Posttraumatic stress disorder in hospitalized terrorist bombing attack victims.

BACKGROUND: Posttraumatic stress disorder (PTSD) is a psychiatric disorder that results from exposure to a traumatic event and consists of intrusive and unwanted recollections; avoidance followed by emotional withdrawal; and heightened physiologic arousal. Hospitalized victims of suicide bombing attacks (SBAs) are unique because of the circumstances and severity of their injuries, which could affect the occurrence and delay the recognition of PTSD. Our objectives were to evaluate the prevalence and severity of PTSD among hospitalized SBA victims and to assess variables of physical injury as risk factors for the development of PTSD. METHODS: Forty-six hospitalized SBA victims were evaluated for PTSD using the PTSD symptom scale self-report questionnaire by phone. Demographic and medical data regarding the severity and type of injury and medical treatment were collected from medical files. Injury Severity Score was used to assess severity of physical injury. RESULTS: Twenty-four of 46 (52.2%) hospitalized SBA victims developed PTSD. Presence of blast lung injury was significantly higher in the PTSD group compared with the non-PTSD group (37.5% versus 9.1%, respectively; p < 0.04). There was no significant difference in Injury Severity Score between PTSD and non-PTSD groups. Blast lung injury and intracranial injury were found to be positive predictors of PTSD (odds ratio, 125 and 25, respectively). No correlation was found between the length of stay, length of intensive care unit stay, or severity of physical injuries and the severity of PTSD. CONCLUSIONS: Hospitalized victims of SBA are considerably vulnerable to develop PTSD. Victims should be monitored closely and treated in conjunction with their physical treatment. Blast lung injury and intracranial injury are predictors of PTSD.

CD40·FasL and CTLA-4·FasL fusion proteins induce apoptosis in malignant cell lines by dual signaling.

Evolution of apoptosis resistance in both lymphoma and leukemia cells is well documented, and induction of apoptosis in malignant cells is a major goal of cancer therapy. Up-regulation of anti-apoptotic signals is one of the mechanisms whereby resistance to apoptosis emerges. We have previously described the fusion proteins CD40·FasL and CTLA-4·FasL, which are formed from two functional membrane proteins and induce apoptosis of activated T cells. The present study explores the potential use of CD40·FasL and CTLA-4·FasL for the killing of malignant cells of lymphatic origin. Using malignant B and T cell lines that differ in surface expression of costimulatory molecules, we found that CTLA-4·FasL induces effective apoptosis of cells expressing CD95 and activates caspases 3, 8, and 9. Only B7-expressing B cells responded to CTLA-4·FasL with rapid abrogation of cFLIP expression. CD40·FasL effectively killed only the T cells that express high levels of CD40L in addition to CD95. In these cells, CD40·FasL significantly diminished cFLIP expression. Importantly, each of the fusion proteins is more potent than its respective components parts, alone or in combination. Thus, the proteins with their two functional ends deliver a pro-apoptotic signal and, in parallel, inhibit an anti-apoptotic signal, thus optimizing the wanted, death-inducing effect. Therefore, these proteins emerge as promising agents to be used for targeted and specific tumor cell killing.

Spontaneous vertebral osteomyelitis due to Staphylococcus epidermidis.

Few reports in the literature have documented 'spontaneous' vertebral osteomyelitis due to Staphylococcus epidermidis. Herein, we describe a case of S. epidermidis lumbar osteomyelitis presenting as progressive back pain, but without a known port of entry or underlying pre-existing high-risk predisposing conditions. A low threshold for the consideration of infectious osteomyelitis is warranted in persons presenting with new, progressive back pain.