Catalytic Oxidation of Benzene over Atomic Active Site AgNi/BCN Catalysts at Room Temperature.

Benzene is the typical volatile organic compound (VOC) of indoor and outdoor air pollution, which harms human health and the environment. Due to the stability of their aromatic structure, the catalytic oxidation of benzene rings in an environment without an external energy input is difficult. In this study, the efficient degradation of benzene at room temperature was achieved by constructing Ag and Ni bimetallic active site catalysts (AgNi/BCN) supported on boron-carbon-nitrogen aerogel. The atomic-scale Ag and Ni are uniformly dispersed on the catalyst surface and form Ag/Ni-C/N bonds with C and N, which were conducive to the catalytic oxidation of benzene at room temperature. Further catalytic reaction mechanisms indicate that benzene reacted with ·OH to produce R·, which reacted with O2 to regenerate ·OH. Under the strong oxidation of ·OH, benzene was oxidized to form alcohols, carboxylic acids, and eventually CO2 and H2O. This study not only significantly reduces the energy consumption of VOC catalytic oxidation, but also improves the safety of VOC treatment, providing new ideas for the low energy consumption and green development of VOC treatment.

In-house ammonia induced lung impairment and oxidative stress of ducks.

Ammonia (NH3) is a toxic gas that in intensive poultry houses, damages the poultry health and induces various diseases. This study investigated the effects of NH3 exposure (0, 15, 30, and 45 ppm) on growth performance, serum biochemical indexes, antioxidative indicators, tracheal and lung impairments in Pekin ducks. A total of 288 one-day-old Pekin male ducks were randomly allocated to 4 groups with 6 replicates and slaughtered after the 21-d test period. Our results showed that 45 ppm NH3 significantly reduced the average daily feed intake (ADFI) of Pekin ducks. Ammonia exposure significantly reduced liver, lung, kidney, and heart indexes, and lowered the relative weight of the ileum. With the increasing of in-house NH3, serum NH3 and uric acid (UA) concentrations of ducks were significantly increased, as well as liver malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX-Px) contents. High NH3 also induced trachea and lung injury, thereby increasing levels of tumor necrosis factor-α (TNF-α) and interleukin-4 (IL-4) in the lung, and decreasing the mRNA expressions of zonula occludens 1 (ZO-1) and claudin 3 (CLDN3) in the lung. In conclusion, in-house NH3 decrease the growth performance in ducks, induce trachea and lung injuries and meanwhile increase the compensatory antioxidant activity for host protection.

Ectopic pregnancy adjacent to iliac vessels managed successfully by minimally invasive treatment using local methotrexate injection: An extremely rare case and literature review.

A case report of successfully treated retroperitoneal ectopic pregnancy (REP) is presented. A 36-year-old woman, gravida 3, para 2, was admitted to hospital for suspected ectopic pregnancy with light vaginal bleeding and mild abdominal pain for 3 days at 45 days of gestation by the last menstrual period.Multiple transvaginal ultrasonography and two times laparoscopic probes led to the diagnosis of REP located to the iliac blood vessels closely. Eventually the patient was cured with the treatment using local methotrexate injection under real-time ultrasound guidance and systemic methotrexate administration. We also summarized another 31 cases of REP to further understand this disease, sharing them to arouse clinical attention for the diagnosis and treatment of REP timely.

Laparoendoscopic Single-Site Technique Contrasted with Conventional Laparoscopy in Cystectomy for Benign Ovarian Cysts.

