5188 lines
243 KiB
XML
5188 lines
243 KiB
XML
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<AbstractText>(--)-alpha-Bisabolol has a primary antipeptic action depending on dosage, which is not caused by an alteration of the pH-value. The proteolytic activity of pepsin is reduced by 50 percent through addition of bisabolol in the ratio of 1/0.5. The antipeptic action of bisabolol only occurs in case of direct contact. In case of a previous contact with the substrate, the inhibiting effect is lost.</AbstractText>
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|
</PublicationTypeList>
|
|
<VernacularTitle>Biochemische Untersuchungen von Kamilleninhaltsstoffen. III. In-vitro-Versuche über die antipeptische Wirkung des (-)-alpha-Bisabolols</VernacularTitle>
|
|
</Article>
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<Country>Germany</Country>
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|
<MedlineTA>Arzneimittelforschung</MedlineTA>
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<NlmUniqueID>0372660</NlmUniqueID>
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<ISSNLinking>0004-4172</ISSNLinking>
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<Chemical>
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<RegistryNumber>0</RegistryNumber>
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<NameOfSubstance UI="D006454">Hemoglobins</NameOfSubstance>
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</Chemical>
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<Chemical>
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<RegistryNumber>0</RegistryNumber>
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|
<NameOfSubstance UI="D012717">Sesquiterpenes</NameOfSubstance>
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</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>42HK56048U</RegistryNumber>
|
|
<NameOfSubstance UI="D014443">Tyrosine</NameOfSubstance>
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|
</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>5V2JDO056X</RegistryNumber>
|
|
<NameOfSubstance UI="D014238">Trichloroacetic Acid</NameOfSubstance>
|
|
</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>EC 3.4.23.1</RegistryNumber>
|
|
<NameOfSubstance UI="D010434">Pepsin A</NameOfSubstance>
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</Chemical>
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<CitationSubset>IM</CitationSubset>
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<MeshHeadingList>
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<MeshHeading>
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<DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
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</MeshHeading>
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<MeshHeading>
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|
<DescriptorName UI="D006454" MajorTopicYN="N">Hemoglobins</DescriptorName>
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|
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeading>
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|
<MeshHeading>
|
|
<DescriptorName UI="D006863" MajorTopicYN="N">Hydrogen-Ion Concentration</DescriptorName>
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|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName>
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|
</MeshHeading>
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|
<MeshHeading>
|
|
<DescriptorName UI="D008722" MajorTopicYN="N">Methods</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D010434" MajorTopicYN="N">Pepsin A</DescriptorName>
|
|
<QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName>
|
|
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D010946" MajorTopicYN="N">Plants, Medicinal</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D012717" MajorTopicYN="N">Sesquiterpenes</DescriptorName>
|
|
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D013056" MajorTopicYN="N">Spectrophotometry, Ultraviolet</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D014238" MajorTopicYN="N">Trichloroacetic Acid</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
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|
<DescriptorName UI="D014443" MajorTopicYN="N">Tyrosine</DescriptorName>
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|
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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</MeshHeading>
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</MeshHeadingList>
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</MedlineCitation>
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<History>
