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Biomedical subjects

R Nakamura

Publications and source records attributed to R Nakamura.

At least 541 records · Page 30Linked to original sources
PubMed1975

Synchronization error in bilateral simultaneous flexion of elbows.

Using 7 left- and 7 right-handed subjects, the difference in time between left and right arms in the initiation of bilateral simultaneous flexion of elbows (synchronization error) was measured under three conditions: response to a sound stimulus with a warning signal, response to a sound stimulus without a warning signal, and self-initiated trial (option). The absolute value of synchronization errors depended upon experimental conditions. In conditions 'with warning' and 'option' the dominance shown in performance of left-handed subjects was the mirror-image of that shown by the right-handed subjects. The right biceps muscle responded faster in left-handed subjects and vice versa. Right-handed subjects showed rather a constant value in their dispersion of synchronization errors.

Adult↗
PubMed1975

Study of periodontal disease and coenzyme Q.

A 25-year old Caucasian with uniquely severe and chronic periodontal disease, requiring extraction of all teeth, was treated with hexahydrocoenzyme Q4 which functions like naturally occurring coenzyme Q10 in gingival tissue. During the fourth and fifth examinations after the seventh and eighth weeks of treatment, three dentists separately and independently scored clinical improvements of five symptoms by significances of essentially P less than 0.01 to P less than 0.001. The initial benefit of the treatment was observed at the second examination after three weeks of treatment. The administration of coenzyme Q could be an important therapeutic adjunct to periodontal therapy for certain patients.

Adult↗
PubMed1974

Study of CoQ10-enzymes in gingiva from patients with periodontal disease and evidence for a deficiency of coenzyme Q10.

The specific activities of both the succinate dehydrogenase-coenzyme Q(10) reductase and the DPNH-cytochrome c reductase [NADH:(acceptor)oxidoreductase, EC 1.6.99.3] were determined in mitochondria from 40 diseased gingival biopsies from patients with periodontal disease and from 24 control biopsies from nondiseased areas (clinically evaluated) of gingival tissues from the same mouths of the patients from whom the diseased gingival tissues were taken. The control tissue was taken during normal surgical procedures, such as for gingival recontouring and tuberosity removal. The diseased gingival biopsies showed a mean specific activity for the succinate dehydrogenase-coenzyme Q(10) reductase which was higher (P < 0.02) than that of the control biopsies, and which increased (P < 0.01) when the assays utilized exogenous coenzyme Q(3), and corresponded to an average deficiency of coenzyme Q(10)-enzyme activity of 35%. About 60% of the 40 diseased gingival tissues showed a deficiency of coenzyme Q(10) at its site in this succinate-coenzyme Q(10) enzyme. Of the 24 control tissues, 20% showed deficiencies of coenzyme Q(10). As a group, the control tissues showed no deficiency of coenzyme Q(10). No deficiency of coenzyme Q(10) at its site in DPNH-cytochrome c reductase was observed for either the control or diseased gingival tissues, as groups or individually.

Adolescent↗
PubMed1974

Effect of coenzyme Q on serum levels of creatine phosphokinase in preclinical muscular dystrophy.

Coenzyme Q(10) (CoQ(10)) exists in human tissue, and is indispensable to mitochondrial enzymes of respiration. CoQ was administered to children with preclinical muscular dystrophy, CoQ enzymology was emphasized, and serum creatine phosphokinase, CPK, (ATP:creatine N-phosphotransferase, EC 2.7.3.2) was repeatedly monitored.A 40-week treatment of an infant, 1-2 years of age, reduced serum CPK (P < 0.001; total CPK assays, 76). A 40-week treatment of a boy, 3-5 years of age, reduced serum CPK (P < 0.01); treatment through 80 weeks reduced CPK (P < 0.001; total CPK assays, 118). This response of preclinical dystrophy to CoQ implies a deficiency of CoQ in skeletal muscle that was actually found previously by assay of the activity of the succinate dehydrogenase:coenzyme Q(10) reductase of the rectus abdominis. The relationships among a CoQ deficiency in muscle, serum CPK, and use of CPK in muscle are uncertain; however, restoration of CoQ enzyme activity in muscle by oral administration of CoQ could lead to increased use of CPK in muscle to form phosphocreatine from creatine and ATP, with a corresponding decrease in serum levels of CPK. The great excess of CPK in serum comes from deteriorating muscle in which CPK is below normal.

Child, Preschool↗