Ji-Geng Yan

Vibration injury damages arterial endothelial cells

Prolonged exposure to hand‐transmitted vibration can cause debilitating neural and vascular dysfunction in humans. It is unclear whether the pathophysiology involves simultaneous or sequential injury of arteries and nerves. The mechanism of vibration injury was investigated in a rat tail model, containing arteries and nerves structurally similar to those in the human hand. Tails were selectively vibrated for 1 or 9 days with the remainder of the animal at rest. One vibration bout of 4 h/day, 60 HZ, 5 g (49 m/s2) acceleration, injured endothelial cells. Injury was signaled by elevated immunostaining for NFATc3 transcription factor. Electron microscopy revealed that vibration for 9 days produced loss and thinning of endothelial cells, with activated platelets coating the exposed subendothelial tissue. Endothelial cells and arterial smooth muscle cells contained double membrane–limited, swollen processes indicative of vasoconstriction‐induced damage. Laser doppler surface recording demonstrated that 5 min of vibration significantly diminished tissue blood perfusion. These findings indicate that early injury involves vasoconstriction and denuding of the arterial endothelium.

Vibration-induced disruption of retrograde axoplasmic transport in peripheral nerve.

Hand‐arm vibration syndrome (HAVS) results from excessive exposure to hand‐transmitted vibration. Whether the peripheral nerve damage characteristic of HAVS is a direct result of vibration or is secondary to vascular insufficiency remains unclear. The purpose of this study was to explore the effect of vibration exposure on axoplasmic transport in peripheral nerves and soleus motor neurons. Sciatic nerves and motor neurons from rats following two 5‐h periods of vibration exposure demonstrated disruption in retrograde transport compared to normal. After 10 days of vibration (5 h/day), axoplasmic transport failed to recover within 24–48 h in most rats. This study demonstrates that disrupted axoplasmic transport is an early consequence of short‐term vibration exposure. The effects of vibration on axoplasmic transport also appear to be cumulative. This study provides a new biological way to evaluate measures to prevent early vibration injury. Muscle Nerve, 2005

Persistent reduction of conduction velocity and myelinated axon damage in vibrated rat tail nerves

Prolonged hand‐transmitted vibration exposure in the workplace has been recognized for almost a century to cause neurodegenerative and vasospastic disease. Persistence of the diseased state for years after cessation of tool use is of grave concern. To understand persistence of vibration injury, the present study examined recovery of nerve conduction velocity and structural damage of myelinated axons in a rat tail vibration model. Both 7 and 14 days of vibration (4 h/day) decreased conduction velocity. The decrease correlated directly with the increased percentage of disrupted myelinated axons. The total number of myelinated axons was unchanged. During 2 months of recovery, conduction velocity returned to control level after 7‐day vibration but remained decreased after 14‐day vibration. The rat tail model provides insight into understanding the persistence of neural deficits in hand–arm vibration syndrome. Muscle Nerve, 2009

Upregulation of Specific mRNA Levels in Rat Brain After Cell Phone Exposure

Adult Sprague-Dawley rats were exposed to regular cell phones for 6 h per day for 126 days (18 weeks). RT-PCR was used to investigate the changes in levels of mRNA synthesis of several injury-associated proteins. Calcium ATPase, Neural Cell Adhesion Molecule, Neural Growth Factor, and Vascular Endothelial Growth Factor were evaluated. The results showed statistically significant mRNA up-regulation of these proteins in the brains of rats exposed to cell phone radiation. These results indicate that relative chronic exposure to cell phone microwave radiation may result in cumulative injuries that could eventually lead to clinically significant neurological damage.

The correlation between calcium absorption and electrophysiological recovery in crushed rat peripheral nerves

The correlation between calcium ion (Ca2+) concentration and electrophysiological recovery in crushed peripheral nerves has not been studied. Observing and quantifying the Ca2+ intensity in live normal and crushed peripheral nerves was performed using a novel microfine tearing technique and Calcium Green‐1 Acetoxymethyl ester stain, a fluorescent Ca2+ indicator. Ca2+ was shown to be homogeneously distributed in the myelinated sheaths. After a crush injury, there was significant stasis in the injured zone and the portion distal to the injury. The Ca2+ has been almost completely absorbed after 24 weeks in the injured nerve to be similar to the controls. The process of the calcium absorption was correlated with the Compound Muscle Action Potential recovery process of the injured nerves. This correlation was statistically significant (r = −0.81, P < 0.05). The better understanding of this process will help us to improve nerve regeneration after peripheral nerve injury.

Cortical plasticity induced by different degrees of peripheral nerve injuries: a rat functional magnetic resonance imaging study under 9.4 Tesla

Background Major peripheral nerve injuries not only result in local deficits but may also cause distal atrophy of target muscles or permanent loss of sensation. Likewise, these injuries have been shown to instigate long-lasting central cortical reorganization. Methods Cortical plasticity changes induced after various types of major peripheral nerve injury using an electrical stimulation technique to the rat upper extremity and functional magnetic resonance imaging (fMRI) were examined. Studies were completed out immediately after injury (acute stage) and at two weeks (subacute stage) to evaluate time affect on plasticity. Results After right-side median nerve transection, cortical representation of activation of the right-side ulnar nerve expanded intra-hemispherically into the cortical region that had been occupied by the median nerve representation After unilateral transection of both median and ulnar nerves, cortical representation of activation of the radial nerve on the same side of the body also demonstrated intra-hemispheric expansion. However, simultaneous electrical stimulation of the contralateral uninjured median and ulnar nerves resulted in a representation that had expanded both intra- and inter-hemispherically into the cortical region previously occupied by the two transected nerve representations. Conclusions After major peripheral nerve injury, an adjacent nerve, with similar function to the injured nerve, may become significantly over-activated in the cortex when stimulated. This results in intra-hemispheric cortical expansion as the only component of cortical plasticity. When all nerves responsible for a certain function are injured, the same nerves on the contralateral side of the body are affected and become significantly over-activated during a task. Both intra- and inter-hemispheric cortical expansion exist, while the latter dominates cortical plasticity.

