The crystal structure of dipotassium iron(III) {hydrogen bis­[hydrogenphosphate(V)]} difluoride, K2Fe[H(HPO4)2]F2, obtained by hydro­thermal synthesis, was determined from single‐crystal X‐ray diffraction data. The structure is characterized by K+ cations and hydrogen‐bonded {[Fe[H(HPO4)2]F2]2−}n chains, which consist of centrosymmetric Fe[F2O4] octa­hedra linked to their four neighbouring phosphate tetra­hedra via common O corners, developing a three‐dimensional structure.

No abstract

The relationship between body mass index and pressure ulcers in critically ill patients is controversial. We aimed to investigate the association between body mass index and pressure ulcers by analysing data from the Medical Information Mart for Intensive Care IV (version 2.0) database. Eligible data (21 835 cases) were extracted from the database (2008‐2019). The association between body mass index and pressure ulcers in critically ill patients was investigated by adjusting multivariate trend analysis, restricted cubic spline analysis, and segmented linear models. Subgroup analyses and sensitivity analyses were used to ensure the stability of the results. Trend analysis and restricted cubic spline analysis showed an approximate U‐shaped correlation between body mass index and the occurrence of pressure ulcers in critically ill patients, with the risk of pressure ulcers decreasing rapidly with increasing body mass index (8.6% decrease per unit) after adjusting for relevant factors; the trend reached its minimum at a body mass index of 27.5 kg/m2, followed by a slow increase in the risk of pressure ulcers with increasing body mass index (1.4% increase per unit). Among the subgroups, the highest overall risk of pressure ulcers and the risk of severe pressure ulcers were significantly higher in the underweight group than in the other subgroups, and the risk associated with the overweight group was the lowest. There is a U‐shaped association between body mass index and pressure ulcers in critically ill patients, and being underweight and obese both increase the risk of pressure ulcers. The risk is highest among underweight patients and lowest among overweight patients (but not patients of normal weight), necessitating targeted prevention strategies for critically ill patients with different body mass indexes.

<div>Abstract<p>Centrosomal Aurora-A (Aur-A) kinase ensures proper spindle assembly and accurate chromosome segregation in mitosis. Overexpression of Aur-A leads to centrosome amplification, aberrant spindle, and consequent genetic instability. In the present study, Aur-A was found to be overexpressed in laryngeal squamous cell carcinoma (LSCC). Moreover, Aur-A expression was adversely correlated with median survival, and further identified as a potential independent factor for disease prognosis. Suppression of Aurora kinase activity chemically or genetically led to LSCC Hep2 cell cycle arrest and apoptotic cell death. Importantly, we found that Aur-A increases cell migration and this novel function was correlated with Akt1 activation. The enhanced cell migration induced by Aur-A overexpression could be abrogated by either small-molecule Akt1 inhibitor or short interfering RNA. VX-680, a selective Aurora kinase inhibitor, decreased Akt1 phosphorylation at Ser⁴⁷³ and inhibited cell migration, but failed to do so in constitutive active Akt1 (myr-<i>Akt1</i>)–overexpressed cells. Moreover, our data suggested that overexpression of Aur-A kinase might also contribute to radioresistance of LSCC. Inhibiting Aur-A by VX-680 induced expression of p53 and potently sensitized cells to radiotherapy, leading to significant cell death. Ectopic overexpression of Aur-A, however, reduced p53 level and rendered cells more resistant to irradiation. Taken together, we showed that Aur-A kinase, a negative prognostic marker, promotes migration and reduces radiosensitivity in laryngeal cancer cells. [Cancer Res 2007;67(21):10436–44]</p></div>

<div>Abstract<p>Centrosomal Aurora-A (Aur-A) kinase ensures proper spindle assembly and accurate chromosome segregation in mitosis. Overexpression of Aur-A leads to centrosome amplification, aberrant spindle, and consequent genetic instability. In the present study, Aur-A was found to be overexpressed in laryngeal squamous cell carcinoma (LSCC). Moreover, Aur-A expression was adversely correlated with median survival, and further identified as a potential independent factor for disease prognosis. Suppression of Aurora kinase activity chemically or genetically led to LSCC Hep2 cell cycle arrest and apoptotic cell death. Importantly, we found that Aur-A increases cell migration and this novel function was correlated with Akt1 activation. The enhanced cell migration induced by Aur-A overexpression could be abrogated by either small-molecule Akt1 inhibitor or short interfering RNA. VX-680, a selective Aurora kinase inhibitor, decreased Akt1 phosphorylation at Ser⁴⁷³ and inhibited cell migration, but failed to do so in constitutive active Akt1 (myr-<i>Akt1</i>)–overexpressed cells. Moreover, our data suggested that overexpression of Aur-A kinase might also contribute to radioresistance of LSCC. Inhibiting Aur-A by VX-680 induced expression of p53 and potently sensitized cells to radiotherapy, leading to significant cell death. Ectopic overexpression of Aur-A, however, reduced p53 level and rendered cells more resistant to irradiation. Taken together, we showed that Aur-A kinase, a negative prognostic marker, promotes migration and reduces radiosensitivity in laryngeal cancer cells. [Cancer Res 2007;67(21):10436–44]</p></div>