[Effects of a fall intervention program for elderly patients with dementia based on person-centered care on care staff].

AIM: This study aimed to clarify the effects of a fall prevention intervention that focused on the characteristics of falls among elderly patients with dementia and was based on person-centered care in geriatric facilities on care staff. METHODS: This study was conducted between May 2016 and January 2017, and the subjects were classified into two groups: the intervention group, consisting of members who had participated in a three-month education training program, and the control group, consisting of members who provided the usual care. The study period was nine months divided as follows: training period (three months), fall prevention practice (three months), and follow-up period (three months). The quality of care was measured using the Nursing Quality Indicator for Preventing Falls (NQIPFD), and the assessment scale of health care professionals' recognition of the successful Interdisciplinary Team Approach in Health Care Facilities for the Elderly was also used. In total, the care staff members were evaluated four times: once to obtain baseline values before training, and again after the training period, after the fall prevention practice, and after the follow-up period. The results were analyzed using an analysis of variance (fixed factors = group and time, random factor = subjects, and covariance = years of experience working at the geriatric facility and type of job). RESULTS: There were 50 care staff subjects in the intervention group and 69 people in the control group. The results of the analysis of variance indicated that there was a significant difference in the NQIPFD between baseline 68.60 (±9.09) and follow-up 70.02 (±9.88) in the intervention group. With regard to the differences by intervention, the effect size of the dementia knowledge scale scores was 0.243 higher than the others, which was significant (p<0.01). CONCLUSIONS: The results showed that the participation of care staff in a fall intervention program to support elderly patients with dementia based on person-centered care significantly improved the NQIPFD and other measured factors. These findings suggest that the program fostered positive effects among the care staff.

Role of fusional convergence amplitude in postoperative phoria maintenance in children with intermittent exotropia.

PURPOSE: To examine the role of fusional convergence amplitude in postoperative phoria maintenance in childhood intermittent exotropia [X(T)]. METHODS: The medical records of 29 children aged 15 years or younger (mean age, 10.8 ± 2.4 years) and treated with monocular recession-resection for X(T) were reviewed retrospectively. The patients' fusional convergence amplitude (break point/total amplitudes), physiologic diplopia, and phoria maintenance (presence/absence of phoria maintenance and ability to maintain phoria) were assessed. The presence of phoria maintenance was confirmed by a cover test, and the ability to maintain phoria was quantified using the Bagolini red filter bar. Correlations of the amplitude size with the presence and ability of phoria maintenance were investigated. RESULTS: A significant correlation was seen between fusional amplitude (break point/total) and ability to maintain phoria at near and at far (break point: P < .05 at near/P < .01 at far; total: P < .05 at near/far). Neither the break point amplitude nor the total amplitude significantly differed between the patients with phoria maintenance and those without it (break point: P = .71 at near, P = .29 at far; total: P = .98 at near, P = .85 at far). Phoria maintenance correlated with the suppression of physiologic diplopia during phoria (P < .01). The deviation angle did not significantly correlate with fusional amplitude either at near (P = .58) or at far (P = .27). CONCLUSIONS: In childhood X(T), fusional amplitude plays a role in enforcing the patient's ability to maintain phoria. However, sufficient fusional amplitude does not guarantee fully functioning fusion if suppression is present during phoria.

Influence of Test Distance on Stereoacuity in Intermittent Exotropia.

AIMS: To investigate influence of test distance on stereoacuity in intermittent exotropia (X[T]) using the same test conditions for both near and far distances. METHODS: Subjects were 38 consecutive patients with X(T). All the patients were between ages 6 and 15 years and had decimal visual acuity of 1.0 or better. Another inclusion criterion was presence of phoric condition at near and far distances. Stereoacuity was measured at a near distance of 40 cm and at a far distance of 5 m. The following test conditions were used for both test distances: separation of the two eyes using polarized glasses, and a target with a random dot pattern. All the stereograms had the same subtended angle of 2.5º, and binocular disparity of 480, 240, 120, and 60 arcsec. We used two stereogram types with crossed and uncrossed disparities. RESULTS: Far stereoacuity of 38 subjects measured with the crossed disparity was significantly worse than near stereoacuity (P<0.05, Wilcoxon signed-ranks test), although 30 (78.9%) of the 38 subjects showed no differences in stereopsis between the near and far distances. Far stereoacuity of 38 cases measured with the uncrossed disparity was significantly worse than at near (P<0.05, Wilcoxon signed-ranks test), although 20 (52.6%) of the 38 subjects showed no differences between stereoacuity at near and far. In comparison of stereoacuity with crossed disparity and uncrossed disparity, stereoacuity with crossed disparity was significantly better than that with uncrossed disparity both at near and far (P<0.05, Wilcoxon signed-ranks test). CONCLUSIONS: Stereoacuity in X(T) was different according to test distance when measured controlling subtended angle of stereogram at both distances. Far stereoacuity was significantly worse than near stereoacuity when measured using test targets with both crossed and uncrossed disparities. Additionally, stereoacuity measured with crossed disparity was better than that with uncrossed disparity at both distances.

