OBJECTIVE: This systematic review aimed to determine the effects of maternal exposure to bisphosphonates (BPs) during pregnancy on neonatal outcomes. It aimed to disclosfe the impact of BPs on neonates and identify aspects that require further investigation.
METHODS: A comprehensive search of PubMed, Science Direct, LILACS, EMBASE, and Web of Science was conducted until August 2022, with no time restrictions. The selection criteria included studies published in English that evaluated pregnant women who were exposed to BPs.
RESULTS: From an initial pool of 2169 studies, 13 met the inclusion criteria for this systematic review. These studies collectively included 106 women (108 pregnancies) who were exposed to BPs either before orduring pregnancy. A summary of the key characteristics of the selected studies and the risk of bias assessment are provided. Exposure to BPs occurs at various stages of pregnancy, with different indications for BP treatment. The most frequently reported neonatal outcomes were spontaneous abortion, congenital malformations, hypocalcemia, preterm birth, and low birth weight.
CONCLUSIONS: Although previous reports have linked BPs before or during pregnancy with adverse neonatal outcomes, these associations should be interpreted with caution. Given the complexity of these findings, further research is necessary to provide more definitive insights to guide clinical decisions regarding the use of BPs in pregnant women.

OBJECTIVE: Organisms and cellular viability are of paramount importance to living creatures. Disruption of the balance between cell survival and apoptosis results in compromised viability and even carcinogenesis. One molecule involved in keeping this homeostasis is serum-glucocorticoid regulated kinase (SGK) 1. Emerging evidence points to a significant role of SGK1 in cell growth and survival, cell metabolism, reproduction, and life span, particularly in prenatal programming and reproductive senescence by the same token. Whether the hormone inducible SGK1 kinase is a major driver in the pathophysiological processes of prenatal programming and reproductive senescence?
METHODS: The PubMed/Medline, Web of Science, Embase/Ovid, and Elsevier Science Direct literature databases were searched for articles in English focusing on SGK1 published up to July 2023 RESULT: Emerging evidence is accumulating pointing to a pathophysiological role of the ubiquitously expressed SGK1 in the cellular and organismal viability. Under the regulation of specific hormones, extracellular stimuli, and various signals, SGK1 is involved in several biological processes relevant to viability, including cell proliferation and survival, cell migration and differentiation. In line, SGK1 contributes to the development of germ cells, embryos, and fetuses, whereas SGK1 inhibition leads to abnormal gametogenesis, embryo loss, and truncated reproductive lifespan.
CONCLUSIONS: SGK1 integrates a broad spectrum of effects to maintain the homeostasis of cell survival and apoptosis, conferring viability to multiple cell types as well as both simple and complex organisms, and thus ensuring appropriate prenatal development and reproductive lifespan.

Hyperglycemia is the diagnostic feature of diabetes mellitus (DM), and during pregnancy, hyperglycemia has numerous serious implications for organogenesis and fetal growth. Each type of DM has different neonatal implications based on pathogenesis, length of disease, and comorbidities. Currently, limited attention is given to the woman\'s type of DM when evaluating risks for neonates. The diagnosis of infant of a diabetic mother is not sufficient because of the varying pathophysiology of diabetes classifications and associated neonatal outcomes. By expanding the diagnosis to include the woman\'s classification and glucose control, maternity and neonatal care providers could develop plans of care based on potential neonatal outcomes, including anticipatory guidance for families. In this commentary, we propose a more specific diagnosis, rather than infant of a diabetic mother, to better serve these infants.

Organisms may retain nonfunctional anatomical features as a consequence of evolutionary natural selection. Resultant atavistic and vestigial anatomical structures have long been a source of perplexity. Atavism is when an ancestral trait reappears after loss through an evolutionary change in previous generations, whereas vestigial structures are remnants that are largely or entirely functionless relative to their original roles. While physicians are cognizant of their existence, atavistic and vestigial structures are rarely emphasized in anatomical curricula and can, therefore, be puzzling when discovered incidentally. In addition, the literature is replete with examples of the terms atavistic and vestigial being used interchangeably without careful distinction between them. We provide an overview of important atavistic and vestigial structures in the head, neck, and spine that can serve as a reference for anatomists and clinical neuroscientists. We review the literature on atavistic and vestigial anatomical structures of the head, neck, and spine that may be encountered in clinical practice. We define atavistic and vestigial structures and employ these definitions consistently when classifying anatomical structures. Pertinent anatomical structures are numerous and include human tails, plica semilunaris, the vomeronasal organ, levator claviculae, and external ear muscles, to name a few. Atavistic and vestigial structures are found throughout the head, neck, and spine. Some, such as human tails and branchial cysts may be clinically symptomatic. Literature reports indicate that their prevalence varies across populations. Knowledge of atavistic and vestigial anatomical structures can inform diagnoses, prevent misrecognition of variation for pathology, and guide clinical interventions.

