Exosomal CTHRC1 from cancer-associated fibroblasts facilitates endometrial cancer progression via ITGB3/FAK signaling pathway.

The emerging tumor microenvironment (TME) is a complex and constantly evolving entity. Cancer-associated fibroblasts (CAFs) are a vital component of the TME with diverse functions. They interact closely with cancer cells through reciprocal signaling and play a crucial role in tumor progression. Exosomes, which contain diverse biological information, are identified as an important mediator of cell-cell communication. This study aimed to investigate how CAF-derived exosomes promote metastasis of endometrial cancer (EC). Our findings revealed that CAF-derived exosomes significantly enhanced EC cell proliferation and migration compared to normal fibroblast-derived exosomes. Quantitative proteomics analysis of CAF/NF-derived exosomes demonstrated differential expression of CTHRC1, a protein overexpressed in multiple tumors, promoting cancer progression through enhanced cell migration and invasion. Exosomal overload of CTHRC1 significantly contributes to EC cell migration. Mechanically, we determined that ITGB3 was immunoprecipitated by CTHRC1 and phosphorylated FAK on Tyr397, which was important for exosomal CTHRC1 mediated migratory ability of EC cells. Overexpression of CTHRC1 in secreted exosomes promotes the metastatic ability of EC cells in mouse models and may be eliminated by Defactinib, an inhibitor of FAK Tyr397 phosphorylation. Moreover, overexpression of CTHRC1 was increased in EC patients, elevating with cancer progression, and correlated with negative tumor prognosis. Our results revealed that CAF mediated endometrial cancer progression is related to high levels of CTHRC1 and exosomal CTHRC1 derived from CAF may be a promising therapeutic strategy for metastatic endometrial cancer.

The P286R mutation of DNA polymerase ε activates cancer-cell-intrinsic immunity and suppresses endometrial tumorigenesis via the cGAS-STING pathway.

Endometrial carcinoma (EC) is a prevalent gynecological tumor in women, and its treatment and prevention are significant global health concerns. The mutations in DNA polymerase ε (POLE) are recognized as key features of EC and may confer survival benefits in endometrial cancer patients undergoing anti-PD-1/PD-L1 therapy. However, the anti-tumor mechanism of POLE mutations remains largely elusive. This study demonstrates that the hot POLE P286R mutation impedes endometrial tumorigenesis by inducing DNA breakage and activating the cGAS-STING signaling pathway. The POLE mutations were found to inhibit the proliferation and stemness of primary human EC cells. Mechanistically, the POLE mutants enhance DNA damage and suppress its repair through the interaction with DNA repair proteins, leading to genomic instability and the upregulation of cytoplasmic DNA. Additionally, the POLE P286R mutant also increases cGAS level, promotes TBK1 phosphorylation, and stimulates inflammatory gene expression and anti-tumor immune response. Furthermore, the POLE P286R mutation inhibits tumor growth and facilitates the infiltration of cytotoxic T cells in human endometrial cancers. These findings uncover a novel mechanism of POLE mutations in antagonizing tumorigenesis and provide a promising direction for effective cancer therapy.

SMYD3 promotes endometrial cancer through epigenetic regulation of LIG4/XRCC4/XLF complex in non-homologous end joining repair.

Endometrial cancer (EC) stands as one of the most prevalent malignancies affecting the female genital tract, witnessing a rapid surge in incidence globally. Despite the well-established association of histone methyltransferase SMYD3 with the development and progression of various cancers, its specific oncogenic role in endometrial cancer remains unexplored. In the present study, we report that the expression level of SMYD3 is significantly upregulated in EC samples and associated with EC progression. Through meticulous in vivo and in vitro experiments, we reveal that depletion of SMYD3 curtails cell proliferation, migration, and invasion capabilities, leading to compromised non-homologous end joining repair (NHEJ) and heightened sensitivity of EC cells to radiation. Furthermore, our pathway enrichment analysis underscores the pivotal involvement of the DNA damage repair pathway in regulating EC progression. Mechanistically, in response to DNA damage, SMYD3 is recruited to these sites in a PARP1-dependent manner, specifically methylating LIG4. This methylation sets off a sequential assembly of the LIG4/XRCC4/XLF complex, actively participating in the NHEJ pathway and thereby fostering EC progression. Notably, our findings highlight the promise of SMYD3 as a crucial player in NHEJ repair and its direct correlation with EC progression. Intriguingly, pharmacological intervention targeting SMYD3 with its specific inhibitor, BCI-121, emerges as a potent strategy, markedly suppressing the tumorigenicity of EC cells and significantly enhancing the efficacy of radiotherapy. Collectively, our comprehensive data position SMYD3 as a central factor in NHEJ repair and underscore its potential as a promising pharmacological target for endometrial cancer therapy, validated through both in vitro and in vivo systems.

