229 research outputs found
Reexamining the effects of gestational age, fetal growth, and maternal smoking on neonatal mortality
BACKGROUND: Low birth weight (<2,500 g) is a strong predictor of infant mortality. Yet low birth weight, in isolation, is uninformative since it is comprised of two intertwined components: preterm delivery and reduced fetal growth. Through nonparametric logistic regression models, we examine the effects of gestational age, fetal growth, and maternal smoking on neonatal mortality. METHODS: We derived data on over 10 million singleton live births delivered at ≥ 24 weeks from the 1998–2000 U.S. natality data files. Nonparametric multivariable logistic regression based on generalized additive models was used to examine neonatal mortality (deaths within the first 28 days) in relation to fetal growth (gestational age-specific standardized birth weight), gestational age, and number of cigarettes smoked per day. All analyses were further adjusted for the confounding effects due to maternal age and gravidity. RESULTS: The relationship between standardized birth weight and neonatal mortality is nonlinear; mortality is high at low z-score birth weights, drops precipitously with increasing z-score birth weight, and begins to flatten for heavier infants. Gestational age is also strongly associated with mortality, with patterns similar to those of z-score birth weight. Although the direct effect of smoking on neonatal mortality is weak, its effects (on mortality) appear to be largely mediated through reduced fetal growth and, to a lesser extent, through shortened gestation. In fact, the association between smoking and reduced fetal growth gets stronger as pregnancies approach term. CONCLUSIONS: Our study provides important insights regarding the combined effects of fetal growth, gestational age, and smoking on neonatal mortality. The findings suggest that the effect of maternal smoking on neonatal mortality is largely mediated through reduced fetal growth
Nicotine Acts on Growth Plate Chondrocytes to Delay Skeletal Growth through the α7 Neuronal Nicotinic Acetylcholine Receptor
BACKGROUND: Cigarette smoking adversely affects endochondral ossification during the course of skeletal growth. Among a plethora of cigarette chemicals, nicotine is one of the primary candidate compounds responsible for the cause of smoking-induced delayed skeletal growth. However, the possible mechanism of delayed skeletal growth caused by nicotine remains unclarified. In the last decade, localization of neuronal nicotinic acetylcholine receptor (nAChR), a specific receptor of nicotine, has been widely detected in non-excitable cells. Therefore, we hypothesized that nicotine affect growth plate chondrocytes directly and specifically through nAChR to delay skeletal growth. METHODOLOGY/PRINCIPAL FINDINGS: We investigated the effect of nicotine on human growth plate chondrocytes, a major component of endochondral ossification. The chondrocytes were derived from extra human fingers. Nicotine inhibited matrix synthesis and hypertrophic differentiation in human growth plate chondrocytes in suspension culture in a concentration-dependent manner. Both human and murine growth plate chondrocytes expressed alpha7 nAChR, which constitutes functional homopentameric receptors. Methyllycaconitine (MLA), a specific antagonist of alpha7 nAChR, reversed the inhibition of matrix synthesis and functional calcium signal by nicotine in human growth plate chondrocytes in vitro. To study the effect of nicotine on growth plate in vivo, ovulation-controlled pregnant alpha7 nAChR +/- mice were given drinking water with or without nicotine during pregnancy, and skeletal growth of their fetuses was observed. Maternal nicotine exposure resulted in delayed skeletal growth of alpha7 nAChR +/+ fetuses but not in alpha7 nAChR -/- fetuses, implying that skeletal growth retardation by nicotine is specifically mediated via fetal alpha7 nAChR. CONCLUSIONS/SIGNIFICANCE: These results suggest that nicotine, from cigarette smoking, acts directly on growth plate chondrocytes to decrease matrix synthesis, suppress hypertrophic differentiation via alpha7 nAChR, leading to delayed skeletal growth
Recommended from our members
Timing of singleton births by onset of labour and mode of birth in NHS maternity units in England, 2005-2014: A study of linked birth registration, birth notification, and hospital episode data
BACKGROUND: Maternity care has to be available 24 hours a day, seven days a week. It is known that obstetric intervention can influence the time of birth, but no previous analysis at a national level in England has yet investigated in detail the ways in which the day and time of birth varies by onset of labour and mode of giving birth.
METHOD: We linked data from birth registration, birth notification, and Maternity Hospital Episode Statistics and analysed 5,093,615 singleton births in NHS maternity units in England from 2005 to 2014. We used descriptive statistics and negative binomial regression models with harmonic terms to establish how patterns of timing of birth vary by onset of labour, mode of giving birth and gestational age.
RESULTS: The timing of birth by time of day and day of the week varies considerably by onset of labour and mode of birth. Spontaneous births after spontaneous onset are more likely to occur between midnight and 6am than at other times of day, and are also slightly more likely on weekdays than at weekends and on public holidays. Elective caesarean births are concentrated onto weekday mornings. Births after induced labours are more likely to occur at hours around midnight on Tuesdays to Saturdays and on days before a public holiday period, than on Sundays, Mondays and during or just after a public holiday.
