No abstract

The response of metal−organic frameworks (MOFs) toward external stimuli, such as light, heat, and electrons, usually involves a local change in their structures. Although diffraction methods allow for monitoring of the overall dynamics of the crystal structure, the local environment on each crystal and specific position within the crystal remains largely unknown. Here, the collective change in the pores of MOF single crystals was visualized by scanning transmission electron microscopy (STEM) with an interpretable resolution of 4.7 Å to give a clear observation of each individual pore. The local evolvement occurred before the deterioration of image resolution; therefore, the maintenance of overall image resolution does not guarantee the preservation of structure integrity. The local evolvement in response to electron irradiation was quantitatively analyzed and was found to be dependent on both the lattice plane and specific position in the crystal. The crystal shrunk gradually as the electron dose increased. This was likely attributed to the displacement of the molecular building blocks in the MOF backbone. The displacements were inhomogeneous across the individual crystal, corroborating with the local twisting and rotation of the crystal. This STEM method provided an example for the spatial and temporal study of the local structure evolvement of MOFs under stimuli.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder characterized by progressive destruction of lung tissues and airway obstruction. COPD is currently the third leading cause of death worldwide and there is no curative treatment available so far. Cigarette smoke (CS) is the major risk factor for COPD. Yet, only a relatively small percentage of smokers develop the disease, showing that disease susceptibility varies significantly among smokers. As smoking cessation can prevent the disease in some smokers, quitting smoking cannot halt the progression of COPD in others. Despite extensive research efforts, cellular and molecular mechanisms of COPD remain elusive. In particular, the disease susceptibility and smoking cessation effects are poorly understood. To address these issues in this work, we develop a multiscale network model that consists of nodes, which represent molecular mediators, immune cells and lung tissues, and edges describing the interactions between the nodes. Our model study identifies several positive feedback loops and network elements playing a determinant role in the CS-induced immune response and COPD progression. The results are in agreement with clinic and laboratory measurements, offering novel insight into the cellular and molecular mechanisms of COPD. The study in this work also provides a rationale for targeted therapy and personalized medicine for the disease in future.