26 research outputs found
Testosterone Amplifies the Negative Valence of an Agonistic Gestural Display by Exploiting Receiver Perceptual Bias
Many animals communicate by performing elaborate displays that are incredibly extravagant and wildly bizarre. So, how do these displays evolve? One idea is that innate sensory biases arbitrarily favour the emergence of certain display traits over others, leading to the design of an unusual display. Here, we study how physiological factors associated with signal production influence this process, a topic that has received almost no attention. We focus on a tropical frog, whose males compete for access to females by performing an elaborate waving display. Our results show that sex hormones like testosterone regulate specific display gestures that exploit a highly conserved perceptual system, evolved originally to detect \u27dangerous\u27 stimuli in the environment. Accordingly, testosterone makes certain gestures likely to appear more perilous to rivals during combat. This suggests that hormone action can interact with effects of sensory bias to create an evolutionary optimum that guides how display exaggeration unfolds
Epidemiology and Characteristics of Gastric Carcinoma in Childhood : An Analysis of Data from Population-Based and Clinical Cancer Registries
(1) Background: Gastric carcinoma is an exceptionally rare tumor in childhood. Little is
known about the etiology, epidemiology, and clinical features of pediatric gastric carcinomas. This
analysis aimed to fill this gap by increasing knowledge about the occurrence of gastric carcinoma in
childhood. (2) Material and methods: Data from gastric carcinoma cases diagnosed between 2000
and 2017/2018 were retrieved from the Surveillance, Epidemiology, and End Results Program (SEER)
and the German Center for Cancer Registry Data. Data from patients <20 years of age were analyzed
for patient- and tumor-related characteristics. In addition, clinical data from patients with gastric
carcinoma registered in the German Registry for Rare Pediatric Tumors (STEP) were analyzed for
diagnostics, therapy, and outcome. (3) Results: Ninety-one cases of gastric carcinoma, mainly in
adolescents, were identified in the epidemiologic cancer registries. Among patients with recorded
staging data, advanced tumor stages were common (66.7%). Within the follow-up period covered,
63.7% of patients with clinical follow-up data died. Eight pediatric patients with gastric carcinoma
were enrolled in the STEP registry, among whom two were patients with hereditary CDH1 mutations
and another was a patient with PeutzâJeghers syndrome. Three patients were found to have distinctly
decreased immunoglobulin concentrations. All four patients in whom complete resection was
achieved remained in remission. Three of the other four patients died despite multimodal therapy. (4) Conclusions: A combination of Helicobacter pylori infection and tumor predisposition and/or
immunodeficiency appears to promote the development of gastric carcinoma in childhood. While
patients with localized disease stages have a good chance of achieving durable remission through
complete resection, patients with stage IV carcinomas face a dismal prognosis, highlighting the need
to develop new strategies such as mutation-guided treatments
Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation.
