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Recent eLetters

Displaying 1-10 letters out of 214 published

  1. Mahatma Gandhi National Rural Employment Guarantee Act (MGNREGA)and Women's empowerment in India

    Nair et al (1) have highlighted some important issues related to Mahatma Gandhi National Rural Employment Guarantee Act (MGNREGA), using qualitative techniques. Provision under MNREGA includes an ambitious project of the Government of India to provide guaranteed wage employment to the rural population of India with a minimum of 100 days in a year. However, several flaws have been identified in its implementation (2). The issues identified at the Government level are a) poor planning and administrative skill, b) lack of focus on objectives, c) lack of adequate man power, d) difficulty in funding the scheme, e) discrimination, f) corruption and irregularities, g) lack of safety measures; and at the public level are a) inadequate awareness, b) no purposive spending c) being unorganized.

    The scheme is implemented at the village by active participation of village local self administering body i.e. Gram Panchayat. The Gram Panchayat has to plan, organize and implement the scheme effectively. It has been observed that the panchayats, except those in Karnataka and, to some extent, in West Bengal, have no experience at all in planning large- scale programme. Problems related to corruption in implementing the programmes exist and no real asset was being created by the scheme. (3)

    One of the objectives of the scheme to strengthen women empowerment may go unrealized. Under this scheme, cases of discrimination against women and people from "backward" groups are reported from several regions of the country.(4). While some states such as Kerala and erstwhile Andhra Pradesh have registered high percentage of women workers getting enrolled in the scheme, other states have registered a very low percentage of women availing benefit under MGNREGA. In some regions only a few job cards are issued when the applicants are women, or there are delays in the issue of cards. Women are sometimes told that manual labour under the MGNREGA is not meant for women and they could not participate in the works as it entailed digging and removing soil. In some states, only the powerful groups having strong lobby with the Government among the work force get large number of job cards.

    The actual funds that reach the beneficiaries are very little compared to the funds allocated for welfare schemes. The condition of women workforce in the insurgency hit areas is worse. Lesser women in these areas (44%) are employed as compared to the national average of 48%.(5). Nair et al (1) have highlighted another issue of child neglect among the women workers. Hence, creches have to be set up to enable women carrying their children to the work site during their work. In the work place usually women workers lay their children in cradles tied around tree branches. Hence, absence of the facility for creche may restrict the women to come forward to demand for work.

    Another problem related to the payment was that payment to the workers under MGNREGA was made in cash in some states such as Tamilnadu, instead of through banks or post office accounts.(6) This leads to a situation whereby chances of giving less payment to the worker increases. At present, the payment has been channelized to the bank account of the workers directly thereby reducing this discrimination. Despite these measures, more efforts need to be put under the scheme to promote women in the workforce for better income generation and empowerment..

    References 1. Nair M, Ariana P, Webster P.Impact of mothers' employment on infant feeding and care: a qualitative study of the experiences of mothers employed through the Mahatma Gandhi National Rural Employment Guarantee Act. BMJOpen 2014;4:e004434 doi:10.1136/bmjopen-2013-004434 2. Chaarlas LJ, Velmurugan JM. Mahtama Gandhi National Rural Employment Guarantee Act, 2005 (MGNREGA): Issues and Challenges. http://www.ijmra.us/project%20doc/IJPSS_JUNE2012/IJMRA-PSS1123.pdf (accessed on4.4.14) 3. Singh S. Plan panel highlights problems in NREGA. http://www.livemint.com/Politics/GQCl7OUte0QkFutGbdTV9M/Plan-panel- highlights-problems-in-NREGA.html. Jan 15, 2010. 4. http:/www.policyproposalfor india.com/article.php?article- id=169&languageid=1 5. htpp://www.livemint.com/2011/09/21191111/less-than-9-households- could.htm/ 6. Ramesh. Pay Wages for Rural Job Scheme through Banks and POs accounts. The New Indian Express dated 8th Dec, 2011; page 6.

