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The Cochrane Database of Systematic... Dec 2020The introduction and advancement of enteral feeds for preterm or low birth weight infants is often delayed because of concerns that early full enteral feeding will not... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The introduction and advancement of enteral feeds for preterm or low birth weight infants is often delayed because of concerns that early full enteral feeding will not be well tolerated or may increase the risk of necrotising enterocolitis. Early full enteral feeding, however, might increase nutrient intake and growth rates; accelerate intestinal physiological, metabolic, and microbiomic postnatal transition; and reduce the risk of complications associated with intravascular devices for fluid administration. OBJECTIVES: To determine how early full enteral feeding, compared with delayed or progressive introduction of enteral feeds, affects growth and adverse events such as necrotising enterocolitis, in preterm or low birth weight infants.
SEARCH METHODS
We used the standard search strategy of Cochrane Neonatal to search Cochrane Central Register of Controlled Trials; MEDLINE Ovid, Embase Ovid, Maternity & Infant Care Database Ovid, the Cumulative Index to Nursing and Allied Health Literature, and clinical trials databases, conference proceedings, and the reference lists of retrieved articles for randomised controlled trials and quasi-randomised trials to October 2020.
SELECTION CRITERIA
Randomised controlled trials that compared early full enteral feeding with delayed or progressive introduction of enteral feeds in preterm or low birth weight infants.
DATA COLLECTION AND ANALYSIS
We used the standard methods of Cochrane Neonatal. Two review authors separately assessed trial eligibility, evaluated trial quality, extracted data, and synthesised effect estimates using risk ratios (RR), risk differences, and mean differences (MD) with 95% confidence intervals (CI). We used the GRADE approach to assess the certainty of evidence.
MAIN RESULTS
We included six trials. All were undertaken in the 2010s in neonatal care facilities in India. In total, 526 infants participated. Most were very preterm infants of birth weight between 1000 g and 1500 g. Trials were of good methodological quality, but a potential source of bias was that parents, clinicians, and investigators were not masked. The trials compared early full feeding (60 mL/kg to 80 mL/kg on day one after birth) with minimal enteral feeding (typically 20 mL/kg on day one) supplemented with intravenous fluids. Feed volumes were advanced daily as tolerated by 20 mL/kg to 30 mL/kg body weight to a target steady-state volume of 150 mL/kg to 180 mL/kg/day. All participating infants were fed preferentially with maternal expressed breast milk, with two trials supplementing insufficient volumes with donor breast milk and four supplementing with preterm formula. Few data were available to assess growth parameters. One trial (64 participants) reported a slower rate of weight gain (median difference -3.0 g/kg/day), and another (180 participants) reported a faster rate of weight gain in the early full enteral feeding group (MD 1.2 g/kg/day). We did not meta-analyse these data (very low-certainty evidence). None of the trials reported rate of head circumference growth. One trial reported that the mean z-score for weight at hospital discharge was higher in the early full enteral feeding group (MD 0.24, 95% CI 0.06 to 0.42; low-certainty evidence). Meta-analyses showed no evidence of an effect on necrotising enterocolitis (RR 0.98, 95% CI 0.38 to 2.54; 6 trials, 522 participants; I² = 51%; very low-certainty evidence).
AUTHORS' CONCLUSIONS
Trials provided insufficient data to determine with any certainty how early full enteral feeding, compared with delayed or progressive introduction of enteral feeds, affects growth in preterm or low birth weight infants. We are uncertain whether early full enteral feeding affects the risk of necrotising enterocolitis because of the risk of bias in the trials (due to lack of masking), inconsistency, and imprecision.
Topics: Body Weight; Enteral Nutrition; Enterocolitis, Necrotizing; Fluid Therapy; Humans; Infant Formula; Infant, Newborn; Infant, Premature; Infant, Very Low Birth Weight; Milk, Human; Randomized Controlled Trials as Topic; Weight Gain
PubMed: 33368149
DOI: 10.1002/14651858.CD013542.pub2 -
Nature Communications Jan 2016The domestic dog is becoming an increasingly valuable model species in medical genetics, showing particular promise to advance our understanding of cancer and...
The domestic dog is becoming an increasingly valuable model species in medical genetics, showing particular promise to advance our understanding of cancer and orthopaedic disease. Here we undertake the largest canine genome-wide association study to date, with a panel of over 4,200 dogs genotyped at 180,000 markers, to accelerate mapping efforts. For complex diseases, we identify loci significantly associated with hip dysplasia, elbow dysplasia, idiopathic epilepsy, lymphoma, mast cell tumour and granulomatous colitis; for morphological traits, we report three novel quantitative trait loci that influence body size and one that influences fur length and shedding. Using simulation studies, we show that modestly larger sample sizes and denser marker sets will be sufficient to identify most moderate- to large-effect complex disease loci. This proposed design will enable efficient mapping of canine complex diseases, most of which have human homologues, using far fewer samples than required in human studies.
