[Analysis of factors associated with proximal junctional kyphosis after surgery for Lenke type 5 adolescent idiopathic scoliosis].

Objective: To investigate the risk factors associated with the development of proximal junctional kyphosis (PJK) after posterior spinal fusion for in children with Lenke type 5 adolescent idiopathic scoliosis (AIS). Methods: It was a retrospective case-control study that included medical records of 98 children with Lenke type 5 AIS who underwent posterior orthopedic surgery under general anesthesia at the Honghui Hospital Affiliated to Xi'an Jiaotong University from January 2013 to December 2018. There were 23 males and 75 females with a mean age of (14.5±2.2) years (10-18 years). Patients were divided into PJK and non-PJK groups according to whether the posterior junctional angle (PJA) was greater than 10° and increased for more than 10° from the preoperative period at the the last follow-up. Univariate analysis was used to analyze the correlation of general data of the children with occurrence of PJK after the operation. Multivariate logistic regression analysis was used to analyze the risk factors of postoperative PJK. Results: There were 35 cases in the PJK group and 63 cases in the non-PJK group. The PJK and non-PJK groups were followed up for (35.6±7.3) months and (36.4±7.5) months, respectively, and the difference was not statistically significant (P=0.637). There was no statistically significant difference between the two groups in general data such as gender, age, and body mass index (all P>0.05), while there were statistically significant differences between the two groups in upper instrumented vertebrea (UIV) location and junctional area posterior ligamentous complex (PLC) injury (all P<0.05). The results of univariate analysis showed that UIV location at T10-T12, junctional area PLC injury, preoperative coronal thoracic curve (TC), preoperative and final follow-up PJA, and preoperative and final follow-up pelvic incidence-lumbarlordosis (PI-LL) were correlated with postoperative PJK (OR=2.50, 5.37, 0.92, 1.12, 1.32, 1.06, 3.35, all P<0.05). Multifactorial logistic regression analysis showed that UIV located at T10-T12 (OR=2.346, 95%CI: 1.582-3.481, P=0.001), junctional area PLC injury (OR=5.112, 95%CI: 1.283-20.418, P=0.023) and last follow-up PI-LL (OR=1.826, 95%CI: 1.558-24.745, P=0.012) were risk factors for the occurrence of postoperative PJK in children with Lenke type 5 AIS. Conclusions: Postoperative UIV fixation to the thoracolumbar segment, PLC injury in the junctional area and excessive postoperative PI-LL in children with Lenke type 5 AIS may be the risk factors for the occurrence of PJK after the operation. It is suggested that avoidance of UIV selection to the thoracolumbar segment, intraoperative protection of the PLC located near the UIV and restoration of a good PI-LL relationship may reduce the incidence of PJK.

[The development of artificial cervical disc replacement from the perspective of orthopedic bionic therapy].

The modern surgical treatment of cervical degenerative disc disease can be traced back to the advent of anterior cervical decompression and fusion.With the emergence of fusion-related complications,different scholars have promoted the gradual transformation of cervical degenerative disc diseases from "fusion fixation" to "non-fusion reconstruction" through in-depth fusion with materials science,engineering mechanics and other disciplines.The innovation of this treatment concept is consistent with the original intention of "structural remodeling,functional reconstruction,maximum repair and reconstruction of the morphology and function of skeletal muscle system" in orthopedic bionic treatment,which is essentially in line with the "bionic alternative therapy" in orthopedic bionic therapy.This paper focuses on the surgical treatment of cervical degenerative disc diseases,reviews the development history of artificial cervical disc replacement,analyzes the evolution from orthopedic biomimetic therapy,and explores a new direction for the design of artificial cervical disc prostheses and the treatment of cervical degenerative disc diseases in the future.

Impact of different regenerative techniques and materials on the healing outcome of endodontic surgery: a systematic review and meta-analysis.

