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Ferroptosis is a term that describes one form of regulated non-apoptotic cell death. It’s triggered by iron-dependent accumulation of lipid peroxides. Emerging evidence suggests a link between ferroptosis and the pathophysiological processes of neurological disorders, including stroke, degenerative diseases, neurotrauma, and cancer. Hemorrhagic stroke, also known as intracerebral hemorrhage (ICH), belongs to a devastating illness for its high level in morbidity and mortality. Currently, there are few established treatments and limited knowledge about the mechanisms of post-ICH neuronal death. The secondary brain damage after ICH is mainly attributed to oxidative stress and hemoglobin (Hb) lysate, including iron, which leads to irreversible damage to neurons. Therefore, ferroptosis is becoming a common trend in research of neuronal death after ICH. Accumulative data suggest the inhibition of ferroptosis may effectively prevent neuronal ferroptosis, thereby reducing secondary brain damage after ICH in animal models. Ferroptosis has a close relationship with oxidative damage and iron metabolism. In this review lies in revealing the pathological pathways and regulation mechanism of ferroptosis following ICH, then offer the potential intervention strategies to mitigate neuron death and dysfunction after ICH.

Microglia are the resident immune cells of the central nervous system (CNS). It is well established that microglia are activated and polarized to acquire different inflammatory phenotypes, either pro-inflammatory or anti-inflammatory phenotypes, which act as a critical component in the neuroinflammation following intracerebral hemorrhage (ICH). Microglia produce pro-inflammatory mediators at the early stages after ICH onset, anti-inflammatory microglia with neuroprotective effects appear to be suppressed. Previous research found that driving microglia towards an anti-inflammatory phenotype could restrict inflammation and engulf cellular debris. The principal objective of this review is to analyze the phenotypes and dynamic profiles of microglia as well as their shift in functional response following ICH. The results may further the understanding of the body’s self-regulatory functions involving microglia following ICH. On this basis, suggestions for future clinical development and research are provided.

As a significant constituent in biosphere, bacteria have a great influence on human activity. The detection of pathogen bacteria is closely related to the human health. However, the traditional methods for detection of pathogenic bacteria are time-consuming and difficult for quantification, although they are practical and reliable. Therefore, novel strategies for rapid, sensitive, and cost-effective detection are in great demand. Aptamer is a kind of oligonucleotide that selected by repeated screening in vitro or systematic evolution of ligands by exponential enrichment (SELEX) technology. Over the past years, owing to high affinity and specificity of aptamers, a variety of aptamer-based biosensors have been designed and applied for pathogen detection. In this review, we have discussed the recent advances on the applications of aptamer-based biosensors in detection of pathogenic bacteria. In addition, we also point out some problems in current methods and look forward to the further development of aptamer-based biosensors for pathogen detection.

MicroRNAs (miRNAs) are a type of endogenous non-coding short-chain RNA, which plays a crucial role in the regulation of many essential cellular functions, including cellular migration, proliferation, invasion, autophagy, oxidative stress, apoptosis, and differentiation. The lung can be damaged by pathogenic microorganisms, as well as physical or chemical factors. Research has confirmed that miRNAs and lung cell apoptosis can affect the development and progression of several lung diseases. This article reviews the role of miRNAs in the development of lung disease through regulating host cell apoptosis.

As emerging alternatives to natural enzymes, nanoscale materials featuring enzyme‐like catalytic behaviors (nanozymes) exhibit some attractive merits including robust activity, low cost, and easy‐to‐regulate performance. These merits have enabled them to be intensively used in the biomedical field in recent years. To remedy the lack of catalytic selectivity in most nanozymes, deoxyribonucleic acid (DNA) chains with specific recognition functions are utilized to integrate with nanozymes to produce various nanozyme–DNA combinations via adsorption/desorption. In the formed combinations, the DNA component provides the molecular/ionic recognition role, and the nanozyme part offers response with catalytically amplified signals, enabling them to detect analytes and biomarkers selectively and sensitively. To highlight this interesting topic, here we made a critical review of the interactions between nanozymes and DNA and their applications in biosensing and disease diagnosis. First, strategies for the conjugation of DNA chains onto nanozyme surface were introduced briefly. Then, the interactions between DNA and nanozymes were summarized in detail, where flexible modulations of nanozyme activity by DNA adsorption/desorption as well as various factors were analyzed, and potential impacts caused by nanozymes on the recognition characteristics of DNA chains were pointed out. After that, typical applications of DNA‐mediated nanozyme modulation in toxic ion sensing, health risk factor monitoring, and biomedical diagnosis were introduced. In the end, prospects of the combination of nanozymes and DNA chains were presented, and future challenges of the emerging field were also discussed, to attract more interest and effort to advance this promising area. This critical review highlights the interactions between nanozymes and deoxyribonucleic acid (DNA) and their applications in biosensing and disease diagnosis. First, strategies for the conjugation of DNA chains onto nanozyme surfaces are introduced briefly. Then, the interactions between DNA and nanozymes are summarized in detail, where flexible modulations of nanozyme activity by DNA adsorption/desorption as well as various factors are analyzed, and potential impacts caused by nanozymes on the recognition characteristics of DNA chains are pointed out. After that, typical applications of DNA‐mediated nanozyme modulation in toxic ion sensing, health risk factor monitoring, and biomedical diagnosis are introduced. In the end, prospects of the combination of nanozymes and DNA chains are presented, and future challenges of the emerging field are also discussed.

