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Background and aimThere is a widely held and influential view that physical activity begins to decline at adolescence. This study aimed to identify the timing of changes in physical activity during childhood and adolescence.MethodsLongitudinal cohort study (Gateshead Millennium Study) with 8 years of follow-up, from North-East England. Cohort members comprise a socioeconomically representative sample studied at ages 7, 9, 12 and 15 years; 545 individuals provided physical activity data at two or more time points. Habitual total volume of physical activity and moderate-to-vigorous intensity physical activity (MVPA) were quantified objectively using the Actigraph accelerometer over 5–7 days at the four time points. Linear mixed models identified the timing of changes in physical activity across the 8-year period, and trajectory analysis was used to identify subgroups with distinct patterns of age-related changes.ResultsFour trajectories of change in total volume of physical activity were identified representing 100% of all participants: all trajectories declined from age 7 years. There was no evidence that physical activity decline began at adolescence, or that adolescent declines in physical activity were substantially greater than the declines during childhood, or greater in girls than boys. One group (19% of boys) had relatively high MVPA which remained stable between ages 7 and15 years.ConclusionsFuture policy and research efforts to promote physical activity should begin well before adolescence, and should include both boys and girls.

Although CT scans are very useful clinically, potential cancer risks exist from associated ionising radiation, in particular for children who are more radiosensitive than adults. We aimed to assess the excess risk of leukaemia and brain tumours after CT scans in a cohort of children and young adults. In our retrospective cohort study, we included patients without previous cancer diagnoses who were first examined with CT in National Health Service (NHS) centres in England, Wales, or Scotland (Great Britain) between 1985 and 2002, when they were younger than 22 years of age. We obtained data for cancer incidence, mortality, and loss to follow-up from the NHS Central Registry from Jan 1, 1985, to Dec 31, 2008. We estimated absorbed brain and red bone marrow doses per CT scan in mGy and assessed excess incidence of leukaemia and brain tumours cancer with Poisson relative risk models. To avoid inclusion of CT scans related to cancer diagnosis, follow-up for leukaemia began 2 years after the first CT and for brain tumours 5 years after the first CT. During follow-up, 74 of 178 604 patients were diagnosed with leukaemia and 135 of 176 587 patients were diagnosed with brain tumours. We noted a positive association between radiation dose from CT scans and leukaemia (excess relative risk [ERR] per mGy 0·036, 95% CI 0·005–0·120; p=0·0097) and brain tumours (0·023, 0·010–0·049; p<0·0001). Compared with patients who received a dose of less than 5 mGy, the relative risk of leukaemia for patients who received a cumulative dose of at least 30 mGy (mean dose 51·13 mGy) was 3·18 (95% CI 1·46–6·94) and the relative risk of brain cancer for patients who received a cumulative dose of 50–74 mGy (mean dose 60·42 mGy) was 2·82 (1·33–6·03). Use of CT scans in children to deliver cumulative doses of about 50 mGy might almost triple the risk of leukaemia and doses of about 60 mGy might triple the risk of brain cancer. Because these cancers are relatively rare, the cumulative absolute risks are small: in the 10 years after the first scan for patients younger than 10 years, one excess case of leukaemia and one excess case of brain tumour per 10 000 head CT scans is estimated to occur. Nevertheless, although clinical benefits should outweigh the small absolute risks, radiation doses from CT scans ought to be kept as low as possible and alternative procedures, which do not involve ionising radiation, should be considered if appropriate. US National Cancer Institute and UK Department of Health.

BackgroundAccelerated infant weight gain in individuals born full term is linked to cardiovascular risk in adulthood, but data in those born preterm are inconsistent.ObjectiveTo investigate the association between weight gain in infancy and childhood with later markers of the metabolic syndrome in adolescents who were born preterm.Study designLongitudinal cohort study.SettingChildren born preterm with regular assessments of infant growth had auxology, body composition (dual X-ray absorptiometry), blood pressure, insulin sensitivity and lipid profile determined in adolescence.ResultsWe reviewed 153 children (mean gestation 30.8 weeks, median birth weight 1365 g) of whom 102 consented to venepuncture at a median age of 11.5 years. Adolescent height and weight standard deviation scores (SDS) were similar to population averages (0.01±0.92 and 0.3±1.2, respectively) and did not differ between infants when grouped according to degree of catch-up in weight gain in the immediate postdischarge period to 12 weeks of age. There were no significant associations between infant weight gain (change in weight SDS adjusted for length) and later metabolic outcome. However, there were strong associations between more rapid childhood weight gain (after 1 year of age) and subsequent body composition (higher fat mass %, fat mass index and waist circumference) and metabolic markers (higher fasting insulin, blood pressure and lower insulin sensitivity).ConclusionsThe association of rapid weight gain on health is time critical in those born preterm; in early infancy, this does not impact on metabolic status in adolescence, in contrast to rapid weight gain in childhood, which should be discouraged. However, given the critical importance of brain growth in the neonatal period and infancy, further research is needed before strategies that discourage infant weight gain or catch-up can be recommended for infants born preterm.

