PURPOSE: The lateralization of cognitive functions in crossed aphasia in dextrals (CAD) has been explored and compared mainly with cases of aphasia with left hemisphere damage. However, comparing the neuropsychological aspects of CAD and aphasia after right brain damage in left-handers (ARL) could potentially provide more insights into the effect of a shift in the laterality of handedness or language on other cognitive organization. Thus, this case study compared two cases of CAD and one case of ARL. MATERIALS AND METHODS: The following neuropsychological measures were obtained from three aphasic patients with right brain damage (two cases of CAD and one case of ARL); language, oral and limb praxis, and nonverbal cognitive functions (visuospatial neglect and visuospatial construction). RESULTS: All three patients showed impaired visuoconstructional abilities, whereas each patient showed a different level of performances for oral and limb praxis, and visuospatial neglect. CONCLUSION: Based on the analysis of these three aphasic patients' performances, we highlighted the lateralization of language, handedness, oral and limb praxis, visuospatial neglect and visuospatial constructive ability in aphasic patients with right brain damage.
Aged ; Aphasia/*etiology/*physiopathology ; Brain Injuries/*complications ; Cognition/*physiology ; Female ; Functional Laterality/*physiology ; Humans ; Male ; Middle Aged

Macrophages are important for the first line of defense against microbial pathogens. Integrin CD11b, which is encoded by Itgam, is expressed on the surface of macrophages and has been implicated in adhesion, migration, and cell-mediated cytotoxicity. However, the functional impact of CD11b on the inflammatory responses of macrophages upon microbial infection remains unclear. Here, we show that CD11b deficiency resulted in increased susceptibility to sepsis induced by methicillin-resistant Staphylococcus aureus (MRSA) infection by enhancing the pro-inflammatory activities of macrophages. Upon infection with MRSA, the mortality of Itgam, knockout mice was significantly higher than that of control mice, which is associated with increased production of TNF-α and IL-6. In response to MRSA, both bone marrowderived macrophages and peritoneal macrophages lacking CD11b produced elevated amounts of pro-inflammatory cytokines and nitric oxide. Moreover, CD11b deficiency upregulated IL-4-induced expression of anti-inflammatory mediators such as IL-10 and arginase-1, and an immunomodulatory function of macrophages to restrain T cell activation. Biochemical and confocal microscopy data revealed that CD11b deficiency augmented the activation of NF-κB signaling and phosphorylation of Akt, which promotes the functional activation of macrophages with pro-inflammatory and immunoregulatory phenotypes, respectively. Overall, our experimental evidence suggests that CD11b is a critical modulator of macrophages in response to microbial infection.