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PurposeBased on the transactional theory of stress and coping, this study aims to understand the daily impact of coronavirus disease 2019 (COVID-19) on employee goal progress. In particular, the authors explore how COVID-19 induces anxiety related to task setbacks that consequently influences one's goal progress.Design/methodology/approachA daily diary study was conducted with a total of 558 observations from 60 participants. The data were analyzed using multilevel path analysis with random slopes.FindingsThe perceived risk of COVID-19 infection was positively associated with COVID-19 task setback anxiety, which in turn improved end-of-day goal progress. Lower employee conscientiousness strengthened the relationship between perceived risk of COVID-19 infection and COVID-19 task setback anxiety, and lower supervisor bottom-line mentality strengthened the relationship between COVID-19 task setback anxiety and end-of-day goal progress.Practical implicationsAlthough COVID-19 task setback anxiety results in higher end-of-day goal progress, the authors recommend caution as the cost of coping exists. Thus, supervisors should focus on supporting the employees rather than having a bottom-line mentality.Originality/valueThis study advances stress and coping literature by examining how employees appraise and cope with COVID-19 in work context. The authors demonstrate that a perceived risk of COVID-19 induces task setbacks related to anticipatory anxiety, which in turn influences employee outcomes. In addition, the authors identify employee conscientiousness and supervisor bottom-line mentality as a boundary condition of this process.

Chalcones compounds have been investigated to exhibit anticancer activity through various physiological modes of action. In order to develop chalcone compounds with novel anticancer-related modes of action, diverse chalcone compounds were designed and synthesized. Variously substituted poly-methoxy chalcone compounds 1–17 were prepared, and their structures were identified using high-resolution mass spectrometry (HR/MS) and nuclear magnetic resonance (NMR) experiments. Long-term survival clonogenic assay was applied to evaluate their anti-cancer abilities and revealed that their GI50 values ranged between 1.33 and 172.20 μM. When MCF-7SC cells were treated with various concentrations of compound 14, reduced cell viability and induced apoptosis in MCF-7SC cells were observed in a dose-dependent manner. Wound healing assay demonstrated that compound 14 prevented the MCF7-SC migrated cells at non-lethal concentrations after 12 and 24 h of exposure. The efficiency of compound 14 on the levels of Epithelial-mesenchymal transition (EMT) markers was accessed by the western blot analysis. For the concrete understanding of anticancer properties at the molecular level, in vitro kinase assays on 12 cancer related proteins were carried out. Glycogen synthase kinase 3 beta (GSK3β) was most effectively inhibited by compound 14 with 89% inhibitory activity at 10 µM against GSK3β. The binding mode of compound 14 with GSK3β was reinforced through in silico experiments, which demonstrated compound 14 binds with GSK3β at binding affinity ranged between − 7.5 kcal/mol and − 6.8 kcal/mol. SwissADME analysis provided the druggability and leadlikeness of compound 14, which unveiled drug development possibilities of chalcone compound 14.

C14H13NO5, monoclinic, P21 (no. 4), a = 4.6967(7) Å, b = 10.7175(16) Å, c = 12.945(2) Å, β = 94.827(8)°, V = 649.30(17) Å3, Z = 2, R gt (F) = 0.0577, wR ref (F 2) = 0.1302, T = 223(2) K.

C20H21F2NO4, triclinic, P 1 ‾ $P‾{1}$ (no. 2), a = 8.6363(11) Å, b = 9.9144(11) Å, c = 11.8734(15) Å, α = 81.891(4)°, β = 72.889(4)°, γ = 80.972(3)°, V = 954.7(2) Å3, Z = 2, R gt (F) = 0.0466, wR ref (F 2) = 0.1339, T = 223(2) K.

C19H14N2O5 ⋅ CH3OH, monoclinic, P21/c (no. 14), a = 7.9074(3) Å, b = 20.4341(7) Å, c = 11.0406(4) Å, β = 92.6004(16)°, V = 1783.85(11) Å3, Z = 4, Rgt (F) = 0.0467, wR ref(F 2) = 0.1260, T = 223(2) K.

