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Academic literature on the topic 'Activine B'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Activine B"

Klotz, B., L. Seefried, R. Ebert, and F. Jakob. "Activin-Antagonisten in der Therapie der Osteoporose." Osteologie 20, no. 03 (2011): 217–21. http://dx.doi.org/10.1055/s-0037-1619996.

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ZusammenfassungActivin A ist ein Polypeptid mit vielfältigen biologischen Wirkungen auf die Regulation der Fertilität, die Pluripotenz und Differenzierung von Stammzellen, die Differenzierung von Neuronen, Inselzellen und Immunzellen und die Regulation des Stoffwechsels. Activin gehört zu den Liganden der Familie der TGFβ- Superfamilie. Die Activine A, B und C binden an die Typ-II-BMP-Rezeptoren (Activin-Rezeptor IIA [ActRIIA] und IIB [ActRIIB]) und rekrutieren spezifische Typ-I-Rezeptoren (activin receptor-like kinase 2 [ALK2], 4 [ALK4] und 7 ]ALK7]). Da der ActRIIB auch andere Faktoren wie z. B. Myostatin (GDF8) und die Bone Morphogenetic Proteins 7 und 2 (BMP-7, BMP-2) bindet, konkurrieren diese Liganden um den Rezeptor. Im Alter findet man erhöhte Activin- Spiegel im Serum. Activin-Antagonisten verändern die Balance zwischen den verschiedenen Liganden und verursachen eine veränderte Genregulation an allen Zellen, die entsprechende Signalsysteme exprimieren. Ein ACTIIIGG- Fusionsprotein mit Activin-antagonistischer Wirkung wird unter dem Namen Sotatercept (ACE-011) bereits klinisch als Medikament gegen die Tumor-induzierte und die Chemotherapie- induzierte Anämie erprobt und präklinisch für die Therapie der Osteoporose entwickelt. Am Knochen entfaltet der Antagonist eine duale Wirkung, er zeigt ausgeprägte anabole Effekte und verringert die Knochenresorption. In einem Mausmodell der Androgendefizienz werden zudem eine anabole Wirkung am Muskel und eine Verringerung des Fettgewebes beschrieben. Weitere Studien sind auf dem Weg, um sicherzustellen, dass das vielversprechende Medikament bei der Anwendung am Menschen neben der Effizienz auch ein gutes Sicherheits- und Nebenwirkungsprofil besitzt. Wenn es die Klinikreife erreicht, wird es unser therapeutisches Arsenal zur Behandlung der Osteoporose und möglicherweise auch der Sarkopenie wesentlich bereichern.

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Olsen, Oddrun Elise, Hanne Hella, Samah Elsaadi, Carsten Jacobi, Erik Martinez-Hackert, and Toril Holien. "Activins as Dual Specificity TGF-β Family Molecules: SMAD-Activation via Activin- and BMP-Type 1 Receptors." Biomolecules 10, no. 4 (March 29, 2020): 519. http://dx.doi.org/10.3390/biom10040519.

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Activins belong to the transforming growth factor (TGF)-β family of multifunctional cytokines and signal via the activin receptors ALK4 or ALK7 to activate the SMAD2/3 pathway. In some cases, activins also signal via the bone morphogenetic protein (BMP) receptor ALK2, causing activation of the SMAD1/5/8 pathway. In this study, we aimed to dissect how activin A and activin B homodimers, and activin AB and AC heterodimers activate the two main SMAD branches. We compared the activin-induced signaling dynamics of ALK4/7-SMAD2/3 and ALK2-SMAD1/5 in a multiple myeloma cell line. Signaling via the ALK2-SMAD1/5 pathway exhibited greater differences between ligands than signaling via ALK4/ALK7-SMAD2/3. Interestingly, activin B and activin AB very potently activated SMAD1/5, resembling the activation commonly seen with BMPs. As SMAD1/5 was also activated by activins in other cell types, we propose that dual specificity is a general mechanism for activin ligands. In addition, we found that the antagonist follistatin inhibited signaling by all the tested activins, whereas the antagonist cerberus specifically inhibited activin B. Taken together, we propose that activins may be considered dual specificity TGF-β family members, critically affecting how activins may be considered and targeted clinically.

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Schneyer, Alan, Amy Schoen, Alicia Quigg, and Yisrael Sidis. "Differential Binding and Neutralization of Activins A and B by Follistatin and Follistatin Like-3 (FSTL-3/FSRP/FLRG)." Endocrinology 144, no. 5 (May 1, 2003): 1671–74. http://dx.doi.org/10.1210/en.2002-0203.

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Modulation of activin and other TGFβ superfamily signaling is the primary mechanism of action for both follistatin (FS) and FS-like 3 (FSTL-3). However, most studies of these ligands use activin A due to its wide availability. We have now tested the ability of FS288 and FSTL-3 to bind and neutralize activin B relative to activin A. Activin B bound to both FS and FSTL-3 at a potency approximately 10-fold lower than that of activin A. Moreover, whereas both activins had similar biological activity in 293 cell reporter assays, FS and FSTL-3 were approximately 3-fold more effective in neutralizing activin A relative to activin B. These results suggest that neutralization of activins A and B by FS and FSTL-3 are not identical, so that the relative activity of each activin in tissues where both are produced, such as in the ovary, could be quite different. In addition, biological systems that use primarily activin B, but which have been examined in vitro using activin A, may need to be reevaluated to determine the actual physiologic roles of FS or FSTL-3.

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Vänttinen, Teemu, Tiina Kuulasmaa, Jianqi Liu, and Raimo Voutilainen. "Expression of Activin/Inhibin Receptor and Binding Protein Genes and Regulation of Activin/Inhibin Peptide Secretion in Human Adrenocortical Cells." Journal of Clinical Endocrinology & Metabolism 87, no. 9 (September 1, 2002): 4257–63. http://dx.doi.org/10.1210/jc.2002-020460.

