University of Tabuk

Surgery remains a major contributor to healthcare costs and mortality from perioperative complications, yet long term national mortality trends are poorly defined.

A population based analysis of U.S. mortality data (1999-2024) was conducted using the CDC WONDER database. High risk surgical deaths were identified by ICD-10 code Y83. Age adjusted mortality rates (AAMRs) were calculated, and Joinpoint regression estimated annual percentage changes (APCs).

Among 470,098 deaths, men comprised 54.7 %, with 76.0 % occurring in medical facilities. National AAMR declined from 8.1 (1999) to 3.4 (2015), rose to 7.9 (2021), then fell to 3.2 (2024). Mortality was highest among men, non Hispanic Black and American Indian/Alaska Native groups, and in non-metropolitan areas; Marked state level variation was observed, with the highest AAMRs in Mississippi, New Mexico, Wyoming, North Dakota, and West Virginia.

U.S. surgical mortality showed a three phase pattern of decline, rise, and reduction, with persistent demographic and state/regional disparities requiring targeted policy action.

Diabetic retinopathy (DIR) is a predominant diabetic microvascular complication that may cause vision loss. Retinal inflammation and angiogenesis contribute largely to the neuronal degeneration in DIR. The current study is aiming to test the effect of oral betanin doses in protection from DIR in rats along with a network pharmacology study to investigate an assumption that betanin may inhibit nuclear factor-κ B (NF-κB). Three rat groups were assigned as vehicle, DIR, and DIR + Betanin 100 mg/kg. Molecular docking indicated the possible binding between betanin and NF-κB while the bioinformatic study highlighted a relation between this possible inhibition and suppression of NOD-like receptor pyrin domain-containing protein 3/vascular endothelial growth factor (NLRP3/VEGF) axis. The rat experimental study validated this assumption and indicated a protective effect for betanin on rat retinas as shown by routine hematoxylin and eosin staining (retinal thickness and ganglion cell count) and periodic acid-Schiff staining that was mediated through mitigating expression/protein level for of NF-κB, NLRP3, TNF-α, IL-6 and VEGF proteins. Immunohistochemistry showed that betanin was able to suppress retinal content of the glial fibrillary acidic protein (GFAP). In conclusion, the current study indicated that betanin was a good candidate for DIR in rats through suppression of the inflammatory cascade and may be suggested for diabetic patients if appropriated clinical studies will be available.