162 research outputs found

    Solute distribution in porous rhyolite as evaluated by sequential centrifugation

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    International audiencePore water in a porous rhyolite, having a porosity of 27% and pore radii ranging from >25 μm to 0.008 μm, was centrifugally extracted stepwise with increasing centrifugal speed to examine the potential variations of the compositions of pore water and their relationships to reaction and transport occurring in the rock. The rock was soaked for from 1 h to 7 days in an aqueous solution prior to centrifugation. To evaluate the effect of adsorption under minimum effect of dissolution, Li+ and Br− were added to the solution as tracer ions. As centrifugal speed increased, water was extracted in order of large to small pores and the thickness of residual water film became thinner. The concentrations of ions dissolving from the rock (Na+, K+, Ca2+, etc.) after 7 days of immersion were relatively constant in pores of 1−10 μm radii and exponentially increased by 3−100 fold with decreasing pore radius to 0.1 μm. These ions are dissolved from the rock and transported toward the exterior of the rock by diffusion. The calculation using a reactive-transport equation showed that the observed concentration changes reflect the change in solute distribution profile with pore size. The concentration of Si after 7 days of immersion was approximately constant or slightly decreased with increasing centrifugal speed, which appears to be controlled by the solubility. The concentration of Li+ decreased with increasing centrifugal speed after 1 h of immersion but the trend changed after 7 days of reaction. Initial behaviour of Li+ is explained by adsorption on pore walls, and the change of trend is explained by desorption of that previously adsorbed, slight amounts of dissolution, and inflow from the outside of the rock. The change in concentration of Br− with increasing centrifugal speed was small, probably because Br− was not adsorbed on the surfaces. The sequential centrifugation thus provides information on the solute distribution associated with reaction and transport occurring in rock pores

    A Single-institution Study on Predictors of Short-term Progression from Mild Cognitive Impairment in Parkinson’s Disease to Parkinson’s Disease with Dementia

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    Background: Patients with non-demented Parkinson’s disease (PD) sometime have mild cognitive impairment (MCI), and mild cognitive impairment in Parkinson’s disease (PD-MCI) may convert to Parkinson’s disease with dementia (PDD) within several years. Cognitive impairment also occurs in the early stages of the disease, gradually progressing to lower quality of life and instrumental activities of daily living. It is important to elucidate the predictors of progression from PD-MCI to PDD via longitudinal studies. Methods: This was a single center, case-control study. We analysed data from 49 patients with PD-MCI diagnosed as level I using the Movement Disorder Society PD-MCI criteria at baseline who had completed 1.5 years of follow-up. We defined patients who progressed to PDD as patients with progressive PD-MCI and patients who did not progress to PDD as patients with non-progressive PD-MCI. Depression, apathy, sleep disorders, constipation, light-headedness, hallucinations, impulse control disorders (ICDs) and impulsive-compulsive behaviors (ICBs) at baseline were statistically analysed as predictors of progression. Results: Of the 49 PD-MCI patients, 33 did not convert to PDD (non-progressive PD-MCI), and 16 converted to PDD (progressive PD-MCI). The Mini-Mental State Examination (MMSE) score, light-headedness and ICDs were elucidated as predictors of progressive PD-MCI via a multivariate logistic regression model. The adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for each item were MMSE score, OR 0.324, 95% CI 0.119-0.882, P = 0.027; light-headedness, OR 27.665, 95% CI 2.263-338.185, P= 0.009; and ICDs, OR 53.451, 95% CI 2.298-291.085, P = 0.010. Conclusion: Cognitive function, ICDs and light-headedness may be risk factors for the development of PDD in PD-MCI patients

    Inhibition of Plasminogen Activator Inhibitor- 1 Attenuates Transforming Growth Factor- β-Dependent Epithelial Mesenchymal Transition and Differentiation of Fibroblasts to Myofibroblasts

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    Transforming growth factor-β (TGF-β) is central during the pathogenesis of pulmonary fibrosis, in which the plasminogen activator inhibitor-1 (PAI-1) also has an established role. TGF-β is also known to be the strongest inducer of PAI-1. To investigate the link between PAI-1 and TGF-β in fibrotic processes, we evaluated the effect of SK-216, a PAI-1-specific inhibitor, in TGF-β-dependent epithelial-mesenchymal transition (EMT) and fibroblast to myofibroblast differentiation. In human alveolar epithelial A549 cells, treatment with TGF-β induced EMT, whereas co-treatment with SK-216 attenuated the occurrence of EMT. The inhibition of TGF-β-induced EMT by SK-216 was also confirmed in the experiment using murine epithelial LA-4 cells. Blocking EMT by SK-216 inhibited TGF-β-induced endogenous production of PAI-1 and TGF-β in A549 cells as well. These effects of SK-216 were not likely mediated by suppressing either Smad or ERK pathways. Using human lung fibroblast MRC-5 cells, we demonstrated that SK-216 inhibited TGF-β-dependent differentiation of fibroblasts to myofibroblasts. We also observed this inhibition by SK-216 in human primary lung fibroblasts. Following these in vitro results, we tested oral administration of SK-216 into mice injected intratracheally with bleomycin.We found that SK-216 reduced the degree of bleomycin-induced pulmonary fibrosis in mice. Although the precise mechanisms underlying the link between TGF-β and PAI-1 regarding fibrotic process were not determined, PAI-1 seems to act as a potent downstream effector on the pro-fibrotic property of TGF-β. In addition, inhibition of PAI-1 activity by a PAI-1 inhibitor exerts an antifibrotic effect even in vivo. These data suggest that targeting PAI-1 as a downstream effector of TGF-β could be a promising therapeutic strategy for pulmonary fibrosis

    Recurrent transient thyrotoxicosis with painless thyroiditis--a case report.

