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Journal of Current Ophthalmology 2023To review the concept of plateau iris and summarize the recent evidence on its diagnosis and management. (Review)
Review
PURPOSE
To review the concept of plateau iris and summarize the recent evidence on its diagnosis and management.
METHODS
This is a narrative review on the plateau iris. A literature review was conducted in PubMed, Google Scholar, and Scopus databases using keywords: angle-closure glaucoma, glaucoma, nonpupillary block glaucoma, plateau iris, and plateau iris management.
RESULTS
This review defined the current knowledge about plateau iris. First of all, the anatomy and epidemiology were discussed. Then, we outlined the available evidence on the diagnosis of plateau iris and its differential diagnosis. Conclusively, the treatment options were mentioned.
CONCLUSIONS
Plateau iris is a condition in which nonpupillary block mechanisms are responsible for intraocular pressure elevation and angle closure attack when a patent peripheral iridotomy has removed the relative pupillary block. An anteriorly positioned ciliary body causes mechanical obstruction of trabecular meshwork in these patients. It is usually seen in younger patients with angle closure and is diagnosed by gonioscopic examination and imaging modalities such as Ultrasound biomicroscopy. Despite the known mechanism of plateau iris, there is no consensus over treatment. Low-dose pilocarpine and Argon laser peripheral iridoplasty are nonsurgical treatments for these patients, but their effects are short-term. Cataract extraction with/without endocyclophotocoagulation (ECP), endocycloplasty, excisional goniotomy, and transscleral cyclophotocoagulation are alternative treatments. Patients should be examined periodically for further progression or recurrence of plateau iris. In cases of glaucoma unresponsive to conventional medical treatments, surgical treatments such as trabeculectomy and drainage devices should be considered.
PubMed: 37680292
DOI: 10.4103/joco.joco_319_22 -
Pharmacological Research Sep 2023Microglia are the resident immune cells of the central nervous system, undertaking surveillance role and reacting to brain homeostasis and neurological diseases. Recent...
Microglia are the resident immune cells of the central nervous system, undertaking surveillance role and reacting to brain homeostasis and neurological diseases. Recent studies indicate that microglia modulate epilepsy-induced neuronal activities, however, the mechanisms underlying microglia-neuron communication in epilepsy are still unclear. Here we report that epileptic neuronal hyperexcitability activates microglia and drives microglial ATP/ADP hydrolyzing ectoenzyme CD39 (encoded by Entpd1) expression via recruiting the cAMP responsive element binding protein (CREB)-regulated transcription coactivator-1 (CRTC1) from cytoplasm to the nucleus and binding to CREB. Activated microglia in turn suppress epileptic neuronal hyperexcitability in a CD39 dependent manner. Disrupting microglial CREB/CRTC1 signaling, however, decreases CD39 expression and diminishes the inhibitory effect of microglia on epileptic neuronal hyperexcitability. Overall, our findings reveal CD39-dependent control of epileptic neuronal hyperexcitability by microglia is through an excitation-transcription coupling mechanism.
Topics: Humans; Microglia; Brain; Signal Transduction; Epilepsy
PubMed: 37541638
DOI: 10.1016/j.phrs.2023.106881 -
Neurobiology of Disease Oct 2023Epilepsy is one of the most common neurological disorders. Neuroinflammation involving the activation of microglia and astrocytes constitutes an important and common...
Epilepsy is one of the most common neurological disorders. Neuroinflammation involving the activation of microglia and astrocytes constitutes an important and common mechanism in epileptogenesis. Transient receptor potential melastatin 2 (TRPM2) is a calcium-permeable, non-selective cation channel that plays pathological roles in various inflammation-related diseases. Our previous study demonstrated that Trpm2 knockout exhibits therapeutic effects on pilocarpine-induced glial activation and neuroinflammation. However, whether TRPM2 in microglia and astrocytes plays a common pathogenic role in this process and the underlying molecular mechanisms remained undetermined. Here, we demonstrate a previously unknown role for microglial TRPM2 in epileptogenesis. Trpm2 knockout in microglia attenuated kainic acid (KA)-induced glial activation, inflammatory cytokines production and hippocampal paroxysmal discharges, whereas Trpm2 knockout in astrocytes exhibited no significant effects. Furthermore, we discovered that these therapeutic effects were mediated by upregulated autophagy via the adenosine monophosphate activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway in microglia. Thus, our findings highlight an important deleterious role of microglial TRPM2 in temporal lobe epilepsy.
