Association between cognitive impairments and anxiety disorders following traumatic brain injury

This study examined the association between cognitive impairment and anxiety disorders following traumatic brain injury (TBI). Sixty-six participants recruited from a rehabilitation hospital completed the Structured Clinical Interview for the DSM–IV (Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition) and cognitive tests at one year post injury. Prevalence of anxiety disorder was 27.3%. Logistic regression analyses revealed that the attention/working memory, information processing, and executive functions models were significantly associated with anxiety disorder. The memory model was not significant. Processing speed emerged as the strongest model associated with anxiety disorder. The role of cognitive impairment in the etiology of anxiety disorders after TBI is discussed, and treatment implications are explored.     

The impact of chemokine receptor CX3CR1 deficiency during respiratory infections with Mycobacterium tuberculosis or Francisella tularensis

Recruitment of immune cells to infection sites is a critical component of the host response to pathogens. This process is facilitated partly through interactions of chemokines with cognate receptors. Here, we examine the importance of fractalkine (CX3CL1) receptor, CX3CR1, which regulates function and trafficking of macrophages and dendritic cells, in the host''s ability to control respiratory infections with Mycobacterium tuberculosis or Francisella tularensis. Following low-dose aerosol challenge with M. tuberculosis, CX3CR1^−/− mice were no more susceptible to infection than wild-type C57BL/6 mice as measured by organ burden and survival time. Similarly, following inhalation of F. tularensis, CX3CR1^−/− mice displayed similar organ burdens to wild-type mice. CX3CR1^−/− mice had increased recruitment of monocytes and neutrophils in the lung; however, this did not result in increased abundance of infected monocytes or neutrophils. We conclude that CX3CR1-deficiency affects immune-cell recruitment; however, loss of CX3CR1 alone does not render the host more susceptible to M. tuberculosis or F. tularensis.