Following a multi-disciplinary approach integrating information from several experimental models we have collected new evidence supporting, expanding and redesigning the AOP \"Disrupted laminin/int-β1 interaction leading to decreased cognitive function\". Investigations in vitro in rabbit and rat neurospheres and in vivo in mice exposed to EGCG (epigallocatechin-gallate) during neurodevelopment are combined with in vitro evaluations in neural progenitor cells overexpressing int-β1 and literature information from int-β1 deficiency models. We have discovered for the first time that neural progenitor cells from intrauterine growth restricted (IUGR) animals overexpress int-β1 at gene and protein level and due to this change in prenatal brain programming they respond differently than control neurospheres to the exposure of EGCG, a compound triggering neural progenitor cell migration alterations. We have also identified that EGCG developmental exposure has deleterious effects on neuronal branching and arborization in vitro and in vivo. Our results warn that a thorough developmental neurotoxicity characterization of this and other catechin-based food supplements is needed before recommending their consumption during pregnancy.

It is very complicated to give correct answer to the question \"How to define human life?\" Nowadays dilemmas consider the respect of human life from the birth to death involve not just biology but also other sciences like philosophy, theology, sociology, psychology, law and politics. These sciences evaluate the topic from different points of view. Integration of all of these perspectives could result with a proper definition. The principal purpose of this paper is to try to determine when a human individual begins. If this proves to be too difficult, we might have to settle for a specific stage in the reproductive process before which it would be impossible to say with any plausibility that a human individual exists. It is necessary to return the moral dimension of observation to the science of life. The point is to reconcile the universal ethical principles concerning the absolute value of life with the everyday challenges and dilemmas. It is our deepest conviction that life has an absolute value and that there always remains something indestructible and substantial in life, which may neither be evaluated by anything final, nor completely reduced to the material biological equivalent and the genetic substratum.

OBJECTIVE: Reactivation of embryonic ζ-globin is a promising strategy for genetic treatment of α-thalassaemia. However, quantification of ζ-globin as a quantitative trait in α-thalassaemia carriers and patients remains incompletely understood. In this study, we aimed to set up a reliable approach for the quantification of ζ-globin in α-thalassaemia carriers, followed by a population study to investigate its expression patterns.
METHODS: ζ-globin was purified as monomers from cord blood haemolysate of a Hb Bart\'s fetus, followed by absolute protein quantification, which was then tested by in-house ELISA system and introduced as protein standard. It was then used for large-scale quantification in peripheral blood samples from 6179 individuals. Finally, liquid chromatography-tandem mass spectrometry (LC-MS/MS) introduced as an independent validating approach by measuring ζ-globin expression in a second cohort of 141-SEA/αα carriers.
RESULTS: The ELISA system was proved sensitive in distinguishing individuals with varied extent of ζ-globin. Large scale quantitative study of this --SEA/αα carrier cohort indicated the high diversity of ζ-globin expression ranging from 0.00155 g/L to 1.48778 g/L. Significant positive correlation between ELISA and LC-MS/MS (R=0.400, p<0.001) was observed and it is more sensitive in distinguishing the samples with extreme expression of ζ-globin (R=0.650, p<0.001).
CONCLUSIONS: Our study has reported reliable approaches for the quantification of ζ-globin and presented the expression patterns of ζ-globin among the --SEA/αα carrier population, which might lay a foundation on subsequent genotype-phenotype studies on mechanisms of delayed haemoglobin switch in α-thalassaemia.

