Development of Professional Care Program for Nurses in Dementia Wards and Its Educational Effects.

PURPOSE: To develop an education program for nurses specializing in dementia care, and to investigate its effects. METHODS: An intervention study of nurses was conducted using a quasi-experiment with 3 randomly assigned groups. Participants were 51 nurses from a psychiatric hospital dementia ward, divided into an intervention program group (17 nurses), a knowledge-acquisition-only group (16 nurses), and a usual-care group (18 nurses) as controls. The program group intervention comprised 3 frameworks: motivation for achieving the task, acquisition of professional knowledge required for dementia care, and sharing of successful experiences based on professional knowledge. The knowledge-acquisition-only group received only the acquisition of professional knowledge framework, and the usual-care group received only the usual-care framework. The intervention period was 3 months. RESULTS: Post-intervention, the program group had a significantly greater sense of self-efficacy associated with professional knowledge and significantly greater self-efficacy associated with practice compared with the knowledge-acquisition-only and the usual-care groups. Professional knowledge was acquired by 80% of the program group, compared with 70% of the knowledge-acquisition-only group. A co-occurrence network diagram of the multivariate analysis results produced by text mining of the descriptive data indicated that nurses provided care for symptoms specific to different diseases based on their pathological mechanisms. CONCLUSION: Program implementation led to the acquisition of deeper knowledge and greater self-efficacy by sharing expertise-based practices and successful experiences, compared with desk-based learning in a single workshop lecture, suggesting the program's usefulness in clinical practice.

Glucose-responsive Insulinoma with Insulin Hypersecretion Suppressed by Metformin.

In type 2 diabetes mellitus, metformin suppresses excessive insulin secretion in relation to the intake of glucose. We herein report the case of a 45-year-old man with glucose-responsive insulinoma whose responsive hypoglycemia was alleviated by metformin. The patient had a history of a postprandial loss of consciousness, resulting in hospital admission. He refused surgery and diazoxide administration. A 75-g oral glucose tolerance test after metformin administration revealed the suppression of glucose-responsive insulin hypersecretion and responsive hypoglycemia. Pancreatic head duodenectomy was performed, which alleviated the symptoms. Metformin administration in patients with glucose-responsive insulinoma may therefore be effective for preventing responsive hypoglycemia and hyperinsulinemia.

Anesthetic management of a patient with congenital insensitivity to pain with anhidrosis by coadministration of remifentanil.

BACKGROUND: Congenital insensitivity to pain with anhidrosis (CIPA) is a rare autosomal recessive disease characterized by unexplained fever, systemic insensitivity to pain, anhidrosis, and mental distress. Anesthetic management is challenging because autonomic dysfunction can induce perioperative complications. Only a few reports of anesthetic management of CIPA patients have been published. We herein present a case of successful management of the same patient on two occasions using small doses of fentanyl and remifentanil. CASE PRESENTATION: A 37-year-old man with CIPA underwent two orthopedic operations. We were able to balance the dose of remifentanil to avoid the extremes of hyperalgesia when the dose is too low and shivering when the dose is too high. CONCLUSION: To our knowledge, no reports have described the anesthetic management of CIPA patients with remifentanil. We consider anesthetic management with coadministration of remifentanil to be potentially useful for such patients.

Long-term amiodarone treatment causes cardioselective hypothyroid-like alteration in gene expression profile.