Inhibitory Effect of Oleic Acid on Octanoylated Ghrelin Production.

Ghrelin is a growth hormone-releasing peptide that also displays orexigenic activity. Since serine-3 acylation with octanoylate (octanoylation) is essential for the orexigenic activity of ghrelin, suppression of octanoylation could lead to amelioration or prevention of obesity. To enable the exploration of inhibitors of octanoylated ghrelin production, we developed a cell-based assay system using AGS-GHRL8 cells, in which octanoylated ghrelin concentration increases in the presence of octanoic acid. Using this assay system, we investigated whether fatty acids contained in foods or oils, such as acetic acid, stearic acid, oleic acid, linoleic acid, and α-linolenic acid, have inhibitory effects on octanoylated ghrelin production. Acetic acid did not suppress the increase in octanoylated ghrelin production in AGS-GHRL8 cells, which was induced by the addition of octanoic acid. However, stearic acid, oleic acid, linoleic acid, and α-linolenic acid significantly suppressed octanoylated ghrelin production, with the effect of oleic acid being the strongest. Additionally, oleic acid decreased the serum concentration of octanoylated ghrelin in mice. The serum concentration of des-acyl ghrelin (without acyl modification) was also decreased, but the decrease was smaller than that of octanoylated ghrelin. Decreased octanoylated ghrelin production likely resulted from post-translational ghrelin processing, as there were no significant differences in gene expression in the stomach between oleic acid-treated mice and controls. These results suggest that oleic acid is a potential inhibitor of octanoylated ghrelin production and that our assay system is a valuable tool for screening compounds with suppressive effects on octanoylated ghrelin production.

Bladder pain relief by HMGB1 neutralization and soluble thrombomodulin in mice with cyclophosphamide-induced cystitis.

High mobility group box 1 (HMGB1), one of damage-associated molecular patterns (DAMPs), plays roles in not only inflammation but also processing of somatic pain. Given that no evidence for roles of HMGB1 in visceral pain signaling is available, we asked if HMGB1 participates in bladder pain accompanying cystitis caused by cyclophosphamide in mice, using the anti-HMGB1 neutralizing antibody and recombinant human soluble thrombomodulin (rhsTM) that sequesters HMGB1 and promotes its degradation by thrombin. Cyclophosphamide, administered i.p., caused bladder pain-like nociceptive behavior and referred hyperalgesia accompanying cystitis symptoms including increased bladder weight, an indicator of edema, in mice. The cyclophosphamide-induced bladder pain and referred hyperalgesia, but not increased bladder weight, were prevented by i.p. preadministration of the anti-HMGB1 neutralizing antibody or rhsTM. HMGB1, given i.p., facilitated the bladder pain and referred hyperalgesia caused by a subeffective dose of cyclophosphamide, an effect blocked by rhsTM. In the cyclophosphamide-treated mice, HMGB1 levels greatly decreased in the bladder tissue, particularly in the urothelial cells, but did not change in the plasma. Low molecular weight heparin, known to inhibit the receptor for advanced glycation end products (RAGE), but not lipopolysaccharide from Rhodobacter sphaeroides, an inhibitor of toll-like receptor 4 (TLR4), blocked the cyclophosphamide-induced bladder pain and referred hyperalgesia. Thus, our data indicate involvement of HMGB1 in the cyclophosphamide-induced bladder pain signaling, but not cystitis itself, and suggest that targeting HMGB1 with rhsTM or blocking RAGE might serve as a novel therapeutic strategy for the management of bladder pain.

Recombinant human soluble thrombomodulin prevents peripheral HMGB1-dependent hyperalgesia in rats.

