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M Walker

Publications and source records attributed to M Walker.

At least 19 recordsLinked to original sources

Paternal age and birth defects: how strong is the association?

BACKGROUND: Although the association between maternal age and the risks of birth defects has been well studied, the evidence from population data linking paternal age with birth defects was limited and inconsistent. METHODS: We conducted a population-based retrospective cohort study of 5,213,248 subjects from the 1999-2000 birth registration data of the USA. Multiple logistic regressions were used to estimate the independent effect of paternal age on all birth defects and 21 specific defects groups after adjusting for potential confounding of maternal age, race, education, marital status, parity, prenatal care initiation, maternal smoking and alcohol drinking during pregnancy. RESULTS: A total of 77,514 (1.5%) birth defects were recorded in the study cohort. The adjusted odds ratios were 1.04 (1.01, 1.06), 1.08 (1.04, 1.12), 1.08 (1.02, 1.14) and 1.15 (1.06, 1.24), respectively, for infants born to fathers 30-35, 40-44, 45-49 and over 50 years (test for trend, P = 0.0155), when compared with those infants born to fathers aged 25-29 for any birth defect. Advanced paternal age was associated with increased risks of heart defects, tracheo-oesophageal fistulaoesophageal atresia, other musculoskeletal/integumental anomalies, Down's syndrome and other chromosomal anomalies. Fathers under 25 years of age were also at increased risks of spina bifida/meningocele, microcephalus, omphalocele/gastroschisis and other musculoskeletal/integumental anomalies. CONCLUSIONS: Infants born to older fathers have a slightly increased risk of birth defects. Young paternal age is also associated with slightly increased risk of several selected birth defects in their offspring. However, given the weak association, paternal age appears to play a small role in the aetiology of birth defects.

Adult↗

Use of intravenous immunoglobulin for treatment of recurrent miscarriage: a systematic review.

BACKGROUND: Intravenous immunoglobulin (IVIG) is a fractionated blood product whose off-label use for treating a variety of conditions, including spontaneous recurrent miscarriage, has continued to grow in recent years. Its high costs and short supply necessitate improved guidance on its appropriate applications. OBJECTIVE: We conducted a systematic review of randomised controlled trials evaluating IVIG for treatment of spontaneous recurrent miscarriage. SEARCH STRATEGY: A systematic search strategy was applied to Medline (1966 to June 2005) and the Cochrane Register of Controlled Trials (June 2005). SELECTION CRITERIA: We included all randomised controlled trials comparing all dosages of IVIG to placebo or an active control. DATA COLLECTION AND ANALYSIS: Two investigators independently extracted data using a standardised data collection form. Measures of effect were derived for each trial independently, and studies were pooled based on clinical and methodologic appropriateness. MAIN RESULTS: We identified eight trials involving 442 women that evaluated IVIG therapy used to treat recurrent miscarriage. Overall, IVIG did not significantly increase the odds ratio (OR) of live birth when compared with placebo for treatment of recurrent miscarriage (OR 1.28, 95% CI 0.78-2.10). There was, however, a significant increase in live births following IVIG use in women with secondary recurrent miscarriage (OR 2.71, 95% CI 1.09-6.73), while those with primary miscarriage did not experience the same benefit (OR 0.66, 95% CI 0.35-1.26). AUTHOR'S CONCLUSIONS: IVIG increased the rates of live birth in secondary recurrent miscarriage, but there was insufficient evidence for its use in primary recurrent miscarriage.

Abortion, Habitual↗

An association analysis of the HLA gene region in latent autoimmune diabetes in adults.

