Novel artificial hip joint: A layer of alumina on Ti-6Al-4V alloy formed by micro-arc oxidation.

In many hip replacement surgeries, monolithic alumina is used as a femoral head due to its high wear resistance. However, it is liable to fracture under load bearing operations in artificial joints. We propose a promising way to overcome this limitation by forming a dense alumina layer onto a relatively tough substrate such as Ti-6Al-4V alloy to obtain high wear resistance on a material that can sustain relatively high toughness. For this purpose, Al metal powders were deposited onto Ti-6Al-4V alloy by cold spraying in N2 atmosphere. Interfacial adhesion between Al and the Ti alloy was improved by the formation of a reaction layer of Al3Ti between them by heating at 640 °C for 1h in air. Subsequently, micro-arc oxidation treatment was performed to oxidize Al. The oxidized layer was composed of an outer porous layer of γ-alumina and inner-most dense layer of α-alumina. The α-alumina layer was almost fully densified and exhibited high Vickers hardness almost equal to that of alumina ceramics used as the femoral head. Thus, the newly developed dense alumina/Ti alloy can be potentially used to produce the reliable bearing surfaces of artificial hip joint.

Neonatal lethality of neural crest cell-specific Rest knockout mice is associated with gastrointestinal distension caused by aberrations of myenteric plexus.

RE1-silencing transcription factor (REST), also known as NRSF (neuron-restrictive silencer factor), is a well-known transcriptional repressor of neural genes. Rest null mice have embryonic lethality which prevents further investigations of the functions of the Rest gene in vivo. We studied neonatal but not embryonic lethality that was characterized by gastrointestinal tract dilation in the neural crest cell (NCC)-specific Rest conditional knockout (CKO) mice. While no histological abnormalities except the thinning of the digestive tract as a consequence of the gas accumulation were found in the digestive tract of the mutant mice, they do not have proper gastric retention after oral dye administration and the reduction of acetylcholinesterase (AChE) activity in NCC-derived myenteric plexus in the stomach was detected. High CO2 concentration in the dilated digestive tract of the Rest CKO mice indicates a failure of gut function by underdeveloped cholinergic transmission in the enteric nervous system. The observed gastrointestinal distension phenotype provides a model for understanding the genetic and molecular basis of NCC defects in humans.