Objective: To compare the laparoendoscopic single-site (LESS) technique with conventional laparoscopy in cystectomy for benign ovarian cysts. Materials and methods: A retrospective analysis was performed at Yixing People's Hospital from April 2020 until December 2021. Results: Thirty-seven patients using the LESS technique were compared with a control group of 45 patients who underwent a traditional laparoscopic ovarian cystectomy. There was no statistically significant difference in the perioperative hemoglobin level changes, cyst rupture rate, postoperative recovery of exhausting time, or pain score at 24 hours after surgery between the 2 groups (P > 0.05). The mean operating time was significantly longer in the LESS group than that of the control group (88.38 ± 30.57 minutes vs 59.44 ± 24.22 minutes; P = 0.001). However, the length of postoperative hospital stay was significantly shorter in the LESS group (3.70 ± 0.57 days vs 4.38 ± 0.86 days; P = 0.001). In addition, total hospitalization expenses were higher in the LESS group (14,709.78 ± 1618.63 yuan vs 12,676.73 ± 1411.78 yuan; P = .001) and the satisfaction score was also significantly higher in the LESS group (z = -2.272; P = 0.023). After a follow-up time of 12 to 24 months, no patient in either group showed wound infection, umbilical hernia, or recurrent cysts. Conclusions: The LESS technique for benign ovarian cystectomy is safe, feasible, and equally effective compared with the multiport laparoscopic oophorocystectomy. Although it currently costs more, patients with benign ovarian cysts are highly satisfied with the LESS technique.

HOXD-AS2-STAT3 feedback loop attenuates sensitivity to temozolomide in glioblastoma.

AIMS: Glioblastoma multiforme (GBM) is the deadliest glioma and its resistance to temozolomide (TMZ) remains intractable. Long non-coding RNAs (lncRNAs) play crucial roles in that and this study aimed to investigate underlying mechanism of HOXD-AS2-affected temozolomide sensitivity in glioblastoma. METHODS: We analyzed and validated the aberrant HOXD-AS2 expression in glioma specimens. Then we explored the function of HOXD-AS2 in vivo and in vitro and a clinical case was also reviewed to examine our findings. We further performed mechanistic experiments to investigate the mechanism of HOXD-AS2 in regulating TMZ sensitivity. RESULTS: Elevated HOXD-AS2 expression promoted progression and negatively correlated with prognosis of glioma; HOXD-AS2 attenuated temozolomide sensitivity in vitro and in vivo; The clinical case also showed that lower HOXD-AS2 sensitized glioblastoma to temozolomide; STAT3-induced HOXD-AS2 could interact with IGF2BP2 protein to form a complex and sequentially upregulate STAT3 signaling, thus forming a positive feedback loop regulating TMZ sensitivity in glioblastoma. CONCLUSION: Our study elucidated the crucial role of the HOXD-AS2-STAT3 positive feedback loop in regulating TMZ sensitivity, suggesting that this could be provided as a potential therapeutic candidate of glioblastoma.

Anti-PD-1 immunotherapy combined with stereotactic body radiation therapy and GM-CSF for the treatment of advanced malignant PEComa: A case report.

Background: Perivascular epithelioid cell neoplasm (PEComa) is a rare mesenchymal tumour. Due to its low incidence, a standard treatment regimen for PEComa has not yet been established. Radiotherapy has a synergistic effect with PD-1 inhibitors and GM-CSF. We treated advanced malignant PEComa with a triple regimen of PD-1 inhibitor, SBRT and GM-CSF to provide better therapeutic effect. Case presentation: A 63-year-old woman was diagnosed with malignant PEComa after presenting with postmenopausal vaginal bleeding. Despite two surgeries, the neoplasm eventually metastasized throughout the body. We formulated triple therapy with SBRT, a PD-1 inhibitor, and GM-CSF for the patient. The patient's local symptoms were controlled at the radiotherapy site, and the lesions at the unirradiated sites were also relieved. Conclusions: For the first time, a triple regimen of PD-1 inhibitor, SBRT and GM-CSF was used in the treatment of malignant PEComa and achieved good efficacy. Considering the lack of prospective clinical studies in PEComa, we believe that this triple therapy is a good-quality regimen for advanced malignant PEComa.

Snail inhibits metastasis via regulation of E­cadherin and is associated with prognosis in colorectal cancer.

The overall survival (OS) rate of patients with colorectal cancer (CRC) remains low due to the lack of clear prognostic markers. Therefore, the identification of valuable prognostic markers is urgently required. Snail and E-Cadherin (E-Cad) are important protein molecules in the EMT process and play a crucial role in tumor invasion and metastasis. The present study investigated the clinical significance of Snail and E-cad expression in CRC. Compared with those in adjacent tissue, the expression levels of Snail and E-cad were significantly increased and decreased, respectively, in CRC. Moreover, low Snail and high E-cad expression were associated with clinicopathological features and longer OS time. Furthermore, Snail and E-cad could predict the prognosis of patients with CRC. Reverse transcription-qPCR, Western blotting, Wound scratch assay, High content cell migration experiment, which showed that low Snail or high E-cad expression inhibited invasion and metastasis of CRC. In conclusion, Snail can promote CRC invasion and metastasis by regulating E-cad. Snail and E-cad expression constitute a novel prognostic marker for CRC, and the present study revealed a greater combined effect of Snail and E-cad as effective prognostic markers in CRC for the first time.

