Sentences with phrase «normal dogs with the mutation»

Not exact matches

All dogs with AHE were homozygous for this mutation, 15/41 healthy AH control dogs were heterozygous carriers while 26/41 normal healthy AH dogs were wild type.

So, one of the mysteries of Doberman vWD that has puzzled scientists for years, how affected dogs can end up with a small amount of completely normal vWf, is cleared up by understanding this type of mutation.

Normal kidneys reabsorb the Amino Acid cystine so that only small amounts pass into the urine, while dogs with mutations of both copies of the SLC3A1 gene fail to reabsorb cystine allowing large amounts to pass into the urine, hence the name cystinuria.

Dogs with two copies of the mutation have CEA, those with one are normal carriers and those with none are clear.

Dogs affected with Type I vWD have a mutation which allows normal vWF to be produced part of the time, so even dogs with two copies of the defective gene (affected dogs) have some minimal amount of normal Dogs affected with Type I vWD have a mutation which allows normal vWF to be produced part of the time, so even dogs with two copies of the defective gene (affected dogs) have some minimal amount of normal dogs with two copies of the defective gene (affected dogs) have some minimal amount of normal dogs) have some minimal amount of normal vWF.

Normal / Normal littermates of dogs with the mutation, if of equal quality, should be given preference for breeding.

The affected dogs (A) are homozygous for the dodecamer repeat expansion mutation with multiple dodecamer repeats, carrier (C) dogs have the normal and mutated allele and clear dogs (WT) have three copies of the repeat [8]

Dogs with the mutation would best be bred to those that are Normal / Normal.

The photoreceptors of dogs that carry this mutation develop normally, in contrast to those of dogs with XLPRA2, and remain morphologically and functionally normal until young adulthood, indicating the C - terminal of the RPGR protein is not essential for functional and structural differentiation of rods and cones.

In young affected dogs retinal structure, rhodopsin expression and photoreceptor activation is normal; disease progression is characterized by regions of initial focal photoreceptor degeneration surrounded by areas of structurally normal retina, which interestingly is very similar to the phenotypes of humans with RHO mutations [24].

Because this material appears to be more abundant in affected Swedish vallhund dogs compared to other forms of PRA with primary photoreceptor death or compared to the normal aging canine retinas, we suspect that the autofluorescent material is intimately associated with the disease - causing gene mutation.