A Self-Healing Crystal That Repairs Multiple Cracks.

We report both cracking and self-healing in crystals occurring during a thermal phase transition, followed by a topochemical polymerization. A squaramide-based monomer was designed where the azide and alkyne units of adjacent molecules are positioned favorably for a topochemical click reaction. The monomer undergoes spontaneous single-crystal-to-single-crystal (SCSC) polymerization at room temperature via regiospecific 1,3-dipolar cycloaddition, yielding the corresponding triazole-linked polymer in a few days.

Molecular insight into the structural and functional aspects of arene Ru(II) complexes bearing bulky thiourea ligands.

Herein we report four new arene ruthenium(II) complexes [Ru(η-p-cymene)(L1)кCl] (C1), [Ru(η-benzene)(L1)кCl] (C2) where L1 is N-((2,6-dimethylphenyl)carbamothioyl)benzamide (L1), and [Ru(η-p-cymene)(L2)кCl] (C3), [Ru(η-benzene)(L2)кCl] (C4) where L2 is N-((2,6-diisopropylphenyl)carbamothioyl)benzamide (L2) which were synthesized and evaluated for biological activity. The monodentate coordination of thione sulphur (S) to ruthenium ion along with two terminal chloride was confirmed by X-Ray diffraction analysis thus revealing a typical "piano-stool" pseudo tetrahedral geometry. DPPH radical scavenging activity showed that ligands were less efficient however on complex formation it showed significant efficacy with C4 showing the highest activity.

Two Structurally Different Polymers from a Single Monomer.

We designed and synthesized a malonamide-derived monomer, containing azide and alkyne units, for topochemical polymerization to yield nylon (n,3). This monomer on crystallization gave two concomitant polymorphs and . Both the polymorphs show crystal packings that are suitable for topochemical azide-alkyne cycloaddition polymerization.

Microglia specific deletion of miR-155 in Alzheimer's disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures.

Alzheimer's Disease (AD) is characterized by the accumulation of extracellular amyloid-β (Aβ) as well as CNS and systemic inflammation. Microglia, the myeloid cells resident in the CNS, use microRNAs to rapidly respond to inflammatory signals. MicroRNAs (miRNAs) modulate inflammatory responses in microglia, and miRNA profiles are altered in Alzheimer's disease (AD) patients.