Topics: Animals; Body Size; Dog Diseases; Dogs; Female; Genome-Wide Association Study; Genotype; Humans; Male; Phenotype; Quantitative Trait Loci
PubMed: 26795439
DOI: 10.1038/ncomms10460 -
Irish Journal of Medical Science Feb 2017The participation of inflammation in the progression of cancer for many years have been the subject of research. (Review)
Review
BACKGROUND
The participation of inflammation in the progression of cancer for many years have been the subject of research.
METHODS
In the 19th century, there was evidence that an acute inflammation may inhibit the development of cancer. However, chronic inflammation affects the progression of the disease.
RESULTS
Today, it is known that inflammation and cancer use similar mechanisms of development such as severe cell proliferation or angiogenesis. It has been shown that prolonged presence of inflammatory cells and factors in the tumor microenvironment can accelerate its growth and inhibit apoptosis of transformed cells.
CONCLUSION
In this article we present a brief history of the discovery mechanisms and potential links between acute and chronic inflammation and cancer.
Topics: Apoptosis; Cell Proliferation; Disease Progression; Humans; Inflammation; Neoplasms; Neovascularization, Pathologic
PubMed: 27156054
DOI: 10.1007/s11845-016-1464-0 -
Pharmacological Research Sep 2020Spermidine, as a natural component from polyamine members, is originally isolated from semen and also existed in many natural plants, and can be responsible for cell... (Review)
Review
Spermidine, as a natural component from polyamine members, is originally isolated from semen and also existed in many natural plants, and can be responsible for cell growth and development in eukaryotes. The supplementation of spermidine can extend health and lifespan across species. Although the elevated levels of polyamines and the regulation of rate-limiting enzymes for polyamine metabolism have been identified as the biomarkers in many cancers, recent epidemiological data support that an increased uptake of spermidine as a caloric restriction mimic can reduce overall mortality associated with cancers. The possible mechanisms between spermidine and cancer development may be related to the precise regulation of polyamine metabolism, anti-cancer immunosurveillance, autophagy, and apoptosis. Increased intake of polyamine seems to suppress tumorigenesis, but appears to accelerate the growth of established tumors. Based on these observations and the absolute requirement for polyamines in tumor growth, spermidine could be a rational target for chemoprevention and clinical therapeutics of cancers.
Topics: Animals; Antineoplastic Agents; Apoptosis; Autophagy; Biomarkers, Tumor; Cell Proliferation; Humans; Neoplasms; Predictive Value of Tests; Signal Transduction; Spermidine
PubMed: 32461185
DOI: 10.1016/j.phrs.2020.104943 -
International Journal of Nanomedicine 2023Aptamers are widely applied to diagnosis and therapy because of their targeting. However, the current progress of research into aptamers for the treatment of eye... (Review)
Review
Aptamers are widely applied to diagnosis and therapy because of their targeting. However, the current progress of research into aptamers for the treatment of eye disorders has not been well-documented. The current literature on aptamers was reviewed in this study. Aptamer-related drugs and biochemical sensors have been evaluated for several eye disorders within the past decade; S58 targeting TGF-β receptor II and pegaptanib targeting vascular endothelial growth factor (VEGF) are used to prevent fibrosis after glaucoma filtration surgery. Anti-brain-derived neurotrophic factor aptamer has been used to diagnose glaucoma. The first approved aptamer drug (pegaptanib) has been used to inhibit angiogenesis in age-related macular degeneration (AMD) and diabetic retinopathy (DR), and its efficacy and safety have been demonstrated in clinical trials. Aptamers, including E10030, RBM-007, AS1411, and avacincaptad pegol, targeting other angiogenesis-related biomarkers have also been discovered and subjected to clinical trials. Aptamers, such as C promoter binding factor 1, CD44, and advanced end products in AMD and DR, targeting other signal pathway proteins have also been discovered for therapy, and biochemical sensors for early diagnosis have been developed based on aptamers targeting VEGF, connective tissue growth factor, and lipocalin 1. Aptamers used for early detection and treatment of ocular tumors were derived from other disease biomarkers, such as CD71, nucleolin, and high mobility group A. In this review, the development and application of aptamers in eye disorders in recent years are systematically discussed, which may inspire a new link between aptamers and eye disorders. The aptamer development trajectory also facilitates the discovery of the pathogenesis and therapeutic strategies for various eye disorders.
