Neurite Outgrowth on Electrospun Nanofibers with Uniaxial Alignment: The Effects of Fiber Density, Surface Coating, and Supporting Substrate

Distal sensory-motor polyneuropathy is one of the most frequent diabetic complications. However, few therapies address the etiology of neurodegeneration in the peripheral nervous systems of diabetic patients. Several metabolic mechanisms have been proposed as etiologies of this polyneuropathy. In this study, we revisited one of those mechanisms, the polyol pathway, and investigated the curative effects of a novel strong aldose reductase inhibitor, ranirestat, in streptozotocin-induced diabetic rats with preexisting polyneuropathy. Twelve weeks after the onset of diabetes, rats which had an established polyneuropathy were treated once daily with a placebo, ranirestat, or epalrestat, over 6 weeks. Before and after the treatment, nerve conduction velocities and thermal perception threshold of hindlimbs were examined. After the treatment, intraepidermal fiber density was evaluated. As an ex vivo assay, murine dorsal root ganglion cells were dispersed and cultured with or without 1 μmol/l ranirestat for 48 hours. After the culture, neurite outgrowth was quantified using immunological staining. Sensory nerve conduction velocity increased in diabetic rats treated with ranirestat (43.3±3.6 m/s) compared with rats treated with placebo (39.8±2.3). Motor nerve conduction velocity also increased in the ranirestat group (45.6±3.9) compared with the placebo group (38.9±3.5). The foot withdrawal latency to noxious heating was improved in the ranirestat group (17.7±0.6 seconds) compared with the placebo group (20.6±0.6). The decrease in the intraepidermal fiber density was significant in the diabetic placebo group (21.6±1.7/mm) but not significant in the diabetic ranirestat group (26.2±1.2) compared with the nondiabetic placebo group (30.3±1.5). Neurite outgrowth was promoted in the neurons supplemented with ranirestat (control 1446±147 μm/neuron, ranirestat 2175±149). Ranirestat improved the peripheral nervous dysfunctions in rats with advanced diabetic polyneuropathy. Ranirestat could have potential for regeneration in the peripheral nervous system of diabetic rats.

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Prenylated quinolinecarboxylic acid compound-18 prevents sensory nerve fiber outgrowth through inhibition of the interleukin-31 pathway

PLoS ONE ◽

10.1371/journal.pone.0246630 ◽

2021 ◽

Vol 16 (2) ◽

pp. e0246630

Author(s):

Masato Ogura ◽

Kumiko Endo ◽

Toshiyuki Suzuki ◽

Yoshimi Homma

Keyword(s):

Neurite Outgrowth ◽

Nerve Fiber ◽

Sensory Nerve ◽

Skin Lesions ◽

Janus Kinase ◽

Sensory Nerves ◽

Fiber Density ◽

Stat3 Phosphorylation ◽

Sensory Nerve Fiber ◽

Quinolinecarboxylic Acid

Interleukin-31 (IL-31) is involved in excessive development of cutaneous sensory nerves in atopic dermatitis (AD), leading to severe pruritus. We previously reported that PQA-18, a prenylated quinolinecarboxylic acid (PQA) derivative, is an immunosuppressant with inhibition of p21-activated kinase 2 (PAK2) and improves skin lesions in Nc/Nga mice as an AD model. In the present study, we investigate the effect of PQA-18 on sensory nerves in lesional skin. PQA-18 alleviates cutaneous nerve fiber density in the skin of Nc/Nga mice. PQA-18 also inhibits IL-31-induced sensory nerve fiber outgrowth in dorsal root ganglion cultures. Signaling analysis reveals that PQA-18 suppresses phosphorylation of PAK2, Janus kinase 2, and signal transducer and activator of transcription 3 (STAT3), activated by IL-31 receptor (IL-31R), resulting in inhibition of neurite outgrowth in Neuro2A cells. Gene silencing analysis for PAK2 confirms the requirement for STAT3 phosphorylation and neurite outgrowth elicited by IL-31R activation. LC/MS/MS analysis reveals that PQA-18 prevents the formation of PAK2 activation complexes induced by IL-31R activation. These results suggest that PQA-18 inhibits the IL-31 pathway through suppressing PAK2 activity, which suppresses sensory nerve outgrowth. PQA-18 may be a valuable lead for the development of a novel drug for pruritus of AD.

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Oriented collagen as a potential cochlear implant electrode surface coating to achieve directed neurite outgrowth

European Archives of Oto-Rhino-Laryngology ◽

10.1007/s00405-011-1775-8 ◽

2011 ◽

Vol 269 (4) ◽

pp. 1111-1116 ◽

Cited By ~ 8

Author(s):

Stefan Volkenstein ◽

John E. Kirkwood ◽

Edwina Lai ◽

Stefan Dazert ◽

Gerald G. Fuller ◽

...

Keyword(s):

Cochlear Implant ◽

Neurite Outgrowth ◽

Electrode Surface ◽

Surface Coating

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Exploring electrospun nanofibers for physically unclonable functions: a scalable and robust method toward unique identifiers

Journal of Physics D Applied Physics ◽

10.1088/1361-6463/ac4767 ◽

2021 ◽

Author(s):

Jing Bai ◽

Ye Tian ◽

Yinjing Wang ◽

Jiangyu Fu ◽

Yanyan Cheng ◽

...

