sample) for the mitochondrial D-loop region comprised between positions 15,372 and 16,083 using suggested primers and PCR conditions, and to compare their results against a reference sequence. Twenty-one participating laboratories reported a total of 67.5% concordant results, 15% non-concordant results, and 17.5% no results. The hair sample analysis presented more difficulty to the participants than the bloodstain analysis, with a high percentage (29%) failing to obtain a result. The high level of participation showed the interest of the community in the analysis of dog forensic samples but the results reveal that crucial methodological issues need to be addressed and further training is required in order to respond proficiently to the demands of forensic casework.
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http://dx.doi.org/10.1016/j.fsigen.2009.04.008DOI Listing
December 2009

Prothrombotic and hemorrhagic effects of aspirin.

Clin Appl Thromb Hemost 2009 Oct 3;15(5):523-8. Epub 2008 Jul 3.

Laboratoire d'Hématologie Université Victor Segalen Bordeaux 2, Bordeaux, France.

Aspirin remains the most widely used drug for prevention of vascular events. Recent observational epidemiological evidence has raised the concern that aspirin withdrawal for treatment noncompliance, surgery, or side effects can carry an increased thrombotic risk. The delay to the thrombotic event was between 7 to 30 days in most reports and most frequently 7 to 10 days. The mechanism underlying this effect remains poorly understood. Using an in vivo model of laser-induced thrombosis, aspirin injected in 1 single dose of 100 mg/kg body weight has also shown a prothrombotic activity in the rat 8 to 10 days after injection in the normal rat. The hypothesis was made that minimal concentrations of aspirin or ultra-low dose aspirin (ULDA) could induce this effect. ULDA showed prothrombotic properties in the same model of induced thrombosis that were very similar to those described after aspirin withdrawal, but the effect was observed only 1 hour after aspirin administration. This prothrombotic effect of ULDA is very similar to the effect observed after COX 2 selective inhibition with NS 398. The administration of both the selective COX 2 inhibitor and ULDA did not produce further changes. In conclusion, the prothrombotic effects described in recent observational studies are likely produced by a direct effect of aspirin, whose putative mechanism involving COX 2 inhibition remains poorly understood.
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http://dx.doi.org/10.1177/1076029608319945DOI Listing
October 2009

Reverse effect of aspirin: is the prothrombotic effect after aspirin discontinuation mediated by cyclooxygenase 2 inhibition?

Pathophysiol Haemost Thromb 2007 6;36(1):40-4. Epub 2008 Mar 6.

Laboratoire d'Hématologie, UFR des Sciences Pharmaceutiques, Université Victor Segalen Bordeaux 2, Bordeaux, France.

Background: While aspirin is the drug most often used to prevent cardiovascular complications, its discontinuation induces an increased risk of acute coronary syndrome and ischemic stroke in some patients.

Objectives: We hypothesized that infinitesimal concentrations of aspirin could persist in plasma after its discontinuation, thereby inducing a prothrombotic effect that could be due to a modification in the mechanism of action of aspirin via the cyclooxygenase 1 (COX-1) and COX-2 pathways.

Methods And Results: We studied the effects of ultra-low-dose aspirin (ULDA) as well as those of sc-560 and ns-398, specific COX-1 and COX-2 inhibitors, on induced hemorrhagic time and in a model of laser-induced thrombosis in rats. In the laser-induced thrombosis model, ULDA treatment increased the number of emboli and the duration of embolization, thereby confirming its prothrombotic effect described in previous publications. This effect was also observed in rats pretreated with sc-560 but not in those pretreated with ns-398.

Conclusions: We demonstrated that ULDA induced a prothrombotic effect in the rats studied. This strongly suggests that a very small amount of aspirin could remain in the patient's blood after aspirin therapy, leading to cardiovascular complications. This effect may be mediated by the COX-2 pathway.
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http://dx.doi.org/10.1159/000112638DOI Listing
May 2008

Modifications produced by selective inhibitors of cyclooxygenase and ultra low dose aspirin on platelet activity in portal hypertension.

World J Gastroenterol 2007 Oct;13(38):5065-70

Universidad Maimónides, Buenos Aires, Argentina.

Aim: To study the mechanism involved in the potentially beneficial effect of ultra low dose aspirin (ULDA) in prehepatic portal hypertension, rats were pretreated with selective COX 1 or 2 inhibitors (SC-560 or NS-398 respectively), and subsequently injected with ULDA or placebo.

Methods: Portal hypertension was induced by portal vein ligation. Platelet activity was investigated with an in-vivo model of laser induced thrombus production in mesenteric circulation and induced hemorrhagic time (IHT). Platelet aggregation induced by ADP and dosing of prostanoid products 6-keto-PGF1alpha, TXB2, PGE2 and LTB4 were also performed.