    Conflict of Interest:

    None declared

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  2. Relationship between NSAID use and AF

    The results of population study " Non-steroidal anti-inflammatory drugs and the risk of atrial fibrillation: a population-based follow-up study", indicates a potential relationship between NSAID use an atrial fibrillation in elderly people. However a simple reflexion about the conclusions came to my mind: Why were the patients using NSAID ? Obviously we must think about the relationship between AF and the condition to which NSAID prescription was indicated. A systemic inflammatory disease with secondary cardiac manifestation for example, would justify that findings.

    Conflict of Interest:

    None declared

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  3. Response to: "The smoking habit of a close friend or family member--how deep is the impact? A cross-sectional study"

    Dear Editor, Understanding the impact of social and familial behaviour on smoking behaviour is undoubtedly a Public Health priority. We read with great interest the article by Saari et al [1] assessing the impact of smoking habits of close friends and family members. The authors reported that women who had a smoker as a close friend in school had a greater likelihood of being a smoker themselves in adulthood (OR 5.1, 95% CI 2.6 to 10.0), but this effect was not found in men. Interestingly, for men, having family members in childhood who smoked increased the likelihood of becoming smokers in adulthood (OR not given, reported as >2.0), but not in women. First, we appreciate the authors' recognition of the importance of social and peer groups in shaping smoking behaviour, especially among school age children. Despite much of the research attention falling on parent-child influences, it remains an important pathway for initiation of smoking behaviour. We wish however to highlight several important limitations in the manuscript. There were several key confounders which were not adequately covered in the study. Deprivation indicators such as household income, parental income or geographic location are all key risk factors for smoking and could heavily confound the results [2,3]. Other well-established confounders such as alcohol intake and anxiety or stress levels [4,5] were also not considered. The authors could be more transparent about several aspects of their method. Self-perceived health, for example, was not relevant to the central research question and the impact of the result was not discussed. Furthermore, the responses were also regrouped into "very good" and not-"very good" which is misleading and the authors could simply present all five categories as reported. Notwithstanding the irrelevance to the research question, all reasons for such reclassifications should be discussed, as well as whether alternative groupings would produce comparable 'positive' results. In order to isolate the effects of close-friend smoking from parental-smoking, a stratified analysis of parental-smoker and non-parental-smoker children could have been conducted - which would help to answer the central research question and strengthen the study. Finally, the authors should be far more circumspect in their conclusions. They claim that "the impact of [a close friend] is greater than [parents or siblings] in school age when it comes to smoking behaviour in adults," however their results show that childhood friends affected adult smoking behaviour in women only. In contrast, childhood family affected adult smoking behaviour only in men. By stretching the conclusion to be too general the paper misses the opportunity to highlight this interesting and enlightening contrast which has practical implications for Public Health efforts to engage populations in nuanced ways. The authors note that traditional methods of smoking cessation action may be ineffective. Study participants received annual smoking cessation interventions but this did not affect smoking behaviour. This fact would support the authors' suggestion that existing smoking cessation campaigns need something 'new' in order to increase their effectiveness - such as a focus on peer-led or social-network-based initiatives. In closing, although there are several aspects of the manuscript which require further clarification, the paper raises interesting and important questions about the effects of childhood social networks on smoking behaviour and highlights important sociological issues to public health departments and practitioners. We look forward to further research in this area. References 1 Saari AJ, Kentala J, Mattila KJ. The smoking habit of a close friend or family member--how deep is the impact? A cross-sectional study. BMJ Open 2014;4:e003218. doi:10.1136/bmjopen-2013-003218 2 Kleinschmidt I, Hills M, Elliott P. Smoking behaviour can be predicted by neighbourhood deprivation measures. J Epidemiol Community Heal 1995;49:S72-S77. doi:10.1136/jech.49.Suppl_2.S72 3 Shohaimi S. Residential area deprivation predicts smoking habit independently of individual educational level and occupational social class. A cross sectional study in the Norfolk cohort of the European Investigation into Cancer (EPIC-Norfolk). J Epidemiol Community Heal 2003;57:270-6. doi:10.1136/jech.57.4.270 4 Byrne DG, Byrne AE, Reinhart MI. Personality, stress and the decision to commence cigarette smoking in adolescence. J Psychosom Res 1995;39:53-62. doi:10.1016/0022-3999(94)00074-F 5 Steptoe A, Wardle J, Pollard TM, et al. Stress, social support and health-related behavior: A study of smoking, alcohol consumption and physical exercise. J Psychosom Res 1996;41:171-80. doi:10.1016/0022-3999(96)00095-5