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Activins and inhibins are glycoprotein hormones produced mainly in gonads but also in other organs. They are believed to be important para/autocrine regulators of various cell functions. We investigated activin/inhibin receptor and binding protein gene expression and the regulation of activin/inhibin secretion in human adrenal cells. RT-PCR revealed inhibin/activin α-, βA/B-subunit, follistatin, activin type I/II receptor, and inhibin receptor (betaglycan and inhibin-binding protein) mRNA expression in fetal and adult adrenals and cultured adrenocortical cells. Cultured cells secreted activin A and inhibin A/B as determined by specific ELISAs. ACTH stimulated inhibin A/B secretion in fetal (1.8- and 1.8-fold of control, respectively) and in adult cells (3.4- and 1.7-fold of control, respectively) without significant effect on activin A. 8-bromoadenosine cAMP (protein kinase A activator) increased activin A and inhibin A/B secretion in the human adrenocortical NCI-H295R cell line (32-, 17-, and 3-fold of control, respectively). 12-O-tetradecanoyl phorbol-13-acetate (protein kinase C activator) stimulated both activin A and inhibin A secretion (764- and 32-fold of control, respectively), and activin treatment increased inhibin B secretion in these cells (25-fold of control). In conclusion, human adrenocortical cells produce dimeric activins and inhibins. ACTH stimulates inhibin secretion and decreases activin/inhibin secretion ratio, probably via the protein kinase A signal transduction pathway. This, together with the adrenocortical activin/ inhibin receptor and binding protein expression, suggests a physiological role for activins and inhibins in the human adrenal gland.

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Merino, R., D. Macias, Y. Ganan, J. Rodriguez-Leon, A. N. Economides, C. Rodriguez-Esteban, J. C. Izpisua-Belmonte, and J. M. Hurle. "Control of digit formation by activin signalling." Development 126, no. 10 (May 15, 1999): 2161–70. http://dx.doi.org/10.1242/dev.126.10.2161.

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Major advances in the genetics of vertebrate limb development have been obtained in recent years. However, the nature of the signals which trigger differentiation of the mesoderm to form the limb skeleton remains elusive. Previously, we have obtained evidence for a role of TGFbeta2 in digit formation. Here, we show that activins A and B and/or AB are also signals involved in digit skeletogenesis. activin betaA gene expression correlates with the initiation of digit chondrogenesis while activin betaB is expressed coincidently with the formation of the last phalanx of each digit. Exogenous administration of activins A, B or AB into the interdigital regions induces the formation of extra digits. follistatin, a natural antagonist of activins, is expressed, under the control of activin, peripherally to the digit chondrogenic aggregates marking the prospective tendinous blastemas. Exogenous application of follistatin blocks physiological and activin-induced digit formation. Evidence for a close interaction between activins and other signalling molecules, such as BMPs and FGFs, operating at the distal tip of the limb at these stages is also provided. Chondrogenesis by activins is mediated by BMPs through the regulation of the BMP receptor bmpR-1b and in turn activin expression is upregulated by BMP signalling. In addition, AER hyperactivity secondary to Wnt3A misexpression or local administration of FGFs, inhibits activin expression. In correlation with the restricted expression of activins in the course of digit formation, neither activin nor follistatin treatment affects the development of the skeletal components of the stylopod or zeugopod indicating that the formation of the limb skeleton is regulated by segment-specific chondrogenic signals.

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Young, J. M., S. Henderson, C. Souza, H. Ludlow, N. Groome, and A. S. McNeilly. "Activin B is produced early in antral follicular development and suppresses thecal androgen production." REPRODUCTION 143, no. 5 (May 2012): 637–50. http://dx.doi.org/10.1530/rep-11-0327.

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Little is known about the role of activin B during folliculogenesis. This study investigated the expression levels of activin/inhibin subunits (βA, βB, and α), steroid enzyme, and gonadotrophin receptors in theca (TC) and granulosa cells (GC) by QPCR and activin A and B and inhibin A protein levels in follicular fluid (FF) of developing sheep follicles during estrus and anestrus. The effect of activin B on androgen production from primary TC cultures in vitro was also assessed. During folliculogenesis, in anestrus and estrus, FF activin B concentrations and thecal and GC activin βB mRNA levels decreased as follicle diameter increased from 1–3 to >6 mm regardless of estrogenic status. Estrogenic preovulatory follicles had reduced concentrations of FF activins B and A, and TC and GCs expressed higher levels of activin βA mRNA at 3–4 mm, and TCs more inhibin α mRNA at >4 mm stages of development compared with nonestrogenic follicles. Activin B decreased androstenedione production from primary TCs in vitro, an effect blocked by inhibin A. Thus, sheep follicles 1–3 mm in diameter contained high FF levels of activin B, which decreased as the follicle size increased, and, like activin A, suppressed thecal androgen production in vitro, an effect blocked by inhibin. Furthermore, the theca of large estrogenic follicles expressed high levels of inhibin α and activin βA mRNA suggesting local thecal derived inhibin A production. This would inhibit the negative effects of thecal activins B and A ensuring maximum androgen production for enhanced estradiol production by the preovulatory follicle(s).

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Wu, Hui, Michael Wu, Yi Chen, Carolyn A. Allan, David J. Phillips, and Mark P. Hedger. "Correlation between Blood Activin Levels and Clinical Parameters of Type 2 Diabetes." Experimental Diabetes Research 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/410579.

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Aims. Activins A and B, and their binding protein, follistatin, regulate glucose metabolism and inflammation. Consequently, their role in type 2 diabetes (T2D) was examined.Methods. Blood was taken from fasted participants (34 males; 58 females; 50–75 years) with diabetes or during an oral glucose tolerance test (OGTT). Clinical parameters were assessed, and blood assayed for activins, follistatin, and C-reactive protein.Results. Serum levels of activin A (93.3 ± 27.0 pg/mL, mean ± SD), B (81.8 ± 30.8 pg/mL), or follistatin (6.52 ± 3.15 ng/mL) were not different (P>0.05) between subjects with normal OGTT (n=39), impaired glucose tolerance and/or fasting glucose (n=17), or T2D (n=36). However, activin A and/or activin B were positively correlated with parameters of insulin resistance and T2D, including fasting glucose (P<0.001), fasting insulin (P=0.02), glycated hemoglobin (P=0.003), and homeostasis model assessment of insulin resistance (HOMA-IR;P<0.001). Follistatin was positively correlated with HOMA-IR alone (P=0.01).Conclusions. These data indicate that serum measurements of activin A, B, or follistatin cannot discriminate risk for T2D in individual patients, but the activins display a positive relationship with clinical parameters of the disease.

