The Clinical Efficacy of Botulinum Toxin Injections to the Upper Lumbrical Muscles for Clenched Fist Deformity in Chronic Stroke Patients.

Objective: Post-stroke hemiplegic patients with a spastic clenched fist deformity that was caused by upper motor neuron syndrome often have problems with hygiene and nursing. Botulinum toxin-A (BTX-A) had been given for treatment of such patients to relieve spasticity by targeting finger joint muscles, such as the flexor digitorum superficialis and flexor digitorum profundus. However, some of these patients do not have satisfactory outcomes.

Proposal for a New Exercise Method for Dysphagia with Velopharyngeal Inadequacy: A Case of Bickerstaff's Brainstem Encephalitis.

Bickerstaff's brainstem encephalitis is an autoimmune disease with the primary lesion situated in the brainstem and three cardinal signs: ophthalmoplegia; ataxia; and impaired consciousness. A 68-year-old man was started on rehabilitation exercise 3 months after onset of Bickerstaff's brainstem encephalitis, due to remnant dysarthria and dysphagia (Functional Oral Intake Scale, level 5) after the cardinal signs of Bickerstaff's brainstem encephalitis resolved. Exercise involved using a straw in the anterior midline between the dorsal tongue and hard palate.

Fundamentals of prions and their inactivation (review).

Prion is an infectious particle composed of an abnormal isoform of the prion protein (PrPSc) and causes prion diseases such as bovine spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) and scrapie. Host cells express cellular prion protein (PrPC), which plays roles in normal functions such as anti-oxidative stress. PrPSc is derived from PrPC and produced by conformational conversion.

Role of cellular prion proteins in the function of macrophages and dendritic cells.

The cellular isoform of prion proteins (PrPC) is expressed in hematopoietic stem cells, granulocytes, T and B lymphocyte natural killer cells, platelets, monocytes, dendritic cells, and follicular dendritic cells, which may act as carrier cells for the spread of its abnormal isoform (PrPSc) before manifesting transmissible spongiform encephalopathies (TSEs). In particular, macrophages and dendritic cells seem to be involved in the replication of PrPSc after ingestion. In addition, information on the role of PrPC during phagocytotic activity in these cells has been obtained.

Prion protein suppresses perturbation of cellular copper homeostasis under oxidative conditions.

Prion protein (PrP) binds copper and exhibits superoxide dismutase-like activity, while the roles of PrP in copper homeostasis remain controversial. Using Zeeman graphite furnace atomic absorption spectroscopy, we quantified copper levels in immortalized PrP gene (Prnp)-deficient neuronal cells transfected with Prnp and/or Prnd, which encodes PrP-like protein (PrPLP/Dpl), in the presence or absence of oxidative stress induced by serum deprivation. In the presence of serum, copper levels were not significantly affected by the expression of PrP and/or PrPLP/Dpl, whereas serum deprivation induced a decrease in copper levels that was inhibited by PrP but not by PrPLP/Dpl.