Correlation between pupillary size and depth of focus after the implantation of extended depth of focus intraocular lenses.

PURPOSE: To evaluate whether depth of focus after the implantation of extended depth of focus (EDoF) intraocular lenses (IOLs) correlates with pupillary size. METHODS: This retrospective case series study evaluated eyes undergoing cataract surgery with implantation of EDoF IOLs. At least one month postoperatively, the depth of focus (DoF) was measured to determine the correlation with pupillary size, age, anterior chamber depth (ACD), axial length (AXL), and corneal spherical aberrations (SA). RESULTS: The study evaluated 64 eyes of 49 patients. The mean depth of focus was 2.67 diopters (D). The mean preoperative photopic pupil size was 3.36 mm. A significant negative association was found between preoperative photopic pupil size and depth of focus (r = 0.30, Pearson's correlation coefficient) and between preoperative mesopic pupil size and depth of focus (r = 0.274, Pearson's correlation coefficient).

Boosting the Faraday Efficiency of Electrochemical Ammonia Synthesis via the Strain Effect Induced by Interfacial Hybrid Formation between BN and Carbon Nanotubes.

The electrochemical nitrogen reduction reaction (eNRR) is a highly promising alternative to the Haber-Bosch (H-B) process, but its commercial development is limited by the high bond energy of N2 molecules and the presence of the competitive hydrogen evolution reaction (HER). Here, a metal-free composite electrocatalyst of boron nitride (h-BNNs) and carbon nanotubes (CNTs) was explored through the interfacial hybridization of h-BNNs and CNTs, which showed a highly improved eNRR Faraday efficiency (FE) of 63.9% and an NH3 yield rate of 36.5 µg h-1 mgcat.-1 at -0.691 V (vs RHE). New chemical bonds of C-B and C-N were observed, indicating a strong interaction between CNTs and h-BNNs. According to the Raman spectra and the optimized model of h-BNNs/CNTs, an obvious strain effect between h-BNNs and CNTs was supposed to play a significant role in the highly improved FE, compared with the FE of h-BNNs alone (4.7%). Density functional theory (DFT) calculations further showed that h-BNNs/CNTs had lower energy barriers in eNRR, giving them higher N2 to NH3 selectivity, while h-BNNs have lower energy barriers in the HER. This work shows the important role of the strain effect in boosting the selectivity in the eNRR process.

p32/OPA1 axis-mediated mitochondrial dynamics contributes to cisplatin resistance in non-small cell lung cancer.

Cisplatin resistance is a major obstacle in the treatment of non-small cell lung cancer (NSCLC). p32 and OPA1 are the key regulators of mitochondrial morphology and function. This study aims to investigate the role of the p32/OPA1 axis in cisplatin resistance in NSCLC and its underlying mechanism. The levels of p32 protein and mitochondrial fusion protein OPA1 are higher in cisplatin-resistant A549/DDP cells than in cisplatin-sensitive A549 cells, which facilitates mitochondrial fusion in A549/DDP cells. In addition, the expression of p32 and OPA1 protein is also upregulated in A549 cells during the development of cisplatin resistance. Moreover, p32 knockdown effectively downregulates the expression of OPA1, stimulates mitochondrial fission, decreases ATP generation and sensitizes A549/DDP cells to cisplatin-induced apoptosis. Furthermore, metformin significantly downregulates the expressions of p32 and OPA1 and induces mitochondrial fission and a decrease in ATP level in A549/DDP cells. The co-administration of metformin and cisplatin shows a significantly greater decrease in A549/DDP cell viability than cisplatin treatment alone. Moreover, D-erythro-Sphingosine, a potent p32 kinase activator, counteracts the metformin-induced downregulation of OPA1 and mitochondrial fission in A549/DDP cells. Taken together, these findings indicate that p32/OPA1 axis-mediated mitochondrial dynamics contributes to the acquired cisplatin resistance in NSCLC and that metformin resensitizes NSCLC to cisplatin, suggesting that targeting p32 and mitochondrial dynamics is an effective strategy for the prevention of cisplatin resistance.

