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Jonsson, Björn
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Publications (10 of 26) Show all publications
Derraik, J. G., Ahlsson, F., Lundgren, M., Jonsson, B. & Cutfield, W. S. (2016). First-borns have greater BMI and are more likely to be overweight or obese: a study of sibling pairs among 26 812 Swedish women. Journal of Epidemiology and Community Health, 70(1), 78-81
Open this publication in new window or tab >>First-borns have greater BMI and are more likely to be overweight or obese: a study of sibling pairs among 26 812 Swedish women
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2016 (English)In: Journal of Epidemiology and Community Health, ISSN 0143-005X, E-ISSN 1470-2738, Vol. 70, no 1, p. 78-81Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: A number of large studies have shown phenotypic differences between first-borns and later-borns among adult men. In this study, we aimed to assess whether birth order was associated with height and BMI in a large cohort of Swedish women.

METHODS: Information was obtained from antenatal clinic records from the Swedish National Birth Register over 20 years (1991-2009). Maternal anthropometric data early in pregnancy (at approximately 10-12 weeks of gestation) were analysed on 13 406 pairs of sisters who were either first-born or second-born (n=26 812).

RESULTS: Early in pregnancy, first-born women were of BMI that was 0.57 kg/m(2) (2.4%) greater than their second-born sisters (p<0.0001). In addition, first-borns had greater odds of being overweight (OR 1.29; p<0.0001) or obese (OR 1.40; p<0.0001) than second-borns. First-borns were also negligibly taller (+1.2 mm) than their second-born sisters. Of note, there was a considerable increase in BMI over the 18-year period covered by this study, with an increment of 0.11 kg/m(2) per year (p<0.0001).

CONCLUSIONS: Our study corroborates other large studies on men, and the steady reduction in family size may contribute to the observed increase in adult BMI worldwide.

National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:uu:diva-269652 (URN)10.1136/jech-2014-205368 (DOI)000369959800014 ()26311896 (PubMedID)
Available from: 2015-12-17 Created: 2015-12-17 Last updated: 2017-12-01Bibliographically approved
Albertsson-Wikland, K., Kriström, B., Lundberg, E., Aronson, A. S., Gustafsson, J., Hagenäs, L., . . . Aman, J. (2014). Growth hormone dose-dependent pubertal growth: a randomized trial in short children with low growth hormone secretion. Hormone Research in Paediatrics, 82(3), 158-170
Open this publication in new window or tab >>Growth hormone dose-dependent pubertal growth: a randomized trial in short children with low growth hormone secretion
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2014 (English)In: Hormone Research in Paediatrics, ISSN 1663-2818, E-ISSN 1663-2826, Vol. 82, no 3, p. 158-170Article in journal (Refereed) Published
Abstract [en]

BACKGROUND/AIMS: Growth hormone (GH) treatment regimens do not account for the pubertal increase in endogenous GH secretion. This study assessed whether increasing the GH dose and/or frequency of administration improves pubertal height gain and adult height (AH) in children with low GH secretion during stimulation tests, i.e. idiopathic isolated GH deficiency.

METHODS: A multicenter, randomized, clinical trial (No. 88-177) followed 111 children (96 boys) at study start from onset of puberty to AH who had received GH 33 µg/kg/day for ≥1 year. They were randomized to receive 67 µg/kg/day (GH(67)) given as one (GH(67×1); n = 35) or two daily injections (GH(33×2); n = 36), or to remain on a single 33 µg/kg/day dose (GH(33×1); n = 40). Growth was assessed as heightSDSgain for prepubertal, pubertal and total periods, as well as AHSDS versus the population and the midparental height.

RESULTS: Pubertal heightSDSgain was greater for patients receiving a high dose (GH(67), 0.73) than a low dose (GH(33×1), 0.41, p < 0.05). AHSDS was greater on GH(67) (GH(67×1), -0.84; GH(33×2), -0.83) than GH(33) (-1.25, p < 0.05), and heightSDSgain was greater on GH(67) than GH(33) (2.04 and 1.56, respectively; p < 0.01). All groups reached their target heightSDS.