Anaplastic large cell lymphoma (ALCL) is a rare, aggressive, non-Hodgkin's lymphoma that is characterized by CD30 expression and disease onset in young patients. About half of ALCL patients bear the t(2;5)(p23;q35) translocation, which results in the formation of the nucleophosmin-anaplastic lymphoma tyrosine kinase (NPM-ALK) fusion protein (ALCL ALK(+)). However, little is known about the molecular features and tumour drivers in ALK-negative ALCL (ALCL ALK(-)), which is characterized by a worse prognosis. We found that ALCL ALK(-), in contrast to ALCL ALK(+), lymphomas display high miR-155 expression. Consistent with this, we observed an inverse correlation between miR-155 promoter methylation and miR-155 expression in ALCL. However, no direct effect of the ALK kinase on miR-155 levels was observed. Ago2 immunoprecipitation revealed miR-155 as the most abundant miRNA, and enrichment of target mRNAs C/EBPÎČ and SOCS1. To investigate its function, we over-expressed miR-155 in ALCL ALK(+) cell lines and demonstrated reduced levels of C/EBPÎČ and SOCS1. In murine engraftment models of ALCL ALK(-), we showed that anti-miR-155 mimics are able to reduce tumour growth. This goes hand-in-hand with increased levels of cleaved caspase-3 and high SOCS1 in these tumours, which leads to suppression of STAT3 signalling. Moreover, miR-155 induces IL-22 expression and suppresses the C/EBPÎČ target IL-8. These data suggest that miR-155 can act as a tumour driver in ALCL ALK(-) and blocking miR-155 could be therapeutically relevant. Original miRNA array data are to be found in the supplementary material (Table S1).This work was supported by the SCRI-LIMCR GmbH, the âJubilĂ€umsfond der Ăsterreichischen Nationalbankâ (grant-no. 14856 to O.M.), R.G. was supported by grant SFB P021 from the Austrian Science Funds (FWF), L.K. was supported by grant FWF, P26011, R.M. was supported by FWF grants SFB F28 and SFB F47. S.D.T. is a Senior Lecturer supported with funding from Leukemia and Lymphoma Research.This is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1002/path.453
Die Funktion des Ehebruchs in ausgewÀhlten MÀren des Mittelalters
Diese Forschungsarbeit widmet sich der Funktion des Ehebruchs in neun ausgewaÌhlten MaÌren des Mittelalters, die im Zeitraum von etwa 1250 bis 1500 entstanden sind. Ein gattungsgeschichtlicher UÌberblick, der nennenswerte Forschungsliteratur beruÌcksichtigt, zeigt zunaÌchst die unterschiedlichen Gestaltungsvarianten einer Ehebruchssituation im MaÌre und wie das erzaÌhlerische Potential, das diesem Motiv innewohnt, zu Unterhaltungszwecken oder unter dem Aspekt einer glaubhaften Verhaltenslehre fuÌr den Rezipienten genutzt werden kann. Die daran anschlieĂende Textanalyse zielt darauf ab, konkrete Varianten der Thematik in den neun ausgewaÌhlten MaÌren herauszuarbeiten und den jeweiligen Ehebruch auf seine moÌgliche Funktion zu untersuchen. Die sich daraus ergebenden thematischen ZusammenhaÌnge und einige wiederkehrende Handlungselemente werden im letzten Teil der Arbeit eroÌrtert und die ausgewaÌhlten MaÌren des Textkorpus dadurch erneut miteinander verglichen
Epidemiology and Characteristics of Gastric Carcinoma in Childhood-An Analysis of Data from Population-Based and Clinical Cancer Registries
Hypoxia Inducible Lipid Droplet Associated protein inhibits Adipose Triglyceride Lipase.
Elaborate control mechanisms of intracellular triacylglycerol (TAG) breakdown are critically involved in the maintenance of energy homeostasis. Hypoxia inducible lipid droplet associated protein (HILPDA)/Hypoxia inducible gene-2 (Hig-2) has been shown to affect intracellular TAG levels, yet, the underlying molecular mechanisms are unclear. Here, we show that HILPDA inhibits adipose triglyceride lipase (ATGL), the enzyme catalyzing the first step of intracellular TAG hydrolysis. HILPDA shares structural similarity with G0/G1 switch gene 2 (G0S2), an established inhibitor of ATGL. HILPDA inhibits ATGL activity in a dose-dependent manner with an IC50 value of 2 M. ATGL inhibition depends on the direct physical interaction of both proteins and involves the N- terminal, hydrophobic region of HILPDA and the N-terminal, patatin-domain containing segment of ATGL. Finally, confocal microscopy combined with Foerster resonance energy transfer-fluorescence lifetime imaging microscopy (FRET-FLIM) analysis indicated that HILPDA and ATGL colocalize and physically interact intracellularly. These findings provide a rational biochemical explanation for the tissue-specific increased TAG accumulation in HILPDA overexpressing transgenic mouse models
Epidemiology and Characteristics of Gastric Carcinoma in Childhood—An Analysis of Data from Population-Based and Clinical Cancer Registries
