Friend or foe? Using eye-tracking technology to investigate the visual discrimination ability of giant pandas
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PROVIDER: S-EPMC11336681 | biostudies-literature | 2023 May
REPOSITORIES: biostudies-literature
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Project description:The impact of invasion on diversity varies widely and remains elusive. Despite the considerable attempts to understand mechanisms of biological invasion, it is largely unknown whether some communities' characteristics promote biological invasion, or whether some inherent characteristics of invaders enable them to invade other communities. Our aims were to assess the impact of one of the massive plant invaders of Scandinavia on vascular plant species diversity, disentangle attributes of invasible and noninvasible communities, and evaluate the relationship between invasibility and genetic diversity of a dominant invader. We studied 56 pairs of Heracleum persicum Desf. ex Fisch.-invaded and noninvaded plots from 12 locations in northern Norway. There was lower native cover, evenness, taxonomic diversity, native biomass, and species richness in the invaded plots than in the noninvaded plots. The invaded plots had nearly two native species fewer than the noninvaded plots on average. Within the invaded plots, cover of H. persicum had a strong negative effect on the native cover, evenness, and native biomass, and a positive association with the height of the native plants. Plant communities containing only native species appeared more invasible than those that included exotic species, particularly H. persicum. Genetic diversity of H. persicum was positively correlated with invasibility but not with community diversity. The invasion of a plant community by H. persicum exerts consistent negative pressure on vascular plant diversity. The lack of positive correlation between impacts and genetic diversity of H. persicum indicates that even a small founder population may cause high impact. We highlight community stability or saturation as an important determinant of invasibility. While the invasion by H. persicum may decrease susceptibility of a plant community to further invasion, it severely reduces the abundance of native species and makes them more vulnerable to competitive exclusion.
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Project description:The PGC1 family (Peroxisome proliferator-activated receptor γ (PPARγ) coactivators) of transcriptional coactivators are considered master regulators of mitochondrial biogenesis and function. The PGC1α isoform is expressed especially in metabolically active tissues, such as the liver, kidneys and brain, and responds to energy-demanding situations. Given the altered and highly adaptable metabolism of tumor cells, it is of interest to investigate PGC1α in cancer. Both high and low levels of PGC1α expression have been reported to be associated with cancer and worse prognosis, and PGC1α has been attributed with oncogenic as well as tumor suppressive features. Early in carcinogenesis PGC1α may be downregulated due to a protective anticancer role, and low levels likely reflect a glycolytic phenotype. We suggest mechanisms of PGC1α downregulation and how these might be connected to the increased cancer risk that obesity is now known to entail. Later in tumor progression PGC1α is often upregulated and is reported to contribute to increased lipid and fatty acid metabolism and/or a tumor cell phenotype with an overall metabolic plasticity that likely supports drug resistance as well as metastasis. We conclude that in cancer PGC1α is neither friend nor foe, but rather the obedient servant reacting to metabolic and environmental cues to benefit the tumor cell.
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Project description:The role of fibronectin (FN) in tumorigenesis and malignant progression has been highly controversial. Cancerous FN plays a tumor-suppressive role, whereas it is pro-metastatic and associated with poor prognosis. Interestingly, FN matrix deposited in the tumor microenvironments (TMEs) promotes tumor progression but is paradoxically related to a better prognosis. Here, we justify how FN impacts tumor transformation and subsequently metastatic progression. Next, we try to reconcile and rationalize the seemingly conflicting roles of FN in cancer and TMEs. Finally, we propose future perspectives for potential FN-based therapeutic strategies.
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Project description:ARID1A belongs to a class of chromatin regulatory proteins that function by maintaining accessibility at most promoters and enhancers, thereby regulating gene expression. The high frequency of ARID1A alterations in human cancers has highlighted its significance in tumorigenesis. The precise role of ARID1A in cancer is highly variable since ARID1A alterations can have a tumor suppressive or oncogenic role, depending on the tumor type and context. ARID1A is mutated in about 10% of all tumor types including endometrial, bladder, gastric, liver, biliopancreatic cancer, some ovarian cancer subtypes, and the extremely aggressive cancers of unknown primary. Its loss is generally associated with disease progression more often than onset. In some cancers, ARID1A loss is associated with worse prognostic features, thus supporting a major tumor suppressive role. However, some exceptions have been reported. Thus, the association of ARID1A genetic alterations with patient prognosis is controversial. However, ARID1A loss of function is considered conducive for the use of inhibitory drugs which are based on synthetic lethality mechanisms. In this review we summarize the current knowledge on the role of ARID1A as tumor suppressor or oncogene in different tumor types and discuss the strategies for treating ARID1A mutated cancers.
