Objective. To investigate the clinical features of dermatomyositis (DM) and clinically amyopathic DM (CADM) patients

Although complexation of hydrophilic guests inside the cavities of hydrophobic hosts is considered to be unlikely, we demonstrate herein the complexation between γ- and β-cyclodextrins (γ- and β-CDs) with an archetypal polyoxometalate (POM)--namely, the [PMo12O40](3-) trianion--which has led to the formation of two organic-inorganic hybrid 2:1 complexes, namely [La(H2O)9]{[PMo12O40]⊂[γ-CD]2} (CD-POM-1) and [La(H2O)9] {[PMo12O40]⊂[β-CD]2} (CD-POM-2), in the solid state. The extent to which these complexes assemble in solution has been investigated by (i) (1)H, (13)C, and (31)P NMR spectroscopies and (ii) small- and wide-angle X-ray scattering, as well as (iii) mass spectrometry. Single-crystal X-ray diffraction reveals that both complexes have a sandwich-like structure, wherein one [PMo12O40](3-) trianion is encapsulated by the primary faces of two CD tori through intermolecular [C-H···O═Mo] interactions. X-ray crystal superstructures of CD-POM-1 and CD-POM-2 show also that both of these 2:1 complexes are lined up longitudinally in a one-dimensional columnar fashion by means of [O-H···O] interactions. A beneficial nanoconfinement-induced stabilizing effect is supported by the observation of slow color changes for these supermolecules in aqueous solution phase. Electrochemical studies show that the redox properties of [PMo12O40](3-) trianions encapsulated by CDs in the complexes are largely preserved in solution. The supramolecular complementarity between the CDs and the [PMo12O40](3-) trianion provides yet another opportunity for the functionalization of POMs under mild conditions by using host-guest chemistry.

No abstract

Human deficiencies of iron (Fe) and zinc (Zn) are worldwide problems. Biofortification of wheat could reduce Fe and Zn deficiencies in societies that depend on wheat consumption. This study investigated the effects of foliar application of Fe with or without Zn on the concentrations of Fe and Zn in grain and especially in flour of three wheat cultivars. On average, grain Fe concentration was increased significantly from 29.5 mg kg(-1) in the control to 37.8, 35.9, or 34.9 mg kg(-1) by application of FeSO4, ferric citrate plus ZnSO4, or ferric citrate, respectively. As expected, grain Zn concentration was increased from 29.0 mg kg(-1) in the control to 45.7 or 39.6 mg kg(-1) by application of ferric citrate plus ZnSO4 or a complex of micronutrients. Although the Fe and Zn concentrations in flour were inherently lower than in bran and shorts made by experimental mill, the concentrations in flour were simultaneously increased from 10.4 to 12.4 mg kg(-1) for Fe and from 11.8 to 17.4 mg kg(-1) for Zn by application of ferric citrate plus ZnSO4. Importantly, Fe was peripherally localized within grain fractions and strictly limited to transport to endosperm, making it more difficult to increase the quantity of Fe in flour products by foliar Fe application, but the situation with Zn is promising because Zn is more readily transported to the endosperm than Fe. The current study increases the understanding of agronomic biofortification.

A proper DNA damage response (DDR) is essential to maintain genome integrity and prevent tumorigenesis. DNA double-strand breaks (DSBs) are the most toxic DNA lesion and their repair is orchestrated by the ATM kinase. ATM is activated via the MRE11–RAD50–NBS1 (MRN) complex along with its autophosphorylation at S1981 and acetylation at K3106. Activated ATM rapidly phosphorylates a vast number of substrates in local chromatin, providing a scaffold for the assembly of higher-order complexes that can repair damaged DNA. While reversible ubiquitination has an important role in the DSB response, modification of the newly identified ubiquitin-like protein ubiquitin-fold modifier 1 and the function of UFMylation in the DDR is largely unknown. Here, we found that MRE11 is UFMylated on K282 and this UFMylation is required for the MRN complex formation under unperturbed conditions and DSB-induced optimal ATM activation, homologous recombination-mediated repair and genome integrity. A pathogenic mutation MRE11(G285C) identified in uterine endometrioid carcinoma exhibited a similar cellular phenotype as the UFMylation-defective mutant MRE11(K282R). Taken together, MRE11 UFMylation promotes ATM activation, DSB repair and genome stability, and potentially serves as a therapeutic target.