Offspring Mortality Research Articles

Fathers' Alcohol Consumption and Long-Term Risk for Mortality in Offspring.

This study examined associations between fathers' alcohol consumption and risk for total and cause-specific mortality in offspring. We examined the associations between fathers' alcohol consumption and total and cause-specific mortality in adult offspring. Fathers' alcohol consumption was associated with increased risk of alcohol-related mortality in offspring. The association appeared to be weaker for causes of death in which alcohol plays a smaller, or less direct, role. Data on fathers' alcohol consumption, and offspring's risky use of alcohol, smoking, mental health and contact with police/childcare authorities were collected among 46,284 men (sons) aged 18-20 years, during conscription for compulsory military training in 1969/70. Data on offspring mortality were obtained from the National Cause of Death register, 1971-2008. The mortality outcomes included total mortality, alcohol-related causes of death and violent causes of death (categorized into suicides vs violent/external causes excluding suicides). Compared to sons whose fathers never used alcohol, the risk for total and alcohol-related mortality among sons increased with the father's consumption level. The risk of violent death was significantly elevated among sons whose fathers drank alcohol occasionally or often, but the risk of suicide increased in the highest consumption category only. After adjustment for covariates, the results remained for alcohol-related mortality whereas they were significantly attenuated, or disappeared, for total mortality, violent death and suicide. Fathers' alcohol consumption is associated with increased risk of alcohol-related mortality in the offspring. Alcohol use among fathers also increases the offspring's risk of later total mortality, suicide and violent death, but these associations appear to be mediated or confounded by factors related to parental drinking and/or adverse childhood psychosocial circumstances.

Placental Abruption and Child Mortality

Placental abruption causes asphyxia and leads to high perinatal mortality. Our objective was to study the overall mortality and causes of death among children born after placental abruption. Data on children born from singleton pregnancies complicated by placental abruption between 1987 and 2005 were collected from the Finnish Medical Birth Register, the Hospital Discharge Register, and the Cause-of-Death Register. A reference group consisted of children born from pregnancies without placental abruption. After excluding stillbirths, the final study sample comprised 3888 children born after placental abruption (index children) and 12 530 referent children. The main outcome measure was overall mortality. By the end of 2013, there were 280 deaths among the index children and 107 deaths among the referent children. Compared with the referent children, the overall mortality among the index children was significantly increased (hazard ratio: 8.70; 95% confidence interval 6.96-10.90). During the neonatal period (0-27 days) the mortality was nearly 15-fold (14.8; 10.9-20.0), birth-related asphyxia being the leading cause of death (108; 34-341). The mortality remained high during days 28 to 365 (10.3; 4.83-21.8) and beyond 365 days (1.70; 1.03-2.79). Furthermore, the overall mortality was increased among the index children born at 32 to 36 + 6 gestational weeks (2.77; 1.54-4.98) and at ≥37 weeks (4.98; 3.54-6.99) and among children with a birth weight of 2500 g or more (5.94; 4.33-8.14). The impact of abruption on offspring mortality extends far beyond the perinatal period. This is mainly due to birth-related asphyxia and prematurity-related consequences.

Offspring fitness and the optimal propagule size in a fluctuating environment

Propagule size is an important maternal effect on offspring fitness and phenotype in birds and other oviparous animals. The performance of propagules often increases with size, but a fluctuating environment may introduce temporal variation in the optimal phenotype. Understanding these mechanisms will provide novel insights into the eco‐evolutionary dynamics of life history strategies in parental reproductive investment. We investigated the interaction between propagule size (measured as egg volume) and environmental conditions on offspring mortality and phenotype in a Norwegian house sparrow population. Increased propagule size reduced offspring mortality in early life, with more pronounced effects under heavy precipitation. However, the optimal propagule size for low offspring mortality until recruitment shifted from large to small as temperature increased. Propagule size had no significant effect on fledgling body mass and tarsus length. These results reveal a potential for eco‐evolutionary dynamics in propagule size, as populations adapt to fluctuating environmental conditions. The ultimate outcome of this dynamic process will also depend on variation in parental fitness and tradeoffs with other life‐history traits, particularly clutch size.