SMYD2 inhibition-mediated hypomethylation of Ku70 contributes to impaired nonhomologous end joining repair and antitumor immunity.

DNA damage repair (DDR) is a double-edged sword with different roles in cancer susceptibility and drug resistance. Recent studies suggest that DDR inhibitors affect immune surveillance. However, this phenomenon is poorly understood. We report that methyltransferase SMYD2 plays an essential role in nonhomologous end joining repair (NHEJ), driving tumor cells adaptive to radiotherapy. Mechanically, in response to DNA damage, SMYD2 is mobilized onto chromatin and methylates Ku70 at lysine-74, lysine-516, and lysine-539, leading to increased recruitment of Ku70/Ku80/DNA-PKcs complex. Knockdown of SMYD2 or its inhibitor AZ505 results in persistent DNA damage and improper repair, which sequentially leads to accumulation of cytosolic DNA, and activation of cGAS-STING pathway and triggers antitumor immunity via infiltration and activation of cytotoxic CD8+ T cells. Our study reveals an unidentified role of SMYD2 in regulating NHEJ pathway and innate immune responses, suggesting that SMYD2 is a promising therapeutic target for cancer treatment.

Loss of the receptors ER, PR and HER2 promotes USP15-dependent stabilization of PARP1 in triple-negative breast cancer.

Poly(ADP-ribose) polymerase 1 (PARP1) is essential for the progression of several types of cancers. However, whether and how PARP1 is stabilized to promote genomic stability in triple-negative breast cancer (TNBC) remains unknown. Here, we demonstrated that the deubiquitinase USP15 interacts with and deubiquitinates PARP1 to promote its stability, thereby stimulating DNA repair, genomic stability and TNBC cell proliferation. Two PARP1 mutations found in individuals with breast cancer (E90K and S104R) enhanced the PARP1-USP15 interaction and suppressed PARP1 ubiquitination, thereby elevating the protein level of PARP1. Importantly, we found that estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) inhibited USP15-mediated PARP1 stabilization through different mechanisms. ER bound to the USP15 promoter to suppress its expression, PR suppressed the deubiquitinase activity of USP15, and HER2 abrogated the PARP1-USP15 interaction. The specific absence of these three receptors in TNBC results in high PARP1 levels, leading to increases in base excision repair and female TNBC cell survival.

Development and Clinical Trial of a New Orthopedic Surgical Robot for Positioning and Navigation.

Robot-assisted orthopedic surgery has great application prospects, and the accuracy of the robot is the key to its overall performance. The aim of this study was to develop a new orthopedic surgical robot to assist in spinal surgeries and to compare its feasibility and accuracy with the existing orthopedic robot. A new type of high-precision orthopedic surgical robot (Tuoshou) was developed. A multicenter, randomized controlled trial was carried out to compare the Tuoshou with the TiRobot (TINAVI Medical Technologies Co., Ltd., Beijing) to evaluate the accuracy and safety of their navigation and positioning. A total of 112 patients were randomized, and 108 patients completed the study. The position deviation of the Kirschner wire placement in the Tuoshou group was smaller than that in the TiRobot group (p = 0.014). The Tuoshou group was better than the TiRobot group in terms of the pedicle screw insertion accuracy (p = 0.016) and entry point deviation (p < 0.001). No differences were observed in endpoint deviation (p = 0.170), axial deviation (p = 0.170), sagittal deviation (p = 0.324), and spatial deviation (p = 0.299). There was no difference in security indicators. The new orthopedic surgical robot was highly accurate and optimized for clinical practice, making it suitable for clinical application.

Nickel clusters accelerating hierarchical zinc indium sulfide nanoflowers for unprecedented visible-light hydrogen production.

