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039). The ADCm values in IDH-mutant (Mut) patients were higher than those of IDH-Wt patients (p less then 0.0004). The value of ADC ≥ 0.99 × 10-3 mm2/s emerged as a "cut-off" to differentiate the mutation state. In the overall group, a positive relationship between the ADCm values and OS was detected (p = 0.003; r = 0.62). Adding quantitative measures of ADC values to conventional MR imaging could be used routinely as a noninvasive marker of specific molecular patterns.The corneal fibrotic responses to corneal damage often lead to severe corneal opacification thereby resulting in severe visual impairment or even blindness. The persistence of corneal opacity depends heavily on the activity of corneal myofibroblast. Myofibroblasts are opaque and synthesize a disorganized extracellular matrix (ECM) and thus promoting opacification. Cluster of differentiation 147 (CD147), a member of the immunoglobulin superfamily, is known to play important roles in the differentiation process from fibroblast to myofibroblast in damaged cornea and may therefore be an effective target for treatment of corneal opacity. Here, we examined the therapeutic efficacy of novel CD147 inhibiting verbenone derivative SP-8356 ((1S,5R)-4-(3,4-dihydroxy-5-methoxystyryl)-6,6-dimethylbicyclo[3.1.1]hept-3-en-2-one) on corneal fibrosis. Topical SP-8356 significantly reduced corneal haze and fibrosis in the alkali-burned cornea. In detail, SP-8356 inhibited both alpha-smooth muscle actin (α-SMA) expressing myofibroblast and its ECM-related products, such as matrix-metalloproteinase-9 and collagen type III and IV. Similar to SP-8356, topical corticosteroid (prednisolone acetate, PA) also reduced the ECM-related products and opacification. However, prednisolone acetate failed to decrease the population of α-SMA-positive corneal myofibroblast. In conclusion, SP-8356 is capable enough to prevent corneal haze by preventing pathological fibrosis after severe corneal damage. Therefore, SP-8356 could be a potentially promising therapeutic drug for corneal fibrosis.Three-dimensional porous carbon is considered as an ideal electrode material for supercapacitors (SCs) applications owing to its good conductivity, developed pore structure, and excellent connectivity. Herein, using longan shell as precursor, 3-dimensional porous carbon with abundant and interconnected pores and moderate heteroatoms were obtained via simple carbonization and potassium hydroxide (KOH) activation treatment. The electrochemical performances of obtained 3-dimensional porous carbon were investigated as electrode materials in symmetric SCs with aqueous and solid electrolytes. The optimized material that is named after longan shell 3-dimensional porous carbon 800 (LSPC800) possesses high porosity (1.644 cm3 g-1) and N content (1.14 at %). In the three-electrode measurement, the LSPC800 displays an excellent capacitance value of 359 F g-1. Besides, the LSPC800 also achieves splendid specific capacitance (254 F g-1) in the two electrode system, while the fabricated SC employing 1 M Li2SO4 as electrolyte acquires ultrahigh power density (15930.38 W kg-1). Most importantly, LSPC800 electrodes are further applied into the SC adopting the KOH/polyvinyl alcohol (PVA) gel electrolyte, which reaches up to an outstanding capacitance of 313 F g-1 at 0.5 A g-1. In addition, for the all-solid-state SC, its rate capability at 50 A g-1 is 72.73% and retention at the 10,000th run is 93.64%. Evidently, this work is of great significance to the simple fabrication of 3-dimensional porous carbon and further opens up a way of improving the value-added utilization of biomass materials, as well as proving that the biomass porous carbons have immense potential for high-performance SCs application.BACKGROUND the RIGENERA trial assessed the efficacy of granulocyte-colony stimulating factor (G-CSF) in the improvement of clinical outcomes in patients with severe acute myocardial infarction. However, there is no evidence available regarding the long-term safety and efficacy of this treatment. METHODS in order to evaluate the long-term effects on the incidence of major adverse events, on the symptom burden, on the quality of life and the mean life expectancy and on the left ventricular (LV) function, we performed a clinical and echocardiographic evaluation together with an assessment using the Minnesota Living with Heart Failure Questionnaire (MLHFQ) and the Seattle Heart Failure Model (SHFM) at 10-years follow-up, in the patients cohorts enrolled in the RIGENERA trial. RESULTS thirty-two patients were eligible for the prospective clinical and echocardiography analyses. A significant reduction in adverse LV remodeling was observed in G-CSF group compared to controls, 9% vs. find more 48% (p = 0.030). The New York Heart Association (NYHA) functional class was lower in G-CSF group vs. controls (p = 0.040), with lower burden of symptoms and higher quality of life (p = 0.049). The mean life expectancy was significantly higher in G-CSF group compared to controls (15 ± 4 years vs. 12 ± 4 years, p = 0.046. No difference was found in the incidence of major adverse events. CONCLUSIONS this longest available follow-up on G-CSF treatment in patients with severe acute myocardial infarction (AMI) showed that this treatment was safe and associated with a reduction of adverse LV remodeling and higher quality of life, in comparison with standard-of-care treatment.There is indication that nutritional supplements protect retinal cells from degeneration. In a previous study, we demonstrated that dietary supplementation with an association of forskolin, homotaurine, spearmint extract and B vitamins efficiently counteracts retinal dysfunction associated with retinal ganglion cell (RGC) death caused by optic nerve crush. We extended our investigation on the efficacy of dietary supplementation with the use of a mouse model in which RGC degeneration depends as closely as possible on intraocular pressure (IOP) elevation. In this model, injecting the anterior chamber of the eye with methylcellulose (MCE) causes IOP elevation leading to RGC dysfunction. The MCE model was characterized in terms of IOP elevation, retinal dysfunction as determined by electrophysiological recordings, RGC loss as determined by brain-specific homeobox/POU domain protein 3A immunoreactivity and dysregulated levels of inflammatory and apoptotic markers. Except for IOP elevation, dysfunctional retinal parameters were all recovered by dietary supplementation indicating the involvement of non-IOP-related neuroprotective mechanisms of action.
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