334 research outputs found

    Treatment of non-tuberculosis mycobacteria skin infections

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    Non-tuberculosis mycobacteria (NTM) skin infections have become increasingly prevalent in recent years, presenting a unique challenge in clinical management. This review explored the complexities of NTM infections localized to the superficial tissues and provided valuable insights into the optimal therapeutic strategies. The antibiotic selection should base on NTM species and their susceptibility profiles. It is recommended to adopt a comprehensive approach that considers the unique characteristics of superficial tissues to improve treatment effectiveness and reduce the incidence of adverse reactions, infection recurrence, and treatment failure. Infection control measures, patient education, and close monitoring should complement the treatment strategies to achieve favorable outcomes in managing NTM skin infections. Further efforts are warranted to elucidate factors and mechanisms contributing to treatment resistance and relapse. Future research should focus on exploring novel treatment options, innovative drug development/delivery platforms, and precise methodologies for determining therapeutic duration. Longitudinal studies are also needed to assess the long-term safety profiles of the integrated approaches

    Wnt3a: functions and implications in cancer

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    Abstract Wnt3a, one of Wnt family members, plays key roles in regulating pleiotropic cellular functions, including self-renewal, proliferation, differentiation, and motility. Accumulating evidence has suggested that Wnt3a promotes or suppresses tumor progression via the canonical Wnt signaling pathway depending on cancer type. In addition, the roles of Wnt3a signaling can be inhibited by multiple proteins or chemicals. Herein, we summarize the latest findings on Wnt3a as an important therapeutic target in cancer.http://deepblue.lib.umich.edu/bitstream/2027.42/113235/1/40880_2015_Article_52.pd

    Functional division of the dorsal striatum based on a graph neural network

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    The dorsal striatum, an essential nucleus in subcortical areas, has a crucial role in controlling a variety of complex cognitive behaviors; however, few studies have been conducted in recent years to explore the functional subregions of the dorsal striatum that are significantly activated when performing multiple tasks. To explore the differences and connections between the functional subregions of the dorsal striatum that are significantly activated when performing different tasks, we propose a framework for functional division of the dorsal striatum based on a graph neural network model. First, time series information for each voxel in the dorsal striatum is extracted from acquired functional magnetic resonance imaging data and used to calculate the connection strength between voxels. Then, a graph is constructed using the voxels as nodes and the connection strengths between voxels as edges. Finally, the graph data are analyzed using the graph neural network model to functionally divide the dorsal striatum. The framework was used to divide functional subregions related to the four tasks including olfactory reward, "0-back" working memory, emotional picture stimulation, and capital investment decision-making. The results were further subjected to conjunction analysis to obtain 15 functional subregions in the dorsal striatum. The 15 different functional subregions divided based on the graph neural network model indicate that there is functional differentiation in the dorsal striatum when the brain performs different cognitive tasks. The spatial localization of the functional subregions contributes to a clear understanding of the differences and connections between functional subregions

    Characteristic Analysis from Excessive to Deficient Syndromes in Hepatocarcinoma Underlying miRNA Array Data

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    Traditional Chinese medicine (TCM) treatment is regarded as a safe and effective method for many diseases. In this study, the characteristics among excessive, excessive-deficient, and deficient syndromes of Hepatocellular carcinoma (HCC) were studied using miRNA array data. We first calculated the differentially expressed miRNAs based on random module t-test and classified three TCM syndromes of HCC using SVM method. Then, the weighted miRNA-target networks were constructed for different TCM syndromes using predicted miRNA targets. Subsequently, the prioritized target genes of upexpression network of TCM syndromes were analyzed using DAVID online analysis. The results showed that there are distinctly different hierarchical cluster and network structure of TCM syndromes in HCC, but the excessive-deficient combination syndrome is extrinsically close to deficient syndrome. GO and pathway analysis revealed that the molecular mechanisms of excessive-deficient and deficient syndromes of HCC are more complex than excessive syndrome. Furthermore, although excessive-deficient and deficient syndromes have similar complex mechanisms, excessive-deficient syndrome is more involved than deficient syndrome in development of cancer process. This study suggested that miRNAs might be important mediators involved in the changing process from excessive to deficient syndromes and could be potential molecular markers for the diagnosis of TCM syndromes in HCC

    Brain White Matter Impairment in Patients with Spinal Cord Injury

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    It remains unknown whether spinal cord injury (SCI) could indirectly impair or reshape the white matter (WM) of human brain and whether these changes are correlated with injury severity, duration, or clinical performance. We choose tract-based spatial statistics (TBSS) to investigate the possible changes in whole-brain white matter integrity and their associations with clinical variables in fifteen patients with SCI. Compared with the healthy controls, the patients exhibited significant decreases in WM fractional anisotropy (FA) in the left angular gyrus (AG), right cerebellum (CB), left precentral gyrus (PreCG), left lateral occipital region (LOC), left superior longitudinal fasciculus (SLF), left supramarginal gyrus (SMG), and left postcentral gyrus (PostCG) (p<0.01, TFCE corrected). No significant differences were found in all diffusion indices between the complete and incomplete SCI. However, significantly negative correlation was shown between the increased radial diffusivity (RD) of left AG and total motor scores (uncorrected p<0.05). Our findings provide evidence that SCI can cause not only direct degeneration but also transneuronal degeneration of brain WM, and these changes may be irrespective of the injury severity. The affection of left AG on rehabilitation therapies need to be further researched in the future

    Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway

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    Tangshen formula (TSF), a formula of Chinese herbal medicine, improves lipid metabolism in humans and animals with diabetic kidney disease. However, the effect and mechanism of TSF on nonalcoholic fatty liver disease (NAFLD) remain unclear. The activation of autophagy appears to be a potential mechanism for improving NAFLD. In the present study, we examined the therapeutic effect of TSF on hepatic steatosis and sought to explore whether its effect is related to activating autophagy. Here, we showed that TSF treatment significantly attenuated hepatic steatosis in both high-fat diet (HFD) and methionine choline-deficient diet (MCDD)-fed mice. Meanwhile, TSF reduced lipid accumulation in palmitate (PA)-stimulated HepG2 cells and primary mouse hepatocytes. Furthermore, TSF increased Sirtuin 1 (SIRT1) expression and promoted autophagy activation in vivo. TSF also improved PA-induced suppression of both SIRT1 expression and SIRT1-dependent autophagy, thereby alleviating intracellular lipid accumulation in vitro. In addition, TSF increased SIRT1 expression and induced autophagy in an adenosine monophosphate-activated protein kinase (AMPK)-dependent manner. Moreover, SIRT1 knockdown abolished the autophagy-inducing and lipid-lowering effects of TSF. In conclusion, TSF improved lipid accumulation and hepatic steatosis by inducing the AMPK/SIRT1 pathway-mediated autophagy
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