Combined cell grafting and VPA administration facilitates neural repair through axonal regeneration and synaptogenesis in traumatic brain injury.

Neuronal regeneration and functional recovery are severely compromised following traumatic brain injury (TBI). Treatment options, including cell transplantation and drug therapy, have been shown to benefit TBI, although the underlying mechanisms remain elusive. In this study, neural stem cells (NSCs) are transplanted into TBI-challenged mice, together with olfactory ensheathing cells (OECs) or followed by valproic acid (VPA) treatment. Both OEC grafting and VPA treatment facilitate the differentiation of NSCs into neurons (including endogenous and exogenous neurons) and significantly attenuate neurological functional defects in TBI mice. Combination of NSCs with OECs or VPA administration leads to overt improvement in axonal regeneration, synaptogenesis, and synaptic plasticity in the cerebral cortex in TBI-challenged mice, as shown by retrograde corticospinal tract tracing, electron microscopy, growth-associated protein 43 (GAP43), and synaptophysin (SYN) analyses. However, these beneficial effects of VPA are reversed by local delivery of N-methyl-D-aspartate (NMDA) into tissues surrounding the injury epicenter in the cerebral cortex, accompanied by a pronounced drop in axons and synapses in the brain. Our findings reveal that increased axonal regeneration and synaptogenesis evoked by cell grafting and VPA fosters neural repair in a murine model of TBI. Moreover, VPA-induced neuroprotective roles are antagonized by exogenous NMDA administration and its concomitant decrease in the number of neurons of local brain, indicating that increased neurons induced by VPA treatment mediate axonal regeneration and synaptogenesis in mice after TBI operation. Collectively, this study provides new insights into NSC transplantation therapy for TBI.

Exercise protects intestinal epithelial barrier from high fat diet- induced permeabilization through SESN2/AMPKα1/HIF-1α signaling.

Over-nutrition and a sedentary lifestyle are associated with increased intestinal permeability. This condition promotes obesity and associated metabolic disorders. Sestrin2 (SESN2) is a stress-inducible protein thought to promote the survival and recovery of epithelial cells and act as a positive regulator in exercise-induced improvements of glycolipid metabolism. Here we aimed to test the hypothesis that chronic exercise can protect intestinal barrier function against high-fat diet induced permeabilization through SESN2. WT and SESN2-/- mice were randomly assigned to five groups, fed with either normal chow or high fat diet (HFD), and provided with or without exercise training for 15-week. Metabolic parameters, fecal microbiota composition, and intestinal barrier integrity were assessed. The role of the gut microbiota was investigated by administering a mixture of broad-spectrum antibiotics (ABX). Fifteen-week HFD feeding induced dysmetabolism, dysbiosis and gut barrier dysfunctions in the WT mice. These effects were exaggerated in SESN2-/- mice. Chronic aerobic exercise significantly reversed HFD-induced pathologic changes, while SESN2 ablation weakened the protective effects of exercise. ABX did not abolish the differences in gut barrier function between WT and SESN2-/- mice. We speculated that SESN2 may protect intestinal integrity partly independent of gut microbiome. Combining ex vivo and in vivo approaches, we demonstrated that SESN2/pAMPK-Thr172/HIF-1α pathway may play an important role in exercise- improved intestinal permeability. Taken together, our study demonstrated that HFD and SESN2-KO have synergistic effects on intestinal homeostasis. SESN2 is crucial in exercise-improved intestinal permeability.

Serum Intestinal Metabolites are Raised in Patients with Psoriasis and Metabolic Syndrome.