Perinatal health outcomes and care among asylum seekers and refugees: a systematic review of systematic reviews

BackgroundGlobal migration is at an all-time high with implications for perinatal health. Migrant women, especially asylum seekers and refugees, represent a particularly vulnerable group. Understanding the impact on the perinatal health of women and offspring is an important prerequisite to improving care and outcomes. The aim of this systematic review was to summarise the current evidence base on perinatal health outcomes and care among women with asylum seeker or refugee status.MethodsTwelve electronic database, reference list and citation searches (1 January 2007–July 2017) were carried out between June and July 2017. Quantitative and qualitative systematic reviews, published in the English language, were included if they reported perinatal health outcomes or care and clearly stated that they included asylum seekers or refugees. Screening for eligibility, data extraction, quality appraisal and evidence synthesis were carried out in duplicate. The results were summarised narratively.ResultsAmong 3415 records screened, 29 systematic reviews met the inclusion criteria. Only one exclusively focussed on asylum seekers; the remaining reviews grouped asylum seekers and refugees with wider migrant populations. Perinatal outcomes were predominantly worse among migrant women, particularly mental health, maternal mortality, preterm birth and congenital anomalies. Access and use of care was obstructed by structural, organisational, social, personal and cultural barriers. Migrant women’s experiences of care included negative communication, discrimination, poor relationships with health professionals, cultural clashes and negative experiences of clinical intervention. Additional data for asylum seekers and refugees demonstrated complex obstetric issues, sexual assault, offspring mortality, unwanted pregnancy, poverty, social isolation and experiences of racism, prejudice and stereotyping within perinatal healthcare.ConclusionsThis review identified adverse pregnancy outcomes among asylum seeker and refugee women, representing a double burden of inequality for one of the most globally vulnerable groups of women. Improvements in the provision of perinatal healthcare could reduce inequalities in adverse outcomes and improve women’s experiences of care. Strategies to overcome barriers to accessing care require immediate attention. The systematic review evidence base is limited by combining heterogeneous migrant, asylum seeker and refugee populations, inconsistent use of definitions and limited data on some perinatal outcomes and risk factors. Future research needs to overcome these limitations to improve data quality and address inequalities.Systematic registrationSystematic review registration number: PROSPERO CRD42017073315.

Complete brood failure in an altricial bird is almost always associated with the sudden and permanent disappearance of a parent

A central goal in evolutionary ecology is to identify factors that explain variation in reproductive success, i.e. in the number of offspring produced. In altricial birds, a substantial part of this variation is determined by the number of nestlings that die before fledging, but surprisingly little is known about the proximate causes of offspring mortality during the nestling period. We used a uniquely comprehensive dataset of parental nestbox visits from seven breeding seasons to investigate the association between parental behaviour and nestling mortality in a population of blue tits (Cyanistes caeruleus). In almost all nests that suffered complete brood mortality one of the parents had suddenly disappeared during the nestling stage. In contrast, parental disappearance in nests with partial brood mortality was rare and equally common as in nests with no brood loss. With few exceptions, parents that disappeared during the nestling stage were never observed again and never returned to breed. In contrast, parents that remained after their partner disappeared were equally likely to be observed again or return to breed as parents of nests where both parents stayed. Visit rates at nests where a parent would disappear did not differ from those at nests where both parents stayed. Taken together, our results show that - in contrast to partial brood failure - complete brood failure is almost always associated with the sudden and permanent disappearance of one of the parents, probably due to predation. Partial and complete brood mortality should be treated as distinct processes that have different underlying causes.

Association Between Vitamin D Supplementation During Pregnancy and Offspring Growth, Morbidity, and Mortality

