cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1270473.v35
title: Inhibitory mechanism of FAT4 gene expression in response to actin dynamics during Src-induced carcinogenesis

description: Oncogenic transformation is characterized by morphological changes resulting from alterations in actin dynamics and adhesive activities. Emerging evidence suggests that the protocadherin FAT4 acts as a tumor suppressor in humans, and reduced <em>FAT4</em> gene expression has been reported in breast and lung cancers and melanoma. However, the mechanism controlling<em> FAT4</em> gene expression is poorly understood. In this study, we show that transient activation of the Src oncoprotein represses <em>FAT4</em> mRNA expression through actin depolymerization in the immortalized normal human mammary epithelial cell line MCF-10A. Src activation causes actin depolymerization via the MEK/Erk/Cofilin cascade. The MEK inhibitor U0126 blocks the inhibitory effect of Src on<em> FAT4</em> mRNA expression and Src-induced actin depolymerization. To determine whether actin dynamics act on the regulation of <em>FAT4</em> mRNA expression, we treated MCF-10A cells with the ROCK inhibitor Y-27632. Y-27632 treatment decreased <em>FAT4</em> mRNA expression. This suppressive effect was blocked by siRNA-mediated knockdown of Cofilin1. Furthermore, simultaneous administration of Latrunculin A (an actin depolymerizing agent), Y-27632, and Cofilin1 siRNA to the cells resulted in a marked reduction of <em>FAT4</em> mRNA expression. Intriguingly, we also found that<em> FAT4</em> mRNA expression was reduced under both low cell density and low stiffness conditions, which suggests that mechanotransduction affects <em>FAT4</em> mRNA expression. Additionally, we show that siRNA-mediated FAT4 knockdown induced the activity of the Hippo effector YAP/TAZ in MCF-10A cells. Taken together, our results reveal a novel inhibitory mechanism of <em>FAT4</em> gene expression through actin depolymerization during Src-induced carcinogenesis in human breast cells.
DOI: 10.6084/m9.figshare.1270464
title: EXTRAVASACIÓN DE QUIMIOTERAPIA VESICANTE, CURA EN AMBIENTE HÚMEDO

description: En la extravasación de un vía venosa periférica parte del líquido infundido sale de la vena y se distribuye por los tejidos. Este hecho que no tiene importancia clínica en la mayoría de los casos se hace especialmente relevante cuando se trata de quimioterapia y más aún si ésta es vesicante. En este caso el fármaco extravasado produce necrosis de los tejidos y aunque se apliquen los antídotos pertinentes pueden producirse úlceras. La variabilidad de las lesiones depende del tipo de fármaco ya que se distribuyen en dos grupos en función del antídoto que precisen. Por otra parte la incidencia de extravasación de citostáticos en total es baja (entre el 0,01-7%) siendo la incidencia de extravasación de vesicantes aún menor. El objetivo de este trabajo es describir un caso y así poder establecer pautas de cura eficaces para un grupo de heridas muy especiales, con una baja incidencia pero con un curso muy agresivo. Para ello hemos hecho el seguimiento de un paciente que acude al hospital 9 días después del tratamiento de quimioterapia con una lesión en el antebrazo izquierdo sugestiva de extravasación tardía de un fármaco vesicante. Tras dos semanas de tratamiento con un total de 7 valoraciones presenciales de la lesión y 4 curas en ambiente húmedo (Hidrogel y espuma de poliuretano) la lesión cicatriza completamente. Por lo tanto, en este caso, la preparación del lecho de la herida y la cura en ambiente húmedo fue suficiente para conseguir la cicatrización completa de la lesión.
DOI: 10.6084/m9.figshare.1270467
title: Tweet DB #profes2014

description: A sqlite db containing tweets tagged as #profes2014
DOI: 10.6084/m9.figshare.1279394.v176
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.
DOI: 10.6084/m9.figshare.1270467.v1
title: Tweet DB #profes2014

description: A sqlite db containing tweets tagged as #profes2014
DOI: 10.6084/m9.figshare.1270469.v1
title: 1000 Backlinks to adobe.com (12-Dec-2014) -- varocarbas.com

description: High quality backlinks to adobe.com. The retrieval process was completed on 12-Dec-2014.
DOI: 10.6084/m9.figshare.1270473.v37
title: Inhibitory mechanism of FAT4 gene expression in response to actin dynamics during Src-induced carcinogenesis