In the title compound, C

In the title compound, C16H12O2, the dihedral angle formed between the plane of the chromenone ring system (r.m.s. deviation = 0.031 Å) and the pendant benzene ring is 31.09 (5)°. In the crystal, weak C—H...O hydrogen bonds link the molecules into C(6) chains propagating along the a-axis direction.

There is accumulating evidence that compounds containingN-acylhydrazone or 4-chromenone moieties can be active against multiple cancer cell types, yet the combined effect of these chemical groups is unclear. This study aimed to develop more effective anti-cancer compounds by combining 4-chromenone andN-acylhydrazone. Thirteen derivatives were designed, synthesized, and characterized, and their structures were identified using nuclear magnetic resonance spectroscopy and high-resolution mass spectrometry. Most of the derivatives exhibited moderate to high efficacy in inhibiting the clonogenicity of HCT116 colon cancer cells. In particular, derivative12, (E)-N'-((6-methoxy-4-oxo-4H-chromen-3-yl)methylene)isonicotinohydrazide, strongly inhibited clonogenicity (GI50 = 34.8 μM) of HCT116 cells and aurora kinase A (aurA) activity in vitro (IC50 = 1.4 μM). In silico docking experiment predicted that derivative12interacts with aurA based on computational docking and calculations of binding free energy. When derivative12was exposed to HCT116 cells, the phosphorylation of aurA at Thr288 was dose-dependently decreased within 60 min. Further analysis showed that derivative12destroyed the mitotic spindle in HCT116 cells. These results suggest that derivatives of 4-chromenone combined withN-acylhydrazone are feasible in the development of selective aurA inhibitor and could be considered potential chemotherapeutic agents.

In the title compound, C20H22N2O4, two benzene rings bearing methoxy substituents are connected by a central acetylpyrazoline ring: the dihedral angle between the benzene rings is 83.7 (1)°. In the crystal, pairwise C—H...O hydrogen bonds generate inversion dimers and additional weak C—H...O interactions link the dimers into chains propagating along the c-axis direction.

In the title compound, C

The structure of the isoflavone compound, 3-(2,3-dihydrobenzo[b][1,4]dioxin-6-yl)-6,7-dimethoxy-4H-chromen-4-one (5), was elucidated by 2D-NMR spectra, mass spectrum and single crystal X-ray crystallography. Compound 5, C19H16O6, was crystallized in the monoclinic space group P21/c with the cell parameters, a = 12.0654(5) &Aring, b =11.0666(5) &Aring, c = 23.9550(11) &Aring, &beta, = 101.3757(16)&deg, V = 3135.7(2) &Aring, 3, and Z = 8. The asymmetric unit of compound 5 consists of two independent molecules 5I and 5II. Both molecules exhibit the disorder of each methylene group present in their 1,4-dioxane rings with relative occupancies of 0.599(10) (5I) and 0.812(9) (5II) for the major component A, and 0.401(10) (5I) and 0.188(9) (5II) for the minor component B, respectively. Each independent molecule revealed remarkable discrepancies in bond lengths, bond angles and dihedral angles in the disordered regions of 1,4-dioxane rings. The common feature of the molecules 5I and 5II are a chromone ring and a benzodioxin ring, which are more tilted towards each other in 5I than in 5II. An additional difference between the molecules is seen in the relative disposition of two methoxy substituents. In the crystal, the molecule 5II forms inversion dimers which are linked into chains along an a-axis direction by intermolecular C&ndash, H⋯O interactions. Additional C&ndash, H⋯O hydrogen bonds connected the molecules 5I and 5II each other to form a three-dimensional network. Hirshfeld surface analysis evaluated the relative intermolecular interactions which contribute to each crystal structure 5I and 5II. Western blot analysis demonstrated that compound 5 inhibited the TNF&alpha, induced phosphorylation of IKK&alpha, /&beta, resulting in attenuating further downstream NF-&kappa, B signaling. A molecular docking study predicted the possible binding of compound 5 to the active site of IKK&beta, Compound 5 showed an inhibitory effect on the clonogenicity of HCT116 human colon cancer cells. These results suggest that compound 5 can be used as a platform for the development of an anti-cancer agent targeting IKK&alpha

