Spectrally tunable near-infrared photoluminescence in MP3O9:Cr3+ (M = Al, Ga, In) phosphate phosphors.

Modulation of the octahedral crystal field environment of Cr3+ is an effective approach to achieve tunable emission. Here, we prepared a series of broadband MP3O9:Cr3+ (M = Al, Ga, In) near-infrared (NIR) phosphors, and cubic AlP3O9:Cr3+ (APO-c:Cr3+) and monoclinic AlP3O9:Cr3+ (APO-m:Cr3+) phosphors were prepared by controlling the synthesis temperature. The emission wavelength was tuned from 787 nm for APO-c:Cr3+ to 894 nm for monoclinic InP3O9:Cr3+ (IPO:Cr3+) by regulating the M ion and reducing the crystal field intensity. Excitingly, the MP3O9:Cr3+ (M = Al, Ga, In) family shows excellent thermal stability; the emission intensity of APO-c:Cr3+, APO-m:Cr3+ and monoclinic GaP3O9:Cr3+ (GPO:Cr3+) can still maintain 95.6%, 86% and 86% of that at room temperature when heating to 423 K, respectively. An NIR LED device was prepared by incorporating GPO:Cr3+ and a blue light LED, demonstrating the potential application in night vision and non-destructive testing.

An efficient and thermally stable Cr3+-activated Y2GdSc2Al2GaO12 garnet phosphor for NIR spectroscopy applications.

Near-infrared (NIR) spectroscopy realized by an NIR phosphor-converted light-emitting diode (pc-LED) as a light source has aroused considerable interest due to its numerous merits and widespread application scenarios. Nevertheless, developing NIR emitting phosphors with high performance is still the top priority. Here, we report a new Y2GdSc2Al2GaO12:Cr3+ (YGSAG:Cr3+) garnet phosphor, which demonstrates a broadband emission peaking at 754 nm with a full width at half maximum (FWHM) of around 120 nm in the range of 650-1200 nm. The YGSAG:0.08Cr3+ sample irradiated by blue light exhibits the most intense emission intensity, leading to a high absorption efficiency of 49.54%. In addition, compared with room temperature, the integrated PL intensity of the sample can still be maintained at 90.97% at 423 K. Benefitting from the outstanding optical properties, the as-manufactured NIR pc-LED device driven by a 100 mA current represents a high NIR output power of 35.14 mW and a photoelectric efficiency of 12.51%. These results verify that the as-synthesized YGSAG:Cr3+ phosphor possesses great potential for the applications of NIR spectroscopy.

Broadband Near-Infrared Luminescence in Garnet Y3Ga3MgSiO12: Cr3+ Phosphors.

Broadband near-infrared (NIR) phosphors are the critical component of phosphor converted NIR light-emitting diode (LED) light sources. However, there are still a lack of NIR phosphors with excellent external quantum efficiency (EQE) and thermal stability. Here, we report a highly efficient broadband NIR phosphor Y3Ga3MgSiO12: Cr3+. The optimized phosphor yields an internal quantum efficiency (IQE) and an EQE of 79.9 and 33.7%, respectively. The integrated emission intensity still remains at 84.4% of that at room temperature when heated to 423 K. A broadband NIR LED lamp was made by combining as-prepared phosphor and a blue InGaN LED chip, which shows an output power of 89.8 mW with a photoelectric conversion efficiency of 17.1% driven at 525 mW input power. Our research provides a promising NIR phosphor with high efficiency broadband for the NIR light source.

Transcellular Transport Behavior of the Intact Polymeric Mixed Micelles with Different Polymeric Ratios.