    Conflict of Interest:

    None declared

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  4. Correction to "UK multiple sclerosis risk-sharing scheme: a new natural history dataset and an improved Markov model"

    With regret we need to inform you of a typo in the data description in our paper. The number of EDSS scores in the BCMS data used for the Markov Model is N=7255. N=7335 is incorrect. Therefore the first sentence in the 'Results' section of the abstract should read "The BCMS untreated cohort contributed 7255 EDSS scores [...]". The first sentence in the second paragraph of 'RESULTS Data description' should read: "The natural history BCMS comparator dataset comprised of 898 patient profiles with 7255 EDSS scores [...]". This does not affect any of the analyses or results but is a typo that will not match with future publications.

    Conflict of Interest:

    Dr Jacqueline Palace has received support for scientific meetings and honorariums for advisory work from Merck Serono, Biogen Idec, Novartis, Teva, Chugai Pharma and Bayer Schering, and unrestricted grants from Merck Serono, Novartis, Biogen Idec and Bayer Schering. Her hospital trust receives funds for her role as clinical lead for the RSS, and she has received grants from the MS society and Guthie Jackson Foundation for unrelated research studies.

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  5. Correction- Author Affiliatons

    Authors were inadvertently affiliated.

    The correct affiliations of authors should be:

    Israel Amirav1,2 Michael T. Newhouse5 , Anthony Luder1, Asaf Halamish3, Hamza Omar4, Miguel Gorenberg4

    1. Pediatric Department, Ziv Medical Center, Faculty of Medicine, Bar-Ilan University, Safed, Israel

    2. Pediatric Department, University of Alberta, Edmonton, Canada

    3. Technosaf, Karkur, Israel

    4. Nuclear Medicine Department, Ziv Medical Center, Safed, Israel

    5. Firestone Institute for Respiratory Health, St Joseph's Hospital, McMaster University, Hamilton, Ontario, Canada

    Conflict of Interest:

    None declared

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  6. Long term effectiveness of community based lifestyle intervention needs to be studied with robust study design

    Sir, While reading this article, we have noticed the following issues which need to be considered before arriving at any conclusion:

    1. The study does not fit into the definition of cohort study.1 As only Complete Health Improvement Programme (CHIP) intervention group was followed and studied. Hence "cohort study" term is loosely used by the authors in the title.

    2. The authors did not mention about size and characteristics of population in the study area. This limits the interpretation of generalizability of study results even to local population.

    3. Parent study showed that 790 participants completed the 30 days CHIP intervention but why only 323(41%) were approached for the study is not described in the study.2 This fact should be considered before making any interpretation about internal validity of the study, as this sample size was not justified.

    4. Standard measurement procedure of biometric indicators would have helped the reader to validate the study findings. This information is lacking in this article.

    5. Authors did not describe the baseline demographic characteristics of the study participants.This information would have helped the readers to understand the possible confounders, the effect modifiers and interpreting the study results.

    6. The study reports that there was significant improvement in biometrics among high risk participants but deterioration of indices among low risk participants. This can be explained by phenomenon of regression to mean. Hence, results / conclusion of the study should be interpreted with caution.

    7. In the result section authors mentioned that improvement in weight is around 1.6% and that is statistically significant. But 95% CI includes null value (-2.84 to 0.24) which makes it statistically not significant.

    8. Authors lost the opportunity to find the differential impact of intervention between the groups (obese/non-obese, hypertensive/ non- hypertensive) by using chi square test.