CONCLUSION: Pubertal heightSDSgain and AHSDS were dose dependent, with greater growth being observed for the GH(67) than the GH(33) randomization group; however, there were no differences between the once- and twice-daily GH(67) regimens.

National Category
Pediatrics
Identifiers
urn:nbn:se:uu:diva-238294 (URN)10.1159/000363106 (DOI)000345448500003 ()25170833 (PubMedID)
Available from: 2014-12-11 Created: 2014-12-11 Last updated: 2017-12-05Bibliographically approved
Jonsson, P., Jonsson, B. & Eeg-Olofsson, O. (2014). Psychological and social outcome of epilepsy in well-functioning children and adolescents. A 10-year follow-up study. European journal of paediatric neurology, 18(3), 381-390
Open this publication in new window or tab >>Psychological and social outcome of epilepsy in well-functioning children and adolescents. A 10-year follow-up study
2014 (English)In: European journal of paediatric neurology, ISSN 1090-3798, E-ISSN 1532-2130, Vol. 18, no 3, p. 381-390Article in journal (Refereed) Published
Abstract [en]

Background: From a population based study of epilepsy in Swedish children a subgroup designated well-functioning with an epilepsy diagnosis in 1997 was worked up from a medical point of view 10 years later. Aim: To describe the psychological and social outcome in this subgroup. Methods: Thirty-one patients aged 11-22 years and their parents/partners responded to a questionnaire according to Achenbach System of Empirically Based Assessment (ASEBA) to evaluate behavioural and emotional problems, and social competence. Results: Active epilepsy, diagnosed in 32%, was related to attention problems, somatic complaints, and school problems. Polytherapy, used in 16%, was related to attention problems and aggressive behaviour. School problems were found in six of seven children younger than 18 years. Internalizing, externalizing, and 'other' syndromes were found in 29% of the individuals, but a grouping of these syndromes in the clinical range only in two (6.5%), a girl with generalized tonic clonic seizures alone, and a boy with structural focal epilepsy. Both had active epilepsy and were treated with polytherapy. All ten individuals with Rolandic epilepsy were classified as normal. The answers to the ASEBA questionnaire of individuals and parents/partners were inconsistent, and parents generally stated more problems than the individuals. Summary.: This 10-year follow-up study of psychological and social outcome in well-functioning children and adolescents with childhood onset epilepsy shows some emotional, behavioural, and social problems. Thus, early information to increase knowledge about epilepsy and associated psychological co-morbidities in order to decrease risk of low self-esteem, social anxiety, and depression later in life is of importance.

Keywords
Childhood epilepsy, Adolescent epilepsy, Well-functioning individuals, Internalizing and externalizing problems, ASEBA
National Category
Pediatrics Neurology
Identifiers
urn:nbn:se:uu:diva-228046 (URN)10.1016/j.ejpn.2014.01.010 (DOI)000336695500019 ()
Available from: 2014-07-07 Created: 2014-07-03 Last updated: 2017-12-05Bibliographically approved
Ahlsson, F., Diderholm, B., Ewald, U., Jonsson, B., Forslund, A. H., Stridsberg, M. & Gustafsson, J. (2013). Adipokines and their relation to maternal energy substrate production, insulin resistance and fetal size. European Journal of Obstetrics, Gynecology, and Reproductive Biology, 168(1), 26-29
Open this publication in new window or tab >>Adipokines and their relation to maternal energy substrate production, insulin resistance and fetal size
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2013 (English)In: European Journal of Obstetrics, Gynecology, and Reproductive Biology, ISSN 0301-2115, E-ISSN 1872-7654, Vol. 168, no 1, p. 26-29Article in journal (Refereed) Published
Abstract [en]

OBJECTIVE:

The role of adipokines in the regulation of energy substrate production in non-diabetic pregnant women has not been elucidated. We hypothesize that serum concentrations of adiponectin are related to fetal growth via maternal fat mass, insulin resistance and glucose production, and further, that serum levels of leptin are associated with lipolysis and that this also influences fetal growth. Hence, we investigated the relationship between adipokines, energy substrate production, insulin resistance, body composition and fetal weight in non-diabetic pregnant women in late gestation.

