Angiotensinogen gene null-mutant mice lack homeostatic regulation of glomerular filtration and tubular reabsorption

Angiotensinogen gene null-mutant mice lack homeostatic regulation of glomerular filtration and tubular reabsorption. Chronic volume depletion by dietary salt restriction causes marked decrease in glomerular filtration rate (GFR) with little increase in urine osmolality in angiotensinogen gene null mutant (Agt−/−) mice. Moreover, urine osmolality is insensitive to both water and vasopressin challenge. In contrast, in normal wild-type (Agt+/+) mice, GFR remains remarkably constant and urine osmolality is adjusted promptly. Changes in volume status also cause striking divergence in renal structure between Agt−/− and Agt+/+ mice. Thus, in contrast to the remarkably stable glomerular size of Agt+/+ mice, glomeruli of Agt−/− mice are atrophied during a low salt and hypertrophied during a high salt diet. Moreover, the renal papilla, a structure unique to mammals and essential for urine diluting and concentrating mechanisms, is hypoplastic in Agt−/− mice. Thus, angiotensin is essential for the two fundamental homeostatic functions of the mammalian kidney, namely stable GFR and high urine diluting and concentrating capacity during alteration in extracellular fluid (ECF) volume. This is not only accompanied by angiotensin’s tonic effects on renal vasomotor tone and tubule transporters, but also accomplished through its capacity to affect the structure of both the glomerulus and the papilla directly or indirectly

Enormous shrinkage of carbon nanotubes by supersonic stress and low-acceleration electron beam irradiation

The authors demonstrated a new method for inducing enormous shrinkage in single-walled carbon nanotube bundles by applying low energy electron beam irradiation along with supersonic vibration, and a maximum shrinkage rate of −100% cm2/C was obtained under electron acceleration of 1 keV. The characteristic feature of the shrunken single-walled carbon nanotubes was a wavy deformation that affected the entire bundle. The authors believe that a uniaxial stress induced by the supersonic vibration broke the equilibrium of the internal stress and allowed the uniform accumulation of defects under low energy electron beam excitation. The wavy deformation of the single-walled carbon nanotubes resulted in the enormous shrinkage of the bundle

Influence of locational states of submicron fibers added into matrix on mechanical properties of plain-woven Carbon Fiber Composite

The aim of this study was to show the influence of locational states of submicron fibers added into epoxy matrix on mechanical properties of modified plane-woven carbon fiber reinforced plastic (CFRP). To change the locational states of submicron fibers, two kinds of fabrication processes were applied in preparing specimen by hand lay-up method. Submicron fibers were simply added into epoxy resin with ethanol after they were stirred by a dispersion process using homogenizer to be located far from the interface between reinforcement and matrix. In contrast, submicron fibers were attached onto the carbon fibers by injecting from a spray nozzle accompanying with ethanol to be located near the interface, after they were tentatively contained in ethanol. The plain-woven CFRP plates were fabricated by hand lay-up method and cured at 80 degree-C for 1 hour and then at 150 degree-C for 3 hours. After curing, the plain-woven CFRP plates were cut into the dimension of specimen. Tensile shear strength and Mode-II fracture toughness of CFRP were determined by tensile lap-shear test and End-notched flexure(ENF) test, respectively. When submicron fibers were located far from the interface between carbon fibers and epoxy resin, tensile shear strength and Mode-II fracture toughness of CFRP were improved 30% and 18% compared with those of unmodified case. The improvement ratio in modified case was rather low (about few percentages) in the case where submicron fibers were located near the interface. The result suggested that crack propagation should be prevented when submicron fibers were existed far from the interface due to the effective stress state around the crack tip

Research Update: Nickel filling in nanofeatures using supercritical fluid and its application to fabricating a novel catalyst structure for continuous growth of nanocarbon fibers

A novel catalyst structure for continuous growth of nanocarbon fibers is proposed. In this structure, catalyst nanofibers are embedded in a membrane that separates the growth ambient into carbon-supplying and carbon-precipitating environments. The catalyst nanofibers pierce through the membrane so that carbon source gas is supplied only to one end of the catalyst fibers and nanocarbon fibers grow continuously at the other end. To realize this structure, self-supporting anodized alumina was used as a membrane, and its nano-through-holes were filled with catalyst Ni in supercritical CO2 fluid. Direct carbon growth from the Ni nanofibers was confirmed using this catalyst structure

