Isokinetic strength of knee extension and flexion was measured in patients with Parkinson's disease, to clarify whether muscle weakness is inherent to the disease. To counteract normal variation among subjects, we selected patients with symptoms completely or largely confined to one side and compared sides for each patient. The affected side was weaker than the other in both slow and fast movements very early in the disease. In more advanced disease, the difference between sides diminished at the slow speed but remained significant at the faster speed. These observations suggest that weakness is inherent to Parkinson's disease and influenced by movement speed.
We compared isokinetic muscle strength between initial and subsequent measurements in patients who could repeat the same testing later. Patients were divided into two groups according to changes in clinical condition between the times of the first and the subsequent measurements. Although isokinetic muscle strength is likely to depend on movement velocity in the early stages of Parkinson's disease, it may be influenced by bradykinesia, as the disease progresses. Speed-force correlation seen in these patients may give clues to the understanding of the pathophysiology of bradykinesia.

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MAP kinase cascades play a pivotal role in many aspects of cellular functions, and are evolutionarily conserved from yeast to mammals. MAP kinase pathways are composed of three kinases: a MAP kinase (MAPK), MAPK kinase (MAPKK), and a MAPK kinase kinase (MAPKKK). MEKK1 is a 196-kD protein serine-threonine kinase that has been cloned as a mammalian homologue of Ste11 and Byr2 MAPKKK in yeast. MEKK1 gene disruption by homologous recombination defined its role of JNK and ERK activations and cell survival by some specific stimuli. MEKK1 deficient cells also showed unexpected roles of cell migration. MEKK1 is associated with actin fibers and focal adhesions, localizing MEKK1 to sites critical in the control of cell adhesion and migration. MEKK1 is required for activation of the cysteine protease calpain and cleavage of spectrin and talin, proteins linking focal adhesions to the cytoskeleton. In MEKK1 knockout mice, the absence of this kinase was sufficient to prevent the cardiac hypertrophy induced by G a q and elevated levels of apoptosis and inflammatory lesions by pressure overload. Thus, MEKK1 is a logical target for drug development in pathological conditions including heart diseases.

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The purpose of this study using a crossover design was to evaluate the effects of physical exercise on mental function of elderly persons. We also investigated self-efficacy to examine the effect of their psychological aspect on continuation of exercise.
The subjects were 22 community-dwelling elderly persons who were utilizing a geriatric day-care facility. Assessments included the Geriatric Depression Scale (GDS), the Mini Mental State Examination (MMSE), the Tokyo Metropolitan Institute of Gerontology Index of Competence as an index for activity of daily living (ADL), the Self-Management Skill Scale, and the Self Efficacy for Health Promotion Scale.
Level of depression, cognition and ADL were maintained during the physical exercise intervention, but it's effect on mental function could not be determined. There were no significant differences between changes at the intervention and nonintervention period in mental state (GDS, MMSE) and ADL.
Measured values of the Self Efficacy for Health Promotion Scale significantly correlated with change ratio of ADL, but those of the GDS and MMSE did not correlate with scales of self-efficacy. In order to evaluate psychological factors affecting continuation of exercise, we need to investigate not only self-efficacy but also their recognition and understanding about the purpose of physical exercise, their daily-life background, and their desire to be independent.

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A rare case of hereditary spherocytic elliptocytosis was reported. The proband of 25 years-old-female had hemolytic anemia and abdominal pain. The blood smear and scanning electron microscopy revealed the presence mostly of ovalocytes and small number of microsherocyte and microcyte. The father also had the same red cell morphology, but hemolysis was compensated.
The red cell membrane protein analysis by SDS-PAGE revealed the deficiency of spectrin in the proband and protein 4.1 in her father. Splenectomy was performed in the proband, and hemolytic anemia improved.

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