Vitrectomy using 0.025% povidone-iodine irrigation for treating post-traumatic endophthalmitis due to intraocular foreign bodies: Two case reports

Traumatic eye injury-related endophthalmitis is a serious traumatic complication that threatens the vision of many patients worldwide. Herein, we present two cases of traumatic endophthalmitis that underwent 0.025% povidone-iodine treatment and hoped to introduce the bactericidal effect of 0.025% povidone-iodine in balanced salt solution PLUS (0.025% PI-BSS PLUS) and its use in vitrectomy for traumatic endophthalmitis. The 0.025% PI-BSS PLUS solution is bactericidal and nontoxic when used as an irrigation solution in pars plana vitrectomy. The two cases of traumatic endophthalmitis were resolved by pars plana vitrectomy using 0.025% PI-BSS PLUS

Green Synthesis of Carbon Dots from Grapefruit and Its Fluorescence Enhancement

In this study, undoped carbon quantum dots (UCQDs, UCQDs-peel) and N-doped carbon dots (NCQDs) were prepared by a facile one-pot environmentally friendly hydrothermal method using grapefruit as carbon sources in the absence and presence of area, respectively. The structure, morphology, and fluorescence properties of three samples were characterized by Fourier transform infrared spectroscopy (FT-IR), transmission electron microscopy (TEM), and photoluminescence (PL). It was found that three types of CQDs could emit blue fluorescence with different intensities when irradiated with ultraviolet light. Compared to the luminescence properties of UCQDs, NCQDs, and UCQDs-peel, it can be seen that the fluorescence intensity of NCQDs was strongest due to the presence of NH and C-N bonds

Astaxanthin Attenuates Hypertensive Vascular Remodeling by Protecting Vascular Smooth Muscle Cells from Oxidative Stress-Induced Mitochondrial Dysfunction

Oxidative stress aggravates mitochondrial injuries and accelerates the proliferation of vascular smooth muscle cells (VSMCs), which are important mechanisms contributing to vascular remodeling in hypertension. We put forward the hypothesis that Astaxanthin (ATX), known to possess strong features of antioxidant, could attenuate vascular remodeling by inhibiting VSMC proliferation and improving mitochondrial function. The potential effects of ATX were tested on spontaneously hypertensive rats (SHRs) and cultured VSMCs that injured by angiotensin II (Ang II). The results showed that ATX lowered blood pressure, reduced aortic wall thickness and fibrosis, and decreased the level of reactive oxygen species (ROS) and H2O2 in tunica media. Moreover, ATX decreased the expression of proliferating cell nuclear antigen (PCNA) and ki67 in aortic VSMCs. In vitro, ATX mitigated VSMC proliferation and migration, decreased the level of cellular ROS, and balanced the activities of ROS-related enzymes including NADPH oxidase, xanthine oxidase, and superoxide dismutase (SOD). Besides, ATX mitigated Ca2+ overload, the overproduction of mitochondrial ROS (mtROS), mitochondrial dysfunction, mitochondrial fission, and Drp1 phosphorylation at Ser616. In addition, ATX enhanced mitophagy and mitochondrial biosynthesis by increasing the expression of PINK, parkin, mtDNA, mitochondrial transcription factor A (Tfam), and PGC-1α. The present study indicated that ATX could efficiently treat vascular remodeling through restraining VSMC proliferation and restoring mitochondrial function. Inhibiting mitochondrial fission by decreasing the phosphorylation of Drp1 and stimulating mitochondrial autophagy and biosynthesis via increasing the expression of PINK, parkin, Tfam, and PGC-1α may be part of its underlying mechanisms

Carbonic Anhydrase I modifies SOD1-induced motor neuron toxicity in Drosophila via ER stress pathway

