Acantholytic invasive squamous cell carcinoma: tumor diameter, invasion depth, grade of differentiation, surgical margins, perineural invasion, recurrence and death rate.

BACKGROUND: Squamous cell carcinoma (SCC) may present with or without the feature of acantholysis. METHODS: Investigate invasive acantholytic SCC by microscopic maximum tumor surface diameter, depth of invasion, grade of differentiation, perineural invasion (PNI) and percentage of acantholysis. Assess recurrence following excision. RESULTS: A total of 1658 consecutive invasive SCC cases were examined, comprising 4.9% acantholytic SCC. Median tumor microscopic maximum diameter was 8 mm for acantholytic SCC and 7.3 mm for non-acantholytic SCC. Median tumor invasion depth was 1.0 mm for acantholytic SCC and 1.5 mm for non-acantholytic SCC. Well, moderate and poor differentiation were not significantly different between acantholytic SCC and non-acantholytic SCC. One PNI case was found in 82 acantholytic SCC cases. A total of 77 acantholytic SCC cases were followed up over a median 25 months finding histologic proven recurrence at three acantholytic SCC excision sites. CONCLUSIONS: Acantholytic SCC were more likely to be located on head sites with less median depth than non-acantholytic SCC. Increasing percentage of acantholysis within acantholytic SCC was not associated with a shift towards poor differentiation. Histologic margins of 1.2 mm may adequately excise small acantholytic SCC. No recorded deaths, low PNI and low recurrence rates suggests acantholytic SCC is low-risk.

Maternal medium-chain acyl-CoA dehydrogenase deficiency identified by newborn screening.

Prior to the advent of expanded newborn screening, sudden and unexplained death was often the first and only symptom of medium-chain acyl-CoA dehydrogenase deficiency (MCADD). With the use of tandem mass spectrometry, infants can now be identified and treated before a life threatening metabolic decompensation occurs. Newborn screening has also been shown to detect previously undiagnosed maternal inborn errors of metabolism. We have now diagnosed two women with MCADD following the identification of low free carnitine in their newborns. While one of the women reported prior symptoms of fasting intolerance, neither had a history of metabolic decompensation or other symptoms consistent with a fatty acid oxidation disorder. These cases illustrate the importance of including urine organic acid analysis and an acylcarnitine profile as part of the confirmatory testing algorithm for mothers when low free carnitine is identified in their infants.

Reduced calcium uptake by rat brain mitochondria and synaptosomes in response to aging.

Synaptosomes were isolated from cerebral cortex of 3-, 18- and 24-month-old male, Fisher 344 rats and 45Ca2+ uptake was measured at 1, 3, 5, 15 and 30 s time periods following 65 mM KCl depolarization. Identical experiments were performed in which 5 mM KCl was added to examine age-related changes in resting 45Ca2+ accumulation by synaptosomes. Both 'fast-' and 'slow-phase' voltage-dependent 45Ca2+ uptake were significantly reduced in synaptosomes from 18- and 24- vs 3-month-old rats. No age-related change in resting (5 mM KCl) 45Ca2+ accumulation was observed. ATP-dependent and respiration-linked 45Ca2+ uptake was examined in mitochondria isolated from whole brains of 3- and 28-month-old male, hooded Long-Evans rats. Both ATP-dependent and glutamate-malate-ADP stimulated 45Ca2+ uptake by mitochondria were markedly reduced in response to aging. Respiratory control ratios were the same for 3- and 28-month-old mitochondria, suggesting that the decrement in 45Ca2+ uptake was not caused by an age-related decline in respiratory activity of mitochondria. The results of this study show that both voltage-dependent calcium entry into presynaptic nerve terminals and calcium uptake by mitochondria in brain decline with advanced aging. Age-related changes in cytosolic calcium levels could underlie, at least in part, cellular decrements in brain observed with aging.

45Ca2+ uptake into rat whole brain synaptosomes unaltered by dihydropyridine calcium antagonists.

Voltage-dependent 45Ca2+ uptake into rat whole brain synaptosomes was measured after 3-s KCl-induced depolarization to investigate possible inhibitory effects of calcium antagonists, nitrendipine, nimodipine, and nisoldipine. At a Ca2+ concentration of 1.2 mM, nitrendipine, in concentrations ranging from 0.1 nM to 10 microM, had no effect on 45Ca2+ uptake. When the Ca2+ concentration was lowered to 0.06 and 0.12 mM, nitrendipine, 10 microM, inhibited 45Ca2+ uptake in response to 109 mM KCl depolarization. However, in a separate concentration response study, nitrendipine, nimodipine, and nisoldipine, 0.1 nM to 10 microM, failed to alter the uptake of 45Ca2+ (0.06 mM Ca2+) into 30 mM KCl-depolarized synaptosomes. The high concentrations of these agents required to depress 45Ca2+ uptake indicate that the dihydropyridine calcium antagonists are considerably less potent in brain tissue than in peripheral tissue.

Light-dependent modifications in the metabolic responses of squash seedlings.

Light-induced modifications in lipoxidase metabolism and chlorophyll formation in the cotyledon of squash (Cucurbita moscata) seedlings were determined. The enzyme activity decreased as light intensity increased, but chlorophyll continued to accumulate long after lipoxidase activity had virtually disappeared. Considering the differences in the levels of irradiance required to manifest the optimal responses, and also from the results obtained with ultraviolet and red, far-red light treatments, any causal relationship between lipoxidase disappearance and chlorophyll synthesis was ruled out.The observed light-saturation phase in the chlorophyll synthesis, indicated that chlorophyll formation was initially controlled by the phytochrome system. No similar saturation stage for the enzyme responses was observed.The sensitivity of lipoxidase to prolonged light exposures suggested a strong correlation with the known photoreactions presumed to be controlled by the high energy reactive-phytochrome system. Lipoxidase metabolism is, therefore, suggested as a biochemical index for the photomorphogenic reactions similar to the ones induced by the high energy reaction.