As a typical two-dimensional (2D) metal chalcogenides and visible-light responsive semiconductor, zinc indium sulfide (ZnIn2S4) has attracted much attention in photocatalysis. However, the high recombination rate of photogenerated electrons and holes seriously limits its performance for hydrogen production. In this work, we report in-situ photodeposition of Ni clusters in hierarchical ZnIn2S4 nanoflowers (Ni/ZnIn2S4) to achieve unprecedented photocatalytic hydrogen production. The Ni clusters not only provide plenty of active sites for reactions as evidenced by in-situ photoluminescence measurement, but also effectively accelerate the separation and migration of the photogenerated electrons and holes in ZnIn2S4. Consequently, the Ni/ZnIn2S4 composites exhibit good stability and reusability with highly enhanced visible-light hydrogen production. In particular, the best Ni/ZnIn2S4 photocatalyst exhibits an unprecedented hydrogen production rate of 22.2 mmol·h-1·g-1, 10.6 times that of the pure ZnIn2S4 (2.1 mmol·h-1·g-1). And its apparent quantum yield (AQY) is as high as 56.14% under 450 nm monochromatic light. Our work here suggests that depositing non-precious Ni clusters in ZnIn2S4 is quite promising for the potential practical photocatalysis in solar energy conversion.

Size effect of bifunctional gold in hierarchical titanium oxide-gold-cadmium sulfide with slow photon effect for unprecedented visible-light hydrogen production.

Gold nanoparticles (Au NPs) with surface plasmonic resonance (SPR) effect and excellent internal electron transfer ability have widely been combined with semiconductors for photocatalysis. However, the in-depth effects of Au NPs in multicomponent photocatalysts have not been completely understood. Herein, ternary titanium oxide-gold-cadmium sulfide (TiO2-Au-CdS, TAC) photocatalysts, based on hierarchical TiO2 inverse opal photonic crystal structure with different Au NPs sizes have been designed to reveal the SPR effect and internal electron transfer of Au NPs in the presence of slow photon effect. It appears that the SPR effect and internal electron transfer ability of Au NPs, depending on their sizes, play a synergistic effect on the photocatalytic enhancement. The ternary TAC-10 photocatalyst with ~ 10 nm Au NPs demonstrates an unprecedented hydrogen evolution rate of 47.6 mmolh-1g-1 under visible-light, demonstrating ~ 48% enhancement comparing to the sample without slow photon effect. In particular, a 9.83% apparent quantum yield under 450 nm monochromatic light is achieved for TAC-10. A model is proposed and finite-difference time-domain (FDTD) simulations reveal the size influence of Au NPs in ternary TAC photocatalysts. This work suggests that the rational design of bifunctional Au NPs coupling with slow photon effect could largely promote hydrogen production from visible-light driven water splitting.

Renal cell carcinoma choroidal metastasis recorded by smartphone with interface eyepiece adapter mounted on slit lamp: A case report.

RATIONALE: Ocular metastasis of renal cell carcinoma (RCC) is rare, and mainly located on the choroid. We report a choroidal metastasis from RCC, which was recorded by a smartphone with an interface eyepiece adapter mounted on a slit lamp. PATIENT CONCERNS: A 45-year-old female presented with 1-month history of painless occlusion of the vision field on the left eye, who had undergone right nephrectomy for RCC 19 months ago. DIAGNOSES: A smooth, hemispherical and brown protrusion was found behind the pupil nasally. An enhanced computed tomography scan of the orbit showed a slightly high-density hemispherical nodule involving the nasal portions of the left eyeball, the enhancement of the lesion was obvious and homogeneous. A metastatic choroidal space-occupying lesion from RCC was highly suspected according to the clinical and radiological findings. INTERVENTIONS: The patient was advised to undergo further treatment, such as radiotherapy. OUTCOMES: The images of choroid metastasis were recorded by the smartphone with the interface eyepiece adapter mounted on the slit lamp handily. CONCLUSIONS: The smartphone with an interface eyepiece adapter mounted on the slit lamp can be widely used to record the precious images in the clinic in a timely manner.

A comparison of the bilateral decompression via unilateral approach versus conventional approach transforaminal lumbar interbody fusion for the treatment of lumbar degenerative disc disease in the elderly.

