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Background Cardiovascular diseases (CVDs) and diabetes mellitus (DM) are top two chronic comorbidities that increase the severity and mortality of COVID‐19. However, how SARS‐CoV‐2 alters the progression of chronic diseases remain unclear. Methods We used adenovirus to deliver h‐ACE2 to lung to enable SARS‐CoV‐2 infection in mice. SARS‐CoV‐2’s impacts on pathogenesis of chronic diseases were studied through histopathological, virologic and molecular biology analysis. Results Pre‐existing CVDs resulted in viral invasion, ROS elevation and activation of apoptosis pathways contribute myocardial injury during SARS‐CoV‐2 infection. Viral infection increased fasting blood glucose and reduced insulin response in DM model. Bone mineral density decreased shortly after infection, which associated with impaired PI3K/AKT/mTOR signaling. Conclusion We established mouse models mimicked the complex pathological symptoms of COVID‐19 patients with chronic diseases. Pre‐existing diseases could impair the inflammatory responses to SARS‐CoV‐2 infection, which further aggravated the pre‐existing diseases. This work provided valuable information to better understand the interplay between the primary diseases and SARS‐CoV‐2 infection.

The study introduced a finite element model of DQ75t-28m bridge crane metal structure and made finite element static analysis to obtain the stress response of the dangerous point of metal structure in the most extreme condition. The simulated samples of the random variable and the stress of the dangerous point were successfully obtained through the orthogonal design. Then, we utilized BP neural network nonlinear mapping function trains to get the explicit expression of stress in response to the random variable. Combined with random perturbation theory and first-order second-moment (FOSM) method, the study analyzed the reliability and its sensitivity of metal structure. In conclusion, we established a novel method for accurately quantitative analysis and design of bridge crane metal structure.

ObjectiveBy exploring the effects of miR-29a-5p knockout on neurological damage after acute ischemic stroke, we aim to deepen understanding of the molecular mechanisms of post-ischemic injury and thus provide new ideas for the treatment of ischemic brain injury.MethodsmiR-29a-5p knockout rats and wild-type SD rats were subjected to transient middle cerebral artery occlusion (MCAO). miR-29a levels in plasma, cortex, and basal ganglia of ischemic rats, and in plasma and neutrophils of ischemic stroke patients, as well as hypoxic glial cells were detected by real-time PCR. The infarct volume was detected by TTC staining and the activation of astrocytes and microglia was detected by western blotting.ResultsThe expression of miR-29a-5p was decreased in parallel in blood and brain tissue of rat MCAO models. Besides, miR-29a-5p levels were reduced in the peripheral blood of acute stroke patients. Knockout of miR-29a enhanced infarct volume of the MCAO rat model, and miR-29a knockout showed M1 polarization of microglia in the MCAO rat brain. miR-29a knockout in rats after MCAO promoted astrocyte proliferation and increased glutamate release.ConclusionKnockout of miR-29a in rats promoted M1 microglial polarization and increased glutamate release, thereby aggravating neurological damage in experimental stroke rat models.

Background Inflammation is a complex physiological and pathological process. Although many types of inflammation are well characterized, their physiological functions are largely unknown. tRNA aspartic acid methyltransferase 1 (TRDMT1) has been implicated as a stress‐related protein, but its intrinsic biological role is unclear. Methods We constructed a Trdmt1 knockout rat and adopted the LPS‐induced sepsis model. Survival curve, histopathological examination, expression of inflammatory factors, and protein level of TLR4 pathway were analyzed. Results Trdmt1 deletion had no obvious impact on development and growth. Trdmt1 deletion slightly increased the mortality during aging. Our data showed that Trdmt1 strongly responded in LPS‐treated rats, and Trdmt1 knockout rats were vulnerable to LPS treatment with declined survival rate. We also observed more aggravated tissue damage and more cumulative functional cell degeneration in LPS‐treated knockout rats compared with control rats. Further studies showed upregulated TNF‐α level in liver, spleen, lung, and serum tissues, which may be explained by enhanced p65 and p38 phosphorylation. Conclusions Our data demonstrated that Trdmt1 plays a protective role in inflammation by regulating the TLR4‐NF‐κB/MAPK‐TNF‐α pathway. This work provides useful information to understand the TRDMT1 function in inflammation.