Effects of training service dogs on service members with PTSD: A pilot-feasibility randomized study with mixed methods.

This pilot-feasibility randomized control trial examined effects of an adjunctive short-term service dog training program (SDTP) for service members in out-patient treatment for PTSD. Twenty-nine volunteer participants were randomly assigned to either the SDTP (n = 12) or waitlist (n = 17); 20 participants were available for post-treatment evaluation. SDTP protocol consisted of six structured one-hour sessions with a dog-trainer conducted over two weeks, intended to train a service dog to help a fellow Veteran.

Type I Second Degree Atrioventricular Block in a Woman With Remote Repair of a Ventricular Septal Defect.

In a 45-year-old woman with syncope, an electrocardiogram revealed intermittent asymptomatic type I second degree atrioventricular block, right bundle branch block and left anterior fascicular block. An echocardiogram documented concentric left ventricular hypertrophy and right ventricular dilatation and hypokinesia. Because the patient did not have second degree atrioventricular block at the time of an electrophysiological study, the atrioventricular node, the left posterior fascicle, and the His bundle all remain potential sites for the type I second degree atrioventricular block on her initial electrocardiogram.

Selective Toxicity of a Highly Potent Camptothecin Analogue: A Pilot Study with Glioblastoma Multiforme Cells.

Background/aim: We developed a novel camptothecin analogue, CPT417, that yields reduced toxicity compared to other analogues used in chemotherapeutic regimens. In this pilot study, we assessed the activity of CPT417 against glioblastoma multiforme (GBM) cells and glioma stem cells.

Materials And Methods: The human U251 GBM cell line and normal human astrocytes were cultured in parallel for clonogenic survival analysis following exposure to increasing concentrations of CPT417.

Traumatic brain injury causes platelet adenosine diphosphate and arachidonic acid receptor inhibition independent of hemorrhagic shock in humans and rats.

Background: Coagulopathy in traumatic brain injury (CTBI) is a well-established phenomenon, but its mechanism is poorly understood. Various studies implicate protein C activation related to the global insult of hemorrhagic shock or brain tissue factor release with resultant platelet dysfunction and depletion of coagulation factors. We hypothesized that the platelet dysfunction of CTBI is a distinct phenomenon from the coagulopathy following hemorrhagic shock.

Early platelet dysfunction in a rodent model of blunt traumatic brain injury reflects the acute traumatic coagulopathy found in humans.

Acute coagulopathy is a serious complication of traumatic brain injury (TBI) and is of uncertain etiology because of the complex nature of TBI. However, recent work has shown a correlation between mortality and abnormal hemostasis resulting from early platelet dysfunction. The aim of the current study was to develop and characterize a rodent model of TBI that mimics the human coagulopathic condition so that mechanisms of the early acute coagulopathy in TBI can be more readily assessed.