Purple Rehmannia: Investigation of the activation of R2R3-MYB transcription factors involved in anthocyanin biosynthesis.

Engineering anthocyanin biosynthesis in herbs could provide health-promoting foods for improving human health. Rehmannia glutinosa is a popular medicinal herb in Asia, and was a health food for the emperors of the Han Dynasty (59 B.C.). In this study, we revealed the differences in anthocyanin composition and content between three Rehmannia species. On the 250, 235 and 206 identified MYBs in the respective species, six could regulate anthocyanin biosynthesis by activating the ANTHOCYANIDIN SYNTHASE (ANS) gene expression. Permanent overexpression of the Rehmannia MYB genes in tobacco strongly promoted anthocyanin content and expression levels of NtANS and other genes. A red appearance of leaves and tuberous/roots was observed, and the total anthocyanin content and the cyanidin-3-O-glucoside content were significantly higher in the lines overexpressing RgMYB41, RgMYB42, and RgMYB43 from R. glutinosa, as well as RcMYB1 and RcMYB3 in R. chingii and RhMYB1 from R. henryi plants. Knocking out of RcMYB3 by CRISPR/Cas9 gene editing resulted in the discoloration of the R. chingii corolla lobes, and decreased the content of anthocyanin. R. glutinosa overexpressing RcMYB3 displayed a distinct purple color in the whole plants, and the antioxidant activity of the transgenic plants was significantly enhanced compared to WT. These results indicate that Rehmannia MYBs can be used to engineer anthocyanin biosynthesis in herbs to improve their additional value, such as increased antioxidant contents.

Neutralizing IL-8 potentiates immune checkpoint blockade efficacy for glioma.

Malignant gliomas are largely refractory to immune checkpoint blockade (ICB) therapy. To explore the underlying immune regulators, we examine the microenvironment in glioma and find that tumor-infiltrating T cells are mainly confined to the perivascular cuffs and express high levels of CCR5, CXCR3, and programmed cell death protein 1 (PD-1). Combined analysis of T cell clustering with T cell receptor (TCR) clone expansion shows that potential tumor-killing T cells are mainly categorized into pre-exhausted/exhausted and effector CD8+ T subsets, as well as cytotoxic CD4+ T subsets. Notably, a distinct subpopulation of CD4+ T cells exhibits innate-like features with preferential interleukin-8 (IL-8) expression. With IL-8-humanized mouse strain, we demonstrate that IL-8-producing CD4+ T, myeloid, and tumor cells orchestrate myeloid-derived suppressor cell infiltration and angiogenesis, which results in enhanced tumor growth but reduced ICB efficacy. Antibody-mediated IL-8 blockade or the inhibition of its receptor, CXCR1/2, unleashes anti-PD-1-mediated antitumor immunity. Our findings thus highlight IL-8 as a combinational immunotherapy target for glioma.

IFN-γ Facilitates Corneal Epithelial Cell Pyroptosis Through the JAK2/STAT1 Pathway in Dry Eye.

