Laser Rescanning for Enhancing Mechanical Properties of Laser-Directed Energy-Deposited High-Manganese Steels.

This study investigates the effects of laser deposition and laser rescanning (LR) on the microstructure and mechanical properties of high-manganese steel (HMnS) deposited by laser-directed energy deposition (L-DED) comprising 24 wt.% Mn. Four types of laser deposition and LR strategies were investigated: unidirectional L-DED scanning without laser rescanning, L-DED scanning with 90° alterations in the laser scanning path on each layer without laser rescanning, unidirectional L-DED with laser rescanning in the same direction, and L-DED with laser rescanning with 90° alterations in the laser scanning path. The L-DED-processed HMnS had only a few small pores and exhibited a microstructure without any serious defects such as cracks. Additionally, a strong fibrous texture along the <101>/building direction of the fully austenite phase was found. The mechanical properties (microhardness and tensile strength) of HMnS were improved by the LR with a grain refinement effect and fine solidification cell size due to the significantly faster solidification rate in LR than that in L-DED.

Direct activation of guinea pig vagal afferent neurons by FMRFamide.

Vagus nerve comprises two distinct kinds of nerves, nodose and jugular ganglionic nerves. We tested pharmacological difference between two vagal nerves in the responsiveness to FMRFamide. The response probability to FMRFamide was significantly higher in nodose than jugular nerves in intracellular calcium measurement. Nodose nerves also depolarized membrane potential to FMRFamide more than jugular nerves did, in patch-clamp recording, although the probability of action potential discharge was same in both nerves. The inward current induced by FMRFamide was characterized as mixed cations. These results suggest that FMRFamide may act as an activator and modulator of vagal sensory nerves for treating symptoms in visceral diseases.

Long-term changes in expressions of spinal glutamate transporters after spinal cord injury.

Glutamate is a major excitatory transmitter in the central nervous system that may produce cellular injury when its concentration is abnormally increased in the synaptic cleft. Glial glutamate transporters GLAST and GLT-1, which are responsible for clearing synaptic glutamate into glial cells, play an important role in the regulation of the glutamate concentration in the synaptic cleft. However, there has been no report on long-term changes in the levels of glutamate transporters following spinal cord injury. Spinal cord injury (SCI) was induced at T12 by a New York University (NYU) impactor. Segments of the spinal cord at T9-10, L1-2, L4-5 and at the epicenter were removed after SCI, and Western blots for GLAST, GLT-1 and EAAC1 were performed. GLAST and GLT-1 were significantly decreased in the epicenter from 1day up to 8weeks after SCI. GLT-1 was significantly decreased in the spinal segments rostral to the injury site, and GLAST expression was significantly increased in the L4-5 region of the spinal cord for 8weeks. Because strategies to modulate the regulation of glutamate transporters may be applied, the present data serve as a reference for further research, although the long-term roles of glutamate transporters in pathological processes caused by SCI are not clear.