Congenital anomalies are a leading cause of perinatal and infant mortality. Advances in care have improved the prognosis for some congenital anomaly groups and subtypes, but there remains a paucity of knowledge about survival for many others, especially beyond the first year of life. We estimated survival up to 20 years of age for a range of congenital anomaly groups and subtypes. Information about children with at least one congenital anomaly, delivered between 1985 and 2003, was obtained from the UK Northern Congenital Abnormality Survey (NorCAS). Anomalies were categorised by group (the system affected), subtype (the individual disorder), and syndrome according to European Surveillance of Congenital Anomalies (EUROCAT) guidelines. Local hospital and national mortality records were used to identify the survival status of liveborn children. Survival up to 20 years of age was estimated by use of Kaplan-Meier methods. Cox proportional hazards regression was used to examine factors that affected survival. 13 758 cases of congenital anomaly were notified to NorCAS between 1985 and 2003. Survival status was available for 10 850 (99·0%) of 10 964 livebirths. 20-year survival was 85·5% (95% CI 84·8–86·3) in individuals born with at least one congenital anomaly, 89·5% (88·4–90·6) for cardiovascular system anomalies, 79·1% (76·7–81·3) for chromosomal anomalies, 93·2% (91·6–94·5) for urinary system anomalies, 83·2% (79·8–86·0) for digestive system anomalies, 97·6% (95·9–98·6) for orofacial clefts, and 66·2% (61·5–70·5) for nervous system anomalies. Survival varied between subtypes within the same congenital anomaly group. The proportion of terminations for fetal anomaly increased throughout the study period (from 12·4%, 9·8–15·5, in 1985 to 18·3%, 15·6–21·2, in 2003; p<0·0001) and, together with year of birth, was an independent predictor of survival (adjusted hazard ratio [HR] for proportion of terminations 0·95, 95% CI 0·91–0·99, p=0·023; adjusted HR for year of birth 0·94, 0·92–0·96, p<0·0001). Estimates of survival for congenital anomaly groups and subtypes will be valuable for families and health professionals when a congenital anomaly is detected, and will assist in planning for the future care needs of affected individuals. BDF Newlife.

Recognising overweight and obesity is critical to prompting action, and consequently preventing and treating obesity. The present study examined the association between parental perceptions of child weight status and child's diet. Participants were members of the Gateshead Millennium Study. Parental perception of their child's weight status was assessed using a questionnaire and compared against International Obesity Task Force cut-offs for childhood overweight and obesity when the children were aged 6-8 years old. Diet was assessed at age 6-8years old using the FAST (Food Assessment in Schools Tool) food diary method. The association between parental perception and dietary patterns as defined by Principal Components Analysis, was assessed using multivariate regression after adjustment for child's gender, child's weight status, maternal body mass index (BMI), maternal education and deprivation status. Of the 361 parents who provided complete data on confounders and on their perception of their child's weight status, 63 (17%) parents perceived their child as being of 'normal' weight or 'overweight' when they were actually 'overweight' or 'obese', respectively. After adjustment for confounders, parents who misperceived their child's weight had children with a lower 'healthy' dietary pattern score compared to children whose parents correctly perceived their weight (β = -0.88; 95% CI: -1.7, -0.1; P-value = 0.028). This association was found despite higher consumption of reduced sugar carbonated drinks amongst children whose parents incorrectly perceived their weight status compared to children whose parents perceived their weight correctly (52.4% vs. 33.6%; P-value = 0.005). In conclusion, children whose parents did not correctly perceive their weight status scored lower on the 'healthy' dietary pattern. Further research is required to define parents' diets based on their perception status and to examine if a child's or parent's diet mediates the association between parental perception and child weight.

