PubMed Health⌕ Search

Biomedical subjects

U C Yeo

Publications and source records attributed to U C Yeo.

8 recordsLinked to original sources
PubMed2000

Psoralen-ultraviolet A-induced erythema: sensitivity correlates with the concentrations of psoralen in suction blister fluid.

Since the advent of psoralen-ultraviolet A (PUVA) therapy, the value of plasma 8-methoxypsoralen (8-MOP) concentrations to predict PUVA-induced erythema has been widely investigated. Plasma 8-MOP concentrations have not been proportional to, and cannot alone predict, the degree of PUVA-induced erythema. We assumed that PUVA-induced erythema was related more closely to psoralen concentrations in the skin tissue rather than those within blood vessels. This study was designed to investigate the correlations between the 8-MOP concentrations in suction blister fluid (SBF) and in plasma, with the degree of PUVA-induced erythema. 8-MOP concentrations in plasma and SBF were measured in 15 vitiligo patients and 11 volunteers. Blood and SBF samples were collected 2 h after taking 8-MOP, and 8-MOP concentrations in plasma and SBF were quantified using reverse-phase high-performance liquid chromatography. Eleven volunteers were phototested using a series of doses of ultraviolet A at the time of sampling. The erythema responses were estimated visually to determine the minimal phototoxic dose (MPD). SBF 8-MOP concentrations showed a weak positive correlation with plasma 8-MOP concentrations, which means that we could not predict the exact SBF 8-MOP concentrations using the plasma 8-MOP concentrations. The MPD showed a better correlation with the log of the SBF 8-MOP concentration than with that of the plasma 8-MOP concentration. These results show that plasma 8-MOP concentration cannot represent the exact SBF 8-MOP concentration, and that SBF 8-MOP concentrations, which are representative of the skin tissue 8-MOP level, are more closely related to the erythemal sensitivity during PUVA therapy.

Adolescent↗
PubMed1999

Arginine in the beginning of the 1A rod domain of the keratin 10 gene is the hot spot for the mutation in epidermolytic hyperkeratosis.

Keratin intermediate filaments are expressed in specific type I/type II pairs in the stage of differentiation of keratinocytes. The mutations in the keratin genes expressed in the epidermis are etiologically responsible for several epidermal genetic skin diseases, such as epidermolysis bullosa simplex, epidermolytic hyperkeratosis (EHK), ichthyosis bullosa of Siemens, palmoplantar keratoderma, pachyonchia congenita and white sponge nevus. The mutations of keratins 1/10 which are expressed in spinous and granular layers are confirmed to cause EHK. There are several trials to correlate between the clinical phenotypes and sites of mutations of the keratin genes. One of these is that EHK is divided into two groups: the palms and soles involvement (PS) group and the non-palms and soles (NPS) group. So far the PS group had the mutations in the keratin 1 and the NPS group in keratin 10. Most of the mutations of the NPS group were reported in the beginning of the 1A rod domain and over 2/3 of the mutations in the 1A rod domain were the base pair substitution of arginine. Here we find two different mutations in two unrelated Korean kindreds classified as NPS group-R156C and R156H-in the 1A rod domain of keratin 10. Our results are compatible with the above classification and suggest that the arginine in the beginning of the 1A rod domain is the hot spot for the mutation of the keratin 10 gene.

Arginine↗
PubMed1999

Serum concentration of the soluble interleukin-2 receptor in vitiligo patients.

Serum levels of sIL-2R can be used to monitor in vivo immune activation and its elevation have been shown to be correlated with T cell mediated immune disease such as atopic dermatitis, psoriasis, lymphoma and systemic sclerosis. Vitiligo is the disease of depigmentation caused by destruction of melanocytes, and there have been extensive studies on the immune pathogenesis. If the pathogenesis of vitiligo is correlated with the activation of T lymphocytes, the change of IL-2R will be detected compared with that of normal control. Therefore we sought the change in sIL-2R to determine whether T lymphocytes from patients with vitiligo show abnormal biological behavior. The quantitation of sIL-2R was done by sandwich enzyme-linked immunosorbent assay (ELISA) from the sera of 79 vitiligo patients and 40 normal controls. The results were summarized as following. The sIL-2R level in vitiligo patients (671.91 +/- 368.59 U/ml) was significantly increased compared with that of controls (370.8 +/- 71.8 U/ml; P < 0.005). According to clinical types, sIL-2R level in focal type of vitiligo patients was significantly higher than those in other types (segmental or generalized; P < 0.05). The sIL-2R level in patients less than 1 year duration was significantly higher than in patients more than 1 year duration (P < 0.05). The sIL-2R levels were not significantly different between active and inactive group. There was no significant differences among sIL-2R levels according to sex or age of onset. Our study showed that sIL-2R level was higher in vitiligo patients compared with that of normal controls, so the activation of T lymphocytes would be an important component in the pathogenesis of vitiligo. The higher sIL-2R levels in recent onset group would suggest that sIL-2R level might be an acute immunologic marker in vitiligo patients.

