Microdensitometry, or microspectrophotometry, is the measurement of the concentration or mass of a chromophore in microscopically defined regions, and is governed by well-established laws of physics. Initially it proved of value in Feulgen cytophotometry of the relative amounts of DNA in individual nuclei of isolated cells. It has now achieved wide applicability to the measurement of cellular biochemical activity by means of stoichiometric chromogenic reactions. The validity of some of these measurements has been confirmed by comparative biochemical and microdensitometric assays. Thus microdensitometry, even of heterogeneously distributed chromophores, can be precise, provided that the technique is operated with due regard to its limitations within the laws of physics. The potential errors include: variation in thickness of tissue sections (path-length); scatter; glare; diffraction; occlusion of light by optically dense particles; and the inhomogeneity error. However, under correct conditions for the cytochemical reactions and for operating the microdensitometer, these potential errors become small or negligible. Thus the highly sensitive cytochemical bioassay of thyrotropin exemplifies the precision that can be achieved by controlled use of microdensitometry.
{"title":"Microdensitometry.","authors":"L. Bitensky","doi":"10.32388/2zzghk","DOIUrl":"https://doi.org/10.32388/2zzghk","url":null,"abstract":"Microdensitometry, or microspectrophotometry, is the measurement of the concentration or mass of a chromophore in microscopically defined regions, and is governed by well-established laws of physics. Initially it proved of value in Feulgen cytophotometry of the relative amounts of DNA in individual nuclei of isolated cells. It has now achieved wide applicability to the measurement of cellular biochemical activity by means of stoichiometric chromogenic reactions. The validity of some of these measurements has been confirmed by comparative biochemical and microdensitometric assays. Thus microdensitometry, even of heterogeneously distributed chromophores, can be precise, provided that the technique is operated with due regard to its limitations within the laws of physics. The potential errors include: variation in thickness of tissue sections (path-length); scatter; glare; diffraction; occlusion of light by optically dense particles; and the inhomogeneity error. However, under correct conditions for the cytochemical reactions and for operating the microdensitometer, these potential errors become small or negligible. Thus the highly sensitive cytochemical bioassay of thyrotropin exemplifies the precision that can be achieved by controlled use of microdensitometry.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73085954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Peptide metabolism.","authors":"","doi":"10.32388/v70kdd","DOIUrl":"https://doi.org/10.32388/v70kdd","url":null,"abstract":"Peptide Metabolism modifications of peptides.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2020-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79601849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-05-30DOI: 10.1002/9780470720158.CH14
H. Papoušek, M. Papoušek
Our previous studies on learning and on cognitive development in preverbal human infants indicated that motor activity and social interaction played particularly important roles in the cognitive development of infants. Closer analysis has revealed that motor activity and social interaction have some underlying common regulatory mechanisms. These mechanisms can be detected more easily in infants than in older subjects. An attempt to synthesize our observations led us to the concept that there is a fundamental cognitive process in the integration of adaptive behaviour. This concept may help to elucidate the motivational and emotional aspects of social interaction, the role of mothers or other caretakers in their interactions with infants, and the unfavourable effects of early social deprivation of different types on cognitive development. Some of the assumptions on which this concept is based have been corroborated by analyses of adult-infant interaction.
{"title":"Cognitive aspects of preverbal social interaction between human infants and adults.","authors":"H. Papoušek, M. Papoušek","doi":"10.1002/9780470720158.CH14","DOIUrl":"https://doi.org/10.1002/9780470720158.CH14","url":null,"abstract":"Our previous studies on learning and on cognitive development in preverbal human infants indicated that motor activity and social interaction played particularly important roles in the cognitive development of infants. Closer analysis has revealed that motor activity and social interaction have some underlying common regulatory mechanisms. These mechanisms can be detected more easily in infants than in older subjects. An attempt to synthesize our observations led us to the concept that there is a fundamental cognitive process in the integration of adaptive behaviour. This concept may help to elucidate the motivational and emotional aspects of social interaction, the role of mothers or other caretakers in their interactions with infants, and the unfavourable effects of early social deprivation of different types on cognitive development. Some of the assumptions on which this concept is based have been corroborated by analyses of adult-infant interaction.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89506996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-05-30DOI: 10.1002/9780470720936.CH10
