LIVIVO - Search results -

Search results

Result 1 - 10 of total 240

Search options

Article: Eosinophilic Cholangitis with Poor Prognosis after Corticosteroid- and Ursodeoxycholic Acid-Related Remission of Peripheral and Peribiliary Eosinophilia.

Shimomura, Takahito / Nakajima, Tomoki / Nakashima, Toshiaki / Morimoto, Yasutaka / Yamaoka, Junko / Shibuya, Akiko / Ohno, Tomoyuki / Yoshida, Norimasa / Kishimoto, Mitsuo / Konishi, Eiichi / Tanaka, Hideo / Moriguchi, Michihisa / Itoh, Yoshito

Case reports in gastroenterology

2021 Volume 15, Issue 1, Page(s) 232–243

Abstract: A 79-year-old man presented with high fever, marked eosinophilia, altered biochemical liver function tests (LFT) with predominance of biliary enzymes, and severe wall thickening of the gallbladder. Magnetic resonance cholangiopancreatography (MRCP) ... ...

Abstract	A 79-year-old man presented with high fever, marked eosinophilia, altered biochemical liver function tests (LFT) with predominance of biliary enzymes, and severe wall thickening of the gallbladder. Magnetic resonance cholangiopancreatography (MRCP) suggested cholecystitis, without signs of biliary strictures. Laparoscopic cholecystectomy and exploratory liver excision revealed eosinophilic cholangitis and cholecystitis, complicated with hepatitis and portal phlebitis. Prednisolone monotherapy rapidly improved peripheral eosinophilia, but not LFT. Liver biopsy showed that infiltrating eosinophils were replaced by lymphocytes and plasma cells. Treatment with ursodeoxycholic acid improved LFT abnormalities. Nevertheless, after 2 months, transaminase-dominant LFT abnormalities appeared. Transient prednisolone dose increase improved LFT, but biliary enzymes' levels re-elevated and jaundice progressed. The second and third MRCP within a 7-month interval showed rapid progression of biliary stricture. The repeated liver biopsy showed lymphocytic, not eosinophilic, peribiliary infiltration and hepatocellular reaction to cholestasis. Eighteen months after the first visit, the patient died of hepatic failure. Autopsy specimen of the liver showed lymphocyte-dominant peribiliary infiltration and bridging fibrosis due to cholestasis. Though eosinophil-induced biliary damage was an initial trigger, repeated biopsy suggested that lymphocytes played a key role in progression of the disease. Further studies are needed to elucidate the relationship between eosinophils and lymphocytes in eosinophilic cholangitis.
Language	English
Publishing date	2021-02-18
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2440540-1
ISSN	1662-0631
ISSN	1662-0631
DOI	10.1159/000512420
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article: Analysis of mechanisms of epidermal proliferation induced by intracutaneous injection of cholera toxin by the use of site-specifically mutated cholera toxins.

Yamaoka, J / Imamura, S

Journal of dermatological science

1998 Volume 16, Issue 3, Page(s) 182–190

Abstract: Intracutaneous injection of cholera toxin (CT) into rabbits increases vascular permeability and induces epidermal proliferation. To understand the mechanisms of these effects on the skin, we evaluated the involvement of the ADP-ribosyltransferase ... ...

Abstract	Intracutaneous injection of cholera toxin (CT) into rabbits increases vascular permeability and induces epidermal proliferation. To understand the mechanisms of these effects on the skin, we evaluated the involvement of the ADP-ribosyltransferase activity of the A subunit of CT and receptor-binding interactions between GM1-ganglioside and the B subunit of CT. We constructed two mutant CTs, E112K and W88K, by site-directed mutagenesis. Mutant CT-E112K, in which glutamic acid at position 112 (E112) of the A subunit of CT was replaced by lysine, has been shown to have lost its biological activity on Chinese hamster ovary (CHO) cells because of its abolished ADP-ribosyltransferase activity. Mutant CT-W88K, in which tryptophan at position 88 (W88) of the B subunit of CT was replaced by lysine, has been shown to have lost its binding ability to GM1-ganglioside. Intracutaneous injection of these mutant CTs evoked less vascular permeability and less epidermal proliferation than recombinant wild-type CT. These results suggest that: (1) the ADP-ribosyltransferase activity carried by E112 of the A subunit of CT; and (2) the binding ability to GM1-ganglioside via W88 of the B subunit of CT are essential for these effects of CT on the skin.
MeSH term(s)	Animals ; CHO Cells ; Capillary Permeability/drug effects ; Cell Division/drug effects ; Chemical Phenomena ; Chemistry, Physical ; Cholera Toxin/chemistry ; Cholera Toxin/genetics ; Cholera Toxin/pharmacology ; Cricetinae ; Epidermal Cells ; Epidermis/drug effects ; Injections, Intradermal ; Mutagenesis, Site-Directed ; Mutation/physiology ; Rabbits ; Recombinant Proteins
Chemical Substances	Recombinant Proteins ; Cholera Toxin (9012-63-9)
Language	English
Publishing date	1998-03
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1024446-3
ISSN	0923-1811
ISSN	0923-1811
DOI	10.1016/s0923-1811(97)00050-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2870: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Rapid changes in substance P signaling and neutral endopeptidase induced by skin-scratching stimulation in mice.

