Dependence of new environmental nano organic semiconductor nickel-(II)-tetraphenyl-21H,23H-porphyrin films on substrate type for energy storage applications.

Characterization of organic nickel-(II)-tetraphenyl-21H,23H-porphyrin films as a function of substrate type was performed for energy storage applications and consequently environmental enhancement. Nickel-(II)-tetraphenyl-21H,23H-porphyrin films show an amorphous phase. They have a crystallite size of 8-11 nm. Strain caused a shift of different humps' positions. The measured transmittance has high values within the range of 85-91%, and the absorption coefficient values were included within the high-absorption region. Both optical gap and fundamental gap, refractive index, carrier-concentration-to-effective-mass ratio and lattice dielectric constant were calculated, and they were found to be increased, except refractive index and lattice dielectric constant. The obtained data indicated that nickel-(II)-tetraphenyl-21H,23H-porphyrin films are a candidate for energy storage applications.

Masson tumor as a neck mass.

INTRODUCTION: A Masson's tumor is a benign, intravascular tumor, typically located in the fingers. Histologically, a Masson's tumor is characterized by an intravascular endothelial papillary projection associated with thrombi, without atypia or necrosis. The CD 31 and CD 34 stains are the most efficient immunohistological markers to identify the vascular origin. CASE SUMMARY: A 54-year-old man presented with a right lateral neck mass for 3 weeks. The CT scan of the neck showed an oval, well-circumscribed cystic mass, measuring 20mm×9mm, situated over the right sternocleidomastoid muscle, with a peripheral vessel draining into the right anterior jugular vein. The mass was excised surgically, and a pathological report indicated a thrombosed material inside the lumen of a small vein with a differentiated papillary structure; neither nuclear atypia nor necrosis were seen. The patient had an uncomplicated recovery and completed 8 months of follow-up appointments without any evidence of recurrence. DISCUSSION: Intravascular papillary endothelial hyperplasia (IPEH) can be differentiated from angiosarcoma by lack of extension to the perivascular tissue and absence of necrosis and atypia. The pathogenesis is still unknown; surgical excision is the method of treatment. This is an extremely rare presentation of Masson's tumor.

Investigation of belinostat-induced genomic instability by molecular cytogenetic analysis and pathway-focused gene expression profiling.

Histone deacetylases (HDACs), which regulate transcription and specific functions such as tumor suppression by p53, are frequently altered in tumors and have a contentious role in carcinogenesis. HDAC inhibitors, which have a long history of use in psychiatry and neurology, have recently been tested as possible treatments for tumors. Belinostat received regulatory approval in the USA on July 3, 2014, for use against peripheral T-cell lymphoma. However, the unavailability of information on belinostat genotoxicity in normal cells and the molecular mechanisms involved in the genetic instability after exposure to belinostat encouraged us to conduct this study. Our data showed that the exposure of mice to belinostat at the recommended human doses induced chromosome breakage, whole-chromosome lagging, and oxidative DNA damage in bone marrow cells in a dose-dependent manner. The expression levels of 84 genes involved in the DNA damage signaling pathway were evaluated by using an RT2 Profiler PCR array. Belinostat exposure altered the expression of 25 genes, with statistically significant changes observed in 17 genes. The array results were supported by RT-PCR and western blotting experiments. Collectively, our results showed that belinostat exposure caused oxidative DNA damage and downregulated the expression of genes involved in DNA damage repair, which may be responsible for belinostat-induced genomic instability. Thus, the clinical usage of this drug should be weighed against the hazards of carcinogenesis, and the observed genotoxicity profile of belinostat may support further development of efficient HDAC inhibitors with weaker genotoxicity.

Blocking of cytokines signalling attenuates evoked and spontaneous neuropathic pain behaviours in the paclitaxel rat model of chemotherapy-induced neuropathy.

BACKGROUND: Chemotherapy-induced peripheral neuropathic pain (CIPNP) is a serious dose-limiting neurotoxic effect of cancer drug treatment. The underlying mechanism(s) of this debilitating condition, which lacks effective drug treatment, is incompletely understood. However, neural-immune interactions, involving increased expression and release of cytokines, are believed to be involved. Here, we examined, in the paclitaxel rat model of CIPNP, whether plasma levels of 24 cytokines/chemokines change after paclitaxel treatment, and whether blocking of signalling of some of those cytokines would reverse/attenuate behavioural signs of CIPNP. METHODS: To achieve these objectives luminex, pharmacological and behavioural experiments were performed on male Wistar rats (250-300 g) 31 days after the last injection of paclitaxel (1 mg/kg, i.p. on four alternate days) as well as on control (vehicle-treated) rats. RESULTS: Compared with control rats, plasma levels of IL-1α, IL-1ß, IL-6, TNF-α, INF-γ and MCP-1 were significantly upregulated in paclitaxel-treated rats. Blocking of TNF-α signalling with etanercept (2 mg/kg, i.p.) or IL-1ß with IL-1 receptor antagonist (IL-1ra; 3 mg/kg, i.p.), significantly attenuated established mechanical and cold hypersensitivity as well as spontaneous pain behaviour (spontaneous foot lifting) 24 and 48 h postdrug treatment. Pharmacological blockade of MCP-1/CCL2 signalling with a highly selective CCR2 receptor antagonist (S504393, 5 mg/kg, i.p.) also significantly reduced evoked, but not spontaneous, pain behaviours of CIPNP in paclitaxel-treated rats at the same time points. CONCLUSIONS: The findings support the notion that cytokines/chemokines, particularly TNF-α, IL-1 and MCP-1, are involved in the pathophysiology of CIPNP and suggest that strategies that target their inhibition may be effective in treating CIPNP. SIGNIFICANCE: This study demonstrates that paclitaxel-treated rats exhibit, in addition to indices of mechanical and cold hypersensitivity, a behavioural sign of spontaneous pain, the principal compliant of patients with neuropathic pain. This was accompanied by upregulation in plasma levels of key cytokines/chemokines (IL-1α, IL-1ß, IL-6, TNF-α, INF-γ and MCP-1) 31 days post-treatment. However, it is noteworthy that cytokine release, rather than nerve injury per se, may be causative of NP in this model of CIPNP. Nevertheless, our findings that pharmacological blockade of TNF-α, IL-1ß and MCP-1 attenuated both evoked and spontaneous pain suggest that strategies that target inhibition of these cytokines may be effective in treating CIPNP.