Keyword(s):

Electrospun Nanofibers ◽

Orientation Distribution ◽

Dark Field ◽

Fiber Density ◽

Scale Invariant ◽

Optimal Point ◽

Physical Unclonable Functions ◽

Physically Unclonable Functions ◽

Mean Size ◽

Field Reflectance

Abstract Optical physical unclonable functions (PUFs) have great potentials in the security identification of Internet of Things. In this work, electrospun nanofibers are proposed as a candidate for a nanoscale, robust, stable and scalable PUF. The dark-field reflectance images of the polymer fibers are quantitatively analyzed by Hough transform. We find that the fiber length and orientation distribution reach an optimal point as the fiber density grows up over 850 in 400 x 400 pixels for a polyvinylpyrrolidone nanofiber based PUF device. Subsequently, we test the robustness and randomness of the PUF pattern by using the fiber amount as an encoding feature, generating a reconstruction success rate over 80% and simultaneously an entropy of 260 bits within a mean size of 4 cm2. A scale-invariant algorithm is adopted to identify the uniqueness of each pattern on a 256-sensor device. Furthermore, thermo-, moisture as well as photostability of the authentication process are systematically investigated by comparing polyacrylonitrile to polyvinylpyrrolidone system.

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Therapeutic Benefit of Extended Thymosinβ4 Treatment Is Independent of Blood Glucose Level in Mice with Diabetic Peripheral Neuropathy

Journal of Diabetes Research ◽

10.1155/2015/173656 ◽

2015 ◽

Vol 2015 ◽

pp. 1-13 ◽

Cited By ~ 11

Author(s):

Lei Wang ◽

Michael Chopp ◽

Longfei Jia ◽

Xuerong Lu ◽

Alexandra Szalad ◽

...

Keyword(s):

Blood Glucose ◽

Peripheral Neuropathy ◽

Sciatic Nerve ◽

Neurite Outgrowth ◽

Diabetic Peripheral Neuropathy ◽

Diabetic Mice ◽

Drg Neurons ◽

Fiber Density ◽

Intraepidermal Nerve Fiber Density

Peripheral neuropathy is a chronic complication of diabetes mellitus. To investigated the efficacy and safety of the extended treatment of diabetic peripheral neuropathy with thymosinβ4 (Tβ4), male diabetic mice (db/db) at the age of 24 weeks were treated with Tβ4 or saline for 16 consecutive weeks. Treatment of diabetic mice with Tβ4 significantly improved motor (MCV) and sensory (SCV) conduction velocity in the sciatic nerve and the thermal and mechanical latency. However, Tβ4 treatment did not significantly alter blood glucose levels. Treatment with Tβ4 significantly increased intraepidermal nerve fiber density. Furthermore, Tβ4 counteracted the diabetes-induced axon diameter and myelin thickness reductions and theg-ratio increase in sciatic nerve. In vitro, compared with dorsal root ganglia (DRG) neurons derived from nondiabetic mice, DRG neurons derived from diabetic mice exhibited significantly decreased neurite outgrowth, whereas Tβ4 promoted neurite growth in these diabetic DRG neurons. Blockage of the Ang1/Tie2 signaling pathway with a neutralized antibody against Tie2 abolished Tβ4-increased neurite outgrowth. Our data demonstrate that extended Tβ4 treatment ameliorates diabetic-induced axonal degeneration and demyelination, which likely contribute to therapeutic effect of Tβ4 on diabetic neuropathy. The Ang1/Tie2 pathway may mediate Tβ4-induced axonal remodeling.

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Quantitative Diameter Measurements of Chromatin and TMV Fibers in the Freeze-Dried State

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100102936 ◽

1988 ◽

Vol 46 ◽

pp. 170-171

Author(s):

B. D. Athey ◽

A. L. Stout ◽

M. F. Smith ◽

J. P. Langmore

Keyword(s):

Reliable Method ◽

Fiber Diameter ◽

Quantitative Agreement ◽

One Dimension ◽

Fiber Axis ◽

Two Dimensional ◽

Fiber Density ◽

Variable Diameter ◽

Freeze Dried ◽

Expected Values

Although there is general agreement that Inactive chromosome fibers consist of helically packed nucleosomes, the pattern of packing is still undetermined. Only one of the proposed models, the crossed-linker model, predicts a variable diameter dependent on the length of DNA between nucleosomes. Measurements of the fiber diameter of negatively-stained and frozen- hydrated- chromatin from Thyone sperm (87bp linker) and Necturus erythrocytes (48bp linker) have been previously reported from this laboratory. We now introduce a more reliable method of measuring the diameters of electron images of fibrous objects. The procedure uses a modified version of the computer program TOTAL, which takes a two-dimensional projection of the fiber density (represented by the micrograph itself) and projects it down the fiber axis onto one dimension. We illustrate this method using high contrast, in-focus STEM images of TMV and chromatin from Thyone and Necturus. The measured diameters are in quantitative agreement with the expected values for the crossed-linker model for chromatin structure

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