BACKGROUND: Bilateral decompression via unilateral approach (BDUA) is an effective surgical approach for treating lumbar degenerative diseases. However, no studies of prognosis, especially the recovery of the soft tissue, have reported using BDUA in an elderly population. The aims of these research were to investigate the early efficacy of the bilateral decompression via unilateral approach versus conventional approach transforaminal lumbar interbody fusion (TLIF) for the treatment of lumbar degenerative disc disease in the patients over 65 years of age, especially in the perioperative factors and the recovery of the soft tissue. METHODS: The clinical data from 61 aging patients with lumbar degenerative disease who received surgical treatment were retrospectively analyzed. 31 cases who received the lumbar interbody fusion surgery with bilateral decompression via unilateral approach (BDUA) were compared with 30 cases who received conventional approach transforaminal lumbar interbody fusion. The radiographic parameters were measured using X-ray including lumbar lordosis angle and fusion rate. Japanese Orthopedic Association (JOA), Visual Analogue Scale (VAS) and Oswestry Disability Index (ODI) scores were used to evaluate the clinical outcomes at different time points. Fatty degeneration ratio and area of muscle/vertebral body were used to detect recovery of soft tissue. RESULTS: The BDUA approach group was found to have significantly less intraoperative blood loss(p < 0.05) and postoperative drainage(p < 0.05) compared to conventional approach transforaminal lumbar interbody fusion group. Symptoms of spinal canal stenosis and nerve compression were significantly relieved postoperatively, as compared with the preoperative state. However, the opposite side had a lower rate of fatty degeneration (9.42 ± 3.17%) comparing to decompression side (11.68 ± 3.08%) (P < 0.05) six months after surgery in the BDUA group. While there were no significant differences (P > 0.05) in two sides of conventional transforaminal lumbar interbody fusion approach group six months after surgery. CONCLUSIONS: Bilateral decompression via unilateral approach (BDUA) is able to reduce the intraoperative and postoperative body fluid loss in the elderly. The opposite side of decompression in BDUA shows less fatty degeneration in 6 months, which indicates better recovery of the soft tissue of the aging patients.

Escherichia coli templated iron oxide biomineralization under oscillation.

Motility is significant in organisms. Studying the influence of motility on biological processes provides a new angle in understanding the essence of life. Biomineralization is a representative process for organisms in forming functional materials. In the present study, we investigated the biomineralization of iron oxides templated by Escherichia coli (E. coli) cells under oscillation. The formation of iron oxide minerals with acicular and banded morphology was observed. The surface charge of E. coli cells contributed to the biomineralization process. The surface components of E. coli cells including lipids, carbohydrates and proteins also have roles in regulating the formation and morphology of iron oxide minerals. As-prepared mineralized iron oxide nanomaterials showed activity in photocatalytic degradation of methylene blue as well as in electrocatalytic hydrogen evolution reaction. This study is helpful not only in understanding motility in biological processes, but also in developing techniques for fabricating functional nanomaterials.

Diosmetin enhances the sensitivity of radiotherapy by suppressing homologous recombination in endometrial cancer.

Radiotherapy is an essential treatment for endometrial cancer (EC), especially in advanced, metastatic, and recurrent cases. Combining radiotherapy, which mainly causes DNA double-strand breaks (DSBs), with small molecules targeting aberrantly activated homologous recombination (HR) repair pathways holds great potential for treating ECs in advanced stages. Here, we demonstrate that diosmetin (DIO), a natural flavonoid, suppresses HR, therefore inhibiting cell proliferation and enhancing the sensitivity of EC to radiotherapy. Clonogenic experiments revealed that combining DIO and X-ray significantly inhibited the viability of EC cells compared to cells treated with diosmetin or X-ray alone. The survival fraction of EC cells decreased to 40% when combining 0.4 Gy X-ray and 4 µM DIO; however, each treatment alone only caused death in approximately 15% and 22% of cancer cells, respectively. Further mechanistic studies showed that diosmetin inhibited the recruitment of RPA2 and RAD51, two critical factors involved in the HR repair pathway, upon the occurrence of DSBs. Thus, we propose that a combination of diosmetin and irradiation is a promising therapeutic strategy for treating endometrial cancer.

Triptolide impairs genome integrity by directly blocking the enzymatic activity of DNA-PKcs in human cells.