Purpose: Psoriasis is an immune-mediated chronic inflammatory disease. Metabolic syndrome (MetS) is characterized by central obesity, hypertension, dyslipidemia, diabetes and insulin resistance (IR). Increasing evidence indicates that psoriasis is associated with MetS. This study aimed to explore some metabolite indexes which could evaluate the severity or predict the risk of psoriasis patients associated with MetS. Patients and methods: It was a case-control study conducted in Beijing Hospital of Traditional Chinese Medicine. Sixty healthy volunteers (HC), 100 patients with psoriasis (Ps), 100 patients with MetS (MetS) and 80 patients with both psoriasis and MetS (Ps+MetS) were entered between January 2016 and December 2018. Blood samples were taken after at least 12 hours fasting and the contents of trimethylamine N-oxide (TMAO), carnitine, choline and betaine in serum were measured by Liquid Chromatography Mass Spectrometry (LC-MS/MS). Besides, the serum levels of low-density lipoprotein (LDL), high-density lipoprotein (HDL), cholesterol (CHO), triglyceride (TG), blood glucose (BG), creatinine (Cr), urea nitrogen (BUN), uric acid (UA) were determined. Results: The non-healthy groups had different degrees of dyslipidemia, Ps-MetS> Ps >MetS. Compared with HC, the Ps had a higher level of TG; The MetS had the lowest level of HDL; The Ps+Mets had the highest level of TG and CHO. The Ps and Ps+MetS both had high level of UA, but there was no difference between the two groups. As for intestinal metabolites, the Ps had significant differences in TMAO, carnitine, and betaine in comparison with HC. The MetS had the highest level of TMAO. There was positive correlation between PASI and TMAO and betaine. Conclusions: TMAO and betaine could serve as indexes reflecting the severity of psoriasis. TG, CHO, LDL and UA could serve as risk factors of MetS in psoriatic patients.

Conventional ultrasonography and elastosonography in diagnosis of malignant thyroid nodules: A systematic review and meta-analysis.

Purpose: To evaluate the diagnostic value of conventional ultrasound and elastosonography in malignant thyroid nodules by meta-analysis. Methods: The literature included in the Cochrane Library, PubMed, and Embase were searched by using "elastosonography, ultrasonography, thyroid nodules" as the keywords. The clinical studies using elastosonography and conventional ultrasound to diagnose thyroid nodules were selected, and histopathology of thyroid nodules was used as reference standards. The quality evaluation and heterogeneity test were performed on the literature that met the requirements, the combined specificity and sensitivity were pooled, and a comprehensive ROC curve analysis was performed. The Quality Assessment of Diagnostic Accuracy Studies (QUADAS) tool was utilized to evaluate the quality of each included study. Meta-DiSc version 1.4, StataSE 12 and Review Manager 5.4 were used. Results: A total of nine studies assessed 3066 thyroid nodules (2043 benign and 1023 malignant). The pooled sensitivity, specificity, PLR, NLR, and DOR of conventional ultrasound for the diagnose of malignant thyroid nodules were 0.833 (95% CI 0.809-0.855), 0.818 (95% CI 0.801-0.835), 4.85 (95% CI 4.36-5.39), 0.20 (95% CI 0.17-0.23), and 29.38 (95% CI 23.28-37.08), respectively, with an AUC of 0.9068. Also, the pooled sensitivity, specificity, PLR, NLR, and DOR of elastosonography were 0.774 (95% CI 0.741-0.804), 0.737 (95% CI 0.715-0.758), 3.14(95% CI 2.85-3.47), 0.29 (95% CI 0.25-0.34), and 9.35 (95% CI 7.63-11.46), respectively, with an AUC of 0.8801. Three studies provided data regarding the conventional ultrasound and elastosonography. The pooled sensitivity, specificity, PLR, NLR, DOR, and AUC were 0.902 (95% CI 0.870-0.928), 0.649 (95% CI 0.616-0.681), 2.72 (95% CI 2.46-3.00), 0.14 (95% CI 0.11-0.19), 25.51 (95%CI 17.11-38.03), and 0.9294. Conclusion: The existing evidence shows that elastosonography cannot completely replace conventional ultrasound in the diagnosis of malignant thyroid nodules, and the combination of elastosonography and conventional ultrasound gives a better diagnostic precision. Systematic review registration: www.crd.york.ac.uk, identifier PROSPERO CRD42022375808.