Topics: Humans; Vascular Endothelial Growth Factor A; Ophthalmology; Macular Degeneration; Aptamers, Nucleotide; Diabetic Retinopathy; Glaucoma; Acceleration
PubMed: 37551274
DOI: 10.2147/IJN.S418115 -
Minerva Pediatrics Dec 2021Pediatric obesity is a growing and alarming global health problem and represents an important determinant of morbidity. Since nutrition plays an important role in... (Review)
Review
Pediatric obesity is a growing and alarming global health problem and represents an important determinant of morbidity. Since nutrition plays an important role in regulating growth and development, the excess weight gain related to overnutrition can affect growth patterns, bone maturation and pubertal development. The purpose of this review was to summarize the current knowledge about the effect of primary obesity on linear growth and pubertal development in children and adolescents. Evidence about regulatory hormones and adipokines that may be involved in the physiology of childhood growth in the context of obesity were also discussed. The most recent literature confirms previous studies indicating that linear growth is accelerated (mainly due to longer trunks rather than longer legs) and bone age is advanced in prepubertal children with obesity, while there is a reduction of pubertal height gain and attainment of normal adult height. Conflicting results are reported on the timing of puberty, specifically in boys. Indeed, previous studies suggested earlier onset of puberty in obese girls and overweight boys, and a delayed puberty in obese boys. Conversely, the most recent studies show more consistently an earlier onset and completion of pubertal development also in boys with obesity. Considering the false belief of health associated with transient taller stature in children and the adverse outcomes related to early puberty, interventions on diet and physical activity are urgently needed to tackle the epidemics of childhood obesity in public health and clinical setting.
Topics: Adolescent; Adult; Body Height; Body Weight; Child; Female; Humans; Male; Overweight; Pediatric Obesity; Puberty
PubMed: 34309346
DOI: 10.23736/S2724-5276.21.06543-5 -
Clinical Epigenetics Aug 2021In the first study of its kind, we examine the association between growth and development in early life and DNAm age biomarkers in mid-life. (Comparative Study)
Comparative Study
BACKGROUND
In the first study of its kind, we examine the association between growth and development in early life and DNAm age biomarkers in mid-life.
METHODS
Participants were from the Medical Research Council National Survey of Health and Development (n = 1376). Four DNAm age acceleration (AgeAccel) biomarkers were measured when participants were aged 53 years: AgeAccelHannum; AgeAccelHorvath; AgeAccelLevine; and AgeAccelGrim. Exposure variables included: relative weight gain (standardised residuals from models of current weight z-score on current height, and previous weight and height z-scores); and linear growth (standardised residuals from models of current height z-score on previous height and weight z-scores) during infancy (0-2 years, weight gain only), early childhood (2-4 years), middle childhood (4-7 years) and late childhood to adolescence (7-15 years); age at menarche; and pubertal stage for men at 14-15 years. The relationship between relative weight gain and linear growth and AgeAccel was investigated using conditional growth models. We replicated analyses from the late childhood to adolescence period and pubertal timing among 240 participants from The National Child and Development Study (NCDS).
RESULTS
A 1SD increase in relative weight gain in late childhood to adolescence was associated with 0.50 years (95% CI 0.20, 0.79) higher AgeAccelGrim. Although the CI includes the null, the estimate was similar in NCDS [0.57 years (95% CI - 0.01, 1.16)] There was no strong evidence that relative weight gain and linear growth in childhood was associated with any other AgeAccel biomarker. There was no relationship between pubertal timing in men and AgeAccel biomarkers. Women who reached menarche ≥ 12 years had 1.20 years (95% CI 0.15, 2.24) higher AgeAccelGrim on average than women who reached menarche < 12 years; however, this was not replicated in NCDS and was not statistically significant after Bonferroni correction.
CONCLUSIONS
Our findings generally do not support an association between growth and AgeAccel biomarkers in mid-life. However, we found rapid weight gain during pubertal development, previously related to higher cardiovascular disease risk, to be associated with older AgeAccelGrim. Given this is an exploratory study, this finding requires replication.
Topics: Adolescent; Adult; Age Factors; Aging; Biomarkers; Birth Weight; Body Height; Body Mass Index; Child; Child Development; Child, Preschool; DNA Methylation; Female; Humans; Infant; Infant, Newborn; Male; Middle Aged; United Kingdom; Weight Gain; Young Adult
PubMed: 34372922
DOI: 10.1186/s13148-021-01138-x -
Ecology Jul 2021Organismal locomotion mediates ecological interactions and shapes community dynamics. Locomotion is constrained by intrinsic and environmental factors and integrating...
