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Richard B. Borgens

Bio: Richard B. Borgens is an academic researcher from Purdue University. The author has contributed to research in topics: Spinal cord & Spinal cord injury. The author has an hindex of 49, co-authored 125 publications receiving 6136 citations.


Papers
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Journal ArticleDOI
20 Aug 1982-Science
TL;DR: The regrowth reported here in mice is probably similar to the scattered clinical reports of fingertips regeneration in children, and presents a model system with which to explore the controls of wound healing and tissue reconstruction in mammals.
Abstract: Mice will replace the tip of a foretoe when it is amputated distal to the last interphalangeal joint. Amputation of the digit more proximal to the joint does not result in regrowth of the foretoe. Though this growth shares certain similarities with the epimorphic regeneration of amphibian limbs, the two processes are not the same. The regrowth reported here in mice is probably similar to the scattered clinical reports of fingertips regeneration in children, and presents a model system with which to explore the controls of wound healing and tissue reconstruction in mammals.

226 citations

Journal ArticleDOI
07 Aug 1981-Science
TL;DR: Enhanced regeneration was observed in the severed giant reticulospinal neurons and processes from giant axons with swollen irregular tips, indicating active growth, were seen in or across the spinal lesion in most of the electrically treated animals.
Abstract: After a weak, steady electric current of approximately 10 microamperes was imposed across the completely severed spinal cord of the larval lamprey Petromyzon marinus, enhanced regeneration was observed in the severed giant reticulospinal neurons. The current was applied with implanted wick electrodes for 5 to 6 days after transection (cathode distal to lesion). The spinal cords were examined 44 to 63 days after the operation by means of intracellular fluorescent dye injections and electrophysiology. Extracellular stimulation of whole cords showed that action potentials in most of the electrically treated preparations were conducted in both directions across the lesion, but they were not conducted in either direction in most of the sham-treated controls. In most of the electrically treated animals, processes from giant axons with swollen irregular tips, indicating active growth, were seen in or across the lesion. Only a few of the sham-treated controls showed these features. It is possible that these facilitated regenerative responses were mediated by the effects of the artificially applied electric fields on the natural steady current of injury entering the spinal lesion.

200 citations

Journal ArticleDOI
TL;DR: Electrical currents near regenerating newt limbs were measured with a recently developed vibrating probe and suggest that the endogenous stump currents play some causal role in initiating regeneration of amputated adult frog limbs.
Abstract: Electrical currents near regenerating newt limbs were measured with a recently developed vibrating probe. Steady currents with local surface densities of 10 to 100 muA/cm2 or more leave the end of the stump during the first 5-10 days after amputation and are balanced by currents with densities of only 1-3 muA/cm2 that enter the intact skin around the stump. They are immediately dependent upon the entry of sodium ions into this skin and are therefore inferred to be skin-driven. The outward currents are comparable in direction, density, duration, and position to artificially imposed currents previously found sufficient to induce significant regeneration of amputated adult frog limbs. This comparison suggests that the endogenous stump currents play some causal role in initiating regeneration.

170 citations

Journal ArticleDOI
TL;DR: A more comprehensive and inclusive discussion of secondary injury is provided, especially in studies of the central nervous system (CNS), without attempts to place the molecular events in the context of progressive systemic and tissue-level changes.
Abstract: Secondary injury is a term applied to the destructive and self-propagating biological changes in cells and tissues that lead to their dysfunction or death over hours to weeks after the initial insult (the “primary injury”). In most contexts, the initial injury is usually mechanical. The more destructive phase of secondary injury is, however, more responsible for cell death and functional deficits. This subject is described and reviewed differently in the literature. To biomedical researchers, systemic and tissue-level changes such as hemorrhage, edema, and ischemia usually define this subject. To cell and molecular biologists, “secondary injury” refers to a series of predominately molecular events and an increasingly restricted set of aberrant biochemical pathways and products. These biochemical and ionic changes are seen to lead to death of the initially compromised cells and “healthy” cells nearby through necrosis or apoptosis. This latter process is called “bystander damage.” These viewpoints ...

170 citations

Journal ArticleDOI
TL;DR: Using an in vitro guinea pig spinal cord injury model, polyethylene glycol (PEG), a hydrophilic polymer, can significantly accelerate and enhance the membrane resealing process to restore membrane integrity following controlled compression, suggesting membrane repair to be an effective target in reducing ROS genesis.
Abstract: Membrane disruption and the production of reactive oxygen species (ROS) are important factors causing immediate functional loss, progressive degeneration, and death in neurons and their processes after traumatic spinal cord injury. Using an in vitro guinea pig spinal cord injury model, we have shown that polyethylene glycol (PEG), a hydrophilic polymer, can significantly accelerate and enhance the membrane resealing process to restore membrane integrity following controlled compression. As a result of PEG treatment, injury-induced ROS elevation and lipid peroxidation (LPO) levels were significantly suppressed. We further show that PEG is not an effective free radical scavenger nor does it have the ability to suppress xanthine oxidase, a key enzyme in generating superoxide. These observations suggest that it is the PEG-mediated membrane repair that leads to ROS and LPO inhibition. Furthermore, our data also imply an important causal effect of membrane disruption in generating ROS in spinal cord injury, suggesting membrane repair to be an effective target in reducing ROS genesis.