BACKGROUND: Regenerative techniques are increasingly applied in endodontic surgery, but different materials used in regenerative techniques may have varying impacts on wound healing. OBJECTIVES: This study evaluated the effects of different regenerative techniques and materials on the outcome of endodontic surgery. PARTICIPANTS: patients with persistent periapical lesions, treated with root-end surgery. CONTROL: endodontic surgery without the use of regenerative techniques/materials. INTERVENTION: endodontic surgery with the use of regenerative techniques/materials. OUTCOME: combined clinical and radiographic results. METHODS: PubMed, Web of Science, Embase, SinoMed and the CENTRAL Cochrane were searched up to 10th July 2020, followed by a manual search. Detailed eligibility criteria were applied. Cochrane's risk-of-bias tool 2.0 was used to assess the risk of bias of the eligible studies. Meta-analysis was conducted using RevMan software. Subgroup analyses were performed based on the regenerative materials used in endodontic surgery. RESULTS: Eleven eligible randomized controlled trials (RCTs) were included in the meta-analysis: two had a low risk of overall bias, and nine had some concerns of overall bias. Generally, the use of regenerative techniques significantly improved the outcome of endodontic surgery (risk ratio [RR]: 0.42; 95% confidence interval [CI], 0.26-0.68; P < 0.001). On subgroup analysis, the use of expanded polytetrafluoroethylene (e-PTFE) membranes alone had no added benefits (RR: 2.00; 95% CI, 0.22-18.33; P = 0.54). The application of collagen membranes or autologous platelet concentrates (APCs) alone was associated with a trend for better outcomes (RR: 0.51; 95% CI, 0.20-1.25; P = 0.14) (RR: 0.55; 95% CI, 0.18-1.71; P = 0.30). The combined use of collagen membranes and bovine-derived hydroxyapatite significantly improved the outcome (RR: 0.35; 95% CI, 0.17-0.75; P = 0.007). DISCUSSION: This systematic review evaluated the effects of collagen membranes, e-PTFE membranes, APCs and bone grafting materials, providing detailed information about the risks and benefits of using each regenerative technique/material or its combination in endodontic surgery. CONCLUSIONS: Regenerative techniques improve periapical lesion healing after endodontic surgery. The combined use of collagen membranes and bovine-derived hydroxyapatite may be beneficial as an adjunct to endodontic surgery. In contrast, the positive efficacy of e-PTFE membranes or APCs alone remains doubtful.

[Clinical observation of single-segment cervical adjacent segment disease treated with artificial cervical disc replacement].

Objective: To investigate the clinical outcomes and radiographic results of artificial cervical disc replacement (ACDR) for cervical adjacent segment disease (ASD). Methods: The clinical data of 28 patients with single-segment cervical ASD treated with ACDR in Xi 'an Honghui Hospital from December 2013 to July 2016 were retrospectively analyzed. There were 19 males and 9 females with a mean age of (46±7) years (36-63 years). Preoperative, postoperative 1 month and postoperative 24 months of clinical and radiographic outcomes were recorded and compared. The clinical outcome mainly includes Japanese orthopedic association (JOA), Neck Disability Index (NDI%), Odom score and complications. Imaging assessment mainly included range of motion (ROM) of cervical spine, surgical segment ROM, Cobb angle of surgical segment, degree of adjacent disc degeneration, heterotopic ossification, and prosthesis related image parameters. Results: In terms of clinical outcome, the average JOA score was 12.7±1.5 before surgery, 14.0±1.0 one month after surgery, 15.8±0.9 24 months after surgery, and the improvement rate of JOA was 75%±19%. The mean NDI% was 27.0%±2.8% before surgery, 20.5%±1.6% one month after surgery, and 15.3%±2.8% 24 months after surgery; the difference before and after treatment was statistically significant (F=159.101, P<0.01). Twenty patients were classified with excellent Odom score and 8 patients with good Odom score at the final follow-up. The total ROM of cervical spine, operation segment ROM, operation segment Cobb angle were all improved significantly after the operation (F=4.633, 6.063, 26.952, all P<0.05). There was a statistical difference in Miyazaki classification between adjacent discs above ACDR and below the fusion segment 24 months after surgery (µ(c)=2.12, P=0.034). The incidence of heterotopic ossification was 14.3%. The results of displacement degree of prosthesis were as follow: coronal plane (0.30±0.11) mm, sagittal plane (0.28±0.10) mm; subsidence of the prosthesis: (0.27±0.09) mm. No prosthesis loosening was observed. Conclusions: The clinical outcome of revision of cervical ASD by ACDR is satisfactory. The risk of intervertebral disc degeneration in adjacent segments is significantly lower than that of ACDF due to the presence of certain motor function postoperatively.

