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Visual evoked sensory (VEP) and event-related potentials (ERP) were assessed in 29 adolescents with insulin-dependent diabetes mellitus (IDDM) and in 29 controls matched for age and gender. Data were compared with clinical and psychometric measures, age at onset, duration of disease, and metabolic control. Analysis revealed no latency differences for the first cortical VEP component (P50) but a steadily increasing latency delay for subsequent VEP (N80, P100, N150, P200) and ERP components (P300) in the IDDM group compared to healthy controls. IDDM subjects showed highly significant latency prolongations (p < 0.001) for P100, N150 and P200 and P300 compared with healthy controls. A pathological VEP/ERP latency delay of more than 3 SD above the reference value range was observed in 21 IDDM patients (72.4%). Psychometric outcome measures in IDDM subjects showed no significant performance deficits on the Raven SPMs relative to non-diabetic controls. In contrast to VEP and ERP anomalies, which were highly interrelated, there was no tendency for neurophysiological and psychometric abnormalities to be contemporarily present. Neither electrophysiological nor psychometric measures were correlated with age at onset, IDDM duration, quality of metabolic control, or the presence of peripheral neuropathy. These findings give evidence that 1) higher cognitive functions are frequently affected in adolescents even with prepubertal IDDM onset, 2) neurophysiological ERP analysis seems to detect minor neurocognitive restrictions, presently not affecting psychometric outcome, 3) altered neurophysiological parameters were present in more than 70% of IDDM subjects studied, and 4) functional CNS disturbances affecting neurocognition are apparently not correlated with metabolic parameters previously thought to be important predictors of CNS outcome, suggesting the presence of multifactorial influences affecting neurocognition in IDDM subjects.

Capric (C10:0), lauric (C12:0), myristic (C14:0), palmitic (C16:0), stearic (C18:0) and arachidic (C20:0) acids were compared for their toxic effects upon cultured rat heart muscle and endothelioid cells. The free fatty acids (FFA) were found to albumin (6:1) and tested at 5 x 10(-5)M. Reduction of cell viability (51Cr release) and in situ mitochondrial and lysosomal labilization were used as indices of injury. Reduction in viability of both cell types was produced by palmitic, stearic or arachidic acids, but only after exposures of from 12 to 36 h. These FFA also produced needle-like cytoplasmic inclusions. Mitochondria and lysosomes were labilized after shorter exposures. Capric, lauric and myristic acids, were relatively non-toxic, and protected endothelioid cell lysosomes from labilization.

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