ObjectiveTo analyze the stress contribution of different cement volume to the adjacent vertebral endplates in percutaneous kyphoplasty (PKP) so as to explore the possible mechanism of adjacent vertebral fractures after PKP.Methods The three-dimensional finite element model of osteoporotic thoracolumbar vertebral compression fractures was established to simulate vertebral body partial restoration (80％) with PKP.During the process,two doses of bone cement ( polymethylmethacrylate,PMMA) were filled in the vertebral body (4.0 ml bone cement filling 15％ of the vertebral body volume and 8.0 ml bone cement filling 30％ of the vertebral body volume).Endplate stress under conditions of axial compression,flexion and extension was analyzed. ResultsRegarding the two filling doses in PKP,the adjacent vertebral endplate stress under the above-mentioned conditions was all increased at T11 and L1 vertebral body compared with that before operation.Meanwhile,endplate stress had positive correlation with the cement volume and the stress concentrated largely in the anterior and middle parts of endplate.ConclusionsThe stress of adjacent vertebral endplate is positively correlated with cement volume,with anterior and middle parts of endplate as the stress concentration.The probability of adjacent vertebral fractures shows a rising trend with the increase of cement volume in PKP.

Long non-coding RNAs (lncRNAs) can promote or inhibit the occurrence and development of pancreatic cancer,lung cancer,gastric cancer and breast cancer by regulating the expression of protein,signal pathway and cell cycle in different ways.Further studies of mechanisms of different lncRNAs in tumors may provide new methods for the diagnosis and treatment of cancers.

Female ; Humans ; Infant ; Mothers ; Serotonin ; Object Attachment ; Surveys and Questionnaires ; Depression, Postpartum

Humans ; Sleep, REM ; Memory ; Sleep ; REM Sleep Behavior Disorder

BACKGROUND: Systemic lupus erythematosus (SLE) is a complex autoimmune disease, and the mechanism of SLE is yet to be fully elucidated. The aim of this study was to explore the role of two-pore segment channel 2 (TPCN2) in SLE pathogenesis. METHODS: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to detect the expression of TPCN2 in SLE. We performed a loss-of-function assay by lentiviral construct in Jurkat and THP-1 cell. Knockdown of TPCN2 were confirmed at the RNA level by qRT-PCR and protein level by Western blotting. Cell Count Kit-8 and flow cytometry were used to analyze the cell proliferation, apoptosis, and cell cycle of TPCN2-deficient cells. In addition, gene expression profile of TPCN2-deficient cells was analyzed by RNA sequencing (RNA-seq). RESULTS: TPCN2 knockdown with short hairpin RNA (shRNA)-mediated lentiviruses inhibited cell proliferation, and induced apoptosis and cell-cycle arrest of G2/M phase in both Jurkat and THP-1 cells. We analyzed the transcriptome of knockdown-TPCN2-Jurkat cells, and screened the differential genes, which were enriched for the G2/M checkpoint, complement, and interleukin-6-Janus kinase-signal transducer and activator of transcription pathways, as well as changes in levels of forkhead box O, phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin, and T cell receptor pathways; moreover, TPCN2 significantly influenced cellular processes and biological regulation. CONCLUSION TPCN2 might be a potential protective factor against SLE.
Apoptosis/genetics* ; Cell Division ; Humans ; Jurkat Cells ; Lupus Erythematosus, Systemic/genetics* ; RNA, Small Interfering/genetics*

Irinotecan is an anticancer topoisomerase I inhibitor that acts as a prodrug of the active metabolite, SN-38. Unfortunately, the limited utility of irinotecan is attributed to its pH-dependent stability, short half-life and dose-limiting toxicity. To address this problem, a novel trivalent PEGylated prodrug (PEG-[Irinotecan]₃) has been synthesized and its full-profile pharmacokinetics, antitumor activity and toxicity compared with those of irinotecan. The results show that after intravenous administration to rats, PEG-[Irinotecan]₃ undergoes stepwise loss of irinotecan to form PEG-[Irinotecan]_3‒x (x = 1,2) and PEG-[linker] during which time the released irinotecan undergoes conversion to SN-38. As compared with conventional irinotecan, PEG-[Irinotecan]₃ displays extended release of irinotecan and efficient formation of SN-38 with significantly improved AUC and half-life. In a colorectal cancer-bearing model in nude mice, the tumor concentrations of irinotecan and SN-38 produced by PEG-[Irinotecan]₃ were respectively 86.2 and 2293 times higher at 48 h than produced by irinotecan. In summary, PEG-[Irinotecan]₃ displays superior pharmacokinetic characteristics and antitumor activity with lower toxicity than irinotecan. This supports the view that PEG-[Irinotecan]₃ is a superior anticancer drug to irinotecan and it has entered the phase II trial stage.