Purpose: To investigate the effect of gamma interferon (IFN-γ) on corneal epithelial pyroptosis in an experimental dry eye (DE) model and explore the underlying molecular mechanisms. Methods: Experimental DE was established in adult wild-type (WT) C57BL/6 mice and Ifng-knockout mice on a C57BL/6 background by subcutaneous injection of scopolamine (1.5 mg/0.3 mL, three times per day) and exposure to desiccating stress. An immortalized human corneal epithelial cell line (HCE-T) was treated with IFN-γ under hyperosmolar conditions. Corneal epithelial defects, tear production, and conjunctival goblet cells were detected by fluorescein sodium staining, the phenol red cotton test, and periodic acid-Schiff staining. The mRNA expression was measured by quantitative real-time PCR. Changes in protein expression were analyzed by Western blotting and immunofluorescence staining. Cell Counting Kit-8 and lactate dehydrogenase assays and in situ TUNEL staining were used to assess cell death. Results: The expression of IFNG and its related genes was increased in the corneas of DE mice, whereas genetic deletion of Ifng ameliorated desiccating stress-induced dry eye symptoms. We further found that IFN-γ activated the JAK2/STAT1 signaling pathway inducing corneal epithelial pyroptosis. Topical application of a STAT1 inhibitor in vivo or siRNA targeting STAT1 in vitro suppressed pyroptosis of corneal epithelial cells. In addition, the production of reactive oxygen species (ROS) was elevated in DE, and a reduction in excessive ROS release prevented pyroptosis. Conclusions: The increase in IFN-γ participates in the pathogenesis of dry eye and promotes corneal epithelial pyroptosis by activating the JAK2/STAT1 signaling pathway. Oxidative stress might be in downstream of JAK2/STAT1, thereby contributing to pyroptosis.

Outcomes and risk factors for failure of trabeculectomy in glaucomatous patients in Southwest China: a 325 eyes analysis.

AIM: To evaluate the outcomes and elucidate the failure factors for trabeculectomy with mitomycin C (MMC) in Southwest Chinese patients. METHODS: A retrospective correlational study was conducted on the glaucomatous patients who underwent initial trabeculectomy with MMC in Southwest Hospital and had been followed up for 1-3y. A complete success for surgery is defined as a postoperative intraocular pressure (IOP) >5 and ≤21 mm Hg and 20% reduction of IOP compared to preoperative, without IOP-lowering medications. A qualified success for surgery is defined as the abovementioned postoperative IOP with or without IOP-lowering medications. The primary outcomes were IOP, the number of IOP-lowering medications, and cumulative success rate. The secondary outcomes included best corrected visual acuity (BCVA), mean deviation (MD) of visual field, major complications, and risk factors for surgical failure. RESULTS: A total of 325 eyes of 261 glaucomatous patients had been included in our study. Both the mean IOP and the number of IOP-lowering medications were significantly decreased from 32.9±12.0 to 16.4±5.7 mm Hg (P<0.0001) and 3.0±0.9 to 0.9±1.0 (P<0.0001), respectively, at the last visit. The cumulative complete success rate and qualified success rate were 77.8% and 92.0% at 1-year follow-up, and 47.2% and 77.7% at 3-year follow up. There were no significant differences in surgical outcomes between primary angle-closure glaucoma (PACG) and primary open angle glaucoma (POAG). In PACG patients, the success rates of trabeculectomy were comparable with those of phacotrabeculectomy. Hypertension (HR=1.904, P=0.011), encapsulated bleb (HR=2.756, P<0.001), and more preoperative topical medications (HR=2.475, P=0.008) were risk factors for surgical failure. CONCLUSION: The qualified success rate of trabeculectomy with MMC in glaucomatous patients in the cohort is 92.0% at 1-year, and 77.7% at 3-year follow up. Hypertension, encapsulated bleb, and more preoperative topical medications are associated with surgical failure.

AKR1C1 Protects Corneal Epithelial Cells Against Oxidative Stress-Mediated Ferroptosis in Dry Eye.