STUDY DESIGN:

Twenty pregnant women with normal glucose tolerance were investigated at 36 weeks of gestation at Uppsala University Hospital. Levels of adipokines were related to rates of glucose production and lipolysis, maternal body composition, insulin resistance, resting energy expenditure and estimated fetal weights. Rates of glucose production and lipolysis were estimated by stable isotope dilution technique.

RESULTS:

Median (range) rate of glucose production was 805 (653-1337)μmol/min and that of glycerol production, reflecting lipolysis, was 214 (110-576)μmol/min. HOMA insulin resistance averaged 1.5±0.75 and estimated fetal weights ranged between 2670 and 4175g (-0.2 to 2.7 SDS). Mean concentration of adiponectin was 7.2±2.5mg/L and median level of leptin was 47.1 (9.9-58.0)μg/L. Adiponectin concentrations (7.2±2.5mg/L) correlated inversely with maternal fat mass, insulin resistance, glucose production and fetal weight, r=-0.50, p<0.035, r=-0.77, p<0.001, r=-0.67, p<0.002, and r=-0.51, p<0.032, respectively. Leptin concentrations correlated with maternal fat mass and insulin resistance, r=0.76, p<0.001 and r=0.73, p<0.001, respectively. There was no correlation between maternal levels of leptin and rate of glucose production or fetal weight. Neither were any correlations found between levels of leptin or adiponectin and maternal lipolysis or resting energy expenditure.

CONCLUSION:

The inverse correlations between levels of maternal adiponectin and insulin resistance as well as endogenous glucose production rates indicate that low levels of adiponectin in obese pregnant women may represent one mechanism behind increased fetal size. Maternal levels of leptin are linked to maternal fat mass and its metabolic consequences, but the data indicate that leptin lacks a regulatory role with regard to maternal lipolysis in late pregnancy.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-189671 (URN)10.1016/j.ejogrb.2012.12.009 (DOI)000319244400005 ()23280283 (PubMedID)
Available from: 2013-01-03 Created: 2013-01-03 Last updated: 2017-12-06Bibliographically approved
Englund, A., Jonsson, B., Zander, C. S., Gustafsson, J. & Annerén, G. (2013). Changes in mortality and causes of death in the Swedish Down syndrome population. American Journal of Medical Genetics. Part A, 161A(4), 642-649
Open this publication in new window or tab >>Changes in mortality and causes of death in the Swedish Down syndrome population
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2013 (English)In: American Journal of Medical Genetics. Part A, ISSN 1552-4825, E-ISSN 1552-4833, Vol. 161A, no 4, p. 642-649Article in journal (Refereed) Published
Abstract [en]

During the past few decades age at death for individuals with Down syndrome (DS) has increased dramatically. The birth frequency of infants with DS has long been constant in Sweden. Thus, the prevalence of DS in the population is increasing. The aim of the present study was to analyze mortality and causes of death in individuals with DS during the period 19692003. All individuals with DS that died between 1969 and 2003 in Sweden, and all individuals born with DS in Sweden between 1974 and 2003 were included. Data were obtained from the Swedish Medical Birth Register, the Swedish Birth Defects Register, and the National Cause of Death Register. Median age at death has increased by 1.8 years per year. The main cause of death was pneumonia. Death from congenital heart defects decreased. Death from atherosclerosis was rare but more frequent than reported previously. Dementia was not reported in any subjects with DS before 40 years of age, but was a main or contributing cause of death in 30% of the older subjects. Except for childhood leukemia, cancer as a cause of death was rare in all age groups. Mortality in DS, particularly infant mortality, has decreased markedly during the past decades. Median age at death is increasing and is now almost 60 years. Death from cancer is rare in DS, but death from dementia is common.