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Albano, R. M., N. Groome, and J. C. Smith. "Activins are expressed in preimplantation mouse embryos and in ES and EC cells and are regulated on their differentiation." Development 117, no. 2 (February 1, 1993): 711–23. http://dx.doi.org/10.1242/dev.117.2.711.

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Members of the activin family have been suggested to act as mesoderm-inducing factors during early amphibian development. Little is known, however, about mesoderm formation in the mammalian embryo, and as one approach to investigating this we have studied activin expression during early mouse development. Activins are homo- or heterodimers of the beta A or beta B subunits of inhibin, itself a heterodimer consisting of one of the beta subunits together with an alpha subunit. Our results indicate that the oocyte contains mRNA encoding all three subunits, and antibody staining demonstrates the presence of both alpha and beta protein chains. From the fertilized egg stage onwards, alpha subunit protein cannot be detected, so the presence of beta subunits reflects the presence of activin rather than inhibin. Maternal levels of activin protein decline during early cleavage stages but increase, presumably due to zygotic transcription (see below), in the compacted morula. By 3.5 days, only the inner cell mass (ICM) cells of the blastocyst express activin, but at 4.5 days the situation is reversed; activin expression is confined to the trophectoderm. Using reverse transcription-PCR, neither beta A nor beta B mRNA was detectable at the two-cell stage but transcripts encoding both subunits were detectable at the morula stage, with beta B mRNA persisting into the blastocyst. We have also analyzed activin and inhibin expression in ES and EC cells. Consistent with the observation that activins are expressed in the ICM of 3.5-day blastocysts, we find high levels of beta A and beta B mRNA in all eight ES cell lines tested. F9 EC cells express only activin beta B, together with low levels of the inhibin alpha chain. When ES and EC cells are induced to differentiate, levels of activin fall dramatically. These results are consistent with a role for activins in mesoderm formation and other steps of early mouse development.

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Andrzejewski, Danielle, Melissa L. Brown, Nathan Ungerleider, Amy Burnside, and Alan L. Schneyer. "Activins A and B Regulate Fate-Determining Gene Expression in Islet Cell Lines and Islet Cells From Male Mice." Endocrinology 156, no. 7 (May 11, 2015): 2440–50. http://dx.doi.org/10.1210/en.2015-1167.

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TGFβ superfamily ligands, receptors, and second messengers, including activins A and B, have been identified in pancreatic islets and proposed to have important roles regulating development, proliferation, and function. We previously demonstrated that Fstl3 (an antagonist of activin activity) null mice have larger islets with β-cell hyperplasia and improved glucose tolerance and insulin sensitivity in the absence of altered β-cell proliferation. This suggested the hypothesis that increased activin signaling influences β-cell expansion by destabilizing the α-cell phenotype and promoting transdifferentiation to β-cells. We tested the first part of this hypothesis by treating α- and β-cell lines and sorted mouse islet cells with activin and related ligands. Treatment of the αTC1-6 α cell line with activins A or B suppressed critical α-cell gene expression, including Arx, glucagon, and MafB while also enhancing β-cell gene expression. In INS-1E β-cells, activin A treatment induced a significant increase in Pax4 (a fate determining β-cell gene) and insulin expression. In sorted primary islet cells, α-cell gene expression was again suppressed by activin treatment in α-cells, whereas Pax4 was enhanced in β-cells. Activin treatment in both cell lines and primary cells resulted in phosphorylated mothers against decapentaplegic-2 phosphorylation. Finally, treatment of αTC1-6 cells with activins A or B significantly inhibited proliferation. These results support the hypothesis that activin signaling destabilized the α-cell phenotype while promoting a β-cell fate. Moreover, these results support a model in which the β-cell expansion observed in Fstl3 null mice may be due, at least in part, to enhanced α- to β-cell transdifferentiation.

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Tang, Pei, Xueer Wang, Min Zhang, Simin Huang, Chuxi Lin, Fang Yan, Ying Deng, Lu Zhang, and Lin Zhang. "Activin B Stimulates Mouse Vibrissae Growth and Regulates Cell Proliferation and Cell Cycle Progression of Hair Matrix Cells through ERK Signaling." International Journal of Molecular Sciences 20, no. 4 (February 15, 2019): 853. http://dx.doi.org/10.3390/ijms20040853.

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Activins and their receptors play important roles in the control of hair follicle morphogenesis, but their role in vibrissae follicle growth remains unclear. To investigate the effect of Activin B on vibrissae follicles, the anagen induction assay and an in vitro vibrissae culture system were constructed. Hematoxylin and eosin staining were performed to determine the hair cycle stages. The 5-ethynyl-2′-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays were used to examine the cell proliferation. Flow cytometry was used to detect the cell cycle phase. Inhibitors and Western blot analysis were used to investigate the signaling pathway induced by Activin B. As a result, we found that the vibrissae follicle growth was accelerated by 10 ng/mL Activin B in the anagen induction assay and in an organ culture model. 10 ng/mL Activin B promoted hair matrix cell proliferation in vivo and in vitro. Moreover, Activin B modulates hair matrix cell growth through the ERK–Elk1 signaling pathway, and Activin B accelerates hair matrix cell transition from the G1/G0 phase to the S phase through the ERK–Cyclin D1 signaling pathway. Taken together, these results demonstrated that Activin B may promote mouse vibrissae growth by stimulating hair matrix cell proliferation and cell cycle progression through ERK signaling.

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Dissertations / Theses on the topic "Activine B"

Gineste, Aurélie. "Fer et immunité innée : vers une meilleure compréhension des mécanismes développés par l'hôte pour réduire le fer accessible aux pathogènes." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30117/document.