Purpose: To evaluate the precise mode of cell death and to investigate the molecular mechanism underlying the initiation of inflammation in dry eye disease (DED). Methods: C57BL/6 mice were injected with scopolamine subcutaneously and exposed to desiccating stress to establish a DED mouse model. An immortalized human corneal epithelial cell line (HCEC) was cultured under hyperosmolarity (500 mOsM). Protein expressions were measured using western blot assay and immunofluorescence staining. mRNA expression was analyzed by RNA-sequencing and quantitative RT-PCR. Transmission electron microscopy was used to observe the intracellular ultrastructure. Intracellular Fe2+ was detected by a FerroOrange fluorescent probe. Flow cytometry was used to evaluate the cellular reactive oxygen species and lipid peroxidation. Results: Marked changes in ferroptosis-related markers expression, intracellular iron accumulation, and lipid peroxidation were observed in corneal epithelial cells of DED models. When excessive oxidative stress was suppressed, ferroptosis induced by hyperosmolarity in HCECs was restrained, as indicated by decreased iron content and lipid peroxidation levels. Moreover, AKR1C1 was upregulated by the activation of NRF2 in HCECs under hyperosmolarity. When AKR1C1 was knocked down, cell viability was decreased, accompanied by increased lipid peroxidation, whereas overexpression of AKR1C1 produced the opposite results. It was observed consistently that corneal defects and the inflammatory response were promoted after inhibition of AKR1C1 in vivo. Conclusions: Excessive oxidative stress-induced ferroptosis participates in DED pathogenesis. The expression of AKR1C1 is triggered by NRF2 to decrease ferroptosis-induced cell damage and inflammation in HCECs. These findings may provide potential makers targeting ferroptosis and AKR1C1 for DED therapy.

A comparative study on the model of PM2.5 direct or indirect interaction with bronchial epithelial cells.

The impact of PM2.5 on epithelial cells is a pivotal process leading to many lung pathological changes and pulmonary diseases. In addition to PM2.5 direct interaction with epithelia, macrophages that engulf PM2.5 may also influence the function of epithelial cells. However, among the toxic researches of PM2.5, there is a lack of evaluation of direct or indirect exposure model on human bronchial epithelial cell against PM2.5. In this present research, PM2.5-exposed human bronchial epithelial cell line (BEAS-2B) serves as the direct interaction model. By contrast, a PM2.5-stimulated co-culture model of macrophages and epithelial cells based on the transwell system was adopted as indirect stimulation model. By comparing these two models of interaction, we examined the viability of BEAS-2B and mRNA/protein expression profile of oxidative stress and inflammatory response-related transcription factors Nrf2, NF-kB, and according inflammatory indicators such as IL-1, IL-6, and IL-8, with a view to evaluating the effects of different interaction models of PM2.5 on epithelial cell damage in vitro. Our results indicated that under the same doses, the direct stimulation model of PM2.5 could inhibit the viability of BEAS-2B. Furthermore, the indirect stimulation model strengthen inflammation response of epithelia under the higher concentration of PM2.5 and induce epithelia to undergo EMT under the lower concentration of PM2.5. Overall, we have found that macrophage involvement may protect epithelia from PM2.5 cytotoxic effect, while it strengthens the inflammation response and induce epithelia to undergo EMT.

Comprehensive omics analyses profile genesets related with tumor heterogeneity of multifocal glioblastomas and reveal LIF/CCL2 as biomarkers for mesenchymal subtype.

Rationale: Around 10%-20% patients with glioblastoma (GBM) are diagnosed with more than one tumor lesions or multifocal GBM (mGBM). However, the understanding on genetic, DNA methylomic, and transcriptomic characteristics of mGBM is still limited. Methods: In this study, we collected nine tumor foci from three mGBM patients followed by whole genome sequencing, whole genome bisulfite sequencing, RNA sequencing, and immunohistochemistry. The data were further examined using public GBM databases and GBM cell line. Results: Analysis on genetic data confirmed common features of GBM, including gain of chr.7 and loss of chr.10, loss of critical tumor suppressors, high frequency of PDGFA and EGFR amplification. Through profiling DNA methylome of individual tumor foci, we found that promoter methylation status of genes involved in detection of chemical stimulus, immune response, and Hippo/YAP1 pathway was significantly changed in mGBM. Although both CNV and promoter methylation alteration were involved in heterogeneity of different tumor foci from same patients, more CNV events than promoter hypomethylation events were shared by different tumor foci, implying CNV were relatively earlier than promoter methylation alteration during evolution of different tumor foci from same mGBM. Moreover, different tumor foci from same mGBM assumed different molecular subtypes and mesenchymal subtype was prevalent in mGBM, which might explain the worse prognosis of mGBM than single GBM. Interestingly, we noticed that LIF and CCL2 was tightly correlated with mesenchymal subtype tumor focus in mGBM and predicted poor survival of GBM patients. Treatment with LIF and CCL2 produced mesenchymal-like transcriptome in GBM cells. Conclusions: Together, our work herein comprehensively profiled multi-omics features of mGBM and emphasized that components of extracellular microenvironment, such as LIF and CCL2, contributed to the evolution and prognosis of tumor foci in mGBM patients.