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<PubMedPubDate PubStatus="pubmed">
|
|
<Year>1975</Year>
|
|
<Month>9</Month>
|
|
<Day>1</Day>
|
|
</PubMedPubDate>
|
|
<PubMedPubDate PubStatus="medline">
|
|
<Year>1975</Year>
|
|
<Month>9</Month>
|
|
<Day>1</Day>
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|
<Hour>0</Hour>
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|
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|
</PubMedPubDate>
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<Year>1975</Year>
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|
<Month>9</Month>
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<PublicationStatus>ppublish</PublicationStatus>
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<ArticleId IdType="pubmed">21</ArticleId>
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</ArticleIdList>
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</PubmedArticle>
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<PubmedArticle>
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<MedlineCitation Status="MEDLINE" Owner="NLM">
|
|
<PMID Version="1">22</PMID>
|
|
<DateCompleted>
|
|
<Year>1976</Year>
|
|
<Month>01</Month>
|
|
<Day>26</Day>
|
|
</DateCompleted>
|
|
<DateRevised>
|
|
<Year>2020</Year>
|
|
<Month>02</Month>
|
|
<Day>25</Day>
|
|
</DateRevised>
|
|
<Article PubModel="Print">
|
|
<Journal>
|
|
<ISSN IssnType="Print">0004-4172</ISSN>
|
|
<JournalIssue CitedMedium="Print">
|
|
<Volume>25</Volume>
|
|
<Issue>9</Issue>
|
|
<PubDate>
|
|
<Year>1975</Year>
|
|
<Month>Sep</Month>
|
|
</PubDate>
|
|
</JournalIssue>
|
|
<Title>Arzneimittel-Forschung</Title>
|
|
<ISOAbbreviation>Arzneimittelforschung</ISOAbbreviation>
|
|
</Journal>
|
|
<ArticleTitle>[Demonstration of tumor inhibiting properties of a strongly immunostimulating low-molecular weight substance. Comparative studies with ifosfamide on the immuno-labile DS carcinosarcoma. Stimulation of the autoimmune activity for approx. 20 days by BA 1, a N-(2-cyanoethylene)-urea. Novel prophylactic possibilities].</ArticleTitle>
|
|
<Pagination>
|
|
<MedlinePgn>1369-79</MedlinePgn>
|
|
</Pagination>
|
|
<Abstract>
|
|
<AbstractText>A report is given on the recent discovery of outstanding immunological properties in BA 1 [N-(2-cyanoethylene)-urea] having a (low) molecular mass M = 111.104. Experiments in 214 DS carcinosarcoma bearing Wistar rats have shown that BA 1, at a dosage of only about 12 percent LD50 (150 mg kg) and negligible lethality (1.7 percent), results in a recovery rate of 40 percent without hyperglycemia and, in one test, of 80 percent with hyperglycemia. Under otherwise unchanged conditions the reference substance ifosfamide (IF) -- a further development of cyclophosphamide -- applied without hyperglycemia in its most efficient dosage of 47 percent LD50 (150 mg kg) brought about a recovery rate of 25 percent at a lethality of 18 percent. (Contrary to BA 1, 250-min hyperglycemia caused no further improvement of the recovery rate.) However this comparison is characterized by the fact that both substances exhibit two quite different (complementary) mechanisms of action. Leucocyte counts made after application of the said cancerostatics and dosages have shown a pronounced stimulation with BA 1 and with ifosfamide, the known suppression in the post-therapeutic interval usually found with standard cancerostatics. In combination with the cited plaque test for BA 1, blood pictures then allow conclusions on the immunity status. Since IF can be taken as one of the most efficient cancerostatics--there is no other chemotherapeutic known up to now that has a more significant effect on the DS carcinosarcoma in rats -- these findings are of special importance. Finally, the total amount of leucocytes and lymphocytes as well as their time behaviour was determined from the blood picture of tumour-free rats after i.v. application of BA 1. The thus obtained numerical values clearly show that further research work on the prophylactic use of this substance seems to be necessary and very promising.</AbstractText>
|
|
</Abstract>
|
|
<AuthorList CompleteYN="Y">
|
|
<Author ValidYN="Y">
|
|
<LastName>Ardenne</LastName>
|
|
<ForeName>M</ForeName>
|
|
<Initials>M</Initials>
|
|
</Author>
|
|
<Author ValidYN="Y">
|
|
<LastName>Reitnauer</LastName>
|
|
<ForeName>P G</ForeName>
|
|
<Initials>PG</Initials>
|
|
</Author>
|
|
</AuthorList>
|
|
<Language>ger</Language>
|
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<PublicationTypeList>
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<PublicationType UI="D003160">Comparative Study</PublicationType>
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<PublicationType UI="D004740">English Abstract</PublicationType>
