J1-160 and J1-180 are oligodendrocyte-secreted nonpermissive substrates for cell adhesion.

The glia-derived J1 extracellular matrix glycoproteins have been referred to as J1-160/J1-180 (the developmentally late appearing lower molecular weight group) and J1-200/J1-220 (the developmentally early appearing higher molecular group immunochemically related to tenascin). Members of the two groups show distinct cross-reactivities. To characterize the structural and functional differences between these J1 glycoproteins, two monoclonal antibodies were generated which recognize only the members of the lower molecular weight group. The two antibodies detect immunochemical similarities among the members of the lower molecular weight group, but do not react with J1/tenascin. J1-160 and J1-180 are specifically expressed by differentiated oligodendrocytes in culture and by myelin of the central nervous system and have not been found in the peripheral nervous system nor in any other organ of the adult mice tested. Electron microscopic examination of rotary-shadowed J1-160 and J1-180 reveals, respectively, dimeric and trimeric (tribrachion) kink-armed rodlike structures, which are linked by disulfide bridges. J1-160/J1-180 are nonpermissive substrates for the attachment and spreading of early postnatal small cerebellar neurons, astrocytes, and fibroblasts. In a mixture with laminin, J1-160/J1-180 are nonpermissive substrates for neurons, but not for astrocytes or fibroblasts. The repulsive effect toward neurons can be neutralized by one of the monoclonal antibodies, but not by the other. These observations are discussed in the context of cell interactions during regeneration in the mammalian nervous system.

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Permeability Enhancing and Chemotactic Activities of Lower Molecular Weight Degradation Products of Human Fibrinogen

Thrombosis and Haemostasis ◽

10.1055/s-0038-1650136 ◽

1981 ◽

Vol 45 (01) ◽

pp. 090-094 ◽

Cited By ~ 52

Author(s):

Katsuo Sueishi ◽

Shigeru Nanno ◽

Kenzo Tanaka

Keyword(s):

Molecular Weight ◽

Degradation Products ◽

Electron Microscopic Observation ◽

Chemotactic Activity ◽

Lower Molecular Weight ◽

Electron Microscopic ◽

Human Fibrinogen ◽

Rabbit Skin ◽

Molecular Weights ◽

Active Fragments

SummaryFibrinogen degradation products were investigated for leukocyte chemotactic activity and for enhancement of vascular permeability. Both activities increased progressively with plasmin digestion of fibrinogen. Active fragments were partially purified from 24 hr-plasmin digests. Molecular weights of the permeability increasing and chemotactic activity fractions were 25,000-15,000 and 25,000 respectively. Both fractions had much higher activities than the fragment X, Y, D or E. Electron microscopic observation of the small blood vessels in rabbit skin correlated increased permeability with the formation of characteristic gaps between adjoining endothelial cells and their contraction.These findings suggest that lower molecular weight degradation products of fibrinogen may be influential in contributing to granulocytic infiltration and enhanced permeability in lesions characterized by deposits of fibrin and/or fibrinogen.

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The electron microscopic autoradiographic localization of α-bungarotoxin binding sites within the central nervous system of the rat

Brain Research ◽

10.1016/0006-8993(78)90185-3 ◽

1978 ◽

Vol 142 (1) ◽

pp. 152-159 ◽

Cited By ~ 87

Author(s):

Stephen P. Hunt ◽

Jakob Schmidt

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Binding Sites ◽

Electron Microscopic ◽

The Central Nervous System

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Anti-programmed cell death-1 (PD-1) monoclonal antibodies involve reversible cranial dura matter

Oxford Medical Case Reports ◽

10.1093/omcr/omab077 ◽

2021 ◽

Vol 2021 (9) ◽

Author(s):

Hiroshi Kataoka ◽

Daisuke Shimada ◽

Hitoki Nanaura ◽

Kazuma Sugie

Keyword(s):

Central Nervous System ◽

Cell Death ◽

Nervous System ◽

Monoclonal Antibodies ◽

Programmed Cell Death ◽

Adverse Effects ◽

Neuromuscular Disorders ◽

Neurological Complications ◽

Programmed Cell Death 1 ◽

The Central Nervous System

ABSTRACT This case is the first document to describe a patient receiving anti-programmed cell death 1 (PD-1) antibodies which showed cranial dura matter involvement. According to the increasing use of anti-PD-1 monoclonal antibodies, adverse effects can occur in several organs since its ligand PD-L1 and PD-L2 are expressed in a wide variety of tissues. The estimated rate of neurological complications is 1–4.2% of patients, and neuromuscular disorders are the most common. Adverse effects on the central nervous system including encephalitis are less frequent. Here, a patient receiving anti-PD-1 antibodies showed cranial dura matter involvement, and the dura enhancement on MRI was resolved by withdrawal of the treatment with anti-PD-1 antibodies only.

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Immunology of Multiple Sclerosis

10.1093/med/9780199341016.003.0004 ◽

2016 ◽

Author(s):

Laura Piccio ◽

Anne H. Cross

Keyword(s):

Multiple Sclerosis ◽

Central Nervous System ◽

Nervous System ◽

Monoclonal Antibodies ◽

B Lymphocytes ◽

Autoimmune Disorder ◽

Innate Immune ◽

Immune Systems ◽

The Central Nervous System ◽

Multiple Sclerosis Treatment

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system that targets myelin but affects both white matter and gray matter. Multiple sclerosis is thought to be mediated by cells of the adaptive and innate immune systems. CD4+ T lymphocytes of the Th1 and Th17 subtypes are believed to be critical for the initiation of multiple sclerosis. Treatment with monoclonal antibodies that deplete B lymphocytes has proven that B cells are critical to relapse development in multiple sclerosis. While immunopathophysiology is clearly important in MS, whether multiple sclerosis is truly an autoimmune disorder and the target or targets of the autoimmunity remain unknown.

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Edward George Gray. 11 January 1924 – 14 August 1999

Biographical Memoirs of Fellows of the Royal Society ◽

10.1098/rsbm.2002.0009 ◽

2002 ◽

Vol 48 ◽

pp. 151-165

Author(s):

R.W. Guillery

Keyword(s):

Nervous System ◽

Three Dimensional ◽

Electron Microscopic ◽

Early Application ◽

Microscopic Appearance ◽

Wide Range ◽

Neural Tissues ◽

Synaptic Junctions ◽

The Central Nervous System ◽

Electron Microscopic Appearance

George Gray was an early contributor to our knowledge of the electron microscopic appearance of the central nervous system. He was skilful with the difficult techniques for preparing the tissues, worked rapidly, and was an astute observer. Sitting with him in the dark, staring at a dim image that George was moving rapidly as he searched for significant detail, could be an exciting experience. He had clear ideas about features that mattered and could quickly relate the two-dimensional electron microscopic images to the three-dimensional neural structures under investigation. He is best known for his detailed and perceptive description of synaptic junctions in the mammalian neocortex, and his name is still linked to two distinct junctional types (Gray's type 1 and Gray's type 2), now recognized as generally distinguishing excitatory from inhibitory junctions. He studied a wide range of neural tissues, played a significant role in the early isolation of ‘synaptosomes’, contributed greatly to the rapid advance of knowledge that accompanied the early application of the electron microscope to neural tissues, and influenced a great many later fine-structural studies of the nervous system.

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