BACKGROUND AND PURPOSE: High-mobility group box 1 (HMGB1), a nuclear protein, is actively or passively released during inflammation. Recombinant human soluble thrombomodulin (rhsTM), a medicine for treatment of disseminated intravascular coagulation (DIC), sequesters HMGB1 and promotes its degradation. Given evidence for involvement of HMGB1 in pain signalling, we determined if peripheral HMGB1 causes hyperalgesia, and then asked if rhsTM modulates the HMGB1-dependent hyperalgesia. EXPERIMENTAL APPROACH: Mechanical nociceptive threshold and swelling in rat hindpaw were determined by the paw pressure test and by measuring paw thickness, respectively, and HMGB1 levels in rat hindpaw plantar tissue, dorsal root ganglion (DRG) and serum were determined by Western blotting or elisa. KEY RESULTS: Intraplantar (i.pl.) administration of HMGB1 rapidly evoked paw swelling and gradually caused hyperalgesia in rats. Systemic administration of rhsTM abolished HMGB1-induced hyperalgesia, and partially blocked paw swelling. LPS, administered i.pl., rapidly produced mild paw swelling, and gradually caused hyperalgesia. The anti-HMGB1 neutralizing antibody abolished LPS-induced hyperalgesia, but partially inhibited paw swelling. rhsTM at a high dose, 10 mg kg(-1) , prevented both hyperalgesia and paw swelling caused by LPS. In contrast, rhsTM at low doses, 0.001-1 mg kg(-1) , abolished the LPS-induced hyperalgesia, but not paw swelling. HMGB1 levels greatly decreased in the hindpaw, but not DRG. Serum HMGB1 tended to increase after i.pl. LPS in rats pretreated with vehicle, but not rhsTM. CONCLUSION AND IMPLICATIONS: These data suggest that peripheral HMGB1 causes hyperalgesia, and that rhsTM abolishes HMGB1-dependent hyperalgesia, providing novel evidence for therapeutic usefulness of rhsTM as an analgesic.

Two phases of calcium requirement during starfish meiotic maturation.

During meiosis in oocytes of the starfish, Asterina pectinifera, a Ca(2+) transient has been observed. To clarify the role of Ca(2+) during oocyte maturation in starfish, an intracellular Ca(2+) blocker, TMB-8, was applied. The oocyte maturation induced by 1-methyladenine (1-MA) was blocked by 100 microM TMB-8. Reinitiation of meiosis with germinal vesicle breakdown (GVBD) and the following chromosome condensation did not take place. Maturation-promoting factor (MPF) activity did not increase and GVBD and chromosome condensation did not occur. Ca(2+) transient observed immediately after 1-MA application in control oocytes was also blocked by TMB-8. When calyculin A, which activate the MPF directly, was applied to the oocytes instead of 1-MA in seawater containing 100 microM TMB-8, GVBD and chromosome condensation were blocked. Cytoplasmic transplantation studies confirmed that MPF was activated, although TMB-8 blocked GVBD. These results show that TMB-8 blocked the increase of MPF activity induced by 1-MA and the process of active MPF inducing GVBD and subsequent chromosome condensation. Together with the above phenomena, it is conceivable that there are two phases of Ca(2+) requirement during starfish oocyte maturation. These are the activation of MPF, moreover, GVBD, and the subsequent chromosome condensation.

Calyculin A causes the activation of histone H1 kinase and condensation of chromosomes in unfertilized sea urchin eggs independently of the maturation-promoting factor.

Calyculin A is known to inhibit the type-1 and type-2A phosphatases. We previously reported that calyculin A induces contractile ring formation in unfertilized sea urchin eggs, an increase in histone H(1) kinase activity, and chromosome condensation in the calyculin A-treated unfertilized eggs, and the changes induced by calyculin A are not affected by emetine, an inhibitor of protein synthesis. These observations suggest that the mechanism by which histone H(1) kinases are activated by calyculin A is different from that of maturation-promoting factor (MPF), which is activated by a molecular modification of existed cdc2 and newly synthesized cyclin B. We report here that no cyclin B was detected by immunoblotting of unfertilized calyculin A-treated eggs. In addition, no DNA synthesis was induced by calyculin A. As well, butyrolactone I (an inhibitor of cdc2 and cdk2 kinase) had no effect on the increase in histone H(1) kinase activity nor the chromosome condensation, both of which were induced by calyculin A. Thus, we conclude that calyculin A induces histone H(1) phosphorylation in an MPF-independent manner through inhibition of type-1 phosphatase, and that the chromosome condenses as a result of histone H(1) phosphorylation.