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  • 1
    Abstract: Memories about sensory experiences are tightly linked to the context in which they were formed. Memory contextualization is fundamental for the selection of appropriate behavioral reactions needed for survival, yet the underlying neuronal circuits are poorly understood. By combining trans-synaptic viral tracing and optogenetic manipulation, we found that the ventral hippocampus (vHC) and the amygdala, two key brain structures encoding context and emotional experiences, interact via multiple parallel pathways. A projection from the vHC to the basal amygdala mediates fear behavior elicited by a conditioned context, whereas a parallel projection from a distinct subset of vHC neurons onto midbrain-projecting neurons in the central amygdala is necessary for context-dependent retrieval of cued fear memories. Our findings demonstrate that two fundamentally distinct roles of context in fear memory retrieval are processed by distinct vHC output pathways, thereby allowing for the formation of robust contextual fear memories while preserving context-dependent behavioral flexibility.
    Type of Publication: Journal article published
    PubMed ID: 27773481
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  • 2
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; INHIBITOR ; IONIZING-RADIATION ; tumor ; AGENTS ; CELL ; Germany ; tumor growth ; DEATH ; NEW-YORK ; PROTEIN ; PROTEINS ; radiation ; DNA ; IMPACT ; DOWN-REGULATION ; MUTANT ; PROGRESSION ; MALIGNANCIES ; resistance ; CELL-DEATH ; INDUCED APOPTOSIS ; EFFICIENT ; p53 ; PATHOGENESIS ; DAMAGE ; REGION ; REGIONS ; DNA-DAMAGE ; CISPLATIN ; CHILDREN ; GLIOMAS ; MULTIFORME ; TP53 ; AGENT ; MALIGNANCY ; ONCOLOGY ; TUMOR-SUPPRESSOR ; TUMOR-GROWTH ; GLIOMA ; GLIOMA-CELLS ; MALIGNANT GLIOMA ; MALIGNANT GLIOMAS ; GRADE ; LEVEL ; HISTONE DEACETYLASE INHIBITORS ; cell death ; DNA damage ; PHASE ; SUPPRESSOR ; glioblastoma multiforme ; GLIOBLASTOMA-MULTIFORME ; USA ; HUMAN BRAIN-TUMORS ; GLIOBLASTOMA ; PROMOTES ; correlates ; response ; SIRNA ; tumor suppressor ; CORRELATE ; TRANSIT ; DNA-DAMAGE-RESPONSE ; sensitize ; GENE ING1 ; ING1 isoforms ; P33(ING1) ; PLANT HOMEODOMAIN
    Abstract: Impaired tumor suppressor functions, such as deficient p53, are characteristic for glioblastoma multiforme (GBM) and can cause resistance to DNA-damaging agents like cisplatin. We have recently shown that the INhibitor of Growth 1 (ING1) tumor suppressor is down-regulated in malignant gliomas and that the decrease of ING1 expression correlates with histological grade of malignancy, suggesting a role for ING1 in the pathogenesis and progression of malignant gliomas. Based on this background, the purpose of our current study was to examine the potential impact of ING1 protein levels on DNA-damage response in GBM. Using LN229 GBM cells, which express ING1 proteins and harbor mutant TP53, we are the first to show that DNA damage by cisplatin or ionizing radiation differentially induced the two major ING1 splicing isoforms. The p47(ING1a) supercript stop isoform, that promotes deacetylation of histones, thus formation of heterochromatic regions of DNA, which are less susceptible to DNA damage, was preferentially induced by 〉 50-fold. This might represent a response to protect DNA from damage. Also, ING1 knockdown by siRNA accelerated transit of cells through G(1) phase, consistent with ING1 serving a tumor suppressor function, and caused cells to enter apoptosis more rapidly in response to cisplatin. Our results indicate that malignant gliomas may down-regulate ING1 to allow more efficient tumor growth and progression. Also, ING1 down-regulation may sensitize GBM cells with deficient p53 to treatment with cisplatin
    Type of Publication: Journal article published
    PubMed ID: 17763999
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  • 3
    ISSN: 1432-1076
    Keywords: Total body bone mineral ; Mineralisation ; Male puberty
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The bone mineral content of the distal forearm (BMC) using single-photon absorptiometry and total body bone mineral (TBBM) using dual-photon absorptiometry were determined in 19 normal boys at different pubertal stages. A highly significant correlation between BMC and TBBM was seen (r=0.78, P〈0.001) with a standard error of estimate (SEE) of 13%. Subgroups of early and late pubertal stages did not show any significant differences in the regression lines indicating an identical relationship between BMC and TBBM at various stages of pubertal development although great changes in bone mineral content take place. Due to high accuracy and reproducibility of both methods, which are non-invasive and harmless, measurement of BMC is suitable to estimate changes in total mineral content of the body. This may be of importance in various diseases with disturbance in growth and bone metabolism.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1076
    Keywords: Cushing syndrome ; Primary adrenocortical nodular dysplasia ; Adrenal stimulating immunoglobulins ; Autoimmune involvement ; Familial occurrence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cushing syndrome due to primary adrenocortical nodular dysplasia was diagnosed in two patients, aged 3 years 9 months and 9.5 years. Subsequently, adrenalectomy was performed and followed by steroid replacement. In both cases, the adrenals were normal or only slightly enlarged and showed adrenocortical nodular dysplasia histologically. Small lymphocytic infiltrates consisting of T-cells and class II MHC positive macrophages were present in adrenal specimens of both the patients. Samples of protein A sepharose purified serum immunoglobulins from both children stimulated adrenocortical DNA synthesis and cortisol production in cultured guinea-pig adrenal segments in vitro in a dose dependent fashion. Adrenal stimulating immunoglobulins were also demonstrated in serum specimens of both patients' mothers. However, none of them had overt signs of adrenal disease. Our data support the view that autoimmune mechanisms may be involved in primary adrenocortical nodular dysplasia.
    Type of Medium: Electronic Resource
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