Triptolide is a multi-functional natural small molecular compound extracted from a traditional Chinese medicinal herb. Triptolide and its derivatives exhibit cytotoxicity through inducing DNA damage, therefore increasing sensitivity to DNA-damage based chemotherapy or radiotherapy in different types of cells. However, the regulatory mechanism of genotoxicity by triptolide, and the loss of genome integrity induced by triptolide are not fully understood. Here, we measured the effects of triptolide on genome integrity in a human fibroblast line HCA2-hTERT using the neutral comet assay. We demonstrated that treating cells with triptolide induced genomic instability in HCA2-hTERT cells. Furthermore, we observed the accumulation of γH2AX foci in triptolide treated cells than control cells at 24 h post ionizing radiation. Further mechanistic studies indicated that triptolide inhibited the enzymatic activity of DNA-PKcs, the critical nonhomologous end joining factor. In vitro kinase activity assays showed that triptolide suppressed the kinase activity of DNA-PKcs and molecular docking also predicted a potential interaction between triptolide and DNA-PKcs. As a consequence, we found that triptolide treatment enhanced the interaction between DNA-PKcs and KU80 and hampered the following recruitment of 53BP1. Altogether, our finding provides a new perspective about the toxicity of triptolide in non-cancer cells and highlights the necessity of taking genome effects of triptolide and its derivatives into consideration in the future clinical and research applications.

MiR-23b functions as an oncogenic miRNA by downregulating Mcl-1S in lung cancer cell line A549.

It has been reported that microRNA-23b (miR-23b) plays a role in multiple cancers, while its impact on lung cancer has not been comprehensively known. Our study explored the probable impacts of miR-23b on lung cancer cells. Expression of miR-23b was assessed by reverse transcription quantitative polymerase chain reaction. After miR-23b mimic, inhibitor, and their own control were transfected into A549 cells, cell viability, migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) were investigated through different experimental methods. The targeting contact between miR-23b and myeloid cell leukemia-1 (Mcl-1) was investigated applying dual-luciferase activity assay. In addition, the modulatory impacts of miR-23b on the splicing variants of Mcl-1 (Mcl-1S and Mcl-1L) were explored. MiR-23b was highly expressed in lung cancer cells compared with normal lung cells. Increased expression of miR-23b promoted A549 cell viability, migration, invasion, and EMT. However, miR-23b silencing produced the opposite results. Mcl-1 has been proven to be a specialized target of miR-23b. Compared with the reduction of Mcl-1S induced by miR-23b overexpression, Mcl-1L showed negligible interaction with miR-23b. Moreover, the antitumor activities of miR-23b silencing were alleviated by Mcl-1S silencing. The blockage of Janus kinase/signal transducer and activator of transcription protein (JAK/STAT) and Wnt/ß-catenin induced by miR-23b silencing was reversed by Mcl-1S silencing. MiR-23b might be an up-and-coming biomarker of lung cancer. In addition, miR-23b was involved in the tumor-promoting effects and the mobilization of JAK/STAT and Wnt/ß-catenin pathways through the reduction of Mcl-1S.

cGAMP inhibits tumor growth in colorectal cancer metastasis through the STING/STAT3 axis in a zebrafish xenograft model.

The leading cause of mortality due to colorectal cancer (CRC) is highly associated with the development of liver metastases. Recently, we described cGAMP that is closely related to the metastatic state wherein the progress of metastatic tumors is associated with favorable outcomes in a zebrafish xenograft model. cGAMP was administered and the expression levels of type-I interferons were induced amongst tumor tissues to illuminate the overall measure of the induced STING/STAT3 axis in colorectal liver metastases. Furthermore, cGAMP-STING dependent STAT3 activation resulted in the inhibition of tumor cell proliferation, viability, and invasion in vitro. The subtotal reduction in tumor growth attributed to a large number of infiltrating inflammatory cells in vivo. We showed that cGAMP inhibited migration through angiogenesis by up-regulating IL-2, TNF-α, and IFN-γ, whereas STAT3 down-regulation inhibited CXCL8, BCL-2, and VEGFA expression. The importance of cGAMP in inhibiting the invasion front of CRC confirmed that the cGAMP dependent activation of STING/STAT3 axis played a key role in the inhibition of tumor progression.

Probing conducting polymers@cadmium sulfide core-shell nanorods for highly improved photocatalytic hydrogen production.