AIMS/HYPOTHESIS: Pathophysiological similarities between latent autoimmune diabetes in adults (LADA) and type 1 diabetes indicate an overlap in genetic susceptibility. HLA-DRB1 and HLA-DQB1 are major susceptibility genes for type 1 diabetes but studies of these genes in LADA have been limited. Our aim was to define patterns of HLA-encoded susceptibility/protection in a large, well characterised LADA cohort, and to establish association with disease and age at diagnosis. MATERIALS AND METHODS: Patients with LADA (n = 387, including 211 patients from the UK Prospective Diabetes Study) and non-diabetic control subjects (n = 327) were of British/Irish European origin. The HLA-DRB1 and -DQB1 genes were genotyped by sequence-specific PCR. RESULTS: As in type 1 diabetes mellitus, DRB1 0301_DQB1 0201 (odds ratio [OR] = 3.08, 95% CI 2.32-4.12, p = 1.2 x 10(-16)) and DRB1 0401_DQB1 0302 (OR = 2.57, 95% CI 1.80-3.73, p = 4.5 x 10(-8)) were the main susceptibility haplotypes in LADA, and DRB1 1501_DQB1 0602 was protective (OR = 0.21, 95% CI 0.13-0.34, p = 4.2 x 10(-13)). Differential susceptibility was conferred by DR4 subtypes: DRB1 0401 was predisposing (OR = 1.79, 95% CI 1.35-2.38, p = 2.7 x 10(-5)) whereas DRB1 0403 was protective (OR = 0.37, 95% CI 0.13-0.97, p = 0.033). The highest-risk genotypes were DRB1 0301/DRB1 0401 and DQB1 0201/DQB1 0302 (OR = 5.14, 95% CI 2.68-10.69, p = 1.3 x 10(-8); and OR = 6.88, 95% CI 3.54-14.68, p = 1.2 x 10(-11), respectively). These genotypes and those containing DRB1 0401 and DQB1 0302 associated with a younger age at diagnosis in LADA, whereas genotypes containing DRB1 1501 and DQB1 0602 associated with an older age at diagnosis. CONCLUSIONS/INTERPRETATION: Patterns of susceptibility at the HLA-DRB1 and HLA-DQB1 loci in LADA are similar to those reported for type 1 diabetes, supporting the hypothesis that autoimmune diabetes occurring in adults is an age-related extension of the pathophysiological process presenting as childhood-onset type 1 diabetes.

Adult↗

Semen quality in a residential, geographic and age representative sample of healthy Chinese men.

BACKGROUND: Population-based study of semen quality is rare in literature. METHODS: Healthy men aged 20-60 years from six Chinese provinces were invited to participate in the study between December 2000 and November 2002. Posters were distributed in the participating counties to enroll 200 subjects from each province. Medians, percentiles, and proportions below lower threshold of the WHO criteria for semen parameters were calculated. Generalized linear models were used to examine the determinants of semen quality. RESULTS: Semen samples from 1191 healthy Chinese men were collected and analysed. The medians (5th and 95th percentiles) were 2.3 ml (1.0-4.5) for semen volume, 65 x 10(6)/ml (20-150) for semen concentration, 154 x 10(6)/ejection (29-421) for sperm count, 19% (5-32) for rapid progressive motility, 46% (29-66) for progressive motility, 67% (47-81) for total motile spermatozoa, 70% (48-88) for sperm viability and 39% (23-76) for normal morphology. Many healthy Chinese men had semen parameter values below the lower threshold of the WHO criteria. Region, age, abstinence duration and season were important determinants of semen quality. CONCLUSIONS: Chinese men have lower values of semen parameters according to WHO standard, and a lower threshold for normal semen parameters for Chinese men should be considered.

Adult↗

The effect of tobacco exposure on the fetal hypothalamic-pituitary-adrenal axis.

OBJECTIVE: Our objective was to determine if maternal smoking is associated with programming of the fetal hypothalamic-pituitary-adrenal (HPA) axis. Cigarette smoking, which induces a state of hypoxia in the fetus, may promote in utero'programming' of the HPA axis. In utero, adaptations to the HPA axis, which become maladaptive later in life, have been hypothesised to contribute to the development of adult cardiovascular disease and metabolic disorders. DESIGN: This was a prospective cohort study of term infants. POPULATION AND SETTING: The study involved 104 infants born by elective caesarean section, 21 of whom were exposed to in utero tobacco and 83 were nonexposed. METHODS: Healthy women with healthy pregnancies were recruited if they were undergoing elective caesarean section. Maternal blood was drawn for cortisol and cotinine in the morning, and the umbilical blood was drawn immediately after delivery of the baby. MAIN OUTCOME MEASURES: Umbilical arterial cortisol and adrenocorticotropin hormone (ACTH) levels. RESULTS: ACTH levels were significantly elevated in smoke-exposed infants [17 (4-22) pmol/l versus 4 (2-11) pmol/l, respectively, P= 0.005], while cortisol levels were similar [182 (130-240) nmol/l versus 192 (127-265) nmol/l, respectively, P= 0.541]. CONCLUSIONS: For the first time, it was shown that infants exposed to in utero tobacco smoke have significantly elevated ACTH levels compared with nonexposed infants. The results of this study warrant further exploration of the effect of smoking on the neonatal HPA axis as a potential set up for 'programming'.

