Child ego state and self-care behavior change in heart failure patients.

BACKGROUND: The psychological characteristics of ego functions interfere with self-care behavior in several diseases. However, the effect of ego functions on self-care behavior after education in heart failure (HF) remains unclear. METHODS: Seventy-one HF patients were enrolled. Patients' scores on the Japanese version of the European Heart Failure Self-care Behaviour Scale (EHFScBS) were measured before and after the HF intervention, and the rate of change was used as an indicator of educational effectiveness. The Tokyo University Egogram New Ver. II was used to assess five types of ego state functions: Critical parent, Nurturing parent, Adult, Free Child, and Adapted Child (AC). RESULTS: A comparison of the five ego states showed that AC scores were significantly lower than those of the other ego states (p < 0.01). Total EHFScBS scores significantly decreased from 33 (26-39) to 16 (14-20) (p < 0.01) after the HF education, and the median rates of change in EHFScBS was -46.2%. Patients with a lower rate of change in EHFScBS were more likely to have low AC scores, as characterized by a lack of compliance and coordination, and were less likely to receive higher education (all p < 0.05). Even after adjustment for covariates, low AC scores were independently associated with low rate of change in EHFScBS (p < 0.01). CONCLUSIONS: Educational behavior change for self-care is less effective in HF patients with an ego state with low AC.

Age-related changes in rat genioglossus, geniohyoid and masseter muscles.

OBJECTIVES: The aim of this study was to elucidate age-related changes from adult to middle age in the contractile properties of the masseter, genioglossus and geniohyoid muscles of the rat. MATERIALS AND METHODS: We analysed the expressions of myosin heavy chain (MyHC) mRNAs and proteins as indicators of the contractile properties in these muscles obtained from rats at 6, 12, 18 and 24 months of age using real-time PCR and SDS-PAGE. RESULTS: We found no marked age-related changes in the expressions of MyHC mRNAs and proteins in rat masseter and geniohyoid muscles, suggesting that the biological ageing process does not affect contractile properties in these muscles. However, we found a decrease in the expression of MyHC IIb mRNA with ageing in the rat genioglossus muscle, suggesting that biological ageing process induces at least some fast-to-slow myofibre phenotype transition. CONCLUSION: The biological ageing process from adult to middle age appears to differentially affect different types of craniofacial muscles.

IGF and myostatin pathways are respectively induced during the earlier and the later stages of skeletal muscle hypertrophy induced by clenbuterol, a ß2-adrenergic agonist.

Clenbuterol, a ß2-adrenergic agonist, increases the hypertrophy of skeletal muscle. Insulin-like growth factor (IGF) is reported to work as a potent positive regulator in the clenbuterol-induced hypertrophy of skeletal muscles. However, the precise regulatory mechanism for the hypertrophy of skeletal muscle induced by clenbuterol is unknown. Myostatin, a member of the TGFß super family, is a negative regulator of muscle growth. The aim of the present study is to elucidate the function of myostatin and IGF in the hypertrophy of rat masseter muscle induced by clenbuterol. To investigate the function of myostatin and IGF in regulatory mechanism for the clenbuterol-induced hypertrophy of skeletal muscles, we analysed the expression of myostatin and phosphorylation levels of myostatin and IGF signaling components in the masseter muscle of rat to which clenbuterol was orally administered for 21 days. Hypertrophy of the rat masseter muscle was induced between 3 and 14 days of oral administration of clenbuterol and was terminated at 21 days. The expression of myostatin and the phosphorylation of smad2/3 were elevated at 21 days. The phosphorylation of IGF receptor 1 (IGFR1) and akt1 was elevated at 3 and 7 days. These results suggest that myostatin functions as a negative regulator in the later stages in the hypertrophy of rat masseter muscle induced by clenbuterol, whereas IGF works as a positive regulator in the earlier stages.

Association between the lack of teeth and the expression of myosins in masticatory muscles of microphthalmic mouse.