In order to better promote the application of the polymeric mixed micelles (PMMs) in oral delivery, in addition to focusing on the improvement of micellar structural stability, it is necessary to obtain the absorption characteristics of the intact micellar particles. In this work, the transport behavior across Caco-2 cells of FS/PMMs composed of Pluronic F127 and Solutol HS15 was tracked by encapsulating an environment-responsive probe into the particles. The specific property of the probe is the water-initiated aggregation-caused quenching (ACQ) ability, by which integral particles can be identified accurately. The influence of polymeric ratios (FS) on the transcellular behavior of FS/PMMs was explored and the single pass intestinal perfusion experiment was used to further illustrate it. Moreover, pharmacokinetics parameters were detected to analyze the relationship among FS ratios, transport behavior, and pharmacokinetic parameters. FS ratios were found to hardly affect the endocytosis pathways and intracellular itinerary of FS/PMMs, but do affect the proportion of each path. FS/PMMs with high HS15 content, namely System-I, were found to primarily undergo receptor-mediated endocytosis pathway and be less susceptible to lysosomal degradation, which would lead to more absorption and higher Cmax and AUC than drug suspension. In contrast, despite System-II with high F127 content cannot contribute to drug plasma concentration, it can prolong the in vivo retention time. These findings provided evidence for the role of polymeric ratios in modulating the transcellular absorption and pharmacokinetic parameters of the drug-loaded PMMs, and would be a step forward in helping PMMs' design to enhance oral drug delivery.

Long-chain saturated fatty acids and its interaction with insulin resistance and the risk of nonalcoholic fatty liver disease in type 2 diabetes in Chinese.

Introduction: This study aimed to explore relationships between long-chain saturated fatty acids (LSFAs) and nonalcoholic fatty liver disease (NAFLD) in patients with type 2 diabetes (T2D); and whether insulin action had an interactive effect with LSFAs on NAFLD progression. Methods: From April 2018 to April 2019, we extracted the electronic medical records of 481 patients with T2D who meet the inclusion and exclusion criteria from the Second Affiliated Hospital of Dalian Medical University. Ultrasound was used to estimate NAFLD at admission. Logistic regression analysis were used to estimate odds ratios (OR) and 95% confidence intervals (CI). The additive interaction was carried out to estimate interactions between LSFAs and insulin resistance (IR) in NAFLD patients with T2D. Results: Myristic acid (14:0) and palmitic acid (16:0) were positively associated with the risk of NAFLD (OR for myristic acid (14:0): 7.516, 3.557-15.882 and OR for palmitic acid (16:0): 4.071, 1.987-8.343, respectively). After adjustment for traditional risk factors, these associations were slightly attenuated but still highly significant. Co-presence of myristic acid (14:0)>72.83 µmol/L and IR>4.89 greatly increased OR of NAFLD to 9.691 (4.113-22.833). Similarly, co-presence of palmitic acid (16:0)>3745.43µmol/L and IR>4.89 greatly increased OR of NAFLD to 6.518(2.860-14.854). However, stearic acid (18:0) and risk of NAFLD have no association. Moreover, there was no association between very-long-chain SFAs (VLSFAs) and risk of NAFLD. Discussion: Myristic acid (14:0) and palmitic acid (16:0) were positively associated with the risk of NAFLD in T2D patients in China. High IR amplified the effect of high myristic acid (14:0) and high palmitic acid (16:0) on NAFLD.

Rapid Discovery of Efficient Long-Wavelength Emission Garnet:Cr NIR Phosphors via Multi-Objective Optimization.

High-efficiency long-wavelength emission near-infrared (NIR) phosphors are the key to next-generation LED light sources. However, high-efficiency phosphors usually exhibit narrow-band emission at shorter wavelengths due to the crystal field intensity. In this paper, we utilize multi-objective optimization to discover the NIR phosphor Gd3Mg0.5Al1.5Ga2.5Ge0.5O12:0.04Cr3+. It exhibits a broadband NIR emission from 650 to 1100 nm peaking at 763 nm, with a full width at half maximum (FWHM) of 150 nm, an internal quantum efficiency (IQE)/external quantum efficiency (EQE) of 90%/53.1%, and good thermal stability (85.3% @ 150 °C). The packaging results show that ∼53.2 mW of output power is achieved at 915 mW input power, which suggests promising applications for NIR pc-LED. Our approach is based on the data of emission wavelength (WL) and IQE for garnet:Cr NIR phosphors to construct machine learning models. An active learning strategy is used to make tradeoffs between WL and IQE, and we are able to find the targeted phosphor after only four iterations of synthesis and characterization.

Efficient degradation of Rhodamine B in water by CoFe2O4/H2O2 and CoFe2O4/PMS systems: A comparative study.