CONCLUSION: The timing of births varies by onset of labour and mode of birth and these patterns have implications for midwifery and medical staffing. Further research is needed to understand the processes behind these findings
A parsimonious explanation for intersecting perinatal mortality curves: understanding the effect of plurality and of parity
BACKGROUND: Birth weight- and gestational age-specific perinatal mortality curves intersect when compared across categories of maternal smoking, plurality, race and other factors. No simple explanation exists for this paradoxical observation. METHODS: We used data on all live births, stillbirths and infant deaths in Canada (1991–1997) to compare perinatal mortality rates among singleton and twin births, and among singleton births to nulliparous and parous women. Birth weight- and gestational age-specific perinatal mortality rates were first calculated by dividing the number of perinatal deaths at any given birth weight or gestational age by the number of total births at that birth weight or gestational age (conventional calculation). Gestational age-specific perinatal mortality rates were also calculated using the number of fetuses at risk of perinatal death at any given gestational age. RESULTS: Conventional perinatal mortality rates among twin births were lower than those among singletons at lower birth weights and earlier gestation ages, while the reverse was true at higher birth weights and later gestational ages. When perinatal mortality rates were based on fetuses at risk, however, twin births had consistently higher mortality rates than singletons at all gestational ages. A similar pattern emerged in contrasts of gestational age-specific perinatal mortality among singleton births to nulliparous and parous women. Increases in gestational age-specific rates of growth-restriction with advancing gestational age presaged rising rates of gestational age-specific perinatal mortality in both contrasts. CONCLUSIONS: The proper conceptualization of perinatal risk eliminates the mortality crossover paradox and provides new insights into perinatal health issues
Customized birth weight for gestational age standards: Perinatal mortality patterns are consistent with separate standards for males and females but not for blacks and whites
BACKGROUND: Some currently available birth weight for gestational age standards are customized but others are not. We carried out a study to provide empirical justification for customizing such standards by sex and for whites and blacks in the United States. METHODS: We studied all male and female singleton live births and stillbirths (22 or more weeks of gestation; 500 g birth weight or over) in the United States in 1997 and 1998. White and black singleton live births and stillbirths were also examined. Qualitative congruence between gestational age-specific growth restriction and perinatal mortality rates was used as the criterion for identifying the preferred standard. RESULTS: The fetuses at risk approach showed that males had higher perinatal mortality rates at all gestational ages compared with females. Gestational age-specific growth restriction rates based on a sex-specific standard were qualitatively consistent with gestational age-specific perinatal mortality rates among males and females. However, growth restriction patterns among males and females based on a unisex standard could not be reconciled with perinatal mortality patterns. Use of a single standard for whites and blacks resulted in gestational age-specific growth restriction rates that were qualitatively congruent with patterns of perinatal mortality, while use of separate race-specific standards led to growth restriction patterns that were incompatible with patterns of perinatal mortality. CONCLUSION: Qualitative congruence between growth restriction and perinatal mortality patterns provides an outcome-based justification for sex-specific birth weight for gestational age standards but not for the available race-specific standards for blacks and whites in the United States
Comparative quantification of health risks: Conceptual framework and methodological issues
Reliable and comparable analysis of risks to health is key for preventing disease and injury. Causal attribution of morbidity and mortality to risk factors has traditionally been conducted in the context of methodological traditions of individual risk factors, often in a limited number of settings, restricting comparability. In this paper, we discuss the conceptual and methodological issues for quantifying the population health effects of individual or groups of risk factors in various levels of causality using knowledge from different scientific disciplines. The issues include: comparing the burden of disease due to the observed exposure distribution in a population with the burden from a hypothetical distribution or series of distributions, rather than a single reference level such as non-exposed; considering the multiple stages in the causal network of interactions among risk factor(s) and disease outcome to allow making inferences about some combinations of risk factors for which epidemiological studies have not been conducted, including the joint effects of multiple risk factors; calculating the health loss due to risk factor(s) as a time-indexed "stream" of disease burden due to a time-indexed "stream" of exposure, including consideration of discounting; and the sources of uncertainty
SoccerNet 2023 Challenges Results
peer reviewedThe SoccerNet 2023 challenges were the third annual video understanding
challenges organized by the SoccerNet team. For this third edition, the
challenges were composed of seven vision-based tasks split into three main
themes. The first theme, broadcast video understanding, is composed of three
high-level tasks related to describing events occurring in the video
broadcasts: (1) action spotting, focusing on retrieving all timestamps related
to global actions in soccer, (2) ball action spotting, focusing on retrieving
all timestamps related to the soccer ball change of state, and (3) dense video
captioning, focusing on describing the broadcast with natural language and
anchored timestamps. The second theme, field understanding, relates to the
single task of (4) camera calibration, focusing on retrieving the intrinsic and
extrinsic camera parameters from images. The third and last theme, player
understanding, is composed of three low-level tasks related to extracting
information about the players: (5) re-identification, focusing on retrieving
the same players across multiple views, (6) multiple object tracking, focusing
on tracking players and the ball through unedited video streams, and (7) jersey
number recognition, focusing on recognizing the jersey number of players from
tracklets. Compared to the previous editions of the SoccerNet challenges, tasks
(2-3-7) are novel, including new annotations and data, task (4) was enhanced
with more data and annotations, and task (6) now focuses on end-to-end
approaches. More information on the tasks, challenges, and leaderboards are
available on https://www.soccer-net.org. Baselines and development kits can be
found on https://github.com/SoccerNet
- …