    9. Study only deals with the bi-variate analysis for arriving at the conclusion about impact of the intervention and ignored the scope of confounders, effect modifiers in it. Multivariate analysis addressing all possible confounders would have been necessary to study actual impact of the intervention.

    10. This study dealt with the observations after 3- 5 years follow-up of CHIP intervention, hence findings after 30 day of follow up becomes irrelevant for this article.

    11. Authors mentioned that CHIP can be implemented inexpensively in long term. But cost-effective analysis, costing of intervention, outcome evaluation analysis is necessary to arrive at any conclusion about cost- effectiveness of the intervention.

    12. Authors did comparison between compliant and non-compliant groups to justify zero effect of loss to follow up on overall results. But this cannot be done unless information about baseline demographic characteristics of both the population is provided.

    13. Authors concluded that CHIP intervention was effective after 3 - 5 years after implementation unlike other community based intervention. Between the groups comparison is essential, instead of within group intervention to arrive at his conclusion (Table 1). Also, the effective sample for within group comparison was 33% of actual recruited participants. Hence long term effectiveness of CHIP intervention is questionable in given community itself.

    References:

    1. Leon Gordis. Epidemiology. Philadelphia: Saunders Elsevier. 2009

    2. Morton DP, Rankin P, Morey P, et al. The effectiveness of the Complete Health Improvement Program (CHIP) in Australasia for reducing selected chronic disease risk factors: a feasibility study. N Z Med J 2013;126:43-54.

    Conflict of Interest:

    None declared

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  7. The effect of different criteria on outcomes in ME/CFS trials

    The authors discuss the PACE Trial: "Hence, primary studies and systematic reviews on prognosis and therapy are alternative sources to evaluate the usefulness of different case definitions of CFS/ME. We have identified only one such publication, the PACE trial.(1) Here, participants were diagnosed according to the Oxford- 1991 criteria, Empirical criteria-2007/Reeves and London ME-1994/National Task Force criteria, and then randomised to either standard medical treatment, graded exercise therapy, cognitive behaviour therapy or pacing. The results showed that the effectiveness of the treatments was similar across groups, irrespective of the case definition which had been used."

    This is what has been reported by the PACE Trial investigators. However there appears to be problems with how the criteria were used and operationalized.

    Ellen Goudsmit, one of the co-authors of the London criteria, has posted on PubMed Commons (2): "As a co-author of the London criteria for myalgic encephalomyelitis, I wish it to be known that this study did not use the criteria and that their citation refers to an incomplete and flawed version written by someone without permission from the original authors. It is therefore unclear if there were any patients with ME who participated in this trial." Dr Goudsmit gave more details about her concerns in a comment on another PACE Trial paper (3).

    I also question whether all those defined as having ME in the PACE Trial would all be seen as having ME by others: 97% (329 out of 340) of those that who did not have a psychiatric disorder who satisfied the Oxford criteria for CFS (4,5), which basically just requires chronic fatigue, were classed as satisfying the ME criteria.

    Regarding the Reeves criteria, it is first important to point out that it was the Reeves et al (2003) criteria that were used rather than the Reeves empirical criteria. These criteria were operationalized in a non-standard way in the PACE Trial, as the authors explained: "For the purposes of this study, the four or more symptoms needed to be present within the previous week of the assessment date, rather than the previous 6 months (Reeves et al. 2003)."

    In a trial of chronic fatigue (8), which is not that different from a trial of Oxford criteria CFS, investigators found the following: "Meeting the criteria for chronic fatigue syndrome was the most powerful predictor of poor outcome and this negative effect was enhanced by greater functional impairment or greater perceived negative consequences, but was not further enhanced by both." They are referring to the Fukuda criteria for CFS in this case (9).

    I discuss the heterogeneity of patients in a section of a paper of mine entitled, "Recognize heterogeneity of patients with a diagnosis of ME/CFS" (10).

    References:

    (1) White PD, Goldsmith KA, Johnson AL, et al. Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. Lancet 2011;377:823-36.