Adrenocorticotropic Hormone↗

Syndromic obesity and diabetes: changes in body composition with age and mutation analysis of ALMS1 in 12 United Kingdom kindreds with Alstrom syndrome.

CONTEXT: Alström syndrome (AS) is a monogenic form of infancy-onset obesity and insulin resistance, caused by ALMS1 mutations. The natural history of the insulin resistance is unknown, in particular how this relates to changes in body composition. It is also unclear how ALMS1 mutations relate to the characteristic phenotype. OBJECTIVES: Our objectives were to characterize body composition and metabolic parameters, to establish ALMS1 mutation spectrum of United Kingdom AS patients, and to determine whether a genotype-phenotype correlation exists. DESIGN AND PATIENTS: We conducted a cross-sectional cohort study of 12 unrelated subjects with AS. Age-standardized body composition was assessed by anthropometry and dual-energy x-ray absorptiometry and insulin sensitivity by homeostasis model assessment. The exons and intron-exon boundaries of ALMS1 were directly sequenced. SETTING: The study was performed during the annual Alström Syndrome UK multidisciplinary screening clinic. RESULTS: AS patients have early-onset obesity, but body mass index, waist circumference, and body fat from dual-energy x-ray absorptiometry were negatively correlated with age (r = -0.37, P = 0.2; r = -0.84, P = 0.002; and r = -0.6, P = 0.05). Despite this, insulin resistance increased, demonstrated by raised fasting insulin and fall in homeostasis model assessment insulin sensitivity with age (r = -0.64, P = 0.02). ALMS1 mutations were identified in 10 of 12 patients, with a potential founder mutation in exon 16 present in five [np 10775del (C); Del3592fs/ter3597]. No genotype-phenotype correlation was observed. CONCLUSIONS: We identified mutations in ALMS1 in more than 80% of patients with no genotype-phenotype correlation. In AS, severe childhood obesity, waist circumference, and body fat decrease with age, whereas insulin resistance increases. The abdominal obesity, insulin resistance, diabetes, hypertriglyceridemia, and hypertension suggest that AS could represent a monogenic model for the metabolic syndrome.

Absorptiometry, Photon↗

Reduced beta cell function in offspring of mothers with young-onset type 2 diabetes.

AIMS/HYPOTHESIS: Animal models indicate that even exposure to mild maternal hyperglycaemia in utero is detrimental to the beta cell function of the offspring, but evidence of this in humans is limited. In Europids who are diagnosed with type 2 diabetes before the age of 50 years, the risk of diabetes in the offspring of the diabetic mothers is greatly increased compared with the risk in those born to diabetic fathers. We hypothesised that offspring born to mothers with young-onset type 2 diabetes would have been exposed to mild hyperglycaemia in utero, so we studied the impact of this on their beta cell function. SUBJECTS AND METHODS: We measured beta cell function using early insulin response (EIR) after oral glucose; insulin resistance using HOMA; and HbA(1c) in 568 non-diabetic adult offspring born to parents with type 2 diabetes (mean age 55.8 years), split according to which parent was affected (in 327 it was the mother) and parental age of diagnosis: <50 years (n=117) or > or =50 years. To reduce the impact of genetic susceptibility, the offspring of affected fathers were used as control subjects. RESULTS: Offspring of mothers with young-onset type 2 diabetes had lower EIR (log EIR 4.32, 95% CI [4.14-4.51] vs 4.63 [4.43-4.83] p=0.02) and higher HbA(1c) (4.89% [4.79-4.99] vs 4.68% [4.57-4.79] p=0.02) than the offspring of fathers with young-onset type 2 diabetes. Insulin sensitivity was similar in the two groups. There were no differences in EIR or HbA(1c) between the offspring born to mothers and fathers who were diagnosed after the age of 50 years. CONCLUSIONS/INTERPRETATION: We conclude that the offspring of mothers with young-onset type 2 diabetes have a reduction in beta cell function. This is consistent with exposure to mild maternal hyperglycaemia programming beta cell function.

Adult↗

Gastrazole (JB95008), a novel CCK2/gastrin receptor antagonist, in the treatment of advanced pancreatic cancer: results from two randomised controlled trials.