J. Stephen, T. Wallis, W. Starkey, D. Candy, M. Osborne, S. Haddon
Despite years of study and the accumulation of much potentially relevant information, neither the microbial determinants nor the pathophysiological mechanisms of salmonella-induced enteritis are known with precision. Earlier work is reviewed on the experimental pathology of salmonellosis, the pathophysiology of the disease and the biotyping of salmonella strains in closed rabbit ileal loops. The same strains have been confirmed by us to be (i) invasive and diarrhoeagenic, (ii) invasive and non-diarrhoeagenic, and (iii) non-invasive and non-diarrhoeagenic. At least two mechanisms have been put forward to explain fluid exsorption. One implicates prostaglandins released from polymorphonuclear cells (PMNs) interacting with invading organisms, whereas the second involves salmonella enterotoxin(s). This subject is in a state of confusion and requires clarification. The toxin has been shown by some to bear partial likeness to either cholera toxin (although the evidence is in fact contradictory) or Shiga toxin. Since both 'cholera-like' and 'Shiga-like' toxins are produced by all three biotypes in vitro, production of toxin (of whatever class or subclass) cannot per se be the sole explanation for salmonella-induced fluid secretion. In our experiments the onset of fluid secretion in rabbit ileal loops was coincident with the appearance of large numbers of infiltrating PMNs. We have also shown that organisms from all three biotypes, grown for 6 h in iron-containing but not in iron-deficient media, yielded polymyxin B extracts which are enterotoxic in rabbit ileal loops; culture supernatants were negative. Structural damage occurred to villus tips but not crypts in infected loops, succeeded the onset of fluid secretion, and was not reproduced by polymyxin B enterotoxic extracts. Thus salmonella diarrhoea may be a complex phenomenon with multiple determinants which might include the release of endogenous secretagogues and bacterial enterotoxin(s), if such are shown to be synthesized and released in vivo at appropriate times and in appropriate sites. Structural damage to villus tips leading to shortened villi may also contribute to diarrhoea by altering absorption (tip function)/secretion (crypt function) ratios as well as to the expulsion of those organisms which have not migrated to deeper tissues.
{"title":"Salmonellosis: in retrospect and prospect.","authors":"J. Stephen, T. Wallis, W. Starkey, D. Candy, M. Osborne, S. Haddon","doi":"10.1002/9780470720936.CH10","DOIUrl":"https://doi.org/10.1002/9780470720936.CH10","url":null,"abstract":"Despite years of study and the accumulation of much potentially relevant information, neither the microbial determinants nor the pathophysiological mechanisms of salmonella-induced enteritis are known with precision. Earlier work is reviewed on the experimental pathology of salmonellosis, the pathophysiology of the disease and the biotyping of salmonella strains in closed rabbit ileal loops. The same strains have been confirmed by us to be (i) invasive and diarrhoeagenic, (ii) invasive and non-diarrhoeagenic, and (iii) non-invasive and non-diarrhoeagenic. At least two mechanisms have been put forward to explain fluid exsorption. One implicates prostaglandins released from polymorphonuclear cells (PMNs) interacting with invading organisms, whereas the second involves salmonella enterotoxin(s). This subject is in a state of confusion and requires clarification. The toxin has been shown by some to bear partial likeness to either cholera toxin (although the evidence is in fact contradictory) or Shiga toxin. Since both 'cholera-like' and 'Shiga-like' toxins are produced by all three biotypes in vitro, production of toxin (of whatever class or subclass) cannot per se be the sole explanation for salmonella-induced fluid secretion. In our experiments the onset of fluid secretion in rabbit ileal loops was coincident with the appearance of large numbers of infiltrating PMNs. We have also shown that organisms from all three biotypes, grown for 6 h in iron-containing but not in iron-deficient media, yielded polymyxin B extracts which are enterotoxic in rabbit ileal loops; culture supernatants were negative. Structural damage occurred to villus tips but not crypts in infected loops, succeeded the onset of fluid secretion, and was not reproduced by polymyxin B enterotoxic extracts. Thus salmonella diarrhoea may be a complex phenomenon with multiple determinants which might include the release of endogenous secretagogues and bacterial enterotoxin(s), if such are shown to be synthesized and released in vivo at appropriate times and in appropriate sites. Structural damage to villus tips leading to shortened villi may also contribute to diarrhoea by altering absorption (tip function)/secretion (crypt function) ratios as well as to the expulsion of those organisms which have not migrated to deeper tissues.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80272418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-05-30DOI: 10.1002/9780470719862.CH13
U. Houtsmuller
{"title":"Evaluation of modern foods as sources of lipids. In: lipids, malnutrition & the developing brain.","authors":"U. Houtsmuller","doi":"10.1002/9780470719862.CH13","DOIUrl":"https://doi.org/10.1002/9780470719862.CH13","url":null,"abstract":"","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90316406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-05-30DOI: 10.1002/9780470720752.CH15
M. Karplus, S. Swaminathan, T. Ichiye, W. V. van Gunsteren
