Injectable scaffolds are of great interests for skin regeneration because they can fill irregularly shaped defects through minimally invasive surgical treatments. In this study, an injectable hydrogel from biopolymers is developed and its application as wound dressings is examined. Gelatin-based hydrogels were successfully prepared at body temperature upon blending with low content of gellan, and the synergetic effect on the gel formation was carefully characterized through rheological methods. The electrostatic complexation between gelatin and gellan was confirmed to contribute a continuous hydrogel network. The obtained blend hydrogel demonstrates remarkable shear-thinning and self-recovering properties. For antibacterial purpose, tannic acid was incorporated into the blend hydrogel. In addition, tannic acid-loaded blend hydrogel was verified to accelerate the wound healing on the mice model, significantly than the control groups. Thus, this paper presents a facile approach without chemical modification to construct injectable gelatin-based hydrogels, which have great potential as a wound dressing or tissue scaffold at body temperature.

A combined zero electronic kinetic energy spectroscopy and ion-pair dissociation imaging study of the

N,N-Dimethyl-beta-alanine was found to be a more powerful phosphine-free ligand than the previously reported ligand, N,N-dimethylglycine, in the Pd-catalyzed Heck reaction for a variety of aryl bromides, aryl iodides, and activated aryl chlorides with a practical turnover number of 10(3). Both kinetic and theoretical studies suggested that N,N-dimethyl-beta-alanine led to faster oxidative addition of an aryl halide to Pd than N,N-dimethylglycine. [reaction: see text]

Chronic pain and anxiety symptoms are frequently encountered clinically, but the neural circuit mechanisms underlying the comorbid anxiety symptoms in pain (CASP) in context of chronic pain remain unclear. Using viral neuronal tracing in mice, we identified a previously unknown pathway whereby glutamatergic neurons from layer 5 of the hindlimb primary somatosensory cortex (S1) (GluS1), a well-known brain region involved in pain processing, project to GABAergic neurons in the caudal dorsolateral striatum (GABAcDLS). In a persistent inflammatory pain model induced by complete Freund's adjuvant injection, enhanced excitation of the GluS1→GABAcDLS pathway was found in mice exhibiting CASP. Reversing this pathway using chemogenetic or optogenetic approaches alleviated CASP. In addition, the optical activation of GluS1 terminals in the cDLS produced anxiety-like behaviors in naive mice. Overall, the current study demonstrates the putative importance of a novel GluS1→GABAcDLS pathway in controlling at least some aspects of CASP.