    (2) Goudsmit EM. Comment on: Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. http://www.ncbi.nlm.nih.gov/pubmed/21334061#cm21334061_1177

    (3) Goudsmit EM. RE: Recovery from chronic fatigue syndrome after treatments given in the PACE trial. https://listserv.nodak.edu/cgi- bin/wa.exe?A2=ind1301E&L=CO-CURE&P=R1285&I=-3&d=No+Match%3BMatch%3BMatches

    (4) KindlonT. PACE Trial - 97% of the participants who didn't have a psychiatric disorder satisfied the definition of M.E. used. https://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind1106A&L=CO-CURE&P=R2764&I= -3&d=No+Match%3BMatch%3BMatches&m=21522

    (5) Sharpe MC, Archard LC, Banatvala JE, et al. A report--chronic fatigue syndrome: guidelines for research. J R Soc Med 1991;84:118-21.

    (6) Reeves WC, Lloyd A, Vernon SD, et al; International Chronic Fatigue Syndrome Study Group (2003). Identification of ambiguities in the 1994 chronic fatigue syndrome research case definition and recommendations for resolution. BioMed Central Health Services Research 3, 25.

    (7) White PD1, Goldsmith K, Johnson AL, Chalder T, Sharpe M. Recovery from chronic fatigue syndrome after treatments given in the PACE trial. Psychol Med. 2013;43:2227-35. doi: 10.1017/S0033291713000020.

    (8) Darbishire L1, Seed P, Ridsdale L. Predictors of outcome following treatment for chronic fatigue. Br J Psychiatry. 2005;186:350-1.

    (9) Fukuda, K., Straus, S. E., Hickie, I., et al (1994) The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Annals of Internal Medicine. 1994;121:953-959.

    (10) Kindlon T. Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Bulletin of the IACFS/ME. 2011;19(2):59-111.

    Conflict of Interest:

    I do various types of voluntary work for the Irish ME/CFS Association

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  8. A Dutch research protocol on advance care planning in COPD patients: a critical revision.

    Dear Editor, we are very interested in the manuscript of Houben and colleagues concerning the research protocol on the efficacy of advance care planning on the quality of end-of-life care and communication in patients with chronic obstructive pulmonary disease (COPD). Before writing this letter we have carefully revised the paper and deeply discussed about its strengths and limitations. Overall, we agree with the discussion that Authors have written and we think that this protocol would be able in assessing both primary and secondary outcomes. However, in hour modest opinion there are some points that have been not adequately discussed and that need to be at the least mentioned in order to make the described protocol more suitable for a contemporary research. Authors correctly hypothesize that structured advance care planning (ACP) by a trained nurse, in collaboration with the patient's physician, can improve quality of end-of-life care communication, as well as quality of end-of-life care and quality of dying for patients with COPD. Furthermore, they stated that structured ACP would not result in increased symptoms of anxiety or depression. The described protocol has been well built around the initial hypothesis. Nevertheless, considering that the end-of-life care is the main topic of the manuscript, we would like to highlight that in the paper there is mention neither of comorbidities nor of the concept of the system medicine. Effectively, there are strong evidences that let suppose that the enrolled patients will be not only COPD patients, but subjects suffering from several comorbidities such as skeletal muscle dysfunction, nutritional abnormalities, cardiovascular complications, metabolic complications and osteoporosis (1, 2). Therefore, a contemporary research protocol on COPD might have more likelihood of impact if it will be approached on the concept of system medicine, mainly considering that a COPD patient that is going to consider his end-of-life care will be of course a complex patient (3, 4). In any case, a COPD-centric approach is justified by the worldwide prevalence and increasing burden of this disease (5). However, in this context we believe that a modern protocol carried out on ACP in COPD patients should be based on the newest GOLD guidelines at the enrolment phase, since this would allow better characterizing the exacerbation profile of enrolled patients and since COPD exacerbations are now recognized as a strong predictor of subsequent exacerbations and mortality. Finally, it would be of interest to have more details concerning the elements of structured ACP intervention compared with those reported in Box 1.