Gastrin has been shown to be a growth stimulant in pancreatic cancer cells. Gastrazole is a potent and selective gastrin receptor antagonist. Two randomised blinded trials were conducted to assess the effect of gastrazole in advanced pancreatic cancer. Patients with biopsy-proven, inoperable pancreatic carcinoma were recruited. Trial A compared protracted venous infusion (PVI) gastrazole with PVI placebo, whereas trial B compared PVI gastrazole with PVI fluorouracil (5-FU). Eighteen patients were randomised in trial A. Gastrazole produced significantly better survival compared to placebo (median 7.9 months vs 4.5 months; 1-year survival: 33 vs 11%, respectively; log rank P=0.02). No difference in toxicity was seen between gastrazole and placebo, except central venous catheter and pump complications. Ninety-eight patients were randomised in trial B. No significant survival difference was detected between gastrazole and 5-FU (median: 3.6 vs 4.2 months; 1-year survival: 13.2 vs 26.2%, respectively; log rank P=0.42). Toxicity of gastrazole was mild with significantly less diarrhoea (P=0.03), stomatitis (P<0.001) and hand- foot syndrome (P<0.001) compared to 5-FU. Quality of life (QoL) assessment showed similar QoL between gastrazole and 5-FU at baseline and no significant differences occurred with treatment either between arms or within arms. Compared to placebo, patients with advanced pancreatic cancer treated with gastrazole appeared to live longer, albeit in a very small trial and will require confirmation with large-scale randomised data. However, it did not produce survival advantage over PVI 5-FU. Lack of toxicity for gastrazole may allow its combination with cytotoxic drugs.

Adult↗

Chk1-dependent slowing of S-phase progression protects DT40 B-lymphoma cells against killing by the nucleoside analogue 5-fluorouracil.

Chk1 plays a crucial role in the DNA damage and replication checkpoints in vertebrates and may therefore be an important determinant of tumour cell responses to genotoxic anticancer drugs. To evaluate this concept we compared the effects of the nucleoside analogue 5-fluorouracil (5FU) on cell cycle progression and clonogenic survival in DT40 B-lymphoma cells with an isogenic mutant derivative in which Chk1 function was ablated by gene targeting. We show that 5FU activates Chk1 in wild-type DT40 cells and that 5FU-treated cells accumulate in the S phase of the cell cycle due to slowing of the overall rate of DNA replication. In marked contrast, Chk1-deficient DT40 cells fail to slow DNA replication upon initial exposure to 5FU, despite equivalent inhibition of the target enzyme thymidylate synthase, and instead accumulate progressively in the G1 phase of the following cell cycle. This G1 accumulation cannot be reversed rapidly by exogenous thymidine or removal of 5FU, and is associated with increased incorporation of 5FU into genomic DNA and severely diminished clonogenic survival. Taken together, these results demonstrate that a Chk1-dependent replication checkpoint which slows S phase progression can protect tumour cells against the cytotoxic effects of 5FU.

Cell Cycle↗

Common variations in the ALMS1 gene do not contribute to susceptibility to type 2 diabetes in a large white UK population.

AIMS/HYPOTHESIS: Alström syndrome is a rare monogenic disorder characterised by retinal dystrophy, deafness and obesity. Patients also have insulin resistance, central obesity and dyslipidaemia, thus showing similarities with type 2 diabetes. Rare mutations in the ALMS1 gene cause severe gene disruption in Alström patients; however, ALMS1 gene polymorphisms are common in the general population. The aim of our study was to determine whether common variants in ALMS1 contribute to susceptibility to type 2 diabetes in the UK population. METHODS: Direct sequencing was performed on coding regions and intron/exon boundaries of the ALMS1 gene in 30 unrelated probands with type 2 diabetes. The linkage disequilibrium (LD; D' and r2) and haplotype structure were examined for the identified variants. The common (minor allele frequency [MAF] >5%) single-nucleotide polymorphisms tagging the common haplotypes (tagged SNPs [tSNPs]) were identified and genotyped in 1985 subjects with type 2 diabetes, 2,047 control subjects and 521 families. RESULTS: We identified 18 variants with MAF between 6 and 38%. Three SNPs efficiently tagged three common haplotypes (rs1881245, rs3820700 and rs1320374). There was no association (all p > 0.05) between the tSNPs and type 2 diabetes in the case-control study and minor alleles of the tSNPs were not overtransmitted to probands with type 2 diabetes in the family study. CONCLUSIONS/INTERPRETATION: Common variations in the ALMS1 gene were not associated with type 2 diabetes in a large study of a white UK population.

Adult↗

Pregnancy-induced hypertension is associated with lower infant mortality in preterm singletons.

