cis-Dichloridobis(1,10-phenanthroline)cobalt(II) dimethyl­formamide solvate

In the title complex, [CoCl2(C12H8N2)2]·C3H7NO, which has twofold rotation symmetry, the CoII cation is coordinated by two 1,10-phenanthroline (phen) mol­ecules and two chloride ligands in a distorted octa­hedral geometry. In the crystal structure, a cavity is created by six complex mol­ecules connected by C—H⋯π inter­actions and non-classical C—H⋯Cl hydrogen bonds. The cavities are occupied by the disordered dimethyl­formamide solvent mol­ecule. The C and N atoms of the C—N bond in the solvent mol­ecule also lie on a crystallographic twofold rotation axis; the remaining atoms of the solvent are statistically disordered (ratio 0.5:0.5) about this axis

Biphenyl-3,3′-dicarb­oxy­lic acid

The asymmetric unit of the title compound, C14H10O4, contains one half mol­ecule, the complete mol­ecule being generated by a twofold axis. The two benzene rings form a dihedral angle of 43.11 (5)°. Inter­molecular O—H⋯O hydrogen bonds link the mol­ecules into one-dimensional zigzag chains. These chains are further connected into two-dimensional supra­molecular layers by weak π–π stacking inter­actions between neighbouring benzene rings, with centroid–centroid distances of 3.7648 (8) Å

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies

Secreted protein acidic and rich in cysteine (SPARC) is associated with nasopharyngeal carcinoma metastasis and poor prognosis

<p>Abstract</p> <p>Background</p> <p>The aim of the present study was to analyse the expression of Secreted protein acidic and rich in cysteine (SPARC) in nasopharyngeal carcinoma (NPC) specimens, and to evaluate its correlation with clinicopathologic features, including survival of patients with NPC</p> <p>Methods</p> <p>NPC tissue microarrays (TMAs) were constructed from Sun Yat-sen University Cancer Center (SYSUCC), another three centers on mainland China, Singapore and Hong Kong. Using quantitative RT-PCR and Western-blotting techniques, we detected mRNA and protein expression of SPARC in NPC cell lines and immortalized nasopharyngeal epithelial cells (NPECs) induced by Bmi-1 (NPEC2 Bmi-1). The difference of SPARC expression in the cell lines was tested using a <it>t</it>-test method. The relationship between the SPARC expression and clinicopathological data was assessed by chi-square. Survival analysis was estimated using the Kaplan-Meier approach with log-rank test. Univariate and multivariate analyses of clinical variables were performed using Cox proportional hazards regression models.</p> <p>Results</p> <p>The expression levels of SPARC mRNA and protein were markedly higher in NPC cell lines than in NPEC2 Bmi-1. Especially, the expression levels of SPARC mRNA and protein were much lower in the 6-10B than in the 5-8 F (<it>P </it>= 0.002, <it>P </it>= 0.001). SPARC immunostaining revealed cytoplasmic localization in NPC cells and no staining in the stroma and epithelium.</p> <p>In addition, high level of SPARC positively correlated with the status of distant metastasis (<it>P </it>= 0.001) and WHO histological classification (<it>P </it>= 0.023). NPC patients with high SPARC expression also had a significantly poorer prognosis than patients with low SPARC expression (log-rank test, <it>P </it>< 0.001), especially patients with advanced stage disease (log-rank, <it>P </it>< 0.001). Multivariate analysis suggested that the level of SPARC expression was an independent prognostic indicator for the overall survival of patients with NPC (<it>P </it>< 0.001).</p> <p>Conclusions</p> <p>SPARC expression is common in NPC patients. Our data shows that elevated SPARC expression is a potential unfavorable prognostic factor for patients with NPC.</p

Expression of indoleamine 2,3-dioxygenase in nasopharyngeal carcinoma impairs the cytolytic function of peripheral blood lymphocytes

<p>Abstract</p> <p>Background</p> <p>Tumor-specific cytotoxic T cells and infiltrating lymphocytes are frequently found in tumor tissues in patients with nasopharyngeal carcinoma (NPC). Most patients with NPC, however, especially those with advanced stages, have a poor clinical prognosis despite conventional immunotherapy. The aim of this work was to examine the effect of indoleamine 2,3-dioxygenase (IDO), an immunosuppressive enzyme, on the lymphocyte function in NPC.</p> <p>Methods</p> <p>The NPC cell line CNE2 was treated by interferon-γ (IFNγ) and the levels of IDO expression was analyzed by Western blotting and reverse phase high-performance liquid chromatography (HPLC). Lymphocytes from health human exposed to the milieu created by IDO-positive CNE2 cells and the lymphocyte cytotoxicity to target tumor cells was analyzed by standard lactate dehydrogenase (LDH) release assay. Additionally, expression of IDO was determined by Immunohistochemical assay in the tumor tissues form clinically evaluated NPC.</p> <p>Results</p> <p>IDO expression was acutely induced in the NPC cell line CNE2 by low dose interferon-γ (IFNγ) or by co-incubation with activated lymphocytes. Exposure to the milieu created by IDO-positive CNE2 cells did not promote lymphocyte death, but lymphocyte cytotoxicity against target tumor cells was impaired. The suppression of lymphocyte cytotoxic function was fully restored when the conditioned medium was replaced by fresh medium for 24 h. In additionally, the IDO-positive cells were found scattered in the tumor tissues from patients with NPC.</p> <p>Conclusion</p> <p>Altogether, these findings suggest that IDO-mediated immunosuppression may be involved in the tumor immune evasion, and that blocking IDO activity in tumor cells may help to re-establish an effective anti-tumor T cell response in NPC.</p

Frequency Diverse Array MIMO Radar Adaptive Beamforming with Range-Dependent Interference Suppression in Target Localization

Conventional multiple-input and multiple-output (MIMO) radar is a flexible technique which enjoys the advantages of phased-array radar without sacrificing its main advantages. However, due to its range-independent directivity, MIMO radar cannot mitigate nondesirable range-dependent interferences. In this paper, we propose a range-dependent interference suppression approach via frequency diverse array (FDA) MIMO radar, which offers a beamforming-based solution to suppress range-dependent interferences and thus yields much better DOA estimation performance than conventional MIMO radar. More importantly, the interferences located at the same angle but different ranges can be effectively suppressed by the range-dependent beamforming, which cannot be achieved by conventional MIMO radar. The beamforming performance as compared to conventional MIMO radar is examined by analyzing the signal-to-interference-plus-noise ratio (SINR). The Cramér-Rao lower bound (CRLB) is also derived. Numerical results show that the proposed method can efficiently suppress range-dependent interferences and identify range-dependent targets. It is particularly useful in suppressing the undesired strong interferences with equal angle of the desired targets