In this work, a comparative study of efficient degradation of Rhodamine B (RhB) in CoFe2O4/H2O2 and CoFe2O4/PMS systems was performed. Batch experiments indicated that the RhB degradation rate of CoFe2O4/H2O2 system reached 95.5% at 90 min under the condition of 0.5 g L-1 of CoFe2O4 dosage, 10 mM of H2O2 concentration and 3.0 of initial pH. At certain conditions of initial pH = 7.0, 0.3 g L-1 of CoFe2O4 dosage, 7 mM of PMS concentration, CoFe2O4/PMS system could completely degrade RhB within 90 min. EPR and quenching experiments indicated that •OH was the main active species of CoFe2O4/H2O2 system, and •OH, SO4•-, •O2- and 1O2 participated in RhB degradation of CoFe2O4/PMS system. The circulate of Co(II)/Co(III) and Fe(II)/Fe(III) on the CoFe2O4 surface promoted the formation of free radical species in the two system. In CoFe2O4/PMS system, the formed •O2- and SO5•- realized the generation of non-free radical species (1O2). The LC-MS results indicated that N-de-ethylation, chromophore cleavage, opening rings and mineralization were the main steps for the RhB degradation of the two systems. After five cycles of degradation experiment, the CoFe2O4/H2O2 and CoFe2O4/PMS systems still maintained the high degradation rate (85.2% and 92.4%) and low mass loss (2.7% and 3.09%). In addition, CoFe2O4/PMS system had better potential value for the actual water and multi-pollutant degradation than CoFe2O4/H2O2 system. Finally, the toxicity analysis and cost assessment of the two oxidation systems were preliminarily evaluated.

Use of Eggshell-Catalyzed Biochar Adsorbents for Pb Removal from Aqueous Solution.

Eggshell is a cheap and environmentally friendly calcium source. In this study, Ca-modified biochar adsorbents (CEA) were prepared by 1:10, 1:2, and 1:1 mass ratio of the eggshell and Eupatorium adenophorum. The CEA-2 sample prepared with a 1:2 mass ratio showed a maximum Pb adsorption capacity (97.74 mg·g-1) at the conditions of an initial pH of 7.0, an adsorbent dosage of 0.5 g·L-1, and a contact time of 8.0 h. The kinetic and isotherm studies indicated that the adsorption process of the CEA-2 sample had monolayer adsorption characteristics, which was controlled together by intraparticle and interface diffusion. Thermodynamic studies indicated that the adsorption process of CEA-2 was spontaneous (ΔG 0 <0) and endothermic (ΔH 0 > 0). X-ray diffraction and scanning electron microscopy analyses showed a uniform distribution of Ca-Pb precipitation on the CEA-2 surface, which proved that chemical precipitation was the main adsorption mechanism. Fourier transform infrared spectra found that CEA-2 had abundant active groups, especially nitrogen-containing functional groups, which could adsorb Pb through a surface complexation reaction. The Brunauer-Emmett-Teller surface area of CEA-2 was found to be 621 m2·g-1, and such developed pores could ensure the smooth diffusion of Pb. Finally, the effect of coexisting cation and anion experiment and the cyclic regeneration experiment indicated that CEA-2 had prominent stability and reusability for Pb adsorption.

Multiobjective Machine Learning-Assisted Discovery of a Novel Cyan-Green Garnet: Ce Phosphors with Excellent Thermal Stability.

Ce-doped garnet phosphors play an important role in the white light-emitting diode (LED) family. In the past years, a lot of trial-and-error experiments guided by experience to discover phosphors suitable for white LEDs have been presented. The working temperature of phosphors may reach 200 °C in white LEDs, and so, the exploration of phosphors with excellent thermal stability at the desired wavelength continues to be a challenge. In the present study, to discover novel cyan-green garnet:Ce phosphors, wavelength and thermal stability machine learning models were built by constructing reasonable features. Among the 171,636 compounds with garnet structures predicted by our models, 25 samples were selected for preparation and characterization by multiobjective optimization based on active learning. Lu1.5Sr1.5Al3.5Si1.5O12:Ce performed the best with excellent thermal stability (≥60% emission intensity was retained at 640 K) and exhibited emission peaks of about 505 nm, and it is a very promising phosphor for future applications, especially in high-temperature operating environments.