OBJECTIVE: To assess the association between pregnancy-induced hypertension (PIH) and infant mortality. DESIGN: Retrospective cohort study. SETTING: Birth and infant death registration dataset of the USA. POPULATION: A total of 17,432,987 eligible, liveborn singleton births in 1995-2000. METHODS: Multivariate logistic regression was applied to evaluate the association between PIH and infant mortality, with adjustment of potential confounders. MAIN OUTCOME MEASURES: Infant death (0-364 days) and its three components: early neonatal death (0-6 days), late neonatal death (7-27 days), and postneonatal death (28-364 days). RESULTS: There was a significant reduction in infant mortality associated with PIH in early preterm infants (OR = 0.59, 95% CI: 0.56-0.63) and in late preterm infants (OR = 0.80, 95% CI: 0.73-0.87), but a significant increase in term infants (OR = 1.08, 95% CI: 1.02-1.14). Both in early preterm and late preterm births, early neonatal mortality (OR = 0.38, 95% CI: 0.34-0.42; OR = 0.68, 95% CI: 0.61-0.77) and late neonatal mortality (OR = 0.59, 95% CI: 0.50-0.70; OR = 0.76, 95% CI: 0.61-0.96) were decreased in infants born to mothers with PIH compared with those born to mothers with normal blood pressure. The PIH-associated reduction in neonatal mortality among preterm singletons was stronger in small-for-gestational-age infants than in normal growth infants and stronger in infants born to nulliparous women than in those born to multiparous women. CONCLUSIONS: PIH is associated with lower risk of infant death in preterm births but higher risk in term births.

Adult↗

Neonatal mortality and morbidity in vertex-vertex second twins according to mode of delivery and birth weight.

OBJECTIVE: To assess the risk of neonatal mortality and morbidity in vertex-vertex second twins according to mode of delivery and birth weight. STUDY DESIGN: Data from a historical cohort study based on a twin registry in the US (1995-1997) were used. Multivariate logistic regression was used to control for maternal age, race, marital status, cigarette smoking during pregnancy, parity, medical complications, gestational age, and other confounders. RESULTS: A total of 86 041 vertex-vertex second twins were classified into two groups: second twins delivered by cesarean section after cesarean delivery of first twin (C-C) (43.0%), second twins whose co-twins delivered vaginally (V-X) (57.0%). In infants of birth weight>or=2500 g group, the risks of noncongenital anomaly-related death (adjusted odds ratio (aOR): 4.64, 95% confidence interval (95% CI): 1.90, 13.92), low Apgar score (aOR: 2.39, 95% CI: 1.43, 4.14), and ventilation use (aOR: 1.31, 95% CI: 1.18, 1.47) were higher in the V-X group compared with the C-C group. No asphyxia-related neonatal deaths occurred in C-C group, whereas the incidence of this death was 0.04% in the V-X group. CONCLUSION: The risks of neonatal mortality and morbidity are increased in vertex-vertex second twins with birth weight>or=2500 g whose co-twins delivered vaginally compared with second twins delivered by cesarean section after cesarean delivery of first twin.

Adult↗

GAD antibodies in probands and their relatives in a cohort clinically selected for Type 2 diabetes.

AIMS: A subset of patients who present as if they have Type 2 diabetes have positive pancreatic autoantibodies, and have been referred to as having latent autoimmune diabetes in adults (LADA). We assessed the prevalence and clinical characteristics of patients with glutamic acid decarboxylase antibodies (GADA) in a cohort clinically selected for Type 2 diabetes and determined the presence of diabetes and GADA in their first-degree relatives. METHODS: GADA were measured in 2059 subjects, not known to be related, and clinically selected as having Type 2 diabetes for genetic studies. Clinical characteristics were compared in GADA positive and GADA negative subjects. Diabetes and GAD antibody status were compared in 208 first-degree relatives of GADA positive and GADA negative probands. RESULTS: Of the subjects, 136 (7%) were GADA positive. Compared with the GADA negative subjects, they were slimmer (P < 0.001), diagnosed at a younger age (P = 0.011) and progressed to insulin faster (P < 0.001). Thirty-three per cent of GADA positive subjects had a first-degree relative with diabetes compared with 42% of GADA negative subjects (P = 0.034). The overall prevalence of GADA was similar in the first-degree relatives of GADA positive and GADA negative probands (4 v 5%), and 19 of 22 (86%) diabetic relatives of GADA positive probands were GADA negative. CONCLUSION: Despite clinically selecting a Type 2 diabetes cohort, 7% were GADA positive with an altered phenotype. These GADA positive patients had a strong family history of non-autoimmune diabetes. This suggests that, in this subgroup of patients, autoimmune pancreatic beta-cell destruction occurs on a background of Type 2 diabetes genetic susceptibility.

