Predictors of Track Test Performance in Drivers with Stroke.

AIM: To identify in-house assessment criteria to predict outcomes of driving tests in patients with stroke who wish to resume driving. MATERIAL AND METHODS: A total of 181 patients with stroke who attended Fukui General Hospital (as outpatients or inpatients) between 2003 and 2015 and who had no obvious motor impairment were included in the study. All subjects underwent a neuropsychological examination, a driving simulator test, and a track test at a driving school. Based on their performance in the track test, the subjects were divided into capable drivers (CD group) and incapable drivers (ID group). Intergroup differences in test results were evaluated. Logistic regression analysis was performed using age and outcomes of Trail-Making Tests A and B, and Symbol Digit Modalities Test (SDMT) as independent variables and track test performance as the dependent variable. RESULTS: The ID group performed worse than the CD group in most aspects of the neuropsychological examination. There was no significant difference between the two groups with respect to any component of the driving simulator test. SDMT values were extracted from the logistic regression analysis, with an Odds Ratio of 1.05 (p=0.028). On receiver operating characteristic curve analysis (with the area under the curve of 0.76), at the SDMT achievement rate < 37.3%, there was a sensitivity of 65% and specificity of 79% for the identification of driving inability. CONCLUSION: Neuropsychological tests are useful for evaluating the ability of patients with stroke to resume driving. In particular, SDMT is the most suitable test for predicting driving test outcomes.

Cisplatin differently affects amino terminal and carboxyl terminal domains of HSP90.

The 90-kDa heat shock protein (HSP90) is a molecular chaperone that assists in the folding and assembly of proteins in the cytosol. We previously demonstrated that the antineoplastic reagent, cisplatin, inhibits the aggregation prevention activity of mammalian HSP90. We now show that cisplatin binds both the amino terminal and carboxyl terminal domains of the human HSP90 and differently affects these two domains. Cisplatin blocks the aggregation prevention activity of HSP90C, but not HSP90N. In contrast, cisplatin induces a conformational change in HSP90N, but not HSP90C. These results indicate that cisplatin modulates the HSP90 activities through two different mechanisms using the two distinct binding sites of the HSP90 molecule.

The induction mechanism of the molecular chaperone HSP70 in the gastric mucosa by Geranylgeranylacetone (HSP-inducer).

To elucidate the induction mechanism of HSP70 by geranylgeranylacetone (GGA), we investigated GGA specific binding proteins using a GGA-affinity column. Alteration of chaperone activity of HSP70 and binding affinity of HSP70 to heat shock factor-1 (HSF-1) was evaluated in the presence or absence of GGA. The binding domain of HSP70 to GGA was also analyzed. A 70-kDa protein eluted by 10 mM GGA from the GGA-affinity column was identical to constitutively expressed HSP70 on immunoblotting. GGA-binding domain of HSP70 was C-terminal of the protein as peptide-binding domain (HSP70C). The chaperone activity of HSP70 and recombinant HSP70C was suppressed by GGA. Furthermore, dissociation of the HSP70 from HSF-1 was observed in the presence of GGA. GGA preferentially binds to the C-terminal of HSP70 which binds to HSF-1. After dissociation of HSP70, free HSF-1 could acquire the ability to bind to HSE (the promoter region of HSP70) gene.

Expression of reelin in the dorsal cochlear nucleus of the mouse.

The cytoarchitecture of dorsal cochlear nucleus (DCN), characterized by a distinct laminar structure similar to the cerebellar cortex of the normal mouse, is known to be disrupted in the Reelin-deficient mouse, reeler. Here, we have reexamined both the cytoarchitecture and myeloarchitecture of this nucleus and described expression pattern of Reelin protein during perinatal periods. Reelin-immunopositive granule cells were firstly recognized in the external granular layer of the DCN at embryological day 16 (E16). Next, we examined the cytoarchitecture of the DCN of the normal and reeler mice with Ca2+/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha) immunostaining. CaMKIIalpha-immunoreactive cartwheel cells were laminarly distributed in the layer II of the normal DCN, but scattered throughout the reeler DCN. Injection of retrograde tracer, Fluoro-Gold (FG) into the inferior colliculus of the reeler mouse resulted in that retrogradely labeled neurons in the DCN were radially scattered instead of being confined to a single layer as seen in the normal mouse. To examine whether CaMKIIalpha-immunopositive cartwheel cells are neurons projecting to the inferior colliculus or not, double labeling with CaMKIIalpha immunohistochemistry and retrograde labeling with an injection of FG into the inferior colliculus were made, which revealed that CaMKIIalpha-immunoreactive cartwheel cells do not send axons to the inferior colliculus. The present findings imply that Reelin may have some roles in the formation of laminar structures of the DCN.