Patients with AMD have higher NLR compared with controls, and NLR correlates with disease severity. NLR may be used as a biomarker of inflammation in AMD.

Although cigarette smoking has no effect on cell polymorphism and polymegethism, the results suggest that smoking reduces endothelial cell count.

During surgery, changes in intraocular pressure (IOP) can be observed resulting from several factors, such as airway manipulations and drugs used. We aimed to investigate the effects of sugammadex and neostigmine on IOP, hemodynamic parameters, and complications after extubation. Our study comprised 60 patients, aged 18-65 years, with a risk status of the American Society of Anesthesiologists I-II who underwent arthroscopic surgery under general anesthesia. The patients were randomly assigned into two groups. At the end of the surgery, the neuromuscular block was reversed using neostigmine (50 μg/kg) plus atropine (15 μg/kg) in Group 1, and sugammadex (4 mg/kg) in Group 2. Neuromuscular blockade was monitored using acceleromyography and a train-of-four mode of stimulation. IOP was measured before induction and at 30 seconds, 2 minutes, and 10 minutes after extubation. A Tono-Pen XL applanation tonometer was used to measure IOP. This showed that elevation in IOP of patients reversed using sugammadex was similar to that recorded in patients reversed using neostigmine-atropine. When heart rate was compared, there was a significant difference between basal values and those obtained at 30 seconds and 10 minutes after extubation in the neostigmine-atropine group. Extubation time (time from withdrawal of anesthetic gas to extubation) was significantly shorter in the sugammadex group (p = 0.003) than in the neostigmine-atropine group. The postextubation IOP values of the sugammadex group were similar to the neostigmine-atropine group. Extubation time (time from withdrawal of anesthetic gas to extubation) was significantly shorter in the sugammadex group (p = 0.003) than in the neostigmine-atropine group.

Ochratoxin A (OTA) is a carcinogenic mycotoxin, which is produced by Aspergillus and Penicillium genera of fungi and commonly contaminates food and feed. We and others have previously shown that OTA causes sustained activation of PI3K/AKT and MAPK/ERK1-2 signaling pathways in different cell types and animal models. Given the close relationship between cellular signaling activity and protein stability, we were curious whether increased PI3K/AKT and MAPK/ERK1-2 signaling may be the result of OTA-stimulated alterations in proteolytic activity. We show that both of the major proteolytic systems, autophagy, and the ubiquitin-proteasome system (UPS), are activated upon OTA exposure in human kidney proximal tubule HK-2 and mouse embryonic fibroblast (MEF) cells. OTA stimulates transient autophagic activity at early time points of treatment but autophagic activity subsides after 6 h even in the sustained presence of OTA. Interestingly, OTA exposure also results in increased cell death in wild-type MEF cells but not in autophagy-halted Atg5-deficient cells, suggesting that autophagy exerts a pro-death effect on OTA-induced cytotoxicity. In addition, prolonged OTA exposure decreased ubiquitinated protein levels by increasing proteasomal activity. Using purified and cellular proteasomes, we observed enhanced chymotrypsin-, caspase-, and trypsin-like activities of the 26S but not the 20S proteasome in the presence of OTA. However, in the cellular context, increased proteasomal activity depended on prior induction of autophagy. Our results suggest that autophagy and subsequent UPS activation are responsible for sustained activation of PI3K/AKT and MAPK/ERK1-2 pathways through regulating the levels of critical phosphatases VHR/DUSP3, DUSP4, and PHLPP, which are known to be involved in OTA toxicity and carcinogenicity.

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