Whether vitamin D supplementation during pregnancy is beneficial and safe for offspring is unclear. To systematically review studies of the effects of vitamin D supplementation during pregnancy on offspring growth, morbidity, and mortality. Searches of Medline, Embase, and the Cochrane Database of Systematic Reviews were conducted up to October 31, 2017. Key search terms were vitamin D, pregnancy, randomized controlled trials, and offspring outcomes. Randomized clinical trials of vitamin D supplementation during pregnancy and offspring outcomes. Two authors independently extracted data, and the quality of the studies was assessed. Summary risk ratio (RR), risk difference (RD) or mean difference (MD), and 95% CI were calculated using fixed-effects or random-effects meta-analysis. Main outcomes were fetal or neonatal mortality, small for gestational age (SGA), congenital malformation, admission to a neonatal intensive care unit, birth weight, Apgar scores, neonatal 25-hydroxyvitamin D (25[OH]D) and calcium concentrations, gestational age, preterm birth, infant anthropometry, and respiratory morbidity during childhood. Twenty-four clinical trials involving 5405 participants met inclusion criteria. Vitamin D supplementation during pregnancy was associated with a lower risk of SGA (RR, 0.72; 95% CI, 0.52 to 0.99; RD, -5.60%; 95% CI, -0.86% to -10.34%) without risk of fetal or neonatal mortality (RR, 0.72; 95% CI, 0.47 to 1.11) or congenital abnormality (RR, 0.94; 95% CI, 0.61 to 1.43). Neonates with prenatal vitamin D supplementation had higher 25(OH)D levels (MD, 13.50 ng/mL; 95% CI, 10.12 to 16.87 ng/mL), calcium levels (MD, 0.19 mg/dL; 95% CI, 0.003 to 0.38 mg/dL), and weight at birth (MD, 75.38 g; 95% CI, 22.88 to 127.88 g), 3 months (MD, 0.21 kg; 95% CI, 0.13 to 0.28 kg), 6 months (MD, 0.46 kg; 95% CI, 0.33 to 0.58 kg), 9 months (MD, 0.50 kg; 95% CI, 0.01 to 0.99 kg), and 12 months (MD, 0.32 kg; 95% CI, 0.12 to 0.52 kg). Subgroup analysis by doses showed that low-dose vitamin D supplementation (≤2000 IU/d) was associated with a reduced risk of fetal or neonatal mortality (RR, 0.35; 95% CI, 0.15 to 0.80), but higher doses (>2000 IU/d) did not reduce this risk (RR, 0.95; 95% CI, 0.59 to 1.54). Vitamin D supplementation during pregnancy is associated with a reduced risk of SGA and improved infant growth without risk of fetal or neonatal mortality or congenital abnormality. Vitamin D supplementation with doses of 2000 IU/d or lower during pregnancy may reduce the risk of fetal or neonatal mortality.

Lethal trap created by adaptive evolutionary response to an exotic resource.

Global transport of organisms by humans provides novel resources to wild species, which often respond maladaptively. Native herbivorous insects have been killed feeding on toxic exotic plants, which acted as 'ecological traps'1-4. We document a novel 'eco-evolutionary trap' stemming from the opposite effect; that is, high fitness on an exotic resource despite lack of adaptation to it. Plantago lanceolata was introduced to western North America by cattle-ranching. Feeding on this exotic plant released a large, isolated population of the native butterfly Euphydryas editha from a longstanding trade-off between maternal fecundity and offspring mortality. Because of this release-and despite a reduced insect developmental rate when feeding on this exotic-Plantago immediately supported higher larval survival than did the insects' traditional host, Collinsia parviflora 5 . Previous work from the 1980s documented an evolving preference for Plantago by ovipositing adults 6 . We predicted that if this trend continued the insects could endanger themselves, because the availability of Plantago to butterflies is controlled by humans, who change land management practices faster than butterflies evolve 6 . Here we report the fulfilment of this prediction. The butterflies abandoned Collinsia and evolved total dependence on Plantago. The trap was set. In 2005, humans withdrew their cattle, springing the trap. Grasses grew around the Plantago, cooling the thermophilic insects, which then went extinct. This local extinction could have been prevented if the population had retained partial use of Collinsia, which occupied drier microhabitats unaffected by cattle removal. The flush of grasses abated quickly, rendering the meadow once again suitable for Euphydryas feeding on either host, but no butterflies were observed from 2008 to 2012. In 2013-2014, the site was naturally recolonized by Euphydryas feeding exclusively on Collinsia, returning the system to its starting point and setting the stage for a repeat of the anthropogenic evolutionary cycle.