MiR-204 reduces apoptosis in rats with myocardial infarction by targeting SIRT1/p53 signaling pathway.

OBJECTIVE: The aim of this study was to investigate the influence of micro ribonucleic acid (miR)-204 on rats with myocardial infarction by targeting the silent information regulator 1 (SIRT1)/p53 signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into three groups, including: sham-operation group (n=12), model group (n=12) and miR-204 mimics group (n=12). The rats in the sham-operation group only underwent thoracotomy, without myocardial infarction injury. Meanwhile, the rats in model group and miR-204 mimics group were utilized to establish the models of myocardial infarction, and then, intervened with normal saline and miR-204 mimics, respectively. The morphology of myocardial tissues was observed via hematoxylin-eosin (HE) staining. Immunofluorescence was performed to detect the expression of Caspase-3. Target genes of miR-204 were analyzed using bioanalysis software. Western blotting (WB) assay was applied to measure the relative protein expression of SIRT1. MiR-204 expression and the messenger RNA (mRNA) expressions of SIRT1 and p53 were measured via quantitative Polymerase Chain Reaction (qPCR). Furthermore, cell apoptosis was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: HE staining showed that the morphology of myocardial tissues was normal in sham-operation group. Severe myocardial tissue injury was visible in model group, and the injury was relieved in miR-204 mimics group when compared with model group. The results manifested that the positive expression of Caspase-3 in cardiac tissues increased remarkably in the model group and miR-204 mimics group in comparison with sham-operation group (p<0.05). Meanwhile, it was evidently lower in miR-204 mimics group than model group (p<0.05). Based on the analysis via bioanalysis software, SIRT1 was the target gene of miR-204. WB results revealed that the relative protein expression level of SIRT1 was elevated notably in the other two groups compared with the 2sham-operation group (p<0.05). However, it was markedly lowered in miR-204 mimics group in contrast with model group (p<0.05). QRT-PCR results demonstrated that the model group and miR-204 mimics group exhibited distinctly lower expression of miR-204 but higher mRNA expressions of SIRT1 and p53 than sham-operation group (p<0.05). However, miR-204 mimics group exhibited prominently higher expression of miR-204 but lower mRNA expressions of SIRT1 and p53 than model group (p<0.05). Finally, the results of TUNEL assay demonstrated that the apoptosis rate increased remarkably in the model group and miR-204 mimics group when compared with sham-operation group (p<0.05). However, it decreased notably in miR-204 mimics group in comparison with model group (p<0.05). CONCLUSIONS: MiR-204 reduces the apoptosis level in rats with myocardial infarction via targeted inhibition of the SIRT1/p53 signaling pathway.

Suberoylanilide hydroxamic acid attenuates epidural fibrosis via inhibiting myofibroblast differentiation and increasing fibroblast apoptosis.

OBJECTIVE: Epidural fibrosis represents a fatal stage of failed back surgery syndrome (FBSS) of known and idiopathic etiology, but no valid therapy is presently available. Previous evidence demonstrated that suberoylanilide hydroxamic acid (SAHA), a histone deacetylases inhibitor, has antifibrotic and anti-inflammatory potential. Current studies have proved that SAHA inhibits myofibroblast differentiation and increases fibroblast apoptosis to attenuate epidural fibrosis. The purpose of this study was to investigate the effect and mechanism of SAHA on repressing epidural fibrosis. PATIENTS AND METHODS: First, the levels of acetylation of histone and α-tubulin in adult human fibroblasts (AHF) and human epidural fibroblasts (HEF) were analyzed following SAHA and transforming growth factor-ß(TGF-ß) treatment. Then, mRNA and protein obtained from human fibroblasts following TGF-ß activation and SAHA treatment in vitro culture were used to test the influence of SAHA on the activation and apoptosis of fibroblasts, so as to further explore the related mechanism of SAHA. Then, a laminectomy model was established in rats to observe the therapeutic effect of SAHA on epidural scar tissue. RESULTS: The present research proved that the increases of HDAC 3 and α-tubulin were observed in AHF and HEF after TGF-ß administration, but SAHA decreased HDAC 3 and α-tubulin expressions. In addition, cell study demonstrated that SAHA inhibited fibroblast activation via decreasing TGF-ß function and accelerated apoptosis by promoting cleaved-caspase-3. In the epidural fibrosis model, it was found that SAHA weakened scar hyperplasia and collagen deposition, and effectively inhibited the process of epidural fibrosis. CONCLUSIONS: These results indicated that SAHA inhibited HDAC 3 expression, decreased TGF-ß effect, and enhanced caspase-3 in fibroblasts, leading reduction of myofibroblast activation and apoptosis elevation. Hence, SAHA ameliorated epidural fibrosis development.

