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Succinate dehydrogenase inhibitor (SDHI) is an important fungicide to control grain diseases. For this reason, a series of novel pyrazole‐4‐carboxamide derivatives with an N‐methoxy group were designed and synthesized. All the target compounds were characterized by 1H NMR, 13C NMR, and HRMS. The compound 3c was further confirmed by X‐ray diffraction, which crystallized in the triclinic system, space group P‐1, Z = 2. The fungicidal activity results indicated that most of these compounds possessed good activity against Sclerotinia sclerotiorum at 50 ppm. Especially, compound 3h exhibited the best activity with the EC50 is 7.80 μg/mL, which is comparable with the positive control bixafen (EC50 = 6.70 μg/mL). Furthermore, the physicochemical properties, molecular docking simulation, ADMET analyses, DFT of compounds 3h, 3k and two commercial SDHIs, isoflucypram and pydiflumetofen, were investigated in this study. [ABSTRACT FROM AUTHOR]

Primary localized tracheobronchial amyloidosis ( TBA) is a rare respiratory tract dysfunction, which is a heterogeneous group of diseases involving abnormal extracellular deposition of amyloid and autologous fibrillar protein material in β-pleated sheets. A 64-year-old man was referred to our hospital because of hemoptysis. Physical examination showed decreased breath sounds in the right lung on auscultation. Chest computed tomography scan displayed multiple nodules with varied size in main bronchia around bilateral hilus of the lung. After admission, bronchoscopy was performed for this patient, and roughness of mucosa in trachea and multiple nodules in respiratory tract were observed. Through further tissue biopsy, the diagnosis of primary TBA was confirmed. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies in our lab have identified pre-B-cell colony enhancing factor (PBEF) as a novel biomarker in acute lung injury. This study continues to elucidate the underlying molecular mechanism of PBEF in the pathogenesis of acute lung injury in pulmonary cell culture models. Our results revealed that IL-1β induced PBEF expression in pulmonary vascular endothelial cells at the transcriptional level and a −1535 T-variant in the human PBEF gene promoter significantly attenuated its binding to an IL-1β-induced unknown transcription factor. This may underlie the reduced expression of PBEF and thus the lower susceptibility to acute lung injury in −1535T carriers. Furthermore, overexpression of PBEF significantly augmented IL-8 secretion and mRNA expression by more than 6-fold and 2-fold in A549 cells and HPAEC, respectively. It also significantly augmented IL-1β-mediated cell permeability by 44% in A549 cells and 65% in endothelial cells. The knockdown of PBEF expression significantly inhibited IL-1β-stimulated IL-8 secretion and mRNA level by 60% and 70%, respectively, and the knockdown of PBEF expression also significantly attenuated IL-1β-induced cell permeability by 29% in epithelial cells and 24% in endothelial cells. PBEF expression also affected the expression of two other inflammatory cytokines (IL-16 and CCR3 genes). These results suggest that PBEF is critically involved in pulmonary vascular and epithelial inflammation and permeability, which are hallmark features in the pathogenesis of acute lung injury. This study lends further support to our finding that PBEF is a potential new target in acute lung injury. [Copyright &y& Elsevier]

Abstract: Identification of pre-B-cell colony-enhancing factor (PBEF) interacting partners may reveal new molecular mechanisms of PBEF in the pathogenesis of acute lung injury (ALI). The interactions between PBEF and NADH dehydrogenase subunit 1(ND1), ferritin light chain and interferon induced transmembrane 3 (IFITM3) in human pulmonary vascular endothelial cells were identified and validated. ND1, ferritin and IFITM3 are involved in oxidative stress and inflammation. Overexpression of PBEF increased its interactions and intracellular oxidative stress, which can be attenuated by rotenone. The interaction modeling between PBEF and ND1 is consistent with the corresponding experimental finding. These interactions may underlie a novel role of PBEF in the pathogenesis of ALI. Structured summary: MINT-6538697: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with NADH1 (uniprotkb:P03886) by two hybrid (MI:0018) MINT-6538811, MINT-6538868: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with interferon-induced transmembrane protein 3 (uniprotkb:Q01628) by anti bait coimmunoprecipitation (MI:0006) MINT-6538787, MINT-6538841: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with NADH1 (uniprotkb:P03886) by anti bait coimmunoprecipitation (MI:0006) MINT-6538755: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with γ-glutamyl-transferase (uniprotkb:P19440) by two hybrid (MI:0018) MINT-6538799, MINT-6538862: PBEF (uniprotkb:P43490) physically interacts (MI:0218)with Ferritin light chain (uniprotkb:P02792) by anti bait coimmunoprecipitation (MI:0006) MINT-6538769: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with E2L6 (uniprotkb:O14933) by two hybrid (MI:0018) MINT-6538741: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with Adenosine A2aR (uniprotkb:P29274) by two hybrid (MI:0018) MINT-6538727: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with interferon-induced transmembrane protein 3 (uniprotkb:Q01628) by two hybrid (MI:0018) MINT-6538712: PBEF (uniprotkb:P43490) physically interacts (MI:0218) with Ferritin light chain (uniprotkb:P02792) by two hybrid (MI:0018) [Copyright &y& Elsevier]

The C=N double bond in the title compound, C(15)H(13)BrN(2)O(2), is transE configured and the dihedral angle between the aromatic ring planes is 22.3 (1)°. The crystal structure is stabilized by intra-molecular O-H⋯O and inter-molecular N-H⋯O hydrogen bonds.

In the title compound, C(13)H(9)BrO(2), the dihedral angle between the aromatic ring planes is 53.6 (1)°. The crystal structure is stabilized by intra-molecular O-H⋯O and inter-molecular C-H⋯O hydrogen bonding and C-H⋯π inter-actions.