Adolescent↗
PubMed1999

Activating mutation of GS alpha in McCune-Albright syndrome causes skin pigmentation by tyrosinase gene activation on affected melanocytes.

McCune-Albright syndrome (MAS) is a sporadic disease characterized by café-au-lait spots, polyostotic fibrous dysplasia and hyperfunctional endocrinopathies. To elucidate the mechanism of skin pigmentation, melanocytes, keratinocytes and fibroblasts were primary cultured from the café-au-lait spot of a MAS patient. Then, mutational analysis and morphologic evaluation were performed. Also, cAMP level and tyrosinase gene expression in cultured cells were determined. Only Gsalpha mutation was found in affected melanocytes and the cAMP level in affected melanocytes was higher than that of normal melanocytes. The mRNA expression of tyrosinase gene was increased in the affected melanocytes. This study suggests that skin pigmentation of MAS results from activating mutation of Gsalpha in melanocytes and the mechanism involves the c-AMP-mediated tyrosinase gene activation.

Base Sequence↗
PubMed1998

A case of hydroa vacciniforme with unusual ear mutilation.

A 22 year-old man visited our department with a 18-year-history of recurrent vesicular eruption on his skin when exposed to the sun. History revealed that the skin lesions developed as vesicles at first, then over the next several days, they formed crusts and healed with scarring. We were able to induce skin lesions by a repetitive UV-A provocation test. By the clinical and histologic features of the induced lesions, the case was diagnosed as hydroa vacciniforme (HV). However, no vesicular lesions were found on physical examination. Instead, in addition to varioliform scarring, we found various unusual clinical manifestations: burn-like lesions and crusts, flexion contracture of the digitum, and ear lobe mutilation. The ear lobe mutilation, which had not been reported previously in HV, was especially interesting.

Adult↗
PubMed1998

Mutations in the 1A rod domain segment of the keratin 9 gene in epidermolytic palmoplantar keratoderma.

Palmoplantar keratodermas (PPK) constitute a heterogeneous group of diseases marked by the thickening of palms and soles of affected individuals. They are divided into autosomal dominant and autosomal recessive groups by the mode of transmission. The autosomal dominantly transmitted group is further divided into epidermolytic (EPPK, Voerner) and non-epidermolytic (NEPPK, Unna-Thost) types according to the histopathologic findings. Recent development of molecular approaches has confirmed that EPPK and NEPPK are caused by the mutations in keratin 9 and 1 genes, respectively. We have studied three families of EPPK to find the mutation in the keratin 9 gene. DNA sequence analyses revealed single base changes in sequences encoding the highly conserved 1A rod domain segment of the keratin 9 gene in two of the three families. These mutations caused Arg (CGG) to Glu (CAG; R162Q) and Arg (CGG) to Try (TGG; R162W) substitutions. The same arginine position has been mutated in the keratin 10 gene in epidermolytic hyperkeratosis, the keratin 14 gene in epidermolysis bullosa simplex, and the keratin 9 gene in hereditary EPPK in Western patients. In this study we show that unrelated Korean patients have similar mutations.

Arginine↗
PubMed1993

Piroxicam photosensitivity associated with vesicular hand dermatitis.

A case of piroxicam photosensitivity in a 42-year-old man is reported. While he was taking piroxicam, eczematous skin lesions on sun-exposed skin and vesicular hand dermatitis on the finger webs and palms developed. He showed a lowered minimal erythema dose (MED) to UVA when a rechallenge with piroxicam was attempted. Photopatch testing with piroxicam was positive.

Adult↗