Aerobic Exercise Improves Mitochondrial Function in Sarcopenia Mice Through Sestrin2 in an AMPKα2-Dependent Manner.

Sarcopenia, the age-related loss of skeletal muscle mass and function, contributes to high morbidity and mortality in the older population. Regular exercise is necessary to avoid the initiation and progression of sarcopenia, in which the underlying molecular mechanism is still not clear. Our data revealed that the outcomes induced by sarcopenia, including muscle mass and strength loss, decreased cross-sectional area of gastrocnemius fiber, chronic inflammation, and increased dysfunctional mitochondria, were reversed by regulation exercise. Knockout or silencing of Sestrin2 (Sesn2) resulted in imbalanced mitochondrial fusion and fission, mitochondrial biogenesis, and mitophagy damage in vivo and in vitro, which was attenuated by aerobic exercise or overexpression of Sesn2. Moreover, we found that the effects of Sesn2 on mitochondrial function are dependent on AMP-activated protein kinase α2 (AMPKα2). This study indicates that aerobic exercise alleviates the negative effects resulting from sarcopenia via the Sesn2/AMPKα2 pathway and provides new insights into the molecular mechanism by which the Sesn2/AMPKα2 signaling axis mediates the beneficial impact of exercise on sarcopenia.

Mitochondrial Dynamics Mediated by DRP1 and MFN2 Contributes to Cisplatin Chemoresistance in Human Ovarian Cancer SKOV3 cells.

Cisplatin (DDP) is the first-line chemotherapeutic agent for ovarian cancer. However, the development of DDP resistance seriously influences the chemotherapeutic effect and prognosis of ovarian cancer. It was reported that DDP can directly impinge on the mitochondria and activate the intrinsic apoptotic pathway. Herein, the role of mitochondrial dynamics in DDP chemoresistance in human ovarian cancer SKOV3 cells was investigated. In DDP-resistant SKOV3/DDP cells, mitochondrial fission protein DRP1 was down-regulated, while mitochondrial fusion protein MFN2 was up-regulated. In accordance with the expression of DRP1 and MFN2, the average mitochondrial length was significantly increased in SKOV3/DDP cells. In DDP-sensitive parental SKOV3 cells, downregulation of DRP1 and upregulation of mitochondrial fusion proteins including MFN1,2 and OPA1 occurred at day 2~6 under cisplatin stress. Knockdown of DRP1 or overexpression of MFN2 promoted the resistance of SKOV3 cells to cisplatin. Intriguingly, weaker migration capability and lower ATP level were detected in SKOV3/DDP cells. Respective knockdown of DRP1 in parental SKOV3 cells or MFN2 in SKOV3/DDP cells using siRNA efficiently reversed mitochondrial dynamics, migration capability and ATP level. Moreover, MFN2 siRNA significantly aggravated the DDP-induced ROS production, mitochondrial membrane potential disruption, expression of pro-apoptotic protein BAX and Cleaved Caspase-3/9 in SKOV3/DDP cells. In contrast, DRP1 siRNA alleviated DDP-induced ROS production, mitochondrial membrane potential disruption, expression of pro-apoptotic protein BAX and Cleaved Caspase-3/9 in SKOV3 cells. Thus, these results indicate that mitochondrial dynamics mediated by DRP1 and MFN2 contributes to the development of DDP resistance in ovarian cancer cells, and will also provide a new strategy to prevent chemoresistance in ovarian cancer by targeting mitochondrial dynamics.

Downregulation of miR-146a promotes tumorigenesis of cervical cancer stem cells via VEGF/CDC42/PAK1 signaling pathway.