Keywords
Down syndrome, mortality, morbidity, epidemiology, trends, causes of death
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-199710 (URN)10.1002/ajmg.a.35706 (DOI)000316631300003 ()
Available from: 2013-05-13 Created: 2013-05-13 Last updated: 2017-12-06Bibliographically approved
Hyllienmark, L., Alstrand, N., Jonsson, B., Ludvigsson, J., Cooray, G. & Wahlberg-Topp, J. (2013). Early Electrophysiological Abnormalities and Clinical Neuropathy: A prospective study in patients with type 1 diabetes. Diabetes Care, 36(10), 3187-3194
Open this publication in new window or tab >>Early Electrophysiological Abnormalities and Clinical Neuropathy: A prospective study in patients with type 1 diabetes
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2013 (English)In: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 36, no 10, p. 3187-3194Article in journal (Refereed) Published
Abstract [en]

OBJECTIVEThe aim of this study was to elucidate whether subclinical nerve dysfunction as reflected by neurophysiological testing predicts the development of clinical neuropathy in patients with type 1 diabetes.RESEARCH DESIGN AND METHODSFifty-nine patients were studied twice with neurophysiological measurements at baseline and at follow-up. At baseline, patients were 15.5 3.22 years (range 7-22 years) of age, and duration of diabetes was 6.8 3.3 years. At follow-up, patients were 20-35 years of age, and disease duration was 20 +/- 5.3 years (range 10-31 years).RESULTSAt baseline, patients showed modestly reduced nerve conduction velocities and amplitudes compared with healthy subjects, but all were free of clinical neuropathy. At follow-up, clinical neuropathy was present in nine (15%) patients. These patients had a more pronounced reduction in peroneal motor nerve conduction velocity (MCV), median MCV, and sural sensory nerve action potential at baseline (P < 0.010-0.003). In simple logistic regression analyses, the predictor with the strongest association with clinical neuropathy was baseline HbA(1c) (R-2 = 48%, odds ratio 7.9, P < 0.002) followed by peroneal MCV at baseline (R-2 = 38%, odds ratio 0.6, P < 0.006). With the use of a stepwise forward analysis that included all predictors, first baseline HbA(1c) and then only peroneal MCV at baseline entered significantly (R-2 = 61%). Neuropathy impairment assessment showed a stronger correlation with baseline HbA(1c) ( = 0.40, P < 0.002) than with follow-up HbA(1c) ( = 0.034, P < 0.007).CONCLUSIONSEarly defects in nerve conduction velocity predict the development of diabetic neuropathy. However, the strongest predictor was HbA(1c) during the first years of the disease.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-210193 (URN)10.2337/dc12-2226 (DOI)000324749500060 ()
Available from: 2013-11-04 Created: 2013-11-04 Last updated: 2017-12-06Bibliographically approved
Fetuga, B., Ogunlesi, T., Olanrewaju, D., Jonsson, B. & Albertsson-Wikland, K. (2013). Growth in prepubertal Nigerian children is highly dependent on socio-economic status. Acta Paediatrica, 102(8), 824-831
Open this publication in new window or tab >>Growth in prepubertal Nigerian children is highly dependent on socio-economic status
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2013 (English)In: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 102, no 8, p. 824-831Article in journal (Refereed) Published
Abstract [en]

Aim To relate height, weight and body mass index (BMI) of prepubertal children in Sagamu, Nigeria, to parental socio-economic class (SEC). Methods Cross-sectional study of 1606 children aged 5-11years from eight public and eight private primary schools. Height, weight and BMI from 1557 prepubertal children were standardized using two references: US-CDC birth cohorts 1929-1974 and Swedish birth cohort 1974. Results Children in private schools were taller and heavier than those in public schools (p<0.0001). Most children (73.2%) belonged to lower SEC, 17.6% to middle and 9.2% to upper. HeightSDS, weightSDS and BMISDS increased with increasing parental SEC. Upper SEC children were taller and heavier with higher BMIs than those from lower SEC (p<0.0001). HeightSDS, weightSDS and BMISDS were below 0' in all SEC and gender groups (all p<0.002). Younger children were taller and heavier than the older (p<0.0001). Conclusion Fathers/mothers with higher education/occupation had taller and heavier children with higher BMI than other groups. Children in private schools were taller and heavier than children in public schools. Disparities in parental SEC still constrain optimal child growth in Nigeria: whereas height and weight of children of upper SEC were close to the US-CDC29-74 reference mean, they were still below Swedish74 reference mean representing more optimal growth.

