The Construction Of A Business Model For Intellectually Disabled Workers

The Japanese welfare system has undergone rapid change. A law has been enacted that requires the handicapped to work in order to be independent from government assistance. However, it is difficult for the intellectually disabled (ID) to earn a living wage because of a lack of understanding with respect to their ability and communication skills. Our organization conducts business with ID individuals such as those with autism. The business model for the income of our organization and the ID individuals concerned was successfully constructed through an understanding and application of the characteristics of ID individuals. This paper shows the current environment affecting the ID and presents our strategic and successful business model that is designed to enable them to achieve a realistic livelihood

The Effect of Medical Cooperation in the CKD Patients: 10-Year Multicenter Cohort Study

Introduction: While chronic kidney disease (CKD) is one of the most important contributors to mortality from non-communicable diseases, the number of nephrologists is limited worldwide. Medical cooperation is a system of cooperation between primary care physicians and nephrological institutions, consisting of nephrologists and multidisciplinary care teams. Although it has been reported that multidisciplinary care teams contribute to the prevention of worsening renal functions and cardiovascular events, there are few studies on the effect of a medical cooperation system. Methods: We aimed to evaluate the effect of medical cooperation on all-cause mortality and renal prognosis in patients with CKD. One hundred and sixty-eight patients who visited the one hundred and sixty-three clinics and seven general hospitals of Okayama city were recruited between December 2009 and September 2016, and one hundred twenty-three patients were classified into a medical cooperation group. The outcome was defined as the incidence of all-cause mortality, or renal composite outcome (end-stage renal disease or 50% eGFR decline). We evaluated the effects on renal composite outcome and pre-ESRD mortality while incorporating the competing risk for the alternate outcome into a Fine-Gray subdistribution hazard model. Results: The medical cooperation group had more patients with glomerulonephritis (35.0% vs. 2.2%) and less nephrosclerosis (35.0% vs. 64.5%) than the primary care group. Throughout the follow-up period of 5.59 +/- 2.78 years, 23 participants (13.7%) died, 41 participants (24.4%) reached 50% decline in eGFR, and 37 participants (22.0%) developed end-stage renal disease (ESRD). All-cause mortality was significantly reduced by medical cooperation (sHR 0.297, 95% CI 0.105-0.835, p = 0.021). However, there was a significant association between medical cooperation and CKD progression (sHR 3.069, 95% CI 1.225-7.687, p = 0.017). Conclusion: We evaluated mortality and ESRD using a CKD cohort with a long-term observation period and concluded that medical cooperation might be expected to influence the quality of medical care in the patients with CKD

Localization of endogenous VASH2 in glomeruli.

<p>(A) The mRNA level of VASH2 in the kidney cortex from wild-type mice was assessed by real-time PCR. VASH2 expression was increased in diabetic condition compared with non-diabetic mice kidney. n = 6 for each group. *<i>P</i><0.05 versus wild-type mice. (B) VASH2 expression is detected with immunofluorescence for β-galactosidase. No immunoreactivity in glomeruli is seen in wild-type mice (left panel), whereas glomeruli from non-diabetic and diabetic VAHS2 knockout (VASH2^{<i>LacZ/LacZ</i>}) mice (middle and right panel, respectively) show a β-galactosidase-positive area (original magnification, ×400). (C) Double immunofluorescence for β-galactosidase and markers for glomerular component cells in VASH2 knockout mice show that the localization of β-galactosidase-positive area are consistent with platelet-derived growth factor receptor-β (PDGFRβ)-positive mesangial cells, but not CD31-positive endothelial cells and zonula occludens-1 (ZO-1)-positive podocytes.</p

Alterations of glomerular endothelial area and VEGF-A expression in diabetic VASH2 knockout mice.

<p>(A) The distribution of CD31, a marker for endothelial cells, was determined by immunofluorescence in non-diabetic wild-type, non-diabetic VASH2 knockout, diabetic wild-type, and diabetic VASH2 knockout mice (original magnification, ×400). (B) In quantitative analysis, CD31-positive glomerular endothelial area was expanded in diabetic wild-type mice, but it was significantly prevented in diabetic VASH2 knockout mice. No difference was found in endothelial area between non-diabetic wild-type and non-diabetic VASH2 knockout mice. (C, D) Immunoblot for vascular endothelial growth factor-A (VEGF-A; C) and VEGF receptor-2 (VEGFR2; D). Each lane was loaded with 40 μg of protein obtained from the renal cortex. Each band was scanned and subjected to a densitometric analysis. Increased VEGF-A level induced by diabetes showed no difference between wild-type and VASH2 knockout mice, whereas increased VEGFR2 expression seen in diabetic wild-type mice was significantly suppressed in diabetic VASH2 knockout mice. n = 6 for each group. *<i>P</i><0.05 versus non-diabetic WT or VASH2 knockout mice, ^#<i>P</i><0.05 versus diabetic WT mice. Each column shows the mean ± SE.</p

Urine albumin excretion, renal hypertrophy and creatinine clearance in non-diabetic and diabetic wild-type and VASH2 knockout mice.

