Friend or foe: high bone mineral density on routine bone density scanning, a review of causes and management.
Ontology highlight
ABSTRACT:
SUBMITTER: Gregson CL
PROVIDER: S-EPMC3651616 | biostudies-literature | 2013 Jun
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:IntroductionRecent advances in technology have seen the introduction of remote scanning capabilities become a reality for departments, allowing staff to remotely access, observe and even scan without being by the scanner side. The COVID-19 pandemic has accelerated use of remote working which also aligns with the direction of travel for healthcare more widely. However for technology to succeed it needs to be acceptable for use by radiographers in clinical practice.MethodsFollowing trial of a remote scanning technology, a group of radiographers were surveyed for their views on its use in practice. The survey was based on the Technology Acceptance Model as well as providing opportunity for open feedback on views regarding the technology.ResultsPerceived ease of use was high but appears to have little influence over overall intention to use. Perceived usefulness was lower and demonstrated correlations with attitude towards and intended use of the remote technology, suggesting that this is a key area to address which would positively impact on acceptance. Other considerations that would help support effective implementation were highlighted with the majority stating the technology as friend rather than foe.ConclusionAs an early evaluation of practitioner views on remote scanning within MRI, the results highlight the areas that would benefit from further development before further roll out in practice. A clear vision of its use and robust governance is needed to effectively support its implementation and acceptance by radiographers.Implications for practiceIntroducing remote scanning technology has potential to support training and share skills of experienced radiographers across multiple locations. It has the potential to transform the way MRI departments work and increase safer supervision to enable wider utilization of the support workforce.
| S-EPMC10073644 | biostudies-literature
Project description:OBJECTIVE:Dual-energy X-ray absorptiometry (DXA)-derived bone mineral density (BMD) often fails to predict fragility fractures. Quantitative textural analysis using magnetic resonance imaging (MRI) may potentially yield useful radiomic features to predict fractures. We aimed to investigate the correlation between BMD and texture attributes (TAs) extracted from MRI scans and the interobserver reproducibility of the analysis. METHODS:Forty-nine volunteers underwent lumbar spine 1.5-T MRI and DXA. Three-dimensional (3-D) gray-level co-occurrence matrices were measured from routine sagittal T2 fast spin-echo images using the IBEX software. Twenty-two TAs were extracted from 3-D segmented L3 vertebrae. The estimated concordance coefficient was calculated using linear regression analysis. A Pearson correlation coefficient analysis was performed to evaluate the correlation between BMD and the TAs. Interobserver reproducibility was assessed with the concordance coefficient described by Lin. RESULTS:The results revealed a fair-to-moderate significant correlation between BMD and 13 TAs (r=-0.20 to 0.39; p<0.05). Eight TAs (autocorrelation, energy, homogeneity 1, homogeneity 1.1, maximum probability, sum average, sum variance, and inverse difference normalized) negatively correlated with BMD (r=-0.20 to -0.38; p<0.05), whereas five TAs (dissimilarity, difference entropy, entropy, sum entropy, and information measure corr 1) positively correlated with BMD (r=0.29-0.39; p<0.05). The interobserver agreement was almost perfect for all significant TAs (95% confidence interval, 0.92-1.00; p<0.05). CONCLUSION:Specific TAs could be reliably extracted from routine MRI and correlated with BMD. Our results encourage future evaluation of the potential usefulness of quantitative texture measurements from MRI scans for predicting fragility fractures.
| S-EPMC7442400 | biostudies-literature
Project description:The presence of arterial media calcification, a highly complex and multifactorial disease, puts patients at high risk for developing serious cardiovascular consequences and mortality. Despite the numerous insights into the mechanisms underlying this pathological mineralization process, there is still a lack of effective treatment therapies interfering with the calcification process in the vessel wall. Current anti-calcifying therapeutics may induce detrimental side effects at the level of the bone, as arterial media calcification is regulated in a molecular and cellular similar way as physiological bone mineralization. This especially is a complication in patients with chronic kidney disease and diabetes, who are the prime targets of this pathology, as they already suffer from a disturbed mineral and bone metabolism. This review outlines recent treatment strategies tackling arterial calcification, underlining their potential to influence the bone mineralization process, including targeting vascular cell transdifferentiation, calcification inhibitors and stimulators, vascular smooth muscle cell (VSMC) death and oxidative stress: are they a friend or foe? Furthermore, this review highlights nutritional additives and a targeted, local approach as alternative strategies to combat arterial media calcification. Paving a way for the development of effective and more precise therapeutic approaches without inducing osseous side effects is crucial for this highly prevalent and mortal disease.
| S-EPMC9027727 | biostudies-literature
Project description: Not available
| S-EPMC1124002 | biostudies-literature
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.
| S-EPMC7016990 | biostudies-literature
Project description:Current evidence strongly suggests that aberrant activation of the NF-?B 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-?B signalling can have a profound impact on cellular homeostasis. Here we discuss NFKB1 (p105/p50), one of the five subunits of NF-?B, 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-?B as a potential cancer therapy.
| S-EPMC6162711 | biostudies-literature
Project description:The PGC1 family (Peroxisome proliferator-activated receptor ? (PPAR?) coactivators) of transcriptional coactivators are considered master regulators of mitochondrial biogenesis and function. The PGC1? 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 PGC1? in cancer. Both high and low levels of PGC1? expression have been reported to be associated with cancer and worse prognosis, and PGC1? has been attributed with oncogenic as well as tumor suppressive features. Early in carcinogenesis PGC1? may be downregulated due to a protective anticancer role, and low levels likely reflect a glycolytic phenotype. We suggest mechanisms of PGC1? downregulation and how these might be connected to the increased cancer risk that obesity is now known to entail. Later in tumor progression PGC1? 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 PGC1? is neither friend nor foe, but rather the obedient servant reacting to metabolic and environmental cues to benefit the tumor cell.
| S-EPMC5793199 | biostudies-literature
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:The prevalence and incidence of cancers has risen over the last decade. Available treatments have improved outcomes, yet mortality and morbidity remain high, creating an urgent demand for personalized and new therapy targets. Interferon induced transmembrane protein (IFITM3) is highly expressed in cancers and is a marker of poor prognosis. In this review, we discuss recent advances in IFITM3 biology, the regulatory pathways, and its function within cancer as part of immunity and maintaining stemness. Overexpression of IFITM3 is likely an indirect effect of ongoing inflammation, immune and cancer epithelial-to-mesenchymal (EMT) related pathways i.e., interferons, TGF-β, WNT/β-catenin, etc. However, IFITM3 also influences tumorigenic phenotypes, such as cell proliferation, migration and invasion. Furthermore, IFITM3 plays a key role in cancer growth and maintenance. Silencing of IFITM3 reduces these phenotypes. Therefore, targeting of IFITM3 will likely have implications for potential cancer therapies.
| S-EPMC7753217 | biostudies-literature