Surgical treatment of carotid artery stent infection: a case report.

The most effective treatment for graft infection is still debated, and the success rate of current treatments is low. We herein report the results of surgical treatment and follow-up of a case of infection acquired during carotid stenting with the aim of exploring the most effective treatments for graft infection. We retrospectively analyzed a patient who was admitted in September 2019. This patient underwent debridement, autologous saphenous vein replacement of the common carotid to internal carotid artery, external carotid artery suturing, and continuous negative-pressure wound therapy for carotid stent infection. Ten days after carotid artery revascularization, the growth of granulation tissue in the incision was good, and we decided to suture the neck incision. Five days after removing the stitches, grade A healing was noted. Furthermore, the carotid artery and autologous vein grafts were unobstructed as shown by carotid artery computed tomography angiography reexamination. The patient was monitored for 8 months with no new neurological symptoms and good healing of the incision. Effective treatment of vascular graft infection includes debridement and removal of the infected graft, autologous vein graft revascularization, and negative-pressure wound therapy combined with antibiotic therapy.

Comparison of Ultrasound-Guided Core Needle Biopsy Under the Assistance of Hydrodissection With Fine Needle Aspiration in the Diagnosis of High-Risk Cervical Lymph Nodes: A Randomized Controlled Trial.

A randomized comparison of ultrasound (US)-guided core needle biopsy (CNB) under the assistance of hydrodissection with fine needle aspiration (FNA) was performed to evaluate the feasibility, safety and effectiveness for the diagnosis of high-risk cervical lymph nodes. Patients from December 2018 to May 2020 were randomly assigned to the CNB group and the FNA group at a ratio of 1:1. This study protocol was approved by the Ethics Committee of our hospital and registered in the Chinese Clinical Trial Registry (ChiCTR1800019370). The feasibility of CNB for high-risk cervical lymph nodes was evaluated by observing and recording the separation success rate (SSR) and technical success rate (TSR) of the CNB group. Safety was evaluated by comparing the incidence of major complications in the two groups. The diagnostic efficacy was evaluated by comparing the diagnostic accuracy, sensitivity, and specificity of the two groups. A total of 84 patients (84 lymph nodes) were randomized into the CNB (n = 42) and FNA (n = 42) groups. All patients in the CNB group achieved successful hydrodissection and biopsy. The SSR and TSR were both 100% in the CNB group. There were no major complications during or after the process in the two groups. Compared with the FNA group, the CNB group was significantly superior in terms of diagnostic accuracy and sensitivity (100% vs. 81.0%, P = 0.009; 100% vs. 79.2%, P = 0.035, respectively). The specificity of the two groups was 100%, and there was no significant difference. Compared with FNA, CNB under the assistance of hydrodissection is a feasible and safe method but is more effective for the diagnosis of high-risk cervical lymph nodes. CLINICAL TRIAL REGISTRATION: http://www.medresman.org, ChiCTR1800019370.

miR-129-5p inhibits prostate cancer proliferation via targeting ETV1.

BACKGROUND: Prostate cancer is one of the most commonly diagnosed diseases in males. METHODS: RT-qPCR was used to detect miR-129-5p expression in tumor tissues and adjacent normal tissues from patients with prostate cancer. The cell proliferation assay and colony forming assay were used to study the role of miR-129-5p in mediating prostate cancer cell growth. Bioinformatic analysis and dual luciferase assay were performed to predict and confirm ETV1 as a target gene of miR-129-5p. RESULTS: We found that miR-129-5p levels were decreased significantly in human prostate cancer tissues compared with matched normal tissues from patients with prostate cancer. Overexpression of miR-129-5p suppressed prostate cancer cell growth while antagonist of miR-129-5p promoted cell proliferation in immortal prostate cell line RWPE-1. In addition, elevation of miR-129-5p decreased ETV1 expression in prostate cancer cells while downregulation of miR-129-5p increased ETV1 expression in RWPE-1. Mechanistically, ETV1 is confirmed a direct target of miR-129-5p in prostate cancer cells. Through repression of ETV1 expression, miR-129-5p could inactivate YAP signaling in prostate cancer cells. In addition, overexpression of ETV1 attenuated miR-129-5p induced cell proliferation in prostate cancer cells. Correlation analysis further revealed that there was a negative correlation between miR-129-5p levels and ETV1 mRNA levels in tumor tissues from patients with prostate cancer. CONCLUSION: Our results identified miR-129-5p as a tumor suppressor in prostate cancer via repression of ETV1.

