Solvent-driven luminescence modulation/switching in an iridium(iii) complex containing an aldehyde group.

Complex [Ir(dfppy)2(phca)]PF6 (1) has been synthesized, which contains an aldehyde group in the N^N ligand phca = 1,10-phenanthroline-4-carbaldehyde, with the aim of exploring solvent-driven luminescence modulation/switching in this complex. Complex 1 shows green emission at 514 nm in CH3OH, while orange phosphorescence with the emissions at 516 and 624 nm in CH2Cl2. The solid-state structure of 1 is dependent on the crystallization solvent used, forming a red solid 1R in CH2Cl2, while a yellow solid 1Y in CHCl3. The neighboring [Ir(dfppy)2(phca)]+ cations in solid 1R are held together by ππ stacking interactions, while by van der Waals interactions in solid 1Y. The distinct packing structures of 1R and 1Y lead to their significantly different solid-state luminescence, weak orange phosphorescence for 1R (emission at 620 nm, Φ = 3.3%) and strong yellow phosphorescence for 1Y (emissions at 532 and 558 nm, Φ = 46.6%). Both 1R and 1Y show CH2Cl2/CHCl3-driven phosphorescence switching between orange and yellow, due to their structural interconversion through recrystallization. Moreover, the emission color of 1Y can be reversibly switched between yellow and orange through alternate pressing and recrystallization in CHCl3. This work discusses the relationship among the solvent, the structure and the luminescence modulation/switching of complex 1.

Improvement of sensitive and specific detection of circulating tumor cells using negative enrichment and immunostaining-FISH.

BACKGROUND: Circulating tumor cells (CTCs) provide an opportunity to obtain pivotal biological information required for the development of personalized medicine. However, the current assays of CTCs' detection face serious challenges regarding specificity and sensitivity. METHODS: In this study, we developed a novel strategy that combined negative enrichment (NE), immunocytochemistry CD45 staining and fluorescence in situ hybridization (FISH) to identify, enumerate and characterize CTCs. CTCs were identified as DAPI+/CD45-/Chromosome multiploid. The assay was evaluated with different cancer cell lines including lung, breast, esophageal and gastric cancer. And then, the developed assay was applied in cancer patients to explore the possibility of clinical application and whether CTC number was related to clinicopathological factors. RESULTS: The average recover rate of esophageal cancer cell line Eca-109 using negative enrichment was higher than 80% and the multiploid cells rate of four cancer cell lines were >96%, which demonstrate the NE-FISH platform is favorable for CTCs detection. CTCs count was significantly higher in lung cancer patients than healthy controls and benign lung disease with an area under ROC curve of 0.905 (95% confidence interval 0.866-0.944, P < .001). Using a cutoff value of 2 CTCs, the positive rate of detecting lung, gastric, breast and esophageal cancer patients were 71.33%, 86.21%, 76.77% and 78.35%, respectively. Besides, CTCs could be detected in stage I with the positive rate of 64.15% for lung cancer, 83.33% for gastric cancer, 78.95% for breast cancer and 68.18% for esophageal cancer, which may promote the early diagnose and influence the treatment decision for better management of those cancer in clinic. CONCLUSIONS: Our study showed that CTCs could be detected in diverse cancers using the novel NE-FISH platform with high sensitivity and specificity. Therefore, analysis of CTCs with NE-FISH has a clear potential to improve the management of cancer patients in clinical use.

Celastrol inhibits migration and invasion through blocking the NF-κB pathway in ovarian cancer cells.

Metastatic ovarian cancer is a major clinical challenge with poor prognosis and high mortality. Celastrol is a natural compound that has exhibits antiproliferative activity; however, its effects on metastasis-related phenotypes in ovarian cancer models are unclear. In the current study, the anti-invasive activities and associated signaling pathways of celastrol were determined in ovarian cancer cells. Cell proliferation was tested by MTT assay. Cell migration was detected by wound healing and Transwell assays, while cell invasion was detected by a Matrigel-coated Transwell method. In addition, nuclear factor (NF)-κB and matrix metalloproteinase (MMP) expression was examined by western blotting, and MMP-2/-9 activities were determined by gelatin zymography. At sub-toxic concentrations (<0.5 µM), celastrol inhibited migration and invasion in a concentration-dependent manner in SKOV-3 and OVCAR-3 cells. At the molecular level, celastrol blocked the canonical NF-κB pathway by inhibiting IκBα phosphorylation, and preventing IκBα degradation and p65 accumulation. Furthermore, the expression and activity of the NF-κB target protein MMP-9, but not MMP-2, were inhibited by celastrol. Furthermore, celastrol showed no synergistic effect with MG132, an NF-κB inhibitor. In conclusion, celastrol exhibited significant anti-invasive activities in ovarian cancer cells. Such functions may be mediated via NF-κB pathway blockade. The results of this in vitro study strengthen the value of applying celastrol as a potential clinical intervention modality for delaying ovarian cancer metastasis. This, celastrol warrants further preclinical investigation.

Quality of sperm obtained by penile vibratory stimulation and percutaneous vasal sperm aspiration in men with spinal cord injury.

The aim of this study was to explore sperm chromosomal aneuploidy and DNA integrity in infertile patients with spinal cord injury (SCI). Semen samples were collected from 12 infertile men with SCI by percutaneous vasal sperm aspiration (PVSA) and from 14 male SCI patients by penile vibratory stimulation (PVS). These semen samples as well as samples from 16 donors were analyzed using the hypo-osmotic swelling (HOS) test, the sperm chromatin dispersion test, terminal deoxynucleotidyl transferase-mediated terminal uridine nick-end labeling assay, and multicolor fluorescence in situ hybridization with probes specific for the chromosomes 13, 18, 21, X, and Y. There were significant differences in the percentages of motile sperm, normal morphologic sperm, normal HOS/eosin staining, and sperm DNA fragmentation between the infertile men with SCI and the control group (P < .05 and P < .01). The sperm forward motility was significantly greater in the PVSA group than in the PVS group (P < .01). The number of round cells per milliliter of semen obtained from the 14 SCI patients by PVS was between 1 million and 12 million. The rate of sperm DNA fragmentation, as identified by the sperm chromatin dispersion test, was higher in the PVS group than in the PVSA group (P < .05). The aneuploidy rates for the SCI patients were 1.5- to 1.6-fold higher for chromosomes 13, 18, and 21, and were 2.3- to 2.4-fold higher for chromosomes X and Y than for patients in the control group (P < .001). These results suggest that for men with SCI, the semen quality is poorer, the prevalence of abnormal HOS/eosin staining is greater, and sperm DNA fragmentation and sperm chromosomal aneuploidies are seen at a higher rate compared with healthy, fertile, and normospermic men.