We report three types of conducting polymers (CPs), polyaniline (PANI), polypyrrole (PPY) and poly (3,4-ethylenedioxythiophene) (PEDOT) to modify the surface of the CdS nanorods to probe their photocorrosion inhibition and photocatalytic hydrogen production. Various characterizations, such as high resolution transmission electron microscopy (HRTEM), X-ray photoelectron spectroscopy (XPS), cyclic voltammetry (CV) and density function theory (DFT) calculations have been conducted to reveal the intrinsic structure of the as-constructed CPs@CdS (@ means CPs at the surface of CdS) core-shell nanorods. The results show that the PANI and PPY shells with abundant N and C atoms can significantly enhance the binding energy of Cd and S atoms on the surface of the CdS nanorods. However, there is no obvious enhancement of binding energy at the interface of the PEDOT shell and the CdS nanorods core. Therefore, PANI@CdS and PPY@CdS possess stronger driving force than PEDOT@CdS to inject the photogenerated holes in conducting polymer shells. As a result, the polyaniline (PANI) modified PANI@CdS core-shell nanorods demonstrate the most effectively enhanced hydrogen production rate of ∼9.7 mmol h-1 g-1 and effective photocorrosion inhibition in 30 h without deactivation under visible-light irradiation. The hydrogen production performance of PPY@CdS is not effectively promoted owing to the weak transmittance of light for the PPY shell. The PEDOT shell cannot improve the hydrogen production and stability property of the CdS nanorods. This work could shed some light on conducting polymers modifying metal sulfides nanostructures that is of inconceivable significance for effective photocorrosion inhibition and highly enhanced photocatalytic activities.

A stable, reusable, and highly active photosynthetic bioreactor by bio-interfacing an individual cyanobacterium with a mesoporous bilayer nanoshell.

An individual cyanobacterium cell is interfaced with a nanoporous biohybrid layer within a mesoporous silica layer. The bio-interface acts as an egg membrane for cell protection and growth of outer shell. The resulting bilayer shell provides efficient functions to create a single cell photosynthetic bioreactor with high stability, reusability, and activity.

Evaluation of MR issues for the latest standard brands of orthopedic metal implants: plates and screws.

PURPOSE: The study was performed to evaluate magnetic resonance (MR) issues for the latest standard brands of plates and screws used in orthopedic surgery at a 1.5-T MR system, including the safety and metallic artifacts. METHODS: The plates and screws (made of titanium alloy and stainless steel materials, according to the latest standard brands) were assessed for displacement in degrees, MRI-related heating and artifacts at a 1.5-T MR system. The displacement in degrees of the plates and screws was evaluated on an angel-measurement instrument at the entrance of the MR scanner. The MRI-related heating was assessed on a swine leg fixed with a plate by using a "worst-case" pulse sequence. A rectangular water phantom was designed to evaluate metallic artifacts of a screw on different sequences (T1/T2-weighted FSE, STIR, T2-FSE fat saturation, GRE, DWI) and then artifacts were evaluated on T2-weighted FSE sequence by modifying the scanning parameters including field of view (FOV), echo train length (ETL) and bandwidth to identify the influence of parameters on metallic artifacts. 15 volunteers with internal vertebral fixation (titanium alloy materials) were scanned with MR using axial and sagittal T2-FSE, sagittal T2-FSE fat suppression and STIR with conventional and optimized parameters, respectively. Then all images were graded by two experienced radiologists having the experience of more than 7 years under double-blind studies that is neither of them knew which was conventional parameter group and optimized parameter group. RESULTS: The average deflection angle of titanium alloy and stainless steel implants were 4.3° and 7.7°, respectively, (less than 45°) which indicated that the magnetically induced force was less than the weight of the object. The deflection angle of the titanium alloy implants was less than the stainless steel one (t=9.69, P<0.001). The average temperature changes of titanium alloy before and after the scan was 0.48°C and stainless steel implants was 0.74°C, respectively, with the background temperature changes of 0.24°C. The water phantom test indicated that the DWI sequence produced largest artifacts, while FSE pulse sequence produced smallest artifacts. And T2-weighted FSE fat saturation sequence produced larger artifacts than STIR sequence. The influence of the scanning parameters on metallic artifacts was verified that metallic artifacts increased with longer echo train length and bigger FOV, while decreased with larger bandwidth. The interreader agreement was good or excellent for each set of images graded with Cohen's Kappa statistic. Image grading of axial and sagittal T2-FSE with optimized parameters were significantly superior to that with conventional parameters (grade, 3.3±0.5 vs 2.7±0.6, P=0.003; 3.2±0.4 vs 1.9±0.7, P=0.001) and image of STIR sequence received a better grade than T2-FSE FS sequence (grade, 3.4±0.5 vs 1.7±0.6, P<0.001). CONCLUSIONS: The latest standard plates and screws used in orthopedic surgery do not pose an additional hazard or risk to patients undergoing MR imaging at 1.5-T or less. Though artifacts caused by them cannot be ignored because of their relatively large size, it is possible to be minimized by choosing appropriate pulse sequences and optimizing scanning parameters, such as FSE and STIR sequence with large bandwidth, small FOV and appropriate echo train length.