The long-term cardiac effects of amiodarone resemble many aspects of hypothyroidism. The anti-arrhythmic potential of amiodarone may therefore be the result of a drug-induced, local hypothyroid-like condition. To investigate this controversial issue, we compared gene expression profiles in the hearts of rats treated with amiodarone with those of rats with hypothyroidism. Wistar male rats were assigned to 3 groups (n=6-8): Control, systemic hypothyroidism (hypothyroidism) and amiodarone treatment (amiodarone, 150 mg/kg/day, p.o., 4 weeks). Electrocardiogram (ECG) recordings, gene profiling by DNA microarray and Northern blotting were carried out. Amiodarone, like hypothyroidism, caused significant prolongation of RR and QT intervals in ECGs. Microarray analysis of 8435 genes in the left ventricular myocardium revealed a significant similarity in expression profiles between hypothyroidism and amiodarone (R=0.63, p<0.00001). The gene expression profiles of hypothyroidism and amiodarone showed closer correlation when top 100 up-regulated and 100 down-regulated genes in hypothyroidism (total 200 genes) were analyzed (R=0.78, p<0.00001). Northern blots of left ventricular myocardium showed a parallel decrease in mRNAs for myosin heavy chain (MHC)-alpha and a parallel increase for myosin heavy chain (MHC)-beta in hypothyroidism and amiodarone. In the liver and pituitary, in contrast, Northern blots showed quite different changes in the transcripts of the representative T3-responsive genes in the hypothyroidism and amiodarone. In conclusion, long-term treatment with amiodarone causes cardioselective hypothyroid-like alterations in gene expression profiles. The potent anti-arrhythmic activity of amiodarone may be attributable, in part at least, to this unique transcriptional remodeling.

Release of thioredoxin from Saccharomyces cerevisiae with environmental stimuli: solubilization of thioredoxin with ethanol.

Thioredoxin is crucial for the maintenance of the redox status of cells of all types. Mammalian thioredoxin is secreted from various types of cells, although the mechanism underlying has not yet been clarified. Previously, we demonstrated that thioredoxin was released from Saccharomyces cerevisiae after treatment with ethanol. In this paper, we show that as well as ethanol, low-pH shock and hypoosmotic shock release thioredoxin. Low-molecular-weight proteins in yeast cells were preferentially released by treatment with ethanol and low-pH shock. A cell wall integrity pathway seems partially involved in the hypoosmotic shock-induced release of thioredoxin. Considerable amounts of thioredoxin were present in the insoluble fractions of the cells, a portion of which was associated with lipid microdomains that are resistant to nonionic detergent at 4 degrees C. The intracellular localization of thioredoxin may influence the efficiency of its release from yeast cells with ethanol.

Efficient extraction of thioreodoxin from Saccharomyces cerevisiae by ethanol.

Thioredoxin, an antioxidant protein, is a promising molecule for development of functional foods because it protects the gastric mucosa and reduces the allergenicity of allergens. To establish a method for obtaining an ample amount of yeast thioredoxin, we found here that thioredoxin is released from Saccharomyces cerevisiae by treatment with 20% ethanol. We also found that Japanese sake contains a considerable amount of thioredoxin.

Unique regulation of thyroid hormone metabolism during fasting in the house musk shrew (Suncus murinus, Insectivora: Soricidae).

The active hormone, 3,3',5-triiodothyronine (T3) is derived from thyroxine (T4) by the action of iodothyronine 5'-deiodinases (5'-D). By now two types of 5'-D have been identified; Type 1 (D1) and type 2 (D2). A relative contribution of these isotypes to the circulating T3 levels in the human remains to be determined whereas a number of reports indicate that, under physiological conditions, D1 plays a major role in maintaining circulating T3 levels in rodents. In both human and rodents, sickness and starvation reduce serum T3 concentration mainly through decrease in D1 activity. Recently, we found that the house musk shrew (Suncus murinus, Insectivora: Soricidae) has a different tissue distribution of D1 activity. Because compared to rodents D1 activity in the shrew was found only in liver at a much reduced level, D2 rather than D1 may play a role in the maintenance of serum T3. Therefore, we questioned how D1 and D2 activities change in fasted shrews and how these changes affect circulating thyroid hormone levels. We thus starved shrews for 24, 48 or 72 h and measured changes in serum concentration of T3, T4, and 3,3',5'-triiodothyronine (reverse T3, rT3) and D1 activities as well as its mRNA expression in liver. D2 activities were also measured in brown adipose tissue (BAT) and cerebral cortex of shrews. Unlike in human and rodents, T3 levels in shrews remained constant during fasting while T4 levels tended to decrease, resulting in an increase in its T3/T4 ratio. On the other hand, changes in rT3 levels were similar to those in human and rodents, being elevated with fasting. D1 mRNA and its activity were significantly reduced in the liver whereas D2 activities in BAT and cerebral cortex were increased by fasting. These results indicated that fasting in shrews also reduced hepatic D1 activity but it did not affect circulating T3 levels. The increased T3/T4 ratio together with increased D2 activity in BAT and cerebral cortex with fasting suggest that D2 rather than D1 is responsible for the maintenance of T3 levels in the house musk shrew.