Yamaoka, Junichi / Kawana, Seiji

Journal of dermatological science

2007 Volume 48, Issue 2, Page(s) 123–132

Abstract: Background: Skin-scratching is a commonly seen behavior in patients with pruritus which sometimes exacerbates original lesions. Substance P (SP) signaling may play a predominant role in the pathophysiology induced by skin-scratching, however, it has not ...

Abstract	Background: Skin-scratching is a commonly seen behavior in patients with pruritus which sometimes exacerbates original lesions. Substance P (SP) signaling may play a predominant role in the pathophysiology induced by skin-scratching, however, it has not been well-elucidated. Objectives: To clarify changes in SP, its receptor NK-1R and a degradating enzyme neutral endopeptidase (NEP) induced by skin-scratching stimulation in mice. Methods: After skin-scratching stimulation was given to mice, changes in SP signaling were investigated as follows. Mast cell degranulation was examined with toluidine blue staining. SP-immunoreactive nerve fibers and the expressions of NK-1R and NEP were examined with immunofluorescence. Protein contents of SP and the enzymatic activity of NEP were examined with an ELISA and a colorimetric assay, respectively. Results: After skin-scratching stimulation, mast cells significantly degranulated within several minutes. SP-immunoreactive nerve fibers disappeared immediately from sensory nerve fibers, indicating the quick secretion and the depletion of SP. Both protein contents of SP and NEP activity in skin decreased dramatically soon after skin-scratching stimulation and thereafter they returned to the basal level within a week. The expression of NK-1R was significantly upregulated in epidermal basal keratinocytes after several days, in which NEP and NK-1R were well-coexpressed. Blocking NK-1R by an NK-1R antagonist suppressed scratching-induced decreases in SP-immunoreactive nerve fibers and in NEP activity. Conclusions: The present study clarified changing patterns of factors involved in SP signaling and NEP induced by skin-scratching stimulation. These findings provide basic and useful information to understand the pathophysiology of scratching-associated pruritic skin diseases.
MeSH term(s)	Animals ; Cell Degranulation/physiology ; Dermatitis, Contact/physiopathology ; Dinitrofluorobenzene ; Male ; Mast Cells/physiology ; Mice ; Mice, Inbred ICR ; Neprilysin/metabolism ; Neurokinin-1 Receptor Antagonists ; Physical Stimulation ; Pruritus/physiopathology ; Receptors, Neurokinin-1/metabolism ; Skin/metabolism ; Skin Physiological Phenomena ; Substance P/metabolism
Chemical Substances	Neurokinin-1 Receptor Antagonists ; Receptors, Neurokinin-1 ; Substance P (33507-63-0) ; Dinitrofluorobenzene (D241E059U6) ; Neprilysin (EC 3.4.24.11)
Language	English
Publishing date	2007-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1024446-3
ISSN	0923-1811
ISSN	0923-1811
DOI	10.1016/j.jdermsci.2007.06.007
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2870: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: A transient unresponsive state of self-scratching behaviour is induced in mice by skin-scratching stimulation.

Yamaoka, Junichi / Kawana, Seiji

Experimental dermatology

2007 Volume 16, Issue 9, Page(s) 737–745

Abstract: When mice were scratched with brushes on their dorsal skins, they began to scratch themselves with their hind paws. Thus, self-scratching behaviour was induced in mice in response to skin-scratching stimulation. If the second skin-scratching stimulation ... ...