(1) Background: Gastric carcinoma is an exceptionally rare tumor in childhood. Little is known about the etiology, epidemiology, and clinical features of pediatric gastric carcinomas. This analysis aimed to fill this gap by increasing knowledge about the occurrence of gastric carcinoma in childhood. (2) Material and methods: Data from gastric carcinoma cases diagnosed between 2000 and 2017/2018 were retrieved from the Surveillance, Epidemiology, and End Results Program (SEER) and the German Center for Cancer Registry Data. Data from patients <20 years of age were analyzed for patient- and tumor-related characteristics. In addition, clinical data from patients with gastric carcinoma registered in the German Registry for Rare Pediatric Tumors (STEP) were analyzed for diagnostics, therapy, and outcome. (3) Results: Ninety-one cases of gastric carcinoma, mainly in adolescents, were identified in the epidemiologic cancer registries. Among patients with recorded staging data, advanced tumor stages were common (66.7%). Within the follow-up period covered, 63.7% of patients with clinical follow-up data died. Eight pediatric patients with gastric carcinoma were enrolled in the STEP registry, among whom two were patients with hereditary CDH1 mutations and another was a patient with Peutz–Jeghers syndrome. Three patients were found to have distinctly decreased immunoglobulin concentrations. All four patients in whom complete resection was achieved remained in remission. Three of the other four patients died despite multimodal therapy. (4) Conclusions: A combination of Helicobacter pylori infection and tumor predisposition and/or immunodeficiency appears to promote the development of gastric carcinoma in childhood. While patients with localized disease stages have a good chance of achieving durable remission through complete resection, patients with stage IV carcinomas face a dismal prognosis, highlighting the need to develop new strategies such as mutation-guided treatments
European larch sapwood: A model for predicting the cambial age and for a more accurate dating
International audienceEuropean larch (Larix decidua Mill.) holds significant importance as a forest tree species throughout the Alps and in certain regions of central Europe. Its extensive use as construction timber has made it a subject of substantial interest in dendroarchaeological studies aimed at understanding the long-term interactions between human societies and forests. Precise dating of felling phases, accurate estimation of the age of harvested wood, and information on the geographical origin of wood play a crucial role when it comes to characterize these interactions. In this study, we compiled a large dataset of L. decidua samples from across the European Alps to provide a robust statistical model that predicts the cambial age of L. decidua trees based on the number of heartwood rings. By extension, this model can be used to estimate the number of sapwood rings so as to approximate the felling date and to more precise date archaeological larch timber. The model requires almost complete heartwood sequences (<5 missing rings) to achieve accurate estimations. Our results also evidence that the ratio between the number of sapwood and heartwood rings varies across the Alps. At the same time, the indicator developed in this work is not suitable for a determination of wood origin, raising doubts about the effectiveness of attempts aimed at dendroprovenancing L. decidua based on sapwood
Hypoxia-inducible lipid droplet-associated protein inhibits adipose triglyceride lipase
Elaborate control mechanisms of intracellular triacylglycerol (TAG) breakdown are critically involved in the maintenance of energy homeostasis. Hypoxia-inducible lipid droplet-associated protein (HILPDA)/hypoxia-inducible gene-2 (Hig-2) has been shown to affect intracellular TAG levels, yet, the underlying molecular mechanisms are unclear. Here, we show that HILPDA inhibits adipose triglyceride lipase (ATGL), the enzyme catalyzing the first step of intracellular TAG hydrolysis. HILPDA shares structural similarity with G0/G1 switch gene 2 (G0S2), an established inhibitor of ATGL. HILPDA inhibits ATGL activity in a dose-dependent manner with an IC50 value of âŒ2 ÎŒM. ATGL inhibition depends on the direct physical interaction of both proteins and involves the N-terminal hydrophobic region of HILPDA and the N-terminal patatin domain-containing segment of ATGL. Finally, confocal microscopy combined with Förster resonance energy transfer-fluorescence lifetime imaging microscopy analysis indicated that HILPDA and ATGL colocalize and physically interact intracellularly. These findings provide a rational biochemical explanation for the tissue-specific increased TAG accumulation in HILPDA-overexpressing transgenic mouse models