Research subject-1
“Postoperative neural plasticity and neurotization in the facial reanimation using lengthening temporalis myoplasty”
The lengthening temporalis myoplasty (Labbe 2000)is a new temporalis transfer
technique for facial reanimation. The concept of this technique is to transfer
the whole temporalis without turning over itself, which makes more natural
direction of the cheek/oral commissure movements. Since temporalis is innervated
by trigeminal nerve,“biting” is necessary for facial movement, however
there are several cases who acquired a natural smile without biting or
even the recovery of palpebral area. These facts suggest the postoperative
neural plasticity and neurotization occurred.
Rat models of the lengthening temporalis myoplasty is made to investigate
the postoperative neural plasticity and neurotization of this technique
using the neural tracers and electrophysiological tests etc.
Research subject-2
“Facial nerve reconstruction with multiple neural sources using end-to-side nerve graft”
We have reported a new technique for facial nerve reconstruction using single nerve graft material with end-to-side coaptation of recipient branches, and animal models of this method that support the efficacy of this technique as well. For better facial muscle regeneration, we also use additional hypoglossal or masseteric nerve. The use of multiple neural source to induce double innervation of facial muscles is relatively new concept and most of the mechanism of it is still unknown. Rat facial nerve reconstruction models of this technique is made to investigate the efficacy and reconstructed neural network using the neural tracers and electrophysiological tests etc.
Research subject-3
“Stress and wound healing”
For diabetes mellitus, a cause of intractable ulcer, stress is quite likely
to influence various hormones, thereby increasing symptoms. Animal experiments
have shown elevated levels of various hormones such as plasma corticosterone,
hormonal releasing factors, cytokines such as IL-6, catecholamines, blood
sugar and neutral fats under conditions of restraint stress. Clinically,
antidepressants are administered to patients with diabetes mellitus for
analgesia because of damage to blood vessels nourishing nerves and the
resultant neuropathic pain. In addition, it has been demonstrated that
psychological care aimed at reducing stress promotes healing. Stress is
assumed to increase blood glucocorticoids, inducing neuronal death in the
brain, thereby exacerbating the progression of neural network breakdown
in patients with depression. Brain-derived neurotrophic factors (BDNFs)
play an important role in the growth and survival of nerve cells. It has
been revealed that when BDNF production is increased after administration
of antidepressants, nerve cell differentiation is promoted. Interrelationships
between antidepressants and BDNFs as well as the acceleration of neural
network restoration/formation have been suggested.
Based on the concept that there are close relationships between stress
and tissue injury, and anti-stress drugs and tissue regeneration, and stress
having an effect on wound healing as described above, we have established
the hypothesis that “stress delays wound healing, and anti-stress drugs
promote healing” and are conducting basic animal experiments to validate
this hypothesis. Many patients with intractable skin ulcers are in a depressive
state. Our research, using mouse models, is aimed at demonstrating the
possibility that anti-stress drugs, i.e. antidepressants, would improve
not only depression but also ulcers.