Abstract	When mice were scratched with brushes on their dorsal skins, they began to scratch themselves with their hind paws. Thus, self-scratching behaviour was induced in mice in response to skin-scratching stimulation. If the second skin-scratching stimulation was given within a few days, the induction of the second self-scratching behaviour was significantly suppressed compared with the first one. Thereafter, mice gradually recovered from this unresponsive state within a week. Thus, a transient unresponsive state of self-scratching behaviour is induced by skin-scratching stimulation. Pretreatment with a tachykinin receptor NK-1R antagonist L-703606 or capsaicin significantly suppressed self-scratching behaviour, while pretreatment with a neutral endopeptidase inhibitor phosphoramidon significantly enhanced it. Pretreatment with a calcitonin gene-related peptide (CGRP) receptor antagonist CGRP(8-37) did not affect the following self-scratching behaviour. From these results, it is suggested that substance P (SP) signalling through its receptor NK-1R at least in part mediates the induction of self-scratching behaviour. After skin-scratching stimulation, immunoreactivity of SP both in the peripheral nerve fibres and in the dorsal root ganglion (DRG) neurons was significantly decreased and was well-correlated with suppression of self-scratching behaviour. From these findings, it is suggested that the induction of unresponsive states of self-scratching behaviour may be at least in part caused by the depleted states of SP in peripheral nerve fibres and/or in DRG neurons. The induction of a transient unresponsive state after skin-scratching may possibly happen also in patients with pruritus. Thus, further studies to elucidate the precise mechanisms are required.
MeSH term(s)	Analgesics, Non-Narcotic/pharmacology ; Animals ; Behavior, Animal/physiology ; Calcitonin Gene-Related Peptide/pharmacology ; Calcitonin Gene-Related Peptide/physiology ; Capsaicin/pharmacology ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred ICR ; Peptide Fragments/pharmacology ; Physical Stimulation/methods ; Pruritus/physiopathology ; Quinuclidines/pharmacology ; Self Stimulation/drug effects ; Self Stimulation/physiology ; Signal Transduction/physiology ; Skin Physiological Phenomena/drug effects ; Substance P/physiology
Chemical Substances	Analgesics, Non-Narcotic ; Peptide Fragments ; Quinuclidines ; calcitonin gene-related peptide (8-37) (119911-68-1) ; L 703606 (144425-84-3) ; Substance P (33507-63-0) ; Calcitonin Gene-Related Peptide (83652-28-2) ; Capsaicin (S07O44R1ZM)
Language	English
Publishing date	2007-09
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1130936-2
ISSN	1600-0625 ; 0906-6705
ISSN (online)	1600-0625
ISSN	0906-6705
DOI	10.1111/j.1600-0625.2007.00593.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 3508: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Effect of epinastine hydrochloride on murine self-scratching behavior after skin-scratching stimulation.

Yilinuer, Halifu / Yamaoka, Junichi / Kawana, Seiji

Archives of dermatological research

2010 Volume 302, Issue 1, Page(s) 19–26

Abstract: The itch-scratch cycle aggravates chronic inflammatory skin diseases. We have previously reported that mice begin to scratch themselves within several minutes after skin-scratching stimulation. This is associated with an increase in release of substance ... ...

