Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present 10 patients with autosomal dominant transmission of a pigmentary pattern characterized by facial, lip, extremity, buttock, and palmoplantar small, discrete hyperpigmented macules. None of the patients had lesions of the oral mucosa or internal organ system abnormalities. These patients' pigmentary pattern can resemble the ones seen in other lentiginosis syndromes. Those most closely mimicked--the Peutz-Jeghers syndrome, the centrofacial lentiginosis syndrome, and Carney's syndrome--all have associated internal abnormalities. We believe the pattern of pigmentation in these 10 black patients is distinct.
Arch Dermatol 1989 Sep
PMID:Inherited patterned lentiginosis in blacks. 267 48

This report describes a 25-year-old white woman with lentigines, cutaneous myxomas, bilateral atrial myxomas, and cerebral artery aneurysms. We believe this case to be the fifth reported case of this unusual association in the medical literature, with the additional finding of a central nervous system aneurysm. In the past this association has been described under the mnemonics NAME syndrome and LAMB syndrome. We propose that these mnemonics be dropped because the particular features encompassed within this syndrome are unclear. We suggest that "cutaneous lentiginosis with atrial myxomas" is an adequate description of this syndrome.
J Am Acad Dermatol 1986 Aug
PMID:Cutaneous lentiginosis with atrial myxomas. 373 90

We report the second case of atrial myxoma associated with livedoid macules representing an embolic phenomenon. This case of atrial myxoma was of the sporadic type with no associated syndrome (such as the LAMB or NAME syndrome or Carney complex). A skin biopsy specimen from fading livedoid macules on the extremities showed a myxoid embolus inside dermal vessels, a diagnostic clue to the presence of an atrial myxoma. The histologic features of such lesions should alert the clinician to the presence of an otherwise silent atrial myxoma. Early surgical intervention may prevent the onset of severe neurologic deficits in such patients.
J Am Acad Dermatol 1995 May
PMID:Atrial myxoma with livedoid macules as its sole cutaneous manifestation. 772 49

The aim of this study was to investigate in human skin in vivo the role of nitric oxide in maintaining resting vascular tone, in the vasodilatation caused by local warming and by ultraviolet B light exposure, and in the response to exogenous calcitonin gene-related peptide (CGRP). Cutaneous blood flow was assessed by planimetry of the visible erythema or pallor and by laser Doppler flowmetry. Intradermal injection of the inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl ester (L-NAME; 25 nmol), into forearm skin produced a visible pallor and a reduction of blood flow at a controlled ambient temperature of 21 degrees C. The control, NG-nitro-D-arginine methyl ester (D-NAME; 25 nmol) or NG-monomethyl-L-arginine (L-NMMA; 25 nmol) did not cause pallor or reduce blood flow. L-NAME and L-NMMA caused dose- and time-dependent increases in pallor, and reductions in cutaneous blood flow in skin that had been locally warmed by immersion in water at 45 degrees C and in skin that had been exposed to ultraviolet B light. D-NAME and D-NMMA at comparable concentrations did not have the effects on skin blood flow observed with the L forms. L-NAME and L-NMMA both inhibited the increased blood flow in human skin caused by the intradermal injection of CGRP (12.5 or 25 pmol). The reduction of CGRP-induced increase of blood flow by L-NAME was reversed by L-arginine. Neither D-NAME nor D-NMMA inhibited the increase in blood flow caused by CGRP. Neither L-NAME nor L-NMMA inhibited the increase in blood flow in human skin caused by the intradermal injection of prostaglandin E2 (63 pmol). The data show that nitric oxide is involved in the maintenance of resting blood flow in human skin and also in the cutaneous vasodilator responses to local warming, ultraviolet B irradiation, or injection of CGRP.
J Invest Dermatol 1996 Jan
PMID:Inhibitors of nitric oxide synthase in human skin. 859 60