Results: The portal hypertensive group receiving a placebo showed a decreased in vivo platelet activity with prolonged IHT, an effect that was normalized by ULDA. SC-560 induced a mild antithrombotic effect in the normal rats, and an unmodified effect of ULDA. NS-398 had a mild prothrombotic action in portal hypertensive rats, similar to ULDA, but inhibited a further effect when ULDA was added. An increased 6-keto-PGF1alpha was observed in portal hypertensive group that was normalised after ULDA administration. TXA2 level after ULDA, remained unchanged.

Conclusion: These results suggest that the effect of ULDA on platelet activity in portal hypertensive rats, could act through a COX 2 pathway more than the COX 1, predominant for aspirin at higher doses.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434635PMC
http://dx.doi.org/10.3748/wjg.v13.i38.5065DOI Listing
October 2007

Modifications produced by indomethacin and L-NAME in the effect of ultralow-dose aspirin on platelet activity in portal hypertension.

Pathophysiol Haemost Thromb 2006 ;35(5):357-63

Facultad de Medicina, Universidad Maimónides, Buenos Aires, Argentina.

In our previous study, we demonstrated the effect of ultralow-dose aspirin (ULDA) on platelet activity and bleeding in rats with portal hypertension (PHT) produced by portal vein ligation (PVL). This paper reports modifications in this effect caused by blocking NO production by nitro arginine methyl ester (NAME) and cyclooxygenase (COX) activity with indomethacin. PVL rats and sham-operated controls were treated with placebo, indomethacin or NAME and 30 min thereafter with placebo or ULDA treatment. Platelet activity was studied by a model of in vivo laser-induced thrombus production in the mesenteric circulation, induced hemorrhage time (IHT) and platelet aggregation ex vivo induced by adenosine diphosphate in an aggregometer. The PVL group receiving placebo showed a decreased platelet activity with prolonged IHT, an effect that was reversed by ULDA. Indomethacin induced a decreased platelet activity in the control rats and a prolonged IHT. In PHT with ULDA, in vivo platelet activity was enhanced but the normalization of IHT observed in rats without indomethacin was blunted. The addition of NAME normalized the diminished in vivo platelet aggregation and increased the IHT observed in PVL animals. These changes decreased the effect of ULDA in both sham-operated and PVL animals. The effect of indomethacin was more clearly modified by ULDA than the effect of NAME, thus suggesting that modifications in the COX pathway might alter the effect of ULDA. The simultaneous administration of indomethacin and ULDA could inhibit its beneficial effect on bleeding in rats with PHT.
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http://dx.doi.org/10.1159/000097689DOI Listing
March 2007

Platelet aggregation in portal hypertension and its modification by ultra-low doses of aspirin.

Pathophysiol Haemost Thromb 2005 ;34(1):29-34

Catedra de Fisiopatologia, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Buenos Aires, Argentina.

Aspirin (ASA) is widely accepted as antithrombotic drug, but several reports point out that its use in ultra-low doses (ULD) has prothrombotic properties. In this study, we evaluate the effect of portal hypertension in rats on platelet aggregation in an in vivo arterial thrombosis model induced by a laser beam. Portal hypertension was produced by calibrated stenosis of the portal vein. ASA in ULD was injected to both control and portal hypertensive groups. Platelet aggregation induced by ADP, prothrombin time, activated partial thromboplastin time, fibrinogen and induced hemorrhagic time test were also performed. Portal hypertensive rats showed a diminished number of emboli and duration of embolization in the laser procedure and an increase in induced hemorrhagic time. These changes were reverted by one injection of ASA at ULD. This observation could be of importance for primary prevention or the treatment of recurrence in upper digestive tract hemorrhage in portal hypertensive patients.
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http://dx.doi.org/10.1159/000088545DOI Listing
January 2006

Results of the 2003-2004 GEP-ISFG collaborative study on mitochondrial DNA: focus on the mtDNA profile of a mixed semen-saliva stain.

Forensic Sci Int 2006 Jul 21;160(2-3):157-67. Epub 2005 Oct 21.

Instituto Nacional de Toxicología y Ciencias Forenses, Servicio de Biología, Barcelona, Spain.

