Habitat destruction, a key determinant of species loss, can be characterized by two components, patch loss and patch fragmentation, where the former refers to the reduction in patch availability, and the latter to the division of the remaining patches. Classical metacommunity models have recently explored how food web dynamics respond to patch loss, but the effects of patch fragmentation have largely been overlooked. Here we develop an extended patch-dynamic model that tracks the patch occupancy of the various trophic links subject to colonization-extinction-predation dynamics by incorporating species dispersal with patch connectivity. We found that, in a simple food chain, species at higher trophic level become extinct sooner with increasing patch loss and fragmentation due to the constraint in resource availability, confirming the trophic rank hypothesis. Yet, effects of fragmentation on species occupancy are largely determined by patch loss, with maximal fragmentation effects occurring at intermediate patch loss. Compared to the spatially explicit simulations that we also performed, the current model with pair approximation generates similar community patterns especially in spatially clustered landscapes. Overall, our extended framework can be applied to model more complex food webs in fragmented landscapes, broadening the scope of existing metacommunity theory.

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Aim To translate and test the psychometric properties of a Chinese version scale to measure the Fear of Activity in patients with Coronary Artery Disease. Design A cross‐sectional design. Methods The translation of the scale to measure Fear of Activity in Patients with Coronary Artery Disease included three steps, forward‐back translation, expert discussion and pilot survey. The internal consistency and test–retest reliability were used to assess the reliability of the Chinese version scale of the Fear of Activity. Content, construct, criterion, and known‐group validity of the scale were also evaluated. Data Sources A total of 275 patients with Coronary Artery Disease were recruited from a university‐affiliated hospital in Guangzhou, southern China. Results The overall content validity index of the Chinese version scale of the Fear of Activity in Patients with Coronary Artery Disease was 0.90. Principal component analyses extracted four factors with a cumulative variance contribution of 57.5%. There is a strong correlation ( r = 0.83) between this scale and Tampa Scale for Kinesiophobia Heart. The total scores of the Chinese version scale of the Fear of Activity in female patients were higher than those in male patients with Coronary Artery Disease, indicating that the scale was able to distinguish the differences between low and high score groups. The Internal consistency and test–retest reliability coefficients of the scale were 0.74 and 0.82, respectively. Conclusion The Chinese version scale of the Fear of Activity in Patients with Coronary Artery Disease, which consists of 21 items with four dimensions, is a reliable and valid instrument to evaluate the fear of activity in patients with Coronary Artery Disease. Implications for the Profession and/or Patient Care The Chinese version scale of the Fear of Activity in Patients with Coronary Artery Disease can be used to assess the levels of fear of activity in patients with Coronary Artery Disease and explores the factors that influence fear of activity in the population. Impact This study translates and confirms the psychometric properties of the Chinese version scale of the Fear of Activity in Patients with Coronary Artery Disease in China. It is useful in both research and clinical fields to explore the fear of activity and its associated factors in patients with Coronary Artery Disease. Reporting Method The study design followed the guideline of Strengthening the Reporting of Observational Studies in Epidemiology statement. Patient or Public Contribution Patients in a university‐affiliated hospital participated in this study and contributed to data collection.

Over the last decade, oncolytic virus (OV) therapy has shown its promising potential in tumor treatment. The fact that not every patient can benefit from it highlights the importance for defining biomarkers that help predict patients’ responses. As particular self-amplifying biotherapeutics, the anti-tumor effects of OVs are highly dependent on the host factors for viral infection and replication. By using weighted gene co-expression network analysis (WGCNA), we found matrix remodeling associated 8 (MXRA8) is positively correlated with the oncolysis induced by oncolytic virus M1 (OVM). Consistently, MXRA8 promotes the oncolytic efficacy of OVM in vitro and in vivo. Moreover, the interaction of MXRA8 and OVM studied by single-particle cryo-electron microscopy (cryo-EM) showed that MXRA8 directly binds to this virus. Therefore, MXRA8 acts as the entry receptor of OVM. Pan-cancer analysis showed that MXRA8 is abundant in most solid tumors and is highly expressed in tumor tissues compared with adjacent normal ones. Further study in cancer cell lines and patient-derived tumor tissues revealed that the tumor selectivity of OVM is predominantly determined by a combinational effect of the cell membrane receptor MXRA8 and the intracellular factor, zinc-finger antiviral protein (ZAP). Taken together, our study may provide a novel dual-biomarker for precision medicine in OVM therapy.

Aiming at the cells' differentiation phenomenon and senescence problem in liver tissue engineering, this work is designed to synthesize three different chargeable polymers (polypropylene acid (PAAc), polyethylene glycol (PEG), and polypropylene amine (PAAm)) coimmobilized by the insulin-like growth factor 1 (IGF-1) and tumor necrosis factor-α (TNF-α). We explore the hepatocyte differentiation effect and the antisenecence effect of PSt-PAAm-IGF-1/TNF-α biomaterial which was selected from the three different chargeable polymers in bone marrow mesenchymal stem cells (BMSCs). Our work will establish a model for studying the biochemical molecular regulation mechanism and signal transduction pathway of cell senescence in liver tissue engineering, which provide a molecular basis for developing biomaterials for liver tissue engineering.