MicroRNA-370 suppresses SOX12 transcription and acts as a tumor suppressor in bladder cancer.

OBJECTIVE: Dysregulation of microRNA-370 (miR-370) is involved in a variety of cancers, but its roles in bladder cancer (BC) remain largely unexplored. Therefore, we designed this study to explore the role of miR-370 in BC. PATIENTS AND METHODS: We took advantage of biochemical assays, including RT-qPCR, Western blot, CCK-8, flow cytometry, transwell, xenograft tumor formation, and immunohistochemistry (IHC) for research. RESULTS: The expression of miR-370 was found to be downregulated during the development of BC, highly correlating with the malignant transformation of tumors. The overexpression of miR-370 led to enhanced apoptosis in BC cells, while inhibiting cell proliferation, migration, and invasion, effectively blocking cancer metastasis. Additionally, we identified SOX12, a known human oncogene, as a direct target of miR-370, showing that upregulation of SOX12 attenuated miR-370-mediated tumor suppression, promoted tumor growth, and epithelial-mesenchymal transition (EMT) in BC. CONCLUSIONS: Taken together, these findings help to elucidate the roles of miR-370 as a tumor suppressor in BC, providing a potential target for diagnosis and treatment of BC.

Semaphorin-7A contributes to growth, migration and invasion of oral tongue squamous cell carcinoma through TGF-ß-mediated EMT signaling pathway.

OBJECTIVE: Oral tongue squamous cell carcinoma (OTSCC) is the most frequently encountered malignant epithelial tumors. Semaphorin-7A is a membrane-associated/secreted protein that plays an essential role in the migration and progression of human malignancies. We aimed to investigate the mechanisms of Semaphorin-7A in the growth and migration of OTSCC. MATERIALS AND METHODS: The expressions of Semaphorin-7A in cells were tested by RT-PCR, Western blot, and Immunofluorescence, separately. The activities of OTSCC cells (HSC-3 and Tca8113) were analyzed by MTT, following treatment with Semaphorin-7A or PBS. The migration, invasion, and apoptosis of cells were also determined. The protein expressions of epithelial mesenchymal transition (EMT) pathway were analyzed by Western blot, after treated with Semaphorin-7A in vitro and in vivo. Finally, the mouse model of OTSCC was treated with antibody target for Semaphorin-7A (AntiSema-7A), Semaphorin-7A or PBS, then the tumor size was determined, and histopathological examination and western blot was applied for further confirmation. RESULTS: In OTSCC cells, Semaphorin-7A was highly expressed, and Semaphorin-7A promoted growth in multiple metastatic OTSCC cell lines. Further study indicated that Semaphorin-7A resulted in up-regulation of Snail, N-cadherin and Vimentin expression, and downregulating of E-cadherin. In addition, The Ets2-repressor factor (ERF) expression was down-regulated, and transforming growth factor (TGF-ß)-induced EMT was promoted in OTSCC cells. Then, the proteins of collagen types I (CT-I) and fibronectin (FIB) were also up-regulated after Semaphorin-7A treatment. Furthermore, our results indicated that inhibition of Semaphorin-7A by antibody target for Semaphorin-7A (AntiSema-7A) suppressed OTSCC growth and increased survival in a mouse model of OTSCC. Histopathological examination confirmed the inhibitory effects in vivo. CONCLUSIONS: Semaphorin-7A promoted growth and migration of OTSCC by regulating TGF-ß-induced EMT signaling pathway in OTSCC cells, which provided a new interconnection between the Semaphorin-7A and TGF-ß-induced EMT signaling pathway.

Coactosin-like protein CLP/Cotl1 suppresses breast cancer growth through activation of IL-24/PERP and inhibition of non-canonical TGFß signaling.

