Aquatic invertebrate’s Carbohydrate-binding module assists environmental cellulase to immobilize in wetland sediments

Carbohydrate-binding modules (CBMs) are non-catalytic protein domains that bind to carbohydrates, and have been well studied in microorganisms. Endogenous CBMs in aquatic invertebrates, however, have not yet been identified, and little is known about their ecological significance to wetland environments. Using an approach of characterizing a recombinant CBM (CjCel9A) from a brackish bivalve, Corbicula japonica, this work identified CjCel9A-CBM’s cellulose-binding activity. Scatchard plot analysis in the study of CjCel9A-CBM binding to α-cellulose showed a high corresponding partitioning coefficient (Kr) of 20.33, indicating CjCel9A-CBM’s high affinity for cellulose. In addition, this affinity tolerated a high ion concentration buffer system, consistent with C. japonica’s adaption to brackish wetland environments. Moreover, immuno-scanning electron microscopy (immuno-SEM) suggested that CjCel9A-CBM binds to α-cellulose unevenly, which was further determined to be caused by its higher affinity for crystalline cellulose (Cellulose I, mostly seen in plant leaves). Together, these findings suggest that CjCel9A-CBM is capable of immobilizing its associated catalytic domain on environmental crystalline cellulose (i.e., fallen leaves) in wetland sediments. Most importantly, they could provide a reasonable answer to a question recognized broadly in wetland ecologists, namely, why many wetland sediments have constant cellulase activities, although the sediments are being washed almost every day

Investigation For Molecular Mechanism Of Insulin Resistance In Transgenic Mice Expressing A Mutant Shp2

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 1998～2000課題番号: 10671062研究代表者: 前川 聡（滋賀医科大学・医学部・助手

Role of Protein-tyrosine phosphatase on pathogenesis of Metabolic syndrome

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 2004～2006課題番号: 16590876研究代表者: 前川 聡（滋賀医科大学・医学部・助教授

Oberlin partial ulnar nerve transfer for restoration in obstetric brachial plexus palsy of a newborn: case report

An 8 month old male infant with Erb's birth palsy was treated with two peripheral nerve transfers. Except for rapid motor reinnervations, elbow flexion was obtained by an Oberlin's partial ulnar nerve transfer, while shoulder abduction was restored by an accessory-to-suprascapular nerve transfer. The initial contraction of the biceps muscle occurred two months after surgery. Forty months after surgery, elbow flexion reached M5 without functional loss of the ulnar nerve. This case demonstrates an excellent result of an Oberlin's nerve transfer for restoration of flexion of the elbow joint in Erb's birth palsy. However, at this time partial ulnar nerve transfer for Erb's birth palsy is an optional procedure; a larger number of cases will need to be studied for it to be widely accepted as a standard procedure for Erb's palsy at birth

Autophagy as a Therapeutic Target in Diabetic Nephropathy

Diabetic nephropathy is a serious complication of diabetes mellitus, and its prevalence has been increasing worldwide. Therefore, there is an urgent need to identify a new therapeutic target to prevent diabetic nephropathy. Autophagy is a major catabolic pathway involved in degrading and recycling macromolecules and damaged organelles to maintain intracellular homeostasis. The study of autophagy in mammalian systems is advancing rapidly and has revealed that it is involved in the pathogenesis of various metabolic or age-related diseases. The functional role of autophagy in the kidneys is also currently under intense investigation although, until recently, evidence showing the involvement of autophagy in the pathogenesis of diabetic nephropathy has been limited. We provide a systematic review of autophagy and discuss the therapeutic potential of autophagy in diabetic nephropathy to help future investigations in this field

The Pathophysiological Role of Protein Phosphatase 2A (PP2A) in metabolic Syndrome

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 2005～2006課題番号: 17590927研究代表者: 卯木 智（滋賀医科大学・医学部・助手）研究分担者: 前川 聡（滋賀医科大学・医学部・助教授

Hyperglycemia and atherosclerosis : Radical scavenger dysfunction and abnormal gene expression in endothelial cells

科学研究費補助金研究成果報告書研究種目: 一般研究(C)研究期間: 1993～1994課題番号: 05670854研究代表者: 柏木 厚典（滋賀医科大学・医学部・講師）研究分担者: 前川 聡（滋賀医科大学・医学部・助手

Organ specificity of insulin resistance induced by Protein-tyrosine phosphatase

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 2002～2003課題番号: 14571088研究代表者: 前川 聡（滋賀医科大学・医学部・講師）研究分担者: 江川 克哉（滋賀医科大学・医学部・助手

Ketogenic essential amino acids replacement diet ameliorated hepatosteatosis with altering autophagy-associated molecules

AbstractKetogenic amino acid (KAA) replacement diet has been shown to cure hepatic steatosis, a serious liver disease associated with diverse metabolic defects. In this study, we investigated the effects of KAA replacement diet on nutrition sensing signaling pathway and analyzed whether induction of hepatic autophagy was involved. Mice are fed with high fat diet (HFD) or KAA replacement in high-fat diet (30% fat in food; HFD)-fed (HFDKAAR) and sacrificed at 8, 12, 16weeks after initiation of experimental food. Hepatic autophagy was analyzed in protein expression of several autophagy-associated molecules and in light chain-3 green fluorescent protein (LC-3 GFP) transgenic mice. HFDKAAR showed increased AMP-activated protein kinase (AMPK) phosphorylation and enhanced liver kinase B1 (LKB1) expression compared to control HFD-fed mice. The KAA-HFD-induced activation of AMPK was associated with an increased protein expression of sirtuin 1 (Sirt1), decreased forkhead box protein O3a (Foxo3a) level, and suppression of mammalian target of rapamycin (mTOR) phosphorylation compared with the HFD-fed mice. The intervention study revealed that a KAA-replacement diet also ameliorated all the established metabolic and autophagy defects in the HFD-fed mice, suggesting that a KAA-replacement diet can be used therapeutically in established diseases. These results indicate that KAA replacement in food could be a novel strategy to combat hepatic steatosis and metabolic abnormalities likely involvement of an induction of autophagy