{"title":"Local and collective motions in protein dynamics.","authors":"M. Karplus, S. Swaminathan, T. Ichiye, W. V. van Gunsteren","doi":"10.1002/9780470720752.CH15","DOIUrl":"https://doi.org/10.1002/9780470720752.CH15","url":null,"abstract":"","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72650870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2008-05-30DOI: 10.1002/9780470720295.CH8
A. Csapo
{"title":"The 'see-saw' theory of parturition.","authors":"A. Csapo","doi":"10.1002/9780470720295.CH8","DOIUrl":"https://doi.org/10.1002/9780470720295.CH8","url":null,"abstract":"","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72912525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-09-28DOI: 10.1002/9780470514696.CH6
O. Petersen
A few years ago, my laboratory obtained evidence for local agonist-evoked repetitive Ca2+ spikes in single pancreatic acinar cells. We have now confirmed this and shown that regular cytosolic Ca2+ spikes evoked by low concentrations of acetylcholine or inositol 1,4,5-trisphosphate (InsP3) are confined to the secretory granule area at the luminal pole of the cells. The local subcellular signals probably arise because the first internal messenger (InsP3), generated from the basolateral membrane, can diffuse rapidly, whereas the Ca2+ released from the more responsive secretory granule region has a very restricted mobility. Local Ca2+ spikes are useful from an energetic point of view and also help to avoid undesirable activation of Ca(2+)-dependent processes. Another messenger, cyclic ADP-ribose, may also regulate intracellular Ca2+ release. In pancreatic acinar cells cyclic ADP-ribose induces repetitive Ca2+ spikes localized in the secretory granule area; these spikes are blocked by ryanodine, but also by the InsP3 receptor antagonist heparin. Ryanodine abolishes or markedly inhibits agonist-evoked Ca2+ spiking, but enhances the frequency of spikes evoked by internal InsP3 application. These results indicate that both ryanodine and InsP3 receptors are involved in Ca2+ spike generation in pancreatic acinar cells, and that both InsP3 and cyclic ADP-ribose may act as internal messengers.
{"title":"Local calcium spiking in pancreatic acinar cells.","authors":"O. Petersen","doi":"10.1002/9780470514696.CH6","DOIUrl":"https://doi.org/10.1002/9780470514696.CH6","url":null,"abstract":"A few years ago, my laboratory obtained evidence for local agonist-evoked repetitive Ca2+ spikes in single pancreatic acinar cells. We have now confirmed this and shown that regular cytosolic Ca2+ spikes evoked by low concentrations of acetylcholine or inositol 1,4,5-trisphosphate (InsP3) are confined to the secretory granule area at the luminal pole of the cells. The local subcellular signals probably arise because the first internal messenger (InsP3), generated from the basolateral membrane, can diffuse rapidly, whereas the Ca2+ released from the more responsive secretory granule region has a very restricted mobility. Local Ca2+ spikes are useful from an energetic point of view and also help to avoid undesirable activation of Ca(2+)-dependent processes. Another messenger, cyclic ADP-ribose, may also regulate intracellular Ca2+ release. In pancreatic acinar cells cyclic ADP-ribose induces repetitive Ca2+ spikes localized in the secretory granule area; these spikes are blocked by ryanodine, but also by the InsP3 receptor antagonist heparin. Ryanodine abolishes or markedly inhibits agonist-evoked Ca2+ spiking, but enhances the frequency of spikes evoked by internal InsP3 application. These results indicate that both ryanodine and InsP3 receptors are involved in Ca2+ spike generation in pancreatic acinar cells, and that both InsP3 and cyclic ADP-ribose may act as internal messengers.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81701681","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-09-28DOI: 10.1002/9780470513774.CH4
J. Fraser, T. Laurent
The highest concentrations of hyaluronan occur in synovial fluid, vitreous body, skin and certain specialized tissues such as umbilical cord and rooster comb, during fetal development, and in tissue repair and regeneration. The largest amounts are found in the intercellular matrix of skin and musculoskeletal tissues. Turnover in the bloodstream is normally in the range of 0.3-1.0 microgram min-1/kg body weight. Circulating hyaluronan is mostly derived from lymph. Lymph nodes may nevertheless extract as much as 80-90% from peripheral lymph before it can reach the bloodstream. Turnover in peripheral tissues may be effected by degradation in situ, or by transfer into lymph by diffusion or hydrodynamic forces. Hyaluronan is firmly bound in specific association with cells or binding proteins but much of it exists in freely mobilized compartments with a half-life of two days or less, and it is metabolized after transport elsewhere. Metabolic degradation of hyaluronan is principally intracellular and relies on uptake by a receptor which, in contrast with other hyaluronan-binding structures, also binds chondroitin sulphate. It is suggested that this dual specificity may be primarily associated with metabolic degradation of hyaluronan. Uptake and metabolism are primarily effected in liver and lymph node by endothelial cells lining the sinusoids of each. Further studies indicate that in lymph nodes and in spleen, macrophage-like cells intertwined with the endothelial cells also take up hyaluronan. The metabolic cycle from polymer to monosaccharides, acetate and beyond can be completed in vivo within 10 minutes.