Long Non-Coding RNA LINC00511 Accelerates Proliferation and Invasion in Cervical Cancer Through Targeting miR-324-5p/DRAM1 Axis.

PURPOSE: Cervical cancer is the second most prevalent female malignance, and human papillomavirus (HPV) infection is the main pathogenic factor of cervical cancer. Emerging evidence has revealed that a number of long non-coding RNAs (lncRNAs) play critical roles in the tumorigenesis and progression of cervical cancer. The aim of this study was to further investigate the precise role of lncRNA LINC00511 in HPV-negative and HPV-positive cervical cancer cells and explore the potential regulatory mechanism. METHODS: The expression of LINC00511 in cervical cancer and cell lines was examined by RT-PCR. Fluorescence in situ hybridization analysis (FISH) assay was performed to detect the localization of LINC00511 in cervical cancer cells. Loss-of-function experiments of LINC00511 by siRNA interference were performed to assess its effects on HPV-negative and HPV-positive cervical cancer cells. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were used to identify the target of LINC00511. Relative expression of related proteins was detected using Western blot. RESULTS: Herein, the results showed that LINC00511 was significantly up-regulated in cervical cancer and cell lines and mainly distributed in the cytoplasm of cervical cancer cells. Loss-of-function experiments indicated that silencing of LINC00511 inhibited the proliferation and invasion of both HPV-negative and HPV-positive cervical cancer cells, as well as promoted apoptosis by regulating the Bcl-2/Bax axis and Caspase 3 activation. Bioinformatic analysis, dual-luciferase reporter, and RIP assays showed that LINC00511 was a target of miR-324-5p, while DRAM1 was a direct target of miR-324-5p. The expression of miR-324-5p was down-regulated in cervical cancer, while the expression of DRAM1 was up-regulated. Moreover, the expression of LINC00511 was negatively correlated with miR-324-5p expression in cervical cancer tissues and positively correlated with DRAM1. Further, DRAM1 overexpression promoted both HPV-negative and HPV-positive cervical cancer cell proliferation and invasion, which could be reversed by miR-324-5p mimics or si-LINC00511. CONCLUSION: Collectively, these results suggest that LINC00511 functions as a competing endogenous RNA (ceRNA) to regulate the miR-324-5p/DRAM1 axis, leading to HPV-negative and HPV-positive cervical cancer aggravation.

KIF2A promotes the progression via AKT signaling pathway and is upregulated by transcription factor ETV4 in human gastric cancer.

Kinesin family protein 2A (KIF2A), an M-type nonmotile microtubule depolymerase, plays essential roles in development and progression of various human cancers. However, its exact function and the underlying mechanism in tumorigenesis of gastric cancer (GC) haven't been fully elucidated. In the present study, KIF2A was overexpressed in human GC and predicted poor prognosis according to the results of GEPIA analysis. KIF2A was also observed to be upregulated in 82 GC samples compared with paired pericarcinoma tissues. Its overexpression was associated with tumor metastasis (P = 0.047) and Ⅲ stage GC (P = 0.0267). The mRNA and protein expression levels of KIF2A were significantly suppressed in KIF2A specific siRNA transfected GC cells compared with the wild-type and negative control (NC) siRNA transfected cells. Furthermore, the effects of KIF2A on the growth, migration, invasion, and apoptosis of GC cell were evaluated in vitro and the underlying mechanisms were explored. It was found that silencing KIF2A effectively induced the apoptosis, and inhibited the proliferation, migration and invasion capacities of GC cells. Western blot analysis demonstrated that silencing of KIF2A significantly decreased the expression levels of AKT, Cyclin D1 and S6K. Moreover, bioinformatics analysis showed that the promoter (from -414 to -407bp) of KIF2A has the ability to bind to transcription factor ETV4, which was confirmed by bi-luciferase reporter assay using 293T cells. The level of ETV4 was upregulated and positively correlated with KIF2A in human GC tissues. Our results also proved that ETV4 upregulated the expression of KIF2A and blocked the decline of proliferation induced by KIF2A knockdown in MKN-45 and AGS cells. In summary, KIF2A is upregulated by transcription factor ETV4, and its knockdown can effectively inhibit the proliferation and induce the apoptosis of GC cells through the AKT signaling pathway in GC cells, implying that the inhibition of KIF2A expression is a potential target for GC therapy.

