MRI-based clinical-radiomics nomogram model for predicting microvascular invasion in hepatocellular carcinoma.

BACKGROUND: Preoperative microvascular invasion (MVI) of liver cancer is an effective method to reduce the recurrence rate of liver cancer. Hepatectomy with extended resection and additional adjuvant or targeted therapy can significantly improve the survival rate of MVI+ patients by eradicating micrometastasis. Preoperative prediction of MVI status is of great clinical significance for surgical decision-making and the selection of other adjuvant therapy strategies to improve the prognosis of patients. PURPOSE: Established a radiomics machine learning model based on multimodal MRI and clinical data, and analyzed the preoperative prediction value of this model for microvascular invasion (MVI) of hepatocellular carcinoma (HCC). METHOD: The preoperative liver MRI data and clinical information of 130 HCC patients who were pathologically confirmed to be pathologically confirmed were retrospectively studied. These patients were divided into MVI-positive group (MVI+) and MVI-negative group (MVI-) based on postoperative pathology. After a series of dimensionality reduction analysis, six radiomic features were finally selected. Then, linear support vector machine (linear SVM), support vector machine with rbf kernel function (rbf-SVM), logistic regression (LR), Random forest (RF) and XGBoost (XGB) algorithms were used to establish the MVI prediction model for preoperative HCC patients. Then, rbf-SVM with the best predictive performance was selected to construct the radiomics score (R-score). Finally, we combined R-score and clinical-pathology-image independent predictors to establish a combined nomogram model and corresponding individual models. The predictive performance of individual models and combined nomogram was evaluated and compared by receiver operating characteristic curve (ROC). RESULT: Alpha-fetoprotein concentration, peritumor enhancement, maximum tumor diameter, smooth tumor margins, tumor growth pattern, presence of intratumor hemorrhage, and RVI were independent predictors of MVI. Compared with individual models, the final combined nomogram model (AUC: 0.968, 95% CI: 0.920-1.000) constructed by radiometry score (R-score) combined with clinicopathological parameters and apparent imaging features showed the optimal predictive performance. CONCLUSION: This multi-parameter combined nomogram model had a good performance in predicting MVI of HCC, and had certain auxiliary value for the formulation of surgical plan and evaluation of prognosis.

Bone marrow-derived mesenchymal stem cells expressing BMP2 suppress glioma stem cell growth and stemness through Bcl-2/Bax signaling.

Objectives: To find an effective molecule that controls glioma stem cell (GSC) proliferation and differentiation for the development of future therapeutic interventions against glioblastoma. Material and Methods: Bone marrow-derived mesenchymal stem cells (BMSCs) were infected with a lentiviral vector to express BMP2. Cell viability, cell counting, and tumor sphere formation assays, as well as flow cytometry, immunofluorescence staining, and Western blotting were used to investigate the effects of BMSC-BMP2 on GSCs. Results: The results of flow cytometry and the CKK-8 assay showed that BMSC-BMP2 induced GSC apoptosis while inhibiting proliferation. BMSC-BMP2 decreased GSC neurosphere formation and neurospheres' transverse and vertical diameter. Meanwhile, BMSC-BMP2 downregulated GSC Nanog and OCT4 expression levels, suggesting stemness inhibition. Western blotting showed that BMSC-BMP2 increased Bax protein expression and significantly decreased Bcl-2 protein expression. Accordingly, the Bcl-2/Bax ratio increased. Conclusion: BMSC-BMP2 could effectively inhibit GSC proliferation, induce GSC apoptosis, and decrease GSC stemness, thereby providing a novel strategy for treating malignant glioma.

Neuroprotective effect of rhaponticin against Parkinson disease: Insights from in vitro BV-2 model and in vivo MPTP-induced mice model.

Parkinson's disease (PD) is a complex neurodegenerative illness associated with the loss or damage to neurons of the dopaminergic system in the brain. Few therapeutic approaches and considerable side effects of conventional drugs necessitate a new therapeutic agent to treat patients with PD. Rhaponticin is a natural hydroxystilbene, found in herbal plants such as Rheum rhaponticum, and known to have desirable biological activity including anti-inflammatory properties. However, the neuroinflammation on rhaponticin levels has only been investigated partially so far. So, the current study explored whether rhaponticin could ameliorate the pathophysiology observed in both the in vitro microglial BV-2 cells and the in vivo (1-methyl-4-phenyl-1,2,3,5-tetrahydropyridine [MPTP])-mediated PD model. The results show rhaponticin significantly attenuated lipopolysaccharide (LPS)-mediated microglial activation by suppressing nitric oxide synthase in conjunction with abridged reactive oxygen species production together with proinflammatory mediator reduction. In vivo rhaponticin treatment improves motor impairments as well as the loss of dopaminergic neurons in MPTP-treated mice possibly through suppression via mediators of inflammation. Taken together, these results offer evidence that rhaponticin exerts anti-inflammatory effects and neuroprotection in an LPS-induced microglial model and the MPTP-induced mouse models of PD.

Multiflorane suppresses the proliferation, migration and invasion of human glioblastoma by targeting MAPK signalling pathway.