We have studied the possible involvement of nitric oxide (NO) in the contact hypersensitivity reaction. A biphasic response of ear swelling was observed at 2 h (early phase) and 24 h (late phase) after application of the antigen to picryl chloride (PC1)-sensitized CBA/J mice. Intravenous injection of NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), at the time of PC1 challenge, inhibited in a concentration-dependent fashion the antigen-induced contact hypersensitivity reaction. Low-dose (1 mg/kg) L-NAME inhibited the early-phase reaction but not the late-phase reaction. High-dose (250 mg/kg) L-NAME inhibited both early- and late-phase reactions. D-NAME (enantiomer of L-NAME) did not inhibit the antigen-induced ear swelling. High-dose (250 mg/kg) L-arginine increased both early and late phase reactions. D-Arginine (enantiomer of L-arginine) did no increase the antigen-induced ear swelling. L-NAME injection, however, did not suppress phenol-induce irritant inflammation. Treatment of mice undergoing PC1-induced contact hypersensitivity reaction with L-NAME reduced the production of interleukin-2 and interferon-gamma by draining lymph node cells. Treatment with L-arginine, on the other hand increased the production of interleukin-2 and interferon-gamma. These results suggest that NO plays a modulating role in contact hypersensitivity reaction.
J Invest Dermatol 1996 Oct
PMID:Modulation of picryl chloride-induced contact hypersensitivity reaction in mice by nitric oxide. 882 59

The importance of nitric oxide (NO) in mediating macrophage functions has been demonstrated, but production of this potent gas has not been examined in Langerhans cells (LC). Using murine LC purified from epidermal cell suspensions and the recently established LC-like cell line derived from newborn BALB/c epidermis (XS-52), it was shown with reverse transcriptase (RT)-PCR that inducible nitric oxide synthase (iNOS) message is present in these cells. Murine keratinocytes did not contain iNOS message. iNOS mRNA was increased in a concentration-dependent manner by lipopolysaccharide (LPS) in purified murine LC and XS-52 cells, and immunofluorescence using an antibody to iNOS revealed bright cytoplasmic staining in LPS-treated XS-52 cells. Anti-iNOS antibody brightly stained LC on human neonatal foreskin cryosections. An increase in NO production by LPS-treated XS-52 cells over 16 h, as measured by the determination of nitrite levels in culture supernatants using the Griess Reaction, was observed. Interferon-gamma (IFNgamma) did not affect NO production on its own. In the presence of LPS and IFNgamma, NO production was 3 times more than observed with LPS alone. NO production was inhibited by the NOS inhibitor L-NAME. Western blots with anti-iNOS antibody demonstrated an increase in iNOS expression in LPS-treated XS-52 cells that was suppressed by IL-10. NO produced in LC may affect LC functions such as microbicidal activity, antigen presentation, and cytotoxicity and may affect adjacent keratinocytes and melanocytes.
J Invest Dermatol 1996 Dec
PMID:Langerhans cells express inducible nitric oxide synthase and produce nitric oxide. 894 67

Ultraviolet (UV) irradiation is known to induce serious oxidative damage in the skin via lipid peroxidation. Nitric oxide (NO) synthesized by keratinocytes, melanocytes and endothelial cells in response to proinflammatory cytokines and UV radiation, has been reported to prevent UV-induced apoptosis in the skin. We have examined the effects of NO on UVB-induced lipid peroxidation in murine skin in vivo. UVB induced a dose-dependent increase in lipid peroxidation of skin extracts in vitro; however, lipid peroxidation in the skin in vivo remained unaffected at irradiation doses of less than 1.0 J cm-2 and decreased significantly at doses over 1.5 J cm-2 (P < 0.01). Time-delayed inhibition of lipid peroxidation in the skin in vivo was observed after irradiation at 1.5 J cm-2. Administration of N G-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthesis, enhanced lipid peroxidation (P < 0.05), while it suppressed the ear-swelling response (ESR), a biological marker of inflammation. By contrast, administration of sodium nitroprusside, an NO enhancer, suppressed lipid peroxidation (P < 0. 01), while it enhanced the ESR. Expression of inducible nitric oxide synthase (iNOS) was observed from 12 to 48 h postirradiation at doses of 0.4-1.6 J cm-2. The UVB-induced iNOS expression was markedly inhibited by L-NAME, suggesting that iNOS is a major enzyme in the production of NO. These results suggest that NO acts as a mediator of the inflammatory response in UVB-irradiated skin, and that lipid peroxidation is inversely regulated with the NO-mediated inflammatory response in vivo.
Br J Dermatol 2000 Apr
PMID:Protective role of nitric oxide-mediated inflammatory response against lipid peroxidation in ultraviolet B-irradiated skin. 1079 14

