167 research outputs found

    Change of Facial Appearance of Skeletal Class III Corrected by Obwegeser-Dal Pont\u27s Method : Experimental Examination by Moire Topography

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    Obwegeser-Dal Pont法は, 骨格型下顎前突症の外科的矯正治療法として今日広く応用されている方法の一つである。一方, 骨格型下顎前突症に対する外科的矯正治療の大きな目的は, 顎口腔機能および審美性の改善であり, その術後評価は非常に重要である。そこで, Obwegeser-DalPont法を適用した骨格型下顎前突症について, 顔貌の検討を試みた。顔貌の変化を把握する場合, 多くは顔面規格写真や頭部X線規格写真が利用されているが, これらはいずれも二次元的観察方法である。しかし, 顔貌の変化は三次元的に生じていることから, 三次元的観察法による分析が必要不可欠である。そこで, 今回の分析には, 三次元的観察方法として種々の利点を有するMoire Topographyでの検討を試み, 次の結果を得た。1.Obwegeser-Dal Pont法により下顎歯列弓を後方移動した場合, 周囲軟組織もスムーズに後方移動され, 審美的に良好な手術結果が得られていることが確認された。2.本法による軟組織の改善は, 上口唇にもみられることが, 明瞭に確認された。3.手術による顔貌の変化の客観的かつ三次元的把握法としてMoire Topographyは, 非常に有用であることが確認された

    Role of dietary amino acid balance in diet restriction-mediated lifespan extension, renoprotection, and muscle weakness in aged mice.

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    Extending healthy lifespan is an emerging issue in an aging society. This study was designed to identify a dietary method of extending lifespan, promoting renoprotection, and preventing muscle weakness in aged mice, with a focus on the importance of the balance between dietary essential (EAAs) and nonessential amino acids (NEAAs) on the dietary restriction (DR)-induced antiaging effect. Groups of aged mice were fed ad libitum, a simple DR, or a DR with recovering NEAAs or EAAs. Simple DR significantly extended lifespan and ameliorated age-related kidney injury; however, the beneficial effects of DR were canceled by recovering dietary EAA but not NEAA. Simple DR prevented the age-dependent decrease in slow-twitch muscle fiber function but reduced absolute fast-twitch muscle fiber function. DR-induced fast-twitch muscle fiber dysfunction was improved by recovering either dietary NEAAs or EAAs. In the ad libitum-fed and the DR plus EAA groups, the renal content of methionine, an EAA, was significantly higher, accompanied by lower renal production of hydrogen sulfide (H2 S), an endogenous antioxidant. Finally, removal of methionine from the dietary EAA supplement diminished the adverse effects of dietary EAA on lifespan and kidney injury in the diet-restricted aged mice, which were accompanied by a recovery in H2 S production capacity and lower oxidative stress. These data imply that a dietary approach could combat kidney aging and prolong lifespan, while preventing muscle weakness, and suggest that renal methionine metabolism and the trans-sulfuration pathway could be therapeutic targets for preventing kidney aging and subsequently promoting healthy aging

    Protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes.

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    To examine the cell-protective role of podocyte autophagy against glomerular endothelial dysfunction in diabetes, we analyzed the renal phenotype of tamoxifen (TM)-inducible podocyte-specific Atg5-deficient (iPodo-Atg5-/-) mice with experimental endothelial dysfunction. In both control and iPodo-Atg5-/- mice, high fat diet (HFD) feeding induced glomerular endothelial damage characterized by decreased urinary nitric oxide (NO) excretion, collapsed endothelial fenestrae, and reduced endothelial glycocalyx. HFD-fed control mice showed slight albuminuria and nearly normal podocyte morphology. In contrast, HFD-fed iPodo-Atg5-/- mice developed massive albuminuria accompanied by severe podocyte injury that was observed predominantly in podocytes adjacent to damaged endothelial cells by scanning electron microscopy. Although podocyte-specific autophagy deficiency did not affect endothelial NO synthase deficiency-associated albuminuria, it markedly exacerbated albuminuria and severe podocyte morphological damage when the damage was induced by intravenous neuraminidase injection to remove glycocalyx from the endothelial surface. Furthermore, endoplasmic reticulum stress was accelerated in podocytes of iPodo-Atg5-/- mice stimulated with neuraminidase, and treatment with molecular chaperone tauroursodeoxycholic acid improved neuraminidase-induced severe albuminuria and podocyte injury. In conclusion, podocyte autophagy plays a renoprotective role against diabetes-related structural endothelial damage, providing an additional insight into the pathogenesis of massive proteinuria in diabetic nephropathy
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