Publications by authors named "M Sereda"

(1) Background: Tinnitus involves the conscious awareness of a tonal or composite noise for which there is no identifiable corresponding external acoustic source. For many people, tinnitus is a disorder associated with symptoms of emotional distress, cognitive dysfunction, autonomic arousal, behavioural changes, and functional disability. Many symptoms can be addressed effectively using education or cognitive behavioural therapy.

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Cochlear implantation is an effective intervention to restore useful aspects of hearing function in adults with severe-to-profound hearing loss. Tinnitus, the perception of sound in the absence of an external source, is common in people with severe-to-profound hearing loss. Existing evidence suggests cochlear implantation may be effective in reducing the negative impact of tinnitus in this population.

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We extend our recently developed sparse-stochastic fragmented exchange formalism for ground-state near-gap hybrid DFT to calculate absorption spectra within linear-response time-dependent generalized Kohn-Sham DFT (LR-GKS-TDDFT) for systems consisting of thousands of valence electrons within a grid-based/plane-wave representation. A mixed deterministic/fragmented-stochastic compression of the exchange kernel, here using long-range explicit exchange functionals, provides an efficient method for accurate optical spectra. Both real-time propagation as well as frequency-resolved Casida-equation-type approaches for spectra are presented, and the method is applied to large molecular dyes.

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Haplo-insufficiency of the gene encoding the myelin protein PMP22 leads to focal myelin overgrowth in the peripheral nervous system and hereditary neuropathy with liability to pressure palsies (HNPP). Conversely, duplication of PMP22 causes Charcot-Marie-Tooth disease type 1A (CMT1A), characterized by hypomyelination of medium to large caliber axons. The molecular mechanisms of abnormal myelin growth regulation by PMP22 have remained obscure.

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Article Synopsis
  • The peripheral nervous system can regenerate after nerve damage, but achieving full functional recovery is rare and heavily relies on Schwann cells, which help repair nerve damage and support axon regrowth.
  • New research reveals that nerve injury stimulates communication between fat cells and glial cells, with the adipokine leptin playing a crucial role in helping Schwann cells adapt metabolically during recovery.
  • Leptin receptors in Schwann cells help regulate energy processes needed for nerve repair, suggesting that targeting this intercellular communication could improve therapeutic strategies for nerve injuries.
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