We describe a case of a large pedunculated solitary cutaneous myxoma arising on the thigh of a 47-year-old man without evidence of Carney's complex, NAME, or LAMB syndromes. The diagnosis was confirmed by hematoxylin and eosin stain, special stains, and immunocytochemistry studies. The tumor was surgically resected with no evidence of recurrence after 6 months. Solitary cutaneous myxoma should be differentiated histologically from myxoid neurofibroma, neurothekeoma, and ossifying and nonossifying fibromyxoid tumor.
J Am Acad Dermatol 2000 Aug
PMID:Solitary cutaneous myxoma. 1090 28

The aim of this study was to investigate the involvement of nitric oxide (NO) in the modulation of immediate and delayed immunological and nonimmunological reactions in human skin. The NO donor nitroglycerin, 0.1 microgram, and the NO synthase inhibitor, NG-nitro-L-arginine (L-NAME), 0.1 microgram, were injected intracutaneously prior to provocation tests. The following provocation tests were carried out: 8 patients with pollen allergy to birch were provoked by a prick test with the allergen and the volume of the weals was measured; 20 patients with allergy to nickel were provoked with nickel sulfate epicutaneously; and 26 healthy volunteers were provoked with tuberculin (causing delayed immunologic reaction), benzalkonium chloride (irritant contact dermatitis), UV radiation or benzoic acid (nonimmunological contact urticaria). The test reactions were evaluated by planimetry. L-NAME inhibited irritant contact dermatitis (P = 0.020) but augmented immediate immunological reactions (prick test) (P = 0.016). The other test reactions remained unchanged. Nitroglycerin did not affect any of the reactions significantly. The results suggest that NO is involved in immediate immunological reactions and irritant contact dermatitis.
Arch Dermatol Res 2001 Mar
PMID:Nitric oxide participates in prick test and irritant patch test reactions in human skin. 1135 25

Ultraviolet-B-induced erythema (one, two, or four times the minimal erythema dose) was reduced but not abolished by application of 1% indomethacin gel immediately after irradiation of human skin. Continuous synthesis of prostaglandins is reflected by similar levels of indomethacin-mediated inhibition of erythema at any time within 48 h after irradiation. Repeated applications of indomethacin did not increase the inhibition. Twenty-four hours after irradiation with four minimal erythema doses, mean prostaglandin E2 levels in suction blisters were 27.2 ng per ml (SEM 11) compared with 8.6 ng per ml in unirradiated skin (n = 25; p < 0.01). Prosta glandin E2 levels in dermal tissues, sampled by microdialysis (depth 0.6 +/- 0.1 mm), were 310 pg per ml (SEM 123) and 237 pg per ml (SEM 88) in irradiated and unirradiated skin, respectively (n = 7, n.s.). Nitric oxide also made a significant contribution to ultraviolet-B-induced erythema. Ultraviolet erythema was inhibited by L-NAME in a dose-related fashion with 2 mM L-NAME causing total abolition of the response. L-NAME was effective at all time points up to 48 h suggesting that NO was produced continuously. NO was undetectable in suction blister fluid but in dermal microdialysate NO was present at 44.3 ng per ml (SEM 6.2) following ultraviolet B compared with 26.0 ng per ml (SEM 8.0) in unirradiated skin (p < 0.05), approximately 1000 times the molar concentration of prostaglandin E2. These findings confirm prostaglandin E2 and NO to be mediators of ultraviolet-induced erythema. They also show that there is prolonged synthesis of both mediators within the erythemal response and that synthesis of NO is induced by lower doses of ultraviolet B compared with that of prostaglandin E2.
J Invest Dermatol 2001 Oct
PMID:Ultraviolet-B-induced erythema is mediated by nitric oxide and prostaglandin E2 in combination. 1167 27


1 2 Next >>