Colorimetric Signal Readout for the Detection of Volatile Organic Compounds Using a Printable Glass-Based Dielectric Barrier Discharge-Type Helium Plasma Detector.

In this paper, we report on a printable glass-based manufacturing method and a new proof-of-concept colorimetric signal readout scheme for a dielectric barrier discharge (DBD)-type helium plasma photoionization detector. The sensor consists of a millimeter-sized glass chamber manufactured using a printable glass suspension. Plasma inside the chip is generated using a custom-built power supply (900 V and 83.6 kHz), and the detector uses ∼5 W of power. Our new detection scheme is based on detecting the change in the color of plasma after the introduction of target gases. The change in color is first captured by a smartphone camera as a video output. The recorded video is then processed and converted to an image light intensity vs retention time plot (gas chromatogram) using three standard color space models (red, green, blue (RGB), hue, saturation, lightness (HSL), and hue, saturation, value (HSV)) with RGB performing the best among the three models. We successfully detected three different categories of volatile organic compounds using our new detection scheme and a 30-m-long gas chromatography column: (1) straight-chain alkanes (n-pentane, n-hexane, n-heptane, n-octane, and n-nonane), (2) aromatics (benzene, toluene, and ethylbenzene), and (3) polar compounds (acetone, ethanol, and dichloromethane). The best limit of detection of 10 ng was achieved for benzene at room temperature. Additionally, the device showed excellent performance for different types of sample mixtures consisting of three and five compounds. Our new detector readout method combined with our ability to print complex glass structures provides a new research avenue to analyze complex gas mixtures and their components.

Blood suPAR, Th1 and Th17 cell may serve as potential biomarkers for elderly sepsis management.

Although soluble urokinase plasminogen activator receptor (suPAR), T helper (Th)-1 and Th17 cells are separately reported to be dysregulated and correlate with disease severity in several infection-mediated diseases, fewer studies report their interaction and clinical value in sepsis management. Thus, this study aimed to investigate the correlation of blood suPAR with Th1 and Th17 cell proportion, as well as their diagnostic and prognostic value in elderly sepsis patients. Totally, 223 elderly sepsis patients were recruited. Serum suPAR was detected by enzyme-linked immunosorbent assay. Besides, Th1 and Th17 cell proportion from CD4+ T cells were determined by flow cytometry. For sepsis severity evaluation, Acute Physiology and Chronic Health Evaluation (APACHE) II score and the Sequential Organ Failure Assessment (SOFA) score were used. Moreover, survival profile within 28 days was documented. The mean value of suPAR, Th1 cell proportion and Th17 cell proportion was 27.5 ± 15.1 ng/mL, 15.3 ± 4.3% and 4.0 ± 2.3%, respectively. Furthermore, suPAR was positively correlated with Th1 cell proportion, Th17 cell proportion, IFN-γ, IL-17 and TNF-α. Meanwhile, suPAR was positively correlated with APACHE II score and SOFA score, so did Th17 cell proportion. Regarding their prognostic value, suPAR and Th17 cell proportion were superior to differ survivors from deaths than Th1 cell proportion. SuPAR positively correlates with Th1, Th17 cell proportion; and they correlate with increased disease severity and mortality risk in elderly sepsis patients.

Intelligent phase-transition MnO2 single-crystal shell enabling a high-capacity Li-rich layered cathode in Li-ion batteries.

Layered, Li-rich Mn-based oxides (LLMOs) are the most promising next-generation, high-energy batteries due to their relatively high specific capacities and high voltages. However, the practical application of LLMO cathodes is limited by low initial coulombic efficiencies (CEs) and poor cycling performance. Herein, we used the reaction of KMnO4 and MnSO4 under hydrothermal conditions to grow a nano-SCMO shell on the LLMO material surface (SCMO@LLMO). The unique particle/sheet compound structure of the SCMO shell is beneficial to the electrochemical reaction. SCMO has good Li storage characteristics and excellent surface structure stability in the single-crystal phase which further improves the reversible capacity, CE, and cyclic stability of the LLMO cathode. Therefore, the optimal coated sample (feedstock: 2 M KMnO4, SCMO@LLMO-2.0) exhibits a good initial discharge capacity (238.2 mA h g-1 at 1C and 173.8 mA h g-1 at 5C), initial CE (89.6% at 1C and 86.5% at 5C), and cycling performance (capacity retention of 84.67% at 1C and 62.72% at 5C after 200 cycles). This work adopts a hydrothermal method to synthesize a nano-single crystal composite material, laying a foundation for the preparation of the SCMO@LLMO cathodes for LLMO primary battery cathodes with high electrochemical performance.

LncRNA NKILA correlates with the malignant status and serves as a tumor-suppressive role in rectal cancer.