Nuclear progestin receptor (Pgr) knockouts resulted in subfertility in male tilapia (Oreochromis niloticus)

It was documented that 17α, 20β-dihydroxy-4-pregnen-3-one (DHP), a fish specific progestin, might play critical roles in spermatogenesis, sperm maturation and spermiation partially through activating nuclear receptor (Pgr). However, no direct evidence is available to demonstrate the functions of DHP in fish spermatogenesis. To further elucidate the roles of DHP in teleosts, we generated a pgr homozygous mutant line in XY Nile tilapia (Oreochromis niloticus). Pgr gene mutation resulted in the development of a smaller, thinner testis and a lower GSI compared with normal testis. Pgr gene knockout led to irregular arrangement of spermatogenic cysts, decline of sperm count and sperm motility. Significant decrease of spermatocytes and spermatozoa was observed, which was further proved by the PCNA and Ph3 staining. Real-time PCR analysis demonstrated that mutation of pgr gene resulted in a significant up-regulation of steroidogenesis-related genes of cyp17a, cyp11b2, StAR, scc, 20β-HSD, and sf1, and down-regulation of fshb, fshr, oct4, sycp3, cdk1, prm, cyclinB1, cyclinB2 and cdc25 genes. Furthermore, both Immunohistochemistry and Western blotting experiments revealed a remarkable increase of Cyp17a1, Cyp17a2 and Cyp11b2 expressions in the pgr−/− testis. EIA measurement showed that an evident increase of 11-KT level was found in the pgr−/− XY fish. There was a significant increase in the mortality of offspring when crossing pgr−/− XY fish with wild type XX fish. Increased TUNEL staining and enhanced apoptosis maker gene (bax) expressions were also observed. Taken together, our data suggested that DHP-activated physiology via pgr is crucial for the fertility in the XY tilapia.

No evidence for sex-specific effects of the maternal social environment on offspring development in Japanese quail (Coturnix japonica)

The social environment of reproducing females can cause physiological changes, with consequences for reproductive investment and offspring development. These prenatal maternal effects are often found to be sex-specific and may have evolved as adaptations, maximizing fitness of male and female offspring for their future environment. Female hormone levels during reproduction are considered a potential mechanism regulating sex allocation in vertebrates: high maternal androgens have repeatedly been linked to increased investment in sons, whereas high glucocorticoid levels are usually related to increased investment in daughters. However, results are not consistent across studies and therefore still inconclusive. In Japanese quail (Coturnix japonica), we previously found that pair-housed females had higher plasma androgen levels and tended to have higher plasma corticosterone levels than group-housed females. In the current study we investigate whether these differences in maternal social environment and physiology affect offspring sex allocation and physiology. Counter to our expectations, we find no effects of the maternal social environment on offspring sex ratio, sex-specific mortality, growth, circulating androgen or corticosterone levels. Also, maternal corticosterone or androgen levels do not correlate with offspring sex ratio or mortality. The social environment during reproduction therefore does not necessarily modify sex allocation and offspring physiology, even if it causes differences in maternal physiology. We propose that maternal effects of the social environment strongly depend upon the type of social stimuli and the timing of changes in the social environment and hormones with respect to the reproductive cycle and meiosis.

Low fertility, fecundity and numbers of mated female offspring explain the lower reproductive success of the parasitic mite Varroa destructor in African honeybees

Although Varroa destructor is the most serious ecto-parasite to the honeybee, Apis mellifera L., some honeybee populations such as Apis mellifera scutellata in Kenya can survive mite infestations without treatment. Previously, we reported that grooming behaviour could be a potential tolerant mechanism expressed by this honeybee subspecies towards mite infestation. However, both hygienic and grooming behaviours could not explain the lower mite-infestation levels recorded in these colonies. Here, we investigated the involvement of other potential resistant mechanisms including suppression of mite reproduction in worker brood cells of A. m. scutellata to explain the low mite numbers in their colonies. High infertility rates (26-27%) and percentages of unmated female offspring (39-58%) as well as low fecundity (1.7-2.2, average offspring produced) were identified as key parameters that seem to interact with one another during different seasons to suppress mite reproduction in A. m. scutellata colonies. We also identified offspring mortality in both sexes and absence of male offspring as key factors accounting for the low numbers of mated daughter mites produced in A. m. scutellata colonies. These results suggest that reduced mite reproductive success could explain the slow mite population growth in A. m. scutellata colonies.