description: Oncogenic transformation is characterized by morphological changes resulting from alterations in actin dynamics and adhesive activities. Emerging evidence suggests that the protocadherin FAT4 acts as a tumor suppressor in humans, and reduced <em>FAT4</em> gene expression has been reported in breast and lung cancers and melanoma. However, the mechanism controlling<em> FAT4</em> gene expression is poorly understood. In this study, we show that transient activation of the Src oncoprotein represses <em>FAT4</em> mRNA expression through actin depolymerization in the immortalized normal human mammary epithelial cell line MCF-10A. Src activation causes actin depolymerization via the MEK/Erk/Cofilin cascade. The MEK inhibitor U0126 blocks the inhibitory effect of Src on<em> FAT4</em> mRNA expression and Src-induced actin depolymerization. To determine whether actin dynamics act on the regulation of <em>FAT4</em> mRNA expression, we treated MCF-10A cells with the ROCK inhibitor Y-27632. Y-27632 treatment decreased <em>FAT4</em> mRNA expression. This suppressive effect was blocked by siRNA-mediated knockdown of Cofilin1. Furthermore, simultaneous administration of Latrunculin A (an actin depolymerizing agent), Y-27632, and Cofilin1 siRNA to the cells resulted in a marked reduction of <em>FAT4</em> mRNA expression. Intriguingly, we also found that<em> FAT4</em> mRNA expression was reduced under both low cell density and low stiffness conditions, which suggests that mechanotransduction affects <em>FAT4</em> mRNA expression. Additionally, we show that siRNA-mediated FAT4 knockdown induced the activity of the Hippo effector YAP/TAZ in MCF-10A cells. Taken together, our results reveal a novel inhibitory mechanism of <em>FAT4</em> gene expression through actin depolymerization during Src-induced carcinogenesis in human breast cells.
DOI: 10.6084/m9.figshare.1270441.v1
title: Gaussian Job Archive for C3H6I2Zn

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1270473.v36
title: Inhibitory mechanism of FAT4 gene expression in response to actin dynamics during Src-induced carcinogenesis

description: Oncogenic transformation is characterized by morphological changes resulting from alterations in actin dynamics and adhesive activities. Emerging evidence suggests that the protocadherin FAT4 acts as a tumor suppressor in humans, and reduced <em>FAT4</em> gene expression has been reported in breast and lung cancers and melanoma. However, the mechanism controlling<em> FAT4</em> gene expression is poorly understood. In this study, we show that transient activation of the Src oncoprotein represses <em>FAT4</em> mRNA expression through actin depolymerization in the immortalized normal human mammary epithelial cell line MCF-10A. Src activation causes actin depolymerization via the MEK/Erk/Cofilin cascade. The MEK inhibitor U0126 blocks the inhibitory effect of Src on<em> FAT4</em> mRNA expression and Src-induced actin depolymerization. To determine whether actin dynamics act on the regulation of <em>FAT4</em> mRNA expression, we treated MCF-10A cells with the ROCK inhibitor Y-27632. Y-27632 treatment decreased <em>FAT4</em> mRNA expression. This suppressive effect was blocked by siRNA-mediated knockdown of Cofilin1. Furthermore, simultaneous administration of Latrunculin A (an actin depolymerizing agent), Y-27632, and Cofilin1 siRNA to the cells resulted in a marked reduction of <em>FAT4</em> mRNA expression. Intriguingly, we also found that<em> FAT4</em> mRNA expression was reduced under both low cell density and low stiffness conditions, which suggests that mechanotransduction affects <em>FAT4</em> mRNA expression. Additionally, we show that siRNA-mediated FAT4 knockdown induced the activity of the Hippo effector YAP/TAZ in MCF-10A cells. Taken together, our results reveal a novel inhibitory mechanism of <em>FAT4</em> gene expression through actin depolymerization during Src-induced carcinogenesis in human breast cells.
DOI: 10.6084/m9.figshare.1279394.v177
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.
DOI: 10.6084/m9.figshare.1279394.v178
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.
DOI: 10.6084/m9.figshare.1270406
title: LTSTM data from January 2004

description: This is low temperature STM data from January 2004.
DOI: 10.6084/m9.figshare.1270395
title: LTSTM data from Dec 2003

description: This is low temperature STM data from December 2003
DOI: 10.6084/m9.figshare.1270413.v1
title: Paton Group Poster 2011-12

description: UNDERSTANDING STRUCTURE, REACTIVITY & SELECTIVITY Based at the University of Oxford, the Paton Group uses computation to solve problems in organic and bio-organic chemistry. Trial-and-error is replaced by rational design to aid and enhance chemical synthesis.
DOI: 10.6084/m9.figshare.1270384
title: Gaussian Job Archive for C3H6I2Zn

