Comparative stability of canine and feline hemostatic proteins in freeze-thaw-cycled fresh frozen plasma.

OBJECTIVE: To evaluate the stability of canine and feline hemostatic proteins in freeze-thaw-cycled (FTC) fresh frozen plasma (FFP). DESIGN: Prospective study. SETTING: Veterinary Teaching Hospital. ANIMALS: Nine blood donor dogs and 10 blood donor cats. INTERVENTIONS: Whole blood was collected and separated into packed RBC and plasma units according to standard methods. Each unit of plasma was divided into 2 equal aliquots and frozen (-41 °C). One aliquot from each donor (FTC) was then thawed and then refrozen (-41 °C) until time of analysis. The second aliquot (nonfreeze-thaw-cycled; NFTC) remained frozen until time of analysis. The hemostatic proteins assessed included coagulation factors, anticoagulant factors (antithrombin and Protein C), and adhesive proteins (fibrinogen and von Willebrand Factor). The coagulant activities of factors II, VII, VIII, IX, X, XI, and XII were measured in modified one-stage activated partial thromboplastin time or prothrombin time assays. Antithrombin and Protein C activities were measured in chromogenic substrate assays. Clottable fibrinogen was measured via the Clauss method, and von Willebrand Factor concentration (vWF:Ag) was measured in an ELISA. A paired t-test was utilized to identify differences in factor activity or concentration between FTC FFP and NFTC FFP. MEASUREMENTS AND MAIN RESULTS: No clinically or statistically significant differences (all P>0.05) were identified between FTC FFP and NFTC FFP. CONCLUSIONS: Refreezing FFP within 1 hour of initial thawing appeared to have no deleterious effects on the hemostatic protein activity or content of that unit. Transfusion of FTC FFP is expected to provide the recipient with comparable replacement of hemostatic proteins as FFP that has remained frozen.

Fluid intelligence loss linked to restricted regions of damage within frontal and parietal cortex.

Tests of fluid intelligence predict success in a wide range of cognitive activities. Much uncertainty has surrounded brain lesions producing deficits in these tests, with standard group comparisons delivering no clear result. Based on findings from functional imaging, we propose that the uncertainty of lesion data may arise from the specificity and complexity of the relevant neural circuit. Fluid intelligence tests give a characteristic pattern of activity in posterolateral frontal, dorsomedial frontal, and midparietal cortex. To test the causal role of these regions, we examined fluid intelligence in 80 patients with focal cortical lesions. Damage to each of the proposed regions predicted fluid intelligence loss, whereas damage outside these regions was not predictive. The results suggest that coarse group comparisons (e.g., frontal vs. posterior) cannot show the neural underpinnings of fluid intelligence tests. Instead, deficits reflect the extent of damage to a restricted but complex brain circuit comprising specific regions within both frontal and posterior cortex.

Executive function and fluid intelligence after frontal lobe lesions.

Many tests of specific 'executive functions' show deficits after frontal lobe lesions. These deficits appear on a background of reduced fluid intelligence, best measured with tests of novel problem solving. For a range of specific executive tests, we ask how far frontal deficits can be explained by a general fluid intelligence loss. For some widely used tests, e.g. Wisconsin Card Sorting, we find that fluid intelligence entirely explains frontal deficits. When patients and controls are matched on fluid intelligence, no further frontal deficit remains. For these tasks too, deficits are unrelated to lesion location within the frontal lobe. A second group of tasks, including tests of both cognitive (e.g. Hotel, Proverbs) and social (Faux Pas) function, shows a different pattern. Deficits are not fully explained by fluid intelligence and the data suggest association with lesions in the right anterior frontal cortex. Understanding of frontal lobe deficits may be clarified by separating reduced fluid intelligence, important in most or all tasks, from other more specific impairments and their associated regions of damage.

Goal neglect and Spearman's g: competing parts of a complex task.

In goal neglect, a person ignores some task requirement though being able to describe it. Goal neglect is closely related to general intelligence or C. Spearman's (1904) g (J. Duncan, H. Emslie, P. Williams, R. Johnson, & C. Freer, 1996). The authors tested the role of task complexity in neglect and the hypothesis that different task components in some sense compete for attention. In contrast to many kinds of attentional limits, increasing the real-time demands of one task component does not promote neglect of another. Neither does neglect depend on preparation for different possible events in a block of trials. Instead, the key factor is complexity in the whole body of knowledge specified in task instructions. The authors suggest that as novel activity is constructed, relevant facts, rules, and requirements must be organized into a "task model." As this model increases in complexity, different task components compete for representation, and vulnerable components may be lost. Construction of effective task models is closely linked to g.

Within-modality and cross-modality attentional blinks in a simple discrimination task.

Following up on studies of the "attentional blink," we studied interference between successive target stimuli in visual and auditory modalities. In each experiment, stimuli were two tones and four dots, simultaneously presented for 1,800 msec. Targets were brief intensity changes in either a tone or a dot. Subjects gave unspeeded responses. In four experiments, our results showed interference between targets in the same modality, but not across modalities. We conclude that, under our experimental conditions, restrictions in concurrent target identification are largely modality specific.

Frontal lobe involvement in spatial span: converging studies of normal and impaired function.

Although monkey lesion studies involving the prefrontal cortex commonly report working memory deficits, and neuroimaging studies consistently show prefrontal involvement in such tasks, patients with damage to this region commonly fail to show any working memory impairment. Such a discrepancy may be due to insensitive testing measures for patients, as well as small, yet critical differences between working memory tasks in imaging and patient studies. The current study utilised a more sensitive measure of spatial working memory spans, based either on structured or unstructured spatial arrays. A PET study in normal subjects confirmed that both variants did indeed activate prefrontal cortex. The same tasks were given to frontal lobe patients and closely matched controls. Patients with large frontal lesions were significantly impaired on this task, with those patients with damage to the right dorsolateral prefrontal cortex appearing particularly impaired. This result demonstrates that prefrontal cortex is necessary for normal working memory, even in simple tasks, such as spatial span. It is suggested, however, that the patient deficit reflects strategic or goal-based dysfunction, rather than storage limitations.