Leucocyte profile and offspring production of guinea pig (Cavia cobaya) given Anredera cordifolia leaf extract

The objective of this study was to determine leucocyte and offspring production of guinea pig (Cavia cobaya) giving Anredera cordifolia leaf extract. Materials used were female 16 heads of guinea pig with body weight of 425g. The treatments were an extract of A. cordifolia leaf at doses of 0, 10, 50 and 90 mg/head, designated as T0, T1, T2 and T3, respectively. A. cordifolia leaf extract was administered orally from 10 days prepartum to 10 days postpartum. Blood was taken at 10 days prepartum and 10 days postpartum. Total birth of the offspring was observed. Data were analyzed by analysis of variance and if there was effect of treatment, then continued with Duncan multiple range test and Chi-Square test for fetal production between the given A. cordifolia leaf extract and control. The result showed that there was no significant difference for 10 days prepartum after addition of A cordifolia leaf extract treatment. The postpartum treated showed a total 50 mg/head level increaed for monocytes than that of level 0, 10 and 90 mg/head. Ten days postpartum treatment showed the total increase for leucocyte and monocytes total were 50 and 90 mg/head, respectively compared to 10 mg/head level. Total lymphocyte of 90 mg/head increased compared to level 10 and 50 mg/head. The highest total neutrophil as found at level of 50 mg/head which increased compared to the level of 0 and 10 mg/head. ProvisioningA. cordifolialeaf extract at doses level of 50 and 90 mg/head could increase litter size (P<0.05; χ2=9.267) and decreased offspring mortality (P<0.05; χ2=6.4). In conclusion, by giving 50 mg/head A. cordifolia leaf extract could increase leucocyte profile and offspring production of guinea pig.

Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood.

Premature birth complicates 10%-12% of deliveries. Infection and inflammation are the most common etiologies and are associated with increased offspring morbidity and mortality. We hypothesize that lipopolysaccharide (LPS)-induced maternal inflammation causes direct placenta injury and subsequent injury to the fetal intestine. Pregnant C57Bl6 mice were injected intraperitoneally on day 15.5 with 100μg/kg LPS or saline. Maternal serum, amniotic fluid, placental samples, and ileal samples of offspring were obtained assessed for inflammation and/or injury. Maternal placental ultrasounds were performed. Placental DNA was isolated for microbiome analysis. Maternal injection with LPS caused elevated IL-1β, IL-10, IL-6, KC-GRO, and TNF. Placental tissue showed increased IL-1β, IL-6, and KC-GRO and decreased IL-10, but no changes were observed in amniotic fluid. Placental histology demonstrated LPS-induced increases in mineralization and necrosis, but no difference in placental blood flow. Most placentas had no detectable microbiome. Exposure to maternal LPS induced significant injury to the ilea of the offspring. Lipopolysaccharide causes a maternal inflammatory response that is mirrored in the placenta. Placental histology demonstrates structural changes; however, placental blood flow is preserved. LPS also induces an indirect intestinal injury in the offspring that lasts beyond the neonatal period.

Parental age and offspring mortality: Negative effects of reproductive ageing may be counterbalanced by secular increases in longevity

As parental ages at birth continue to rise, concerns about the effects of fertility postponement on offspring are increasing. Due to reproductive ageing, advanced parental ages have been associated with negative health outcomes for offspring, including decreased longevity. The literature, however, has neglected to examine the potential benefits of being born at a later date. Secular declines in mortality mean that later birth cohorts are living longer. We analyse mortality over ages 30–74 among 1.9 million Swedish men and women born 1938–60, and use a sibling comparison design that accounts for all time-invariant factors shared by the siblings. When incorporating cohort improvements in mortality, we find that those born to older mothers do not suffer any significant mortality disadvantage, and that those born to older fathers have lower mortality. These findings are likely to be explained by secular declines in mortality counterbalancing the negative effects of reproductive ageing.

Parental Imprisonment and Premature Mortality in Adulthood

Rising prison populations worldwide have led to an increasing body of research about the well-being of children of prisoners. Research to date has demonstrated that the consequences of parental imprisonment for children are significant and long lasting, often extending beyond the imprisonment period and into adulthood. However, research examining the association between parental imprisonment and offspring health problems and mortality is lacking. Moreover, no research to date has examined the association between parental imprisonment and premature mortality among adults. Using a Dutch multigenerational sample, this study aimed to extend existing literature by examining the link between parental imprisonment and offspring mortality up to age 65, while controlling for parental criminality. Results indicated that children of imprisoned parents were significantly more likely to die prematurely than children of both non-criminal and criminal but non-imprisoned parents. These findings implicate that the mortality risk is not the consequence of the parental criminal behavior but is specifically related to the incarceration of the parent. Further research is required to examine the mechanisms at play for the increased risk of premature mortality for children of prisoners. This research has important implications for health-related early interventions and criminal justice policy.