Nifedipine pretreatment reduces vibration‐induced vascular damage

A rat‐tail vibration model of hand‐arm vibration was employed to test whether preemptive administration of nifedipine (5 mg/kg) to block vasoconstriction prevents vibration‐induced arterial damage. The tails of vibrated and nifedipine‐pretreated vibrated Sprague‐Dawley rats were exposed continuously to 4 h of 60‐HZ vibration at 49 m/s2 rms. In nonvibrated anesthetized rats, the ventral tail arteries were bathed for 15 min in situ in 1 mM epinephrine or 1 mM norepinephrine to induce structural changes indicative of intense vasoconstriction. Arteries were processed for light and electron microscopy 45 min after treatment. Compared to sham control, 4‐h vibration significantly (P < 0.01) reduced lumen size, generated endothelial disruption (7.0 ± 2.6%), elevated nuclear factor of activated T cells c3 (NFATc3) expression in endothelial and smooth muscle cells, and increased smooth muscle cell vacuolization. The findings demonstrate that blockage of vibration‐induced vasoconstriction with nifedipine prevents acute vascular damage. Smooth muscle and endothelial cells structurally altered by vasoconstriction are rendered susceptible to damage by vibration. Muscle Nerve, 2005

Anatomy of the intermetacarpal ligaments of the carpometacarpal joints of the fingers

In this study, the structure of the retaining ligaments between the proximal metacarpal bones of the fingers was defined. Anatomic dissections were performed on 10 fresh cadavers. Four separate ligaments were found: a dorsal metacarpal ligament, a palmar metacarpal ligament, and 2 interosseous ligaments oriented in a V-shaped configuration. The V-shaped interosseous ligaments were found to be the strongest; along with the palmar and dorsal intermetacarpal ligaments, they form a very strong connection between the bases of the adjacent metacarpals.

Transhemispheric Cortical Plasticity Following Contralateral C7 Nerve Transfer: A Rat Functional Magnetic Resonance Imaging Survival Study

PURPOSE To perform contralateral C7 nerve transfer in a controlled, survival rat functional magnetic resonance imaging model, so as to understand the extent of cortical plasticity after brachial plexus injury and surgical manipulation with this procedure. METHODS A total of 24 rats divided into 3 groups underwent surgery followed by functional magnetic resonance imaging in this study. Group I rats served as sham controls. Group II injury rats underwent complete right brachial plexus root avulsion. Group III repair rats underwent complete right brachial plexus root avulsion and then contralateral C7 nerve transfer to the right median nerve. We assessed cortical response to median nerve stimulation at 0, 3, and 5 months after injury using functional magnetic resonance imaging at 9.4 T. We concurrently performed sensory and motor functional testing. RESULTS We noted a progression in cortical activation in the repair rats over 0, 3, and 5 months. Initially, right median nerve stimulation in the repair group showed complete loss of activation in the contralateral somatosensory cortex. Nerve stimulation at 3 months produced primarily ipsilateral cortical activation; at 5 months, 3 patterns of cortical activation emerged: ipsilateral, bilateral, and contralateral activation. After right median nerve stimulation, injury rats maintained a lack of cortical activation and control rats maintained exclusive contralateral activation throughout all time points. Functional testing revealed a degree of return of sensory and motor function over time in the repair group compared with the injured group. CONCLUSIONS A high degree of transhemispheric cortical plasticity occurred after contralateral C7 nerve transfer. There appears to be a predilection for the rat brain to restore the preinjury somatotopic representation of the brain. CLINICAL RELEVANCE Understanding the cortical changes after nerve injury and repair may lead to specific pharmacologic or behavioral interventions that can improve functional outcomes.

Helicoid end-to-side and oblique attachment technique in repair of the musculocutaneous nerve injury with the phrenic nerve as a donor: an experimental study in rats.

The purpose of this study was to identify if a modified end‐to‐side repair can achieve equal results of nerve regeneration compared to an end‐to‐end repair using donor phrenic nerves in repair of the musculocutaneous nerve and also pulmonary protection. Eighteen rats were divided into three groups of six each comparing two nerve graft techniques: helicoid end‐to‐side plus distal oblique repair vs. traditional end‐to‐end repair, using a donor phrenic nerve. The saphenous nerve was used as a graft between the phrenic nerve and the musculocutaneous nerve. The third group was used as control; the musculocutaneous nerve was transected without any repair. Three months postoperatively, electrophysiology, tetanic force, moist muscle weight, histology, nerve fiber counting, and chest X‐ray were evaluated. All results have shown that this modified end‐to‐side repair was superior to the end‐to‐end repair. The former did not compromise the diaphragm function, but the latter showed an elevation of the diaphragm. Little recovery was seen in the third group. The conclusion is that this modified end‐to‐side repair can replace the traditional end‐to‐end repair using donor phrenic nerves with better results of nerve regeneration without diaphragm compromise.