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<PublicationType UI="D016428">Journal Article</PublicationType>
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</PublicationTypeList>
|
|
<VernacularTitle>Nachweis krebshemmender Eigenschaften einer stark immunstimulierenden Verbindung kleiner Molekülmasse. Versuche am immunlabilen DS-Karzinosarkom im Vergleich mit Ifosfamid. Stimulierung der körpereigenen Abwehr über etwa 20 Tage durch BA 1, einen N-(2-Cyanthylen)-harnstoff. Neue prophylaktische Möglichkeiten</VernacularTitle>
|
|
</Article>
|
|
<MedlineJournalInfo>
|
|
<Country>Germany</Country>
|
|
<MedlineTA>Arzneimittelforschung</MedlineTA>
|
|
<NlmUniqueID>0372660</NlmUniqueID>
|
|
<ISSNLinking>0004-4172</ISSNLinking>
|
|
</MedlineJournalInfo>
|
|
<ChemicalList>
|
|
<Chemical>
|
|
<RegistryNumber>0</RegistryNumber>
|
|
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
|
|
</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>8N3DW7272P</RegistryNumber>
|
|
<NameOfSubstance UI="D003520">Cyclophosphamide</NameOfSubstance>
|
|
</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>8W8T17847W</RegistryNumber>
|
|
<NameOfSubstance UI="D014508">Urea</NameOfSubstance>
|
|
</Chemical>
|
|
<Chemical>
|
|
<RegistryNumber>UM20QQM95Y</RegistryNumber>
|
|
<NameOfSubstance UI="D007069">Ifosfamide</NameOfSubstance>
|
|
</Chemical>
|
|
</ChemicalList>
|
|
<CitationSubset>IM</CitationSubset>
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|
<MeshHeadingList>
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|
<MeshHeading>
|
|
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
|
|
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
|
|
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D002296" MajorTopicYN="N">Carcinosarcoma</DescriptorName>
|
|
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D003520" MajorTopicYN="N">Cyclophosphamide</DescriptorName>
|
|
<QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D004353" MajorTopicYN="N">Drug Evaluation, Preclinical</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D004361" MajorTopicYN="N">Drug Tolerance</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D004906" MajorTopicYN="N">Erythrocyte Count</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D006863" MajorTopicYN="N">Hydrogen-Ion Concentration</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D007069" MajorTopicYN="Y">Ifosfamide</DescriptorName>
|
|
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
|
|
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D007109" MajorTopicYN="N">Immunity</DescriptorName>
|
|
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D007165" MajorTopicYN="N">Immunosuppression</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D007928" MajorTopicYN="N">Lethal Dose 50</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D007958" MajorTopicYN="N">Leukocyte Count</DescriptorName>
|
|
</MeshHeading>
|
|
<MeshHeading>
|
|
<DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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|
</MeshHeading>
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|
<MeshHeading>
|
|
<DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
|
|
</MeshHeading>
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<MeshHeading>
|
|
<DescriptorName UI="D009374" MajorTopicYN="N">Neoplasms, Experimental</DescriptorName>
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<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
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</MeshHeading>
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<MeshHeading>
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<DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName>
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|
</MeshHeading>
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|
<MeshHeading>
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|
<DescriptorName UI="D013268" MajorTopicYN="N">Stimulation, Chemical</DescriptorName>
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|
</MeshHeading>
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|
<MeshHeading>
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|
<DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
|
|
</MeshHeading>
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<MeshHeading>
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|
<DescriptorName UI="D014508" MajorTopicYN="N">Urea</DescriptorName>
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<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
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<Year>1975</Year>
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|
<Month>9</Month>
|
|
<Day>1</Day>
|
|
</PubMedPubDate>
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|