Motherhood, Abortion, and the Medicalization of Poverty.

This article considers the impact of laws and policies that determine who experiences unplanned pregnancy, who has abortions, and how economic status shapes one's response to unplanned pregnancy. There is a well-documented correlation between abortion and poverty: poor women have more abortions than do their richer sisters. Equally well-documented is the correlation between unplanned pregnancy and poverty. Finally, the high cost of motherhood for poor women and their offspring manifests in disproportionately high lifelong rates of poverty, ill-health and mortality for offspring and mothers, alike. Read together, these factors offer a vivid illustration of the medicalization of poverty.

735: Vitamin D supplementation during pregnancy and offspring mortality and morbidity: a systematic review

735: Vitamin D supplementation during pregnancy and offspring mortality and morbidity: a systematic review

724: Interpregnancy BMI changes and offspring mortality following second pregnancy

Obesity in pregnancy is associated with increased risk of neonatal mortality, however the effect of interpregnancy weight change is less understood. We sought to understand the impact of maternal interpregnancy body mass index (BMI) change on second offspring mortality risk. We included 266,971 women with first and second singleton deliveries between 1989 and 2015 from the Utah Population Database. Our exposure was defined as interpregnancy BMI change from date of first delivery to conception date of second pregnancy, derived from best clinical gestational dating of second pregnancy. We categorized exposure as: <-1, [-1, 0], [0, <1 reference], [1, 2], [2-4], ≥4 BMI units (kg/m2). Our outcomes were all-cause age-specific mortality: neonatal (≤ 28 days), infant (≤1 year old) childhood (≤5 years old), and late childhood (5-<18 years old). Analyses were based on Cox proportional hazards stratified by full term (>37 weeks) and preterm (< 37 weeks) deliveries. We assessed all-cause mortality and death from congenital anomalies and early infancy. Cox regression was used to estimate hazard ratios of childhood mortality and all models were adjusted for maternal age, race/ethnicity, maternal education, smoking during pregnancy, diabetes, hypertension, assisted reproduction, interpregnancy interval, maternal BMI prior to first pregnancy, infant sex, gestational age (term or not) and small for gestational age. Among full term deliveries, women with BMI change of 4+ had increased risk of neonatal mortality in their second child (hazard ratio 1.63, 95% confidence interval 1.15, 2.31). There were no differences in infant, early or late childhood mortality by interpregnancy BMI change. Maternal interpregnancy BMI changes of 2 to 3.99 and ≥4 had increased risk of all-cause mortality and mortality associated with congenital anomalies or conditions originating in the perinatal period (ICD10 760-779) in their second child (Table 1). In a large U.S. population study, women with large interpregnancy BMI changes have a significant risk of mortality in their second term offspring. Further studies are needed to assess if maternal post-partum weight change are a modifiable risk factor for adverse childhood outcomes.

Prediction of effects of beef selection indexes on greenhouse gas emissions

Genetic improvement in production efficiency traits can also drive reduction in greenhouse gas emissions. This study used international ‘best-practice’ methodology to quantify the improvements in system-wide CO2 equivalent emissions per unit of genetic progress in the Irish Maternal Replacement (MR) and Terminal (T) beef cattle indexes. Effects of each index trait on system gross emissions (GE) and system emissions intensity (EI) were modelled by estimating effects of trait changes on per-animal feed consumption and associated methane production, per-animal meat production and numbers of animals in the system. Trait responses to index selection were predicted from linear regression of individual bull estimated breeding values for each index trait on their MR or T index value, and the resulting regression coefficients were used to calculate trait-wise responses in GE and EI from index selection. Summed over all trait responses, the MR index was predicted to reduce system GE by 0.810 kg CO2e/breeding cow per year per € index and system EI by 0.009 kg CO2e/kg meat per breeding cow per year per € index. These reductions were mainly driven by improvements in cow survival, reduced mature cow maintenance feed requirements, shorter calving interval and reduced offspring mortality. The T index was predicted to reduce system EI by 0.021 kg CO2e/kg meat per breeding cow per year per € index, driven by increased meat production from improvements in carcass weight, conformation and fat. Implications for incorporating an EI reduction index to the current production indexes and long-term projections for national breeding programs are discussed.

