Motor response with apomorphine sublingual film and levodopa in patients with OFF episodes.

Evaluate timing of motor improvement with carbidopa/levodopa (CD/LD) and apomorphine sublingual film (SL-APO) in patients with Parkinson's disease and OFF episodes. A pooled analysis from two studies assessed Movement Disorder Society Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS-III) scores and investigator-rated FULL ON. At 15 and 30 min following the prescribed first daily CD/LD dose, mean improvements in MDS-UPDRS-III scores were -6.

RAGE ablation attenuates glioma progression and enhances tumor immune responses by suppressing galectin-3 expression.

Background: Malignant gliomas consist of heterogeneous cellular components that have adopted multiple overlapping escape mechanisms that overcome both targeted and immune-based therapies. The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily that is activated by diverse proinflammatory ligands present in the tumor microenvironment. Activation of RAGE by its ligands stimulates multiple signaling pathways that are important in tumor growth and invasion.

Study on the Action Mechanism of Dkk-1, TGF-β1 and TNF-α Expression Levels in Dupuytren's Contracture.

Background: The biological mechanism of Dupuytren's contracture needs to be further studied in order to minimize postoperative recurrence and provide a pathological basis for the development of new therapeutic targets.

Methods: HE staining, immunohistochemistry, PCR and western blotting were performed in pathological palmar aponeurosis specimens and normal palmar aponeurosis tissues for comparative study.

Results: (1) TNF-α expression was up-regulated: TNF-α mRNA was more highly expressed in the pathological tissues of DD patients than in the CT group, P < 0.

RAGE Inhibitors as Alternatives to Dexamethasone for Managing Cerebral Edema Following Brain Tumor Surgery.

Resection of brain tumors frequently causes injury to the surrounding brain tissue that exacerbates cerebral edema by activating an inflammatory cascade. Although corticosteroids are often utilized peri-operatively to alleviate the symptoms associated with brain edema, they increase operative morbidities and suppress the efficacy of immunotherapy. Thus, novel approaches to minimize cerebral edema caused by neurosurgical procedures will have significant utility in the management of patients with brain tumors.

A Coarse-to-Fine Deformable Transformation Framework for Unsupervised Multi-Contrast MR Image Registration with Dual Consistency Constraint.

Multi-contrast magnetic resonance (MR) image registration is useful in the clinic to achieve fast and accurate imaging-based disease diagnosis and treatment planning. Nevertheless, the efficiency and performance of the existing registration algorithms can still be improved. In this paper, we propose a novel unsupervised learning-based framework to achieve accurate and efficient multi-contrast MR image registration.

Local and Systemic Immune Dysregulation Alters Glioma Growth in Hyperglycemic Mice.

Purpose: Unlike most cancers, no clear epidemiological correlation between diabetes (Db) and malignant glioma progression exists. Because hyperglycemia activates proinflammatory pathways through the receptor for advanced glycation endproducts (RAGE), we hypothesized that Db can also promote malignant glioma progression.

Experimental Design: We compared the growth of two phenotypically diverse syngeneic glioma models in control and diabetic mice.

S100B suppression alters polarization of infiltrating myeloid-derived cells in gliomas and inhibits tumor growth.

S100B, a member of the multigene family of Ca-binding proteins, is overexpressed by most malignant gliomas but its biological role in gliomagenesis is unclear. Recently, we demonstrated that low concentrations of S100B attenuated microglia activation through the induction of STAT3. Furthermore, S100B downregulation in a murine glioma model inhibited macrophage trafficking and tumor growth.

Characterization of Arginase Expression in Glioma-Associated Microglia and Macrophages.

Microglia (MG) and macrophages (MPs) represent a significant component of the inflammatory response to gliomas. When activated, MG/MP release a variety of pro-inflammatory cytokines, however, they also secrete anti-inflammatory factors that limit their cytotoxic function. The balance between pro and anti-inflammatory functions dictates their antitumor activity.

Metronomic Doses of Temozolomide Enhance the Efficacy of Carbon Nanotube CpG Immunotherapy in an Invasive Glioma Model.

Even when treated with aggressive current therapies, most patients with glioblastoma survive less than two years. Rapid tumor growth, an invasive nature, and the blood-brain barrier, which limits the penetration of large molecules into the brain, all contribute to the poor tumor response associated with conventional therapies. Immunotherapy has emerged as a therapeutic approach that may overcome these challenges.

RAGE expression in tumor-associated macrophages promotes angiogenesis in glioma.

Interaction of RAGE (the receptor for advanced glycation endproducts) with its ligands can promote tumor progression, invasion, and angiogenesis. Although blocking RAGE signaling has been proposed as a potential anticancer strategy, functional contributions of RAGE expression in the tumor microenvironment (TME) have not been investigated in detail. Here, we evaluated the effect of genetic depletion of RAGE in TME on the growth of gliomas.

Increased expression of stress inducible protein 1 in glioma-associated microglia/macrophages.

Factors released by glioma-associated microglia/macrophages (GAMs) play an important role in the growth and infiltration of tumors. We have previously demonstrated that the co-chaperone stress-inducible protein 1 (STI1) secreted by microglia promotes proliferation and migration of human glioblastoma (GBM) cell lines in vitro. In the present study, in order to investigate the role of STI1 in a physiological context, we used a glioma model to evaluate STI1 expression in vivo.

S100B promotes glioma growth through chemoattraction of myeloid-derived macrophages.

Purpose: S100B is member of a multigenic family of Ca(2+)-binding proteins, which is overexpressed by gliomas. Recently, we showed that low concentrations of S100B attenuated microglia activation through the induction of Stat3. We hypothesized that overexpression of S100B in gliomas could promote tumor growth by modulating the activity of tumor-associated macrophages (TAM).

Intracerebral CpG immunotherapy with carbon nanotubes abrogates growth of subcutaneous melanomas in mice.

Purpose: Recently, we showed that intratumoral delivery of low-dose, immunostimulatory CpG oligodeoxynucleotides conjugated with carbon nanotubes (CNT-CpG) was more effective than free CpG and not only eradicated intracranial (i.c.) gliomas but also induced antitumor immunity that protected mice from subsequent i.

HMGA1 expression in human gliomas and its correlation with tumor proliferation, invasion and angiogenesis.

High-mobility group A1 (HMGA1) protein is an architectural transcription factor widely expressed during embryonic development and tumor progression. The purpose of this research was to investigate the expression of HMGA1 in malignant gliomas with different WHO classification and to study the correlation of HMGA1 expression with tumor proliferation, invasion, and angiogenesis. Expression of HMGA1, Ki-67, MMP-9, VEGF-A, and MVD in malignant gliomas and their correlation were studied in 60 samples of different WHO classification by use of immunohistochemistry, and in 27 randomly selected samples by use of real-time quantitative PCR.

The different HMGA1 expression of total population of glioblastoma cell line U251 and glioma stem cells isolated from U251.

The high-mobility group A1 (HMGA1) protein is a non-histone architectural nuclear factor and participates in diverse biological processes, including gene transcription, embryogenesis, cell cycle regulation, apoptosis, and even neoplastic transformation. In our study, glioma stem cells (GSCs) expressing the surface marker CD133 from human glioblastoma cell line U251 were isolated using MACS column and were analyzed using immunofluorescence and flow cytometry (FCM). The different expression of HMGA1 was detected using real-time RT-PCR and Western blot at transcriptional and translational levels between U251 and isolated GSCs.