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    A case of a 40-year-old woman who was suffering from painless thyroiditis with recurrent transient thyrotoxicosis is reported. Acute exacerbations occurred four times during the past ten years, two after delivery and two after catching a cold. Serum thyroid hormones increased, though radioiodine uptake by the thyroid was very low and no inflammatory signs were observed. The histological findings of the thyroid were of atypical thyroiditis and not consistent with either chronic lymphocytic thyroiditis or subacute thyroiditis. Tanned sheep red cell hemagglutination titers for anti-thyroglobulin antibodies (TRC) and for anti-microsomal antibodies (MHA) were negative or low. The disease seems to be rare and the pathophysiology and etiology are discussed.</p

    Studies on thyroid function in rats with experimentally induced thyroiditis.

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    Function of pituitary-thyroid axis was studied in rats with experimentally induced thyroiditisWistar strain female rats were immunized with homologous thyroid extract in Freund's complete adjuvant and with simultaneous intradermal injection of pertussis vaccine concentrate. They received booster shots at the first and third week after the initial immunization. Serum thyroid hormones and TSH were measured just before, and at weekly intervals after, the initial immunization. Histological examination of the thyroid gland at the second week after immunization showed slight infiltration of macrophages in the thyroid follicles. From the third to the fourth week, massive lymphoid cell infiltration and destruction of follicular architecture developed in all immunized rats. Serum R3 levels slightly decreased during the second week, increased transiently during the third week, then decreased again thereafter. Serum T4 levels decreased slightly durinf the fourth week. Serum TSH levels were not elevated significantly during the third week, but the response to TRH was significantly increased at this time. Basal TSH levels were increased during the fourth week. The TRH test was a sensitive method capable of detecting minimal failure of thyroid function undetected by other routine measuremens of thyroid hormones and TSH.</p

    The Pavlik harness in the treatment of developmentally dislocated hips: results of Japanese multicenter studies in 1994 and 2008

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    AbstractBackgroundIt has already been more than 50years since the Pavlik harness was introduced in Japan, and today the Pavlik harness is widely recognized as the standard initial treatment modality for developmental dysplasia of the hip. We performed a multicenter nationwide questionnaire study concerning the results of Pavlik harness treatment twice in 1994 and 2008.MethodsIn 1994 and in 2008, we sent questionnaires to 12 institutes in Japan specializing mainly in pediatric orthopedics. We compare the results of these two studies and discuss differences in reduction rates, incidence of avascular necrosis in the femoral epiphysis and the percentage of joints with acceptable morphology (Severin grade I+II/total) at skeletal maturity. We statistically assessed these results to see whether there were changes in the treatment outcomes over this 14-year period.ResultsReduction of the dislocated hips was obtained by the Pavlik harness in 80.2% (1990/2481 hips; 1994) and 81.9% (1248/1523 hips; 2008). The incidences of avascular necrosis of the proximal femoral epiphysis in the dysplastic hips were 14.3% (119/835 hips; 1994) and 11.5% (76/663 hips; 2008). The type of avascular necrosis in hips from the 2008 study was determined according to the classification of Kalamchi and MacEwen: 24/69 hips (34.8%) were classified as group I; 20/69 hips (29.0%) as group II; 11/69 hips (15.9%) as group Ill; 14/69 hips (20.3%) as group IV. The percentages of hips with acceptable outcomes at skeletal maturity discerned from Severin X-ray changes (grade I+II/total) were 72.3% (604/835 hips; 1994) and 77.7% (488/628 hips; 2008).ConclusionReduction rates and the incidence of avascular necrosis in 2008 were statistically similar to the results in 1994. The rate of acceptable outcome (Severin grade I+II/total) in 2008 was statistically higher than that of 1994

    The DsbA-L gene is associated with respiratory function of the elderly via its adiponectin multimeric or antioxidant properties