Background: Drosophila models of amyotrophic lateral sclerosis (ALS) have been widely used in understanding molecular mechanisms of ALS pathogenesis as well as discovering potential targets for therapeutic drugs. Mutations in the copper/zinc superoxide dismutase (SOD1) cause ALS by gain of toxic functions and induce toxicity in fly motor neurons. Results: In this study, we have determined that human carbonic anhydrase I (CA1) can alleviate mutant SOD1-induced motor neuron toxicity in the transgenic fly model of ALS. Interestingly, we found that motor neuron expression of CA1 could independently induce locomotion defect as well as decreasing the survival rate. In addition, CA1-induced toxicity in motor neurons is anhydrase activity-dependent. Mechanistically, we identified that both SOD1- and CA1-induced toxicity involve the activation of eIF2α in the ER stress response pathway. Downstream activation of the JNK pathway has also been implicated in the induced toxicity. Conclusion: Our results have confirmed that SOD1-induced toxicity in fly motor neuron also involves endoplasmic reticulum (ER) stress pathway. More importantly, we have discovered a new cellular role that CA1 plays by antagonizing mutant SOD1-induced toxicity in motor neurons involving the ER stress pathway. Such information can be potentially useful for further understanding disease mechanisms and developing therapeutic targets for ALS.&nbsp

Dysregulated bile acid signaling contributes to the neurological impairment in murine models of acute and chronic liver failureResearch in context

Background: Hepatic encephalopathy (HE), a severe neuropsychiatric complication, is associated with increased blood levels of ammonia and bile acids (BAs). We sought to determine (1) whether abnormally increased blood BAs in liver cirrhotic patients with HE is caused by elevation of apical sodium-dependent BA transporter (ASBT)-mediated BA reabsorption; and (2) whether increased BA reabsorption would exacerbate ammonia-induced brain injuries. Methods: We quantitatively measured blood BA and ammonia levels in liver cirrhosis patients with or without HE and healthy controls. We characterized ASBT expression, BA profiles, and ammonia concentrations in a chronic liver disease (CLD) mouse model induced by streptozotocin-high fat diet (STZ-HFD) and an azoxymethane (AOM) - induced acute liver failure (ALF) mouse model. These two mouse models were treated with SC-435 (ASBT inhibitor) and budesonide (ASBT activator), respectively. Findings: Blood concentrations of ammonia and conjugated BAs were substantially increased in cirrhotic patients with HE (n = 75) compared to cirrhotic patients without HE (n = 126). Pharmacological inhibition of the enterohepatic BA circulation using a luminal- restricted ASBT inhibitor, SC-435, in mice with AOM-induced ALF and STZ-HFD -induced CLD effectively reduced BA and ammonia concentrations in the blood and brain, and alleviated liver and brain damages. Budesonide treatment induced liver and brain damages in normal mice, and exacerbated these damages in AOM-treated mice. Interpretation: ASBT mediated BA reabsorption increases intestinal luminal pH and facilitates conversion of intestinal ammonium to ammonia, leading to abnormally high levels of neurotoxic ammonia and cytotoxic BAs in the blood and brain. Inhibition of intestinal ASBT with SC-435 can effectively remove neurotoxic BAs and ammonia from the bloodstream and thus, mitigate liver and brain injuries resulting from liver failure. Keywords: Bile acids, Ammonia, Hepatic encephalopathy, Apical sodium-dependent bile acid transporte

Uniform growth of NiCo2S4 nanoflakes arrays on nickel foam for binder-free high-performance supercapacitors

In this work, ultrathin NiCo2O4 nanosheets have been synthesized through an electrodeposition method together with a further calcination process. By using CH3CSNH2 as sulfur source, the NiCo2O4 was converted into NiCo2S4 via anion exchange reaction (from oxygen to sulfur). Scanning electron microscopy imaging together with the energy-dispersive X-ray spectroscopy mapping indicates the successful transformation from NiCo2O4 to NiCo2S4. The uniform and porous NiCo2S4 architectures show good electrical contact to the current collector and good wettability, which can facilitate the transport for electrons and electrolyte ions. As a result, the as-prepared NiCo2S4 electrode shows a greatly enhanced electrochemical performance than NiCo2O4, with a high specific capacitance (1051Fg(-1) at a current density of 0.5Ag(-1)) and good cycling stability (capacity retention of 85% after 5000 charge/discharge cycles). These impressive performances suggest that the porous NiCo2S4 structures can be used as promising binder-free electrode materials for high-performance supercapacitors