<p>(A) Six weeks after the induction of hyperglycemia, albuminuria in diabetic wild-type (WT) mice (solid circles) was significantly exacerbated compared with that in non-diabetic WT mice (open circles). Although no difference was found in albuminuria between non-diabetic WT and non-diabetic VASH2 knockout mice (open squares), increased albuminuria induced by hyperglycemia was markedly prevented in diabetic VASH2 knockout mice (solid squares). (B, C) The increase in kidney weight-to-body weight ratio (B) and urine volume (C) induced by hyperglycemia did not significantly differ between WT and VASH2 knockout mice. (D) The increase in creatinine clearance (Ccr) level induced by hyperglycemia was significantly prevented in VASH2 knockout mice compared with WT mice. n = 6 for non-diabetic WT, 6 for non-diabetic VASH2 knockout, 10 for diabetic WT, and 8 for diabetic VASH2 knockout mice. *<i>P</i><0.05 versus non-diabetic WT or VASH2 knockout mice, **<i>P</i><0.01 versus non-diabetic WT or VASH2 knockout mice, ^#<i>P</i><0.05 versus diabetic WT mice, ^##<i>P</i><0.01 versus diabetic WT mice. Each column shows the mean ± SE.</p

Characteristics of non-diabetic and diabetic wild-type and VASH2-deficient mice at the end of study.

<p>Characteristics of non-diabetic and diabetic wild-type and VASH2-deficient mice at the end of study.</p

Histological and ultrastructural alterations in diabetic VASH2 knockout mice.

<p>(A) Representative light microscopic images of glomeruli from non-diabetic wild-type, non-diabetic VASH2 knockout, diabetic wild-type, and diabetic VASH2 knockout mice (periodic acid-Schiff staining, original magnification, ×400). (B, C) Diabetes-induced increases in glomerular volume (B) and mesangial matrix index (C) were significantly prevented in VASH2 knockout mice compared with wild-type mice. The mesangial matrix index was defined as the proportion of the glomerular volume occupied by mesangial matrix area (excluding nuclei). (D) Representative transmission electron microscopic images of glomerular capillary tufts from non-diabetic wild-type, non-diabetic VASH2 knockout, diabetic wild-type, and diabetic VASH2 knockout mice (scale bars, 2 μm). Diabetes caused foot process fusion (arrow) and obscured silt-diaphragms. (E) Increased GBM thickness in diabetic wild-type mice was significantly suppressed in diabetic VASH2 knockout mice. (F) The decrease in slit diaphragm density observed in diabetic wild-type mice was also improved in diabetic VASH2 knockout mice. n = 6 for non-diabetic WT, 6 for non-diabetic VASH2 knockout, 10 for diabetic WT, and 8 for diabetic VASH2 knockout mice. *<i>P</i><0.05 versus non-diabetic WT or VASH2 knockout mice, ^#<i>P</i><0.05 versus diabetic WT mice. Each column shows the mean ± SE.</p

The role of VASH2 knockdown in extracellular matrix production in cultured mesangial cells.

<p>Human mesangial cells (HMCs) were cultured under normal glucose (NG, 5.5 mM), NG plus mannitol (MN; NG plus mannitol, 19.5 mM) or high glucose (HG, 25 mM) condition for 24 hours in the presence of negative control siRNA (siCont, 10 nM) or VASH2 siRNA (siVASH2, 10 nM). (A) The expression of VASH2 mRNA relative to 18S rRNA was elevated in HG but not in MN condition. (B, C) Immunoblots for VASH2 and β-actin are shown (B). Each lane was loaded with 20 μg of protein obtained from cultured HMCs. Each band was scanned and subjected to a densitometric analysis (C). Transfection of siVASH2 reduced the level of VASH2 by approximately 80%. (D, E) The amount of type IV collagen α3 (D) and connective tissue growth factor (CTGF; E) relative to 18S rRNA is shown. Increase in these mRNA level caused by HG condition was significantly prevented by transfection of siVASH2. n = 4 for each group. ^§<i>P</i><0.05 versus NG or MN, *<i>P</i><0.05 versus NG with siCont or NG with siVASH2, ^#<i>P</i><0.05 versus HG with siCont. Each column shows the mean ± SE.</p