    References

    1. Cazzola M, Calzetta L, Bettoncelli G, Cricelli C, Romeo F, Matera MG, Rogliani P. Cardiovascular disease in asthma and copd: A population- based retrospective cross-sectional study. Respiratory medicine 2012;106:249-256. 2. Choudhury G, Rabinovich R, Macnee W. Comorbidities and systemic effects of chronic obstructive pulmonary disease. Clin Chest Med 2014;35:101-130. 3. Nici L, ZuWallack R. An official american thoracic society workshop report: The integrated care of the copd patient. Proceedings of the American Thoracic Society 2012;9:9-18. 4. Wilkinson AM, Lynn J. Caregiving for advanced chronic illness patients. Techniques in Regional Anesthesia and Pain Management 2005;9:122-132. 5. Mannino DM, Buist AS. Global burden of copd: Risk factors, prevalence, and future trends. Lancet 2007;370:765-773.

    Conflict of Interest:

    None declared

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  9. Dryad data now available

    Data for this article is now available in the Dryad data repository (doi:10.5061/dryad.7dm1p) and can be viewed here http://datadryad.org/resource/doi:10.5061/dryad.7dm1p

    Conflict of Interest:

    BMJ Open staff member

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  10. Detection of mutations associated with preclinical atherosclerosis during the analysis of the whole mitochondrial genome: next generation sequencing data.

    Dear editor, In recent articles published in BMJ [1-4] a problem of cardiovascular diseases (CVD) genesis was discussed. Certainly, physical activity, psychosocial stress, obesity, hypertension and other traditional risk factors play an important role in development of the CVD. But we believe that molecular genetic defects, particularly mitochondrial genome mutations, might be significant in pathogenesis of cardiovascular diseases [5].

    To detect the spectrum of mitochondrial mutations in individuals, we used a high efficiency pyrosequencing of the whole mitochondrial genome. Whole blood samples were taken from 77 subjects, among them 45 patients had carotid atherosclerosis assessed by ultrasonography [6]; and 32 subjects had no atherosclerotic lesions. DNA was extracted by a phenol chloroform method. Afterwards an enriching of mitochondrial DNA was performed using Qiagen? REPLI-g Mitochondrial Kit. To carry out a high efficiency pyrosequencing of the whole mitochondrial genome, a system Roche 454 GS Junior Titanium (Roche, USA) was used. An analysis of mitochondrial DNA sequence was performed using GS Reference Mapper program. The Cambridge standard sequence NC_012920.1 was used for mapping human mitochondrial genome [7]. Statistical data processing was performed by IBM SPSS Statistics v.21.0.

    A whole genome pyrosequencing gave an opportunity to detect 58 homoplasmic mitochondrial genome mutations in the investigated samples. The frequency of mutations T152C, G185A, G228A, A263G, 3107delN, T489C, A750G, A1811G, A4769G, C7028T , A8860G, A10398G, A11467G, A11719G, A12308G, G12372A and A15326G turned to be significantly higher in patients with atherosclerosis than in healthy study participants. At the same time mitochondrial mutations T4216C, A4917G, G8697A, T10463C, A11251G, A11812G, A12705T, A13368A, A13617C, G14905A, A15607G, G15928A, T16069T, T16126C, C16223T, C16296T, T16311C and T16519C prevailed in healthy individuals. In addition, nine heteroplasmic mutations associated with atherosclerosis were found, namely: 576insC, 8516insA, 8516insC, 8528insA, G9477A, 8930insG, 10958insC, 13047insC ? 13050insC.

