Increase in the size of human neocortex-acquired in evolution-accounts for the unique cognitive capacity of humans. This expansion reflects the evolutionarily enhanced proliferative ability of basal progenitors (BPs), including the basal radial glia and basal intermediate progenitors (bIPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in bIP amplification and cortical expansion. Through epigenetic profiling of sorted bIPs, we show that histone H3 lysine 9 acetylation (H3K9ac) is low in murine bIPs and high in human bIPs. Elevated H3K9ac preferentially increases bIP proliferation, increasing the size and folding of the normally smooth mouse neocortex. H3K9ac drives bIP amplification by increasing expression of the evolutionarily regulated gene, Trnp1, in developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture.
Sternalis muscle is an anatomical variation of the anterior thoracic wall. Its incidence in white population is 4-7%. During a routine dissection of male cadaver, a long flat muscular structure was observed, crossing the anterior thoracic wall, which was composed of two bellies and intermediate tendon. It was located underneath the superficial thoracic fascia and superficially to pectoralis major. Superior belly was oriented parallel and merges with the fibers and fascia of right pectoralis major. Thin long intermediate tendon crossed the sternum. The inferior portion of the muscle was wider and longer than the upper one. Its fibers were oriented perpendicularly to the fibers of left pectoralis major and caudally fused with the anterior layer of the rectus abdominis sheath. The two bellies had different nerve supply by the pectoral nerve (superior belly) and anterior branches of the intercostal nerves (inferior belly). The knowledge of sternalis muscle is important for radiologists and surgeons.
Miscarriage due to fetal tumors is an extremely rare finding, with a varying incidence from 1.7 to 13.5 per 100,000 live births, with central nervous system tumors occupying a minority of these cases. Herein, we report the gross morphological and histological findings of a 17-gestational week spontaneous miscarriage in a 27 year old multi-gravida due to a fourth ventricle choroid plexus papilloma (CPP). The CPP was composed of a pronoun fibro-vascular stroma covered with a dense lining of tall cuboid sparsely ciliated single cell layer with rich in chromatin nuclei. The cytoplasm of the CPP covering cells was intensely colored when compared to the pale cytoplasm of the covering cells of the choroid plexus collected from the lateral ventricle, which also lacked in such pronoun fibrovascular stroma. The fourth ventricle was significantly dilated with parenchymal compression of nervous tissue towards the chondral fetal cranium.
PURPOSES: We aimed to investigate the presence, distribution and abundance of chicken ovalbumin upstream promoter transcription factor 1 (COUP TF1; also known as Nuclear Receptor Subfamily 2 Group F Members 1/2-NR2F1 in the germinative zones of human telencephalon during the fetal period. This transcription factor is of significance for the normal neuronal migration and differentiation of projection neurons in the mouse forebrain. MATERIALS AND METHODS: Brain tissue samples from spontaneously aborted human fetuses aged between 12 and 28 gestational weeks (g.w.) were fixed in paraformaldehyde and histologically investigated. Sections immunostained for COUP TF1 were scanned and its expression in different zones of the occipital lobe of developing pallium was evaluated. COUP-TF1 positive cells were counted and their percentage of all DAPI-stained nuclei was calculated in order to establish the abundance of the COUP-TF1-expressing cells among the total cell population. RESULTS: COUP-TF1 expression was prominent in all investigated zones of the developing human occipital lobe at stage 17 th g.w. In all zones studied, COUP-TF1 positive cells presented a relatively high fraction (~71-95%) of the cells counted with the highest value of 95.24% in the ventricular zone. CONCLUSIONS: The present data on the location, abundance and distribution pattern of COUP TF1 expressing cells in the human occipital lobe provide information on the possibility that this TF might participate to human corticogenesis, similarly to the mouse.
Increase in the size of human neocortex, acquired in evolution, accounts for the unique cognitive capacity of humans. This expansion appears to reflect the evolutionarily-enhanced proliferative ability of basal progenitors (BPs) in mammalian cortex, which may have been acquired through epigenetic alterations in BPs. However, whether or how the epigenome in BPs differs across species is not known. Here, we report that histone H3 acetylation is a key epigenetic regulation in BP amplification and cortical expansion. Through epigenetic profiling of sorted BPs, we show that H3K9 acetylation is low in murine BPs and high in human BPs. Elevated H3K9ac preferentially increases BP proliferation, increasing the size and folding of the normally smooth mouse neocortex. Mechanistically, H3K9ac drives BP amplification by increasing expression of the evolutionarily regulated gene, TRNP1, in the developing cortex. Our findings demonstrate a previously unknown mechanism that controls cortical architecture.
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