Dr. Darrell Richard Smith MD FACS
Ear-Nose and Throat Doctor (ENT)
4912 Higbee Ave Nw Suite 200 Canton OH, 44718About
Dr. Darrell Smith is an ear, nose and throat (ENT) doctor, also known as an otolaryngologist, practicing in Canton, OH. Dr. Smith specializes in diseases and disorders of the ear, nose and throat as well as other parts of the head and neck. Such structures an ENT may work on include the sinuses, larynx (voice box) and mouth in addition to the ear, nose and throat. There are seven areas of expertise that an ENT might specialize in, and these are: allergies; facial reconstructive surgery; head and neck; laryngology; otology/neurotology; pediatric otolaryngology; and rhinology.
Education and Training
Case Western Reserve University School of Medicine 1993
Board Certification
OtolaryngologyAmerican Board of OtolaryngologyABOto
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Activation of nuclear factor-kappaB via endogenous tumor necrosis factor alpha regulates survival of axotomized adult sensory neurons.
- Development of selective axonopathy in adult sensory neurons isolated from diabetic rats: role of glucose-induced oxidative stress.
- Mitochondrial respiratory chain dysfunction in dorsal root ganglia of streptozotocin-induced diabetic rats and its correction by insulin treatment.
- Diminished superoxide generation is associated with respiratory chain dysfunction and changes in the mitochondrial proteome of sensory neurons from diabetic rats.
- Tumor necrosis factor-α elevates neurite outgrowth through an NF-κB-dependent pathway in cultured adult sensory neurons: Diminished expression in diabetes may contribute to sensory neuropathy.
- Sensory neurons derived from diabetic rats have diminished internal Ca2+ stores linked to impaired re-uptake by the endoplasmic reticulum.
- The role of aberrant mitochondrial bioenergetics in diabetic neuropathy.
- Impaired adenosine monophosphate-activated protein kinase signalling in dorsal root ganglia neurons is linked to mitochondrial dysfunction and peripheral neuropathy in diabetes.
- Ciliary neurotrophic factor activates NF-κB to enhance mitochondrial bioenergetics and prevent neuropathy in sensory neurons of streptozotocin-induced diabetic rodents.
- Receptor for advanced glycation end-products (RAGE) activates divergent signaling pathways to augment neurite outgrowth of adult sensory neurons.
- Diabetes impairs an interleukin-1β-dependent pathway that enhances neurite outgrowth through JAK/STAT3 modulation of mitochondrial bioenergetics in adult sensory neurons.
- Ciliary neurotrophic factor reverses aberrant mitochondrial bioenergetics through the JAK/STAT pathway in cultured sensory neurons derived from streptozotocin-induced diabetic rodents.
- Temporal dystrophic remodeling within the intrinsic cardiac nervous system of the streptozotocin-induced diabetic rat model.
- The proinflammatory cytokine, interleukin-17A, augments mitochondrial function and neurite outgrowth of cultured adult sensory neurons derived from normal and diabetic rats.
- Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy.
Treatments
- Hearing Loss
- Allergies
- Ear Infection
- Acid Reflux
- Hyperparathyroidism
- Hay Fever (allergic Rhinitis)
- Ear Wax
- Goiter
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