Pickering emulsion, a kind of emulsion stabilized only by solid particles locating at oil–water interface, has been discovered a century ago, while being extensively studied in recent decades. Substituting solid particles for traditional surfactants, Pickering emulsions are more stable against coalescence and can obtain many useful properties. Besides, they are more biocompatible when solid particles employed are relatively safe in vivo. Pickering emulsions can be applied in a wide range of fields, such as biomedicine, food, fine chemical synthesis, cosmetics, and so on, by properly tuning types and properties of solid emulsifiers. In this article, we give an overview of Pickering emulsions, focusing on some kinds of solid particles commonly serving as emulsifiers, three main types of products from Pickering emulsions, morphology of solid particles and as-prepared materials, as well as applications in different fields.

Diabetic cardiomyopathy is a common cardiac condition in patients with diabetes mellitus, which can result in cardiac hypertrophy and subsequent heart failure, associated with pyroptosis, the pro-inflammatory programmed cell death. MicroRNAs (miRNAs), small endogenous non-coding RNAs, have been shown to be involved in diabetic cardiomyopathy. However, whether miRNAs regulate pyroptosis in diabetic cardiomyopathy remains unknown. Our study revealed that mir-30d expression was substantially increased in streptozotocin (STZ)-induced diabetic rats and in high-glucose-treated cardiomyocytes as well. Upregulation of mir-30d promoted cardiomyocyte pyroptosis in diabetic cardiomyopathy; conversely, knockdown of mir-30d attenuated it. In an effort to understand the signaling mechanisms underlying the pro-pyroptotic property of mir-30d, we found that forced expression of mir-30d upregulated caspase-1 and pro-inflammatory cytokines IL-1β and IL-18. Moreover, mir-30d directly repressed foxo3a expression and its downstream protein, apoptosis repressor with caspase recruitment domain (ARC). Furthermore, silencing ARC by siRNA mimicked the action of mir-30d: upregulating caspase-1 and inducing pyroptosis. These findings promoted us to propose a new signaling pathway leading to cardiomyocyte pyroptosis under hyperglycemic conditions: mir-30d↑→foxo3a↓→ ARC↓→caspase-1↑→IL-1β, IL-18↑→pyroptosis↑. Therefore, mir-30d may be a promising therapeutic target for the management of diabetic cardiomyopathy.

Owing to their unique chemical and physical properties, hydrogels are attracting increasing attention in both basic and translational biomedical studies. Although the classical hydrogels with static networks have been widely reported for decades, a growing number of recent studies have shown that structurally dynamic hydrogels can better mimic the dynamics and functions of natural extracellular matrix (ECM) in soft tissues. These synthetic materials with defined compositions can recapitulate key chemical and biophysical properties of living tissues, providing an important means to understanding the mechanisms by which cells sense and remodel their surrounding microenvironments. This review begins with the overall expectation and design principles of dynamic hydrogels. We then highlight recent progress in the fabrication strategies of dynamic hydrogels including both degradation-dependent and degradation-independent approaches, followed by their unique properties and use in biomedical applications such as regenerative medicine, drug delivery, and 3D culture. Finally, challenges and emerging trends in the development and application of dynamic hydrogels are discussed.

Seven new indole alkaloids, bruceollines H-N (1-7), three new quassinoids, yadanziolides T-V (10-12), and four known analogues, bruceolline E (8), bruceolline F (9), bruceine D (13), and yadanziolide B (14), were isolated from an ethanol extract of the stems of Brucea mollis. The absolute configurations of compounds 2 and 5 were determined by comparison of their experimental and calculated ECD spectra. The absolute configuration of the known compound 9 was determined by using Mo2(OAc)4-induced CD analysis for the first time. Compounds 10, 13, and 14 exhibited cytotoxic activities with IC50 values of 3.00-5.81 μM.

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Peripheral nerve defect is a common and severe kind of injury in traumatic accidents. Melatonin can improve peripheral nerve recovery by inhibiting oxidative stress and inflammation after traumatic insults. In addition, it triggers autophagy pathways to increase regenerated nerve proliferation and to reduce apoptosis. In this study, we fabricated a melatonin-controlled-release scaffold to cure long-range nerve defects for the first time. 3D manufacture of melatonin/polycaprolactone nerve guide conduit increased Schwann cell proliferation and neural expression in vitro and promoted functional, electrophysiological and morphological nerve regeneration in vivo. Melatonin nerve guide conduit ameliorated immune milieu by reducing oxidative stress, inflammation and mitochondrial dysfunction. In addition, it activated autophagy to restore ideal microenvironment, to provide energy for nerves and to reduce nerve cell apoptosis, thus facilitating nerve debris clearance and neural proliferation. This innovative scaffold will have huge significance in the nerve engineering.

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This study aimed to investigate whether the fatigue induced by sustained motor task in the jaw elevator muscles differed between healthy subjects and patients with temporomandibular disorder (TMD). Fifteen patients with TMD and thirteen age- and sex-matched healthy controls performed a fatigue test consisting of sustained clenching contractions at 30% maximal voluntary clenching intensity until test failure (the criterion for terminating the fatigue test was when the biting force decreased by 10% or more from the target force consecutively for >3 s). The pre- and post-maximal bite forces (MBFs) were measured. Surface electromyographic signals were recorded from the superficial masseter muscles and anterior temporal muscles bilaterally, and the median frequency at the beginning, middle and end of the fatigue test was calculated. The duration of the fatigue test was also quantified. Both pre- and post-MBFs were lower in patients with TMD than in controls (P < 0·01). No significant difference was found in the percentage change in MBF between groups. The duration of the fatigue test in TMD patients was significantly shorter than that of the controls (P < 0·05). Our results suggest that, compared to healthy subjects, patients with TMD become more easily fatigued, but the electromyographic activation process during the fatigue test is similar between healthy subjects and patients with TMD. However, the mechanisms involved in this process remain unclear, and further research is warranted.