Coactosin-like protein (CLP, or Cotl1), is an F-actin-binding protein, whose role in cancer is largely unknown. Here we show that CLP/Cotl1 is highly expressed in a rat epithelial breast cancer cell line (FE1.3) compared with its mesenchymal counterpart (FE1.2). Knockdown of CLP/Cotl1 in FE1.3 cells increased cell proliferation, whereas its overexpression in FE1.2 cells inhibited proliferation in culture and reduced tumor growth in xenograft assays in mice. Mechanistically, we identified two major pathways through which CLP/Cotl1 exerts its suppressive effects. First, CLP/Cotl1 re-expression in FE1.2 and in human MCF7 breast cancer cells induced expression of the growth-suppressor gene interleukin-24 (IL-24), which independently of p53 upregulates the tumor-suppressor genes p53 apoptosis effector related to PMP-22 (PERP) and p21cip1. Second, overexpression of CLP/Cotl1 potentiated the growth-suppressive effect of transforming growth factor-ß1 (TGFß1), leading to downregulation of TGFß-responsive genes vascular growth factor A/B (VEGFA/VEGFB), hypoxia inducing factor 1α (HIF-1α) and trombospondin 1 (TSP1), which mediate various hallmarks of cancer progression including angiogenesis, invasion and metastasis. CLP/Cotl1 inhibited TGFß signaling via a non-canonical signaling involving IL-24-instigated inhibition of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) phosphorylation and subsequent post-transcriptional downregulation of SMAD2 and SMAD4. We also showed that CLP/COTL1 expression sensitizes breast cancer cells to chemotherapeutic drugs, and this was further enhanced by addition of exogenous TGFß1. CLP/Cotl1 expression is lost in many human malignancies including prostate, uterine and breast cancers. Thus, our results uncover a novel tumor-suppressor role for CLP/Cotl1 and identify the downstream effectors interleukin 24 (IL-24)/PERP and IL-24/MAPK/ERK/TGFß as potential targets for precision therapy.

Optimal flexible laryngeal mask airway size in children weighing 10 to 20 kg.

This prospective, randomised study was conducted to assess the effect of flexible laryngeal mask airway (FLMA) size on oropharyngeal leak pressure (OLP) in children at the recommended intracuff pressure. A total of 120 children undergoing elective ophthalmic surgery were randomly assigned to the size 2 FLMA group or size 2.5 FLMA group. The primary measurement was OLP at an intracuff pressure of 40 cmH2O. Secondary outcomes included the incidence of OLP <10 cmH2O, insufficient ventilation, gastric insufflation, insertion time, successful first-attempt insertion rate, fibreoptic view grade and pharyngolaryngeal adverse events. The median OLP was comparable for the size 2 and size 2.5 FLMA (18 cmH2O versus 18 cmH2O, P=0.38). However, the size 2 FLMA group had a higher incidence of OLP <10 cmH2O and insufficient ventilation (13.3% versus 0, P=0.006). In subgroup analyses based on weight, the size 2.5 FLMA had a lower occurrence of OLP <10 cmH2O and insufficient ventilation (27% versus 0, P=0.0046) in children 16-20 kg. We conclude that at a 40 cmH2O intracuff pressure, the OLP with the size 2 and size 2.5 FLMA was similar in children weighing 10-15.9 kg. However, in children weighing 16-20 kg, size 2 devices had a higher incidence of low OLP and insufficient ventilation, so a 2.5 FLMA may be preferable in this subgroup.

Combination of a novel photosensitizer DTPP with 650 nm laser results in efficient apoptosis, arresting cell cycle and cytoskeleton protein changes in lung cancer A549 cells.

Photodynamic therapy (PDT) using photosensitized reaction to produce cytotoxicity was used for cancer therapy in recent years. To study the effectiveness of PDT mediated by a novel photosensitizer (PS), DTPP 5-(4'-(2″-dicarboxymethylamino)acetamidophenyl)-10, 15, 20-triphenylporphyrin, on lung cancer A549 cell lines in vitro, DTPP was employed in different concentrations (2, 4, 6, 8, 10, 12, 15, 20, 25, and 30 µg/ml) and combined with 650 nm laser of different power densities (0.6, 1.2, 2.4, 4.8, 7.2, and 9.6 J/cm(2)) that resulted in obvious inhibition of cell proliferation and apoptosis. Results showed that cell survival rates have a dependent relationship with time and PS concentrations and no significant cytotoxicity was induced by DTPP itself. Apoptosis and cell cycle S arrest were observed; cytoskeleton morphologic observation revealed collapse, sparkling, and shrunken shapes. Apoptosis-related protein caspase-3 overexpression was detected while caspase-9, bcl-2, and cytoskeleton protein beta-catenin were in low levels of expression than the control. Cleavage of beta-catenin by caspase-3 or other proteases from the lysosome might be the main reason for the cytoskeleton collapse as beta-tubulin and actin were at a stable level 12 h after PDT. This paper gives a better understanding of the effectiveness of DTPP-mediated PDT in lung cancer A549 cells both with regard to dosimetry and apoptosis changes.

