R192H variant of PRPF4 might be due to incomplete penetrance or largely variable disease expressivity, both being phenomena frequently observed for RP-associated mutations in splicing factors. For the PRPF31-linked autosomal dominant RP, this has been explained by a modifier gene that modulates PRPF31 transcription. Low expression of the modifier increases wild-type PRPF31 levels to an extent that are sufficient to prevent the development of disease symptoms in heterozygous mutation carriers. It has been proposed that the vulnerability of retinal cells to splicing factor defects arises from an unmet requirement for the production of sufficient amounts of mature retinal mRNAs. Thus, defects in different splicing factors might act together to decrease the level of functional tri-snRNPs below the threshold required in retinal cells. This does not necessarily require a complete loss of the mutant protein from the tri-snRNP, as demonstrated by an RP-causing missense mutation in SNRNP200 which still allows integration of the mutant protein into the tri-snRNP but causes a decrease in splicing efficiency and fidelity. It is possible that a hypomorphic variant in another splicing factor is present in the patient, but not in her daughter, and leads to the manifestation of RP. Moreover, it can not be excluded that the RP of the patient is caused by biallelic mutations in a recessive RP gene, and that p.R192H represents a rare nonpathogenic variant. Support for the notion that a decrease in overall tri-snRNP activity rather than individual splicing factor defects lead to photoreceptor damage comes from a zebrafish mutant of the trisnRNP recycling factor SART3: Although SART3 is an assembly factor that is not itself part of the tri-snRNP, its mutation leads to the reduced expression of photoreceptor mRNAs. Taken together, our data are consistent with a model in which rare mutations of tri-snRNP splicing factors act together to decrease the level of functional tri-snRNPs below the threshold required in retinal cells. Traumatic brain injury is one of the signature injuries in the conflicts with Iraq and Afghanistan. Thirty percent of combat troops of Operation Iraqi Freedom and Operation Enduring Freedom have been diagnosed with mild, moderate, or severe TBI. More TBI cases occur out of the combat zone due to vehicle Trichostatin A purchase crashes, falls, sports, and recreational activities, which account for 84% of the total military TBI cases. The Glasgow Coma Scale is a standard measure to ascertain the initial severity and prognosis of TBI. Mild TBI, which is the most common form of military and civilian TBI, is characterized by loss of consciousness for,30 min and post traumatic amnesia for,24 hr with a GCS of 13–15, and accounts for 77% of the total TBI cases. Diagnosis of mTBI is difficult as the injury may go unnoticed due to the lack of any immediate symptoms and confirmed pathology. Computed tomography and magnetic resonance imaging have limited ability to detect mild brain tissue damage.