The purposes of the present study were to elucidate the influences of the deficiency of teeth on masticatory muscles, such as the masseter, temporalis and digastric muscles and compare the influence among masticatory muscles. We analysed the expressions of myosin heavy chain (MyHC) isoform messenger RNA (mRNA) and protein in these muscles in the microphthalmic (mi/mi) mouse, whose teeth cannot erupt because of a mutation in the mitf gene locus. The expression levels of MyHC mRNA and protein in the masseter, temporalis, digastric, tibialis anterior and gastrocnemius muscles of +/+ and mi/mi mice were analysed with real-time polymerase chain reaction and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, respectively. The mi/mi masseter muscle at 8 weeks of age expressed 4.1-fold (p < 0.05) and 3.3-fold (p < 0.01) more MyHC neonatal mRNA and protein than that in the +/+, respectively; the expression level of MyHC neonatal protein was 19% of the total MyHC protein in the masseter muscle of mi/mi mice. In the digastric muscle, the expression levels of MyHC I mRNA and protein in the mi/mi mice were 4.7-fold (p < 0.05) and 5-fold (p < 0.01) higher than those in the +/+ mice. In the temporalis, tibialis anterior and gastrocnemius muscles, there was no significant difference in the expression levels of any MyHC isoform mRNA and protein between +/+ and mi/mi mice. These results indicate associations between the lack of teeth and the expression of MyHC in the masseter and digastric muscles but not such associations in the temporalis muscle, suggesting that the influence of tooth deficiency varies among the masticatory muscles.

Changes in triacylglycerol-accumulated fiber type, fiber type composition, and biogenesis in the mitochondria of the soleus muscle in obese rats.

Little is known about the effects of obesity on skeletal muscle consisting of approximately 80% type I (slow) fibers, such as that in the soleus muscle, although type I fibers have an enhanced capacity for mitochondrial respiration and fatty acid oxidation. We investigated the effects of obesity on the soleus muscle in the rat. Rats were fed a high-fat diet (protein:fat:carbohydrate = 20:57:23; 508 kcal/100 g) or a control diet (protein:fat:carbohydrate = 20:10:70; 366 kcal/100 g) for 10 weeks. We analyzed the accumulation of intramyocellular triacylglycerol (IMTG), fiber type composition, and the biogenesis and function of the mitochondria in the soleus muscle of the rat during 10 weeks of feeding, using histochemical and real-time polymerase chain reaction analyses. Obesity increased body weight and markedly elevated IMTG levels in type I, but not in type II, fibers of the soleus muscle throughout the feeding period. Obesity also inhibited the biogenesis and function in the mitochondria and altered the fiber type composition in the soleus muscle. The suppression of biogenesis and function in the mitochondria, and the alteration in the fiber type composition may be attributable to the marked IMTG accumulation in the soleus muscle of the rat.

Changes in the lingual muscles of obese rats induced by high-fat diet feeding.

OBJECTIVE: To elucidate the influences of obesity on the properties and volume of lingual (genioglossus and geniohyoid) muscles in obese rats. METHODS: We analysed the accumulation of triacylglycerol and the diameter of myofibres in the lingual muscles using histochemistry, and the MyHC composition using real-time PCR in rats fed a high-fat diet for 10 weeks. In the genioglossus and geniohyoid muscles, the percentage of oil droplet areas in the obesity group were 3.6 and 2.5 times greater than those in the control group, respectively (p<0.025). The diameters of the slow myofibres in the genioglossus and geniohyoid muscles were approximately 20% greater in the obesity group than in the control group (p<0.0001), while that of the fast myofibres in the geniohyoid muscle was approximately 10% greater in the obesity group than in the control group (p<0.0001). No significant difference in the expressions of any of the MyHC isoforms studied was found in any of the muscles studied between the obesity and control groups. CONCLUSION: High-fat diet feeding induced the fat deposition in the myofibre and influenced the structure of the lingual (genioglossus and geniohyoid) muscles.