Adult↗

Epistasis between type 2 diabetes susceptibility Loci on chromosomes 1q21-25 and 10q23-26 in northern Europeans.

Characterisation of the interactions between susceptibility loci (epistasis) is central to a full understanding of the genetic aetiology and the molecular pathology of complex diseases. We have examined, in British and French pedigrees, evidence for epistasis between the type 2 diabetes susceptibility loci on chromosomes 1q21-25 and 10q23-26 using two complementary linkage-based approaches. Joint two-locus linkage analysis of 1q and 10q in British pedigrees provided significant evidence for interaction (P < or = 0.003) when comparing a general epistasis model with multiplicative or additive-effects-only models. Conditional linkage analysis (which models epistasis as a deviation from multiplicativity only) confirmed these findings, with significant LOD score increases at the 1q (P = 0.0002) and 10q (P = 0.0023) loci. These analyses provided sizeable reductions in the 1-LOD support intervals for both loci. Analyses of the British and French pedigrees together yielded comparable, but not enhanced, findings, with significant (P < or = 0.003) evidence for epistasis in joint two-locus linkage analysis, and during conditional linkage analysis significant increases in linkage evidence at the 1q (P = 0.0002) and 10q (P = 0.0036) loci. Our findings of epistasis nevertheless substantiate the evidence for genuine genetic effects at both loci, facilitate endeavours to fine-map these loci in population samples, and support further examination of this interaction at the nucleotide level by providing a robust prior hypothesis.

Chromosomes, Human, Pair 1↗

A laboratory study to determine the effects of universal and rotating ultrasonic inserts on wrist movement and scaling time efficiency of dental hygienists.

PURPOSE: The purpose of this study was to determine if differences existed in range of wrist movements and scaling time efficiency of dental hygienists using a rotating ultrasonic insert when compared with a standard universal insert. METHODS: A convenience sample of 32 consenting experienced dental hygienists who met inclusion criteria was invited to participate. Using a cross-over research design, the 32 participants were randomly assigned to one of the two subgroups. Subgroup A (n = 16) used the rotating universal ultrasonic insert on a typodont, rested for 15 min and the standard universal insert on a different typodont. Subgroup B (n = 16) used the standard universal ultrasonic insert on a typodont, rested for 15 min and the rotating universal ultrasonic insert on a different typodont. Each participant used the rotating and standard universal ultrasonic scaling inserts to remove 2 cm3 artificial calculus from two different typodonts for up to 15 min per insert. Scaling time efficiency was determined using a Modified Volpe-Manhold Calculus Index, measuring the amount of artificial calculus remaining after ultrasonic scaling. While scaling, each participant wore the WristSensor goniometry gloves, which determined changes in wrist movements (flexion and extension and ulnar and radial deviations), measured as a deviation from the neutral position. RESULTS: A paired t-test (P = 0.05) using 30 subjects with useable data, revealed no statistically significant differences between the two different inserts in terms of wrist movements and scaling time efficiency. A multivariate analysis of variance revealed no statistically significant differences in the percentage of time dental hygienists were in high, medium or low-risk posture categories while using the rotating ultrasonic insert compared with the standard universal insert. Based on the results of this laboratory study, dental hygienists using a rotating ultrasonic insert appear to experience no ergonomic advantage in terms of wrist postures or timesavings over a standard insert.

Cross-Over Studies↗

Role of the mitochondrial DNA 16184-16193 poly-C tract in type 2 diabetes.

Recent evidence suggests that polymorphic genetic variation in the non-coding region of mitochondrial DNA (the 16184-16193 polycytosine [poly-C] tract) contributes to the cause of type 2 diabetes, but previous studies only just reached significance. We aimed to investigate this association. We compared patients with type 2 diabetes (n=992) with two independent control groups (n=536, n=1029) from the UK, and saw no difference in the frequency of the 16184-16193 poly-C tract. This finding was confirmed by a meta-analysis of European studies of 1455 patients and 3132 controls (odds ratio 1.16, 95% CI 0.94-1.44). Genetic variation of the 16184-16193 poly-C tract is unlikely to have a major role in the cause of type 2 diabetes.

DNA, Mitochondrial↗