Evaluation of relative potencies of PCB126 and PCB169 for the immunotoxicities in ovalbumin (OVA)-immunized mice.

Dioxin-like polychlorinated biphenyls (PCBs) exert their toxicities by activating the arylhydrocarbon receptor (AhR), a ligand-dependent transcription factor, in a similar manner to the most toxic dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In the present study, we re-evaluated the relative potency (REP) of the toxic members of dioxin-like PCBs, PCB126 (toxic equivalency factor, TEF 0.1) and PCB169 (TEF 0.01) relative to TCDD, focusing our attention on their effects on the immune reactions of mice immunized with ovalbumin (OVA). Thymus involution, IgM production, and IL-5 produced by the splenocytes were examined in addition to CYP1A1 induction, the established index of AhR-activation, in the spleen. PCB126 had an REP value of 0.1 because of its effects on thymus, IgM, IL-5, and CYP1A1 induction in the spleen, although its effect on IgG1 production was weaker. On the other hand, PCB169 had a smaller REP value estimated at less than 0.01 with regard to CYP1A1 induction in the spleen and all examined immunological effects, except for IgM production. The tissue concentrations of PCB169 and TCDD could not explain the reason for the smaller potency of PCB169, since the spleen contained a higher proportion of PCB169 to TCDD than dosed. These results indicate that dioxin-like PCBs, especially PCB169, shows deviating REPs against immune reactions, and also suggest that PCB169-liganded AhR behaves differently from TCDD-liganded AhR in immune cells.

Steroid receptor coactivator-1 deficiency causes variable alterations in the modulation of T(3)-regulated transcription of genes in vivo.

Thyroid hormone exerts its biological effect by binding to a TR. Both liganded and unliganded TRs regulate the transcription of T(3)-responsive genes. Cofactors with activating or repressing function modulate the transcriptional regulation by TRs. We showed that steroid receptor coactivator 1 (SRC-1)-deficient mice (SRC-1(-/-)) exhibit partial resistance to thyroid hormone at the level of the pituitary thyrotrophs. To determine whether SRC-1 deficiency affects globally T(3)-dependent transcriptional regulation, we studied the effects of thyroid hormone deprivation and replacement on the expression of several genes in different tissues of SRC-1(-/-) and wild-type mice (SRC-1(+/+)). Thyroid hormone deficiency was induced by a low iodine diet (LoI) supplemented with propylthiouracil (PTU) for 2 wk. L-T(3) was injected ip for the last 4 d in one group (PTU+T(3) group), and another group (PTU group) received only vehicle. Levels of mRNAs for T(3)-responsive genes were determined by Northern blotting: GH and TSH beta in pituitary; type 1 iodothyronine 5'-deiodinase, spot 14 (S14), and malic enzyme in liver; and sarcoplasmic reticulum calcium adenosine triphosphatase 2 and myosin heavy chain alpha and beta in heart. Serum parameters, TSH, total cholesterol, creatine kinase, and alkaline phosphatase (AP), were also measured. Hypothyroidism produced a comparable increase in TSH beta mRNA in both genotypes, but its suppression by L-T(3) was attenuated in SRC-1(-/-) mice. In contrast, hypothyroidism failed to reduce S14 mRNA levels in SRC-1(-/-) mice. As a consequence, the response to L-T(3) was not observed in these mice. SRC-1 deficiency had no effect on the expression of the rest of the T(3)-responsive genes examined. Of the four serum parameters, the T(3)-mediated decrease in TSH and changes in AP were attenuated in SRC-1(-/-) mice. We conclude that SRC-1 deficiency altered the expression of only some of the T(3)-responsive genes. SRC-1 appears to be involved not only in transcriptional activation by liganded TRs, but also in the suppression by liganded or unliganded TRs. Some of the effects of SRC-1 may be TR isoform specific.