Steel wheels on steel tracks are lower still.Aerodynamic drag can be reduced by streamlined design features. Friction is desirable and important in supplying traction to facilitate motion on land. Most land vehicles rely on friction for accelerating, decelerating and changing direction. Sudden reductions in traction can cause loss of control and accidents. Control
Steering
Most vehicles, with the notable exception of railed vehicles, have at least one steering mechanism. Wheeled vehicles steer by angling their front or rear wheels. The B-52 Stratofortress has a special arrangement in which all four main wheels can be angled. Skids can also be used to steer by angling them, as in the case of a snowmobile. Ships, boats, submarines, dirigibles and aeroplanes usually have a rudder for steering. On an airplane, ailerons are used to bank the airplane for directional control, sometimes assisted by the rudder. Stopping
With no power applied, most vehicles come to a stop due to friction. But it is often required to stop a vehicle faster than by friction alone: so almost all vehicles are equipped with a braking system. Wheeled vehicles are typically equipped with friction brakes, which use the friction between brake pads (stators) and brake rotors to slow the vehicle. Many airplanes have high performance versions of the same system in their landing gear for use on the ground. A Boeing 757 brake, for example, has 3 stators and 4 rotors. The Space Shuttle also uses frictional brakes on its wheels.
The hypothesis of autosomal recessive inheritance of Vici syndrome was strengthened in 2002 with the clinical description of two new cases, one brother and one sister, by Chiyonobu et al. Gene
Vici syndrome is caused by mutations in the gene EPG5 (OMIM # 615068), which encodes an important regulator of the autophagy pathway, the ectopic P-granules autophagy protein 5, involved in the formation of lysosomes. EPG5 is the human homolog of the C.elegans epg5 gene. The gene EPG5 has been cloned for the first time by Nagase et al. by sequencing clones obtained from a size-fractionated fetal brain cDNA library, and was initially named KIAA1632.The EPG5 human gene is located on chromosome 18q12.3, has a length of 119,67Kb (NC_000018.10), consists of 44 exons and is transcriptionally driven from the centromere toward the telomere. The messenger RNA (mRNA) is 12633bp long (NM_020964.2) and contains a CDS of 7740 bp translated into a protein sequence of 2579 amino acids (NP_066015.2) with a molecular weight of 280kDa, presumed. The protein EPG5 is expressed primarily in the central nervous system (CNS), skeletal muscle, heart, thymus, cells of the immune system, lungs and kidneys.Mutations in the EPG5 gene interfere with the autophagy. This appears to be due to a block in the autophagosome-lysosome fusion mechanism. Diagnosis
The diagnostic workup usually includes an MRI of the brain, an EEG, ophthalmic examination and a cardiac ECHO. Muscle biopsy – which is not commonly done – may show storage of abnormal material and secondary mitochondrial abnormalities in skeletal muscle.