Cervical cancer (CC) is a primary gynecological malignancy worldwide. Cancer stem cells (CSCs) possess enhanced tumor-initiating and self-renewing abilities. MicroRNAs (miRNAs) play essential roles in CSCs' tumorigenesis. This study investigated the effects of miR-146a on CSCs' tumorigenesis and invasion. Tumorsphere cells (TCs) were enriched from the HeLa cell line. Real-time PCR, Western blots, ALDH assays, colony formation and invasion assays, luciferase reporter assays and the Xenograft mouse model were used to determine the underlying mechanism of CC. The results showed that TCs displayed higher ALDH activity and miR-146a was upregulated in differentiated TCs. Moreover, miR-146a inhibitor increased colony formation and cell invasion in TCs while miR-146a mimics displayed the opposite roles. An inverse relationship between miR-146a and VEGF expression was found in TCs and the luciferase reporter assay revealed that VEGF was a direct target of miR-146a. Inhibition of VEGF reversed the effects of miR-146a inhibitor on TCs. The activated CDC42/PAK1 signaling was associated with TCs' tumorigenesis and invasion. Furthermore, miR-146a inhibitor-treated TCs promoted tumor growth in nude mice. Altogether, the results suggest that miR-146a modulated TCs' tumor formation and invasion and was associated with VEGF/CDC42/PAK1 signaling. This study provided insight into developing new therapeutic strategies for CC.

[Analysis and Improvement Suggestions on Change of Medical Devices Licensing Items].

Based on the statistics of 350 technical evaluations of changes in licensing items of class Ⅱ passive and active medical devices completed in Henan province from July 2017 to November 2018, this paper summarized and analysed the common problems and requirements listed in the correction notifications of the technical evaluation, and put forward relevant countermeasures or suggestions, with a view to further speeding up the evaluation and approval of medical devices.

Effect of exercise and butyrate supplementation on microbiota composition and lipid metabolism.

The composition and activity of the gut microbiota depend on the host genome, nutrition, and lifestyle. Exercise and sodium butyrate (NaB) exert metabolic benefits in both mice and humans. However, the underlying mechanisms have not been fully elucidated. This study aimed to examine the effect of exercise training and dietary supplementation of butyrate on the composition of gut microbiota and whether the altered gut microbiota can stimulate differential production of short-chain fatty acids (SCFAs), which promote the expression of SESN2 and CRTC2 to improve metabolic health and protect against obesity. C57BL/6J mice were used to study the effect of exercise and high-fat diet (HFD) with or without NaB on gut microbiota. Bacterial communities were assayed in fecal samples using pyrosequencing of 16S rRNA gene amplicons. Western blot was performed using relevant antibodies to detect the protein expressions in liver and HepG2 cell extracts. Exercise and butyrate administration significantly reversed metabolic dysfunctions induced by HFD (P < 0.05). The number of Firmicutes and the proportion of Firmicutes to Bacteroidetes order were predominant in all HFD groups (P = 0.001). Exercise and butyrate supplementation significantly inhibited the relative abundance of lipopolysaccharide-producing phyla (P = 0.001). SESN2 and CRTC2 expression in the liver of mice were significantly increased after exercise (P < 0.05) and/or supplementation of butyrate (P < 0.05). Exercise enhances butyrate-producing fecal bacteria and increases butyrate production and consequently improves lipid metabolism through the butyrate-SESN2/CRTC2 pathway. Excess butyrate may reduce the proportion of probiotics and reverse the metabolic effects.

Hirudin Protects Ang II-Induced Myocardial Fibroblasts Fibrosis by Inhibiting the Extracellular Signal-Regulated Kinase1/2 (ERK1/2) Pathway.