Measurement of coherent polarons in the strongly coupled antiferromagnetically ordered iron-chalcogenide Fe1.02Te using angle-resolved photoemission spectroscopy.

The nature of metallicity and the level of electronic correlations in the antiferromagnetically ordered parent compounds are two important open issues for the iron-based superconductivity. We perform a temperature-dependent angle-resolved photoemission spectroscopy study of Fe(1.02)Te, the parent compound for iron chalcogenide superconductors. Deep in the antiferromagnetic state, the spectra exhibit a "peak-dip-hump" line shape associated with two clearly separate branches of dispersion, characteristics of polarons seen in manganites and lightly doped cuprates. As temperature increases towards the Néel temperature (T(N)), we observe a decreasing renormalization of the peak dispersion and a counterintuitive sharpening of the hump linewidth, suggestive of an intimate connection between the weakening electron-phonon (e-ph) coupling and antiferromagnetism. Our finding points to the highly correlated nature of the Fe(1.02)Te ground state featured by strong interactions among the charge, spin, and lattice and a good metallicity plausibly contributed by the coherent polaron motion.

CD133+ cells with cancer stem cell characteristics associates with vasculogenic mimicry in triple-negative breast cancer.

Vasculogenic mimicry (VM) refers to the unique capability of aggressive tumor cells to mimic the pattern of embryonic vasculogenic networks. In the study we demonstrated that CD133 expression was the highest in triple-negative (TN) breast cancer specimens. Importantly, VM showed statistical correlation with CD133(+) expression. The presence of the close relationship between VM and CD133(+) expression might be central for TN tumor relapse and progression. The TN breast cancer cell line, MDA-MB-231 cells developed a range of colony morphologies paralleling the holoclone, meroclone and paraclone morphologies produced by normal keratinocytes and other epithelial cancer cell lines when plated at clonal densities. Holoclone cells were capable of forming more colonies on soft agar than meroclone cells and paraclone cells, suggesting that holoclone cells had higher self-renew potential and might harbors cancer stem cells (CSCs) subpopulation. Strikingly, it was holoclone that displayed CD133(+) phenotype and formed VM. In addition, holoclone acquired endothelial cell marker vascular endothelial-cadherin expression and upregulated VM mediators matrix metalloproteinase (MMP)-2 and MMP-9 expression. The subpopulation with holoclone morphology, CD133(+) phenotype and CSCs characteristics might have the capacity of transdifferentiation and contributed to VM in TN breast cancer. The related molecular pathways may be used as novel therapeutic targets for the inhibition of angiogenesis and metastasis in TN breast carcinoma.

Friedel-like oscillations from interstitial iron in superconducting Fe(1+y)Te0.62Se0.38.

Using polarized and unpolarized neutron scattering, we show that interstitial Fe in superconducting Fe(1+y)Te(1-x)Se(x) induces a magnetic Friedel-like oscillation that diffracts at Q⊥=(1/2 0) and involves >50 neighboring Fe sites. The interstitial >2µ(B) moment is surrounded by compensating ferromagnetic four-spin clusters that may seed double stripe ordering in Fe(1+y)Te. A semimetallic five-band model with (1/2 1/2) Fermi surface nesting and fourfold symmetric superexchange between interstitial Fe and two in-plane nearest neighbors largely accounts for the observed diffraction.

P-cadherin expression and basal-like subtype in breast cancers.