Integrated Analysis of the m6A-Related lncRNA Identified lncRNA ABALON/miR-139-3p/NOB1 Axis Was Involved in the Occurrence of Lung Cancer.

BACKGROUND: Lung cancer has the characteristics of early metastasis, high recurrence, and high mortality rate despite emerging advances in diagnostic. Early diagnosis can significantly improve the patient's chances of cure and survival. PURPOSE: This study aimed to identify and assess a prognostic lncRNA/miRNA/gene signature in patients with lung cancer. METHODS: Pearson correlation analysis, univariate Cox analysis and LASSO Cox analysis were used to construct a lung cancer prognostic risk model based on m6A-related lncRNA. The interaction between lncRNA-miRNA-gene was verified by luciferase reporter gene experiment. RESULTS: The Pearson correlation analysis determined that 1655 lncRNAs significantly correlated with the expression of m6A genes. A lung cancer prognostic risk model, including 14 m6A-related lncRNAs, was constructed through univariate Cox analysis and least absolute shrinkage and selection operator (LASSO) Cox analysis. ABALON was identified as the key lncRNA through cluster analysis and gene expression difference analysis. CONCLUSION: It was experimentally verified that ABALON acted as a competing endogenous RNA by sponging miR-139-3p and indirectly regulated the expression of NOB1. This study provided a new biological target for the early diagnosis of lung cancer and a new direction for studying the mechanism of lung cancer.

Long non­coding RNA LINC01224 promotes cell proliferation and inhibits apoptosis by regulating AKT3 expression via targeting miR­485­5p in endometrial carcinoma.

Endometrial carcinoma (EC) is the most common cancer in women worldwide, yet little is known about the underlying molecular basis of EC development. LINC01224, a novel long non­coding (lnc)RNA, was recently identified as an oncogene in various types of cancer. However, the function and underlying mechanism of LINC01224 in EC is still unclear. A total of 50 pairs of tumor and adjacent normal tissue from patients with EC, three EC cell lines and one human normal endometrial stromal cell (ESC) line were subjected to reverse transcription­quantitative PCR assay to evaluate the expression levels of LINC01224. Cell Counting Kit­8, colony formation and flow cytometry assays were used to assess cell proliferation and apoptosis. Western blotting was used to measure expression levels of apoptosis­ and proliferation­associated proteins and AKT3 protein. A xenograft model of HEC1A cells was established to validate the in vivo function of LINC01224 in EC tumor growth. Starbase 3.0 database prediction and luciferase reporter and RNA pull­down assays were performed to verify the binding sites between LINC01224 and microRNA (miR)­485­5p and miR­485­5p and AKT3. LINC01224 expression was significantly upregulated in both EC tumor tissue and cell lines. The upregulation of LINC01224 was negatively associated with survival of patients with EC. Functionally, LINC01224 promoted proliferation and inhibited apoptosis of EC cells; LINC01224 directly bound to and downregulated miR­485­5p to elevate the expression levels of AKT3, thereby promoting EC progression. LINC01224 depletion in EC cells hindered tumor growth in a xenograft model. The tumor suppressing effect of LINC01224­knockdown on EC progression was partly rescued by treatment with miR­485­5p inhibitor. The present data demonstrated the expression levels, clinical relevance and functional mechanism of LINC01224 in EC. LINC01224 promoted EC development via sponging miR­485­5p to elevate AKT3 expression levels; this may provide a promising therapeutic target pathway for EC treatment.

Multifocal glioblastoma-two case reports and literature review.