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Le fer est un élément essentiel à de nombreux processus physiologiques fondamentaux. Lors d'une infection, une forte compétition entre l'hôte et l'agent pathogène a lieu ; alors que la bactérie a besoin d'acquérir le fer de l'hôte, pour son développement et sa virulence, l'hôte déploie de nombreux mécanismes pour protéger ses stocks de fer. Il sécrète notamment un peptide capable de moduler l'homéostasie du fer au niveau systémique, l'hepcidine, qui va causer une diminution de la quantité de fer sérique, une rétention intracellulaire du fer et donc une restriction du fer accessible aux pathogènes. Lors d'une inflammation, l'expression de l'hepcidine est décrite dans la littérature pour être principalement induite via l'activation de deux voies de signalisation : la voie STAT3 et la voie BMP/SMAD, l'altération de chacune de ces voies conduisant à un défaut d'induction d'hepcidine. Cependant, nos précédentes observations publiées ont infirmé le rôle de l'IL6, ligand de la voie STAT3, dans la régulation de l'hepcidine en réponse au LPS, et ont suggéré l'implication d'un peptide appartenant à la famille du TGFb, l'activine B, dans la régulation de l'hepcidine via l'activation de la voie BMP/SMAD in vivo. Dans cette étude, nous nous sommes intéressés au rôle de l'activine B dans la régulation de l'hepcidine in vivo, lors d'une infection. Grâce à l'utilisation de souris invalidées pour le gène codant l'activine B (Inhbb-/-), nous avons confirmé que l'activine B était un ligand endogène de la voie BMP/SMAD dans le foie, puisqu'elle induit la phosphorylation des effecteurs SMAD en réponse au LPS. Cependant, nous avons pu clairement démontrer que l'activine B, et donc l'augmentation de la phosphorylation des effecteurs SMAD, ne participaient pas à la régulation de l'hepcidine in vivo, en réponse à l'infection. Nous nous sommes alors intéressés à l'implication de l'IL6 dans la régulation de l'hepcidine. Alors que l'absence d'Il6 n'altère pas l'induction de l'hepcidine in vivo en réponse au LPS, cette cytokine semble jouer un rôle clé pour la réponse de l'hôte lors d'une infection par une bactérie. Dans ce contexte, la littérature décrit l'importance de l'IL6 pour une réponse immunitaire protectrice de l'hôte lors d'une infection. Lors d'une infection, nous proposons donc l'implication d'une nouvelle voie de signalisation dans l'expression de l'hepcidine. De plus, nous suggérons un rôle important de l'IL6, non pas dans la régulation transcriptionnelle de l'hepcidine, mais pour la protection de l'hôte lors d'une infection bactérienne. Enfin, nos résultats montrent qu'un niveau d'activation basal de la voie BMP/SMAD est requis pour une induction d'hepcidine lors d'inflammation, et que l'augmentation de la phosphorylation des effecteurs SMAD observée en réponse à l'inflammation ne participe pas à cette régulation
Iron is essential for several fundamental metabolic processes. During infection, a strong competition between the host and the pathogen occurs; while the bacteria needs to acquire iron from the host, for its growth and virulence, hosts have developed several mechanisms to protect its iron stores. In particular, the host produces a peptide in order to modulate systemic iron homeostasis, hepcidin. Hepcidin decreases the amount of circulating iron, causes intracellular iron retention and thus a restriction of accessible iron to pathogens. During inflammation, hepcidin expression is described in the literature to be mainly mediated through activation of two signaling pathways: the STAT3 and the BMP/SMAD pathways. Impairment of one of these pathways leads to an impaired hepcidin induction. However, our previous published observations did not support the role of IL6, the major ligand of STAT3 pathway, in the regulation of hepcidin in response to LPS, but suggested the involvement of another protein, that belongs to the TGFb family, activin B, in the regulation of hepcidin via the activation of the BMP/SMAD pathway in vivo. In this study, we investigated the role of activin B in the regulation of hepcidin in vivo, during infection. By using knockout mice for the gene encoding activin B (Inhbb-/-), our results suggest that activin B is not involved in the regulation of hepcidin in vivo in response to infection. We then investigated the function of IL6 in the regulation of hepcidin. Although the absence of IL6 does not affect the induction of hepcidin in vivo in response to LPS, this cytokine appears to play a key role in the host response during bacterial infection. Indeed, the literature describes the importance of IL6 for a protective immune response of the host during infection. During infection, we hypothesize that another signaling pathway regulates hepcidin expression. In addition, we suggest an important role of IL6, not in the transcriptional regulation of hepcidin, but for the host protection during a bacterial infection. Finally, our results also show that basal level of BMP/SMAD pathway is required for an appropriate induction of hepcidin during inflammation

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Mahmoud, Abady Maryam. "Modulation of growth factors and cell cycle regulatory molecules in experimental cardiomyopathy." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210244.

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Background: Different types of cardiomyopathies are associated with variable hypertrophic response.

A number of growth factors are thought to play a role in pathologic cardiac remodeling.

Aims: We compared the modulation of the TGF-ƒÒ superfamily and IGF-1 signaling pathways and their target genes, the cell cycle regulatory proteins in tachycardia-induced dilated cardiomyopathy, a model with no detectable hypertrophy and in ischemic cardiomyopathy, a model with a marked hypertrophic reaction.

Methods: In the first study, endomyocardial biopsies were obtained weekly in 15 dogs, during the development of tachycardiomyopaty. Genes involved in the myostatin-TGF-ƒÒ-Activin-A/Smad signaling pathway, p21 and cyclin D were quantified and correlated to echocardiographic measures of hypertrophy. In the second study, myocardial tissue samples were obtained in 8 dogs with a healed myocardial infarction, in 8 dogs with heart failure induced by overpacing and in 7 healthy dogs. We measured gene expression of IGF-1, its receptor (IGF-1R) and cyclins A, B, D1, D2, D3 and E and correlated them to the level of hypertrophy.

Results: Tachycardiomyopathy was characterized by chambers dilation with no identifiable hypertrophy. Ischemic cardiomyopathy was characterized by eccentric hypertrophy. In tachycardiomyopathy, Activin-A mRNA was 4-fold higher than at baseline. Smad7 was overexpressed in severe heart failure; p21, a direct target gene of the Smad pathway was upregulated 8-fold and cyclin D1 was down-regulated. In that model, IGF-1 was overexpressed but neither IGF-1R nor any of the cyclins studied.