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Project description:Jun/JUN is a basic leucine zipper (bZIP) protein and a prototypic member of the activator protein-1 (AP-1) family of transcription factors that can act as homo- or heterodimers, interact with DNA elements and co-factors, and regulate gene transcription. Jun is expressed by both immune and inflammatory cells. Jun is traditionally seen as an oncoprotein that regulates processes involved in transformation and oncogenesis in human tumours. This article examines the traditional view that Jun plays a permissive role in cancer development and progression, whilst exploring emerging evidence supporting Jun's potential to prevent immune cell exhaustion and promote anti-tumour efficacy.
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Project description:Aggregation of misfolded microtubule associated protein tau into abnormal intracellular inclusions defines a class of neurodegenerative diseases known as tauopathies. The consistent spatiotemporal progression of tau pathology in Alzheimer's disease (AD) led to the hypothesis that tau aggregates spread in the brain via bioactive tau "seeds" underlying advancing disease course. Recent studies implicate microglia, the resident immune cells of the central nervous system, in both negative and positive regulation of tau pathology. Polymorphisms in genes that alter microglial function are associated with the development of AD and other tauopathies. Experimental manipulation of microglia function can alter tau pathology and microglia-mediated neuroinflammatory cascades can exacerbate tau pathology. Microglia also exert protective functions by mitigating tau spread: microglia internalize tau seeds and have the capacity to degrade them. However, when microglia fail to degrade these tau seeds there are deleterious consequences, including secretion of exosomes containing tau that can spread to neurons. This review explores the intersection of microglia and tau from the perspective of neuropathology, neuroimaging, genetics, transcriptomics, and molecular biology. As tau-targeted therapies such as anti-tau antibodies advance through clinical trials, it is critical to understand the interaction between tau and microglia.
| S-EPMC9378545 | biostudies-literature
Project description:Current evidence strongly suggests that aberrant activation of the NF-κB signalling pathway is associated with carcinogenesis. A number of key cellular processes are governed by the effectors of this pathway, including immune responses and apoptosis, both crucial in the development of cancer. Therefore, it is not surprising that dysregulated and chronic NF-κB signalling can have a profound impact on cellular homeostasis. Here we discuss NFKB1 (p105/p50), one of the five subunits of NF-κB, widely implicated in carcinogenesis, in some cases driving cancer progression and in others acting as a tumour-suppressor. The complexity of the role of this subunit lies in the multiple dimeric combination possibilities as well as the different interacting co-factors, which dictate whether gene transcription is activated or repressed, in a cell and organ-specific manner. This review highlights the multiple roles of NFKB1 in the development and progression of different cancers, and the considerations to make when attempting to manipulate NF-κB as a potential cancer therapy.
| S-EPMC6162711 | biostudies-literature
Project description:BackgroundA higher chemotherapy completion rate is associated with better outcomes including treatment efficacy and overall survival. Exercise may have the potential to improve relative dose intensity (RDI) by reducing the frequency and severity of chemotherapy-related toxicities. We examined the association between exercise adherence and RDI and possible clinical- and health-related fitness predictors of RDI.MethodsChemotherapy records were extracted from the electronic medical record for patients enrolled in the ENACT trial (n = 105). Chemotherapy completion was assessed using average RDI. A threshold of 85% was established for "high" versus "low" RDI. Logistic regression analyses were used to estimate the associations between the clinical- and health-related fitness predictors of RDI.ResultsPatients with breast cancer (BC) had a significantly higher average RDI (89.8% ± 17.6%) compared with gastrointestinal cancer (GI) (76.8% ± 20.9%, p = 0.004) and pancreatic cancer (PC) (65.2% ± 20.1%, p < 0.001). Only 25% of BC patents required a dose reduction compared to 56.3% of GI and 86.4% of PC patients. Cancer site was significantly associated with RDI. Compared with BC, patients with GI (β = -0.12, p = 0.03) and PC (β = -0.22, p = 0.006) achieved significantly lower RDI. Every 2.72 unit increase in overall exercise adherence led to a significant 7% decrease in RDI (p = 0.001) in GI patients. Metastatic GI patients had a 15% RDI increase for every 2.72 unit increase in exercise adherence (p = 0.04).ConclusionExercise is a supportive therapy that has potential to enhance chemotherapy tolerance and completion. The relationship between exercise adherence and RDI is influenced by factor such as cancer site and treatment type. Special attention must be paid to how exercise is prescribed to ensure that exercise adherence does not negatively affect RDI. Cancer site, exercise dosage, and multimodal interventions to address toxicities are key areas identified for future research.
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