Abstract	The itch-scratch cycle aggravates chronic inflammatory skin diseases. We have previously reported that mice begin to scratch themselves within several minutes after skin-scratching stimulation. This is associated with an increase in release of substance P (SP) from sensory nerve fibers in the skin, and the self-scratching behavior is suppressed by neurokinin-1 receptor (NK-1R) antagonist. Thus, SP may play a pivotal role in self-scratching behavior. The purpose of this study was to investigate the effect of second-generation histamine H(1)-receptor antagonists on self-scratching behavior in mice. After oral administration of epinastine hydrochloride (epinastine) (total dose 50 +/- 5 mg/kg for 7 days) or the vehicle only to ICR mice for 7 days, skin-scratching stimulation was administered to the dorsal skin for 10 min. Self-scratching behavior was recorded by video camera for 10 min. Twenty-four hours later, skin tissue was harvested and stained with toluidine blue. Immunohistochemical staining for SP was performed, and SP and nerve growth factor (NGF) concentrations were measured by enzyme-linked immunosorbent assay. Self-scratching behavior, mast cell degranulation, and NGF concentration decreased, and the length of SP-positive nerve fibers and SP concentrations increased significantly in the epinastine-treated group, when compared with the vehicle control group. We conclude that epinastine inhibits mast cell degranulation by attenuating SP release from sensory nerve fibers, which results in inhibition of self-scratching behavior. These results suggest that second-generation histamine H(1)-receptor antagonists might efficaciously control itch-scratch cycle-related skin diseases.
MeSH term(s)	Administration, Oral ; Animals ; Behavior Control ; Cell Degranulation/drug effects ; Dibenzazepines/administration & dosage ; Histamine H1 Antagonists, Non-Sedating/administration & dosage ; Imidazoles/administration & dosage ; Immunohistochemistry ; Mast Cells/drug effects ; Mast Cells/immunology ; Mast Cells/metabolism ; Mast Cells/pathology ; Mice ; Mice, Inbred ICR ; Nerve Growth Factor/genetics ; Nerve Growth Factor/metabolism ; Pruritus/prevention & control ; Sensory Receptor Cells/drug effects ; Sensory Receptor Cells/immunology ; Sensory Receptor Cells/metabolism ; Sensory Receptor Cells/pathology ; Skin Diseases/drug therapy ; Skin Diseases/immunology ; Skin Diseases/physiopathology ; Substance P/biosynthesis ; Substance P/immunology ; Substance P/metabolism
Chemical Substances	Dibenzazepines ; Histamine H1 Antagonists, Non-Sedating ; Imidazoles ; Substance P (33507-63-0) ; Nerve Growth Factor (9061-61-4) ; epinastine (Q13WX941EF)
Language	English
Publishing date	2010-01
Publishing country	Germany
Document type	Journal Article
ZDB-ID	130131-7
ISSN	1432-069X ; 0340-3696
ISSN (online)	1432-069X
ISSN	0340-3696
DOI	10.1007/s00403-009-1006-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ui VI Zs.10: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Age is a Negative, and Visceral Fat Accumulation is a Positive, Contributor to Hepatic Steatosis, Regardless of the Fibrosis Progression in Non-alcoholic Fatty Liver Disease

Nakajima T / Nakashima T / Yamaoka J / Shibuya A / Itoh Y / Yoshikawa T

Journal of Gastroenterology and Hepatology Research, Vol 1, Iss 11, Pp 315-

2012 Volume 319

Abstract: AIM: Because aging affects fat distribution, we evaluated age-relatedchanges in the deposition of fat in the liver, compared to the visceraland intramuscular fat compartments, in non-alcoholic fatty liverdisease (NAFLD). A “burn-out” phenomenon of ... ...

Abstract	AIM: Because aging affects fat distribution, we evaluated age-relatedchanges in the deposition of fat in the liver, compared to the visceraland intramuscular fat compartments, in non-alcoholic fatty liverdisease (NAFLD). A “burn-out” phenomenon of hepatic steatosis isassociated with progression of fibrosis in NAFLD. We clarified theeffect of progression of fibrosis on steatosis.METHODS: Sixty patients clinically diagnosed as NAFLD, ofwhom 28 were confirmed histologically, and 26 normal subjectswere examined. Platelet counts and serum concentrations of alanineaminotransferase (ALT), ferritin and hyaluronic acid (HA) weremeasured. Hepatic steatosis, visceral fat area (VFA), subcutaneousfat area (SFA) and the multifidus muscle/subcutaneous fat attenuation(MM/F) ratio were evaluated by computed tomography. The ratio ofhepatic fat deposition to VFA, defined as the liver-viscera (LV) index,quantified the ratio of hepatic steatosis to visceral adiposity.RESULTS: In NAFLD patients, univariate analysis showed thedegree of steatosis was correlated positively with VFA, SFA and ALT,and negatively with age, MM/F ratio and HA. Age and VFA retainedsignificance in multivariate analysis. Age was negatively correlatedwith the LV index. Age was negatively correlated with steatosisand the LV index in 17 patients with fibrosis stage 0 or 1 but not innormal subjects.CONCLUSION: Age is a negative, and visceral fat accumulationis a positive, independent contributor to steatosis. Hepatic fibrosisis negatively correlated with steatosis but not an independentcontributor. Fat is distributed less in the liver, relative to the visceralcompartment, with increasing age.
Keywords	Non-alcoholic Fatty liver disease ; Non-alcoholic Steatohepatitis ; Hepatic steatosis ; Visceral fat ; Aging ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Subject code	610
Language	English
Publishing date	2012-12-01T00:00:00Z
Publisher	Thomson Research Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Suppressive effect of zinc ion on iNOS expression induced by interferon-gamma or tumor necrosis factor-alpha in murine keratinocytes.

