Utility of serum chemokine-like factor 1 as a biomarker of severity and prognosis after severe traumatic brain injury: A prospective observational study.

BACKGROUND: Chemokine-like factor 1 (CKLF1) may be involved in the inflammatory response and secondary brain injury after severe traumatic brain injury (sTBI). We determined serum CKLF1 levels of sTBI patients to further investigate the correlation of CKLF1 levels with disease severity, functional prognosis, and 180-day mortality of sTBI. METHODS: Serum CKLF1 levels were measured at admission in 119 sTBI patients and at entry into study in 119 healthy controls. Serum CKLF levels of 50 patients were also quantified at days 1-3, 5, and 7 after admission. Glasgow coma scale (GCS) scores and Rotterdam computerized tomography (CT) classification were utilized to assess disease severity. Extended Glasgow outcome scale (GOSE) scores were recorded to evaluate function prognosis at 180 days after sTBI. Relations of serum CKLF1 levels to 180-day poor prognosis (GOSE scores of 1-4) and 180-day mortality were analyzed using univariate analysis, followed by multivariate analysis. Receiver-operating characteristic (ROC) curve was built to investigate prognostic predictive capability. RESULTS: Serum CKLF1 levels of sTBI patients increased at admission, peaked at day 2, and then gradually decreased; they were significantly higher during the 7 days after sTBI than in healthy controls. Differences of areas under ROC curve (areas under the curve [AUCs]) were not significant among the six time points. Multivariate analysis showed that serum CKLF1 levels were independently correlated with GCS scores, Rotterdam CT classification, and GOSE scores. Serum CKLF1 levels were significantly higher in non-survivors than in survivors and in poor prognosis patients than in good prognosis patients. Serum CKLF1 levels independently predicted 180-day poor prognosis and 180-day mortality, and had high 180-day prognosis and mortality predictive abilities, and their AUCs were similar to those of GCS scores and Rotterdam CT classification. Combination model containing serum CKLF1, GCS scores, and Rotterdam CT classification performed more efficiently than any of them alone in predicting mortality and poor prognosis. The models were visually described using nomograms, which were comparatively stable under calibration curve and were relatively of clinical benefit under decision curve. CONCLUSION: Serum CKLF1 levels are significantly associated with disease severity, poor 180-day prognosis, and 180-day mortality in sTBI patients. Hence, complement CKLF1 may serve as a potential prognostic biomarker of sTBI.

Evolution properties of a complex coherent square Gaussian-Schell-model beam in a uniaxial crystal orthogonal to the optical axis.

The analytical formulas for spectral density, degree of coherence, and effective beam widths of complex coherent square Gaussian-Schell-model (GSM) beams in a uniaxial crystal orthogonal to the optical axis are derived. Based on these analytical formulas, the evolution properties are investigated by a set of numerical examples. It is demonstrated that the complex coherent square GSM beams spread at different rates in the directions parallel and orthogonal to the optical axis due to the anisotropic crystal, but the self-shift effect of the light field is almost unaffected by the fact that the uniaxial crystal is anisotropic. The effect of anisotropy of the uniaxial crystal on the effective width of the beam in the x direction and that in the y direction is completely opposite. The results provide a way for the modulation of the complex coherent square GSM beams and enrich the propagation theory of uniaxial crystal.

Myricetin exhibits anti-glioma potential by inducing mitochondrial-mediated apoptosis, cell cycle arrest, inhibition of cell migration and ROS generation.

The Editors of JBUON issue an Expression of Concern to 'Myricetin exhibits anti-glioma potential by inducing mitochondrial-mediated apoptosis, cell cycle arrest, inhibition of cell migration and ROS generation', by Hu-Guang Li, Jun-Xia Chen, Jun-Hui Xiong, Jin-Wei Zhu, JBUON 2016;21(1):182-190; PMID:27061547. Following the publication of the above article, readers drew to our attention that part of the data was possibly unreliable. We sent emails to the authors with a request to provide the raw data to prove the originality, but received no reply. Therefore, as we continue to work through the issues raised, we advise readers to interpret the information presented in the article with due caution. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

Myricetin exhibits anti-glioma potential by inducing mitochondrial-mediated apoptosis, cell cycle arrest, inhibition of cell migration and ROS generation.

PURPOSE: To study the antiproliferative effects of myricetin in human glioma U251 cells together with assessing its effects on cell cycle, apoptosis, apoptosis-related proteins, reactive oxygen species (ROS) generation and cell migration. METHODS: Cell viability of human glioma cells after myricetin treatment was assessed by MTT assay. Phase-contrast and confocal fluorescence microscopies were used to assess the morphological changes that occured in these cells following myricetin treatment. Flow cytometry using propidium iodide (PI) and Annexin-V FITC as probes was employed to evaluate the effects on cell cycle arrest and apoptosis induction, respectively. The effect of myricetin on intracellular ROS production was measured by flow cytometry with a fluorescent probe CM-DCFH2-DA. RESULTS: Myricetin induced a dose-dependent as well as time-dependent growth inhibitory effect in U251 human glioma cells. Myricetin treatment resulted in U251 cells detachment from adjacent cells making clusters of cells floating in the medium. Detached cells had irregular shape and incapable to maintain their membranes intact. Apoptotic cell death was induced by myricetin treatment as witnessed by fluorescence microscopy. The percentage of early and late apoptotic cells increased from 0.41% and 8.2% to 23.1% and 10.2%, 25.2% and 19.4%, to finally 36.2% and 28.4% after treatment with 15 µM, 60 µM and 120 µM of myricetin, respectively. We also observed a dose-dependent increase in Bax and Bad levels and a dose-dependent decrease in Bcl-2 and Bcl-xl expression levels following myricetin treatment. Cell cycle arrest in G2/M phase of the cell cycle was also induced by the drug treatment. A concentration-dependent ROS generation was also witnessed and a 3-fold increase of ROS production was seen after 60 µM myricetin treatment. CONCLUSION: Myricetin exerts anticancer effects in U251 human glioma cells by inducing mitochondrial-mediated apoptosis, G2/M phase cell cycle arrest, ROS generation and inhibition of cell migration.