Importance: The outbreak of highly contagious COVID-19 has posed a serious threat to human health, especially for those with underlying diseases. However, Impacts of COVID-19 epidemic on HD center and HD patients have not been reported. Objective: To summery an outbreak of COVID-19 epidemic in HD center. Design, Setting, and Participants: We reviewed the epidemic course from the first laboratory-confirmed case of COVID-19 infection on January 14 to the control of the epidemic on March 12 in the HD center of Renmin Hospital of Wuhan University. Total 230 HD patients and 33 medical staff were included in this study Exposures: COVID-19. Main Outcomes and Measures: Epidemiological, clinical, laboratory, and radiological characteristics and outcomes data were collected and analyzed. 19 COVID-19 HD patients, 19 non-COVID-19 HD patients and 19 healthy volunteers were enrolled for further study about the effect of SARS-CoV-2 infection on host immune responses. Results: 42 out of 230 HD patients (18.26%) and 4 out of 33 medical staffs (12.12%) were diagnosed with COVID-19 from the outbreak to March 12, 2020. 13 HD patients (5.65%), including 10 COVID-19 diagnosed, died during the epidemic. Only 2 deaths of the COVID-19 HD patients were associated with pneumonia/lung failure. Except 3 patients were admitted to ICU for severe condition (8.11%), including 2 dead, most COVID-19 diagnosed patients presented mild or none-respiratory symptoms. Multiple lymphocyte populations in HD patients were significantly decreased. HD patients with COVID-19 even displayed more remarkable reduction of serum inflammatory cytokines than other COVID-19 patients. Conclusions and Relevance: HD patients are the highly susceptible population and HD centers are high risk area during the outbreak of COVID-19 epidemic. HD Patients with COVID-19 are mostly clinical mild and unlikely progress to severe pneumonia due to the impaired cellular immune function and incapability of mounting cytokines storm. More attention should be paid to prevent cardiovascular events, which may be the collateral impacts of COVID-19 epidemic on HD patients.

As a projection based three-dimensional printing method, digital light processing bioprinting (DLPBP) has higher printing resolution and is suitable for constructing finer structures to mimic tissues when compared to extrusion based bioprinting. However, there is a lack of understanding about printing behavior during DLPBP. Herein, a photo crosslinking theory for ink was established and a specified amount of light absorber was added to control crosslinking depth. Then, a standardized methodology was established to quantitatively evaluate printing resolution using different parameters. Complex biostructures, such as the ear, hand, and heart, were precisely printed after understanding the mechanism. Additionally, the mechanical properties of printed samples were accurately adjusted by changing the hydrogel concentration, as well as the degree of substitution and photocrosslinking time. The tissue types printed were from ultra-soft tissues, such as liver (6–8 kPa) to soft tissue, such as the skin (0.3–0.4 MPa). A branching vessel with cells in a real tensile modulus was printed as a demonstration. After 1 week of culture, proliferation and function of human umbilical vein endothelial cells were characterized. Overall, we made it possible to print a mimic complex tissue with high precision, required physical properties and functionalized living cells.

A 3D cell culture has developed rapidly in recent years, as cells growing on a flat substrate in a static environment are far from achieving an in vivo status. Currently, researchers have also gradually realized that to achieve cell morphology, structure, and physiological functions in vitro, 3D cell culture should be capable of simulating key features of an in vivo environment, including the interaction of cell–cell, cell–extracellular matrix (ECM), and cell–organ interactions. Herein, the development of the 3D cell culture system related to the following three perspectives is outlined: 1) biomaterial systems with a hydrogel system as the core; 2) biomanufacturing technology with bioprinting as the main means; and 3) culture device systems supported by microfluidic chips and bioreactors. The question is whether 3D cell culture will be as popular as 2D culture in the future. The key may lie in the development of simple and standard protocols for 3D culture.

Background and Purpose: Melatonin is a neurohormone involved in bone homeostasis. Melatonin directs bone remodelling and the role of bone marrow mesenchymal stem cells (BMMSCs) in the regulating melatonin‐mediated bone formation–resorption balance remains undefined.Experimental Approach: Osteoporosis models were established and bone tissue and serum were collected to test the effects of melatonin on bone homeostasis. Melatonin receptors were knocked down, the NF‐κB signalling pathway and receptor activator of NF‐κB ligand (RANKL) expression were investigated. Communication between bone marrow mesenchymal stem cells and osteoclasts was detected with direct‐contact or indirect‐contact system.Key Results: Bone loss and microstructure disorder in mice were reversed after melatonin treatment, as a result of anabolic and anti‐resorptive effects. In vitro, a physiological (low) concentration of melatonin promoted the bone marrow mesenchymal stem cells, osteogenic lineage commitment and extracellular mineralization but had no impact on extracellular matrix synthesis. After MT knockdown, especially MT₂, the positive effects of melatonin on osteogenesis were attenuated. The canonical NF‐κB signalling pathway was the first discovered downstream signalling pathway after MT receptor activation and was found to be down‐regulated by melatonin during osteogenesis. Melatonin suppressed BMMSC‐mediated osteoclastogenesis by inhibiting RANKL production in BMMSCs and this effect only occurred when BMMSCs and osteoclast precursors were co‐cultured in an indirect‐contact manner.Conclusion and Implications: Our work suggests that melatonin plays a crucial role in bone balance, significantly accelerates the osteogenic differentiation of bone marrow mesenchymal stem cells by suppressing the MT₂‐dependent NF‐κB signalling pathway, and down‐regulates osteoclastogenesis via RANKL paracrine secretion.