scholarly journals Placental Dysfunction in Assisted Reproductive Pregnancies: Perinatal, Neonatal and Adult Life Outcomes

2022 ◽  
Vol 23 (2) ◽  
pp. 659
Author(s):  
Claudio Manna ◽  
Valentina Lacconi ◽  
Giuseppe Rizzo ◽  
Antonino De Lorenzo ◽  
Micol Massimiani

Obstetric and newborn outcomes of assisted reproductive technology (ART) pregnancies are associated with significative prevalence of maternal and neonatal adverse health conditions, such as cardiovascular and metabolic diseases. These data are interpreted as anomalies in placentation involving a dysregulation of several molecular factors and pathways. It is not clear which extent of the observed placental alterations are the result of ART and which originate from infertility itself. These two aspects probably act synergically for the final obstetric risk. Data show that mechanisms of inappropriate trophoblast invasion and consequent altered vascular remodeling sustain several clinical conditions, leading to obstetric and perinatal risks often found in ART pregnancies, such as preeclampsia, fetal growth restriction and placenta previa or accreta. The roles of factors such as VEGF, GATA3, PIGF, sFLT-1, sEndoglin, EGFL7, melatonin and of ART conditions, such as short or long embryo cultures, trophectoderm biopsy, embryo cryopreservation, and supraphysiologic endometrium preparation, are discussed. Inflammatory local conditions and epigenetic influence on embryos of ART procedures are important research topics since they may have important consequences on obstetric risk. Prevention and treatment of these conditions represent new frontiers for clinicians and biologists involved in ART, and synergic actions with researchers at molecular levels are advocated.

2020 ◽  
Vol 20 (15) ◽  
pp. 1353-1397 ◽  
Author(s):  
Abhishek Wadhawan ◽  
Mark A. Reynolds ◽  
Hina Makkar ◽  
Alison J. Scott ◽  
Eileen Potocki ◽  
...  

Increasing evidence incriminates low-grade inflammation in cardiovascular, metabolic diseases, and neuropsychiatric clinical conditions, all important causes of morbidity and mortality. One of the upstream and modifiable precipitants and perpetrators of inflammation is chronic periodontitis, a polymicrobial infection with Porphyromonas gingivalis (P. gingivalis) playing a central role in the disease pathogenesis. We review the association between P. gingivalis and cardiovascular, metabolic, and neuropsychiatric illness, and the molecular mechanisms potentially implicated in immune upregulation as well as downregulation induced by the pathogen. In addition to inflammation, translocation of the pathogens to the coronary and peripheral arteries, including brain vasculature, and gut and liver vasculature has important pathophysiological consequences. Distant effects via translocation rely on virulence factors of P. gingivalis such as gingipains, on its synergistic interactions with other pathogens, and on its capability to manipulate the immune system via several mechanisms, including its capacity to induce production of immune-downregulating micro-RNAs. Possible targets for intervention and drug development to manage distal consequences of infection with P. gingivalis are also reviewed.


Author(s):  
Analia Lorena Tomat ◽  
Francisco Javier Salazar

AbstractA substantial body of epidemiological and experimental evidence suggests that a poor fetal and neonatal environment may “program” susceptibility in the offspring to later development of cardiovascular, renal and metabolic diseases.This review focuses on current knowledge from the available literature regarding the mechanisms linking an adverse developmental environment with an increased risk for cardiovascular, renal and metabolic diseases in adult life. Moreover, this review highlights important sex-dependent differences in the adaptation to developmental insults.Developmental programming of several diseases is secondary to changes in different mechanisms inducing important alterations in the normal development of several organs that lead to significant changes in birth weight. The different diseases occurring as a consequence of an adverse environment during development are secondary to morphological and functional cardiovascular and renal changes, to epigenetic changes and to an activation of several hormonal and regulatory systems, such as angiotensin II, sympathetic activity, nitric oxide, COX2-derived metabolites, oxidative stress and inflammation. The important sex-dependent differences in the developmental programming of diseases seem to be partly secondary to the effects of sex hormones. Recent studies have shown that the progression of these diseases is accelerated during aging in both sexes.The cardiovascular, renal and metabolic diseases during adult life that occur as a consequence of several insults during fetal and postnatal periods are secondary to multiple structural and functional changes. Future studies are needed in order to prevent the origin and reduce the incidence and consequences of developmental programmed diseases.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Liyuan Zhou ◽  
Lin Kang ◽  
Xinhua Xiao ◽  
Lijing Jia ◽  
Qian Zhang ◽  
...  