In ischemic cardiomyopathy, IGF-1, IGF-R, and cyclins B, D1, D3 and E gene expression were upregulated.

In tachycardiomyopathy, Activin-A and p21 were inversely correlated to the thickness of the interventricular septum. In normal dogs and in the both models of cardiomyopathy, IGF-1R was correlated to the thickness of the interventricular septum and to cyclins.

Conclusions: Taken together, these results agree with the notion that Activin-A, IGF and cyclins are involved in the modulation of hypertrophic response observed in cardiomyopathies.

Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished

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Elliott, Robert Jeffery. "Active-site variants of Streptomyces griseus protease B with peptide-ligation activity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0022/NQ51857.pdf.

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Addington, Trevor. "Engineering carbohydrate-active enzymes: specificity and activity remodeled." Doctoral thesis, Universitat Ramon Llull, 2009. http://hdl.handle.net/10803/9285.

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To understand and modify the secondary cell walls of plants the project group Enzyme Discovery in Hybrid Aspen for Fiber Engineering (EDEN) was founded composed of nine laboratories with funding from the European Commission. The main target of EDEN´s research is to genetically engineer fiber structure in order to produce transgenic trees with modified properties for the pulp and paper industries.
In this target framework, the Populus tremula x tremuloides xyloglucan endotransglycosylase (PttXET16A) was selected for in-depth study of its transglycosylase activity catalyzing cleavage and reconnection of xyloglucan molecules, which is proposed to be involved in secondary cell wall morphogenesis.
The creation of a family 16 carbohydrate active enzyme -glucanase/XET hybrids were attempted in order to design a chimeric enzyme with one or more of the following altered properties: specificity, activity, and or stability.
The two enzymes, Bacillus licheniformis 1,3-1,4--glucanase and Populus tremula x tremuloides xyloglucan endotransglycosylase, are members of the same enzymatic family and have highly homologous 3-dimensional structures. However, the enzymes exhibit different activities, one a hydrolase the other a transferase; different specificities, one accepts only linear glcosydic substrates while the other branched substrates; and different stabilities.
Hybrid enzyme construction represented an investigational challenge in order to understand what physical characteristics of both enzymes attribute to the specific pattern of activity and specificity observed.
Removal of the 1,3-1,4--glucanase major loop resulted in a folded protein which still maintained some β-glucan hydrolase activity. However, no xyloglucan endotransglycosylase-like activity or specificity was observed. Next, point mutations of the β-sheets forming the enzymatic binding site cleft were mutated to resemble PttXET16A residues. The final chimeric protein neither exhibited XET nor β-glucanase activities. Structural analysis by X-ray crystallography revealed a major unexpected structural rearrangement providing a clear insight for further enzyme engineering.
Amb la finalitat d'entendre i modificar la paret cel·lular secundària de les plantes, es va fundar el grup Enzyme Discovery in Hibrid Aspen for Fibern Engineering (EDEN) composat per nou laboratoris amb la finançament de la Comissió Europea. El principal objectiu de la recerca del grup EDEN és enginyar genèticament l'estructura de fibres per tal de produir arbres transgènics amb propietats modificades per les indústries de la polpa i el paper.
En el marc d'aquest projecte, es va seleccionar el Populus tremula x tremuloides xiloglucà endotransglicosilasa (PttXET16A) per estudiar en profunditat la seva activitat transglicosilasa catalitzant el trencament i la reconnexió de molècules de xiloglucà, el qual sembla estar involucrat en la morfogènesi de la paret cel·lular secundària.
D'aquesta manera, s'intentà crear una família 16 d'híbrids de l'enzim actiu amb carbohidrats -glucanasa/XET per tal de dissenyar un enzim quimèric amb una o més de les propietats següents alterades: especificitat, activitat i/o estabilitat.
Els dos enzims, Bacillus licheniformis 1,3-1,4--glucanasa i Populus tremula x tremuloides xiloglucà endotransglicosilasa, són membres de la mateixa família enzimàtica i tenen una gran homologia en les seves estructures en 3-dimensions. Tot i així, aquests enzims presenten diferents activitats, un presenta activitat hidrolasa i l'altre, transferasa; diferents especificitats, un accepta només substrats glicosílics lineals mentre l'altre, substrats ramificats; i diferents estabilitats.
La construcció d'un enzim híbrid representa un repte en la investigació amb la finalitat d'entendre quines característiques físiques dels dos enzims s'atribueixen al model específic de l'activitat i especificitat observada.
L'extracció del llaç més gran de l'1,3-1,4--glucanasa va resultar en l'obtenció d'una proteïna plegada que encara manté certa activitat hidrolasa del -glucà. Tot i això, no s'observà activitat o especificitat similar a la xiloglucà endotransglicosilasa. A partir d'aquí, es realitzaren mutacions puntuals a diferents punts de les fulles  que formen l'escletxa del lloc d'unió de l'enzim per assemblar-se als residus del PttXET16A. La proteïna quimèrica final tampoc presentava activitat XET ni -glucanasa. L'anàlisi de l'estructura per cristal·lografia de raigs X revelà una major reorganització estructural de l'esperada proveint el nou enzim d'un clar espai intern que obra moltes més portes a l'enginyeria de l'enzim.
Con la finalidad de entender y modificar la pared celular secundaria de las plantas, se fundó el grupo Enzyme Discovery in Hibrid Aspen for Fibern Engineering (EDEN) compuesto por nueve laboratorios con la financiación de la Comisión Europea. El principal objetivo de la búsqueda del grupo EDEN es ingeniar genéticamente la estructura de fibras para producir árboles transgénicos con propiedades modificadas para las industrias de la pulpa y el papel.
En el marco de este proyecto, se seleccionó el Populus tremula x tremuloides xiloglucán endotransglicosilasa (PttXET16A) para estudiar en profundidad su actividad transglicosilasa catalizando la rotura y la reconnexión de moléculas de xiloglucán, el cual parece estar involucrado en la morfogénesis de la pared celular secundaria. De esta forma, se intentó crear una familia 16 de híbridos de la enzima activa con carbohidratos -glucanasa/XET con la finalidad de diseñar una enzima quimérica con una o más de las propiedades siguientes alteradas: especificidad, actividad y/o estabilidad.
Las dos enzimas, Bacillus licheniformis 1,3-1,4--glucanasa y Populus tremula x tremuloides xiloglucà endotransglicosilasa, son miembros de la misma familia enzimática y tienen una gran homología en sus estructuras en 3-dimensiones. Aún así, estas enzimas presentan diferentes actividades, una tiene actividad hidrolasa y la otra, transferasa; diferentes especificidades, una acepta sólo sustratos glicosílicos lineales mientras la otra, sustratos ramificados; y diferentes estabilidades.
La construcción de una enzima híbrida representa un reto dentro de la investigación con la finalidad de entender qué características físicas de las dos enzimas se atribuyen al modelo específico de la actividad y especificidad observada. La extracción del lazo más grande de la 1,3-1,4--glucanasa resultó en la obtención de una proteína plegada que todavía mantiene cierta actividad hidrolasa del -glucán. Aún así, no se observó actividad o especificidad similar a la xiloglucán endotransglicosilasa. A partir de este punto, se realizaron mutaciones puntuales a diferentes puntos de las hojas  que forman la brecha del lugar de unión de la enzima por asemejarse a los residuos del PttXET16A. La proteína quimérica final tampoco presentaba actividad XET ni -glucanasa. El análisis de la estructura por cristalografía de rayos X reveló una mayor reorganización estructural de la esperada proveyendo la nueva enzima de un claro espacio interno que obre muchas más puertas a la ingeniería de la enzima.