[Effect of 1,25-dihydroxyvitamin D3 on posterior transforaminal lumbar interbody fusion in patients with osteoporosis and lumbar disc degenerative disease].

OBJECTIVE: To investigate the role of 1,25-dihydroxyvitamin D3 in the posterior transforaminal lumbar interbody fusion (TLIF) for patients with osteoporosis and lumbar degenerative disease. METHODS: Between November 20ll and October 2012, 44 patients with osteoporosis and lumbar degenerative disease were treated with TLIF and the clinical data were retrospectively analyzed. The patients were divided into 2 groups based on the administration of 1,25-dihydroxyvitamin D3. After TLIF operation, 1,25-dihydroxyvitamin D3 was used in 21 patients (trial group), and was not used in 23 patients (control group). There was no significant difference in gender, age, etiology, affected segment, and disease duration between 2 groups (P > 0.05). Lumbar interbody fusion was observed by X-ray and thin-section CT scan reconstruction of lumbar spine according to Brantigan assessment system at 6 months after operation and last follow-up. Clinical outcome was evaluated by Oswestry disability index (ODI) before and after operation. RESULTS: The patients of 2 groups were followed up 12-27 months (mean, 14.5 months). No fixation loosening or breaking occurred during follow-up. ODI scores in both groups were significantly improved at 6 months after operation and last follow-up (P < 0.05) when compared with preoperative value. Although at preoperation there was no significant difference in ODI score between 2 groups (P > 0.05), ODI score of trial group was significantly lower than that of control group at 6 months after operation and last follow-up (P < 0.05). At 6 months after operation, the interbody fusion rate was 76.19% (16/21) in trial group and 43.48% (10/23) in control group, showing significant difference (χ2 = 3.60, P =0.03); at last follow-up, the fusion rate was 95.24% (20/21) in trial group and 65.22% (15/23) in control group, showing significant difference (χ2 = 4.38, P = 0.02). CONCLUSION: 1,25-dihydroxyvitamin D3 can improve the lumbar interbody fusion rate and general conditions in the patients with osteoporosis and lumbar degenerative disease.

[Src activation required for pERK1/2 activation in focal adhesions in osteoblasts induced by platelet-derived growth factor].

OBJECTIVE: To study the function of platelet-derived growth factor (PDGF) in inducing phosphorylation extracellular signal-regulated kinase 1/2 (pERK1/2) localization in osteoblasts. METHODS: Primary osteoblasts were isolated and cultured from cranial bone of 10 mice at the age of 3 days, weighting 6-9 g without limitation in male and female. The sixth passage osteoblasts were incubated in 1% serum for 12 hours and divided into 2 groups: treated with DMSO (control group) or with PP2 (experimental group) for 30 minutes. Each group was further divided into 2 subgroups according to with or without PDGF (20 ng/ml) stimulation for 10 minutes. pERK1/2 localization was analysized by immunofluorescence staining in osteoblasts pretreated with or without Src inhibitor PP2. The sixth passage osteoblasts were divided into 2 groups treated with DMSO (control group) or with PP2 (experimental group) for 30 minutes. Each group was further divided into two subgroups according to with or without PDGF (20 ng/ml) stimulation for 10 mintues. The ability of osteoblast migration was determined by wound healing assay. The sixth passage osteoblasts were divided into 2 groups treated with DMSO (control group) or 10 micromol/L PP2 (experimental group) for 30 mintues. Each group was further divided into 2 subgroups according to with or without PDGF (20 ng/ml) stimulation. The pERK1/2 was determined by Western blot in osteoblastic cytoskeleton induced by PDGF. RESULTS: Immunofluorescence staining showed pERK1/2 localization in osteoblastic nuclears and focal adhesions after PDGF stimulation. PP2 significantly inhibited ERK1/2 localization in focal adhesions, but not in nuclears. The wound healing assay results showed that PP2 significantly inhibited osteoblast migration induced by PDGF. The result of Western blot demonstrated that pERK1/2 in osteoblastic cytoskeleton was significantly inhibited. CONCLUSION: Src activation is required for pERK1/2 translocalization to focal adhesions and osteoblasts migration.