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Depression in dementia patients is associated with complications such as decreased activities of daily living and decreased quality of life. Because pharmacotherapeutic treatments for depression in dementia patients may have a poor risk-benefit ratio, effective non-pharmacotherapeutic interventions are favourable. However, the development of effective treatments requires the identification of depression-associated factors that can be modified by non-pharmacotherapeutic means in dementia patients. This systematic literature review aimed to identify modifiable factors related to depression and confirm that these factors can be improved by non-pharmacotherapeutic interventions. We searched PubMed, SpringerLink, the Web of Science, and the Cochrane Library for articles published between June 2007 and June 2017. We included studies that investigated causes of depression in dementia patients and excluded studies with unclear dementia diagnostic criteria or operational definitions. Of 9004 records screened, 6 studies were included. The participants included community-dwelling individuals and long-term care facility residents. The severity of dementia varied from mild to severe. After reviewing the studies, we identified five modifiable relevant factors in community-dwelling individuals: (i) pain; (ii) neuropsychiatric symptoms; (iii) cognitive decline; (iv) social isolation; and (v) quality of life. In long-term care facility residents, we identified neuropsychiatric symptoms and quality of life as relevant factors. Our results indicated that non-pharmacological interventions that improve these factors may improve symptoms of depression. A longitudinal study is recommended to clarify the mechanisms underlying depression symptoms and treatment in dementia patients. In addition, further investigation is needed to elucidate the ways in which differing dementia types and severity affect symptoms of depression.

Aim: Patients infected with hepatitis C virus (HCV) genotype 2 are more sensitive to interferon (IFN) therapy than those infected with genotype 1, but 10–20% of patients do not achieve a sustained viral response (SVR) to combination therapy with pegylated (PEG) IFN and ribavirin (RBV). This study examines the prognostic factors associated with SVR in patients infected with HCV genotype 2 treated with PEG IFN and RBV. Methods: We treated 149 patients with chronic hepatitis C caused by HCV genotype 2. The patients received s.c. PEG IFN-α-2b (1.5 µg/kg) and a weekly weight-adjusted dose of RBV (600, 800 and 1000 mg per 80 kg, respectively) for 24 weeks and then prognostic factors associated with the SVR were examined. Results: Among the 149 patients, 138 completed the combination therapy and a sustained viral response was achieved in 71.8% of them. Univariate analysis showed that age, as well as mean RBV and PEG IFN doses were factors affecting the SVR (P = 0.012, =0.021, =0.014). Multivariate analysis identified age and mean PEG IFN dose (P = 0.021, =0.018, respectively) as factors involved in the SVR, but not mean RBV dose. Conclusion: The SVR of patients infected with HCV genotype 2 depended on the dosage of PEG IFN, but not of RBV. Selecting sufficient doses of PEG IFN for combination with RBV is critical for treating such patients.

Background: The aim of this study was to assess the response to dioxin-induced oxidative stress in neonates via lactation in the model we have described previously. Methods: Maternal rats were treated with a single dose of 50 or 100 µmol/kg 1,2,3,4-tetrachlorodibenzo-p-dioxin (TCDD) on the first day postpartum (day 1). Messenger RNA levels of the key anti-oxidant enzymes (AOE), phospholipid hydroperoxide-glutathione peroxidase (PH-GPx), cellular-glutathione peroxidase (cell-GPx), copper-zinc superoxide dismutase (CuZn SOD), manganese superoxide dismutase (Mn SOD) and catalase (CAT) in the neonatal and maternal livers were determined by a competitive reverse transcription− polymerase chain reaction method. Results: Lactational transfer of 1,2,3,4-TCDD induced an inhibition of PH-GPx and cell-GPx mRNA in the neonatal liver on day 2 to 68 (P