Using oocyte essential fatty acid composition to assess spawner reproductive potential under hypersaline conditions

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 584:199-212 (2017) - DOI: https://doi.org/10.3354/meps12366 Using oocyte essential fatty acid composition to assess spawner reproductive potential under hypersaline conditions Julian Döring*, Werner Ekau Leibniz Centre for Tropical Marine Research (ZMT), Fahrenheitstraße 6, 28359 Bremen, Germany *Corresponding author: julian.doering@me.com ABSTRACT: Inversion of estuaries in the dry tropics (i.e. salinity increases upstream) against the backdrop of a globally changing climate is forcing migratory clupeid fish species to adapt quickly to modifications in their spawning habitats to ensure reproductive success. Hatching success and survival probabilities of marine fish eggs and early life stages are prone to impairment under high temperature and elevated salinity conditions. Essential fatty acids affect osmoregulation in marine fish early life stages, and deficiencies can therefore be expected to cause elevated offspring mortality under hyperosmotic conditions, ultimately modifying a stock’s reproductive potential. Here we show that oocytes spawned by bonga shad Ethmalosa fimbriata inside a hypersaline estuary exhibited significantly higher 20:4 (n-6) proportions (1.6 ± 0.7% of total fatty acids) than oocytes spawned under marine conditions (0.6 ± 0.2%). Further, oocyte proportions in 20:4 (n-6), 20:5 (n‑3), and 22:6 (n-3) were positively correlated with water temperature, water salinity, and female reproductive investment (relative batch fecundity, gonado-somatic index, oocyte dry weight). Oocytes spawned during high temperature/high salinity conditions inside the estuary are therefore likely to develop normally under the prevailing conditions. Reproductive potential was determined to be highest in females spawning inside the estuary at the end of the wet season, when temperatures are high and salinities are less stressful due to freshwater input. Results lead to the conclusion that migratory clupeid fishes can maintain their reproductive potential in hypersaline estuaries and lagoons, which potentially allows for sustainable stock sizes. KEY WORDS: Arachidonic acid · Clupeidae · Fatty acids · Maternal effects · Salinity · Temperature · Inverse estuary · Reproductive investment Full text in pdf format Correction PreviousNextCite this article as: Döring J, Ekau W (2017) Using oocyte essential fatty acid composition to assess spawner reproductive potential under hypersaline conditions. Mar Ecol Prog Ser 584:199-212. https://doi.org/10.3354/meps12366 Export citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 584. Online publication date: December 07, 2017 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2017 Inter-Research.

Vagus nerve stimulation in pregnant rats and effects on inflammatory markers in the brainstem of neonates.

BackgroundVagus Nerve Stimulation (VNS) is an FDA-approved method delivering electrical impulses for treatment of depression and epilepsy in adults. The vagus nerve innervates the majority of visceral organs and cervix, but potential impacts of VNS on the progress of pregnancy and the fetus are not well studied.MethodsWe tested the hypothesis that VNS in pregnant dams does not induce inflammatory changes in the cardiorespiratory control regions of the pups’ brainstem, potentially impacting the morbidity and mortality of offspring. Pregnant dams were implanted with stimulators providing intermittent low or high frequency electrical stimulation of the sub-diaphragmatic esophageal segment of the vagus nerve for 6–7 days until delivery. After birth, we collected pup brainstems that included cardio-respiratory control regions and counted the cells labeled for pro-inflammatory cytokines (IL-1β, IL-6, TNFα) and HMGB1.ResultsNeither pup viability nor number of cells labeled for pro-inflammatory cytokines in nTS nor XII was impaired by VNS. We provide evidence suggesting that chronic VNS of pregnant mothers does not impede the progress or outcome of pregnancy.ConclusionsVNS does not cause preterm birth, affect well-being of progeny, or impact central inflammatory processes that are critical for normal cardiovascular and respiratory function in newborns.