167 citations


Cited by
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01 Jan 2010
TL;DR: In this paper, the authors describe a scenario where a group of people are attempting to find a solution to the problem of "finding the needle in a haystack" in the environment.
Abstract: 中枢神経系疾患の治療は正常細胞(ニューロン)の機能維持を目的とするが,脳血管障害のように機能障害の原因が細胞の死滅に基づくことは多い.一方,脳腫瘍の治療においては薬物療法や放射線療法といった腫瘍細胞の死滅を目標とするものが大きな位置を占める.いずれの場合にも,細胞死の機序を理解することは各種病態や治療法の理解のうえで重要である.現在のところ最も研究の進んでいる細胞死の型はアポトーシスである.そのなかで重要な位置を占めるミトコンドリアにおける反応および抗アポトーシス因子について概要を紹介する.

2,716 citations

Journal ArticleDOI
18 Jan 1990-Nature
TL;DR: The capacity for CNS axons to regenerate and elongate within differentiated CNS tissue after the neutralization of myelin-associated neurite growth inhibitors is demonstrated.
Abstract: After lesions in the differentiated central nervous system (CNS) of higher vertebrates, interrupted fibre tracts do not regrow and elongate by more than an initial sprout of approximately 1 mm. Transplantations of pieces of peripheral nerves into various parts of the CNS demonstrate the widespread capability of CNS neurons to regenerate lesioned axons over long distances in a peripheral nerve environment. CNS white matter, cultured oligodendrocytes (the myelin-producing cells of the CNS), and CNS myelin itself, are strong inhibitors of neuron growth in culture, a property associated with defined myelin membrane proteins of relative molecular mass (Mr) 35,000 (NI-35) and 250,000 (NI-250). We have now intracerebrally applied the monoclonal antibody IN-1, which neutralizes the inhibitory effect of both these proteins, to young rats by implanting antibody-producing tumours. In 2-6-week-old rats we made complete transections of the cortico-spinal tract, a major fibre tract of the spinal cord, the axons of which originate in the motor and sensory neocortex. Previous studies have shown a complete absence of cortico-spinal tract regeneration after the first postnatal week in rats, and in adult hamsters and cats. In IN-1-treated rats, massive sprouting occurred at the lesion site, and fine axons and fascicles could be observed up to 7-11 mm caudal to the lesion within 2-3 weeks. In control rats, a similar sprouting reaction occurred, but the maximal distance of elongation rarely exceeded 1 mm. These results demonstrate the capacity for CNS axons to regenerate and elongate within differentiated CNS tissue after the neutralization of myelin-associated neurite growth inhibitors.

1,320 citations

Journal ArticleDOI
TL;DR: The nervous system physiology, the factors that are critical for nerve repair, and the current approaches that are being explored to aid peripheral nerve regeneration and spinal cord repair are reviewed.
Abstract: Nerve regeneration is a complex biological phenomenon. In the peripheral nervous system, nerves can regenerate on their own if injuries are small. Larger injuries must be surgically treated, typically with nerve grafts harvested from elsewhere in the body. Spinal cord injury is more complicated, as there are factors in the body that inhibit repair. Unfortunately, a solution to completely repair spinal cord injury has not been found. Thus, bioengineering strategies for the peripheral nervous system are focused on alternatives to the nerve graft, whereas efforts for spinal cord injury are focused on creating a permissive environment for regeneration. Fortunately, recent advances in neuroscience, cell culture, genetic techniques, and biomaterials provide optimism for new treatments for nerve injuries. This article reviews the nervous system physiology, the factors that are critical for nerve repair, and the current approaches that are being explored to aid peripheral nerve regeneration and spinal cord repair.

1,237 citations

Journal ArticleDOI
TL;DR: Chemistries that Facilitate Nanotechnology Kim E. Sapsford,† W. Russ Algar, Lorenzo Berti, Kelly Boeneman Gemmill,‡ Brendan J. Casey,† Eunkeu Oh, Michael H. Stewart, and Igor L. Medintz .
Abstract: Chemistries that Facilitate Nanotechnology Kim E. Sapsford,† W. Russ Algar, Lorenzo Berti, Kelly Boeneman Gemmill,‡ Brendan J. Casey,† Eunkeu Oh, Michael H. Stewart, and Igor L. Medintz*,‡ †Division of Biology, Department of Chemistry and Materials Science, Office of Science and Engineering Laboratories, U.S. Food and Drug Administration, Silver Spring, Maryland 20993, United States ‡Center for Bio/Molecular Science and Engineering Code 6900 and Division of Optical Sciences Code 5611, U.S. Naval Research Laboratory, Washington, D.C. 20375, United States College of Science, George Mason University, 4400 University Drive, Fairfax, Virginia 22030, United States Department of Biochemistry and Molecular Medicine, University of California, Davis, School of Medicine, Sacramento, California 95817, United States Sotera Defense Solutions, Crofton, Maryland 21114, United States

1,169 citations