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Results for “Pigmentation Disorders”

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At least 1,135 records · Page 63Linked to original sources
PubMed1993

p53 expression in dyskeratosis congenita: a marker for oral premalignancy?

As p53 expression has been associated with malignant disease its presence was assessed in biopsy specimens from dorsal lingual hyperkeratosis, taken over a five year period. p53 expression, using CM1, was assessed using a standard immunoperoxidase technique. p53 was not identified in the first biopsy specimen in 1986 but was identified in all subsequent ones. Only in the latest biopsy specimen was there evidence for dysplasia in haematoxylin and eosin stained sections. It is suggested that p53 expression may be a reliable marker for predicting premalignant change in keratoses occurring in dyskeratosis congenita.

Atrophy↗
PubMed1993

Abnormalities of the auditory brainstem response in vitiligo.

Accumulating evidence suggests that vitiligo is a systemic disease affecting the entire pigmentary system and possibly the melanin-containing cellular elements of the nervous system. In the present paper we comparatively study the auditory brainstem response (ABR) of 30 patients with active vitiligo and 50 healthy human subjects in order to detect possible subclinical abnormalities of the auditory system in this disorder. Our findings reveal a statistically significant (p < 0.01) decrease of the I peak latency and a statistically significant (p < 0.01) increase of the I-III interpeak latency in the patients as compared to the controls. The decrease of the first peak latency may be due to a numerical decrease of active melanocytes in the inner ear which results in an impairment of the ion exchange between the endolymph and perilymph. The increase of the I-III interpeak latency may be explained in terms of an abnormal synaptic activity and transmission of the action potential from the auditory nerve to the superior olive.

Acoustic Stimulation↗
PubMed2000

A quantitative evaluation of pigmented skin lesions using the L*a*b* color coordinates.

The evaluation of pigmentary skin lesions by clinical doctors has been based on subjective and qualitative judgements. Observations have mostly relied on visual inspection, making the effects of treatment difficult to evaluate with any precision. For this reason there is a real need for an objective method to evaluate prognosis after treatment. Recent scientific measurements such as reflectance spectrophotometry and reflectance colorimetry have provided accurate quantitative color information about skin lesions, but these techniques are costly and difficult to apply in the clinical field. The purpose of this study was to develop a simple and cost-effective way of evaluating treatment results. We have developed a software program using the L*a*b* color coordinate system to quantify the effect of treatment and have successfully demonstrated its clinical usefulness. Our method compares the relative color difference between normal skin and skin lesions before and after treatment, instead of measuring the absolute color of skin lesions. The accuracy of our quantitative color analysis was confirmed by the simulated images of hemangioma and ota nevus. Clinical efficacy was also confirmed through a blind test involving 3 clinicians who were asked to grade the treatment effects of 13 cases of hemangioma and 7 cases of ota nevus. These subjective clinical grades correlated well with the treatment results obtained using the proposed color analysis system (Correlation coefficient = 0.84).

Color↗
PubMed1988

Aflatoxin-impaired ability to accumulate oxycarotenoid pigments during restoration in young chickens.

The mechanism by which aflatoxin causes paling in chickens was investigated by measuring its effect on the restoration of pigments in 3-wk-old birds made pale by feeding a white corn-soy diet. Pigment restoration was accomplished by feeding the same diet supplemented with lutein (70 micrograms/g of diet), which is the major oxycarotenoid pigment in chicken diets and tissues. The oxycarotenoids (free, monoester, and diester forms of lutein) in the toe web, liver, serum, and jejunal mucosa of control and aflatoxin-fed (2 micrograms/g of diet) birds were measured by HPLC at 0, 1, 2, 3, 6, and 9 days of repletion. Aflatoxin caused a significant (P less than .05) depression of all forms of lutein in the toe web. In the liver, aflatoxin decreased lutein significantly (P less than .05) but increased lutein monoester and lutein diester. Lutein accumulation in serum and mucosa were inhibited significantly (P less than .05) starting on Days 2 and 3, respectively. These data imply that the normal accumulation of lutein from the diet proceeded into and through the mucosa to the serum to depot sites in the liver and integument, where lutein was acylated to its monoester, which was acylated to its diester. Further, aflatoxin inhibited, apparently independently, the accumulation of lutein by the mucosa, serum, liver, and integument. Pharmacokinetic analysis of the data indicated that both acylation steps in the integument were sensitive to aflatoxin, but the passage of lutein from serum into the integument was not affected.

Aflatoxins↗
PubMed1988

Depletion of oxycarotenoid pigments in chickens and the failure of aflatoxin to alter it.

Aflatoxin, a demonstrated cause of pale bird syndrome in chickens, was investigated for its effects on the depigmentation of chickens placed on a diet low in carotenoids. Chickens were pigmented by feeding for 3 wk a white corn-soy diet supplemented with 50 micrograms free lutein and 0 or 4 micrograms aflatoxin/g diet. Then birds were switched to the same diets unsupplemented with lutein. At 0, 1, 2, 3, 6, and 9 days after switching, jejunal contents and mucosa, serum, liver, and toe web of 4 groups of 10 birds were removed for analysis of their carotenoids by high performance liquid chromatography. In control birds the order of decrease in total lutein was jejunal contents greater than jejunal mucosa greater than serum greater than liver greater than toe web. Aflatoxin did not alter the depletion process, except for minor retardation of lutein depletion in the mucosa and liver. Pharmacokinetic analysis of the data indicated that lutein depletion in the integument was accomplished through three sequential reactions (lutein diester----lutein monoester----lutein----serum lutein) and that aflatoxin had no effect on the reactions. These results imply that aflatoxin induces pale bird syndrome by interfering with the accumulation of pigment by chickens rather than by enhancing the depletion of pigment.

Aflatoxins↗
PubMedDate not supplied

[Atrophic striae].

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Administration, Topical↗
PubMed1954

Carotenaemia.

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Blood↗