Downregulation of miR-139-5p promotes prostate cancer progression through regulation of SOX5.

Altered expression of microRNAs (miRNAs) was involved in prostate cancer progression. However, how miRNAs contributed to prostate cancer development remained unknown. Here, we reported that miR-139-5p levels were decreased in prostate cancer tumor tissues and prostate cancer cell lines. Transfection of miR-139-5p mimics reduced cell proliferation and migration ability of prostate cancer cells. Western blotting and RT-qPCR showed that elevation of miR-139-5p greatly inhibited SOX5 expression in prostate cancer cells. Through regulation of SOX5, enhanced expression of miR-139-5p downregulated TWIST, decreased N-cadherin and Vimentin expression, suggesting inhibition of epithelial-mesenchymal transition (EMT) process. The dual luciferase assay validated that SOX5 was a direct target of miR-139-5p. Additionally, a significant negative correlation between SOX5 mRNA levels and miR-139-5p levels were detected in prostate cancer tumor tissues. Our study indicated that miR-139-5p functioned as a tumor suppressor in prostate cancer cells by regulation of SOX5, and it might be a promising target for prostate cancer patients.

Effect of adjuvant hormone therapy in patients with prostate cancer: A meta-analysis of randomized controlled trials.

OBJECTIVES: To summarize the evidence regarding the treatment effect of adjuvant hormone therapy (AHT) in patients with prostate cancer (PCa). AHT following radiotherapy, chemotherapy, or surgery is widely used in patients with PCa. However, the treatment effect is inconsistent in individual trials. METHODS: The electronic databases including PubMed, EmBase, and Cochrane Library were searched to identify randomized controlled trials (RCTs) in September 2016. RCTs that evaluated the effects of AHT in patients with PCa were included. Hazard ratio (HR) and relative risks (RR) were used to measure the treatment effects of AHT using a random effects model. The analyses were further stratified by factors that could affect the treatment efficacy. RESULTS: A total of 14,594 potential studies were identified, and 27 RCTs were included. Compared with the control group, patients who received AHT were associated with a significant improvement in overall survival (OS) (HR: 0.78; 95% confidence interval [CI]: 0.71-0.85; P <.001), disease-free survival (DFS) (HR: 0.50; 95% CI: 0.39-0.65; P <.001), total mortality (RR: 0.90; 95% CI: 0.85-0.96; P = .001), recurrence (RR: 0.70; 95% CI: 0.60-0.81; P <.001), and disease-specific mortality (RR: 0.70; 95% CI: 0.56-0.87; P <.001). However, no significant difference was observed between AHT and control for response rate (RR: 1.75; 95% CI: 0.91-3.37; P = .095). CONCLUSIONS: The findings of this meta-analysis confirmed that patients who received AHT had a significant improvement in OS, DFS, total mortality, recurrence, and disease-specific mortality. Further, large-scale RCTs are required to evaluate the treatment effect in specific subpopulations.

Intracerebral schwannoma: A case report and literature review.