Growth of bridging carbon nanofibers in cracks formed by heat-treating iron oxide thin sheets in acetylene gas

We produced novel carbon nanofibers (CNFs) by oxidizing high-purity iron foil and then carburizing it in acetylene gas flow. This formed cracks in the heat-treated iron foil with CNFs bridging the two walls of each crack. The CNFs were drawn out from the walls as the crack opened during heat treatment. This will be a new method to grow and arrange carbon nanotubes and nanosheets without using metal nanoparticles or template substrates

Mice lacking nucleotide sugar transporter SLC35A3 exhibit lethal chondrodysplasia with vertebral anomalies and impaired glycosaminoglycan biosynthesis

SLC35A3 is considered an uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) transporter in mammals and regulates the branching of N-glycans. A missense mutation in SLC35A3 causes complex vertebral malformation (CVM) in cattle. However, the biological functions of SLC35A3 have not been fully clarified. To address these issues, we have established Slc35a3–/–mice using CRISPR/Cas9 genome editing system. The generated mutant mice were perinatal lethal and exhibited chondrodysplasia recapitulating CVM-like vertebral anomalies. During embryogenesis, Slc35a3 mRNA was expressed in the presomitic mesoderm of wild-type mice, suggesting that SLC35A3 transports UDP-GlcNAc used for the sugar modification that is essential for somite formation. In the growth plate cartilage of Slc35a3–/–embryos, extracellular space was drastically reduced, and many flat proliferative chondrocytes were reshaped. Proliferation, apoptosis and differentiation were not affected in the chondrocytes of Slc35a3–/–mice, suggesting that the chondrodysplasia phenotypes were mainly caused by the abnormal extracellular matrix quality. Because these histological abnormalities were similar to those observed in several mutant mice accompanying the impaired glycosaminoglycan (GAG) biosynthesis, GAG levels were measured in the spine and limbs of Slc35a3–/–mice using disaccharide composition analysis. Compared with control mice, the amounts of heparan sulfate, keratan sulfate, and chondroitin sulfate/dermatan sulfate, were significantly decreased in Slc35a3–/–mice. These findings suggest that SLC35A3 regulates GAG biosynthesis and the chondrodysplasia phenotypes were partially caused by the decreased GAG synthesis. Hence, Slc35a3−/− mice would be a useful model for investigating the in vivo roles of SLC35A3 and the pathological mechanisms of SLC35A3-associated diseases

Mice lacking nucleotide sugar transporter SLC35A3 exhibit lethal chondrodysplasia with vertebral anomalies and impaired glycosaminoglycan biosynthesis.

SLC35A3 is considered an uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) transporter in mammals and regulates the branching of N-glycans. A missense mutation in SLC35A3 causes complex vertebral malformation (CVM) in cattle. However, the biological functions of SLC35A3 have not been fully clarified. To address these issues, we have established Slc35a3-/-mice using CRISPR/Cas9 genome editing system. The generated mutant mice were perinatal lethal and exhibited chondrodysplasia recapitulating CVM-like vertebral anomalies. During embryogenesis, Slc35a3 mRNA was expressed in the presomitic mesoderm of wild-type mice, suggesting that SLC35A3 transports UDP-GlcNAc used for the sugar modification that is essential for somite formation. In the growth plate cartilage of Slc35a3-/-embryos, extracellular space was drastically reduced, and many flat proliferative chondrocytes were reshaped. Proliferation, apoptosis and differentiation were not affected in the chondrocytes of Slc35a3-/-mice, suggesting that the chondrodysplasia phenotypes were mainly caused by the abnormal extracellular matrix quality. Because these histological abnormalities were similar to those observed in several mutant mice accompanying the impaired glycosaminoglycan (GAG) biosynthesis, GAG levels were measured in the spine and limbs of Slc35a3-/-mice using disaccharide composition analysis. Compared with control mice, the amounts of heparan sulfate, keratan sulfate, and chondroitin sulfate/dermatan sulfate, were significantly decreased in Slc35a3-/-mice. These findings suggest that SLC35A3 regulates GAG biosynthesis and the chondrodysplasia phenotypes were partially caused by the decreased GAG synthesis. Hence, Slc35a3-/- mice would be a useful model for investigating the in vivo roles of SLC35A3 and the pathological mechanisms of SLC35A3-associated diseases