{"title":"Turnover and metabolism of hyaluronan.","authors":"J. Fraser, T. Laurent","doi":"10.1002/9780470513774.CH4","DOIUrl":"https://doi.org/10.1002/9780470513774.CH4","url":null,"abstract":"The highest concentrations of hyaluronan occur in synovial fluid, vitreous body, skin and certain specialized tissues such as umbilical cord and rooster comb, during fetal development, and in tissue repair and regeneration. The largest amounts are found in the intercellular matrix of skin and musculoskeletal tissues. Turnover in the bloodstream is normally in the range of 0.3-1.0 microgram min-1/kg body weight. Circulating hyaluronan is mostly derived from lymph. Lymph nodes may nevertheless extract as much as 80-90% from peripheral lymph before it can reach the bloodstream. Turnover in peripheral tissues may be effected by degradation in situ, or by transfer into lymph by diffusion or hydrodynamic forces. Hyaluronan is firmly bound in specific association with cells or binding proteins but much of it exists in freely mobilized compartments with a half-life of two days or less, and it is metabolized after transport elsewhere. Metabolic degradation of hyaluronan is principally intracellular and relies on uptake by a receptor which, in contrast with other hyaluronan-binding structures, also binds chondroitin sulphate. It is suggested that this dual specificity may be primarily associated with metabolic degradation of hyaluronan. Uptake and metabolism are primarily effected in liver and lymph node by endothelial cells lining the sinusoids of each. Further studies indicate that in lymph nodes and in spleen, macrophage-like cells intertwined with the endothelial cells also take up hyaluronan. The metabolic cycle from polymer to monosaccharides, acetate and beyond can be completed in vivo within 10 minutes.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87585287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2007-09-28DOI: 10.1002/9780470514924.CH12
H. Wille, M. Baldwin, F. Cohen, S. DeArmond, S. Prusiner
The prion protein (PrP) undergoes a profound conformational change when the cellular isoform (PrPc) is converted into the scrapie form (PrPSc). Limited proteolysis of PrPSc produces PrP27-30 which readily polymerizes into amyloid. To study the structure of PrP amyloid, we employed organic solvents that perturb protein conformation. 1,1,1,3,3,3-Hexafluoro-2-propanol (HFIP), which promotes alpha-helix formation, modified the ultrastructure of rod-shaped PrP amyloids, producing flattened ribbons with a more regular substructure. As the concentration of HFIP was increased, the beta-sheet content and proteinase K resistance of PrP27-30 as well as prion infectivity diminished. HFIP reversibly decreased the binding of Congo red dye to the rods, whereas inactivation of prion infectivity was irreversible. In contrast to 10% HFIP, 1,1,1-trifluoro-2-propanol (TFIP) did not inactivate prion infectivity but, similarly to HFIP, TFIP did alter the morphology of the rods and abolished Congo red binding. Our studies separate prion infectivity from the amyloid properties of PrP27-30 and underscore the dependence of prion infectivity on PrPSc conformation. Our results also demonstrate that the specific beta-sheet-rich structures required for prion infectivity are different from those needed for amyloid formation.
{"title":"Prion protein amyloid: separation of scrapie infectivity from PrP polymers.","authors":"H. Wille, M. Baldwin, F. Cohen, S. DeArmond, S. Prusiner","doi":"10.1002/9780470514924.CH12","DOIUrl":"https://doi.org/10.1002/9780470514924.CH12","url":null,"abstract":"The prion protein (PrP) undergoes a profound conformational change when the cellular isoform (PrPc) is converted into the scrapie form (PrPSc). Limited proteolysis of PrPSc produces PrP27-30 which readily polymerizes into amyloid. To study the structure of PrP amyloid, we employed organic solvents that perturb protein conformation. 1,1,1,3,3,3-Hexafluoro-2-propanol (HFIP), which promotes alpha-helix formation, modified the ultrastructure of rod-shaped PrP amyloids, producing flattened ribbons with a more regular substructure. As the concentration of HFIP was increased, the beta-sheet content and proteinase K resistance of PrP27-30 as well as prion infectivity diminished. HFIP reversibly decreased the binding of Congo red dye to the rods, whereas inactivation of prion infectivity was irreversible. In contrast to 10% HFIP, 1,1,1-trifluoro-2-propanol (TFIP) did not inactivate prion infectivity but, similarly to HFIP, TFIP did alter the morphology of the rods and abolished Congo red binding. Our studies separate prion infectivity from the amyloid properties of PrP27-30 and underscore the dependence of prion infectivity on PrPSc conformation. Our results also demonstrate that the specific beta-sheet-rich structures required for prion infectivity are different from those needed for amyloid formation.","PeriodicalId":10218,"journal":{"name":"Ciba Foundation symposium","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2007-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81623727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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