Macrophages, which have functions of engulfing and digesting foreign substances, can clear away harmful matter, including cellular debris and tumor cells. Based on the condition of the internal environment, circulating monocytes give rise to mature macrophages, and when they are recruited into the tumor microenvironment and in suitable conditions, they are converted into tumor-associated macrophages (TAMs). Generally, macrophages grow into two main groups called classically activated macrophages (M1) and alternatively activated macrophages (M2). M2 and a small fraction of M1 cells, also known as TAMs, not only lack the function of phagocytizing tumor cells but also help these tumor cells escape from being killed and help them spread to other tissues and organs. In this review, we introduce several mechanisms by which macrophages play a role in the immune regulation of tumor cells, including both killing factors and promoting effects. Furthermore, the targeted therapy for treating tumors based on macrophages is also referred to in our review. We confirm that further studies of macrophage-focused therapeutic strategies and their use in clinical practice are needed to verify their superior efficacy and potential in cancer treatment.
BackgroundTo isolate and characterization of human spermatogonial stem cells from stem spermatogonium.MethodsThe disassociation of spermatogonial stem cells (SSCs) were performed using enzymatic digestion of type I collagenase and trypsin. The SSCs were isolated by using Percoll density gradient centrifugation, followed by differential surface-attachment method. Octamer-4(OCT4)-positive SSC cells were further identified using immunofluorescence staining and flow cytometry technques. The purity of the human SSCs was also determined, and a co-culture system for SSCs and Sertoli cells was established.ResultsThe cell viability was 91.07% for the suspension of human spermatogonial stem cells dissociated using a two-step enzymatic digestion process. The cells isolated from Percoll density gradient coupled with differential surface-attachement purification were OCT4 positive, indicating the cells were human spermatogonial stem cells. The purity of isolated human spermatogonial stem cells was 86.7% as assessed by flow cytometry. The isolated SSCs were shown to form stable human spermatogonial stem cell colonies on the feeder layer of the Sertoli cells.ConclusionsThe two-step enzyme digestion (by type I collagenase and trypsin) process is an economical, simple and reproducible technique for isolating human spermatogonial stem cells. With little contamination and less cell damage, this method facilitates isolated human spermatogonial stem cells to form a stable cell colony on the supporting cell layer.
Autophagy is an evolutionarily conserved pathway in eukaryotes that delivers unwanted cytoplasmic materials to the lysosome/vacuole for degradation/recycling. Stimulated autophagy emerges as an integral part of plant immunity against intracellular pathogens. In this study, we used turnip mosaic virus (TuMV) as a model to investigate the involvement of autophagy in plant RNA virus infection. The small integral membrane protein 6K2 of TuMV, known as a marker of the virus replication site and an elicitor of the unfolded protein response (UPR), upregulates the selective autophagy receptor gene NBR1 in a UPR-dependent manner. NBR1 interacts with TuMV NIb, the RNA-dependent RNA polymerase of the virus replication complex (VRC), and the autophagy cargo receptor/adaptor protein ATG8f. The NIb/NBR1/ATG8f interaction complexes colocalise with the 6K2-stained VRC. Overexpression of NBR1 or ATG8f enhances TuMV replication, and deficiency of NBR1 or ATG8f inhibits virus infection. In addition, ATG8f interacts with the tonoplast-specific protein TIP1 and the NBR1/ATG8f-containing VRC is enclosed by the TIP1-labelled tonoplast. In TuMV-infected cells, numerous membrane-bound viral particles are evident in the vacuole. Altogether these results suggest that TuMV activates and manipulates UPR-dependent NBR1-ATG8f autophagy to target the VRC to the tonoplast to promote viral replication and virion accumulation.
Background/Aims Indirect pulp capping, pulpotomy, and apexification are three common endodontic treatments for immature traumatized incisors. They all affect tooth root development to some extent. The aim of this retrospective study was to compare the influence of these treatments on root development of immature permanent incisors following dental trauma. Materials and Methods Twenty‐one indirect pulp capping, 48 pulpotomy, and 58 apexification cases with a mean age of 8.4 ± 1.0 years and median follow up of 12 months were included. NIH ImageJ with TurboReg plug‐in was used to correct angular differences between the pre‐operative and recall periapical radiographs, and to calculate variations of root length, dentin wall thickness, and apical closure. Kruskal‐Wallis ANOVA followed by pairwise comparisons was applied to compare the radiographic variations. The type of apical closure was assessed qualitatively and analyzed using Fisher's exact test. Results The apexification group had a lower trend toward apical closure than the other two groups (P < .05). It also showed thinner dentin wall thickness compared with the pulpotomy group (P = .001). There was no significant difference between pulpotomy and indirect pulp capping in the trend to apical closure (P > .05) or dentin wall thickness (P = .775). There was no significant difference in the variation of root length among the three groups (P = .06). There was a moderate correlation between the treatment and the type of apical closure (Cramer's V Coefficient = .375). Pulpotomy tended to form a normal apical constriction rather than a calcific barrier while apexification showed the opposite inclination. Indirect pulp capping had no specific inclination toward any type of apical closure. Conclusions Apexification resulted in an abnormal root development mostly by affecting the dentin wall thickness and apical closure. Pulpotomy was beneficial for normal root development of immature traumatized teeth.
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