Case Report: An Ulceration With a Stalactite Appearance on the Index Finger.

Proteus mirabilis, the most widespread species of all Proteus spp. bacteria, is proven to be one of the most universal pathogens in chronic wounds. In this case, a woman in her 40s consulted a physician about an asymptomatic ulceration with a stalactite appearance at the distal end of the index finger after she was exposed to a needle when vaccinating chickens. The patient did not response to ceftazidime. Physical examination revealed a well-demarcated violescent ulceration with a stalactite appearance at the distal end of the index finger. A biopsy of the lesion showed dense infiltration of multinucleated giant cells, histiocytes, and lymphocytes in the dermis. The result of metagenomics next-generation sequencing (NGS) showed 306 unique sequence reads of P. mirabilis, covering 33.49% of the nucleotide sequences. The pathogen was identified as P. mirabilis, which was resistant to ceftazidime. The patient was treated with ciprofloxacin hydrochloride and improved considerably. This case reported a distinctive cutaneous lesion of P. mirabilis on human infection and showed a successful use of NGS in P. mirabilis.

Circular RNA Cdyl promotes abdominal aortic aneurysm formation by inducing M1 macrophage polarization and M1-type inflammation.

Macrophage polarization plays a crucial role in regulating abdominal aortic aneurysm (AAA) formation. Circular RNAs (circRNAs) are important regulators of macrophage polarization during the development of cardiovascular diseases. How-ever, the roles of circRNAs in regulating AAA formation through modulation of macrophage polarization remain unknown. In the present study, we compared circRNA microarray data under two distinct polarizing conditions (M1 and M2 macrophages) and identified an M1-enriched circRNA, circCdyl. Loss- and gain-of-function assay results demonstrated that circCdyl overexpression accelerated angiotensin II (Ang II)- and calcium chloride (CaCl2)-induced AAA formation by promoting M1 polarization and M1-type inflammation, while circCdyl deficiency showed the opposite effects. RNA pulldown, mass spectrometry analysis, and RNA immunoprecipitation (RIP) assays were conducted to elucidate the underlying mechanisms by which circCdyl regulates AAA formation and showed that circCdyl promotes vascular inflammation and M1 polarization by inhibiting interferon regulatory factor 4 (IRF4) entry into the nucleus, significantly inducing AAA formation. In addition, circCdyl was shown to act as a let-7c sponge, promoting C/EBP-δ expression in macrophages to induce M1 polarization. Our results indicate an important role for circCdyl-mediated macrophage polarization in AAA formation and provide a potent therapeutic target for AAA treatment.

CircRNA Chordc1 protects mice from abdominal aortic aneurysm by contributing to the phenotype and growth of vascular smooth muscle cells.

Circular RNAs (circRNAs) have important potential in modulating vascular smooth muscle cell (VSMC) activity, but their roles in abdominal aortic aneurysm (AAA) are unknown. We performed in situ hybridization and immunohistochemistry and determined that circChordc1 (cysteine and histidine-rich domain containing 1) was markedly downregulated in aneurysm tissue compared with normal arteries. A gene gain and loss strategy was used to confirm that circChordc1 transformed VSMCs into a contracted phenotype and improved their growth, which significantly suppressed aneurysm formation and reduced the risk of rupture in mouse models of angiotensin (Ang) II- and CaCl2-induced AAA. RNA pull-down, immunoprecipitation, and immunoblotting indicated that circChordc1 facilitated the VSMC phenotype and growth determination by binding to vimentin and ANXA2 (annexin A2), which not only increased vimentin phosphorylation to promote its degradation but also promoted the interaction between ANXA2 and glycogen synthase kinase 3 beta (GSK3ß) to induce the nuclear entry of ß-catenin. Thus, our present study revealed that circChordc1 optimized the VSMC phenotype and improved their growth by inducing vimentin degradation and increasing the activity of the GSK3ß/ß-catenin pathway, thereby extenuating vascular wall remodeling and reversing pathological aneurysm progression.