Keywords
BMI, Height, Parental Education, Parental Occupation, Private School, Public School, Socio-economic Status, Weight
National Category
Pediatrics
Identifiers
urn:nbn:se:uu:diva-204767 (URN)10.1111/apa.12290 (DOI)000320777700023 ()
Available from: 2013-08-15 Created: 2013-08-12 Last updated: 2017-12-06Bibliographically approved
Feldt-Rasmussen, U., Brabant, G., Maiter, D., Jonsson, B., Toogood, A., Koltowska-Haggstrom, M., . . . Biller, B. M. K. (2013). Response to GH treatment in adult GH deficiency is predicted by gender, age, and IGF1 SDS but not by stimulated GH-peak. European Journal of Endocrinology, 168(5), 733-743
Open this publication in new window or tab >>Response to GH treatment in adult GH deficiency is predicted by gender, age, and IGF1 SDS but not by stimulated GH-peak
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2013 (English)In: European Journal of Endocrinology, ISSN 0804-4643, E-ISSN 1479-683X, Vol. 168, no 5, p. 733-743Article in journal (Refereed) Published
Abstract [en]

Objective: We studied whether the severity of GH deficiency (GHD) defined as i) GH-peak on stimulation tests (insulin tolerance test (ITT), arginine, and glucagon), ii) number of additional pituitary deficits, or iii) baseline IGF1 SDS could impact the response to GH treatment. We further explored whether iv) IGF1 SDS after 24 months of GH replacement or v) Delta IGF1 SDS from baseline to 24 months was related to the phenotypic response to GH treatment. Design, patients, and measurements: The patient cohort (n=1752; 50% women) was obtained from KIMS (Pfizer International Metabolic Database). The patients were divided into three groups of approximately equal size (tertiles) according to the stimulated GH-peak values and baseline IGF1 SDS and were studied at baseline, 12, and 24 months of GH therapy. Results: Lower baseline IGF1 SDS predicted better response in weight, BMI, total cholesterol, and triglycerides, while IGF1 SDS after 24 months was associated with reduction in waist/hip ratio, total cholesterol, and improved quality of life (QoL). Age-correlated negatively with the response in body weight, BMI, waist, IGF1 SDS, and total and LDL-cholesterol. Response in weight and BMI was greater in men than in women, whereas women showed greater improvement in QoL than men. Patients with more severe GHD as assessed by lower GH-peaks and more pituitary hormone deficiencies had a greater increase in IGF1 SDS. The increase in IGF1 SDS was associated with a reduction in waist/hip ratio and an increase in weight, BMI, and triglycerides. There was no correlation with other lipids, blood pressure, or glucose. Conclusion: Our findings indicate that baseline and 24 months, IGF1 and its degree of increase during GH replacement were more important than stimulated peak GH to predict the phenotypic response.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-200664 (URN)10.1530/EJE-13-0005 (DOI)000318003300011 ()
Available from: 2013-06-03 Created: 2013-06-03 Last updated: 2017-12-06Bibliographically approved
Bolin, K., Sandin, R., Koltowska-Häggström, M., Loftus, J., Prütz, C. & Jonsson, B. (2013). The cost-effectiveness of growth hormone replacement therapy (Genotropin®) in hypopituitary adults in Sweden. Cost Effectiveness and Resource Allocation, 11(1), 24
Open this publication in new window or tab >>The cost-effectiveness of growth hormone replacement therapy (Genotropin®) in hypopituitary adults in Sweden
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2013 (English)In: Cost Effectiveness and Resource Allocation, ISSN 1478-7547, E-ISSN 1478-7547, Vol. 11, no 1, p. 24-Article in journal (Refereed) Published
Abstract [en]

BACKGROUND:

To evaluate the cost-effectiveness of growth hormone (GH) treatment (Genotropin(R)) compared with no GH treatment in adults with GH deficiency in a Swedish societal setting.