Breast cancer is considered as one of the multifactorial diseases. The aim of the current study is to investigate the association between P-cadherin and molecular subtypes of breast cancer, especially the basal-like subtype. Two hundred and thirteen breast-invasive ductal carcinomas were involved in this study. The expressions of P-cadherin were detected via immunohistochemistry. The 213 cases were divided into luminal A, luminal B, HER2 overexpression subtype, and normal breast-like and basal-like subtypes according to the standard of molecular breast cancer subtypes. In addition, the expressions of CK5/6 and CK14 were detected to distinguish between the normal breast-like and the basal-like subtypes. P-cadherin expression was found in 91 cases of 213 breast-invasive ductal carcinomas, with a positive rate of 42.7%. P-cadherin correlated negatively with estrogen receptor (ER) (p=0.001) and progesterone receptor (p=0.001), whereas it positively correlated with histologic grade (p=0.003), NPI (p=0.005), p53 (p=0.038), and Ki67 (p=0.022). P-cadherin expression showed a strong correlation with recurrence and distant metastasis (p=0.009), and invasion of the vascular and soft tissues (p=0.004). Moreover, P-cadherin expression existed in the basal-like and non-basal-like subtypes. During prognosis, P-cadherin expression was associated with decreased disease-free survival in patients (p=0.009) and overall survival (OS) (p=0.005). In addition, multivariate analysis showed that tumor grade (p=0.021), ER (p=0.015), clinical stage (p=0.001), and P-cadherin (p=0.033) were significant predictors of OS. The current data suggest that P-cadherin may be used to distinguish the basal-like subtype and to predict the outcome in view of the relationship with DFS and OS. Furthermore, P-cadherin expression may be useful in making treatment decisions.

Right axillosubclavian vein thrombosis resolved by percutaneous rheolytic thrombectomy in a patient with a recurrent gastrointestinal stromal tumour undergoing imatinib mesylate treatment.

The manifestation and management of spontaneous axillosubclavian vein thrombosis in patients with gastrointestinal stromal tumour (GIST) undergoing oral chemotherapy have never been described. We report a patient with a recurrent GIST who was receiving maintenance imatinib yet developed a right axillosubclavian vein thrombotic occlusion. The occluded vein was unresponsive to systemic anticoagulation but was reopened by percutaneous rheolytic thrombectomy and has shown good long-term patency. Thus, for patients with recurrent GIST undergoing imatinib therapy, axillosubclavian vein thrombosis might manifest as a complication and could be managed with rheolytic thrombectomy, which thoroughly removes intravascular thrombus and effectively re-vascularizes the thrombosed vessel uneventfully.

Sam68 expression and cytoplasmic localization is correlated with lymph node metastasis as well as prognosis in patients with early-stage cervical cancer.

BACKGROUND: This study was aimed at investigating the role and molecular mechanism of Sam68 in cervical cancer lymph node metastasis. MATERIALS AND METHODS: Sam68 expression profile was detected by quantitative polymerase chain reaction, western blotting and immunohistochemical staining. Short hairpin RNA interfering approach was employed to suppress endogenous Sam68 expression in cervical cancer cells to determine its role in metastasis and the possible mechanism. RESULTS: Sam68 expression in cervical cancer was significantly up-regulated at both messenger RNA and protein levels compared with that in normal cervical tissues. The high expression level of Sam68 and its cytoplasmic localization were significantly associated with risk factors including pelvic lymph node metastasis (P < 0.001), and served as independent prognostic factors for predicting shortening of the overall survival time and disease-free survival time in patients with early-stage cervical cancer. Moreover, down-regulation of Sam68 in cervical cancer cells remarkably inhibited cellular motility and invasion. In addition, down-regulation of Sam68 reversed epithelial-mesenchymal transition through inhibiting the Akt/ GSK-3ß/Snail pathway. CONCLUSION: This study demonstrated that Sam68 could induce cervical cancer lymph node metastasis through regulating epithelial-mesenchymal transition, and Sam68 expression profile possessed the potential to serve as predictors of pelvic lymph node metastasis in cervical cancer patients.

Accuracy of CT-guided biopsies in 158 patients with thoracic spinal lesions.

