Fetal Head Compression: Its Possible Role in Neurologic Injury

It is widely assumed that fetal ischemic brain injury during labor derives almost exclusively from severe, systemic hypoxemia with marked neonatal depression and acidemia. Severe asphyxia, however, is one of several causes of perinatal neurological injury and may not be the most common;most neonates diagnosed with hypoxic-ischemic encephalopathy do not have evidence of severe asphyxia. Sepsis, direct brain trauma, and drug or toxin exposure account for some cases, while mechanical forces of labor and delivery that increase fetal intracranial pressure sufficiently to impair brain perfusion may also contribute. Because of bony compliance and mobile suture lines, the fetal skull changes shape and redistributes cerebrospinal fluid during labor according to constraints imposed by contractions, and bony and soft tissue elements of the birth canal as the head descends. These accommodations, including the increase in intracranial pressure, are adaptive and necessary for efficient descent of the head while safeguarding cerebral blood flow. Autonomic reflexes mediated through central receptors normally provide ample protection of the brain from the considerable pressure exerted on the skull. On occasion, those forces, which are transmitted intracranially, may overcome the various adaptive anatomical, cardiovascular, metabolic, and neurological mechanisms that maintain cerebral perfusion and oxygen availability, resulting in ischemic brain injury. Accepting the notion of a potentially adverse impact of fetal head compression suggests that avoidance of excessive uterine activity and of relentless pushing without steady progress in descent may offer protection for the fetal brain during parturition. Excessive head compression should be considered in the differential diagnosis of ischemic encephalopathy.

Review of deep learning and artificial intelligence models in fetal brain magnetic resonance imaging

Central nervous system abnormalities in fetuses are fairly common,happening in 0.1%to 0.2%of live births and in 3%to 6%of stillbirths.So initial detection and categorization of fetal Brain abnormalities are critical.Manually detecting and segmenting fetal brain magnetic resonance imaging(MRI)could be timeconsuming,and susceptible to interpreter experience.Artificial intelligence(AI)algorithms and machine learning approaches have a high potential for assisting in the early detection of these problems,improving the diagnosis process and follow-up procedures.The use of AI and machine learning techniques in fetal brain MRI was the subject of this narrative review paper.Using AI,anatomic fetal brain MRI processing has investigated models to predict specific landmarks and segmentation automatically.All gestation age weeks(17-38 wk)and different AI models(mainly Convolutional Neural Network and U-Net)have been used.Some models'accuracy achieved 95%and more.AI could help preprocess and postprocess fetal images and reconstruct images.Also,AI can be used for gestational age prediction(with one-week accuracy),fetal brain extraction,fetal brain segmentation,and placenta detection.Some fetal brain linear measurements,such as Cerebral and Bone Biparietal Diameter,have been suggested.Classification of brain pathology was studied using diagonal quadratic discriminates analysis,Knearest neighbor,random forest,naive Bayes,and radial basis function neural network classifiers.Deep learning methods will become more powerful as more large-scale,labeled datasets become available.Having shared fetal brain MRI datasets is crucial because there aren not many fetal brain pictures available.Also,physicians should be aware of AI's function in fetal brain MRI,particularly neuroradiologists,general radiologists,and perinatologists.

Electroacupuncture at Baihui (DU20) acupoint upregulates mRNA expression of NeuroD molecules in the brains of newborn rats suffering in utero fetal distress

Neuro D plays a key regulatory effect on differentiation of neural stem cells into mature neurons in the brain.Thus,we assumed that electroacupuncture at Baihui（DU20） acupoint in newborn rats exposed to in utero fetal distress would influence expression of Neuro D.Electroacupuncture at Baihui was performed for 20 minutes on 3-day-old（Day 3） newborn Sprague-Dawley rats exposed to in utero fetal distress;electroacupuncture parameters consisted of sparse and dense waves at a frequency of 2–10 Hz.Real-time fluorescent quantitative PCR results demonstrated that m RNA expression of Neuro D,a molecule that indicates Neuro D,increased with prolonged time in brains of newborn rats,and peaked on Day 22.The level of m RNA expression was similar between Day 16 and Day 35.These findings suggest that electro acupuncture at Baihui acupoint could effectively increase m RNA expression of molecules involved in Neuro D in the brains of newborn rats exposed to in utero fetal distress.

Oligodendrocyte pathology in fetal alcohol spectrum disorders

The pathology of fetal alcohol syndrome and the less severe fetal alcohol spectrum disorders includes brain dysmyelination.Recent studies have shed light on the molecular mechanisms underlying these white matter abnormalities.Rodent models of fetal alcohol syndrome and human studies have shown suppressed oligodendrocyte differentiation and apoptosis of oligodendrocyte precursor cells.Ethanol exposure led to reduced expression of myelin basic protein and delayed myelin basic protein expression in rat and mouse models of fetal alcohol syndrome and in human histopathological specimens.Several studies have reported increased expression of many chemokines in dysmyelinating disorders in central nervous system,including multiple sclerosis and fetal alcohol syndrome.Acute ethanol exposure reduced levels of the neuroprotective insulin-like growth factor-1 in fetal and maternal sheep and in human fetal brain tissues,while ethanol increased the expression of tumor necrosis factor α in mouse and human neurons.White matter lesions have been induced in the developing sheep brain by alcohol exposure in early gestation.Rat fetal alcohol syndrome models have shown reduced axon diameters,with thinner myelin sheaths,as well as reduced numbers of oligodendrocytes,which were also morphologically aberrant oligodendrocytes.Expressions of markers for mature myelination,including myelin basic protein,also were reduced.The accumulating knowledge concerning the mechanisms of ethanol-induced dysmyelination could lead to the development of strategies to prevent dysmyelination in children exposed to ethanol during fetal development.Future studies using fetal oligodendrocyte-and oligodendrocyte precursor cell-derived exosomes isolated from the mother's blood may identify biomarkers for fetal alcohol syndrome and even implicate epigenetic changes in early development that affect oligodendrocyte precursor cell and oligodendrocyte function in adulthood.By combining various imaging modalities with molecular studies,it may be possible to determine which fetuses are at risk and to intervene therapeutically early in the pregnancy.

An Eperimental Study on the Transplantation of Human Fetal Brain Cells into Monkey Models of Parkinson's Disease.

Unilateral administration of methly-phenyl-tetrahydropyridine(MPTP) into the common carotid artery

Identification and analysis of intermediate-size noncoding RNAs in the rhesus macaque fetal brain

Although only about 2%of the human genome has proved to be protein-coding genes,recent advances in genome wide analysis have revealed that the majority of the genome is transcribed,mainly from noncoding segments that were once considered＂junk sequences＂or＂dark matters＂（Liu et al.,2011a;Zhang et al.,2014b）. In addition to the well-characterized housekeeping non- coding RNAs （ncRNAs） （tRNA, rRNA, small nuclear RNA and small nucleolar RNAs） and some small regulatory ncRNAs （microRNAs and small interfering RNAs）, the transcriptome of mammals could also pervasively have been transcribed long noncoding RNAs （lncRNAs, at least 200 nt） （Rinn and Chang, 2012; Xie et al., 2012）.