MiR-193b-5p inhibits proliferation and enhances radio-sensitivity by downregulating the AKT/mTOR signaling pathway in tongue cancer.

BACKGROUND: MicroRNAs (miRNAs) have been found to have functions regulating cell proliferation, differentiation and apoptosis, thereby regulating the occurrence, development and prognosis of tumors. MiR-193b-3p is well-known for its tumorigenic effect, but there are few studies on miR-193b-5p, and its role in tongue cancer has not been reported. METHODS: In the present research, we investigated the specific role of miR-193b-5p in tongue cancer. MiR-193b-5p mimics were transfected into tongue cancer cell lines CAL27 and TCA-8113 to generate miR-193b-5p overexpression cells. CCK-8, clonogenic assay, wound healing assay, transwell and flow cytometry analysis were performed to detect cell proliferation, migration, invasion and apoptosis. RESULTS: Our data showed that the exogenous overexpression of miR-193b-5p blocked the proliferation, inhibited the phosphorylation of AKT and mTOR, and downregulated the levels of Cyclin D1 and P70 of CAL27 and TCA-8113 cells. We predicted that miR-193b-5p suppressed the proliferation of cancer cells by inhibiting the AKT/mTOR pathway. MiR-193b-5p mimics also induced the apoptosis of CAL27 and TCA-8113 cells by inhibiting the expression of Bcl2 and promoting the levels of Active-Caspase3 and Bax. Furthermore, a marked decline in the migration and invasiveness of tongue cancer cells transected with miR-193b-5p mimics was observed. According to the results of western blot, miR-193b-5p downregulated the levels of the epithelial-to-mesenchymal transition (EMT) markers, including N-cad, Vimentin, Snail and Slug, while upregulating E-cad expression level in CAL27 and TCA-8113 cells, suggesting that miR-193b-5p inhibited the migration and invasion by reversing the EMT process. In addition, miR-193b-5p mimics inhibited the formation of clonogenic colonies of CAL27 and TCA-8113 cells after irradiation. CONCLUSIONS: Taken together, miR-193b-5p mimics block cell proliferation, migration and invasion and induce apoptosis by inhibiting the AKT/mTOR signaling pathway; they also reversed EMT progression and inhibited the radio-resistance of tongue cancer cells. Our results provide a potential target for the clinical treatment of human tongue cancer.

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study.

BACKGROUND/AIMS: The roles of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in peri-implantitis are unclear. Here, we used a canine model of peri-implantitis to explore the effects of inhibiting NF-κB with pyrrolidine dithiocarbamate (PDTC) on the inflammatory response in ligature-induced peri-implantitis. METHODS: After successfully establishing the peri-implantitis model, beagles were randomly assigned to normal, model or PDTC groups. ELISA tests were used to determine the levels of interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). Immunohistochemistry was employed to assess the expression of NF-κB p65. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the mRNA levels of TLR4 and NF-κB p65, and western blot analysis was used to measure the protein levels of TLR4 in periodontal tissues from each group. Periodontal ligament fibroblasts (PDLFs) were cultured and subsequently classified into PDLF normal, PDLF model, PDLF LPS, PDLF PDTC, and PDLF LPS + PDTC groups. An immunofluorescence assay was used to measure the expression level of NF-κB p65. The CCK-8 assay and flow cytometry were performed to evaluate cell proliferation and apoptosis. RESULTS: The in vitro results indicated that NF-κB p65 and TLR4 were upregulated in canine periodontal tissues, and PDTC could suppress the expression levels of NF-κB p65 and TLR4. Inflammation could increase TLR4 protein expression in canine periodontal tissue, and PDTC could inhibit the inflammation-induced increase in TLR4 protein expression. These results revealed that PDTC could reverse the LPS-induced increases in the levels of IL-1, IL-6, IL-8 and TNF-α. In vivo, the results demonstrated that PDTC inhibited the LPS-induced NF-κB p65 upregulation, and PDTC could reverse the inhibitory effect of the PDLF model + LPS on the proliferation of periodontal fibroblasts. The results also showed that in the PDLF model, LPS promoted PDLF apoptosis by inducing implant periodontitis in canines, but PDTC inhibited the PDLF apoptosis and relieved implant periodontitis in canines. CONCLUSION: Based on our results, we concluded that PDTC can inhibit the expression of NF-κB and alleviate the inflammatory response induced by LPS, thereby preventing periodontal inflammation and reducing the development of peri-implantitis.

