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Importantly, in our study we sought to determine if reducing senescent cells could lessen the severity of AAA in aged mice. We find that pretreatment of aged mice with oral senolytic agents (dasatinib + quercetin) reduced senescent cell abundance in the arterial walls and surrounding tissues and lessened the severity of AAA in response to angiotensin II administration. These data provide important preliminary evidence supporting a role of senescent cells in age-related AAA formation and progression and suggest that strategies to reduce senescent cell burden hold promise to lessen AAA severity.Pneumonia is among the leading causes of morbidity and mortality worldwide. Due to constant evolution of respiratory bacteria and viruses, development of drug resistance and emerging pathogens, it constitutes a considerable health care threat. To enable development of novel strategies to control pneumonia, a better understanding of the complex mechanisms of interaction between host cells and infecting pathogens is vital. Terfenadine inhibitor Here, we review the roles of host cell and bacterial-derived extracellular vesicles (EVs) in these interactions. We discuss clinical and experimental as well as pathogen-overarching and pathogen-specific evidence for common viral and bacterial elicitors of community- and hospital-acquired pneumonia. Finally, we highlight the potential of EVs for improved management of pneumonia patients and discuss the translational steps to be taken before they can be safely exploited as novel vaccines, biomarkers, or therapeutics in clinical practice.Inflammation is a fundamental element in secondary brain injury (SBI) besides intracerebral hemorrhage (ICH). Pyrin domain that contains 3 inflammasome (NLRP3) was regarded as a key role of the nod-like receptor family and played an important part in the inflammatory response following ICH-induced injury. FUN14 domain containing 1 (FUNDC1) is a kind of mitophagy receptor, which can eliminate mitochondrial dysfunction after hypoxia and mitochondrial stress. Previous research showed that mitophagy prevents inflammation through inhibiting NLRP3 inflammasome pathway. However, the relationship between FUNDC1 and ICH-induced inflammatory response stays uncertain. In this study, we investigate that FUNDC1 inhibit NLRP3 inflammasome activation by promoting mitophagy, thereby alleviate ICH-induced injury. We established ICH model by injecting tail venous blood into the basal ganglia of C57 mice (healthy, male adult). We injected siRNA to knockdown FUNDC1. In order to deeply seek for the mechanisms of FUNDC1 in ICH-induced injury, FUNDC1 was overexpressed by adeno-associated virus (AAV) and mitophagy was suppressed by specific inhibitor (mdivi-1). The protein level of FUNDC1 was upregulated and got peak at 12h after ICH. We noticed that silencing FUNDC1 can suppress mitophagy, promote NLRP3-mediated inflammation and exacerbate ICH injury. Furthermore, the results indicated that mitophagy participated in the inhibitory effect of FUNDC1 on NLRP3-mediated inflammatory response after ICH. Our results showed that FUNDC1 alleviated ICH-induced inflammation in mice by promoting mitophagy. Those data suggested that FUNDC1 may be a potential target for the treatment of ICH.Aging-related especially brain aging-related diseases are heavy health care burdens worldwide. Natural products with antioxidant and anti-inflammatory properties have been studied to prevent brain aging pathogenesis. In the present study we investigated the potential mechanism of dihydromyricetin (DMY), isolated from Ampelopsis grossedentata, against D-galactose (D-Gal)-triggered brain aging of mice. Mice were randomly assigned into five groups (n = 20) control group, D-gal (150 mg/kg) group, D-gal (150 mg/kg) + Puerarin group, D-gal (150 mg/kg) + DMY (168 mg/kg) and D-gal (150 mg/kg) + DMY (42 mg/kg). Morris water maze (MWM) was used to assess spatial cognition and oxidative stress and inflammation index such as advanced glycation end products (AGEs), malondialdehyde (MDA), IL-2 and IL-6 were detected by ELISA. Cellular senescence marker was detected by Western blotting analysis. We found that DMY (42 mg/kg) showed strong neuroprotective effects, evidenced by improved spatial cognition and might be attributed to the alleviated damage of hippocampal neurons. In addition, DMY also suppressed the D-Gal-induced senescence of hippocampal neurons by inhibiting the expressions of p53, p21, and p16. Furthermore, DMY restored the activity of catalase and exhibited a potent inhibitory effect on lipid peroxidation, AGEs and MDA of D-Gal-exposed mice. Moreover, DMY decreased the abundance of IL-6 but increased the abundance of IL-2 of D-Gal-exposed mice. These findings indicated that DMY might protect against brain aging caused by chronic D-Gal exposure by modulating oxidative stress and inflammation-related senescence of hippocampal neurons.Differential diagnosis of Parkinson’s disease (PD), multiple system atrophy (MSA) and progressive supranuclear paralysis (PSP) is challenging. This study aimed to investigate the expression of phosphorylated α-synuclein (p-α-syn) and phosphorylated tau-protein (p-tau) in sural nerves from patients with PD, MSA and PSP to find biomarkers for differential diagnosis. Clinical evaluations and sural nerve biopsies were performed on 8 PD patients, 8 MSA patients, 6 PSP patients and 8 controls (CTRs). Toluidine blue staining was used to observe morphological changes in sural nerves. The deposition of p-α-syn and p-tau was detected by immunohistochemistry with semiquantitative evaluation. Locations of p-α-syn and p-tau were identified by double immunofluorescent staining. In case groups, the density of nerve fibres decreased with swollen or fragmented Schwann cells (SCs). All cases (22/22) but no CTRs (0/8) presented p-α-syn immunoreactivity with gradually decreasing semiquantitative levels among the PD (6.00 ± 2.07), MSA (5.00 ± 2.33) and PSP (3.50 ± 1.52) groups. p-tau aggregates were found in 7/8 MSA (1.88 ± 1.46) and 6/6 PSP (1.67 ± 0.52) patients but not in PD patients or CTRs. There were different expression patterns of p-α-syn and p-tau in PD, MSA and PSP patients. These findings suggest that peripheral sensory nerve injury exists in PD, MSA and PSP patients. With a different expression pattern and level, p-α-syn and p-tau in sural nerves may serve as novel biomarkers for differential diagnosis of PD, MSA and PSP.