Robot-assisted surgical approach to bladder cancer: a decade of progress!

Robot-assisted radical cystectomy (RARC) has gained popularity and proven its efficacy, safety and reproducibility in the last decade. RARC has resulted in less blood loss, enhanced recovery, and shorter hospital stay. RARC has proven to have similar or better postoperative morbidity, mortality and equal oncologic, outcomes. Limiting factors to the acceptance of this surgical approach have included its steep learning curve and the lack of both long-term outcome data. This article systematically reviews the literature comparing the outcomes for RARC (comparisons with open radical cystectomy when performed at the same institution) with a focus on operative, complications, oncologic, functional and survival outcomes.

Smad2 overexpression reduces the proliferation of the junctional epithelium.

The overexpression of the intracellular signaling molecule of the transforming growth factor-beta family (TGF-ß) Smad2 was found to induce apoptosis and inhibit the proliferation rate of oral epithelial cells. Therefore, the aim of this study was to investigate in vivo the effect of Smad2 overexpression on the proliferation rate of the junctional epithelium (JE). Smad2 overexpression was driven by the cytokeratin 14 promoter (K14-Smad2) in transgenic mice. The K14-Smad2 mice were compared with wild-type (WT) mice selected as the control group. Samples were stained with hematoxylin and eosin stains and analyzed by image analysis. Immunohistochemistry was conducted for proliferating cell nuclear antigen (PCNA) and c-Myc as markers of cell proliferation. The expression of cyclin-dependent kinase inhibitors (P15, P21, and P27) was determined by real-time polymerase chain-reaction (RT-PCR). The quantity of phosphorylated retinoblastoma (pRB) was determined with Western blots. The overexpression of Smad2 altered the area of the junctional epithelial cells in one-year-old K14-Smad2 mice. The area was 32,768 (± 3,473) µm(2) for the WT and 24,937.25 (± 1,965) µm(2) for the K14-Smad2 mice. There was a significant difference in the proliferation rates of the JE (PCNA-positive cells) between the WT and K14-Smad2 mice, 20.7% (± 1.1) and 2.1% (± 0.5), respectively. A significant difference in c-Myc expression occurred between experimental and control samples. The K14-Smad2 mice had a mean of 2.3% (± 0.6), and the WT mice had a mean of 20.1% (± 3.6). Smad2 overexpression up-regulated the mRNA expression of P15 by 2.3-fold and that of P27 by 5.5-fold in the K14-Smad2 mice. Finally, the pRB protein showed a 2.3 (± 0.5)-fold increase in K14-Smad2 mice when compared with WT mice. Smad2 overexpression inhibits the proliferation of JE cells by down-regulating c-Myc and up-regulating P15 and P27, which resulted in an increase in pRB, leading to cell-cycle arrest.

Stilbene 5c, a microtubule poison with vascular disrupting properties that induces multiple modes of growth arrest and cell death.

The stilbene derivative, cis-3,4',5-trimethoxy-3'-aminostilbene (stilbene 5c), is a potentially potent antitumor agent that acts via binding to the colchicine-binding site in tubulin. The current studies were designed to investigate the effectiveness of stilbene 5c against the HCT-116 human colon cancer cell line and B16/F10 melanoma cells as well as human endothelial cell tube formation and tumor perfusion. Stilbene 5c produced a time-dependent decrease in cell viability in both cell lines and the capacity of the cells to proliferate was not restored upon removal of the drug. Treatment with stilbene 5c also promoted both senescence and autophagy in both cell lines. TUNEL and annexin 5 staining indicated that apoptosis also occurs in stilbene 5c-treated HCT-116 cells, but not in B16/F10 melanoma cells. DAPI staining revealed morphological changes in the cell nuclei (binucleated and micronucleated cells) indicative of mitotic catastrophe in HCT-116 cells but not in the B16/F10 melanoma cells. p53-null HCT-116 cells demonstrated a similar growth arrest/cell death response to stilbene as p53-wild type HCT-116 cells. Stilbene 5c also completely inhibited human endothelial cell tube formation on Matrigel, consistent with potential anti-angiogenic actions. Using a new method developed for monitoring the pharmacodynamic effects of stilbene 5c in vivo, we found that a single injection of stilbene 5c reduced tumor perfusion by 65% at 4h, returning to baseline by 24h, while subsequent daily injections of stilbene 5c produced progressively larger reductions and smaller rebounds. This work indicates that stilbene 5c could potentially be effective against melanoma and colon cancer through the promotion of multiple modes of growth arrest and cell death coupled with anti-angiogenic and antivascular actions.