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Gretton, Heather Margaret. "Platelet monoamine oxidase type B (MAO-B) activity in psychopathy." Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30619.

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Studies of platelet MAO-B activity have revealed a link between low platelet activity and psychiatric syndromes characterized by an inability to control impulses and to anticipate future consequences of behavior (Oreland, 1980; Gottfries, von Knorring, & Oreland, 1980). These characteristics are fundamental to the construct of psychopathy, and we might therefore expect that psychopathy is associated with low MAO activity. Indeed, some investigators have suggested that low platelet MAO-B activity is a potential marker for vulnerability to psychopathy (Schalling, Asberg, Edman, & Oreland, 1987). However, no study to date has directly examined the association between platelet MAO activity and psychometrically-sound indices of psychopathy. The present study measured platelet MAO-B activity in a sample of 54 male offenders, assessed with the Psychopathy Checklist-Revised (PCL-R; Hare, 1991). PCL-R scores were not significantly related to level of platelet MAO activity. The results are discussed in terms of methodological issues involved in conducting biochemical research.
Arts, Faculty of
Psychology, Department of
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Malicorne, Gilles. "Thiéno (2,3-b) et (3,2-b) pyridines synthèse et activité antibactérienne /." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb376075729.

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Malicorne, Gilles. "Thiéno (2,3-b) et (3,2-b) pyridines : synthèse et activité antibactérienne." Montpellier 2, 1987. http://www.theses.fr/1987MON20277.

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DESMARTIN, VINCENT. "Synthese et activite cholinergique d'imidazo(1,2-b)pyridazines." Strasbourg 1, 1994. http://www.theses.fr/1994STR15050.

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Ludlow, Helen. "Novel and improved immunoassays for Activin B and Inhibin B and their clinical applications." Thesis, Oxford Brookes University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493408.

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The functional roles of inhibin and activin and clinical applications of measuring them in serum have been reported in a large number of publications. Commercial enzyme-linked immunosorbent assays (ELISAs) for inhibin A, inhibin B and activin A are already available on the market globally.

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Czor, Mathias. "Angoisse et activité ludique." Doctoral thesis, Université Laval, 2015. http://hdl.handle.net/20.500.11794/25891.

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Dans cette thèse qui traite du rapport entre l'angoisse et l'activité ludique, nous reprenons les grands thèmes de l'angoisse : existentielle, morale, absurde. Nous explorons ses nombreux traits : la condition humaine, la mortalité, l'absurdité, l'inconnu, le possible, le néant. Nous abordons la liberté qui en constitue une des composantes essentielles. S'y ajoutent des émotions proches de l'angoisse. Cette thèse trace, dans les grandes lignes, la description de ce que le jeu implique, requiert, accomplit, la forme qu'il prend et la place que cette activité, que nous considérons souvent comme à l'opposé du sérieux, occupe dans notre quotidien. Nous offrons différents points de vue sur ses caractéristiques, notamment l'esthétique, l'irréel, le passif, l'actif et le subjectif. Nous faisons également une description de plusieurs jeux, ce qui nous permet d'analyser les différentes attitudes possibles du joueur, qui impliquent sa subjectivité, sa maturité et son besoin de se dépenser dans des circonstances peu dangereuses. Enfin, nous mettons en relation ces deux concepts, angoisse et jeu, qui l'un comme l'autre demandent la liberté. Ce travail s'inspire et partage les écrits d'auteurs anciens et récents qui traitent de ces sujets, dont les incontournables Buytendijk, Caillois, Fink, Gadamer, Heidegger, Huizinga, Kierkegaard et Sartre. Nous y abordons d'importantes facettes de la vie qui amèneront le lecteur à développer et à prendre position sur ses propres définitions de l'angoisse et du ludique. Notre objectif est de mettre en évidence le rôle indispensable du jeu, de ses effets dans la vie humaine et de démontrer son influence sur l'angoisse.
This thesis written about the relation between angst and play, gives the main definitions of angst : existentialism, culpability, absurdity. We explore the traits of angst : human condition, mortality, absurdity, unknown, possibilities and void. We explain many feelings close to angst. This thesis traces wide lines to describe what play implies, requires, achieves, what forms it takes and where this activity that we often consider the opposite of serious takes place in everyday's existence. Also, we describe many characteristics of play, mainly esthetic, unreal, passive, active, subjective. Many games are also explained. We touch different theories about the player, which imply his subjectivity, maturity and his need to spend energy in non-dangerous activities. Then, we show the relation between play and angst, two concepts that require liberty. Inspired by great authors, old and modern, of those we have to mention Buytendijk, Caillois, Fink, Gadamer, Heidegger, Huizinga, Kierkegaard and Sartre ; we describe important parts of life, which will bring the reader to develop and take position on his view of play and angst. This is to show the irreplaceable role of play and its attributes in the human life but even more to push the limits of knowledge on play, and show play's influence on angst.

