Such therapies are now working in a variety of animal experiments and are on the horizon for most major human brain diseases, including cerebral palsy, mental retardation, strokes, tumors, head trauma, spinal cord injury, multiple sclerosis, Lou Gehrig's disease, Alzheimer's disease, Parkinson's disease and scores of less well known neurological defects.
It is well known that defects in a solid could dramatically influence its chemical reactivity.
A number of MOFs have received attention because of their photoluminescence properties and have been recently reviewed.[ 113]–[ 115] It is well known that defects play a considerable role in the optical properties of diverse solid-state materials.[ 114] For example, defect-induced luminescence has been found in Co2+-doped anatase, Cd-rich CdS and ZnS nanoparticles, and Eu2+-doped Sr2MgSi2O7.
Secondly, considering surface roughness, it is well known that crystalline defects inside epitaxial layers increase with the surface roughness of the seed layer.
It is well known that the defects in the middle of the Si energy gap can be called deep level centers, which will lead to an effective minority carrier lifetime reduction.
It is well known that operative defects in the latter bone are frequently painful for long periods and that they often weaken the bone to such an extent that fracture may occur.
It is well known that the defect chemistry of ZnO is complex, with a range of oxygen or zinc defects of varying charges and with concentrations that are interdependent on each other [15, 16].
For brittle materials in engineering, it is well known that the defect structure governs the macroscopic strength.
It is well known that the defect index, say d L is equal to the number of linearly independent solutions which are square summable of the difference equation − Δ ( p ( t ) ∇ x ( t ) ) + q ( t ) x ( t ) = λ x ( t ), t ∈ I (1.3).
It is well known that the defect index of ℒ is equal to the number of linearly independent square integrable solutions of equation L y = λ y for each λ ∈ C ∖ R, where ℂ and ℝ denote the sets of the complex and real numbers.
Although it is well known that ctf4 exhibits defects in sister chromatin cohesion [16], [17], [19], [20], Elg1 was not found previously to be involved in this process.