METHODS:

A Markov-type cost-utility simulation model was constructed and used to simulate, for men and women, morbidity and mortality for GH-treated and -untreated individuals over a 20-year period. The calculations were performed using current available prices concerning morbidity-related healthcare costs and costs for Genotropin(R). All costs and treatment effects were discounted at 3%. Costs were expressed in Euro (1[euro sign] = 9.03 SEK). GH-treated Swedish patients (n = 434) were identified from the KIMS database (Pfizer International Metabolic Database) and untreated patients (n = 2135) from the Swedish Cancer Registry and the Hospital Discharge Registry.

RESULTS:

The results are reported as incremental cost per quality-adjusted life year (QALY) gained, including both direct and indirect costs for GH-treated versus untreated patients. The weighted sum of all subgroup incremental cost per QALY was [euro sign]15,975 and [euro sign]20,241 for men and women, respectively. Including indirect cost resulted in lower cost per QALY gained: [euro sign]11,173 and [euro sign]10,753 for men and women, respectively. Key drivers of the results were improvement in quality of life, increased survival, and intervention cost.

CONCLUSIONS:

The incremental cost per QALY gained is moderate when compared with informal thresholds applied in Sweden. The simulations suggest that GH-treatment is cost-effective for both men and women at the [euro sign]55,371 (SEK 500,000 -- the informal Swedish cost-effectiveness threshold) per QALY threshold.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-209687 (URN)10.1186/1478-7547-11-24 (DOI)24079522 (PubMedID)
Available from: 2013-10-24 Created: 2013-10-24 Last updated: 2017-12-06Bibliographically approved
Fideleff, H. L., Jonsson, B., Koltowska-Häggström, M., Boguszewski, M. C. .., Wilton, P. & Boquete, H. R. (2012). GH deficiency during the transition period: clinical characteristics before and after GH replacement therapy in two different subgroups of patients. Journal of Pediatric Endocrinology & Metabolism (JPEM), 25(1-2), 97-105
Open this publication in new window or tab >>GH deficiency during the transition period: clinical characteristics before and after GH replacement therapy in two different subgroups of patients
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2012 (English)In: Journal of Pediatric Endocrinology & Metabolism (JPEM), ISSN 0334-018X, E-ISSN 2191-0251, Vol. 25, no 1-2, p. 97-105Article in journal (Refereed) Published
Abstract [en]

Objective:

To study two subsets of patients with GH deficiency (GHD) during the transition period: childhood onset GHD (CO-GHD) and patients who develop GHD during the transition phase (TO-GHD) before and after GH replacement.

Patients and measurements:

In 1340 GHD subjects from KIMS (Pfizer International Metabolic Database), CO (n=586) or TO (n=754), background characteristics, anthropometric measurements, IGF-1, lipids and quality of life (QoL) were evaluated at baseline and after 3 years of GH replacement.

Results:

Both groups responded similarly to GH treatment. Changes of clinical outcomes were mainly determined by their value at baseline. Onset of the disease in childhood or transition period did not appear to be a significant predictor of response in any of the clinical outcomes.

Conclusions:

Age at GHD diagnosis was a significant predictor for many outcomes at baseline, but disease onset did not appear as an independent predictor concerning changes after 3 years of GH treatment. The results suggest that GH replacement during the transition period should be considered independently of the onset of the deficiency.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:uu:diva-163759 (URN)10.1515/JPEM.2011.349 (DOI)000305708000014 ()
Available from: 2011-12-14 Created: 2011-12-14 Last updated: 2017-12-08Bibliographically approved
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