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NF45, also referred to as nuclear factor of activated T cells, has been reported to promote the progression of multiple cancer types. However, the expression and physiological significance of NF45 in pancreatic ductal adenocarcinoma (PDAC) remain largely elusive. In this study, we investigated the clinical relevance and potential role of NF45 expression in PDAC development. Western blot analysis revealed that NF45 was remarkably upregulated in PDAC tissues, compared with the adjacent non-tumorous ones. In addition, the expression of NF45 in 122 patients with PDAC was evaluated using immunohistochemistry. In this way, we found that NF45 was abundantly expressed in PDAC tissues, and the expression of NF45 was correlated with tumor size (p = 0.007), histological differentiation (p = 0.033), and TNM stage (p = 0.001). Importantly, patients with low levels of NF45 expression exhibited better postoperative prognosis as compared with those with high NF45 expression. Furthermore, using PDAC cell cultures, we found that interference of NF45 expression using siRNA oligos suppressed PDAC cell proliferation and retarded cell cycle progression. Moreover, depletion of NF45 impaired the levels of cellular cyclin E and proliferating cell nuclear antigen (PCNA). Conversely, overexpression of NF45 facilitated the cell growth and accelerated cell cycle progression. Our results establish NF45 as an important indicator of PDAC prognosis with potential utility as a therapeutic target in this lethal disease.

Sam68 (Src-associated in mitosis of 68 kD) is a KH domain RNA-binding protein. The expression of Sam68 was correlated with kinds of tumors. Yet, the expression mechanisms and physiological significance of Sam68 in ESCC remains unclear. In this study, we clarified a potential role of Sam68 in the treatment of ESCC. Western blot and immunohistochemistry (IHC) analysis revealed that the protein level of Sam68 was higher in ESCC tumor tissues and cell lines. In addition, IHC stain revealed that Sam68 was positively correlated with clinical pathologic variables such as tumor grade and tumor invasion. In addition, Sam68 could be an independent prognostic indicator for patients' overall survival. In vitro studies such as starvation and refeeding assay along with Sam68-shRNA transfection assay demonstrated that Sam68 expression promoted proliferation of ESCC cells. And Sam68 downregulation caused decreased rate of cell growth and colony formation. Reasons are associated with growth arrest of cell cycle at G1/S phase. Moreover, our results clarified that Sam68 could promote ESCC cell proliferation via the activation of Akt/GSK-3β pathway. This research indicated that Sam68 might accelerate the cell cycle progression and be considered as a new therapy target in ESCC.

Leviteracetam (LEV) is a novel antiepileptic drug with improved tolerance and safety, while carbamazepine (CBZ) represents classical antiepileptic drugs. So far, a systemic comparison of the efficacy and side effects of these two drugs is lacking. A literature review on the comparison of leviteracetam versus carbamazepine for patients with epilepsy was performed up to September 2013 using PubMed, EMBASE, the Cochrane Library and ISI web of science. Finally, 3 randomized controlled trials (RCT) studies met the criteria on comparing the efficacy of leviteracetam versus carbamazepine for patients with epilepsy were included for meta-analysis. Stata 11.0 was used to analyze and summarize the respective data. Three RCTs met the entry criteria. The relative risk (RR) and 95% and the confidence interval (CI) of leviteracetam versus carbamazepine for 6- and 12-month seizure free intervals were 1.0 (0.91-1.10) and 0.97 (0.84-1.13), respectively, for therapy discontinuation due to adverse events (AEs) were 0.62 (0.48-0.80) and 1.00 (0.94-2.05), respectively, and for withdrawal after 6- and 12-month treatment were 0.8 (0.64-0.99) and 0.87 (0.74-1.03), respectively. The RR and 95% CI for occurrence of headache, fatigue, diarrhea, vertigo, nasopharyngitis, depression, weight gain and rash were 0.88 (0.73-1.06), 1.08(0.63-1.83), 1.23 (0.66-2.28), 0.92 (0.49-1.71), 0.85 (0.59-1.22), 2.15 (1.26-3.68), 0.69 (0.45-1.04), 0.39 (0.23-0.68), respectively. The major outcomes such as rate of seizure freedom were similar between leviteracetam and carbamazepine. However, leviteracetam led to depression more frequently than carbamazepine, while carbamazepine caused rash more frequently. However, the limited numbers of available RCTs studies and included patients in this study made our results less convincing and accurate.

GABA (gamma-aminobutyric acid)ergic neurons in the spinal dorsal horn have been reported to be divided into distinctive populations, with different cotransmitters and neuropeptides. In this study, we examined the colocalization of enkephalin (ENK) mRNA with GABA in the spinal dorsal horn using the glutamic acid decarboxylase (GAD)(67)-green fluorescence protein (GFP) knock-in mouse. Our approach was to perform in situ hybridization histochemistry to detect mRNA for preproenkephalin (PPE, the precursor protein for ENK), combined with immunohistochemistry for GFP to reveal GABAergic neurons. Quantitative analysis indicated that more than 44.4% (2967/6681) of GFP-immunoreactive neurons showed signals for PPE mRNA in the spinal dorsal horn. While 53.9% (2967/5501) of PPE mRNA-expressing neurons were immunoreactive for GFP. The double-labeled neurons were observed throughout the spinal dorsal horn, although they had a preferential localization in superficial layers. The present results provide a detailed morphological evidence that ENK and GABA colocalized in a subpopulation of neurons in the spinal dorsal horn, which are likely to represent local inhibitory dorsal horn interneurons involved in the modulation of pain transmission.

Astrocyte activation is involved in the neuropathic pain. As a glutamate scavenger, the glutamate transporter-1 (GLT-1) is exclusively expressed on the astrocytes and probably correlates with astrocyte activation. In the present study, we attempted to clarify the temporal changing courses of astrocyte activation and GLT-1 expression, as well as their correlations induced by a neuropathic pain model, namely, spinal nerve ligation (SNL) in which rapidly appearing (<3 days) and persistent (>21 days) mechanical allodynia and thermal hyperalgesia were presented. Immunofluorescent staining showed that GLT-1 was expressed exclusively in most (not all) of the astrocytes, even when the GLT-1 expression reached its peak. The expression of GLT-1 displayed an interesting biphasic change, with an initial up-regulation followed by a down-regulation after SNL. Our results also demonstrated that SNL induced a marked and long-term (>21 days) activation of astrocytes in the ipsilateral spinal dorsal horn. These results suggest that astrocyte activation, the change of GLT-1 expression and the potential relationship between them might play key roles in the induction and/or maintenance of neuropathic pain. The present results provide novel clues in understanding the mechanisms underlying the involvement of astrocytes and GLT-1 in the neuropathic pain.

Four approaches have been explored for the preparation of maleimido-functionalized self-assembled monolayers (SAMs) on silicon. SAMs prepared by self-assembly of maleimido-functionalized alkyltrichlorosilanes (11-maleimido-undecyl-trichlorosilane) on oxide-covered silicon yield higher signals from maleimido functionalities in ATR-IR (attenuated total reflection IR) spectroscopy and XPS (X-ray photoelectron spectroscopy) than the other three methods. The surface composition of maleimido groups was tailored further by the formation of mixed monolayers with nonfunctionalized alkyltrichlorosilanes (decyltrichlorosilane). The order of the alkyl chains within the monolayers only slightly depends on the composition of the mixed monolayers. We utilized the maleimido-terminated SAMs to bind various nucleophilic compounds, alkylamines, alkylthiols, and thiol-tagged DNA oligonucleotides by means of conjugate addition.