BACKGROUND: Inconsistent accuracies of CT-guided thoracic spinal biopsies have been reported in previous studies. PURPOSE: To determine the accuracy of CT-guided thoracic spinal biopsy, to compare the results with those previously reported, and to determine if there are any factors that influence the accuracy of CT-guided thoracic spinal biopsy. MATERIAL AND METHODS: In total, 158 consecutive CT-guided percutaneous thoracic spine procedures (performed at the Department of Spinal Surgery, Xi'an Red Cross Hospital between April 2000 and July 2010) were reviewed. The 158 lesions were categorized by location and radiographic features. Pathological and clinical follow-up were used to determine accuracy. RESULTS: The diagnostic accuracy of CT-guided thoracic spinal biopsy was 90.5% overall. Biopsy of metastatic bone disease (98.2%) was significantly more accurate than biopsies of primary tumors (80.9%) and of hematological malignancies (47.0%) (P < 0.05 and P < 0.005, respectively). The diagnostic accuracy of CT-guided thoracic spinal biopsy was significantly higher for the lower thoracic spine (97.6%) than for the middle (90.0%) or upper thoracic spine (80.4%) (P < 0.05 and P < 0.025, respectively). The diagnostic accuracy was significantly higher for lytic lesions (96.4%) than for sclerotic lesions (81.3%) (P < 0.010). The accuracy of biopsies performed using the transpedicular approach (91.0%) was not significantly different from that of biopsies performed using posterolateral approaches (91.5%) (0.25 < P < 0.5). CONCLUSION: Percutaneous CT-guided thoracic spinal biopsy is a viable alternative to open surgical biopsy. The diagnostic accuracy was not affected by any of the variables except for lesion level, histology, and radiographic features.

Propofol ameliorates doxorubicin-induced oxidative stress and cellular apoptosis in rat cardiomyocytes.

BACKGROUND: Propofol is an anesthetic with pluripotent cytoprotective properties against various extrinsic insults. This study was designed to examine whether this agent could also ameliorate the infamous toxicity of doxorubicin, a widely-used chemotherapeutic agent against a variety of cancer diseases, on myocardial cells. METHODS: Cultured neonatal rat cardiomyocytes were administrated with vehicle, doxorubicin (1µM), propofol (1µM), or propofol plus doxorubicin (given 1h post propofol). After 24h, cells were harvested and specific analyses regarding oxidative/nitrative stress and cellular apoptosis were conducted. RESULTS: Trypan blue exclusion and MTT assays disclosed that viability of cardiomyocytes was significantly reduced by doxorubicin. Contents of reactive oxygen and nitrogen species were increased and antioxidant enzymes SOD1, SOD2, and GPx were decreased in these doxorubicin-treated cells. Mitochondrial dehydrogenase activity and membrane potential were also depressed, along with activation of key effectors downstream of mitochondrion-dependent apoptotic signaling. Besides, abundance of p53 was elevated and cleavage of PKC-δ was induced in these myocardial cells. In contrast, all of the above oxidative, nitrative and pro-apoptotic events could be suppressed by propofol pretreatment. CONCLUSIONS: Propofol could extensively counteract oxidative/nitrative and multiple apoptotic effects of doxorubicin in the heart; hence, this anesthetic may serve as an adjuvant agent to assuage the untoward cardiac effects of doxorubicin in clinical application.

Late proximal coronary artery stenosis complicating percutaneous endovascular catheterisation procedures.

BACKGROUND: Late-onset proximal coronary artery stenosis caused by preceding percutaneous catheterisation procedures remains under-surveyed. METHODS: From 1993, all patients undergoing percutaneous coronary procedures and a second session within 3 years were included except those ever treated by coronary bypass surgery or chest radiotherapy during this 3-year period. Emergence of a new lesion or worsening of an initially insignificant lesion to >50% of diameter stenosis at the never-treated ostial/proximal coronary segment on the follow-up angiogram was defined as late coronary stenosis caused by the previous catheterisation procedure and was analysed. RESULTS: From January 1993 to December 2005, 3240 patients who underwent 5025 procedures met the inclusion criteria. Of them, 23 patients experienced an event of late coronary artery stenosis (overall incidence 0.46%), and interventional procedures, specifically shaped catheters (Voda, XB, Amplatz Left) and atherosclerosis vulnerability correlated with risks of adverse events. Most of these events could be managed by contemporary medical, interventional, or surgical strategies, yet hazards of mortality and long-term restenosis still existed from this catheter-induced complication. CONCLUSIONS: Percutaneous catheterisation procedures could be complicated by late proximal coronary artery stenosis. Thus, when conducting these procedures, operators should select and manipulate catheters with caution, especially in patients with susceptible clinical characteristics.