Topics: Humans; Microglia; AMP-Activated Protein Kinases; Neuroinflammatory Diseases; TRPM Cation Channels; TOR Serine-Threonine Kinases; Autophagy; Calcium Channels
PubMed: 37648036
DOI: 10.1016/j.nbd.2023.106273 -
Annals of Medicine and Surgery (2012) Jun 2024This article discusses the prevalence and impact of pharmacologically-induced mydriasis, a condition where the pupil becomes excessively dilated due to certain drugs. It... (Review)
Review
This article discusses the prevalence and impact of pharmacologically-induced mydriasis, a condition where the pupil becomes excessively dilated due to certain drugs. It highlights the challenges faced by medical professionals in dealing with this condition and the limitations of current treatments, like pilocarpine and dapiprazole, which come with systemic side effects and specific contraindications, limiting their regular use. The article introduces Ryzumvi, a novel ophthalmic solution approved by the US FDA, which effectively reverses mydriasis caused by adrenergic agonists and antimuscarinic drugs. The article provides insights into its mechanism of action, clinical efficacy, pharmacokinetics, safety, and tolerance based on extensive clinical trials. It emphasizes its rapid onset of action and effectiveness in restoring pupils to their initial size. It also underlines the potential for expanded applications, including in pediatric patients, solidifying its importance in the field of ophthalmology. Furthermore, Ryzumvi represents a promising advancement in managing pharmacologically-induced mydriasis, offering swift and effective relief while highlighting the importance of adhering to safety precautions and the continuous research and development efforts in ophthalmology to comprehensively address vision-related disorders and enhance patient outcomes.
PubMed: 38846833
DOI: 10.1097/MS9.0000000000002058 -
FASEB Journal : Official Publication of... Jul 2023Mucin-2 (MUC2) secreted by goblet cells participates in the intestinal barrier, but its mechanism in acute necrotizing pancreatitis (ANP) remains unclear. In acute...
Mucin-2 (MUC2) secreted by goblet cells participates in the intestinal barrier, but its mechanism in acute necrotizing pancreatitis (ANP) remains unclear. In acute pancreatitis (AP) patients, the functions of goblet cells (MUC2, FCGBP, CLCA1, and TFF3) decreased, and MUC2 was negatively correlated with AP severity. ANP rats treated with pilocarpine (PILO) (PILO+ANP rats) to deplete MUC2 showed more serious pancreatic and colonic injuries, goblet cell dysfunction, gut dysbiosis, and bacterial translocation than those of ANP rats. GC-MS analysis of feces showed that PILO+ANP rats had lower levels of butyric acid, isobutyric acid, isovaleric acid, and hexanoic acid than those of ANP rats. The expression of MUC2 was associated with colonic injury and gut dysbiosis. All these phenomena could be relieved, and goblet cell functions were also partially reversed by MUC2 supplementation in ANP rats. TNF-α-treated colonoids had exacerbated goblet cell dysfunction. MUC2 expression was negatively correlated with the levels of pro-inflammatory cytokines (IL-1β and IL-6) (p < .05) and positively related to the expression of tight junction proteins (Claudin 1, Occludin, and ZO1) (p < .05). Downregulating MUC2 by siRNA increased the levels of the pro-inflammatory cytokines in colonoids. MUC2 might maintain intestinal homeostasis to alleviate ANP.
Topics: Rats; Animals; Mucin-2; Pancreatitis, Acute Necrotizing; Dysbiosis; Acute Disease; Cytokines; Homeostasis; Intestinal Mucosa
PubMed: 37249555
DOI: 10.1096/fj.202201998R -
Neural Regeneration Research Oct 2023Epilepsy is a common and serious neurological disease that causes recurrent seizures. The brain damage caused by seizures can lead to depression, anxiety, cognitive... (Review)
Review
Epilepsy is a common and serious neurological disease that causes recurrent seizures. The brain damage caused by seizures can lead to depression, anxiety, cognitive impairment, or disability. In almost all cases chronic seizures are difficult to cure. MicroRNAs are widely expressed in the central nervous system and play important roles in the pathogenesis of several neurological disorders, including epilepsy. A variety of animals (mostly mice and rats) have been used to induce experimental epilepsy using different protocols and miRNA profiling performed. Most of the recent studies reviewed had performed miRNA profiling in hippocampal tissues and a large number of microRNAs were dysregulated when compared to controls. Most notably, miR-132-3p, -146a-5p, -10a-5p, -21a-3p, -27a-3p, -142a-5p, -212-3p, -431-5p, and -155 were upregulated in both the mouse and rat studies. Overexpression of miR-137 and miR-219 decreased seizure severity in a mouse epileptic model, and suppression of miR-451, -10a-5p, -21a-5p, -27a-5p, -142a-5p, -431-5p, -155, and -134 had a positive influence on seizure behavior. In the rat studies, overexpression of miR-139-5p decreased neuronal damage in drug-resistant rats and inhibition of miR-129-2-3p, -27a-3p, -155, -134, -181a, and -146a had a positive effect on seizure behavior and/or reduced the loss of neuronal cells. Further studies are warranted using adult female and immature male and female animals. It would also be helpful to test the ability of specific agomirs and antagomirs to control seizure activity in a subhuman primate model of epilepsy such as adult marmosets injected intraperitoneally with pilocarpine or cynomolgus monkeys given intrahippocampal injections of kainic acid.
PubMed: 37056117
DOI: 10.4103/1673-5374.369093