Journal De Radiologie最新文献

Numerous explorations have been conducted on the determinants of Ghana's environmental quality. However, to the best of my knowledge, there has been no research on the connection between financial inclusion and environmental sustainability in the country. This study was therefore conducted to help fill that gap. In attaining the aforestated goal, econometric techniques that yield valid and reliable outcomes were engaged. From the results, all the series were first differenced stationary and cointegrated in the long run. The DARDL estimator with the support of the conventional ARDL estimator was adopted to explore the marginal effects of the predictors on the explained variable, and from the results, financial inclusion worsened environmental sustainability in the nation via high carbon emissions. Also, foreign direct investments degraded the country's ecological quality validating the pollution haven hypothesis. Finally, trade openness, population growth, and energy consumption were detrimental to environmental sustainability in the nation. On the causal directions amidst the series, unidirectional causalities from financial inclusion and trade openness to carbon effusions were disclosed. Also, feedback causalities between foreign direct investments and carbon emissions; between population growth and carbon effluents; and between energy consumption and carbon exudates were unfolded. The study recommended among others that, financial establishments should not fund the production of carbon-intensive goods, but those that are friendly to the environment. The government can also help to improve environmental sustainability by establishing regulations to mandate financial entities to engage in eco-friendly activities.

Variation in the onset, progression, and severity of symptoms associated with metabolic disorders such as diabetes impairs the diagnosis and treatment of at-risk patients. Diabetes symptoms, and patient variation in these symptoms, are attributed to a combination of genetic and environmental factors, but identifying the genes and pathways that modify diabetes in humans has proven difficult. A greater understanding of genetic modifiers and the ways in which they interact with metabolic pathways could improve the ability to predict a patient's risk for severe symptoms, as well as enhance the development of individualized therapeutic approaches. In this study, we use the Drosophila Genetic Reference Panel to identify genetic variation influencing hyperglycemia associated with loss of Sirt1 function. Through analysis of individual candidate functions, physical interaction networks, and gene set enrichment analysis, we identify not only modifiers involved in canonical glucose metabolism and insulin signaling, but also genes important for neuronal signaling and the innate immune response. Furthermore, reducing the expression of several of these candidates suppressed hyperglycemia, making them potential candidate therapeutic targets. These analyses showcase the diverse processes contributing to glucose homeostasis and open up several avenues of future investigation.

The dentate gyrus (DG) and its primary cell type, the granule cell (GC), are thought to be critical to many cognitive functions. A major neuronal subtype of the DG is the hilar mossy cell (MC). MCs have been considered to play an important role in cognition, but in vivo studies to understand the activity of MCs during cognitive tasks are challenging because the experiments usually involve trauma to the overlying hippocampus or DG, which kills hilar neurons. In addition, restraint typically occurs, and MC activity is reduced by brief restraint stress. Social isolation often occurs and is potentially confounding. Therefore, we used c-fos protein expression to understand when MCs are active in vivo in socially housed adult C57BL/6 mice in their home cage. We focused on c-fos protein expression after animals explored novel objects, based on previous work which showed that MCs express c-fos protein readily in response to a novel housing location. Also, MCs are required for the training component of the novel object location task and novelty-encoding during a food-related task. GluR2/3 was used as a marker of MCs. The results showed that MC c-fos protein is greatly increased after exposure to novel objects, especially in ventral DG. We also found that novel objects produced higher c-fos levels than familiar objects. Interestingly, a small subset of neurons that did not express GluR2/3 also increased c-fos protein after novel object exposure. In contrast, GCs appeared relatively insensitive. The results support a growing appreciation of the role of the DG in novelty detection and novel object recognition, where hilar neurons and especially MCs are very sensitive.

Loss of Kindlin 1 (Kin1) results in the skin blistering disorder Kindler Syndrome (KS), whose symptoms also include skin atrophy and reduced keratinocyte proliferation. Kin1 binds to integrins to modulate their activation and more recently it has been shown to regulate mitotic spindles and cell survival in a Plk1-dependent manner. Here we report that short-term Kin1 deletion in mouse skin results in impaired mitosis, which is associated with reduced acetylated tubulin (ac-tub) levels and cell proliferation. In cells, impaired mitosis and reduced ac-tub levels are also accompanied by reduced microtubule stability, all of which are rescued by HDAC6 inhibition. The ability of Kin1 to regulate HDAC6-dependent cellular ac-tub levels is dependent on its phosphorylation by Plk1. Taken together, these data define a novel role for Kin1 in microtubule acetylation and stability and offer a mechanistic insight into how certain KS phenotypes, such as skin atrophy and reduced cell proliferation, arise.

Patients with chronic obstructive pulmonary disease (COPD) are often at high risk of early death. Identification of prognostic biomarkers for COPD may aid in improving their survival by providing early strengthened therapy for high-risk patients. In the present study, we investigated the prognostic role of hyperuricemia at baseline on the prognosis of patients with COPD. Thirty-four patients with COPD with hyperuricemia were matched (1:2) to 68 patients with COPD without hyperuricemia and of similar age and sex. Data from those patients with COPD were evaluated retrospectively. The role of hyperuricemia on mortality was first analyzed using the Kaplan-Meier method, and multivariate Cox regression model was then used to evaluate the prognostic significance of hyperuricemia in patients with COPD. Hyperuricemia was not associated with other baseline characteristics in patients with COPD. Kaplan-Meier survival curve showed that patients with COPD with hyperuricemia had higher risk of mortality compared with patients with normouricemia, and the P-value for log-rank test was 0.005. In univariate analysis, hyperuricemia was associated with higher risk of mortality in patients with COPD (hazard ratio =2.29, 95% CI =1.07-4.88, P=0.032). In the multivariate analysis, hyperuricemia was independently associated with higher risk of mortality in patients with COPD (hazard ratio =2.68, 95% CI =1.18-6.09, P=0.019). In conclusion, hyperuricemia is a promising biomarker of early mortality in patients with COPD.