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1270395.v1
title: LTSTM data from Dec 2003

description: This is low temperature STM data from December 2003
DOI: 10.6084/m9.figshare.1270406.v1
title: LTSTM data from January 2004

description: This is low temperature STM data from January 2004.
DOI: 10.6084/m9.figshare.1279394.v179
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.
DOI: 10.6084/m9.figshare.1279394.v180
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.
DOI: 10.6084/m9.figshare.1270363
title: Abundance and Activity of 16S rRNA, <i>AmoA</i> and <i>NifH</i> Bacterial Genes During Assisted Phytostabilization of Mine Tailings

description: Mine tailings in semiarid regions are highly susceptible to erosion and are sources of dust pollution and potential avenues of human exposure to toxic metals. One constraint to revegetation of tailings by phytostabilization is the absence of microbial communities critical for biogeochemical cycling of plant nutrients. The objective of this study was to evaluate specific genes as <i>in situ</i> indicators of biological soil response during phytoremediation. The abundance and activity of 16S rRNA, <i>nifH</i>, and <i>amoA</i> were monitored during a nine month phytostabilization study using buffalo grass and quailbush grown in compost-amended, metalliferous tailings. The compost amendment provided a greater than 5-log increase in bacterial abundance, and survival of this compost-inoculum was more stable in planted treatments. Despite increased abundance, the activity of the introduced community was low, and significant increases were not detected until six and nine months in quailbush, and unplanted compost and buffalo grass treatments, respectively. In addition, increased abundances of nitrogen-fixation <i>(nifH)</i> and ammonia-oxidizing <i>(amoA)</i> genes were observed in rhizospheres of buffalo grass and quailbush, respectively. Thus, plant establishment facilitated the short term stabilization of introduced bacterial biomass and supported the growth of two key nitrogen-cycling populations in compost-amended tailings.
DOI: 10.6084/m9.figshare.1279394.v181
title: Early ovariectomy reveals a non-somatic origin of the mammalian anti-A-reactive IgM that reflects developmental malignancy.

description: The germline encoding of a non-immune immunoglobulin M (IgM) molecule in mammals was experimentally documented for the first time as a result of the specifically timed ovariectomy of C57BL/10 mice. The target of this innate antibody involves a trans-species developmental antigen that signifies malignancy when expressed in any non-developmental tissue. Although ovariectomy and castration result in uncontrolled and/or enhanced humoral and cellular immunity involving increased weights of the spleen and thymus with pronounced B and T cell production, the development of mercaptoethanol-sensitive, complement-binding, non-immune anti-A reactivity in murine plasma was not enhanced after an ovariectomy that was performed in C57BL/10 mice prior to the onset of puberty. This non-immune murine anti-A, which is complementary to the trans-species, syngeneic ovarian GalNAc-glycan-bearing glycolipids and distinct from the cross-reactive adaptive anti-A antibody, was strongly downregulated or did not appear in plasma of animals ovariectomized at the age of 20 days. Thus, contrary to our previous view, this reactivity is unlikely to originate from a somatic, primary immune or autoimmune response. All of the murine tissues expressed the species-specific Forssman<i> </i>reactivity, and further A-like structures were identified in the male and female reproductive and endodermal organs by reaction with innate human anti-A antibody, while the murine anti-A was exclusively inhibited by syngeneic ovarian glycolipids. Moreover, the early ovarian tissue, which represents a last evolutionary and/or developmental location, showed a developmental polymorphism characterized by reactivity to the lectin from <i>Dolichos biflorus</i> and the agglutinin from <i>Helix pomatia </i>indicating the functional involvement of the <i>O</i>-GalNAc-determined mucin-type A-like, Tn- and Thomsen-Friedenreich (TF) epitopes that signify malignancy when accumulated and expressed in non-developmental tissues.