Downregulation of MicroRNA-330 Correlates with the Radiation Sensitivity and Prognosis of Patients with Brain Metastasis from Lung Cancer.

BACKGROUND: The present study sought to explore the role of microRNA-330 (miR-330) in predicting the radiation response and prognosis of patients with brain metastasis (BM) from lung cancer (LC). METHODS: Patients with BM from LC were identified and classified into radiation-sensitive and radiation-resistant groups according to the overall survival rate, local and distant recurrence rate after conventional whole-brain radiation therapy. Quantitative realtime polymerase chain reaction (qRT-PCR) was used to detect miR-330 expression in serum. Receiver operating characteristic (ROC) curves were used to evaluate the prognostic value of miR-330 for the radiation sensitivity of brain metastasis from LC. Related clinical factors for radiation sensitivity were assessed by logistic regression analysis, and a survival analysis was conducted using COX regression and the Kaplan-Meier method. RESULTS: MiR-330 exhibited lower expression in the radiation-sensitive group than in the radiation-resistant group. The area under the ROC curve of miR-330 for predicting radiation sensitivity was 0.898 (optimal cut-off value, 0.815), with a sensitivity of 71.7% and a specificity of 90.1%. After radiation therapy, patients with low miR-330 expression, compared to patients with high miR-330 expression, displayed a lower survival rate and a median survival time. MiR-330 expression was correlated with extracranial metastasis, maximum BM diameter, tumor-node-metastasis (TNM) stage and node (N) stage. Logistic regression and COX regression analyses revealed that extracranial metastasis, TNM stage, N stage and miR-330 expression were factors that influenced both radiation sensitivity and individual prognostic factors in patients with BM from LC. CONCLUSIONS: These findings indicate that the downregulation of miR-330 correlates with radiation sensitivity and poor prognosis in patients with BM from LC.

Role of microRNA-21 in radiosensitivity in non-small cell lung cancer cells by targeting PDCD4 gene.

This study aims to explore the effects of microRNA-21 (miR-21) on radiosensitivity in non-small cell lung cancer (NSCLC) by targeting programmed cell deanth 4 (PDCD4) and regulating PI3K/AKT/mTOR signaling pathway. Cancer tissues and adjacent normal tissues were collected from 97 NSCLC patients who received a standard radiotherapy regimen. TUNEL assay was applied to determine cell apoptosis in tissues. The qRT-PCR assay was used to detect the expressions of miR-21 expression and PDCD4 mRNA. The protein expressions of PDCD4 and PI3K/AKT/mTOR signaling pathway-related proteins were determined by Western blotting. Colony formation assay was used to observe the sensitivity to radiotherapy of NSCLC cells. Flow cytometry was adopted to testify cell apoptosis. Compared with adjacent normal tissues, miR-21 expression was significantly increased and the mRNA and protein expressions of PDCD4 were decreased in NSCLC tissues. Higher miR-21 expression was associated with attenuated radiation efficacy and shorter median survival time. PDCD4 was the target gene of miR-21. The miR-21 mimics and siRNA-PDCD4 decreased the sensitivity to radiotherapy and cell apoptosis of A549 and H1299 cells and activated PI3K/AKT/mTOR pathway. The sensitivity of A549 and H1299 cells was strengthened in the miR-21 inhibitors group and the PI3K/AKT/mTOR inhibitors group. The siRNA-PDCD4 could reverse the effects of miR-21 inhibitors on sensitivity to radiotherapy and cell apoptosis of NSCLC cells. Our findings provide strong evidence that miR-21 could inhibit PDCD4 expression and activate PI3K/AKT/mTOR signaling pathway, thereby affecting the radiation sensitivity of NSCLC cells.