Intracranial schwannoma accounts for between 5 and 8% of intracranial tumors, whereas intracerebral schwannoma, a rare disease, accounts for <1% of intracranial schwannomas. In addition to the present case report, a total of 84 cases reported within China and elsewhere were reviewed and summarized, and the age of the tumor onset, the site of disease, imaging results, clinical presentation, pathological classification and prognosis were analyzed. The present case report described a 12-year-old female with an intracerebral schwannoma in the brainstem, who was followed-up for 5 years using magnetic resonance imaging after a surgical resection without recurrence, and clinical symptoms were reported to have completely resolved. The incidence of intracerebral schwannoma was low among cases, and the correct diagnosis was not able to be made preoperatively, and the majority of cases were diagnosed on the basis of postoperative pathology. The majority of cases analyzed were supratentorial, occurring at an age ≤40 according to previous literature. In addition, 33% of patients presented with subtentorial schwannoma, occurring at an age >40. The prognosis was classified as good (patient can live independently) for the majority of patients if surgery was able to completely resect the lesion.

TUG1 promotes prostate cancer progression by acting as a ceRNA of miR-26a.

Previous studies have demonstrated that taurine-upregulated gene 1 (TUG1) was aberrantly expressed and involved in multiple types of cancer; however, the expression profile and potential role of TUG1 in prostate cancer (PCa) remains unclear. The aim of the present study was to evaluate the expression and function of TUG1 in PCa. In the present study, we analyzed TUG1 expression levels of PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR. Knockdown of TUG1 by RNAi was performed to explore its roles in cell proliferation, migration, and invasion. Here we report, for the first time, that TUG1 promotes tumor cell migration, invasion, and proliferation in PCa by working in key aspects of biological behaviors. TUG1 could negatively regulate the expression of miR-26a in PCa cells. The bioinformatics prediction revealed putative miR-26a-binding sites within TUG1 transcripts. In conclusion, our study suggests that long non-coding RNA (lncRNA) TUG1 acts as a functional oncogene in PCa development.

Long non-coding RNA HOTTIP promotes prostate cancer cells proliferation and migration by sponging miR-216a-5p.

Long non-coding RNAs (lncRNAs) are a class of ncRNAs with >200 nts in length that regulate gene expression. The HOXA transcript at the distal tip (HOTTIP) lncRNA plays an important role in carcinogenesis, however, the underlying role of HOTTIP in prostate cancer (PCa) remains unknown. The aim of the present study was to evaluate the expression and function of HOTTIP in PCa. In the present study, we analyzed HOTTIP expression levels of 86 PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR (qPCR). Knockdown or overexpression of HOTTIP was performed to explore its roles in cell proliferation, migration, invasion, and cell cycle. Furthermore, bioinformatics online programs predicted and luciferase reporter assay were used to validate the association of HOTTIP and miR-216a-5p in PCa cells. Our results found that HOTTIP was up-regulated in human primary PCa tissues with lymph node metastasis. Knockdown of HOTTIP inhibited PCa cell proliferation, migration, and invasion. Overexpression of HOTTIP promoted cell proliferation, migration, and invasion of PCa cells. Bioinformatics online programs predicted that HOTTIP sponge miR-216a-5p at 3'-UTR with complementary binding sites, which was validated using luciferase reporter assay. HOTTIP could negatively regulate the expression of miR-216a-5p in PCa cells. Above all, the knockdown of HOTTIP could represent a rational therapeutic strategy for PCa.

Role of miR-613 as a tumor suppressor in glioma cells by targeting SOX9.