NF-κB interacting lncRNA (NKILA) has been found to function as a tumor-suppressive role in various human cancers. However, the role of NKILA in rectal cancer is still unknown. The objective of this study is to investigate the clinical value and biological function of NKILA in rectal cancer. The association between NKILA expression and clinical variables including prognosis was estimated in rectal cancer patients. The gain-of-function study of NKILA in rectal cancer cell was conducted to evaluate the effect of NKILA on cell proliferation, migration, invasion, and NF-κB signaling pathway. The results suggested NKILA expression was decreased in rectal cancer tissues and cells, and correlated with clinical stage, T classification, N classification and M classification. NKILA low-expression was an independent poor prognostic factor in rectal cancer patients. NKILA-inhibited rectal cancer cell proliferation, migration, and invasion via suppressing NF-κB signaling. In conclusion, NKILA serves as an antioncogenic lncRNA in rectal cancer.

Effect of long non-coding RNA Gas5 on proliferation, migration, invasion and apoptosis of colorectal cancer HT-29 cell line.

Objective: This study aims to investigate the effect of long non-coding RNA (lncRNA) Gas5 on proliferation, migration, invasion and apoptosis of colorectal cancer (CRC) HT-29 cell line. Methods: CRC and normal tissues were collected and prepared from a total of 126 CRC patients, and normal intestinal epithelial cell line FHC and CRC cell lines (HCT-8, HT-29, HCT-116 and SW-480) were prepared. Gas5 expression was detected by quantitative reverse transcriptase-polymerase chain reaction. HT-29 cell line exhibiting the lowest Gas5 expression was selected for further experimentation and divided into blank, negative control and pcNDA-Gas5 groups. The cell counting kit-8 assay was used to test cell proliferation. Flow cytometry was applied to examine cell apoptosis. Transwell assay was performed to detect the migration and invasion of HT-29 cells. The mRNA and protein expression of factors in the classical proliferation (Akt/Erk) and apoptosis (caspase-9/caspase-3) pathways were detected. Results: Gas5 expression was lower in CRC tissues compared to the adjacent normal tissues, and is also lower in CRC cell lines than FHC cell line. Gas5 expression was associated with tumor size and TNM staging. Gas5 expression, distant metastasis, tumor differentiation and TNM staging were independent CRC prognostic factors. The results showed that elevated Gas5 expression inhibited proliferation, migration and invasion, but promoted apoptosis of CRC cells. Meanwhile, elevated Gas5 expression inhibited mRNA expression of Akt and Erk and protein expression of p-Akt and p-Erk, which promoted Casp9 mRNA and pho-Casp9 protein expression but inhibited Casp3 mRNA and pho-Casp3 protein expression. Conclusion: The findings indicated that overexpression of lncRNA Gas5 can inhibit the proliferation, migration and invasion but promote apoptosis of CRC cells.

In vivo and in vitro effects of microRNA-124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway.

In this study, we aim to determine the function of miR-124 on gastric cancer (GC) cells and the underlying mechanism that involves jaddeg1 (JAG1) and the Notch signaling pathway. GC tissues and adjacent tissues from 100 patients suffering from GC were selected. GC SGC-7901 and AGS cells were selected and grouped into control, mimic-NC, miR-124 mimic, inhibitor-NC, miR-124 inhibitor, and miR-124 inhibitor + si-JAG1 groups. RT-qPCR and a Western blotting assay were conducted to detect the expression of miR-124, JAG1, and Notch signaling pathway-related proteins (NICD, HES1, and HES5). MTS, wound-healing, transwell assay and flow cytometry were performed to detect cell proliferation, migration, invasion, cell cycle distribution, and apoptosis, respectively. Compared with adjacent tissues, a lower miR-124 expression and higher JAG1 expression were found in GC tissues. JAG1 is a direct target gene of miR-124. Compared with the control group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR-124 mimic group were decreased, while the apoptosis rate was increased and cells were arrested at the G0/G1 phase. Compared with the miR-124 inhibitor group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR-124 inhibitor + si-JAG1 group were decreased, while the apoptosis rate and cell ratio at the G0/G1 phase were increased. The demonstration that miR-124 inhibits GC cell growth supports the concept that miR-124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch signaling pathway.

Possible prognostic significance of p53, cyclin D1 and Ki-67 in the second primary malignancy of patients with double primary malignancies.

Patients with two types of primary cancers are rare. In this study, we investigated the expression of p53, cyclin D1, and Ki-67 in the second primary malignancy. Tissue samples were obtained from the second primary cancer site of 43 patients who met the diagnostic criteria for double primary cancer. p53, cyclin D1 and Ki-67 were determined using immunohistochemistry. Categorical variables were compared using the Chi-squared test; correlation between data scores and histology was calculated using the Spearman's rank-order correlation. The expression rates of p53, cyclin D1 and Ki-67 in the second primary malignancy site were 60.5%, 30.2% and 65.1% respectively. p53 expression showed statistically significant association with tumor occurrence interval, pathological grading and nodal metastasis (p < 0.05). Positive correlation was detected between the expression of cyclin D1 and Ki-67 and the expression of p53 (r = 0.313, p = 0.041; r = 0.319, p = 0.037, respectively). High-expressing p53 or cyclin D second primary malignancies were associated with decreased overall survival (p = 0.040 and p = 0.043, respectively). Ki-67 expression levels did not exhibit statistically significant differences in survival. In conclusion, elevated protein expression of p53, cyclin D1 and Ki-67 in the second primary malignancy is an indicator of more aggressive malignant behavior of the secondary tumor. These markers may have prognostic value in the clinical setting.