In an attempt to elucidate the morphologic changes of normal aging skin, the present study was undertaken in human facial and chest well skin of individuals aged from 4 months to 76 years old. Biopsied skin was studied with light microscope, scanning electron microscope, and transmission electron microscope, using both conventional and tannic acid staining. The morphologic changes in the skin were noted as follow: 1. Structurally, the aged epidermis gradually became somewhat thinner, with flattening of the dermoepidermal interface. The number of melanocytes also decreased. 2. Abnormalities of elastic fibers such as loss of oxytalan fibers were observed from age 30. It was the initial sign of the aging process of elastic fibers, followed by abnormal changes in elaunin and mature elastic fibers. The degree of facial skin abnormality was rather more severe than that of the chest wall skin. 3. In individuals more than 50 years old, the age related changes in mature elastic fibers were more severe. Transmission electron microscopically, the electron density in elastin was irregular. The elastic fibers also showed pores and irregular splitting with fragmentation. Fine granular materials were scattered near the elastin. 4. Scanning electron microscopically, the elastic fibers in young adult skin showd ribbon-like fibers aligned in the same direction. They were either cylindrical or elliptical, having smooth surface. In old skin, the elastic fibers ran in various directions, forming complicated networks. These were larger, more elliptical and more branched than those in young adult skin. In summary, histologic changes of aging are much more prominent in sun-exposed skin(facial skin) than in sun protected skin(chest wall skin). A completely different spectrum of elastic fiber abnormalities was found in individuals more than 30 years old. The result indicates that elastic fiber abnormalities are related to aging skin.
Adult ; Male ; Female ; Humans

No abstract available.
Blood Group Antigens* ; Humans

No abstract available.
Blood Group Antigens* ; Humans

The multiple lentigines syndrome or LEOPARD syndrome is an autosomal dominantly inherited disorder with a variety of abnormalities and a familial occurrence. This syndrome is characterized by the presence of numerous dark brown macules on the skin but not the mucous surface, and by a marked increase in the number of lentigines from birth to puberty. The eponym LEOPARD stands for lentigines, EKG abnormalities, ocular hypertelorism, pulmonary stenosis, abnormalities of the genitalia, retardation of growth and deafness. We report a case of multiple lentigines syndrome in 7-year-old boy. He had numerous pinhead to pea sized, dark brownish macules scattered on the entire body and also had pulmonary stenosis, EKG abnormality, ocular hypertelorism and right exotropia. Interestingly, he also had a labial melanotic macule on the lower lip, which is usually spared in the multiple lentigines syndrome. Histologically, the biopsy specimen taken from the macule revealed an elongation of rete ridges, an increase of melanin pigments in the basal layer and mild inflammatory infiltrates intermingled with the melanophages in the upper dermis.
Adolescent ; Biopsy ; Child ; Deafness ; Dermis ; Electrocardiography ; Eponyms ; Exotropia ; Genitalia ; Humans ; Hypertelorism ; Lentigo ; LEOPARD Syndrome* ; Lip ; Male ; Melanins ; Panthera ; Parturition ; Peas ; Puberty ; Pulmonary Valve Stenosis ; Skin

No abstract available.
Appendicitis* ; Barium* ; Enema*

No abstract available.
Meningitis, Aseptic*

No abstract available.
Asian Continental Ancestry Group* ; Humans ; Humans* ; Sarcoma, Kaposi*

No abstract available.
Acute Kidney Injury* ; Nifedipine* ; Plasma* ; Renin*

In present study, the mechanism for oxygen-glucose deprivation -induced [3H]gamma-aminobutyric acid (GABA) from cerebral cortex slices of the rat was examined. Deprivation of oxygen and glucose(OGD) from Mg2+-free artificial cerebrospinal fluid, induced significant release of [3H]GABA (7.4+/-0.6% of total tissue content) from cerebral cortex slices. OGD-induced release of [3H]GABA was significantly attenuated by tetrodotoxin(TTX)(1 micrometer), Mg2+(1.2 mM), MK-801(10 micrometer), ketamine(10 micrometer), N-methyl-D-aspartate(NMDA) receptor antagonists, (DNQX)(30 micrometer), and 6-cyano-7-nitroquinoxaline-2,3-dione(CNQX)(30 micrometer), kainate/AMPA receptor antagonists, or 6-nitro-7-sulphamoyl-benzo[f]quinoxaline-2, 3-dione(NBQX)(10 micrometer), a selective AMPA receptor blocker. OGD-evoked [3H]GABA release was attenuated by (NG-nitro-L-arginine methyl ester(L-NAME) and 7-nitronidazole, nitric oxide synthase inhibitors, and methylene blue, potentiated by zaprinast, a cGMP phosphodiesterase inhibitor. OGD-induced release of [3H]GABA was inhibited by nipecotic acid, a selective neuronal GABA transporter blocker, and potentiated by DL-2.4-diamino-n-butyric acid(DABA), a neuronal and glial GABA transporter blocker. Dantrolene (30 micrometer) and 1,2-bis (2-aminophenoxy)-ethane-N, N, N', N'-tetraacetic acid tetrakis (acetoxymethyl) ester(BAPTA-AM)(30 micrometer), inhibitors of intracellular Ca2+ release, verapamil(5 micrometer), omega-conotoxinGVIA(100 nM) and omega-agatoxinIVA(100 nM), inhibitors of voltage-dependent Ca2+ channels, significantly attenuated the OGD-induced release of [3H]GABA. These results suggest that glutamate is involved in OGD-evoked [3H]GABA release, and this release is achieved by Ca2+-dependent exocytosis and reversal of transporters, and can be modulated by various neuronal mechanisms.
Animals ; Cerebral Cortex* ; Cerebrospinal Fluid ; Dantrolene ; Exocytosis ; gamma-Aminobutyric Acid ; Glutamic Acid ; Methylene Blue ; Neurons ; Nitric Oxide Synthase ; Oxygen ; Rats* ; Receptors, AMPA

No abstract available.
Thanatophoric Dysplasia*