The prevalence of diabetes mellitus (DM) has been increasing dramatically worldwide, but the pathogenesis is still unknown. A growing amount of evidence suggests that an abnormal developmental environment in early life increases the risk of developing metabolic diseases in adult life, which is referred to as the “metabolic memory” and the Developmental Origins of Health and Disease (DOHaD) hypothesis. The mechanism of “metabolic memory” has become a hot topic in the field of DM worldwide and could be a key to understanding the pathogenesis of DM. In recent years, several large cohort studies have shown that shift workers have a higher risk of developing type 2 diabetes mellitus (T2DM) and worse control of blood glucose levels. Furthermore, a maternal high-fat diet could lead to metabolic disorders and abnormal expression of clock genes and clock-controlled genes in offspring. Thus, disorders of circadian rhythm might play a pivotal role in glucose metabolic disturbances, especially in terms of early adverse nutritional environments and the development of metabolic diseases in later life. In addition, as a peripheral clock, the gut microbiota has its own circadian rhythm that fluctuates with periodic feeding and has been widely recognized for its significant role in metabolism. In light of the important roles of the gut microbiota and circadian clock in metabolic health and their interconnected regulatory relationship, we propose that the “gut microbiota-circadian clock axis” might be a novel and crucial mechanism to decipher “metabolic memory.” The “gut microbiota-circadian clock axis” is expected to facilitate the future development of a novel target for the prevention and intervention of diabetes during the early stage of life.


Author(s):  
Tony McShane ◽  
Peter Clayton ◽  
Michael Donaghy ◽  
Robert Surtees

Various disorders result from genetically determined abnormalities of enzymes, the metabolic consequences of which affect the development or functioning of the nervous system. The range of metabolic disturbances is wide, as is the resultant range of clinical syndromes. Although most occur in children, some can present in adult life, and increasing numbers of affected children survive into adult life. In some, specific treatments are possible or are being developed. The last 20 years has seen a considerable expansion in our understanding of the genetic and metabolic basis for many neurological conditions. Particular clinical presentations of neurometabolic disorders include ataxias, movement disorders, childhood epilepsies, or peripheral neuropathy. Detailed coverage of the entire range of inherited metabolic diseases of the nervous system is available in other texts (Brett 1997; Scriver et al. 2001; Menkes et al. 2005).Treatment is possible for some metabolic diseases. For instance, the devastating neurological effects of phenylketonuria have been recognized for many years. Neonatal screening for this disorder and dietary modification in the developed world has removed phenylketonuria from the list of important causes of serious neurological disability in children. This success has led to new challenges in the management of the adult with phenylketonuria and unexpected and devastating effect of the disorder on the unborn child of an untreated Phenylketonuria mother. More recently Biotinidase deficiency has been recognized as an important and easily treatable cause of serious neurological disease usually presenting with early onset drug resistant seizures. This and some other neurometabolic diseases can be identified on neonatal blood screening although a full range of screening is not yet routine in the United Kingdom. More disorders are likely to be picked up at an earlier asymptomatic stage as the sophistication of screening tests increases (Wilcken et al. 2003; Bodamer et al. 2007).Although individual metabolic disorders are rare, collectively such disorders are relatively common. In reality most clinicians will see an individual condition only rarely in a career. Furthermore, patients with certain rare conditions are often concentrated in specialist referral centres, further reducing the exposure of general and paediatric neurologists to these disorders. A recent study into progressive intellectual and neurological deterioration, PIND, gives some information about the relative frequency and distribution of some childhood neurodegenerative diseases in the United Kingdom (Verity et al. 2000; Devereux et al. 2004). Although primarily designed to identify any childhood cases of variant Creutzfeldt- Jakob disease, the study also provided much information about the distribution of neurometabolic disease in children in the United Kingdom. The commonest five causes of progressive intellectual and neurological deterioration over 5 years were Sanfilippo syndrome, 41 cases, adrenoleukodystrophy, 32 cases, late infantile neuronal ceroid lipofuschinosis, 32 cases, mitochondrial cytopathy, 30 cases, and Rett syndrome, 29 cases. Notably, geographical foci of these disorders were also found and correlate with high rate of consanguinity in some local populations.


