Similarity in Sequential Bilateral Transient Osteoporosis of the Hip

CASE: Three middle-aged men with habitual drinking developed unilateral hip pain and were referred for osteonecrosis of the femoral head (ONFH). Radiographs showed osteopenia, and magnetic resonance imaging (MRI) showed diffuse bone marrow edema (BME). After several months, the patients' symptoms resolved and radiographic images normalized. More than 6 months later, the contralateral side showed the same clinical course. CONCLUSION: Transient osteoporosis of the hip (TOH) resembles ONFH but heals spontaneously. We report 3 rare cases of sequential TOH, similar in that they occurred in middle-aged male habitual drinkers at risk for ONFH, characterized by diffuse BME on MRI and radiographic resolution

Mitochondrial fission in hepatocytes as a potential therapeutic target for nonalcoholic steatohepatitis

[Aim] The mitochondria are highly plastic and dynamic organelles; mitochondrial dysfunction has been reported to play causative roles in diabetes, cardiovascular diseases, and nonalcoholic fatty liver disease (NAFLD). However, the relationship between mitochondrial fission and NAFLD pathogenesis remains unknown. We aimed to investigate whether alterations in mitochondrial fission could play a role in the progression of NAFLD. [Methods] Mice were fed a standard diet or choline-deficient, L-amino acid-defined (CDAA) diet with vehicle or mitochondrial division inhibitor-1. [Results] Substantial enhancement of mitochondrial fission in hepatocytes was triggered by 4 weeks of feeding and was associated with changes reflecting the early stage of human nonalcoholic steatohepatitis (NASH), steatotic change with liver inflammation, and hepatocyte ballooning. Excessive mitochondrial fission inhibition in hepatocytes and lipid metabolism dysregulation in adipose tissue attenuated liver inflammation and fibrogenesis but not steatosis and the systemic pathological changes in the early and chronic fibrotic NASH stages (4- and 12-week CDAA feeding). These beneficial changes due to the suppression of mitochondrial fission against the liver and systemic injuries were associated with decreased autophagic responses and endoplasmic reticulum stress in hepatocytes. Injuries to other liver cells, such as endothelial cells, Kupffer cells, and hepatic stellate cells, were also attenuated by the inhibition of mitochondrial fission in hepatocytes. [Conclusions] Taken together, these findings suggest that excessive mitochondrial fission in hepatocytes could play a causative role in NAFLD progression by liver inflammation and fibrogenesis through altered cell cross-talk. This study provides a potential therapeutic target for NAFLD

ユビサキ ノ チカラ ハッキ ニトモナウ ヒフ セッショク メンセキ ノ ヘンカ

"指先で発揮される力と, その力によって変化する物体との接触面積との関係を調べることにより, 指先の皮膚特性を明らかにし, かつ指先の接触面積情報が摘み力の制御機構に利用されている可能性について検討した。結果は以下に示すとおりである。(1)指先の力発揮に伴い, 接触面積は指数関数的な変化を示し, 性差, 年齢差はみられなかった。(2)各個人の最大接触面積に対する相対接触面積と力発揮との関係では, ほとんどすべての被検者が, ほぼ類似した指数関数的変化曲線を示した。(3)同一個人の5指間の相対接触面積と力発揮との関係では, きわめて類似した指数関数的変化曲線を示し, 特に拇指と人差指では, かなり一致したものであった。(4)これらの結果は, 摘み力の制御に接触面積情報が利用されている可能性を示唆するものであり, 個体間では10%∿20%の誤差はあるが, 相対接触面積に基づく力のスケールが存在する可能性が推察された。このスケールは, 個人内においては, ただひとつであり, どの指も同じスケールを利用している可能性が示唆された。

SURFIN is a polymorphic antigen expressed on Plasmodium falciparum merozoites and infected erythrocytes

The surfaces of the infected erythrocyte (IE) and the merozoite, two developmental stages of malaria parasites, expose antigenic determinants to the host immune system. We report on surface-associated interspersed genes (surf genes), which encode a novel polymorphic protein family, SURFINs, present on both IEs and merozoites. A SURFIN expressed in 3D7 parasites, SURFIN4.2, was identified by mass spectrometric analysis of peptides cleaved off the surface of live IEs with trypsin. SURFINs are encoded by a family of 10 surf genes, including three predicted pseudogenes, located within or close to the subtelomeres of five of the chromosomes. SURFINs show structural and sequence similarities with exported surface-exposed proteins (PvSTP1, PkSICAvar, PvVIR, Pf332, and PfEMP1) of several Plasmodium species. SURFIN4.2 of a parasite other than 3D7 (FCR3S1.2) showed polymorphisms in the extracellular domain, suggesting sequence variability between genotypes. SURFIN4.2 not only was found cotransported with PfEMP1 and RIFIN to the IE surface, but also accumulated in the parasitophorous vacuole. In released merozoites, SURFIN4.2 was present in an amorphous cap at the parasite apex, where it may be involved in the invasion of erythrocytes. By exposing shared polymorphic antigens on IEs and merozoites, the parasite may coordinate the antigenic composition of these attachment surfaces during growth in the bloodstream