We report here a review of the seventh mitochondrial DNA (mtDNA) exercise undertaken by the Spanish and Portuguese working group (GEP) of the International Society for Forensic Genetics (ISFG) corresponding to the period 2003-2004. Five reference bloodstains from five donors (M1-M5), a mixed stain of saliva and semen (M6), and a hair sample (M7) were submitted to each participating laboratory for nuclear DNA (nDNA; autosomal STR and Y-STR) and mtDNA analysis. Laboratories were asked to investigate the contributors of samples M6 and M7 among the reference donors (M1-M5). A total of 34 laboratories reported total or partial mtDNA sequence data from both, the reference bloodstains (M1-M5) and the hair sample (M7) concluding a match between mtDNA profiles of M5 and M7. Autosomal STR and Y-STR profiling was the preferred strategy to investigate the contributors of the semen/saliva mixture (M6). Nuclear DNA profiles were consistent with a mixture of saliva from the donor (female) of M4 and semen from donor M5, being the semen (XY) profile the dominant component of the mixture. Strikingly, and in contradiction to the nuclear DNA analysis, mtDNA sequencing results yield a more simple result: only the saliva contribution (M4) was detected, either after preferential lysis or after complete DNA digestion. Some labs provided with several explanations for this finding and carried out additional experiments to explain this apparent contradictory result. The results pointed to the existence of different relative amounts of nuclear and mtDNAs in saliva and semen. We conclude that this circumstance could strongly influence the interpretation of the mtDNA evidence in unbalanced mixtures and in consequence lead to false exclusions. During the GEP-ISFG annual conference a validation study was planned to progress in the interpretation of mtDNA from different mixtures.
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http://dx.doi.org/10.1016/j.forsciint.2005.09.005DOI Listing
July 2006

Mitochondrial DNA error prophylaxis: assessing the causes of errors in the GEP'02-03 proficiency testing trial.

Forensic Sci Int 2005 Mar;148(2-3):191-8

Unidad de Genética, Facultad de Medicina de la Universidad de Santiago de Compostela, Instituto de Medicina Legal, A Coruña, Galicia-Spain.

We report the results of the Spanish and Portuguese working group (GEP) of the International Society for Forensic Genetics (ISFG) Collaborative Exercise 2002-2003 on mitochondrial DNA (mtDNA) analysis. Six different samples were submitted to the participating laboratories: four blood stains (M1-M2-M3-M4), one mixture blood sample (M5), and two hair shaft fragments (M6). Most of the labs reported consensus results for the blood stains, slightly improving the results of previous collaborative exercises. Although hair shaft analysis is still carried out by a small number of laboratories, this analysis yielded a high rate of success. On the contrary, the analysis of the mixture blood stain (M5) yielded a lower rate of success; in spite of this, the whole results on M5 typing demonstrated the suitability of mtDNA analysis in mixture samples. We have found that edition errors are among the most common mistakes reported by the different labs. In addition, we have detected contamination events as well as other minor problems, i.e. lack of standarization in nomenclature for punctual and length heteroplasmies, and indels. In the present edition of the GEP-ISFG exercise we have paid special attention to the visual phylogenetic inspection for detecting common sequencing errors.
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http://dx.doi.org/10.1016/j.forsciint.2004.06.008DOI Listing
March 2005

[DNA profile in legal practice].

J Soc Biol 2003 ;197(4):329-31

Experts près la Cour d 'Appel de Bordeaux, Université Victor Ségalen Bordeaux 2, 146, rue Léo-Saignat, 33076 Bordeaux Cedex.

This article shows the main advantages and drawbacks of the genetic analysis used by magistrates and police officers. Analyze a cellular trace on the scene of a crime, seek a paternity are some applications.
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June 2004

The 2000-2001 GEP-ISFG Collaborative Exercise on mtDNA: assessing the cause of unsuccessful mtDNA PCR amplification of hair shaft samples.

Forensic Sci Int 2003 Jun;134(1):46-53

Comisara General de Policía Científica, Sección de Biología-ADN, Madrid, Spain.

We report the results of Spanish and Portuguese working group (GEP) of International Society of Forensic Genetics (ISFG) Collaborative Exercise 2001-2002 on mitochondrial DNA (mtDNA) analysis. 64 laboratories from Spain, Portugal and several Latin-American countries participated in this quality control exercise. Five samples were sent to the participating laboratories, four blood stains (M1-M4) and a sample (M5) consisting of two hair shaft fragments. M4 was non-human (Felis catus) in origin; therefore, the capacity of the labs to identify the biological source of this sample was an integral part of the exercise. Some labs detected the non-human origin of M4 by carrying out immuno-diffussion techniques using antihuman serum, whereas others identified the specific animal origin by testing the sample against a set of animal antibodies or by means of the analysis of mtDNA regions (Cyt-b, 12S, and 16S genes). The results of the other three human blood stains (M1-M3) improved in relation to the last Collaborative Exercises but those related to hairs yielded a low rate of success which clearly contrasts with previous results. As a consequence of this, some labs performed additional analysis showing that the origin of this low efficiency was not the presence of inhibitors, but the low quantity of DNA present in these specific hair samples and the degradation. As a general conclusion the results emphasize the need of external proficiency testing as part of the accreditation procedure for the labs performing mtDNA analysis in forensic casework.
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http://dx.doi.org/10.1016/s0379-0738(03)00095-1DOI Listing
June 2003