No abstract available.
Animals ; Embryonic Development* ; Female ; Mice* ; Oviducts* ; Pregnancy

We investigated whether the two variant elements of CRE(TGcCGTCA[5'CRE], TGACcTCA[3'CRE]) in the 5'flanking region of the rat TRH gene, which are different from the CRE consensus sequence(5'-TGACGTCA-3') by one base pair, are responsive to cAMP, and whether the one base pair difference is responsible for the degree of cAMP responsiveness of the gene. When CA 77 cells were stimulated with forskolin and isobutylmethylxanthine for 4 hours, the level of TRH mRNA was increased by only two fold. The transient gene expression study using serial 5'deletion of the TRH gene in PC12 cells showed that the region between-113 and-77, which includes 5'CRE, was crucial for the cAMP resonsiveness. When the plasmid, which contains the 30 bp oligonucleotide including either 5'CRE or 3'CRE ligated to the enhancerless RSV promoter, was transfected into PC12 cells, it did not significantly affect not only the basal transcription but cAMP responsiveness. The 65 bp oligonucleotide including both 5'CRE and 3'CRE, however, increased both of the basal transcription and cAMP-stimulated transcription by 2-3 fold. When the sequence of 5'CRE was converted to that of the CRE consensus by replacing one base pair, the cAMP responsiveness was increased by two fold although the basal transcription was not increased. The one base pair mutant of 3'CRE increased both of the basal and cAMP-stimulated transcription by 3-4 fold. These results suggest that there are the two variant CREs in rat TRH gene, which are relatively weak CRE compared to the CREs of other neuropeptide genes and cooperative for the activation of both the basal and cAMP-stimulated transcription. The one base pair difference of the variant CREs from the CRE consensus sequence is responsible for the weak responsiveness to cAMP.
Animals ; Base Pairing ; Colforsin ; Consensus ; Consensus Sequence ; Cyclic AMP ; Gene Expression ; Neuropeptides ; PC12 Cells ; Plasmids ; Rats ; Response Elements ; RNA, Messenger ; Thyrotropin ; Thyrotropin-Releasing Hormone

No abstract available.
Apolipoprotein C-II* ; Apolipoproteins* ; Hep G2 Cells* ; RNA, Messenger*

No abstract available.
Gastroenteritis* ; Humans* ; Rotavirus*

No abstract available.
Seizures, Febrile*

No abstract available.
Diarrhea* ; Korea*

No abstract available.
Lung*

No abstract available.
Fluorides* ; Osteoblasts*

Nevus sebaceus is a hamartoma that combines epidermal, follicular, sebaceous, and apocrine gland abnormalities. It mostly occurs on the scalp or face and shows characteristically well demarcated yellowish patches or plaque. Clinically several types of cutaneous neoplasms including syringocystadenoma papilliferum, basal cell carcinoma, nodular hidradenoma, syringoma, sebaceous epithelioma, trichilemmoma and apocrine neoplasms have been associated. We herein report a case of nevus sebaceus associated with tubular apocrine adenoma and apocrine poroma of a 11-year-old girl.
Acrospiroma ; Adenoma* ; Apocrine Glands ; Carcinoma ; Carcinoma, Basal Cell ; Child ; Female ; Hamartoma ; Humans ; Nevus* ; Poroma* ; Scalp ; Syringoma

We report a case of vitiligo developed on the sites of DNCB application for the treatment of alopecia areata in a 53-year-old woman. Histopathologic studies of the depigmented patches showed absence of melanin pigmentation at the basal layer of the epidermis and a negative reaction for the Fontana-Masson stain. The current theories explaining vitiligo development after topical sensitizer application are that topical sensitizers induce the vitiligo by a direct cytotoxic effect on the melanocytes, or by unmasking latent vitiligo as a result of the Koebner phenomenon due to contact dermatitis, but the exact mechanism is still unclear.
Alopecia Areata* ; Alopecia* ; Dermatitis, Contact ; Dinitrochlorobenzene* ; Epidermis ; Female ; Humans ; Melanins ; Melanocytes ; Middle Aged ; Pigmentation ; Vitiligo*