Traumatic brain injury (TBI) is often associated with enduring impairments in high-level cognitive functioning, including working memory (WM). We examined WM function in predominantly chronic patients with mild, moderate and severe TBI and healthy comparison subjects behaviorally and, in a small subset of moderate-to-severe TBI patients, with event-related functional magnetic resonance imaging (f MRI), using a visual n-back task that parametrically varied WM load. TBI patients showed severity-dependent and load-related WM deficits in performance accuracy, but not reaction time. Performance of mild TBI patients did not differ from controls; patients with moderate and severe TBI were impaired, relative to controls and mild TBI patients, but only at higher WM-load levels. f MRI results show that TBI patients exhibit altered patterns of activation in a number of WM-related brain regions, including the dorsolateral prefrontal cortex and Broca's area. Examination of the pattern of behavioral responding and the temporal course of activations suggests that WM deficits in moderate-to-severe TBI are due to associative or strategic aspects of WM, and not impairments in active maintenance of stimulus representations. Overall, results demonstrate that individuals with moderate-to-severe TBI exhibit WM deficits that are associated with dysfunction within a distributed network of brain regions that support verbally mediated WM. (JINS, 2004, 10, 724-741.)

The genetic basis for resistance to a number of antibiotics was examined in Rhizobium japonicum . Resistance to penicillin G, neomycin, and chloramphenicol appears to be mediated by an extrachromosomal element similar to that found in the Enterobacteriaceae . Resistance to these antibiotics was eliminated from cells by treatment with acridine orange, and resistance to all three antibiotics could be transferred en bloc to Agrobacterium tumefaciens under conditions excluding transformation or transduction as possible genetic mechanisms.

The concept of "reserve" has traditionally been defined on the basis of a single indicator (e.g., education or intracranial volume) that purports to moderate or buffer the effects of brain damage on different clinical outcomes. While studies have shown modest effects for some indicators, it has left the concept of "reserve" wanting as an explanatory construct. More recently efforts have been made to identify groups of indicators hypothesized to represent a construct for brain or cognitive reserve. These efforts have also proved wanting because of the lack of evidence to justify such a priori groupings of variables into a brain or cognitive reserve construct. This theoretical paper addresses the issue of construct validity (convergent and discriminant) for both brain and cognitive reserve as single or multiple reserve factors. Conceptual models are proposed that are (a) derived from the current extant reserve literature and (b) empirically testable in order to facilitate establishment of construct validity for the commonly used, and perhaps misused, brain and cognitive reserve concepts.

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