父親の養育性と役割取得を促す発達教育プログラムの開発

神戸松蔭女子学院大

父親の家事・育児意識と行動の変容とその要因に関する研究 ―2000 年と2011 年のデータ比較を通して―

本研究は、今日の父親の育児意識・行動の変化と、その変化を規定する要因について、父親の内的特性との関連を検討し、父親の育児参画と養育性、親役割アイデンティティの形成を促し支援の視点について論議することを目的とした。　研究Ⅰでは、方法は、2000 年と2011 年に、父親・母親107 組を対象にアンケート調査を行い、育児意識と行動の変化について検討した。その結果、父親の家事・育児意識と参加度の自己評価は、11 年前に比べ高まっていた。母親の父親も評価高かったが、11 年前に比べ低下していた。　研究Ⅱでは、研究Ⅰにおける2011 年の被験者を対象に、父親の養育経験、不安・愛着に関する質問項目を津付加して調査し、今日の父親の育児意識・行動を規定する要因について検討した。その結果、父親の親との親密性、父親の父親との良好な関係、子ども時代の熱中経験、父親自身の受容的愛着と関連していた。これらの結果をもとに、育児における父親参画の在り方と養育性支援の視点について検討した。　The purpose of this study was to discuss about perspectives of the support in fathers’ child-rearing, comparing the fathers’ consciousness and daily practices of household and child-rearing with presence and eleven years ago. Furthermore we analyzed on relationships with father’s inner factors of their changes.　The method was to use the face-sheet. We gathered the data from 107 father and mother dyads in 2011, and 137 dyads in 2000. The data suggested that fathers’ believes of their roles on household and child-rearing changed from traditional thought to new perspectives. Participation of daily practices increased than eleven years ago. Their wives evaluated them as he father and as husband. The father’s practices were related with their experiences in childhood of intimacy of parents, good relationships with father’s father and exploring interested things in childhood, also related with father’s attachment.　Based on these consequences, we discussed about how to develop the fathers’ nurturance and social support

Pemt deficiency ameliorates endoplasmic reticulum stress in diabetic nephropathy

Phosphatidylethanolamine N-methyltransferase (Pemt) catalyzes the methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) mainly in the liver. Under an obese state, the upregulation of Pemt induces endoplasmic reticulum (ER) stress by increasing the PC/PE ratio in the liver. We targeted the Pemt gene in mice to explore the therapeutic impact of Pemt on the progression of diabetic nephropathy and diabetes, which was induced by the injection of streptozotocin (STZ). Although the blood glucose levels were similar in STZ-induced diabetic Pemt+/+ and Pemt−/−mice, the glomerular hypertrophy and albuminuria in Pemt−/− mice were significantly reduced. Pemt deficiency reduced the intraglomerular F4/80-positive macrophages, hydroethidine fluorescence, tubulointerstitial fibrosis and tubular atrophy. The expression of glucose-regulated protein-78 (GRP78) was enriched in the renal tubular cells in STZ-induced diabetic mice, and this was ameliorated by Pemt deficiency. In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt). The number of apoptotic cells in the renal tubules was significantly reduced in Pemt−/− diabetic mice, and shRNA-Pemt upregulated the phosphorylation of Akt and decreased the cleavage of caspase 3 and 7 in mProx24 cells. Taken together, these findings indicate that the inhibition of Pemt activity ameliorates the ER stress associated with diabetic nephropathy in a model of type 1 diabetes and corrects the functions of the three major pathways downstream of ER stress, i.e. oxidative stress, inflammation and apoptosis

Nuclear Hormone Receptor Expression in Mouse Kidney and Renal Cell Lines

Nuclear hormone receptors (NHRs) are transcription factors that regulate carbohydrate and lipid metabolism, immune responses, and inflammation. Although several NHRs, including peroxisome proliferator-activated receptor-γ (PPARγ) and PPARα, demonstrate a renoprotective effect in the context of diabetic nephropathy (DN), the expression and role of other NHRs in the kidney are still unrecognized. To investigate potential roles of NHRs in the biology of the kidney, we used quantitative real-time polymerase chain reaction to profile the expression of all 49 members of the mouse NHR superfamily in mouse kidney tissue (C57BL/6 and db/m), and cell lines of mesangial (MES13), podocyte (MPC), proximal tubular epithelial (mProx24) and collecting duct (mIMCD3) origins in both normal and high-glucose conditions. In C57BL/6 mouse kidney cells, hepatocyte nuclear factor 4α, chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) and COUP-TFIII were highly expressed. During hyperglycemia, the expression of the NHR 4A subgroup including neuron-derived clone 77 (Nur77), nuclear receptor-related factor 1, and neuron-derived orphan receptor 1 significantly increased in diabetic C57BL/6 and db/db mice. In renal cell lines, PPARδ was highly expressed in mesangial and proximal tubular epithelial cells, while COUP-TFs were highly expressed in podocytes, proximal tubular epithelial cells, and collecting duct cells. High-glucose conditions increased the expression of Nur77 in mesangial and collecting duct cells, and liver x receptor α in podocytes. These data demonstrate NHR expression in mouse kidney cells and cultured renal cell lines and suggest potential therapeutic targets in the kidney for the treatment of DN