BACKGROUND: Multifocal glioblastoma is a rare type of glioblastoma with worse prognosis. In this article, we aimed to report two cases of classical multifocal glioblastoma. CASE PRESENTATION: In case 1, a 47-year-old male presented with dizziness, and once had a sudden loss of consciousness accompanied by convulsion of limbs. Contrast-enhanced MRI showed multiple lesions with heterogeneously ring-enhanced characters in the left hemisphere, diagnosed as multifocal glioblastoma. He underwent a craniotomy of all lesions, concurrent radiotherapy and chemotherapy as well as additional chemotherapy of temozolomide. After 2 cycles, repeat MRI showed that the new lesions already occurred and progressed. Eventually, he abandoned the chemotherapy after the 2 cycles and died 1 year later. In case 2, a 71-year-old male presented with a history of headache, left limb weakness, and numbness. Discontinuous convulsion of limbs once occurred. Contrast-enhanced MRI showed multiple lesions located in the right hemisphere, diagnosed as multifocal glioblastoma. He underwent a right frontoparietal craniotomy of the main lesion. Hemorrhage of the residual tumor and pulmonary artery embolism occurred synchronously. Eventually, his family decided not to pursue any further treatment and opted for hospice care and he passed away within 11 days of surgery. CONCLUSIONS: We reported two cases of typical multifocal glioblastoma. Valid diagnosis is crucial; then, resection of multiple lesions and canonical radio-chemotherapy probably bring survival benefits.

SNHG10 Promotes Cell Proliferation and Migration in Gastric Cancer by Targeting miR-495-3p/CTNNB1 Axis.

BACKGROUND: Long non-coding RNAs have been acknowledged as the crucial regulators in the progression of human cancers, including gastric cancer (GC). Small nucleolar RNA host gene 10 (SNHG10) has been identified as an oncogene in several cancer types. Nonetheless, it is unclear whether SNHG10 exerts functions in GC cells. AIMS: The aims of the current study were to explore the function and underlying mechanism of SNHG10 in GC. METHODS: The expression levels of SNHG10, miR-495-3p and catenin beta 1 (CTNNB1) were detected by RT-qPCR. Loss-of-function assays, including CCK-8, colony formation assay, flow cytometry analysis and transwell assays, were conducted to verify the effect of SHNG10 on the proliferation, apoptosis, migration and invasion of GC cells. Mechanism experiments were performed to identify the downstream molecular mechanism of SNHG10. RESULTS: SNHG10 was expressed at a high level in GC cells. Knockdown of SNHG10 inhibited the proliferation, migration and invasion of GC cells. Silencing of SNHG10 led to the downregulation of core factors of WNT signaling pathway. Knockdown of SNHG10 could decline the expression of CTNNB1 through sequestering miR-495-3p. CONCLUSIONS: SNHG10 promotes the procession of GC through targeting miR-495-3p/CTNNB1 and activating WNT signaling pathway.

A systematic review of multifocal and multicentric glioblastoma.

Multiple glioblastoma multiforme (GBM) is classified as multifocal and multicentric GBM according to whether there is communication between the lesions. Multiple GBM is more genetically heterogeneous, aggressive and resistant to chemoradiotherapy than unifocal GBM, and has a worse prognosis. There is no international consensus on the treatment of multiple GBM. This review discusses some paradigms of multiple GBM and focuses on the heterogeneity spread pathway, imaging diagnosis, pathology, molecular characterization and prognosis of multifocal and multicentric GBM. Several promising therapeutic methods of multiple GBM are also recommended.

Progesterone receptor inhibits the proliferation and invasion of endometrial cancer cells by up regulating Krüppel-like factor 9.

BACKGROUND: Krüppel-like factor 9 (KLF9) is one of the most important members of the KLF family, and is abnormally expressed in many tumors. However, the detailed function of KLF9 in endometrial cancer (EC) was barely investigated. METHODS: In this study, a total of 52 paired EC tissues were recruited to detect the KLF9 expression. Then a serial of phenotypic experiments and mechanism researches were performed. RESULTS: The results showed that KLF9 expression was decreased in EC tissues, and the reduced expression of KLF9 is associated with highly metastatic capacity of EC cells. KLF9 could inhibit the proliferation and invasion of EC cells by inhibiting the Wnt/ß-catenin signaling pathway. Progesterone receptor (PR) could bind to KLF9 promoter and a positive correlation between KLF9 and PR expression was witnessed. CONCLUSIONS: Taken together, the reduction of KLF9 induced by PR might participate in the development of EC and targeting KLF9 may provide a novel strategy for EC management.