2020 ◽  
pp. jech-2019-213572
Author(s):  
Linda Aurpibul ◽  
Éadaoin M Butler ◽  
Antika Wongthanee ◽  
Amaraporn Rerkasem ◽  
Sakda Pruenglampoo ◽  
...  

BackgroundThere is a growing body of evidence showing that early life events are associated with increased risk of cardiovascular and metabolic diseases later in adult life. However, there is a paucity of data in this field from Asian populations. In this study, we examined the association of birth order with obesity risk and cardiometabolic outcomes in young adults in Thailand.MethodsParticipants were the offspring from a birth cohort study in Chiang Mai (northern Thailand), who were followed up at ~20.5 years of age. Clinical assessments included anthropometry, blood pressure, fasting blood samples and carotid intima-media thickness. Insulin sensitivity was estimated using homeostatic model assessment of insulin resistance (HOMA-IR). Participants were stratified into two groups: first-borns and later-borns. Health outcomes between groups were compared using multivariable models adjusting for important confounders, in particular maternal body mass index (BMI).ResultsA total of 559 participants were studied: 316 first-borns (46% males) and 243 later-borns (47% males). Adjusted models showed anthropometric differences, with first-borns being 2.3 kg heavier (p=0.023) with a BMI 0.86 kg/m2 greater (p=0.019) than later-borns. Thus, rates of obesity were higher in first-borns than in later-borns (6.6% vs 2.9%), so that first-borns had an adjusted relative risk of obesity 3.3 times greater than later-borns [95% CI 1.42 to 7.88; p=0.006]. There were no observed differences in cardiovascular or metabolic parameters assessed, including HOMA-IR.ConclusionAs observed in other populations, first-borns in Thailand had greater BMI and an increased risk of obesity in young adulthood. However, we observed no other cardiometabolic differences between first- and later-borns.


1979 ◽  
Author(s):  
W.E. Hathaway ◽  
R.R. Montgomery

For the past several years, factor VIII assays have been performed on the same sample of plasma by the partial thromboplastin time method (PTT-VIII) and the thromboplastin generation time method (TGT-VIII) in a variety of clinical conditions. Mean (range) values for representative subject groups are given.The methods compare well in inflammatory and metabolic diseases like diabetes and nephrosis. However, higher PTT-VIII values are seen in vasculitis, sickle cell disease, the hemolytic-uremic syndrome, thrombosis, and DIC. Lower values for VIII activity were seen by VIII-TGT in a group of vWd variant patients. Obligate carriers of hemophilia were best detected by the VIII-PTT. Lower than expected values for factor VIII were demonstrated in Intensively transfused hemophiliacs by the VIII-PTT. These studies indicate that the level of factor VIII procoagulant activity is significantly different in many clinical situations depending upon the method of measurement.


2016 ◽  
Vol 53 (6) ◽  
pp. 873-890 ◽  
Author(s):  
Olivier Bargain ◽  
Jinan Zeidan
Keyword(s):  

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