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Books on the topic "Activine B"

Wanping, Su, and Lin Tianlong, eds. Huo li wei sheng su B: Active vitamin B. Beijing: Zhongguo qing gong ye chu ban she, 2006.

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Irresistible A, B, Cs. New York: Scholastic Professional Books, 2000.

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Weeks, Stephanie. I like writing!: A B C. Watertown, MA: Charlesbridge Pub., 2001.

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Giampapa, M. S. X-ray activity in the open cluster IC 4665. [Tucson, Ariz.]: National Optical Astronomy Observatories, 1997.

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Giampapa, M. S. X-ray activity in the open cluster IC 4665. [Tucson, Ariz.]: National Optical Astronomy Observatories, 1997.

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Patrick, Lashmar, Paithouski Shawn, and Lickman Jesse, eds. My personal word book: Level B. Hamilton, Ont: Tree House Press, 2005.

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Symposium, International Astronomical Union. Active OB stars: Structure, evolution, mass-loss, and critical limits : proceedings of the 272nd symposium of the International Astronomical Union held in Paris, France, July 19-23, 2010. Cambridge, UK: Cambridge University Press, 2011.

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Activity Book B. McGraw-Hill Education, 2004.

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Barnfield, Fred, and Lisa Saunders. No Problem!: Activity Book B. Macmillan Education, 1989.

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Root, Betty. Skyways Activity Pack B (Skyways). HarperCollins Publishers, 1989.

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Book chapters on the topic "Activine B"

de Yébenes, Virginia G., and Almudena R. Ramiro. "MicroRNA Activity in B Lymphocytes." In Methods in Molecular Biology, 177–92. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-811-9_12.

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Feitelson, Mark. "The DNA Polymerase Activity of HBV." In Molecular Components of Hepatitis B Virus, 123–32. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2573-4_9.

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Frenzel, T., M. Kadic, and M. Wegener. "Mechanical Activity: The Elastic Counterpart of Optical Activity." In NATO Science for Peace and Security Series B: Physics and Biophysics, 403–4. Dordrecht: Springer Netherlands, 2018. http://dx.doi.org/10.1007/978-94-024-1544-5_33.

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Ruzmaikin, Alexander. "Can We Get the Bottom B?" In Helioseismic Diagnostics of Solar Convection and Activity, 49–57. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4377-6_3.

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Slukvin, Igor I., Valentina V. Pilipenko, Victor P. Chernyshov, and Alexey A. Philchenkov. "B-Cell Promoting Activity of Human Colostrum." In Advances in Experimental Medicine and Biology, 153–57. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_31.

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Nakamura, Shinichi, Osamu Yasuhara, Toshio Kawamata, Toru Kimura, Ichiro Akiguchi, Jun Kimura, Masakuni Kameyama, Noriko Nakamura, and Hiroshi Kimura. "Monoamine Oxidase B Activity in Senile Plaque." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 91–94. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_19.

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"Activin B." In Encyclopedia of Cancer, 36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100086.

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"Appendix B." In Palestinian Women’s Activism, 193–96. Syracuse University Press, 2018. http://dx.doi.org/10.2307/j.ctv14h56f.13.

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"Appendix B: Transcription conventions." In Language Activism, 217–18. De Gruyter, 2021. http://dx.doi.org/10.1515/9781501511561-010.

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"B. Calculus." In Magneto-Active Polymers, 265–76. De Gruyter, 2019. http://dx.doi.org/10.1515/9783110418576-014.

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Conference papers on the topic "Activine B"

Moreira*, Joana, Lucília Saraíva, Pedro Brandão*, Joana Almeida, Nair Nazareth, Ivo E. Sampaio-Dias, Vitor Vasconcelos, et al. "Norhierridin B, a new hierridin B-based hydroquinone with improved antiproliferative activity." In 6th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/ecmc2020-07491.

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Ben, Jemni. "From UML Activity Diagrams to Event B." In Information Control Problems in Manufacturing, edited by Bakhtadze, Natalia, chair Dolgui, Alexandre and Bakhtadze, Natalia. Elsevier, 2009. http://dx.doi.org/10.3182/20090603-3-ru-2001.00069.

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Costa, Leonardo, Jürgen Haas, Henriette Rudolph, Saskia Libicher, Sven Jarius, Tobias Tenenbaum, Horst Schroten, and Brigitte Brigitte Wildemann. "The Choroid Plexus Is Permissive for a Preactivated Antigen-Experienced Memory B Cell Subset in Multiple Sclerosis." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.2.

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Background: The role of B cells in multiple sclerosis (MS) is increasingly recognized. B cells undergo compartmentalized redistribution in blood and cerebrospinal fluid (CSF) during active MS, whereby memory B cells accumulate in the CSF. While B-cell trafficking across the blood– brain barrier has been intensely investigated, cellular diapedesis through the blood–CSF barrier (BCSFB) is incompletely understood. Objectives: To investigate how B cells interact with the choroid plexus to transmigrate into the CSF, we isolated circulating B cells from healthy donors (HC) and MS patients, utilized an inverted cell culture filter system of human choroid plexus papilloma (HIBCPP) cells to determine transmigration rates of B-cell subsets, immunofluorescence, and electron microscopy to analyze migration routes, and qRT-PCR to determine cytokines/chemokines mediating B-cell diapedesis. We also screened the transcriptome of intrathecal B cells from MS patients. Results: We found that spontaneous transmigration of HC- and MS-derived B cells was scant yet increased significantly in response to B-cell specific chemokines CXCL-12/CXCL-13, was further boosted upon pre-activation and occurred via paracellular and transcellular pathways. Migrating cells exhibited upregulation of several genes involved in B-cell activation/migration and enhanced expression of chemokine receptors CXCR4/CXCR5 and were predominantly of isotype class switched memory phenotype. This antigen-experienced migratory subset displayed more pronounced chemotactic activities in MS than in HC and was retrieved in intrathecal B cells from patients with active MS. Trafficking of class-switched memory B cells was downscaled in a small cohort of natalizumab-exposed MS patients and the proportions of these phenotypes were reduced in peripheral blood yet were enriched intrathecally in patients who experienced recurrence of disease activity after withdrawal of natalizumab. Conclusion: Our findings highlight the relevance of the BCSFB as an important gate for the entry of potentially harmful activated B cells into the CSF.

