![Mr. Christopher S Lyle MS, CCC-SLP, Speech-Language Pathologist](/fatd/images/avatar.png)
Mr. Christopher S Lyle MS, CCC-SLP
Speech-Language Pathologist
519 LATHAM DR LOWELL AR, 72745About
Dr. Christopher Lyle is a speech language pathologist practicing in LOWELL, AR. Dr. Lyle specializes in speech, language and swallowing disorders in patients. As a speech language pathologist, Dr. Lyle evaluates, diagnoses and treats patients with communication and swallowing troubles. These conditions may be due to developmental delay, brain injury, hearing loss, autism, stroke or other diseases and injuries. Dr. Lyle helps patients make sounds and improve their voices through various methods. Speech language pathologists also work with patients to strengthen muscles used to speak and swallow, and work with individuals and families to help cope with their conditions.
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Expert Publications
Data provided by the National Library of Medicine- The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide.
- Inhibition of cell proliferation and cell cycle progression by specific inhibition of basal JNK activity: evidence that mitotic Bcl-2 phosphorylation is JNK-independent.
- Characterization of vinblastine-induced Bcl-xL and Bcl-2 phosphorylation: evidence for a novel protein kinase and a coordinated phosphorylation/dephosphorylation cycle associated with apoptosis induction.
- Role of c-Jun in cellular sensitivity to the microtubule inhibitor vinblastine.
- Vinblastine-induced apoptosis is mediated by discrete alterations in subcellular location, oligomeric structure, and activation status of specific Bcl-2 family members.
- Superhigh-sensitivity photothermal monitoring of individual cell response to antitumor drug.
- Induction of apoptosis by vinblastine via c-Jun autoamplification and p53-independent down-regulation of p21WAF1/CIP1.
- Distinct signaling pathways of microtubule inhibitors--vinblastine and Taxol induce JNK-dependent cell death but through AP-1-dependent and AP-1-independent mechanisms, respectively.
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