BACKGROUND AND OBJECTIVES: MicroRNA-613 (miR-613), a novel cancer-related microRNA, has been shown to be responsible for the inhibition of tumor development and progression in various cancers. We aimed to investigate the biological function and regulatory mechanisms of miR-613 in gliomas. MATERIALS AND METHODS: miR-613 expression were detected by qRT-PCR assays in glioma tissues and cell lines. Cell Counting Kit-8 (CCK-8) assay, colony formation analysis, wound healing and transwell invasion assays were performed to evaluate cell proliferation, colony formation, migration and invasion abilities. Luciferase reporter assays, qRT-PCR and Western blot were performed to explore the potential targets of miR-613. Xenograft mice model was established to evaluate the effect of miR-613 in vivo. RESULT: The expression levels of miR-613 were significantly downregulated in the glioma tissues and cell lines, and the decreased level was significantly negatively associated with the overall disease-free survival of the patients. Functionally, ectopic expression of miR-613 in glioma cells suppressed the proliferation, colony formation, and migration and invasion of the cells. The sex-determining region Y-box 9 (SOX9) was identified as a direct functional target of miR-613, and its expression was inversely correlated with miR-613 expression in glioma tissues. Moreover, rescue of SOX9 could partially reverse the inhibitory effects of miR-613 on glioma cell proliferation, colony formation, migration, and invasion. Importantly, miR-613 also suppressed tumor growth in vivo by targeting SOX9. CONCLUSION: Taken together, these findings demonstrate that miR-613 functions as a tumor suppressor in glioma cells by directly targeting SOX9.

NGF and PI3K/Akt signaling participate in the ventral motor neuronal protection of curcumin in sciatic nerve injury rat models.

OBJECTIVE: It has been reported that sciatic nerve injury (SNI) leads to degeneration, damage, and apoptosis of motor neurons. Nerve growth factor (NGF) plays a pivotal role in regeneration and reestablishment of neuronal function via activating PI3K/Akt survival signaling pathways. Curcumin owns neuroprotective effect following brain injury. In the present study, we attempt to investigate underlying mechanism of neuroprotective effect of curcumin through elucidating its correlation with NGF and PI3K/Akt signaling pathways in vitro and in vivo. METHODS: PC-12 cells were exposed H2O2 in order to induce neuron cell injury and cells were then treated with curcumin. Caspase-3, NGF level and Akt phosphorylation were determined using flow cytometry and western blotting. Then, cells were treated with NGF specific siRNA followed by measurement of apoptosis, NGF and Akt phosphorylation levels. In animal model, rats were subjected to SNI and then randomly designated into four different groups: curcumin, curcumin + LY294002, curcumin + NGF shRNA, and negative controls and 12 rats in each group (n = 12). After four weeks of continuous treatment, tissue samples were obtained and subjected to TUNEL, NeuN double staining and western blotting. RESULTS: Curcumin significantly reduced the number of apoptotic cells induced by H2O2 and this effect was associated with upregulation of TrkA, Akt and downregulation of p17. ProNGF level was significantly decreased while mature NGF level was increased with curcumin treatment. When NGF was suppressed, anti-apoptotic effect of curcumin was attenuated. In addition, inhibition of PI3K/Akt results in increased apoptotic rate compared to vehicles following curcumin treatment which was reflected by decreased p17, Ki67, and cyclin D1. Suppression of NGF and inhibition of PI3K led to increased neuron cell death through increasing proNGF and decreasing mNGF, Akt, TrkA, p75NTR, and p17. CONCLUSION: Our findings revealed that curcumin exerts its protective effect against injured neurons through stimulating NGF release which further activates TrkA and PI3K/Akt cell survival signaling.

miR-671 promotes prostate cancer cell proliferation by targeting tumor suppressor SOX6.

Prostate cancer is one of the most severe malignancies in men, and many genes and non-coding RNAs, included microRNAs (miRs), have been demonstrated to regulate prostate cancer progression. In the present study, we investigated the role of miR-671 in prostate cancer cell proliferation. We found that miR-671 was significantly upregulated in human prostate cancer tissues and cells. miR-671 overexpression promoted prostate cancer cell proliferation, while its downregulation inhibited prostate cancer cell proliferation, as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, colony formation assays, soft agar growth assays, and bromodeoxyuridine (BrdU) incorporation assays. miR-671 directly targets the 3' untranslated region (UTR) of the tumor suppressor SOX6 (encoding SRY (sex determining region Y)-box 6) to inhibit its expression. Double knockdown of miR-671 and SOX6 promoted PC3 cell proliferation, suggesting that miR-671 promotes prostate cancer cell proliferation by inhibiting SOX6.