Investigation of the effects of laminin present in the basal lamina of the peripheral nervous system on axon regeneration and remyelination using the nerve acellular scaffold

2020 ◽  
Vol 108 (8) ◽  
pp. 1673-1687
Author(s):  
Wanqing Ji ◽  
Bo Hou ◽  
Hengxin Tang ◽  
Meiqin Cai ◽  
Wenhan Zheng
2018 ◽  
Vol 34 (1) ◽  
pp. 495-521 ◽  
Author(s):  
Michele Curcio ◽  
Frank Bradke

After an injury in the adult mammalian central nervous system (CNS), lesioned axons fail to regenerate. This failure to regenerate contrasts with axons’ remarkable potential to grow during embryonic development and after an injury in the peripheral nervous system (PNS). Several intracellular mechanisms—including cytoskeletal dynamics, axonal transport and trafficking, signaling and transcription of regenerative programs, and epigenetic modifications—control axon regeneration. In this review, we describe how manipulation of intrinsic mechanisms elicits a regenerative response in different organisms and how strategies are implemented to form the basis of a future regenerative treatment after CNS injury.


Author(s):  
M.E. Roke ◽  
W.F.E. Brown ◽  
D. Boughner ◽  
L.C. Ang ◽  
G.P.A. Rice

ABSTRACT:Involvement of the peripheral nervous system by amyloidosis is common. It is less well recognized that amyloid can directly infiltrate and weaken skeletal muscle. We report a case of a 73-year-old woman, known to have cardiac amyloidosis, who developed profound weakness secondary to amyloid myopathy. Review of the 8 other well documented cases in the literature has revealed a rather homogeneous syndrome. Proximal weakness, muscle stiffness, pseudohypertrophy and myalgia constitute the principal features. This syndrome usually develops in cases with well recognized generalized amyloidosis. Amyloid is deposited within the basal lamina of blood vessels and muscle fibers.


2011 ◽  
Vol 108 (15) ◽  
pp. 6282-6287 ◽  
Author(s):  
F. M. Bareyre ◽  
N. Garzorz ◽  
C. Lang ◽  
T. Misgeld ◽  
H. Buning ◽  
...  

Author(s):  
S.S. Spicer ◽  
B.A. Schulte

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.


2000 ◽  
Vol 5 (2) ◽  
pp. 3-3
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage

Abstract Lesions of the peripheral nervous system (PNS), whether due to injury or illness, commonly result in residual symptoms and signs and, hence, permanent impairment. The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides) describes procedures for rating upper extremity neural deficits in Chapter 3, The Musculoskeletal System, section 3.1k; Chapter 4, The Nervous System, section 4.4 provides additional information and an example. The AMA Guides also divides PNS deficits into sensory and motor and includes pain within the former. The impairment estimates take into account typical manifestations such as limited motion, atrophy, and reflex, trophic, and vasomotor deficits. Lesions of the peripheral nervous system may result in diminished sensation (anesthesia or hypesthesia), abnormal sensation (dysesthesia or paresthesia), or increased sensation (hyperesthesia). Lesions of motor nerves can result in weakness or paralysis of the muscles innervated. Spinal nerve deficits are identified by sensory loss or pain in the dermatome or weakness in the myotome supplied. The steps in estimating brachial plexus impairment are similar to those for spinal and peripheral nerves. Evaluators should take care not to rate the same impairment twice, eg, rating weakness resulting from a peripheral nerve injury and the joss of joint motion due to that weakness.


2004 ◽  
Author(s):  
G. Galietta ◽  
A. Capasso ◽  
A. Fortuna ◽  
F. Fabi ◽  
P. Del Basso ◽  
...  

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