PURPOSE: Glioblastoma is one common malignant tumors of central nervous system and its treatment is limited by the unavailability of chemotherapeutic agents. This study was therefore undertaken to evaluate the anticancer effects of Multiflorane molecule against the U87 human glioblastoma cells and normal human astrocytes. METHODS: The CCK8 assay was used to determine cell proliferation. Acridine orange (AO)/Ethidium bromide (EB) staining assays were used to detect apoptosis. Transwell assays were used to detect the cell migration and invasion. Western blotting was used to determine protein expression. RESULTS: The results showed Multiflorane inhibited the proliferation of the human U87 cells with little effects on the normal cells. Investigation of the underlying mechanisms showed that Multiflorane induced apoptosis in U87 cells. Multiflorane-induced apoptosis was linked with upregulation of cleaved caspase-3, 8 and 9, as well as cleaved PARP. The Bax protein levels were increased and of Bcl-2 were decreased. Flow cytometric analysis showed that Multiflorane induced G2/M arrest of the U87 glioblastoma cells. Transwell assays showed that the molecule suppressed the migration and invasion of the U87 glioblastoma cells. Additionally, Multiflorane also blocked the phosphorylation of p38 MAPK1 dose-dependently. CONCLUSION: Taken together, Multiflorane may prove beneficial in the treatment of glioblastoma.

Clinical efficacy of MVD combined with PSR in the treatment of primary trigeminal neuralgia.

Clinical efficacy of microvascular decompression (MVD) combined with percutaneous stereotactic radiofrequency rhizotomy (PSR) in the treatment of primary trigeminal neuralgia was investigated. The medical records of 141 patients with primary trigeminal neuralgia admitted to Shandong Provincial Hospital from May 2011 to June 2013 were collected. Among them, 63 patients received MVD surgery and were set as group A, while the other 78 received MVD combined with PSR and were as group B. The efficacy and complication of the two treatment methods were compared. Multivariate logistic regression was performed to analyze the risk factors for treatment efficacy. The total effective rate was 96.15% in group B, higher than that in group A (88.89%), but the difference was not statistically significant (P>0.05). The complications in group B were statistically less than that in group A (P<0.05). Risk factors for the onset of primary trigeminal neuralgia included the degree of decompression, duration of disease, degree of compression, and clinical symptoms. Patients treated with MVD combined with PSR had a better quality of life and lower 5-year recurrence rate than patients treated with MVD (both P<0.05). In conclusion, MVD combined with PSR treatment has good clinical efficacy in primary trigeminal neuralgia and low incidence of complications. The possible risk factors for the onset of primary trigeminal neuralgia include the degree of decompression, duration of disease, degree of compression, and clinical symptoms.

The complete mitochondrial genome sequence of a rat 9L glial neoplasms CNS-1 cell line.

We sequenced a complete mitochondrial genome sequence of a rat 9L glial neoplasms disease CNS-1 cell line for the first time (Accession No. KM657952). The total length of the mitogenome was 16,306 bp and coding 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes. This mitochondrial genome sequence will provide new genetic resource into glial neoplasms disease.

MiRNA-323-5p Promotes U373 Cell Apoptosis by Reducing IGF-1R.

BACKGROUND MicroRNA regulates mammalian cell growth in terms of its proliferation and apoptosis by controlling the expression of target genes. MiRNA-323-5p plays an important role in regulating cell growth and death within various types of cells. The function of miRNA-323-5p and its possible molecular mechanism in human cerebral glioma U373 cells remains to be further confirmed. The aim of this study was to investigate the regulation function of miRNA-323-5p in human glioma U373 cell growth, proliferation, and apoptosis. MATERIAL AND METHODS We used human cerebral glioma U373 cells as the cell model; utilized liposome technology (transfected by Lipofectamine2000) in human cerebral glioma U373 cells to over-express miRNA-323-5p (microRNA used as control group); and selected MTT assay and flow cytometry to detect cell growth, proliferation, and apoptosis. We used RT-PCR and Western blotting techniques to study the expression levels of target insulin-like growth factor 1 (IGF-1) receptor protein in U373 cells transfected with miRNA-323-5p. We used liposome transfection techniques in human cerebral glioma U373 cells to over-express or processed knockdown of IGF-1R by siRNA, and then transferred with miRNA-323-5p, thereby investigating the treated human cerebral glioma U373 cells apoptosis situations. RESULTS The over-expression of miRNA-323-5p inhibited the growth and proliferation of human cerebral glioma U373 cells and promoted its apoptosis. The over-expression of miRNA-323-5p also reduced the IGF-1R level. After processing the knockdown of IGF-1R and then transfection with miRNA-323-5p, U373 cells had enhanced apoptosis. The over-expression of IGF-1R inhibited the cells apoptosis induced by miRNA-323-5p. CONCLUSIONS MiRNA-323-5p inhibited human cerebral glioma U373 cell proliferation and promoted its apoptosis by reducing IGF-1R.

Therapeutic time window and effect of intracarotid neural stem cells transplantation for intracerebral hemorrhage.

This study investigated the therapeutic effect of neural stem cells transplanted via the carotid artery at different times after intracerebral hemorrhage. A great number of 5-bromo-2-deoxyuridine-positive cells were observed surviving and distributed evenly in the perihematoma areas. Phenotypes of grafted cells depended upon time of transplantation, and the later the cells were transplanted, the larger the percentage of cells that differentiated into neurons. Animals treated at 7 and 14 days after injury exhibited the most significant improvements in behavioral tests. Therefore,intracarotid injection allows efficient delivery of cells to the injured hemisphere, especially during the period 7-14 days after injury, and may potentially be applicable in humans.