Structural and Biochemical Maturation of the Fetal Endocrine Pancreas
Emilio Herrera, Robert H. Knopp in Perinatal Biochemistry, 2020
The embryologic origin of the pancreatic islet cells remains a matter of considerable dispute.1 According to one of the current theories they originate from the neuroectoderm as evidenced by the expression in these cells of several molecular markers shared with certain neuronal cells. Examples of such markers are the common ability of islets and neuronal cells for amine precursor uptake and decarboxylation (APUD),2 the expression of tyrosine hydroxylase,3 and the transient expression during embryogenesis of the insulin gene in cells of the neural tube and neural crest.4 A series of other observations, however, argue against this theory and rather favor the idea that the islet cells are derived from the endoderm as it becomes established at the end of gastrulation. This latter idea is supported mainly by experiments employing the quail-chick marker system suggesting that the endocrine cells of both the gut epithelium and the pancreas originate from the endoderm.1
Maturation, Barrier Function, Aging, and Breakdown of the Blood–Brain Barrier
Shamim I. Ahmad in Aging: Exploring a Complex Phenomenon, 2017
Endothelial cells (ECs) and pericytes both contribute to the BM development and induction of the expression of integrins. The EC-derived factors, platelet-derived growth factor-BB (PDGF-BB) and heparin binding-epidermal growth factor (HB-EGF) support growth, and they are critical in tube maturation. The new vessels are formed from preexisting vessels which sprout into the embryonic neuroectoderm. The early vessels have TJs, transporters, transcytotic vesicles, and leukocyte adhesion molecules. The mature BBB vessels come into close contact with cells of the neurovascular units (NVUs) (pericytes, astroglia, neurons), transcytosis is decreased, the regulated efflux transport increased (Obermeier et al. 2013), and maturation is completed.
Clinical Considerations
Stephen W. Carmichael, Susan L. Stoddard in The Adrenal Medulla 1986 - 1988, 2017
Oppedal, Brandtzaeg and Kemshead (1987) evaluated a panel of monoclonal neuroblastoma antibodies histochemically on normal structures from the sympathetic nervous system that are known to be sites of origin of neuroblastomas and related tumors. Comparisons were made with corresponding tumors. Antigen distribution varied among normal structures such as ganglion cells, satellite cells, various nerve fibers, and different cells in the adrenal gland. The neoplasms seem to reflect the normal maturation in the structures derived from the neuroectoderm.
Giant facial congenital melanocytic nevus associated with conjunctival melanoma
Published in Orbit, 2023
Neha Shree, Arpan Gandhi, Sima Das
Congenital nevi are benign nevomelanocytic hyperpigmented macular lesions that are derivatives of the melanoblasts and are present at birth. They are formed by the overgrowth of melanocytes. They are caused by malformations of the neuroectoderm that are comprised of melanocytes and occasionally neural elements, following dysregulated growth and arrest of melanocytes during migration from the neural crest to the skin.1 Congenital melanocytic nevi have been classified into small nevi which are smaller than 1.5 cm, medium-sized congenital melanocytic nevi as those between 1.5 and 19.9 cm, and large or giant congenital melanocytic nevi as those greater than or equal to 20 cm. Giant congenital nevi are more commonly found on the posterior portion of the trunk; the face is is another common location.2 Although giant congenital nevus involving the face and eyelids and progressing to melanoma has been described in the literature,3 giant congenital facial nevus associated with conjunctival melanoma is not reported.
Huge heterotopic brain cyst of the orbit: report of a case and its management
Published in Orbit, 2022
Abbas Bagheri, Mohammad Gozin, Amirreza Veisi, Mozhgan Rezaei Kanavi
Three possible hypotheses have been proposed explaining the origin of heterotopic brain tissue. The first hypothesis is that heterotopic tissue originates from a meningoencephalocele herniated into the orbit during embryogenesis before the development of the bony cranium, and its connection is disrupted afterward. Of note, the absence of a bony defect could not rule out the possibility of this hypothesis because the defect could be anatomically closed after the cell migrations. Encephaloceles or meningoencephalocele are more common in the midline. Similarly, as the most common extracerebral heterotopic neuroglial tissue, nasal glioma is generally located in the midline.6 Residual neuroectodermal tissues with further differentiation are the second possible origin for the heterotopic brain tissue, which may be due to the defect in the separation of the surface ectoderm and neuroectoderm or early migration of the neuroglial cells. The presence of subcutaneous or retroperitoneal heterotopic neuroglial tissue and implanted neural tissue in the endometrium of the cervix of an evacuated fetus is in favor of this hypothesis.26,27 The third hypothesis is teratomatous differentiation of a germline into a specific neuronal cell line that may result in heterotopic neuroglial tissue. An example for this hypothesis is the report of a true astrocytoma in orbit.28 However, because of mature neuronal elements, lack of neoplasia, and the presence of bony defects in some patients, the first hypothesis is more widely accepted in these cases.6
Retinal Flow Density Changes in Early-stage Parkinson’s Disease Investigated by Swept-Source Optical Coherence Tomography Angiography
Published in Current Eye Research, 2021
Yifan Zhang, Dan Zhang, Yuzhu Gao, Li Yang, Yunhan Tao, Hanyue Xu, Shulei Man, Ming Zhang, Yanming Xu
The eye has been referred to as a window to the brain due to its inseparable relationship with the central nervous system (CNS).5 The retina is derived from the neuroectoderm, which shares a lot of similarities with the CNS in embryological origin, vascular supply, and stress response. Visual symptoms have been reported to occur even before neurological impairments in some degenerative diseases. Especially in PD, dry eyes, impaired contrast sensitivity, and color vision have been known to occur as non-motor manifestations of PD.6 Degeneration of the dopaminergic neurons is the landmark of PD, which is not only observed in the CNS but also exhibits in the retina.7 The degeneration of the dopaminergic neurons in the ganglion cell layer offers a reasonable explanation for the observed thinning of the retinal nerve fiber layer, ganglion cell layer, and the inner plexiform layer reported by the previous literature.8
Related Knowledge Centers
- Bone Morphogenetic Protein
- Ectoderm
- Hindbrain
- Midbrain
- Nervous System
- Neural Groove
- Neural Plate
- Neural Tube
- Noggin
- Neural Fold