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Abstract Mutations in fibrillin 1 (FBN1) is the main cause of Marfan syndrome (MFS) with thoracic aortic aneurysm (TAA) as the main complication. Activation of the complement system plays a key role in the formation of thoracic and abdominal aortic aneurysms. However, the role of the complement system in MFS-associated aortic aneurysms remains unclear. In this study, we observed increased levels of complement C3a and C5a in the plasma of MFS patients and mouse, and the increased deposition of the activated complement system product C3b/iC3b was also observed in the elastic fiber rupture zone of 3-month-old MFS mice. The expression of C3a receptor (C3aR) was increased in MFS aortas, and recombinant C3a promoted the expression of cytokines in macrophages. The administration of a C3aR antagonist (C3aRA) attenuated the development of thoracic aortic aneurysms in MFS mice. The increased inflammation response and matrix metalloproteinases activities were also attenuated by C3aRA treatment in MFS mice. Therefore, these findings indicate that the complement C3a/C3aR inhibition alleviates the formation of aortic aneurysm in Marfan syndrome mice.

Abstract During the process of muscle regeneration post‐injury in adults, muscle stem cells (MuSCs) function is facilitated by neighboring cells within the pro‐regenerative niche. However, the precise mechanism triggering the initiation of signaling in the pro‐regenerative niche remains unknown. Using single‐cell RNA sequencing, 14 different muscle cells are comprehensively mapped during the initial stage following injury. Among these, macrophages and fibro‐adipogenic progenitor cells (FAPs) exhibit the most pronounced intercellular communication with other cells. In the FAP subclusters, the study identifies an activated FAP phenotype that secretes chemokines, such as CXCL1, CXCL5, CCL2, and CCL7, to recruit macrophages after injury. Il1rl1, encoding the protein of the interleukin‐33 (IL‐33) receptor, is identified as a highly expressed signature surface marker of the FAP phenotype. Following muscle injury, autocrine IL‐33, an alarmin, has been observed to activate quiescent FAPs toward this inflammatory phenotype through the IL1RL1‐MAPK/NF‐κB signaling pathway. Il1rl1 deficiency results in decreased chemokine expression and recruitment of macrophages, accompanied by impaired muscle regeneration. These findings elucidate a novel mechanism involving the IL‐33/IL1RL1 signaling pathway in promoting the activation of FAPs and facilitating muscle regeneration, which can aid the development of therapeutic strategies for muscle‐related disorders and injuries.

For the purpose that relieves the suffering of the patients and shortens their hospital stay, it is crucial to design and manage the environment control systems reasonably to maintain an appropriate indoor thermal environment. However, all of the current thermal comfort theories are based on a healthy population. There are significant differences in metabolism and clothing thermal resistance between inpatients and healthy people, which are regarded as vital influenced factors on people's thermal comfort. Therefore, these existing thermal comfort models may not be applicable for inpatients. In this paper, the patients' comfort equation was derived by modifying the metabolism and the clothing thermal resistance based on the thermal comfort model of Professor Fanger, and the rationality of the model was tested by using field experiment data obtained in general wards. Validated by t-tests, the value of AMV and PMV calculated by the modified equation is not markedly different on a 5% significant level for all patients lying on bed in winter. Moreover, the typical comfort diagrams of inpatients were established by solving the thermal comfort equation. The results of this study are intended to assist in the formulation of useful guidelines to facilitate the assessment and management of hospital ward thermal environments.

Abstract Background Recently, extensive evidence has clarified the crucial role of circular RNAs (circRNAs) as a pro-tumor or anti-cancer participant in human malignancies. A new circRNA derived from oxysterol binding protein like 10 (OSBPL10) (circOSBPL10) has not been researched in cervical cancer (CC) yet. Methods The expression of molecules was analyzed by RT-qPCR or western blot. Several functional assays were applied to explore the biological influence of circOSBPL10 on CC. The interaction between RNAs was estimated via luciferase reporter, RNA immunoprecipitation and RNA pull-down assays. Results CircOSBPL10 characterized with cyclic structure was revealed to possess elevated expression in CC cells. CircOSBPL10 downregulation elicited suppressive impacts on CC cell proliferation and migration. Interestingly, circOSBPL10 regulated CC progression by interacting with microRNA-1179 (miR-1179). Moreover, ubiquitin conjugating enzyme E2 Q1 (UBE2Q1) targeted by miR-1179 was positively regulated by circOSBPL10 in CC. Furthermore, enhanced UBE2Q1 expression or suppressed miR-1179 level countervailed the repressive effect of circOSBPL10 depletion on the malignant phenotypes of CC cells. Moreover, forkhead box A1 (FOXA1) was confirmed to induce circOSBPL10 expression in CC cells. Conclusions FOXA1-induced circOSBPL10 facilitates CC progression through miR-1179/UBE2Q1 axis, highlighting a strong potential for circOSBPL10 to serve as a promising therapeutic target in CC.