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Molds
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Another study reported elevated levels of neural auto-antibodies and elevated rates of abnormal nerve conduction velocities in a group of 119 patients with chronic health complaints and proven environmental mold exposure in their homes or workplaces.120 These 119 mold exposed patients had a significantly higher rate of auto-antibodies to many nerve proteins compared with a group of 500 controls. Significantly elevated neural auto-antibodies were reported for the following antigens: myelin basic protein, myelin-associated glycoprotein, myelin oligodendrocyte, glycoprotein, glutamate, tubulin, chondroitan sulfate, and neurofilament antigen. Peripheral nerve studies were also made on these 119 mold exposed patients. Abnormal motor and sensory nerve conduction was reported in 55 patients (46%), abnormal motor conduct ion only in 17 patients (14%), abnormal sensory conduction only in 27 patients (23%), and normal nerve conduction in 20 patients (17%).120
Neural Stem Cells and Oligodendrocyte Progenitors in the Central Nervous System
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Jennifer A. Jackson, Diana L. Clarke
The mature oligodendrocyte is characterized by the expression of myelin basic protein (MBP), myelin associated-glycoprotein (MAG) and myelin proteolipid protein (PLP). In vitro analyses suggest that maturation of oligodendrocytes from the precursor stage to the mature cell is identical in culture, even in the absence of neurons, as in intact tissue. Thus the capacity of oligodendrocyte progenitors to differentiate into oligodendrocytes is intrinsic to the lineage.36 However, co-culture with neurons increases myelin gene expression, such as PLP, MBP and MAG.
Environmental factors contribute to skeletal muscle and spinal cord regeneration
Published in David M. Gardiner, Regenerative Engineering and Developmental Biology, 2017
Ophelia Ehrlich, Yona Goldshmit, Peter Currie
The main inhibitory molecules for axonal regeneration after brain injury or SCI that are found in the mammals are myelin debris proteins (myelin-associated glycoprotein [MAG], Nogo-A, and oligodendrocyte myelin glycoprotein [OMgp]), CSPGs, and chemorepulsive guidance molecules (ephrins and semaphorins) (Giger et al. 2010; Rasmussen and Sagasti 2016).
Modulation of myelin formation by combined high affinity with extracellular matrix structure of electrospun silk fibroin nanoscaffolds
Published in Journal of Biomaterials Science, Polymer Edition, 2019
Sha Liu, Changmei Niu, Ziqi Xu, Yingyu Wang, Yunyun Liang, Ying Zhao, Yahong Zhao, Yumin Yang
To further confirm that myelination was expressed, we performed immunofluorescence staining with MAG (red) and NF-200 (green) to examine myelination (Figure 6). Myelin-associated glycoprotein (MAG) is selectively localized in periaxonal Schwann cell membranes and oligodendroglial membranes of myelin sheaths where it function in glia-axon interactions [14]. MAG is a cell adhesion molecule for postnatal neural development and is thought to be involved in the process of myelination. The segregation of MAG staining in the DRG neurons of the SF could be observed, indicating the formation of myelin sheath. However, MAG staining of the control showed the morphology of Schwann cells, suggesting that axons and Schwann cells have not formed myelin yet.