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The heterogeneity of diffuse large B-cell lymphoma (DLBCL) acts as a main barrier to identify the genetic basis of the disease and the choice of treatment. Differentially expressed genes (DEGs) from three mRNA expression profile datasets were screened using GEO2R, and bioinformatics analysis was performed on the DEGs. A total of six upregulated and 13 downregulated DEGs were identified. Among these, two hub genes with a high degree of correlation were selected. FBN1 and TIMP1 were identified via STRING analysis and validated by GEPIA. FBN1 and TIMP1 were highly expressed in DLBCL tissues. FBN1 expression was significantly higher in patients of the Ann Arbor stage group (III-IV), with higher IPI score (3-5), and in the non-GCB group. Patients with high TIMP1 expression were more frequently associated with B symptoms, Ann Arbor stage (III-IV), higher IPI score (3-5) and were in the non-GCB group. Furthermore, FBN1 siRNA decreased FBN1 and TIMP1 expression and downregulation of TIMP1 attenuated TIMP1 expression but not of FBN1. Migration of DLBCL cells reduced when treated with either FBN1 or TIMP1 siRNA. Moreover, FBN1 or TIMP1 siRNA decreased the expression of Wnt target genes. Simultaneous overexpression of TIMP1 resulted in an increase in these proteins. This confirmed that both FBN1 and TIMP1 were positively associated with DLBCL progression. Further analysis revealed that FBN1/TIMP1 interaction could improve DLBCL cell migration and regulate the Wnt signaling pathway. Although the underlying mechanisms regarding the interaction between FBN1 and TIMP1 requires further clarification, they might be potential therapeutic targets for DLBCL therapy.

Single-cell RNA sequencing (scRNA-seq) was recently adopted for exploring molecular programmes and lineage progression patterns of pathogenesis of important diseases. In this study, scRNA-seq was used to identify potential markers for chondrocytes in osteoarthritis (OA) and to explore the function of different types of chondrocytes in OA.

Here we aimed to identify the biomarkers and differentiation of chondrocyte by Single-cell RNA seq analysis. GeneOntology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to identify the function of candidate marker genes in chondrocytes. Protein-protein interaction (PPI) network was constructed to find the hub genes in 3 types of chondrocyte respectively. We also used qRT-PCR to detect the expression level of the candidate marker genes in different types of chondrocyte.

In this study, we characterized the single-cell expression profiling of 480 chondrocyte samples and found hypertrophic chondrocyte (HTC), homeostatic chondrocyte (HomC) and fie biomarkers of chondrocyte were also valuable for estimating OA progression.

This study aims to assess the angiogenic and osteogenic capacity in rabbit sinus model grafted with Deproteinized bovine bone mineral (DBBM) particles soaked in injectable Platelet rich fibrin (iPRF), both of which interacted to form an integrated block.

Among sixteen rabbits, bilateral maxillary sinuses were randomly grafted with either DBBM containing iPRF (iPRF+DBBM group), or DBBM alone (DBBM group). After a 4 and 8-week healing period, animals were sacrificed for micro-CT, histological and immunofluorescence analyses, respectively.

New bone formation in the iPRF+DBBM group was largely observed around the basal bone wall and Schneiderian membrane (SM), which further substitute the bone grafting material in a bidirectional remodeling pattern. Although the ultimate amount of bone volume was of no significant difference between two groups in radiographical image, the expression of ALP and TRAP staining were significantly higher in the experimental group with numerous vascular formations at 4

week. Moreover, the substitution rate of DBBM by new bone formation after 8 weeks was significantly higher in the experimental group. As a result, mature collagen fibers were detected in the larger amount of area in iPRF+DBBM group even at an early stage.

iPRF+DBBM accelerated vascular formation, bone remodeling and substitution of bone graft materials at the early healing period, even though it failed to increase the bone volume in a long-term period. This integrated grafting biomaterial will have great potential in the application of sinus augmentation, which provides a favorable environment for early implant placement.

iPRF+DBBM accelerated vascular formation, bone remodeling and substitution of bone graft materials at the early healing period, even though it failed to increase the bone volume in a long-term period. This integrated grafting biomaterial will have great potential in the application of sinus augmentation, which provides a favorable environment for early implant placement.

Gastric cancer (GC) is a serious threat to human health. We aimed to explore the effects of Wnt1 induced signaling protein 1 (WISP1) on GC.

The WISP1 expressions in GC tissues were detected using immunohistochemistry and qRT-PCR. The connection between GC prognosis and WISP1 expression was analyzed via Pearson’s χ

test. The WISP1 expressions were down-regulated in GC cells through siWISP1 transfection. Colony formation assay and cell counting kit-8 assay were carried out to measure cell colony formation and proliferation, respectively. Flow cytometry was operated to examine the cell cycle and apoptosis. The protein expressions in our study were assessed using western blot. The AKT pathway was blocked by LY294002 treatment and then the cell activities were assessed. Furthermore, GC mice models were established to investigate the effects of WISP1 on GC

.

We found that WISP1 was highly expressed in GC cells and tissues. The up-regulation of WISP1 was related to poor prognosis of GC patients. WISP1 down-regulation reduced colony formation and cell proliferation, resulted cell cycle arrest and promoted cell apoptosis in GC. WISP1 knockdown suppressed AKT/mTOR pathway activity. LY294002 treatment recovered the decreases of colony formation and cell proliferation, arrest of cell cycle and increase of cell apoptosis which were induced by WISP1 knockdown. WISP1 down-regulation repressed GC tumor growth and enhanced tumor apoptosis

.

WISP1 regulated GC cell proliferation and apoptosis

and

through activating AKT/mTOR pathway. WISP1 might be a target in GC therapy.

WISP1 regulated GC cell proliferation and apoptosis in vivo and in vitro through activating AKT/mTOR pathway. Polyinosinic acid-polycytidylic acid cost WISP1 might be a target in GC therapy.