Temperate phages are potential therapeutic agents, but only a few temperate phages infecting multidrug-resistant Acinetobacter baumannii have been identified. In this study, we isolated 5W, a temperate phage that infects multidrug-resistant A. baumannii, from pond water using the enrichment method. A member of the Siphoviridae family, 5W has a narrow host range and infected only four of 19 A. baumannii clinical isolates. It exhibited rapid adsorption (> 90% in 6 min), a latency period of 20 min, and a burst size of ~ 180 plaque-forming units (PFU/cell). 5W contains a linear double-stranded DNA (dsDNA) genome of 43,032 bp with a GC content of 39.85%. The 5W genome contains 61 open reading frames, including lysogen-forming genes, but lacks any known virulence and antibiotic resistance genes. The lysin of 5W is an N-acetyl-β-d-muramidase belonging to the GH_108 family. The α-helical structure and highly positively charged amino acids in the C-terminal region indicate potential antibacterial activity against A. baumannii, and the M/S subunits of the restriction endonuclease are inserted into the lysogenic gene cluster. Comparative genome analysis revealed high similarity with two different prophages in A. baumannii ABCR01, suggesting that 5W may be derived from recombination of other prophages.

To inhibit the growth of bacteria, the DA-PPI nanozyme with enhanced peroxidase-like activity was synthesized. The DA-PPI nanozyme was obtained by depositing high-affinity element iridium (Ir) on the surface of Pd-Pt dendritic structures. The morphology and composition of DA-PPI nanozyme were characterized using SEM, TEM, and XPS. The kinetic results showed that the DA-PPI nanozyme possessed a higher peroxidase-like activity than that of Pd-Pt dendritic structures. The PL, ESR, and DFT were employed to explain the high peroxidase activity. As a proof of concept, the DA-PPI nanozyme could effectively inhibit E. coli (G−) and S. aureus (G+) due to its high peroxidase-like activity. The study provides a new idea for the design of high active nanozymes and their application in the field of antibacterial.

Background: Hematoma is the chief culprit in brain injury following intracranial cerebral hemorrhage (ICH). Noninvasive hematoma clearance could be an option to prevent and alleviate early brain injury after ICH. Peroxisome proliferator-activated receptor γ (PPAR-γ) and nuclear factor-erythroid 2 related factor-2 (Nrf2) facilitate removal of hematoma in ICH. Monascin acts as the natural Nrf2 activator with PPAR-γ agonist, and the long-term effects of monascin following ICH have not been elucidated. Methods: ICH in rats was induced by stereotactic, intrastriatal injection of type IV collagenase. Monascin was administered twice daily by gastric perfusion for 14 days after ICH induction. Long-term neurological scores (T maze, Garcia scales, rotor rod test, and Morris water maze), hematoma volume, as well as iron overload around hematoma and brain atrophy were evaluated at 7, 14, and 28 days after ICH. Results: The results showed that monascin improved long-term neurological deficits, spatial memory performance, learning ability, and brain shrinkage after ICH. Monascin also reduced hematoma volume at 7 days and iron content at 7 and 14 days after ICH. Conclusion: PPAR γ and Nrf2 play a crucial role in hematoma clearance after ICH in rat. As a dual agonist of PPAR γ and Nrf2, monascin improved long-term outcomes by facilitating hematoma clearance, and by attenuating iron overload and brain atrophy after experimental ICH.

Chlamydia psittaci is an important zoonotic factor associated with human and animal atypical pneumonia. Resisting host cell apoptosis is central to sustaining Chlamydia infection in vivo . Chlamydia can secrete inclusion membrane proteins (Incs) that play important roles in their development cycle and pathogenesis. CPSIT_0846 is an Inc protein in C. psittaci identified by our team in previous work. In the current study, we investigated the regulatory role of CPSIT_0846 in HeLa cell apoptosis, and explored potential mechanisms. The results showed that HeLa cells treated with CPSIT_0846 contained fewer apoptotic bodies and exhibited a lower apoptotic rate than untreated cells either with Hoechst 33258 fluorescence staining or flow cytometry with or without induction by staurosporine (STS). CPSIT_0846 could increase the phosphorylation of the extracellular signal-regulated kinases 1/2 (ERK1/2) or stress-activated protein kinases/c-Jun amino-terminal kinases (SAPK/JNK) signaling pathways, and the Bcl-2 associated X protein (Bax)/B cell lymphoma 2 (Bcl-2) ratio, levels of cleaved caspase-3/9 and cleaved Poly-ADP-ribose polymerase (PARP) were significantly up-regulated following inhibition of ERK1/2 or SAPK/JNK pathways with U0126 or SP600125. After carbonyl cyanide 3-chlorophenylhydrazone (CCCP) treatment, the mitochondrial membrane potential (MMP) of cells was significantly decreased in control group, but stable in the CPSIT_0846 treated one, and less cytochrome c (Cyt.c) was released into the cytoplasm. Inhibition of the ERK1/2 or SAPK/JNK pathway significantly decreased the JC-1 red-green fluorescence signal, and promoted Cyt.c discharge into the cytoplasm in HeLa cells treated with CPSIT_0846. In conclusion, CPSIT_0846 can regulate mitochondrial pathway-mediated apoptosis in HeLa cells by activating the ERK/JNK signaling pathway.

Oxidative stress (OS) is induced by the accumulation of reactive oxygen species (ROS) following intracerebral hemorrhage (ICH) and plays an important role in secondary brain injury caused by the inflammatory response, apoptosis, autophagy, and blood-brain barrier (BBB) disruption. This review summarizes the current state of knowledge regarding the pathogenic mechanisms of brain injury after ICH, markers for detecting OS, and therapeutic strategies that target OS to mitigate brain injury.