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The presence of bacterial persisters is a key factor contributing to chronic infection. However, no effective treatment methods are currently available. Thus, a platform is developed, called reactive oxygen species (ROS) bomb, based on microenvironment‐adaptive hydrogel microspheres, to oxidize the cell membranes of persisters in chronic periprosthetic joint infection (PJI). Fenton reagent hydroxy iron oxide (FeOOH) and a glucose oxidase (GOx)/calcium phosphate (CaP) acid‐responsive shell are sequentially induced on the surface of mesoporous polydopamine (PDA) nanoparticles by the PDA‐mediated ion precipitation and interfacial adhesion, followed by the coloaded with glucose into microfluidic hyaluronic acid hydrogel microspheres. Hydroxyl radicals are explosively generated through GOx‐mediated glucose oxidase, H2O2 production, and its Fenton‐like reactions with FeOOH, which also benefit from the weakly acidic microenvironment around persisters, result in the destruction of bacterial cell membrane, and subsequent overflow of cellular contents such as dsDNA, proteins, and K+. The bactericidal rates of methicillin‐resistant Staphylococcus aureus and Staphylococcus epidermidis persisters are up to 99.14% and 98.96%, and the bacterial loads in lesion location are significantly decreased after ROS bombs treated, effectively alleviated the inflammation and bone resorption damage. This work provides a new strategy toward persisters clearance and shows great application potential in other chronic infection‐related diseases. [ABSTRACT FROM AUTHOR]

Addressing adipose niche senescence is crucial for preventing obesity‐related aging. Telomerase reverse transcriptase (TERT) is a promising target for gene therapy, but traditional methods lack precision and safety. A novel mitochondrion‐located TERT (mito‐TERT) activating approach is presented by injectable gene/short‐fiber complexes (gene/fiber‐plexes) to safely reverse adipose niche senescence from mitochondrial enhancement. The gene/fiber‐plexes are prepared from polydopamine‐coated short‐fibers to adsorb cationic dendrimers (PAMAM G3, PG3) carrying TERT plasmids and Coenzyme Q10 (CoQ10), termed PG3‐TERT@CoQ10. Upon intraperitoneal injection, the gene/fiber‐plexes adhere to the peritoneum and release PG3‐TERT@CoQ10, precisely targeting the adipose niche. Transient active oxygen scavenging by CoQ10 activates TERT transfection and endogenous mitochondrion translocation sequentially, enhancing mitochondrial function. In vitro and in vivo studies shows that gene/fiber‐plexes effectively targeted visceral adipose tissue, increased mito‐TERT levels and restored mitochondrial function. In an obese mouse model, they restored adipose tissue homeostasis and metabolic stability. RNA sequencing indicated reduced senescence‐related genes and restored cell cycle. This mito‐TERT activation strategy shows great promise for treating premature aging and metabolic diseases linked to adipose tissue senescence. [ABSTRACT FROM AUTHOR]

Introduction: Hypertension has shown to be an important risk factor for the decline in cognitive function. Aim of our study is to investigate the presence of cognitive impairment of the elders with hypertension and other confounding factors., Methods: This study was conducted on 400 veterans who were matched one-to-one with the confounding factors for assessing the presence of mild cognitive impairment using both MMSE and Montreal Cognitive Assessment (MoCA). The 13 related factors of patient data were studied., Results: The prevalence rate of cognitive impairment was 29.25%. Age (OR 2.679, 95%CI 1.663-6.875), sleep impairment (OR 1.117, 95%CI 1.754-7.422), uncontrolled hypertension (OR 1.522, 95%CI 1.968-4.454), type 2 diabetes (OR 2.464, 95%CI 1.232-4.931), and hyperlipidaemia (OR 1.411, 95%CI 1.221-8.988) are the risk factors for the cognitive deterioration, while the protective factors are high level of education (OR 0.032, 95%CI 0.007-0.149) and regular exercise (OR 0.307, 95%CI 0.115-0.818)., Discussion: Because some vascular disease risk factors, such as hypertension, can be treated effectively, cognitive decline related to these risk factors, and vascular disease per se, may be prevented or its course modified through more aggressive treatment and improved compliance.