Renin–angiotensin system (RAS) blockade is the gold standard for the treatment of diabetic nephropathy. However, patients with diabetes mellitus still have an increased risk of progressive deterioration of renal function associated with albuminuria. de Zeeuw et al.1 published a paper, entitled Selective vitamin D receptor activation with paricalcitol for reduction of albuminuria in patients with type 2 diabetes (VITAL study): a randomised controlled trial, in The Lancet in November 2010. This multinational, placebo‐controlled, double‐blind trial enrolled 281 patients with type 2 diabetes and albuminuria who were receiving angiotensin‐converting enzyme inhibitors or angiotensin receptor blockers to elucidate the efficacy of a vitamin D analogue (19‐nor‐1‐α‐dihydroxyvitamin D2; paricalcitol) on albuminuria. Patients were assigned to receive 24 weeks treatment with placebo or 1 or 2 μg paricalcitol daily. The primary measure of efficacy was the percentage change in geometric mean urinary albumin:creatinine ratio (UACR) from baseline to the last measurement during the treatment period in the combined paricalcitol groups vs the placebo group. The change in UACR from baseline to the last measurement in the 1 and 2 μg paricalcitol‐treated groups was −20% (95% confidence interval [CI] −30 to −8) and −14% (95% CI −24 to −1), respectively (Table 1). The reduction in UACR in the 2 μg paricalcitol‐treated group was sustained throughout the 24‐week treatment period and reversed to baseline values after completion of treatment. However, the primary endpoint was negative: the UACR in the combined paricalcitol groups reduced by 15% compared with placebo (P = 0.071; Figure 1). The UACR fell by 18% in the 2 μg paricalcitol‐treated group and by 11% in the 1 μg paricalcitol‐treated group, but these differences failed to reach statistical significance (P = 0.053 and 0.23, respectively). In the secondary efficacy analysis, 24‐h urine albumin was reduced by −28% (P = 0.009) in the 2 μg paricalcitol‐treated group. Figure 1 Change in the urinary albumin : creatinine ratio (UACR) from baseline to the last measurement during the 24‐week treatment period. Data show the geometric mean of UACR, with error bars representing 95% confidence intervals. ... Table 1 Efficacy analysis of 24 weeks treatment with 1 or 2 μg paricalcitol or placebo (Reprinted from de Zeeuw et al.1, Copyright 2010, with permission from Elsevier.) Several smaller randomized trials have indicated that paricalcitol reduces proteinuria in patients with chronic kidney disease. For example, Alborzi et al.2 showed that administration of 1 and 2 μg paricalcitol for 1 month reduced 24‐h urinary albumin excretion by 48% (P

Background and Methods: The aim of this study was to assess the effect of lactational exposure to dioxins in neonates on the cytochrome P450 1A1 (CYP1A1) induction in the level of gene expression. Maternal rats were treated with a single dose of 50 or 100 μmol/kg 1,2,3,4-tetrachlorodibenzo-p-dioxin (1,2,3,4-TCDD), a low potent congener of dioxins, on the first day post-partum (day 1). Induction of CYP1A1 mRNA expression was quantitatively analyzed by the competitive reverse transcription–polymerase chain reaction (RT–PCR) method. Results: The CYP1A1 mRNA was detectable at extremely low amounts in the liver of control neonates and mothers. The mRNA ratios of CYP1A1 to β-actin in neonates were dose-dependently increased by the treatment of 1,2,3,4-TCDD of their mothers. Its peak occurred on day 6 and was sustained at the same level on day 10. Increases of the ratio with 100 μmol/kg 1,2,3,4-TCDD on day 2, 6 and 10 were 26-, 40- and 40-fold of the appropriate controls, respectively. These levels paralleled the activity of ethoxyresorufin-o-deethylase, representing CYP1A mediated monooxygenase. In the mother, the mRNA ratio was increased only to threefold of the control, 10 days after treatment. Conclusion: Current RT-PCR procedure enabled to assess both constitutive and induced levels of CYP1A1 mRNA in the neonatal rat livers. Although the dose of 1,2,3,4-TCDD selected in this study was about 5000 times higher than the daily intake of dioxins in breast-fed infants, CYP1A1 mRNA was highly induced for a longer period of time in neonatal rats receiving 1,2,3,4-TCDD via lactation than the treated maternal rats.

Personal computers have been helping blind persons to deal with textual information. Recently, however, operating systems based on GUIs have been rapidly spreading in the personal computer environment. Since GUIs utilize many figures and appeal to the eye, they are inherently difficult to adapt for blind persons. For the purpose of providing blind persons with access to a GUI-based operating system, we have proposed and developed a screen reader that works on the basis of keyboard operation and corresponding speech output. This paper first discusses the problems of accessibility of GUIs to blind problems and proposes the use of a screen reader as a solution. Then, the development of a prototype screen reader, the evaluation of the prototype, and the functions of the new screen reader after revision based on evaluations are described. Lastly, the purposes blind persons have for using personal computers and the applications usable with the support of our screen reader are compared. The effectiveness of our approach is discussed. © 1998 Scripta Technica, Syst Comp Jpn, 29(13): 18–27, 1998