Background In many parts of the world policy and research interventions to modify sedentary behavior of children and adolescents are now being developed. However, the evidence to inform these interventions (e.g. how sedentary behavior changes across childhood and adolescence) is limited. This study aimed to assess longitudinal changes in sedentary behavior, and examine the degree of tracking of sedentary behavior from age 7y to 15y. Methods Participants were part of the Gateshead Millennium Study cohort. Measures were made at age 7y ( n  = 507), 9y ( n  = 510), 12y ( n  = 425) and 15y ( n  = 310). Participants were asked to wear an ActiGraph GT1M and accelerometer epochs were defined as sedentary when recorded counts were ≤25 counts/15 s. Differences in sedentary time and sedentary fragmentation were examined using the Friedman test. Tracking was examined using Spearman’s correlation coefficients and trajectories over time were assessed using multilevel linear spline modelling. Results Median daily sedentary time increased from 51.3 % of waking hours at 7y to 74.2 % at 15y. Sedentary fragmentation decreased from 7y to 15y. The median number of breaks/hour decreased from 8.6 to 4.1 breaks/hour and the median bout duration at 50 % of the cumulative sedentary time increased from 2.4 min to 6.4 min from 7y to 15y. Tracking of sedentary time and sedentary fragmentation was moderate from 7y to 15y however, the rate of change differed with the steepest increases/decreases seen between 9y and 12y. Conclusion In this study, sedentary time was high and increased to almost 75 % of waking hours at 15y. Sedentary behavior became substantially less fragmented as children grew older. The largest changes in sedentary time and sedentary fragmentation occurred between 9y to 12y, a period which spans the transition to secondary school. These results can be used to inform future interventions aiming to change sedentary behavior.

Epigenetic markings acquired in early life may have phenotypic consequences later in development through their role in transcriptional regulation with relevance to the developmental origins of diseases including obesity. The goal of this study was to investigate whether DNA methylation levels at birth are associated with body size later in childhood. A study design involving two birth cohorts was used to conduct transcription profiling followed by DNA methylation analysis in peripheral blood. Gene expression analysis was undertaken in 24 individuals whose biological samples and clinical data were collected at a mean ± standard deviation (SD) age of 12.35 (0.95) years, the upper and lower tertiles of body mass index (BMI) were compared with a mean (SD) BMI difference of 9.86 (2.37) kg/m(2). This generated a panel of differentially expressed genes for DNA methylation analysis which was then undertaken in cord blood DNA in 178 individuals with body composition data prospectively collected at a mean (SD) age of 9.83 (0.23) years. Twenty-nine differentially expressed genes (>1.2-fold and p<10(-4)) were analysed to determine DNA methylation levels at 1-3 sites per gene. Five genes were unmethylated and DNA methylation in the remaining 24 genes was analysed using linear regression with bootstrapping. Methylation in 9 of the 24 (37.5%) genes studied was associated with at least one index of body composition (BMI, fat mass, lean mass, height) at age 9 years, although only one of these associations remained after correction for multiple testing (ALPL with height, p(Corrected) = 0.017). DNA methylation patterns in cord blood show some association with altered gene expression, body size and composition in childhood. The observed relationship is correlative and despite suggestion of a mechanistic epigenetic link between in utero life and later phenotype, further investigation is required to establish causality.

