This review describes the rules governing the choices of natural, synthetic or hybrid materials that can be cross-linked into hydrogels for regenerating different target tissues. The new trend of developing advanced hydrogels is also analysed.

An AIE probe was established for reacting with NO and emitting fluorescence in arthritic joints/chondrocytes. This AIE probe is appropriate for detecting the progression of osteoarthritis.

Background: The genetic central dogma (GCD) has been demonstrated its essential function in many biological processes and diseases. However, its roles in the process of osteogenic differentiation of mesenchymal stem cells (MSCs) remain unclear. Methods: In this project, we analyzed an online database of osteogenic differentiation of MSCs after 14 days and 28 days by osteoinductive medium (GSE83770). The differentially expressed genes were screened by GEO2R, with further conducting of KEGG pathways using DAVID. In addition, protein-protein interactions of the enriched pathways were performed using STRING with marked hub genes measured by the CytoHubba. Hub genes were verified by quantitative reverse-transcription polymerase chain reaction. Results: Results showed that six pathways related to GCD, including DNA replication, Aminoacyl-tRNA biosynthesis, Mismatch repair, Ribosome, Spliceosome, and RNA degradation pathways enriched in the early stage (14 days vs. undifferentiated MSCs) of osteogenesis. The Lysosome pathway was highly enriched in the late stage (28 vs. 14 days) of osteogenesis, and Ribosome pathway plays a key role throughout the entire process (28 days vs. undifferentiated MSCs) of osteogenesis. Conclusion: Both DNA replication and protein translation were functionally worked in the early stage of osteogenesis, whereas the Lysosome pathway was the only GCD-related one in the late stage of osteogenesis. The GCD-related Ribosome pathway occupied the entire process of osteogenesis.genetic central dogma, lysosome, mesenchymal stem cells, osteogenic differentiation, ribosome Highlights • We identified six pathways associated with genetic central dogma (DNA replication, Aminoacyl-tRNA biosynthesis, Mismatch repair, Ribosome, Spliceosome, and RNA degradation pathways), which participated in the early stage of osteogenesis (0−14 days). • The Lysosome pathway plays a crucial role in the late stage of osteogenesis (14-28 days), whereas the Ribosome pathway participates in the

The occurrence of microorganisms has been confirmed in the tumor microenvironment (TME) of many different organs. Microorganisms (e.g., phage, virus, bacteria, fungi, and protozoa) present in TME modulate TME to inhibit or promote tumor growth in species-dependent manners due to the special physiological and pathological features of each microorganism. Such microorganism-TME interactions have recently been emulated to turn microorganisms into powerful cancer theranostic agents. To facilitate scientists to explore microorganisms-TME interactions further to develop improved cancer theranostics, here we critically review the characteristics of different microorganisms that can be found in TME, their interactions with TME, and their current applications in cancer diagnosis and therapy. Clinical trials of using microorganisms for cancer theranostics are also summarized and discussed. Moreover, the emerging technology of whole-metagenome sequencing that can be employed to precisely determine microbiota spectra is described. Such technology enables scientists to gain an in-depth understanding of the species and distributions of microorganisms in TME. Therefore, scientists now have new tools to identify microorganisms (either naturally present in or introduced into TME) that can be used as effective probes, monitors, vaccines, or drugs for potentially advancing cancer theranostics to clinical applications.

Background: Bone fracture healing is a time-consuming and high-priority orthopedic problem worldwide. Objectives: Discovering the potential mechanism of bone healing at a time course and transcriptional level may better help manage bone fracture. Methods: In this study, we analyze a time-course bone fracture–healing transcriptional data set in a rat model (GSE592, GSE594, and GSE1371) of Gene Expression Omnibus (GEO). RNA was obtained from female Sprague-Dawley rats with femoral fracture at the initial time (day 3) as well as early (week 1), middle (week 2), and late (week 4) time periods, with nonfracture rats used as control. Gene Ontology (GO) functional analysis and pathway examinations were performed for further measurements of GSEA and hub genes. Results: Results indicated that the four stages of bone fracture healing at the initial, early, middle, and late time periods represent the phases of hematoma formation, callus formation, callus molding, and mature lamellar bone formation, respectively. Extracellular organization was positively employed throughout the four stages. At the hematoma formation phase, the muscle contraction process was downregulated. Antibacterial peptide pathway was downregulated at all phases. The upregulation of Fn1 (initial, early, middle, and late time periods), Col3a1 (initial, early, and middle time periods), Col11a1 (initial and early time periods), Mmp9 (middle and late time periods), Mmp13 (early, middle, and late time periods) and the downregulation of RatNP-3b (initial, early, middle, and late time periods) were possible symbols for bone fracture healing and may use as therapeutic targets. Conclusion: These findings suggest some new potential pathways and genes in the process of bone fracture healing and further provide insights that can be used in targeted molecular therapy for bone fracture healing.

<abstract> <p>As a guanylate binding protein (GBPs) member, GBP3 is immune-associated and may participate in oncogenesis and cancer therapy. Since little has been reported on GBP3 in this field, we provide pan-cancer bioinformatics to investigate the role of GBP3 in human cancers. The GBP3 expression, related clinical outcomes, immune infiltrates, potential mechanisms and mutations were conducted using tools including TIMER2.0, GEPIA2.0, SRING, DAVID and cBioPortal. Results showed an increased risk of high GBP3 in Brain Lower Grade Glioma (LGG) and Lung Squamous Cell Carcinoma (LUSC) and a decreased risk of GBP3 in Sarcoma (SARC) and Skin Cutaneous Melanoma (SKCM) (p ≤ 0.05). GBP3 was negatively correlated with CAFs in Esophageal Adenocarcinoma (ESCA) and positively correlated with CAFs in LGG, LUSC and TGCG (p ≤ 0.05). In addition, GBP3 was positively correlated with CD8+ T cells in Bladder Urothelial Carcinoma (BLCA), Cervical Squamous Cell Carcinoma (CESC), Kidney Renal Clear Cell Carcinoma (KIRC), SARC, SKCM, SKCM-Metastasis and Uveal Melanoma (UVM) (p ≤ 0.05). Potentially, GBP3 may participate in the homeostasis between immune and adaptive immunity in cancers. Moreover, the most frequent mutation sites of GBP3 in cancers are R151Q/^* and K380N. This study would provide new insight into cancer prognosis and therapy.</p> </abstract>

For salt-sensitive hypertension (SSH), salt restriction and angiotensin-converting enzyme (ACE) inhibitors are essential treatments, but their effect on the function of resistance arteries is unclear. Here, we present an intravital study to detect the effect of salt restriction and ACE inhibitors on the function of the mesenteric small artery (MSA) in SSH. Dahl salt-sensitive rats were randomized into the following groups: ACE inhibitor gavage, salt restriction, ACE inhibitor combined with salt restriction, and high-salt diet. After a 12-week intervention, the mesenteric vessels maintained their perfusion in vivo , and the changes in the diameter and blood perfusion of the MSAs to norepinephrine (NE) and acetylcholine (ACh) were detected. Switching from a high-salt diet to a low-salt diet (i.e., salt restriction) attenuated the vasoconstriction of the MSAs to NE and promoted the vasodilatation to ACh, while ACE inhibitor improved the vasodilatation more obviously. Pathologically, changes in local ACE, AT1R, and eNOS expression were involved in these processes induced by a high-salt diet. Our study suggests that salt restriction and ACE inhibitor treatment improve high salt intake-induced MSA dysfunction in SSH, and salt restriction is a feasible and effective treatment. Our findings may provide a scientific basis for the treatment of hypertension.