26 research outputs found

    Coe Genes Are Expressed in Differentiating Neurons in the Central Nervous System of Protostomes

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    Genes of the coe (collier/olfactory/early B-cell factor) family encode Helix-Loop-Helix transcription factors that are widely conserved in metazoans and involved in many developmental processes, neurogenesis in particular. Whereas their functions during vertebrate neural tube formation have been well documented, very little is known about their expression and role during central nervous system (CNS) development in protostomes. Here we characterized the CNS expression of coe genes in the insect Drosophila melanogaster and the polychaete annelid Platynereis dumerilii, which belong to different subgroups of protostomes and show strikingly different modes of development. In the Drosophila ventral nerve cord, we found that the Collier-expressing cells form a subpopulation of interneurons with diverse molecular identities and neurotransmitter phenotypes. We also demonstrate that collier is required for the proper differentiation of some interneurons belonging to the Eve-Lateral cluster. In Platynereis dumerilii, we cloned a single coe gene, Pdu-coe, and found that it is exclusively expressed in post mitotic neural cells. Using an original technique of in silico 3D registration, we show that Pdu-coe is co-expressed with many different neuronal markers and therefore that, like in Drosophila, its expression defines a heterogeneous population of neurons with diverse molecular identities. Our detailed characterization and comparison of coe gene expression in the CNS of two distantly-related protostomes suggest conserved roles of coe genes in neuronal differentiation in this clade. As similar roles have also been observed in vertebrates, this function was probably already established in the last common ancestor of all bilaterians

    Ovarian pregnancy; Relationship to an intrauterine device

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    Ovarian pregnancy is a rare form of ectopic pregnancy in which the gestational sac is implanted within the ovary. The incidence is 0.5 to 3% of all ectopic gestations (1). In contrast to patients with tubal pregnancies, traditional risk factors, such as pelvic inflammatory disease and prior surgical procedure upon the pelvis, may not play a role in the aetiology. In the 2 cases reported hen, it seems that using an intrauterine contraceptive device was an important factor

    Umbilical coiling index: Is it a marker for the foetus at risk?

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    The aim of this study was to determine the relationship between-the number of coils in the umbilical cord and perinatal outcome. The umbilical cords and delivery records of 147 liveborn neonates were prospectively studied. The umbilical coiling index (UCI) of each cord was calculated by dividing the total number of complete umbilical vascular coils by the umbilical cord length, Subjects with UCIs below the 10th percentile, above the 90th percentile, and between the 10th and 90th percentiles were defined as hypocoiled, hypercoiled, and normocoiled, respectively. Several different parameters were used to measure neonatal outcome. The mean UGI was 0.20+/-10 (SD). No relationship was noted between UCI and maternal age, gravidity, parity, oligohydramnios, or birth weight, When we compared the hypocoiled group (n=30) with the normocoiled group (n=87), we detected a statistically significantly higher incidence of meconium staining, interventional delivery, apgar scores, fetal blood pH and intrapartum fetal heart rate disturbances, As a result, we concluded that the UCI has a strong relationship with perinatal outcome and may be used antenatally as a marker for identifying the fetus at risk

    Three cases of diffuse mullerian neoplasia

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    Three cases with simultaneous neoplasms in multiple sites of female reproductive tract, followed up in our university clinic are reported

    Mineralogical and geochemical evidence of late epithermal alteration in the Kisladag porphyry gold deposit, Usak, Western Turkey

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    The Kışladağ porphyry gold deposit is related to Miocene intrusive and sub-volcanic rocks that resulted from an extensional tectonic regime in western Anatolia. The main lithologies of the deposit are quartz-trachytes to quartz-latites and volcanoclastic rocks intruded by sub-volcanic porphyritic rocks. Three different intrusive phases which have been identified from their age, alteration grade and mineralization (IN-1: the oldest intrusion, intense potassic alteration, IN-2/2A: intense clay-quartz alteration, IN-3: the youngest intrusion, weak alteration). IN-1 contains quartz, illite and kaolinite, IN-2Ahas quartz, adularia, illite, kaolinite and smectite. Alunite, jarosite and tourmaline increase in IN-1 and IN-2A; whereas biotite and illite increase in IN-1 and IN-2A, respectively. The volcanoclastic rocks are composed of quartz, alunite and kaolinite/halloysite indicating advanced argillic alteration. Although the microscopic data confirms potassic and phyllic alterations in IN-1 andIN-2A, mineralogical (well crystallized 1M and poorly crystallized 1M d illite, kaolinite/halloysite, alunite, jarosite) and geochemical (K/Ar age data for different grain-sized illite indicating late overprinting at least 5 Ma) data indicate that the early stage alteration phases were overprinted by the late stage epithermal alteration

    Dysregulation of the epithelial barrier by environmental and other exogenous factors

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    The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point‐of‐care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function

    Dysregulation of the epithelial barrier by environmental and other exogenous factors

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    The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point-of-care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function
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