    It should be noted that 29% homoplasmic and 33% heteroplasmic proatherogenic mutations of mitochondrial genome belong to genes coding NADH dehydrogenase subunits; 18% homoplasmic atherogenic mutations are localized in genes coding rRNA subunits and 44% heteroplasmic single- nucleotide insertions are localized in genes coding ATP synthetase subunits. It can be assumed that the defects in NADH dehydrogenase, ATP synthetase and mitochondrial ribosomes may participate in realization of the mechanisms of atherogenesis. Previously, using pyrosequencer PSQTMHS96MA (Biotage, Sweden) we have found 11 heteroplasmic mutations associated with atherosclerosis: 652delG, A1555G, C3256T, T3336C, C5178A, 652insG , G12315A, G14459A, G13513A, G14846A and G15059A [8-10]. In the present study we did not detect the above mutations, possibly due to the fact that an intermediate stage of the whole mitochondrial genome PCR is not necessary for studying separate mutations with a pyrosequenator PSQTMHS96MA. Thus, it can desensitize Roche technology. However, this disadvantage is highly compensated by a high number of mutations associated with atherosclerosis, which can be detected during whole genome pyrosequencing.

    This study was supported by the Russian Ministry of Education and Science.

    References 1. Huynh QL, Blizzard CL, Sharman JE, Magnussen CG, Dwyer T, Venn AJ.Mann J, McLean R, Te Morenga L. The cross-sectional association of sitting time with carotid artery stiffness in young adults. BMJ Open. 2014 Mar 6;4(3):e004384. doi: 10.1136/bmjopen-2013-004384. 2. Tor?n K, Schi?ler L, Giang WK, Novak M, S?derberg M, Rosengren A. A longitudinal general population-based study of job strain and risk for coronary heart disease and stroke in Swedish men. BMJ Open. 2014 Mar 3;4(3):e004355. doi: 10.1136/bmjopen-2013-004355. 3. Wang Z, Hoy WE. Age-dependent decline of association between obesity and coronary heart disease: a cohort study in a remote Australian Aboriginal community. BMJ Open. 2013 Nov 25;3(11):e004042. doi: 10.1136/bmjopen-2013-004042. 4. Joffres M, Falaschetti E, Gillespie C, Robitaille C, Loustalot F, Poulter N, McAlister FA, Johansen H, Baclic O, Campbell N. Hypertension prevalence, awareness, treatment and control in national surveys from England, the USA and Canada, and correlation with stroke and ischaemic heart disease mortality: a cross-sectional study. BMJ Open. 2013 Aug 30;3(8):e003423. doi: 10.1136/bmjopen-2013-003423. 5. Wallace DC. Mitochondrial DNA sequence variation in human evolution anddisease. Proc Natl Acad Sci USA 1994;91(19 (September)):8739-46. Review. 6. Miasoedova VA, Kirichenko TV, Orekhova VA, Sobenin IA, Mukhamedova NM, Martirosian DM, Karagodin VP, Orekhov AN. Study of intima- medial thickness (IMT) of the carotid arteries as an indicator of natural atherosclerosis progress in Moscow population. Patol Fiziol Eksp Ter 2012 Jul-Sep;(3):104-8. Russian. 7. Homo sapiens mitochondrion, complete genome. NCBI Reference Sequence: NC_012920.1. URL: http://www.ncbi.nlm.nih.gov/nuccore/NC_012920 (last accessed date: 15.12.2013). 8. Sazonova M, Budnikov E, Khasanova Z, Sobenin I, Postnov A, Orekhov A. Studies of the human aortic intima by a direct quantitative assay of mutant alleles in the mitochondrial genome. Atherosclerosis. 2009, 204(1):184-190. (Epub 2009 Sep 4). 9. Sobenin IA, Sazonova MA, Postnov AY, Bobryshev YV, Orekhov AN. Changes of mitochondria in atherosclerosis: Possible determinant in the pathogenesis of the disease. Atherosclerosis. 2013 Jan 25. doi:pii: S0021- 9150(13)00041-5.10.1016/j.atherosclerosis.2013.01.006. [Epub ahead of print]. 10. Sobenin IA, Sazonova MA, Postnov AY, Salonen JT, Bobryshev YV, Orekhov AN. Association of mitochondrial genetic variation with carotid atherosclerosis. PLoS One. 2013 Jul 9;8(7):e68070. doi: 10.1371/journal.pone.0068070. Print 2013.

    Conflict of Interest:

    None declared

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