The age at onset of the association between poverty and poor health is not understood. Our hypothesis was that individuals from highest household income (HI), compared to those with lowest HI, will have increased fetal size in the second and third trimester and birth.
Second and third trimester fetal ultrasound measurements and birth measurements were obtained from eight cohorts. Results were analysed in cross-sectional two-stage individual patient data (IPD) analyses and also a longitudinal one-stage IPD analysis.
The eight cohorts included 21 714 individuals. In the two-stage (cross-sectional) IPD analysis, individuals from the highest HI category compared with those from the lowest HI category had larger head size at birth (mean difference 0.22 z score (0.07, 0.36)), in the third trimester (0.25 (0.16, 0.33)) and second trimester (0.11 (0.02, 0.19)). Weight was higher at birth in the highest HI category. In the one-stage (longitudinal) IPD analysis which included data from six cohorts (n=11 062), head size was larger (mean difference 0.13 (0.03, 0.23)) for individuals in the highest HI compared with lowest category, and this difference became greater between the second trimester and birth. Similarly, in the one-stage IPD, weight was heavier in second highest HI category compared with the lowest (mean difference 0.10 (0 .00, 0.20)) and the difference widened as pregnancy progressed. Length was not linked to HI category in the longitudinal model.
The association between HI, an index of poverty, and fetal size is already present in the second trimester.

Consistent with cumulative risk hypotheses of psychopathology, studies examining prenatal adversity and later mental health largely suggest that pre and postnatal stress exposures have summative effects. Fewer data support that a mismatch in stress levels between pre- and postnatal life increases risk (the mismatch hypothesis). In this retrospective cohort study using data from the 1983 Ontario Child Health Study (OCHS), we examined interactions between birth weight status and childhood/adolescent stress to predict major depression in adulthood. Ninety-five participants born at low birth weight (LBW; <2500 g) and 972 normal birth weight (NBW) control participants completed the Composite International Diagnostic Interview Short-Form Major Depression module at 21-34 years of age. A youth risk scale consisting of five stressful exposures (family dysfunction, socioeconomic disadvantage, parental criminality, maternal mental illness, exposure to other life stresses) indexed child/adolescent adversity. Birth weight groups did not differ by childhood risk score nor depression levels. A significant interaction was observed between birth weight and the youth risk scale whereby exposure to increasing levels of exposure to childhood/adolescent adversity predicted increased levels of depression in the NBW group, but lower rates in those born at LBW. Consistent with the mismatch hypothesis, data from a large, longitudinally followed cohort suggest that the mental health of adults born LBW may be more resilient to the adverse effects of childhood/adolescent stress. Taken in the context of previous studies of low birth weight infants, these findings suggest that the nature of associations between gestational stress and later mental health may depend on the magnitude of prenatal stress exposure, as well as the degree of resilience and/or plasticity conferred by their early-life environment.

OBJECTIVE: The goal of this systematic-review and meta-analysis was to assess whether high maternal stress during pregnancy is associated with the development of pediatric pathology.
METHODS: Epidemiological peer-reviewed studies published in English or Spanish assessing associations between maternal stress during pregnancy and psychiatric and medical diseases were selected.
METHODS: We retrieved 73,024 citations; 42 studies meeting inclusion criteria were assessed. Overall sample included 65,814,076 women.
RESULTS: Overall odds ratio for the development of a medical disease was OR=1.24 (CI95=1.11, 1.39), Z=3.85, p<.01. Overall odds ratio for psychiatric disorders was OR=1.28 (CI95=1.06, 1.56), Z=2.54, p<.02. Multivariate meta-analysis showed a significant coefficient for autism spectrum disorder studies, B=0.42, SE=0.16, Z=2.67, p<.01. We found a significant overall effect size for autism spectrum disorder (OR=1.45 [CI95=1.24, 1.70], Z=4.69, p<.01). In terms of medical diseases, studies including obesity and infantile colic presented a significant overall effect size, as OR=1.20 (CI95=1.03, 1.39), Z=2.41, p<.02. The highest effect size was found regarding the first trimester (B=1.62, SE=0.16, Z=9.90, p<.01).
CONCLUSIONS: We concluded that exposure to high levels of stress during pregnancy are associated with autism spectrum disorder, obesity, and infantile colic in offspring.
CONCLUSIONS: Maternal stress during pregnancy should be addressed to tackle its potential impact in health across the life span.