The results support the use of MENs as an effective drug delivery carrier for growth hormone-releasing hormone antagonists in the treatment of human glioblastomas.

Sentinel-2 satellites provide multi-spectral optical remote sensing images with four bands at 10 m of spatial resolution. These images, due to the open data distribution policy, are becoming an important resource for several applications. However, for small scale studies, the spatial detail of these images might not be sufficient. On the other hand, WorldView commercial satellites offer multi-spectral images with a very high spatial resolution, typically less than 2 m, but their use can be impractical for large areas or multi-temporal analysis due to their high cost. To exploit the free availability of Sentinel imagery, it is worth considering deep learning techniques for single-image super-resolution tasks, allowing the spatial enhancement of low-resolution (LR) images by recovering high-frequency details to produce high-resolution (HR) super-resolved images. In this work, we implement and train a model based on the Enhanced Super-Resolution Generative Adversarial Network (ESRGAN) with pairs of WorldView-Sentinel images to generate a super-resolved multispectral Sentinel-2 output with a scaling factor of 5. Our model, named RS-ESRGAN, removes the upsampling layers of the network to make it feasible to train with co-registered remote sensing images. Results obtained outperform state-of-the-art models using standard metrics like PSNR, SSIM, ERGAS, SAM and CC. Moreover, qualitative visual analysis shows spatial improvements as well as the preservation of the spectral information, allowing the super-resolved Sentinel-2 imagery to be used in studies requiring very high spatial resolution.

The etiology of benign prostatic hyperplasia (BPH) is multifactorial, and chronic inflammation plays a pivotal role in its pathogenesis. Growth hormone-releasing hormone (GHRH) is a hypothalamic neuropeptide that has been shown to act as paracrine/autocrine factor in various malignancies including prostate cancer. GHRH and its receptors are expressed in experimental models of BPH, in which antagonists of GHRH suppressed the levels of proinflammatory cytokines and altered the expression of genes related to epithelial-to-mesenchymal transition (EMT). We investigated the effects of GHRH antagonist on prostatic enlargement induced by inflammation. Autoimmune prostatitis in Balb/C mice was induced by a homogenate of reproductive tissues of male rats. During the 8-wk induction of chronic prostatitis, we detected a progressive increase in prostatic volume reaching 92% at week 8 compared with control (P < 0.001). Daily treatment for 1 mo with GHRH antagonist MIA-690 caused a 30% reduction in prostate volume (P < 0.05). Conditioned medium derived from macrophages increased the average volume of spheres by 82.7% (P < 0.001) and elevated the expression of mRNA for N-cadherin, Snail, and GHRH. GHRH antagonist reduced the average volume of spheres stimulated by inflammation by 75.5% (P < 0.05), and TGF-β2 by 91.8% (P < 0.01). The proliferation of primary epithelial cells stimulated by IL-17A or TGF-β2 was also inhibited by 124.1% and 69.9%, respectively. GHRH stimulated the growth of BPH-1 and primary prostate spheres. This study provides evidence that GHRH plays important roles in prostatic inflammation and EMT and suggests the merit of further investigation to elucidate the effects of GHRH antagonists in prostatitis and BPH. chronic prostatic inflammation | neuropeptide | prostatic hyperplasia | targeted therapy | experimental autoimmune prostatitis

The chemokine stromal cell-derived factor-1 (SDF-1) plays a critical role in mobilizing precursor cells in the bone marrow and is essential for efficient vascular regeneration and repair. We recently reported that calcium augments the expression of chemokine receptor CXCR4 and enhances the angiogenic potential of bone marrow derived cells (BMCs). Neovascularization is impaired by aging therefore we suggested that aging may cause defects of CXCR4 expression and cellular responses to calcium. Indeed we found that both the basal and calcium-induced surface expression of CXCR4 on BMCs was significantly reduced in 25-month-old mice compared with 2-month-old mice. Reduced Ca-induced CXCR4 expression in BMC from aged mice was associated with defective calcium influx. Diminished CXCR4 surface expression in BMC from aged mice correlated with diminished neovascularization in an ischemic hindlimb model with less accumulation of CD34+ progenitor cells in the ischemic muscle with or without local overexpression of SDF-1. Intravenous injection of BMCs from old mice homed less efficiently to ischemic muscle and stimulated significantly less neovascularization compared with the BMCs from young mice. Transplantation of old BMCs into young mice did not reconstitute CXCR4 functions suggesting that the defects were not reversible by changing the environment. We conclude that defects of basal and calcium-regulated functions of the CXCR4/SDF-1 axis in BMCs contribute significantly to the age-related loss of vasculogenic responses.