Current techniques for the generation of cell-laden microgels are limited by numerous challenges, including poorly uncontrolled batch-to-batch variations, processes that are both labor- and time-consuming, the high expense of devices and reagents, and low production rates; this hampers the translation of laboratory findings to clinical applications. To address these challenges, we develop a droplet-based microfluidic strategy based on metastable droplet-templating and microchannel integration for the substantial large-scale production of single cell-laden alginate microgels. Specifically, we present a continuous processing method for microgel generation by introducing amphiphilic perfluoronated alcohols to obtain metastable emulsion droplets as sacrificial templates. In addition, to adapt to the metastable emulsion system, integrated microfluidic chips containing 80 drop-maker units are designed and optimized based on the computational fluid dynamics simulation. This strategy allows single cell encapsulation in microgels at a maximum production rate of 10 ml hr-1 of cell suspension while retaining cell viability and functionality. These results represent a significant advance toward using cell-laden microgels for clinical-relevant applications, including cell therapy, tissue regeneration and 3D bioprinting.

Purpose Amyand’s hernia is a rare hernia defined as an inguinal hernia that contains the appendix within the hernia sac. Current treatment of Amyand’s hernia remains controversial. Our study retrospectively reviewed 6 cases of Amyand’s hernia, aiming to provide a reference for the surgical treatment of Amyand's hernia. Methods Six patients diagnosed with Amyand’s hernia from September 2010 to May 2020 were retrospectively enrolled in our study. We summarized clinical data of six patients including the chief complaint, physical examinations, laboratory examinations, imaging examinations, surgical methods, and postoperative treatments and outcomes. Results The diagnosis of six cases with Amyand’s hernia was made during surgery. Two patients had normal appendixes whereas the remaining four patients had appendicitis. Two patients with normal appendix received tension-free mesh repair through the inguinal incision. Among those with inflamed or perforated appendixes, two received mesh repair and the other two did not. The discharge time after surgery of six patients was 9.8 ± 6.1 days. One patient suffered from a wound infection. No additional postoperative complications were detected. Conclusions Computed tomography and ultrasonography are helpful but limited in the definite diagnosis of Amyand’s hernia. The presence of a normal appendix does not require to be resected, but appendicectomy is necessary if the appendix is inflamed. The treatment of Amyand's hernia should be tailored based on the patient's condition and the type of Amyand's hernia.

Purpose. Osteoporosis is a complication of type 2 diabetes, and it is characterized by reduced bone mass, augmented bone fragility, and increased risk of fracture, thus reducing patient quality of life, especially in the elderly. Ferroptosis has been implicated in the pathological process of type 2 diabetic osteoporosis (T2DOP), but the specific underlying mechanisms remain largely unknown. This study clarified the role of activating transcription factor 3 (ATF3) in T2DOP and explored its specific regulatory mechanism, providing a new treatment target for T2DOP. Methods. We cultured hFob1.19 cells in high glucose (HG, 35 mM) and knocked down ATF3 using short hairpin RNA (shRNA). We then measured cell viability, assessed morphology, quantified the expression of ATF3 and glutathione peroxidase 4 (GPX4), detected the levels of reactive oxygen species (ROS) and lipid peroxides, and determined the osteogenic function of osteoblasts. Cystine/glutamate antiporter (system Xc-) activity was evaluated by determining the expression of SLC7A11 and the levels of glutathione (GSH) and extracellular glutamate. We constructed a T2DOP rat model and observed the effect of ATF3 on ferroptosis and T2DOP by knocking down ATF3 using small interfering RNA (siRNA). Then, we evaluated the levels of iron metabolism, lipid peroxidation, and bone turnover in serum, detected the expression of ATF3, SLC7A11, and GPX4 in bone tissues, and assessed bone microstructure using microcomputed tomography. Results. ATF3 expression was increased in osteoblasts under HG condition and in T2DOP rats. Inhibiting the function of ATF3 increased GPX4 levels and reduced the accumulation of ROS and lipid peroxides. These changes inhibited the ferroptosis of osteoblasts and improved osteogenic function. In addition, HG induced ATF3 upregulation, resulting in decreased SLC7A11 expression and lower levels of intracellular GSH and extracellular glutamate. Conclusion. Osteoblast ferroptosis under HG conditions is induced by ATF3-mediated inhibition of system Xc- activity, and these events contribute to T2DOP pathogenesis.