Up-Regulation of MicroRNA-133a Inhibits the MEK/ERK Signaling Pathway to Promote Cell Apoptosis and Enhance Radio-Sensitivity by Targeting EGFR in Esophageal Cancer In Vivo and In Vitro.

This study aims to explore how microRNA-133a (miR-133a) affects cell apoptosis and radio-sensitivity by targeting EGFR via regulating MEK/ERK pathway in esophageal cancer (EC). A total of 358 EC patients were selected and assigned into the resistant and sensitive groups. Human EC KYSE 150 cell line was assigned into the blank, negative control (NC), miR-133a mimic, miR-133a inhibitors, si-EGFR, miR-133a inhibitors + si-EGFR groups after transfection. MiR-133a and EGFR mRNA expressions were detected by qRT-PCR and EGFR, MEK/ERK pathway-related protein expressions were detected by Western blotting. The radio-sensitivity and cell apoptosis were testified by clone formation and flow cytometry. MiR-133a was up-regulated but EGFR was down-regulated in the sensitive group than in the resistant group. Compared with the blank and NC groups, the miR-133a mimic and si-EGFR groups exhibited increased cell apoptosis rate but decreased EGFR, p-MEK1/2, and p-ERK1/2 protein expressions; while opposite trend was observed in the miR-133a inhibitors group. Compared with the miR-133a inhibitors group, the miR-133a inhibitors + si-EGFR group presented reduced cell survival rate, EGFR, p-MEK1/2, and p-ERK1/2 protein expressions but increased cell apoptosis rate. These results indicated that miR-133a could inhibit the MEK/ERK pathway to promote cell apoptosis and enhance radio-sensitivity by targeting EGFR in EC. J. Cell. Biochem. 118: 2625-2634, 2017. © 2017 Wiley Periodicals, Inc.

The impact of smoking on levels of chronic periodontitis-associated biomarkers.

OBJECTIVE: To investigate the effect of smoking on the expression levels of matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and the concentrations of TNF-α and IL-10 in patients with chronic periodontitis (ChP). METHODS: This is an ex-vivo study. Our study consisted of 78 cases, all of which were diagnosed with ChP and were selected according to the inclusion and exclusion criteria. Among these 78 cases, 38 patients were classified into the smoking group (S-ChP group), and 40 patients in the non-smoking group (NS-ChP group). The clinical periodontal parameters of all patients were recorded, including the plaque index (PLI), probing depth (PD), loss of attachment (LA) and sulcus bleeding index (SBI). Serum was collected from forearm blood to establish a Porphyromonas gingivalis (Pg) internalizing KB cell model. Enzyme-linked immunosorbent assay (ELISA) was used to determine the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cell lysis solution as well as IL-10 and TNF-α in the gingival crevicular fluid (GCF). RESULTS: Fewer Pg internalizing KB cell colonies were observed in the NS-ChP group than in the S-ChP group (P<0.01). When 400µL serum was added, there were remarkable differences in the concentrations of MMP-1 and TIMP-1 secreted from the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=-21.71, P<0.01; TIMP-1: t=64.35, P<0.001). Additionally, when 800µL serum was added, there were significant differences in the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=-81.89, P<0.001; MMP-9: t=-15.67, P<0.001; TIMP-1: t=109.4, P<0.001). The TNF-α levels were higher, but the IL-10 levels were lower in the GCF from the ChP patients in the S-ChP group than those in the NS-ChP group (both P<0.001). CONCLUSION: The serum of S-ChP patients can enhance the concentrations of MMP-1 and MMP-9, but reduce TIMP-1 secreted from Pg internalizing KB cells. However, the concentration of TNF-α was increased and IL-10 was decreased. Abnormal concentrations of ChP-associated biomarkers may be conducive to the development and progression of ChP.

Expression of miRNA-26b in the diagnosis and prognosis of patients with non-small-cell lung cancer.