<PubMedPubDate PubStatus="medline">
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|
<Year>1975</Year>
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<Month>9</Month>
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|
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<Hour>0</Hour>
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|
<Month>9</Month>
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<Reference>
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</Reference>
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</Reference>
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<Citation>Am J Kidney Dis. 2011 Feb;57(2):228-34</Citation>
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</Reference>
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<Reference>
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<Citation>Clin J Am Soc Nephrol. 2012 May;7(5):712-9</Citation>
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<ArticleIdList>
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<ArticleId IdType="pubmed">22422536</ArticleId>
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<ArticleIdList>
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</Reference>
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<Reference>
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<ArticleIdList>
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<ArticleId IdType="pubmed">23516690</ArticleId>
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</ArticleIdList>
|
|
</Reference>
|
|
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|
|
</PubmedData>
|
|
</PubmedArticle>
|
|
<PubmedArticle>
|
|
<MedlineCitation Status="MEDLINE" Owner="NLM">
|
|
<PMID Version="1">23</PMID>
|
|
<DateCompleted>
|
|
<Year>1976</Year>
|
|
<Month>01</Month>
|
|
<Day>26</Day>
|
|
</DateCompleted>
|
|
<DateRevised>
|
|
<Year>2020</Year>
|
|
<Month>02</Month>
|
|
<Day>25</Day>
|
|
</DateRevised>
|
|
<Article PubModel="Print">
|
|
<Journal>
|
|
<ISSN IssnType="Print">0004-4172</ISSN>
|
|
<JournalIssue CitedMedium="Print">
|
|
<Volume>25</Volume>
|
|
<Issue>9</Issue>
|
|
<PubDate>
|
|
<Year>1975</Year>
|
|
<Month>Sep</Month>
|
|
</PubDate>
|
|
</JournalIssue>
|
|
<Title>Arzneimittel-Forschung</Title>
|
|
<ISOAbbreviation>Arzneimittelforschung</ISOAbbreviation>
|
|
</Journal>
|
|
<ArticleTitle>Effect of etafenone on total and regional myocardial blood flow.</ArticleTitle>
|
|
<Pagination>
|
|
<MedlinePgn>1400-3</MedlinePgn>
|
|
</Pagination>
|
|
<Abstract>
|
|
<AbstractText>The distribution of blood flow to the subendocardial, medium and subepicardial layers of the left ventricular free wall was studied in anaesthetized dogs under normoxic (A), hypoxic (B) conditions and under pharmacologically induced (etafenone) coronary vasodilation (C). Regional myocardial blood flow was determined by means of the particle distribution method. In normoxia a transmural gradient of flow was observed, with the subendocardial layers receiving a significantly higher flow rate compared with the subepicardial layers. In hypoxia induced vasodilation this transmural gradient of flow was persistent. In contrast a marked redistribution of regional flow was observed under pharmacologically induced vasodilation. The transmural gradient decreased. In contrast to some findings these experiments demonstrate that a considerable vasodilatory capacity exists in all layers of the myocardium and can be utilized by drugs. The differences observed for the intramural distribution pattern of flow under hypoxia and drug induced vasodilation support the hypothesis that this pattern reflects corresponding gradients of regional myocardial metabolism.</AbstractText>
|
|
</Abstract>
|
|
<AuthorList CompleteYN="Y">
|
|
<Author ValidYN="Y">
|
|
<LastName>Flohr</LastName>
|
|
<ForeName>H</ForeName>
|
|
<Initials>H</Initials>
|
|
</Author>
|
|
<Author ValidYN="Y">
|
|
<LastName>Breull</LastName>
|
|
<ForeName>W</ForeName>
|
|
<Initials>W</Initials>
|
|
</Author>
|
|
</AuthorList>
|
|
<Language>eng</Language>
|
|
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|
|
<Grant>
|
|
<GrantID>G0700399</GrantID>
|
|
<Agency>Medical Research Council</Agency>
|
|
<Country>United Kingdom</Country>
|
|
</Grant>
|
|
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<Citation>J Appl Psychol. 2001 Aug;86(4):730-40</Citation>
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<Citation>J Crit Care. 2008 Jun;23(2):167-72</Citation>
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<Citation>Med Educ. 2009 Jan;43(1):50-7</Citation>
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<Citation>Clin Med (Lond). 2009 Oct;9(5):417-20</Citation>
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