In the title compound, C28H28O6, the benzene rings in the resveratrol moiety are connected by a trans C=C double bond, and the hydroxyl group containing a benzene ring and the central benzene ring are linked through a C=(O)—C=C (enone) moiety to form a chalcone unit. An intramolecular O—H...O hydrogen bond generates an S(6) ring motif. In the crystal, pairs of C—H...O hydrogen bonds generate dimers and additional weak C—H...O interactions link the dimers into chains propagating along the b-axis direction.

In the title compound, C

The isoflavone compound 3-(2,3-dihydrobenzo[b][1,4]dioxin-6-yl)-6-methoxy-4H-chromen-4-one (6) was prepared and structurally characterized using NMR, mass spectrum and X-ray crystallography. Compound 6, C18H14O5, was crystallized in the monoclinic space group P21/n with the cell parameters, a = 7.1869(4) &Aring, b = 10.2764(6) &Aring, c = 19.6771(10) &Aring, b = 99.442(2)&deg, V = 1433.57(14) &Aring, 3, Z = 4. In the title compound, the chromenone ring system is slightly twisted from planarity and the dihedral angle formed between the plane of the chromenone ring and benzene ring is 47.75o. Several intermolecular hydrogen bonds make the crystal stabilized in the three-dimensional structure, which was confirmed by Hirshfeld surface analysis. Density functional theory (DFT) calculations at the B3LYP/6-311++G(d,p) level were carried out and the calculated geometric parameters were compared with the experimental results. A frontier molecular orbital calculation was performed to reveal that the energy values of highest occupied molecular orbital (HOMO) and lowest un-occupied molecular orbital (LUMO) were &minus, 5.8223 eV and &minus, 1.8447 eV, and the HOMO&ndash, LUMO energy gap was 3.9783 eV. A clonogenic long-term survival assay of compound 6 against HCT116 human colon cancer cells showed an anti-cancer ability, with GI50 value of 24.9 &mu, M. Docking experiments within the active sites of aurora kinase A and B were carried out to explain the anti-cancer property of compound 6.

Objectives To identify preoperative features that could be used to predict invasive breast cancer in women with a diagnosis of ductal carcinoma in situ (DCIS) at ultrasound (US)-guided 14-gauge core needle biopsy (CNB). Methods A total of 86 DCIS lesions that were diagnosed at US-guided 14-gauge CNB and excised surgically in 84 women were assessed. We retrospectively reviewed the patients’ medical records, mammography, US, and MR imaging. We compared underestimation rates of DCIS for the collected clinical and radiologic variables and determined the preoperative predictive factors for upstaging to invasive cancer. Results Twenty-seven (31.4%) of 86 DCIS lesions were upgraded to invasive cancer. Preoperative features that showed a significantly higher underestimation of DCIS were palpability or nipple discharge ( p = 0.040), number of core specimens less than 5 ( p = 0.011), mammographic maximum lesion size of 25 mm or larger ( p = 0.022), mammographic mass size of 40 mm or larger ( p = 0.046), sonographic mass size of 32 mm or larger ( p = 0.009), lesion size of 30 mm on MR ( p = 0.004), lower signal intensity (SI) on fat-saturated T2-weighted MR images (FS-T2WI) ( p = 0.005), heterogeneous or rim enhancement on MR images ( p = 0.009), and apparent diffusion coefficient (ADC) values lower than 1.04 × 10 −3 mm 2 /s on diffusion-weighted MR imaging (DWI) ( p Conclusion Clinical symptom of palpability or nipple discharge, number of core specimen, mammographic maximum lesion or mass size, SI on FS-T2WI, heterogeneous or rim enhancement on MR, and ADC value may be helpful in predicting the upgrade to invasive breast cancer for DCIS diagnosed at US-guided 14-gauge CNB.