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    Oxidative stress and inflammation play a key role in the age-related decline in the respiratory function. Adipokine in relation to the metabolic and inflammatory systems is attracting growing interest in the field of respiratory dysfunction. The present clinical and experimental studies investigated the role of the disulfide bond-forming oxidoreductase A-like protein (DsbA-L) gene, which has antioxidant and adiponectin multimeric (i.e. activation) properties, on the respiratory function of the elderly. We performed a retrospective longitudinal genotype-phenotype relationship analysis of 318 Japanese relatively elderly participants (mean age ± standard deviation: 67.0 ± 5.8 years) during a health screening program and an in vitro DsbA-L knock-down evaluation using 16HBE14o-cells, a commonly evaluated human airway epithelial cell line. The DsbA-L rs1917760 polymorphism was associated with a reduction in the ratio of forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) and %FEV1 and with the elevation of the prevalence of FEV1/FVC < 70%. We also confirmed that the polymorphism was associated with a decreased respiratory function in relation to a decrease in the ratio of high-molecular-weight adiponectin/total adiponectin (as a marker of adiponectin multimerization) and an increase in the oxidized human serum albumin (as an oxidative stress marker). Furthermore, we clarified that DsbA-L knock-down induced oxidative stress and up-regulated the mucus production in human airway epithelial cells. These findings suggest that the DsbA-L gene may play a role in protecting the respiratory function of the elderly, possibly via increased systemic adiponectin functions secreted from adipocytes or through systemic and/or local pulmonary antioxidant properties

    Prevalence of anemia in patients with chronic kidney disease in Japan: A nationwide, cross-sectional cohort study using data from the Japan Chronic Kidney Disease Database (J-CKD-DB)

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    Background: The Japan Chronic Kidney Disease Database (J-CKD-DB) is a nationwide clinical database of patients with chronic kidney disease (CKD) based on electronic health records. The objective of this study was to assess the prevalence of anemia and the utilization rate of erythropoiesis-stimulating agents (ESAs) in Japanese patients with CKD. Methods: In total, 31, 082 adult outpatients with estimated glomerular filtration rates of 5–60 ml/min/1.73 m2 in seven university hospitals were included this analysis. The proportions of patients with CKD stages G3b, G4, and G5 were 23.5%, 7.6%, and 3.1%, respectively. Results: The mean (standard deviation) hemoglobin level of male patients was 13.6 (1.9) g/dl, which was significantly higher than the mean hemoglobin level of female patients (12.4 (1.6) g/dl). The mean (standard deviation) hemoglobin levels were 11.4 (2.1) g/dl in patients with CKD stage G4 and 11.2 (1.8) g/dl in patients with CKD stage G5. The prevalences of anemia were 40.1% in patients with CKD stage G4 and 60.3% in patients with CKD stage G5. Logistic regression analysis showed that diagnoses of CKD stage G3b (adjusted odds ratio [95% confidence interval]: 2.32 [2.09–2.58]), G4 (5.50 [4.80–6.31]), and G5 (9.75 [8.13–11.7]) were associated with increased prevalence of anemia. The utilization rates of ESAs were 7.9% in patients with CKD stage G4 and 22.4% in patients with CKD stage G5. Conclusions: We determined the prevalence of anemia and utilization rate of ESAs in Japanese patients with CKD using data from a nationwide cohort study

    J-CKD-DB: a nationwide multicentre electronic health record-based chronic kidney disease database in Japan

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    The Japan Chronic Kidney Disease (CKD) Database (J-CKD-DB) is a large-scale, nation-wide registry based on electronic health record (EHR) data from participating university hospitals. Using a standardized exchangeable information storage, the J-CKD-DB succeeded to efficiently collect clinical data of CKD patients across hospitals despite their different EHR systems. CKD was defined as dipstick proteinuria ≥1+ and/or estimated glomerular filtration rate <60 mL/min/1.73 m² base on both out- and inpatient laboratory data. As an initial analysis, we analyzed 39, 121 CKD outpatients (median age was 71 years, 54.7% were men, median eGFR was 51.3 mL/min/1.73 m²) and observed that the number of patients with a CKD stage G1, G2, G3a, G3b, G4 and G5 were 1, 001 (2.6%), 2, 612 (6.7%), 23, 333 (59.6%), 8, 357 (21.4%), 2, 710 (6.9%) and 1, 108 (2.8%), respectively. According to the KDIGO risk classification, there were 30.1% and 25.5% of male and female patients with CKD at very high-risk, respectively. As the information from every clinical encounter from those participating hospitals will be continuously updated with an anonymized patient ID, the J-CKD-DB will be a dynamic registry of Japanese CKD patients by expanding and linking with other existing databases and a platform for a number of cross-sectional and prospective analyses to answer important clinical questions in CKD care

    A type of familial cleft of the soft palate maps to 2p24.2–p24.1 or 2p21–p12

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    Cleft of the soft palate (CSP) and the hard palate are subtypes of cleft palate. Patients with either condition often have difficulty with speech and swallowing. Nonsyndromic, cleft palate isolated has been reported to be associated with several genes, but to our knowledge, there have been no detailed genetic investigations of CSP. We performed a genome-wide linkage analysis using a single-nucleotide polymorphism-based microarray platform and successively using microsatellite markers in a family in which six members, across three successive generations, had CSP. A maximum LOD score of 2.408 was obtained at 2p24.2-24.1 and 2p21-p12, assuming autosomal dominant inheritance. Our results suggest that either of these regions is responsible for this type of CSP
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