OBJECTIVE: To investigate the correlation between miR-26b and non-small-cell lung cancer (NSCLC). MATERIALS & METHODS: NSCLC tissues and normal lung tissues that were more than 7 cm adjacent from tumor were collected from 154 NSCLC patients. Additionally, 63 normal specimens from benign lung disease were selected as the control group. Real-time fluorescent quantitative PCR was used to detect miR-26b expression in tissues. RESULT: miR-26b expression in NSCLC tissues was significantly lower than in other two types of tissues. Receiver operating characteristic curve analysis showed that the area under the curve was 0.856 with sensitivity and specificity of 79.9 and 79.4%, respectively. miR-26b expression was a risk factor for poor prognosis of NSCLC. CONCLUSION: The expression of miR-26b is downregulated in NSCLC tissues, and it might be useful in the diagnosis and prognosis of NSCLC patients.

Effects of CYP3A5 genetic polymorphism and smoking on the prognosis of non-small-cell lung cancer.

OBJECTIVE: We aimed to explore the impacts of the rs776746 polymorphism in the CYP3A5 gene and smoking on the prognosis of non-small-cell lung cancer (NSCLC). MATERIALS AND METHODS: Our study enrolled 104 early NSCLC patients undergoing surgery and 107 advanced NSCLC patients undergoing chemotherapy, hospitalized between December 2009 and December 2012 at the First Affiliated Hospital of Liaoning Medical University. All subjects with complete follow-up data were pathologically diagnosed. The rs776746 polymorphism and different genotypes (*1/*1, *1/*3, and *3/*3) were identified by polymerase chain-reaction restriction fragment-length polymorphism. RESULTS: Clinical response to chemotherapy in NSCLC patients with *1/*1 + *1/*3 genotypes were significantly worse than in those with the *3/*3 genotype (17.78% vs 56.45%, P<0.001), and after Bonferroni adjustment, the differences still showed significance (P c<0.01). The mortality risk of NSCLC patients undergoing chemotherapy with the *3/*3 genotype was 0.617 times those with *1/*1 + *1/*3 genotypes (relative risk [RR] 0.617, 95% confidence interval [CI] 0.402-0.948; P=0.028), while the mortality risk of smoking patients was 1.743 times greater than that of nonsmoker patients (RR 1.743, 95% CI 1.133-2.679; P=0.042). Furthermore, a 3.087-fold mortality risk was found in NSCLC patients undergoing surgery with the *3/*3 genotype compared with those with *1/*1 + *1/*3 genotypes (RR 3.087, 95% CI 1.197-7.961; P=0.020). In NSCLC patients undergoing surgery, the mortality risk of smokers was 1.896 times greater than nonsmokers (RR 1.896, 95% CI 1.040-3.455; P=0.037). CONCLUSION: Our study demonstrated that the CYP3A5 rs776746 polymorphism and smoking may influence the prognosis of NSCLC patients undergoing chemotherapy and surgery.

The Inhibition of the Components from Shengmai Injection towards UDP-Glucuronosyltransferase.

The mechanism of shengmai injection- (SMI-) related drug-drug interaction remains unclear. Evaluation of the inhibition potential of SMI's ingredients towards UDP-glucuronosyltransferases (UGTs) activity will provide a new insight to understand SMI-related drug-drug interaction. In vitro incubation system to model UGT reaction was used. Recombinant UGT isoforms-catalyzed 4-methylumbelliferone (4-MU) glucuronidation and UGT1A4-catalyzed trifluoperazine (TFP) glucuronidation reactions were employed to phenotype the inhibition profile of maidong's components towards the activity of UGT isoforms. Different inhibition potential of maidong's components towards various UGT isoforms was observed. Based on the inhibition kinetic investigation results, ophiopogonin D (OD) noncompetitively inhibited UGT1A6 and competitively inhibited UGT1A8, ophiopogonin D' (OD') noncompetitively inhibited UGT1A6 and UGT1A10, and ruscorectal (RU) exhibited competitive inhibition towards UGT1A4. The inhibition kinetic parameters were calculated to be 20.6, 40.1, 5.3, 9.0, and 0.02 µM, respectively. In combination with our previous results obtained for the inhibition of UGT isoforms by ginsenosides and wuweizi components, the important SMI ingredients exhibiting strong inhibition towards UGT isoforms were highlighted. All the results obtained in the present study provide a new insight to understand SMI-related drug-drug interaction.