Notes

Current Developments in Photoredox-Mediated Radical Conjugate Add-on Reactions: A growing Tool kit for the Giese Response.
PURPOSE To investigate the biophysical meaning of Diffusion Kurtosis Imaging (DKI) parameters via correlations with the perfusion parameters obtained from a long Dynamic Contrast Enhanced MRI scan, in head and neck (HN) cancer. METHODS Twenty two patients with newly diagnosed HN tumor were included in the present retrospective study. Some patients had multiple lesions, therefore a total of 26 lesions were analyzed. DKI was acquired using 5b values at 0, 500, 1000,1500 and 2000 s/mm2. DCE-MRI was obtained with 130 dynamic volumes, with a temporal resolution of 5 s, to achieve a long scan time (>10 min). The apparent diffusion coefficient Dapp and apparent diffusional kurtosis Kapp were calculated voxel-by-voxel, removing the point at b value = 0 to eliminate possible perfusion effects on the parameter estimations. The transfer constants Ktrans and Kep, ve, and the histogram-based entropy (En) and interquartile range (IQR) of each DCE-MRI parameter were quantified. Correlations between all variables were investigated by the Spearman's Rho correlation test. RESULTS Moderate relationships emerged between Dapp and Kep (Rho = - 0.510, p = 0.009), and between Dapp and ve (Rho = 0.418, p = 0.038). En(Kep) was significantly related to Kapp (Rho = 0.407, p = 0.043), while IQR(Kep) showed an inverse association with Dapp (Rho = -0.422, p = 0.035). CONCLUSIONS A weak to intermediate correlation was found between DKI parameters and both Kep and ve. The kurtosis was associated to the intratumoral heterogeneity and complexity of the capillary permeability, expressed by En(Kep). PURPOSE This study aimed to determine a low-dose protocol for digital chest tomosynthesis (DTS). METHODS Five simulated nodules with a CT number of approximately 100 HU with size diameter of 3, 5, 8, 10, and 12 mm were inserted into an anthropomorphic chest phantom (N1 Lungman model), and then scanned by DTS system (Definium 8000) with varying tube voltage, copper filter thickness, and dose ratio. Three radiophotoluminescent (RPL) glass dosimeters, type GD-352 M with a dimension of 1.5 × 12 mm, were used to measure the entrance surface air kerma (ESAK) in each protocol. The effective dose (ED) was calculated using the recorded total dose-area-product (DAP). The signal-to-noise ratio (SNR) was determined for qualitative image quality evaluation. The image criteria and nodule detection capability were scored by two experienced radiologists. The selected low-dose protocol was further applied in a clinical study with 30 pulmonary nodule follow-up patients. RESULTS The average ESAK obtained from the standard default protocol was 1.68 ± 0.15 mGy, while an ESAK of 0.47 ± 0.02 mGy was found for a low-dose protocol. The EDs for the default and low-dose protocols were 313.98 ± 0.72 µSv and 100.55 ± 0.28 µSv, respectively. EGFR inhibitor There were small non-significant differences in the image criteria and nodule detection scoring between the low-dose and default protocols interpreted by two radiologists. The effective dose of 98.87 ± 0.08 µSv was obtained in clinical study after applying the low-dose protocol. CONCLUSIONS The low-dose protocol obtained in this study can substantially reduce radiation dose while preserving an acceptable image quality compared to the standard protocol. Oxidative stress acts as the major causative factor for various age-associated neurodegenerative diseases, triggering cognitive and memory impairments. In the present study, the underlying neuroprotective mechanism governing how shikonin acts against D-galactose (D-gal)-induced memory impairment, neuroinflammation and neuron damage was examined. The results revealed that chronic administration of D-gal [150 mg/kg intraperitoneally (i.p.)] in mice caused cognitive and memory impairments, as determined by Morris water-maze test. Shikonin treatment, however, alleviated D-gal-induced memory impairment and reversed the D-gal-induced neural damage and apoptosis. Furthermore, western blotting and the results of morphological analysis revealed that shikonin treatments markedly reduced D-gal induced neuroinflammation through inhibition of astrocytosis as determined by glial fibrillary acidic protein (GFAP) detection, and downregulating other inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6. Moreover, shikonin treatment led to inhibition of the activation of nuclear factor-κB (NF-κB) and the phosphorylation of mitogen-activated protein kinases (MAPKs), preventing neurodegeneration. Hence, taken together, the results of the present study suggested that shikonin attenuated D-gal-induced memory impairment, neuroinflammation and neurodegeneration, possibly via the NF-κB/mitogen-activated protein kinase (MAPK) pathway. Our data suggest that shikonin could be a promising, endogenous and compatible antioxidant candidate for age-associated neurodegenerative diseases, including Alzheimer's disease. PURPOSE To investigate the expression of extracellular high mobility group box 1 (HMGB1) and the effect of its inhibitor glycyrrhizin (GL) in corneal wound healing. METHODS We treated C57BL/6J mice with GL or PBS before and after establishing a corneal injury model. Fluorescein staining, Ki-67 expression, haze grade, and haematoxylin/eosin (H&E) staining were used to assess treatment efficacy. The expression of HMGB1, NF-κB-p65, the NLRP3 inflammasome, IL-1β, CCL2, CXCL2, TGF-β1, α-SMA, fibronectin, and collagen III and neutrophil influx were examined by immunohistochemical staining, western blot, and RT-qPCR at various time points after corneal injury. RESULTS After corneal injury, HMGB1 transferred from the nucleus to the cytoplasm and was passively released or actively secreted into the corneal stroma from epithelial cells and inflammatory cells; however, this increase was attenuated by GL treatment. Furthermore, GL indirectly attenuated the expression of IL-1β by directly inhibiting extracellular HMGB1 functions, which activated the NF-κB-p65/NLRP3/IL-1β signalling pathway. Moreover, application of GL alleviated the neutrophil infiltration that delays wound healing, accompanied by the downregulation of expression of the chemokines CCL2 and CXCL2. More interestingly, application of GL reduced the degree of haze grade through inactivating extracellular HMGB1 functions that induced TGF-β1 release and myofibroblast differentiation. In addition, fluorescein and H&E staining and Ki-67 levels suggest that GL promotes regeneration of corneal epithelium. CONCLUSIONS After corneal injury, extracellular HMGB1 can be an essential driver to trigger a neutrophil- and cytokine-mediated inflammatory injury amplification loop. The application of GL promotes the cornea to restore transparency and integrity, which may be related to the attenuation of extracellular HMGB1 levels and function.
Read More: https://www.selleckchem.com/EGFR(HER).html