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Bagi, Sujata M., Fatima N. Kudchi, and Shridevi Bagewadi. "Power Quality Improvement using a Shunt Active Power Filter for Grid Connected Photovoltaic Generation System." In 2020 IEEE Bangalore Humanitarian Technology Conference (B-HTC). IEEE, 2020. http://dx.doi.org/10.1109/b-htc50970.2020.9298001.

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Jähne, B. "Spatiotemporal active thermography." In 2004 Quantitative InfraRed Thermography. QIRT Council, 2004. http://dx.doi.org/10.21611/qirt.2004.b.

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Velut, Jerome, Hugues Benoit-Cattin, and Christophe Odet. "Segmentation by Smoothing B-Spline Active Surface." In 2006 International Conference on Image Processing. IEEE, 2006. http://dx.doi.org/10.1109/icip.2006.312457.

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Wei, F. Y., L. Sang, H. L. Zeng, and P. Cui. "B-doped TiO2 nanotubes and its photocatalytic activity." In 2008 2nd IEEE International Nanoelectronics Conference. IEEE, 2008. http://dx.doi.org/10.1109/inec.2008.4585496.

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Oikonomopoulos, A., M. Pantic, and I. Patras. "B-spline polynomial descriptors for human activity recognition." In 2008 IEEE Computer Society Conference on Computer Vision and Pattern Recognition Workshops (CVPR Workshops). IEEE, 2008. http://dx.doi.org/10.1109/cvprw.2008.4563175.

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Huml, Karel, Vladimír Šubr, and Karel Ulbrich. "Computer modelling of 5-fluorouracil conjugate with an N-(2-hydroxypropyl)methacrylamide copolymer in an active cleft of cathepsin B." In VIIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2001. http://dx.doi.org/10.1135/css200104117.

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Wang, Yue, Eam Khwang Teoh, Zujun Hou, and Jiangang Wang. "Object boundary extraction using Active B-Snake Model." In 2008 19th International Conference on Pattern Recognition (ICPR). IEEE, 2008. http://dx.doi.org/10.1109/icpr.2008.4761405.

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Reports on the topic "Activine B"

Corbin, Calvin C., and Carol J. Molnar. Materiel Readiness Support Activity Automation Plan. Appendix B: Survey Report. Fort Belvoir, VA: Defense Technical Information Center, September 1986. http://dx.doi.org/10.21236/ada206763.

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Nettles, Kendall W., and Geoffrey L. Greene. Estrogen Receptor Inhibition of NF- (kappa) B Activity in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada425643.

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Wilson, Andrew. Nuclear Factor-Kappa B Activity in the Host-Tumor Microenvironment of Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada612700.

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Arnett, Clint, Justin Lange, Ashley Boyd, Martin Page, and Donald Cropek. Expression and secretion of active Moringa oleifera coagulant protein in Bacillus subtilis. Engineer Research and Development Center (U.S.), August 2021. http://dx.doi.org/10.21079/11681/41546.

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Cationic polypeptide proteins found in the seeds of the tropical plant Moringa oleifera have coagulation efficiencies similar to aluminum and ferric sulfates without their recalcitrant nature. Although these proteins possess great potential to augment or replace traditional coagulants in water treatment, harvesting active protein from seeds is laborious and not cost-effective. Here, we describe an alternative method to express and secrete active M. oleifera coagulant protein (MO) in Bacillus subtilis. A plasmid library containing the MO gene and 173 different types of secretory signal peptides was created and cloned into B. subtilis strain RIK1285. Fourteen of 440 clones screened were capable of secreting MO with yields ranging from 55 to 122 mg/L of growth medium. The coagulant activity of the highest MO secreting clone was evaluated when grown on Luria broth, and cell-free medium from the culture was shown to reduce turbidity in a buffered kaolin suspension by approximately 90% compared with controls without the MO gene. The clone was also capable of secreting active MO when grown on a defined synthetic wastewater supplemented with 0.5% tryptone. Cell-free medium from the strain harboring the MO gene demonstrated more than a 2-fold reduction in turbidity compared with controls. Additionally, no significant amount of MO was observed without the addition of the synthetic wastewater, suggesting that it served as a source of nutrients for the effective expression and translocation of MO into the medium.

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Crawford, C. L. Interim Report for Crucible-Scale Active Vitrification Testing Envelope B (AZ-102). Office of Scientific and Technical Information (OSTI), August 2002. http://dx.doi.org/10.2172/799370.

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Nielson, Dennis L. Active Heave Compensated Drilling Rig (AHC800) Cruise KN167 -KN168A/B R/V Knorr. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada630360.

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Kancheva, Lyudmila, Petar Nikolov, Tsvetelina Velikova, Ivan Valkov, Rossen Nikolov, and Lyudmila Mateva. Soluble CD14 is Associated with Disease Activity and Severity in Chronic Viral Hepatitis C and B. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, June 2018. http://dx.doi.org/10.7546/crabs.2018.06.17.

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Sitaraman, S., S. Kim, D. Biswas, R. Hafner, and B. Anderson. Definition of Small Gram Quantity Contents for Type B Radioactive Material Transportation Packages: Activity-Based Content Limitations. Office of Scientific and Technical Information (OSTI), October 2010. http://dx.doi.org/10.2172/992291.

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Sitaraman, S., S. Kim, D. Biswas, R. Hafner, and B. Anderson. Definition of "Small Gram Quantity Contents" for Type B Radioactive Material Transportation Packages: Activity-Based Content Limitations, Rev. 1. Office of Scientific and Technical Information (OSTI), July 2011. http://dx.doi.org/10.2172/1117951.

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Rockhold, Mark L. Status Report for Remediation Decision Support Project, Task 1, Activity 1.B ? Physical and Hydraulic Properties Database and Interpretation. Office of Scientific and Technical Information (OSTI), September 2008. http://dx.doi.org/10.2172/1038662.

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