Analysis of bacterial spectrum, activin A, and CD64 in chronic obstructive pulmonary disease patients complicated with pulmonary infections.

BACKGROUND: Pulmonary infections often lead to poor prognoses in patients with chronic obstructive pulmonary disease (COPD). Activin A and CD64 play crucial pathological roles in the development of COPD. AIM: To explore the bacterial spectrum via analysis of activing A levels, CD64 index, and related mechanisms in COPD patients complicated with pulmonary infection. METHODS: Between March 2015 and January 2018, a total of 85 patients with COPD, who also suffered from pulmonary infections, were enrolled in this study as the pulmonary infection group. In addition, a total of 96 COPD patients, without pulmonary infection, were selected as the control group. Sputum samples of patients in the pulmonary infection group were cultivated for bacterial identification prior to administration of antibiotics. The neutrophil CD64 index was measured using flow cytometry, serum activin A levels were detected via an enzyme-linked immunosorbent assay, and activin A, Smad3, TLR4, MyD88, and NFκB protein expression was analyzed by Western blotting. RESULTS: Gram-negative bacteria were identified in 57.65% of the sputum samples in the pulmonary infection group. The most prevalent Gram-negative species were Pseudomonas aeruginosa and Klebsiella pneumoniae. Conversely, Gram-positive bacteria were identified in 41.18% of the sputum samples in the pulmonary infection group. The most common Gram-positive species was Streptococcus pneumoniae. Fungi were identified in 1.17% of the sputum samples in the pulmonary infection group. The CD64 index was significantly higher in the pulmonary infection group (0.91 ± 0.38) than in the control group (0.23 ± 0.14, P < 0.001). The serum activin A levels were significantly higher in the pulmonary infection group (43.50 ± 5.22 ng/mL), compared to the control group (34.82 ± 4.16 ng/mL, P < 0.001). The relative expression levels of activin A, Smad3, TLR4, MyD88, and NFκB were all significantly higher in the pulmonary infection group, compared to the control group (all P < 0.001). CONCLUSION: Pulmonary infections in COPD patients are mainly caused by Streptococcus pneumoniae, Pseudomonas aeruginosa, and Klebsiella pneumoniae. Pulmonary infections can significantly increase neutrophil CD64 index and serum levels of activin A, thereby activating the activin A/Smad3 signaling pathway, which may positively regulate the TLR4/MyD88/NFκB signaling pathway.

Upregulation of silent information regulator 1 alleviates mitochondrial dysfunction in the trigeminal nucleus caudalis in a rat model of chronic migraine.

Although the mechanism of chronic migraine is still unclear, more and more studies have shown that mitochondrial dysfunction plays a possible role in migraine pathophysiology. Silent information regulator 1 (SIRT1) plays a vital role in mitochondrial dysfunction in many diseases. However, there is no research on the role of SIRT1 in mitochondrial dysfunction of chronic migraine. The aim of this study was to explore the role of SIRT1 in mitochondrial dysfunction in chronic migraine. A rat model was established through repeated dural infusions of inflammatory soup for 7 days to simulate chronic migraine attacks. Cutaneous hyperalgesia caused by the repeated infusions of inflammatory soup was detected using the von Frey test. Then, we detected SIRT1 expression in the trigeminal nucleus caudalis. To explore the effect of SIRT1 on mitochondrial dysfunction in chronic migraine rats, we examined whether SRT1720, an activator of SIRT1, altered mitochondrial dysfunction in chronic migraine rats. Repeated infusions of inflammatory soup resulted in cutaneous hyperalgesia accompanied by downregulation of SIRT1. SRT1720 significantly alleviated the cutaneous hyperalgesia induced by repeated infusions of inflammatory soup. Furthermore, activation of SIRT1 markedly increased the expression of peroxisome proliferator-activated receptor gamma-coactivator 1-alpha, transcription factor A, nuclear respiratory factor 1 and nuclear respiratory factor 2 mitochondrial DNA and increased the ATP content and mitochondrial membrane potential. Our results indicate that SIRT1 may have an effect on mitochondrial dysfunction in chronic migraine rats. Activation of SIRT1 has a protective effect on mitochondrial function in chronic migraine rats.

Strong morphological effect of Mn3O4 nanocrystallites on the catalytic activity of Mn3O4 and Au/Mn3O4 in benzene combustion.

Gold nanoparticles (3-4 nm) were deposited on Mn3O4 nanocrystallites with three distinct morphologies (cubic, hexagonal, and octahedral). The resulting structures were characterized, and their activities for benzene combustion were evaluated. The dominant exposed facets for the three kinds of Mn3O4 polyhedrons show the activity order: (103)≈(200)>(101). A similar activity order was derived for the interfaces between the Au and the Mn3O4 facet: Au/(200)≈Au/(103)>Au/(101). The metal-support interactions between the Au nanoclusters and specific facets of the Mn3O4 polyhedrons lead to a unique interfacial synergism in which the electronic modification of the Au nanoparticles and the morphology of the Mn3O4 substrate have a joint effect that is responsible for a significant enhancement in the catalytic activity of the Au/Mn3O4 system.