Halogen bonding should intentionally be used as a powerful tool, comparable with hydrogen bonding, to enhance the binding affinity and also influence the binding selectivity. Rational design of new and potent inhibitors against therapeutic targets through halogen bonding continues to be an exciting area, which will be further elucidated with the combination of various experimental techniques and theoretical calculations in the forthcoming years.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking. We designed this study to investigate the therapeutic effects and mechanisms of melatonin on the secondary brain injury (SBI) after ICH. An in vivo ICH model was induced via autologous whole blood injection into the right basal ganglia in Sprague-Dawley (SD) rats. Primary rat cortical neurons were treated with oxygen hemoglobin (OxyHb) as an in vitro ICH model. The results of the in vivo study showed that melatonin alleviated severe brain edema and behavior disorders induced by ICH. Indicators of blood-brain barrier (BBB) integrity, DNA damage, inflammation, oxidative stress, apoptosis, and mitochondria damage showed a significant increase after ICH, while melatonin reduced their levels. Meanwhile, melatonin promoted further increasing of expression levels of antioxidant indicators induced by ICH. Microscopically, TUNEL and Nissl staining showed that melatonin reduced the numbers of ICH-induced apoptotic cells. Inflammation and DNA damage indicators exhibited an identical pattern compared to those above. Additionally, the in vitro study demonstrated that melatonin reduced the apoptotic neurons induced by OxyHb and protected the mitochondrial membrane potential. Collectively, our investigation showed that melatonin ameliorated ICH-induced SBI by impacting apoptosis, inflammation, oxidative stress, DNA damage, brain edema, and BBB damage and reducing mitochondrial membrane permeability transition pore opening, and melatonin may be a potential therapeutic agent of ICH.

A tadpole shaped poly( -caprolactone) (PCL; M n ) 24 500) was made amphiphilic by grafting the two PCL tails with PEO. In the first step, a macrocyclic PCL was synthesized by ring-opening polymerization of -caprolactone ( CL) initiated by a cyclic tin(IV) dialkoxide and stabilized by local intramolecular photocross-linking. In the second step, the polymerization of a mixture of CL and R-chloro--caprolactone (RCl CL) was resumed with formation of two activated chloride containing PCL tails. In the third step, the chlorides were converted into azides onto which alkynyl end-capped PEO was grafted by the copper-mediated Huisgen's cycloaddition [3 + 2], thus giving a "click" reaction. The thermal properties of the final copolymer and the precursors were analyzed by differential scanning calorimetry. The amphiphilicity of the final copolymer was confirmed by micellization in water.

The development of wearable electronics that can monitor human physiological information demands specially structured materials with excellent stretchability and electrical conductivity. In this study, a new stretchable conductive polypyrrole/polyurethane (PPy/PU) elastomer was designed and prepared by surface diffusion and in situ polymerization of PPy inside and on porous PU substrates. The structures allowed the formation of netlike microcracks under stretching. The netlike microcrack structures make possible the reversible changes in the electrical resistance of PPy/PU elastomers under stretching and releasing cycles. The variations in morphology and chemical structures, stretchability, and conductivity as well as the sensitivity of resistance change under stretching cycles were investigated. The mechanism of reversible conductivity of the PPy/PU elastomer was proposed. This property was then used to construct a waistband-like human breath detector. The results demonstrated its potential as a strain sensor for human health care applications by showing reversible resistance changes in the repeated stretching and contracting motion when human breathes in and out.

Edited by Tamas DalmayKeywords: HOTAIR miR-193a c-KIT Acute myeloid leukemia a b s t r a c t HOTAIR is significantly overexpressed in various cancers and facilitates tumor invasion and metastasis. However, whether HOTAIR plays oncogenic roles in acute myeloid leukemia (AML) is still unknown. Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.