Yamaoka, J / Kume, T / Akaike, A / Miyachi, Y

Journal of dermatological science

2000 Volume 23, Issue 1, Page(s) 27–35

Abstract: Zinc, an essential metal, is a critical component of zinc binding proteins such as zinc fingers, zinc enzymes and metallothioneins. Recently, evidence for its anti-inflammatory property in skin has been accumulating, as shown in the treatment of acne, ... ...

Abstract	Zinc, an essential metal, is a critical component of zinc binding proteins such as zinc fingers, zinc enzymes and metallothioneins. Recently, evidence for its anti-inflammatory property in skin has been accumulating, as shown in the treatment of acne, alopecia and zinc deficiency. In cutaneous inflammations, a large amount of nitric oxide (NO) is produced through induction of inducible nitric oxide synthase (iNOS) under the influence of proinflammatory cytokines, resulting in tissue damages in skin, as clarified in other organs. Therefore, we asked if the effect of zinc on NO production and/or on iNOS expression in keratinocytes may explain the anti-inflammatory property of zinc in skin. Accordingly, we sought to determine in this study whether zinc ion may have effect on IFN-gamma or TNF-alpha induced NO production and iNOS expression in cultured murine keratinocytes. Ten microM of zinc ion remarkably suppressed cytokine-induced NO production in keratinocytes. Furthermore, zinc ion also suppressed cytokine-induced iNOS expression in the protein level as well as in the messenger RNA level. These results suggest the possibility that the suppressive effect of zinc ion on cytokine-induced NO production in keratinocytes may be in part implicated in the anti-inflammatory property of zinc in some of skin disorders.
MeSH term(s)	Animals ; Base Sequence ; Cell Line ; DNA Primers/genetics ; Gene Expression/drug effects ; Interferon-gamma/pharmacology ; Keratinocytes/drug effects ; Keratinocytes/metabolism ; Mice ; Nitric Oxide/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase/metabolism ; Nitric Oxide Synthase Type II ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Recombinant Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha/pharmacology ; Zinc/pharmacology
Chemical Substances	DNA Primers ; RNA, Messenger ; Recombinant Proteins ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39) ; Zinc (J41CSQ7QDS)
Language	English
Publishing date	2000-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1024446-3
ISSN	0923-1811
ISSN	0923-1811
DOI	10.1016/s0923-1811(99)00062-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2870: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Ultraviolet B radiation downregulates inducible nitric oxide synthase expression induced by interferon-gamma or tumor necrosis factor-alpha in murine keratinocyte Pam 212 cells.

Yamaoka, J / Sasaki, M / Miyachi, Y

Archives of dermatological research

2000 Volume 292, Issue 6, Page(s) 312–319

Abstract: Ultraviolet radiation causes inflammation characterized by erythema and swelling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) in the treatment of psoriasis, ...

Abstract	Ultraviolet radiation causes inflammation characterized by erythema and swelling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) in the treatment of psoriasis, chronic severe atopic dermatitis and uremic pruritus. In inflammatory dermatoses, a pathogenic role of nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) has been suggested. To elucidate how UVBR regulates iNOS expression in skin under inflammatory conditions, we investigated the effect of UVBR on NO production and iNOS expression in cultured murine keratinocyte Pam 212 cells stimulated with interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha). Low doses of UVBR significantly suppressed IFN-gamma- or TNF-alpha-induced NO production. UVBR also downregulated IFN-gamma- or TNF-alpha-induced iNOS expression at both the mRNA level and the protein level. These findings suggest the possibility that the down-regulatory effect of UVBR on IFN-gamma- or TNF-alpha-induced iNOS expression may, in part, explain the antiinflammatory and therapeutic properties of UVBR in inflammatory dermatoses.
MeSH term(s)	Animals ; Blotting, Western ; Cell Line ; Dose-Response Relationship, Radiation ; Down-Regulation ; Gene Expression Regulation, Enzymologic/radiation effects ; Interferon-gamma ; Keratinocytes/drug effects ; Keratinocytes/metabolism ; Keratinocytes/radiation effects ; Mice ; Nitric Oxide/analysis ; Nitric Oxide Synthase/biosynthesis ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; RNA, Messenger/analysis ; Tumor Necrosis Factor-alpha ; Ultraviolet Rays
Chemical Substances	RNA, Messenger ; Tumor Necrosis Factor-alpha ; Nitric Oxide (31C4KY9ESH) ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2000-02-23
Publishing country	Germany
Document type	Journal Article
ZDB-ID	130131-7
ISSN	1432-069X ; 0340-3696
ISSN (online)	1432-069X
ISSN	0340-3696
DOI	10.1007/s004030000124
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ui VI Zs.10: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: The effect of ultraviolet B irradiation on nitric oxide synthase expression in murine keratinocytes.

