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With increasing population aging, osteoporosis vertebral compression fractures (OVCFs), resulting in severe back pain and functional impairment, have become progressively common. Percutaneous vertebroplasty (PVP) and percutaneous kyphoplasty (PKP) as minimally invasive procedures have revolutionized OVCFs treatment. However, PVP- and PKP-related complications, such as symptomatic cement leakage and adjacent vertebral fractures, continue to plague physicians. Consequently, progressively more implants for OVCFs have been developed recently to overcome the shortcomings of traditional procedures. Therefore, we conducted a literature review on several new implants for OVCFs, including StaXx FX, Vertebral Body Stenting, Vesselplasty, Sky Bone Expander, Kiva, Spine Jack, Osseofix, Optimesh, Jack, and V-strut. Additionally, this review highlights the individualized applications of these implants for OVCFs. Nevertheless, current clinical studies on these innovative implants remain limited. Future prospective, randomized, and controlled studies are needed to elucidate the effectiveness and indications of these new implants for OVCFs.

Migration and invasion are important characteristics of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs), which are involved in joint damage and contribute to rheumatoid arthritis (RA) pathology. However, the underlying mechanisms remain unclear. Because epithelial–mesenchymal transition (EMT) is a key mechanism related to migration and invasion in cancer cells, we investigated the relationship between EMT and RA-FLSs and explored whether the transforming growth factor β1 (TGF-β1)/Smad signaling pathway is involved. In vivo, fibroblast-like synoviocytes (FLSs) were isolated from the synovium of RA or osteoarthritis (OA) patients and cultured for 4–8 passages. EMT markers were detected by immunofluorescence and Western blotting. RA-FLSs were treated with TGF-β1 or Smad2/3 small interfering RNA (siRNA), EMT markers were detected, and migration and invasion were assessed by Transwell assays. EMT markers could be detected in FLSs; when compared with osteoarthritis fibroblast-like synoviocytes (OA-FLSs), E-cadherin and vimentin decreased, while N-cadherin and α-smooth muscle actin (α-SMA) increased in RA-FLSs. Furthermore, TGF-β1 enhanced migration and invasion by inducing EMT via activating Smad2/3 in RA-FLSs. Phosphorylation of Smad2/3 was accompanied by degradation of Smad3. Silencing Smad2/3 blocked EMT and inhibited the migration and invasion induced by TGF-β1. Matrix metalloproteinase 9 (MMP9) and vimentin were not affected when cells were treated with TGF-β1 or Smad2/3 siRNA. The TGF-β1/Smad signaling pathway is involved in EMT and contributes to migration and invasion in RA-FLSs. Interestingly, vimentin decreased in RA-FLSs, but there is no correlation between vimentin and TGF-β1/Smad signaling pathway. Thus, further research on vimentin should be conducted.

Plants deploy intracellular receptors to counteract pathogen effectors that suppress cell-surface receptor-mediated immunity. To what extent pathogens manipulate also immunity mediated by intracellular receptors, and how plants tackle such manipulation, remains unknown. Arabidopsis thaliana encodes three very similar ADR1 class helper NLRs (ADR1, ADR1-L1 and ADR1-L2), which play key roles in plant immunity initiated by intracellular receptors. Here, we report that Pseudomonas syringae AvrPtoB, an effector with E3 ligase activity, can suppress ADR1-L1- and ADR1-L2-mediated cell death. ADR1, however, evades such suppression by diversification of two ubiquitination sites targeted by AvrPtoB. The intracellular sensor NLR SNC1 interacts with and guards the CCR domains of ADR1-L1 and ADR-L2. Removal of ADR1-L1 and ADR1-L2 or delivery of AvrPtoB activates SNC1, which then signals through ADR1 to trigger immunity. Our work not only uncovers the long sought-after physiological function of SNC1 in pathogen defense, but also that reveals how plants can use dual strategies, sequence diversification and a multiple layered guard-guardee system, to counteract pathogen attack on core immunity functions.

Nonadiabatic alignment by intense nonresonant laser fields is a versatile technique to manipulate the spatial direction of molecules. By solving the time-dependent Schrödinger equation numerically the degree of alignment of the molecules initially in different rotational state are calculated and the results show that the degree of alignment strongly depends on the initial rotational state. Thus, the present study indicates that, for obtaining a high degree of alignment for molecules, appropriate selection of molecular rotational states is necessary.

Objective： Side population （SP） cells may play a crucial role in tumorigenesis and the recurrence of cancer Many kinds of cell lines and tissues have demonstrated the presence of SP cells, including several gastric cancer cell lines. This study is aimed to identify the cancer stem-like cells in the SP of gastric cancer cell line MKN-45. Methods： We used fluorescence activated cell sorting （FACS） to sort SP cells in the human gastric carcinoma cell line MKN-45 （cells labeled with Hoechst 33342） and then characterized the cancer stem-like properties of SP cells. Results： This study found that the SP cells had higher clone formation efficiency than major population （MP） cells. Five stemness-related gene expression profiles, including OCT-4, SOX-2, NANOG, CD44, and adenosine triphosphate （ATP）-binding cassette transporters gene ABCG2, were tested in SP and MP cells using quantitative real-time reverse transcription polymerase chain reaction （RT-PCR）. Western blot was used to show the difference of protein expression between SP and MP cells. Both results show that there was significantly higher protein expression in SP cells than in MP cells. When inoculated into non-obese diabetic/severe combined immunodeficiency （NOD/SCID） mice, SP cells show higher tumorigenesis tendency than MP cells. Conclusions： These results indicate that SP cells possess cancer stem cell properties and prove that SP cells from MKN-45 are gastric cancer stem-like cells.

Aim： To investigate the mechanisms responsible for the protective action of berberine （Ber） against gut damage in endotoxemic mice. Methods： Male BALB/c mice were administered intragastrically with distilled water （0.1 mL/lO g）, Ber （50 mg/kg） alone, yohimbine （2 mg/kg） alone, or Ber （50mg/kg） in combination with yohimbine （2 mg/kg） for 3 d. On the third day, lipopolysaccharide （LPS, 18 mg/kg） or normal saline was intraperitoneally injected one hour after the intragastric administration. Following the treatment, intestinal injury in the ileum was histopathologically accessed; enterocyte apoptosis was examined using TUNEL method; Toll-like receptor 4 （TLR4） mRNA expression was measured using RT-PCR assay; inhibitor protein-KBa （I-KBa） phosphorylation and myeloperoxidase content were examined using Western blloting. The macrophage inflammatory protein-2 （MIP-2） production was measured using ELISA assay. Results： Mice challenged with LPS caused extensive ileum injury, including a significantly increased injury score, decreased intesti- nal villus height, reduced gut mucosal weight and increased intestinal permeability. Furthermore, LPS significantly induced entero- cyte apoptosis, increased TLR4 mRNA expression, I-KBa phosphorylation, MIP-2 production and myeloperoxidase content in the ileum. Pretreatment with Ber significantly alleviated all the alterations in the ileum in the endotoxemic mice. Pretreatment with the a2-adrenoceptor antagonist yohimbine did not block the protective action of Ber against LPS-induced intestinal injury. In addition, treatment with yohimbine alone did not prevent LPS-induced intestinal injury. Conclusion： Pretreatment with Ber provides significant protection against LPS-induced intestinal injury in mice, via reducing entero- cyte apoptosis, inhibiting the TLR4-nuclear factor KB-MIP-2 pathway and decreasing neutrophil infiltration that are independent of a2-adrenoceptors.