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Blast exposure is associated with traumatic brain injury (TBI), neuropsychiatric symptoms, and long-term cognitive disability. We examined a case series of postmortem brains from U.S. military veterans exposed to blast and/or concussive injury. We found evidence of chronic traumatic encephalopathy (CTE), a tau protein-linked neurodegenerative disease, that was similar to the CTE neuropathology observed in young amateur American football players and a professional wrestler with histories of concussive injuries. We developed a blast neurotrauma mouse model that recapitulated CTE-linked neuropathology in wild-type C57BL/6 mice 2 weeks after exposure to a single blast. Blast-exposed mice demonstrated phosphorylated tauopathy, myelinated axonopathy, microvasculopathy, chronic neuroinflammation, and neurodegeneration in the absence of macroscopic tissue damage or hemorrhage. Blast exposure induced persistent hippocampal-dependent learning and memory deficits that persisted for at least 1 month and correlated with impaired axonal conduction and defective activity-dependent long-term potentiation of synaptic transmission. Intracerebral pressure recordings demonstrated that shock waves traversed the mouse brain with minimal change and without thoracic contributions. Kinematic analysis revealed blast-induced head oscillation at accelerations sufficient to cause brain injury. Head immobilization during blast exposure prevented blast-induced learning and memory deficits. The contribution of blast wind to injurious head acceleration may be a primary injury mechanism leading to blast-related TBI and CTE. These results identify common pathogenic determinants leading to CTE in blast-exposed military veterans and head-injured athletes and additionally provide mechanistic evidence linking blast exposure to persistent impairments in neurophysiological function, learning, and memory.

The current literature on mechanisms involved in the pathogenesis of prostatitis/chronic pelvic pain syndrome (CPPS) is reviewed. Based on the literature and own observation it is suggested that, in the pathogenesis of chronic prostatitis are involved several mechanisms, and the mechanism of infection, especially in the later stages of the disease, is not determinative. Author gives his views concerning the chronic prostatitis. He suggests that the disease is laid down by virus (or group of viruses) which exists in the cell during embryonic life. Lifelong effect of virus (or group of viruses) on cells may initiate different chronic inflammatory processes and different pathologic changes in the organism, including prostatitis. Analysis of the literature showed a lack of a complete understanding of the causes and mechanisms of chronic prostatitis, but it also showed that the prostatitis syndrome is no longer a faceless myth. It is a reality, and the new awareness of its importance may give new hope for patients suffering from this intractable pain syndrome Further research in this area will help to better understand the nature of chronic prostatitis and find the best possible solutions in its treatment.

At present ascorbic acid and cyanocobalamin are widely used in medical practice. Often they are administered simultaneously; chemically they are incompatible, as ascorbic acid (redox compound) inactivates cyanocobalamin. The combination of ascorbic acid and cyanocobalamin is the problem of pharmacy. To solve the problem double-layer suppositories containing two incompatible vitamins: ascorbic acid and cyanocobalamin were developed. Pharmaceutical bioavailability of ascorbic acid and cyanocobalamin has been studied using in-vitro methods to develop optimal base for suppositories. As a result of investigations optimal composition and technology of the double-layer suppositories containing ascorbic acid and cyanocobalamin which met requirements has been developed. Sequential release of active compounds and as a result - sequential pharmacologic action is achieved.