Sasaki, M / Yamaoka, J / Miyachi, Y

Experimental dermatology

2000 Volume 9, Issue 6, Page(s) 417–422

Abstract: Nitric oxide (NO), which has several physiological functions in skin, is generated by NO synthase (NOS). NOS has at least three isoforms; endothelial NOS (eNOS), brain NOS (bNOS), and inducible NOS (iNOS). Ultraviolet B (UVB) irradiation has been ... ...

Abstract	Nitric oxide (NO), which has several physiological functions in skin, is generated by NO synthase (NOS). NOS has at least three isoforms; endothelial NOS (eNOS), brain NOS (bNOS), and inducible NOS (iNOS). Ultraviolet B (UVB) irradiation has been reported to stimulate NO production in skin via induction or activation of NOS, however, the exact mechanism of NOS induction by UVB irradiation remains obscure. In this study, we investigated the direct effect of UVB on the expression of NOS isoforms in murine keratinocytes, and found a significant increase in NO production within 48 h. mRNA and protein expressions of bNOS were both enhanced by UVB irradiation in murine keratinocytes, whereas iNOS mRNA expression was suppressed at 4 and 12 h after UVB irradiation. These results suggest that the enhancement of NO production observed after UVB irradiation in murine keratinocytes may be explained in part by the upregulation of bNOS expression, but not iNOS expression.
MeSH term(s)	Animals ; Cells, Cultured ; Dose-Response Relationship, Radiation ; Gene Expression Regulation, Enzymologic/radiation effects ; Isoenzymes/genetics ; Keratinocytes/cytology ; Keratinocytes/enzymology ; Keratinocytes/radiation effects ; Kinetics ; Mice ; Nitric Oxide Synthase/genetics ; Nitric Oxide Synthase Type II ; Transcription, Genetic/radiation effects ; Ultraviolet Rays
Chemical Substances	Isoenzymes ; Nitric Oxide Synthase (EC 1.14.13.39) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, mouse (EC 1.14.13.39)
Language	English
Publishing date	2000-07-07
Publishing country	Denmark
Document type	Journal Article
ZDB-ID	1130936-2
ISSN	1600-0625 ; 0906-6705
ISSN (online)	1600-0625
ISSN	0906-6705
DOI	10.1034/j.1600-0625.2000.009006417.x
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 3508: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Borehole muography of subsurface reservoirs.

Bonneville, Alain / Kouzes, Richard / Yamaoka, Jared / Lintereur, Azaree / Flygare, Joshua / Varner, Gary S / Mostafanezhad, Isar / Guardincerri, Elena / Rowe, Charlotte / Mellors, Robert

Philosophical transactions. Series A, Mathematical, physical, and engineering sciences

2018 Volume 377, Issue 2137

Abstract: Imaging subsurface rock formations or geological objects like oil and gas reservoirs, mineral deposits, cavities or even magmatic plumbing systems under active volcanoes has been for many years a major quest of geoscientists. Since these subsurface ... ...

Abstract	Imaging subsurface rock formations or geological objects like oil and gas reservoirs, mineral deposits, cavities or even magmatic plumbing systems under active volcanoes has been for many years a major quest of geoscientists. Since these subsurface objects cannot be observed directly, different indirect methods have been developed. These methods are all based on variations of certain physical properties of the subsurface materials that can be detected from the ground surface or from boreholes. To determine the density distribution, a new imaging technique using cosmic-ray muon detectors deployed in a borehole has been developed and a first prototype of a borehole muon detector successfully tested. In addition to providing a static image of the subsurface density in three dimensions (or three-dimensional tomography), borehole muography can also inform on the variations of density with time, which recently became of major importance with the injection of large volumes of fluids, mainly water and CO
Language	English
Publishing date	2018-12-10
Publishing country	England
Document type	Journal Article
ZDB-ID	208381-4
ISSN	1471-2962 ; 0080-4614 ; 0264-3820 ; 0264-3952 ; 1364-503X
ISSN (online)	1471-2962
ISSN	0080-4614 ; 0264-3820 ; 0264-3952 ; 1364-503X
DOI	10.1098/rsta.2018.0060
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Bonn / Germany

Z 4' 46/25: Show issues
Z PHI 2: Show issues

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Bonn / Germany

Order via subito

Inter-library loan at ZB MED