Purpose: This study aimed to evaluate the relationship between macular structural changes and visual prognosis after pars plana vitrectomy (PPV) for proliferative diabetic retinopathy. Methods: The study included 60 eyes that had undergone PPV. Macular optical coherence tomography (OCT) findings were classified into 5 groups preoperatively and 10 groups postoperatively. Best-corrected visual acuity (BCVA) were analyzed according to pre- and postoperative OCT. Results: From the preoperative OCT, normal fovea with/without traction, normal fovea with preretinal hemorrhage, and tractional retinal detachment involving fovea showed an increase in BCVA after PPV (all p < 0.05). Normal fovea, epiretinal membrane and macular thickening were common after surgery. Normal fovea, epiretinal membrane and edema outside of the fovea showed good visual prognosis (BCVA >20/50). Subfoveal fibrosis, macular hole, loss of foveal depression, and serous foveal detachment showed poor visual prognosis (BCVA <20/100). Conclusion: Macular structural changes were various after PPV, and visual prognosis correlated with these changes.
Recent studies have highlighted that early enhancement of the glycolytic pathway is a mode of maintaining the pro-inflammatory status of immune cells. Thiamine, a well-known co-activator of pyruvate dehydrogenase complex, a gatekeeping enzyme, shifts energy utilization of glucose from glycolysis to oxidative phosphorylation. Thus, we hypothesized that thiamine may modulate inflammation by alleviating metabolic shifts during immune cell activation. First, using allithiamine, which showed the most potent anti-inflammatory capacity among thiamine derivatives, we confirmed the inhibitory effects of allithiamine on the lipopolysaccharide (LPS)-induced pro-inflammatory cytokine production and maturation process in dendritic cells. We applied the LPS-induced sepsis model to examine whether allithiamine has a protective role in hyper-inflammatory status. We observed that allithiamine attenuated tissue damage and organ dysfunction during endotoxemia, even when the treatment was given after the early cytokine release. We assessed the changes in glucose metabolites during LPS-induced dendritic cell activation and found that allithiamine significantly inhibited glucose-driven citrate accumulation. We then examined the clinical implication of regulating metabolites during sepsis by performing a tail bleeding assay upon allithiamine treatment, which expands its capacity to hamper the coagulation process. Finally, we confirmed that the role of allithiamine in metabolic regulation is critical in exerting anti-inflammatory action by demonstrating its inhibitory effect upon mitochondrial citrate transporter activity. In conclusion, thiamine could be used as an alternative approach for controlling the immune response in patients with sepsis.
Neuroinflammation, which is involved in various inflammatory cascades in nervous tissues, can result in persistent and chronic apoptotic neuronal cell death and programmed cell death, triggering various degenerative disorders of the central nervous system (CNS). The neuroprotective effects of natural compounds against neuroinflammation are mainly mediated by their antioxidant, anti-inflammatory, and antiapoptotic properties that specifically promote or inhibit various molecular signal transduction pathways. However, natural compounds have several limitations, such as their pharmacokinetic properties and stability, which hinder their clinical development and use as medicines. This review discusses the molecular mechanisms of neuroinflammation and degenerative diseases of CNS. In addition, it emphasizes potential natural compounds and their promising nanocarriers for overcoming their limitations in the treatment of neuroinflammation. Moreover, recent promising CNS inflammation-targeted nanocarrier systems implementing lesion site-specific active targeting strategies for CNS inflammation are also discussed.
Compared with the standard operating microscope system, the digitally assisted vitreoretinal surgery system can reduce intraoperative muscle fatigue during surgery, which is more ergonomically advantageous to retinal surgeons.
Purpose: The aim of this study was to evaluate the effect of intravitreal dexamethasone implant fragmentation on clinical outcomes in branch retinal vein occlusion (BRVO)-induced macular edema (ME). Methods: All consecutive patients receiving an intravitreal dexamethasone implant for BRVO-induced ME were divided into two groups depending on whether the implant was intact or had fragmented into two or more pieces on postoperative day 1. Best-corrected visual acuity (BCVA), intraocular pressure (IOP), and central subfield thickness (CST) on spectral-domain optical coherence tomography were measured for 6 months. Results: Among 68 patients, the implant was fragmented in 6 (8.8%) and intact in 62 (91.2%) eyes. The two groups did not differ in BCVA and CST at any time point (all p > 0.05). There was no difference in the ME recurrence rate, frequency of IOP elevation, and cataract progression between the two groups (all p > 0.05). Conclusion: Fragmentation seemed not to influence clinical outcomes of intravitreal dexamethasone implantation during 6 months or to alter the frequency of adverse events.
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