Background Clinical laboratories provide diagnostic testing services to support the effective delivery of care in today’s complex healthcare systems. Processing clinical material and the use of chemicals or radiation presents potential hazard to laboratory workers, from both biological and chemical sources. Nevertheless, the laboratory should be a safe workplace if the identification of possible hazards, clear guidelines, safety rules and infection prevention and control (IPC) precautions are applied and followed. The main aim of this systematic review was to identify, critically appraise and synthesise the research evidence to gain a clear explanation of the implementation and knowledge, attitude and practice (KAP) of IPC guidelines among hospital laboratory staff. Methods For this systematic review we searched MEDLINE, EMBASE, Scopus and CINAHL (EBSCO), PubMed, grey literature, reference lists and citations for studies published between database inception and November, 2021. All qualitative, quantitative and mixed-methods studies whose aim was to explore risk perception and KAP of IPC guidelines among laboratory staff in any healthcare setting were included, without language or date restrictions. Evidence was narratively synthesised into group of themes. The quality of the evidence was assessed with Joanna Briggs Institutes Critical Appraisal Tools. Results After the full-text screening, a total of 34 articles remained and were included in the final review. Thirty papers were considered to be of high quality and the remaining four were considered to be of low quality. The available evidence shows that there was good knowledge, good attitudes and moderate immunisation status, but there was still poor practice of IPC precautions and an inadequate level of training among laboratory workers. Conclusion There is a gap among KAP related to the implementation of IPC guidelines, which indicates that laboratory staff may be at high risk of acquiring infections in the workplace. These findings suggest that training (including IPC precautions, safety policies, safety equipment and materials, safety activities, initial biohazard handling, ongoing monitoring and potential exposure) of laboratory staff to increase their knowledge about IPC precautions could improve their use of these precautions.

Background Cancer is the leading cause of disease-related mortality in children. Causes of leukemia, the most common form, are largely unknown. Growing evidence points to an origin in-utero , when global redistribution of DNA methylation occurs driving tissue differentiation. Methods Epigenome-wide DNA methylation was profiled in surrogate (blood) and target (bone marrow) tissues at birth, diagnosis, remission and relapse of pediatric pre-B acute lymphoblastic leukemia (pre-B ALL) patients. Double-blinded analyses was performed between prospective cohorts extending from birth to diagnosis and retrospective studies backtracking from clinical disease to birth. Validation was carried out using independent technologies and populations. Results The imprinted and immuno-modulating VTRNA2-1 was hypermethylated (FDR<0.05) at birth in nested cases relative to controls in all tested populations (totaling 317 cases and 483 controls), including European and Hispanic ancestries. VTRNA2-1 methylation was stable over follow-up years after birth and across surrogate, target and other tissues ( n =5,023 tissues; 30 types). When profiled in leukemic tissues from two clinical cohorts (totaling 644 cases), VTRNA2-1 methylation exhibited higher levels at diagnosis relative to controls, it reset back to normal levels at remission, and then re-increased to above control levels at relapse. Hypermethylation was significantly associated with worse pre-B ALL patient survival and with reduced VTRNA2-1 expression ( n =2,294 tissues; 26 types), supporting a functional and translational role for VTRNA2-1 methylation. Conclusion This study provides proof-of-concept to detect at birth epigenetic precursors of pediatric pre-B ALL. These alterations were reproducible with different technologies, in three continents and in two ethnicities, and can offer biomarkers for early detection and prognosis as well as actionable targets for therapy. Key points • Precursors of pediatric acute lymphoblastic leukemia may be of epigenetic origin, detectable since birth and affecting patient prognosis. • These epigenetic precursors can be robust over several years and across several populations, ethnicities and surrogate and target tissues.

With a number of studies suggesting associations between early life influences and later chronic disease risk, it is suggested that associations between early growth and later physical activity (PA) may be a mediator. However, conflicting evidence exists for association between birth weight and childhood PA. In addition, it is important to know what other, potentially modifiable, factors may influence PA in children given its' association with childhood and later adiposity. We used the Gateshead Millennium Study (GMS) to identify predictors of childhood PA levels. The GMS is a cohort of 1029 infants born in 1999-2000 in Gateshead in northern England. Throughout infancy and early childhood, detailed information was collected. Assessments at age 9 years included body composition, objective measures of habitual PA and a range of lifestyle factors. Mean total volumes of PA (accelerometer count per minute, cpm) and moderate-vigorous intensity PA (MVPA), and the percentage of time spent in sedentary behaviour (%SB) were quantified and related to potential predictors using linear regression and path analysis. Children aged 8-10 years were included. Significant differences were seen in all three outcome variables between sexes and season of measurement (p<0.001). Restricting children's access to television was associated with decreased MVPA. Increased paternal age was associated with significant increases in %SB (p = 0.02), but not MVPA or total PA. Increased time spent in out of school sports clubs was significantly associated with decreased %SB (p = 0.02). No significant associations were seen with birth weight. A range of factors, directly or indirectly, influenced PA and sedentary behaviour. However, associations differed between the different constructs of PA and %SB. Exploring further the sex differences in PA would appear to be useful, as would encouraging children to join out of school sports clubs.