Organismal locomotion mediates ecological interactions and shapes community dynamics. Locomotion is constrained by intrinsic and environmental factors and integrating these factors should clarify how locomotion affects ecology across scales. We extended general theory based on metabolic scaling and biomechanics to predict the scaling of five locomotor performance traits: routine speed, maximum speed, maximum acceleration, minimum powered turn radius, and angular speed. To test these predictions, we used phylogenetically informed analyses of a new database with 884 species and found support for our quantitative predictions. Larger organisms were faster but less maneuverable than smaller organisms. Routine and maximum speeds scaled with body mass to 0.20 and 0.17 powers, respectively, and plateaued at higher body masses, especially for maximum speed. Acceleration was unaffected by body mass. Minimum turn radius scaled to a 0.19 power, and the 95% CI included our theoretical prediction, as we predicted. Maximum angular speed scaled higher than predicted but in the same direction. We observed universal scaling among locomotor modes for routine and maximum speeds but the intercepts varied; flying organisms were faster than those that swam or ran. Acceleration was independent of size in flying and aquatic taxa but decreased with body mass in land animals, possibly due to the risk of injury large, terrestrial organisms face at high speeds and accelerations. Terrestrial mammals inhabiting structurally simple habitats tended to be faster than those in complex habitats. Despite effects of body size, locomotor mode, and habitat complexity, universal scaling of locomotory performance reveals the general ways organisms move across Earth's complex environments.
Topics: Animals; Biomechanical Phenomena; Body Size; Locomotion; Mammals
PubMed: 33864262
DOI: 10.1002/ecy.3369 -
Annales D'endocrinologie Jun 2017The diagnostic approach to tall stature in children is based on collecting birth data (macrosomia), sizes and family puberty, a family history of constitutional or... (Review)
Review
The diagnostic approach to tall stature in children is based on collecting birth data (macrosomia), sizes and family puberty, a family history of constitutional or pathological tall stature, search for a delay of development, dysmorphia, disproportion, analysis of the growth velocity (normal or accelerated), general examination and assessment of puberty, and bone age. When there is a history of psychomotor retardation, a family history of pathological tall stature, or a disproportion in the clinical examination, the genetic causes of tall stature will be mentioned. The most frequent causes are Marfan syndrome and similar, Sotos syndrome, Beckwith-Wiedemann syndrome, Klinefelter syndrome, and MEN2B. There are many genetic syndromes with tall stature, justifying consultation with the geneticist. When the speed of growth is accelerated, first of all it evokes puberty and early pseudopuberty, obesity and acromegaly. Finally, when the growth velocity is regular, and the parents are of tall stature, it evokes constitutional tall stature: this is the most frequent diagnosis, to retain after having rejected pathological tall statures.
Topics: Acromegaly; Body Height; Child; Gigantism; Growth; Growth Disorders; Humans
PubMed: 28483364
DOI: 10.1016/j.ando.2017.04.006 -
Zoological Science Jun 2021Growth-retarded () mice display primary congenital hypothyroidism due to the hyporesponsiveness of their thyroid glands to thyroid-stimulating hormone (TSH). We examined...
Growth-retarded () mice display primary congenital hypothyroidism due to the hyporesponsiveness of their thyroid glands to thyroid-stimulating hormone (TSH). We examined somatic growth, anterior pituitary development, and hormonal profiles in female mice and normal ones. Although growth in females was suppressed 2 weeks after birth, the measured growth parameters and organ weights gradually increased and finally reached close to the normal levels. mice exhibited delayed eye and vaginal openings and remained in a state of persistent diestrus thereafter, plasma estrogen levels being lower than those in normal mice. mice that received normal-donor thyroids showed accelerated growth and their body weights increased up to the sham-normal levels, indicating the importance of early thyroid hormone supplementation. In the anterior pituitary, there were fewer growth hormone (GH) and prolactin (PRL) cells in mice than in normal mice as examined at 12 weeks after birth, but the numbers of these cells did not differ from those in normal mice after 24 weeks. mice had more TSH cells than normal mice until 48 weeks. Plasma GH levels in mice were lower than those in normal mice at 2 weeks, but did not differ substantially after 5 weeks. Compared with normal mice, mice had significantly lower plasma PRL and thyroxine levels, but notably higher TSH levels until 48 weeks. These findings indicate that thyroid hormone deficiency in mice causes delayed development and growth, and inappropriate development of GH, PRL and TSH cells, followed by the abnormal secretion of hormones by these pituitary cells.
Topics: Animals; Congenital Hypothyroidism; Female; Growth Hormone; Mice; Organ Size; Pituitary Gland; Prolactin; Thyroid Gland; Thyroid Hormones; Thyrotropin
PubMed: 34057348
DOI: 10.2108/zs200063