BACKGROUND Myocardial fibrosis is closely related to all types of cardiovascular diseases. Hirudin is widely used in the prevention and treatment of cardiovascular diseases and cancers. In this study, we examined the potential role(s) and mechanism of hirudin in angiotensin II (Ang II)-induced myocardial fibrosis. MATERIAL AND METHODS The viability of myocardial fibroblasts, and reactive oxygen species (ROS) rates were measured respectively using cell counting kit-8 (CCK-8) and flow cytometry. Malondialdehyde (MDA) content, the activities of lactate dehydrogenase (LDH), and superoxide dismutase (SOD) were detected by the respective kits. The mRNA and protein levels of fibrosis-related factors were separately assessed by qRT-PCR and western blot. RESULTS Our data revealed that hirudin suppressed the viability of myocardial fibroblasts, and that it relieved the proliferation induced by Ang II in a dose-dependent manner. We also found that hirudin reduced ROS production, LDH activity, and MDA content; however, it enhanced SOD activity. Moreover, while hirudin significantly downregulated the levels of matrix metalloproteinase-2 (MMP-2), MMP-9, fibronectin (FN), transforming growth factor beta 1 (TGF-ß1), collagen-I (COL-I), and COL-III, it upregulated the expression level of tissue inhibitor of metalloproteinases-2 (TIMP-2). Furthermore, phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) was decreased by hirudin, compared to the Ang-II group. CONCLUSIONS Hirudin depressed Ang II-induced myocardial fibroblasts via inhibiting oxidative stress, regulating fibrosis-related factors, and repressing the ERK1/2 pathway.

MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer.

Increasing evidence has demonstrated that miRNAs play a critical role in tumor development and progression. Previous studies have revealed that miR-106a is abnormally expressed in various cancers. However, its function and underlying mechanism in cervical cancer (CC) remains unknown. In this study, we confirmed that the expression of miR-106a was significantly upregulated in both CC cell lines and tissues by qRT-PCR. The increased expression of miR-106a was obviously associated with adverse prognostic features. Moreover, we demonstrated that miR-106a was a novel independent prognostic marker for predicting the 5-year survival of CC patients. The ectopic overexpression of miR­106a promoted cell migration, invasion and invasion-related gene expression, while downregulated miR-106a reversed the effect. In addition, miR-106a regulated tissue inhibitor of metalloproteinase (TIMP)2 by directly binding to its 3'-UTR, leading to the indution of the expression of matrix metalloproteinases (MMPs). In clinical samples of CC, miR-106a was inversely correlated with TIMP2, which was downregulated in CC. Alteration of TIMP2 expression at least partially abolished the migration, invasion and MMP expression of miR-106a in CC cells. In conclusion, our data indicated that miR-106a promoted the migration, invasion and MMP expression of CC by targeting TIMP2, and may represent a novel potential therapeutic target and prognostic marker for CC.

Emission Spectrometry for the Detection of Methane Based on Gas Ionization Discharge Microplasma at Room Temperature.

A microplasma-generating device was developed by using needle-plate electrode discharge with the incorporation a Pt/carbon nanotube (CNT) nanocomposite-decorated FTO electrode. When an alternating current voltage of 1.32 kV and a low power consumption of 13 W in nitrogen (N2) carrier gas are applied, the system can be applied to detect methane at room temperature. The main characteristic lines were assigned to CH, C2 and Hα during the discharge process of CH4 at room temperature.The emission intensity of C2 at 516 nm is linear with the concentration of CH4 from 0.5% to 4.0% (φ), and the detection limit (S/N=3) is 0.19% (φ). The emission intensity of Hα at 656 nm is linear with the concentration of CH4 from 0.1% to 3.0%(φ)with the detection limit (S/N=3) is 0.03% (φ). The relative standard deviation (RSD) is less than 2% from 11 repetitive analyses using 3.2% CH4. The Pt/CNT nanocomposite-modified FTO electrode exhibited enhanced sensing performance with precise, repeatability and linear correlation compared with that of the pure MWNT/FTO electrode and bare FTO electrode. When CH4 were discharged in air, the emission spectra of CH4 was different from that in N2. It was found that C2 peak was disappeared and the Hα intensity was also liner to the concentration of CH4 in the range of 0.5%～4%. The established system exhibited advantages with small size, simple fabrication and operation at room temperature compared to other detection system.

Effect of exogenous phytohormones treatment on glycyrrhizic acid accumulation and preliminary exploration of the chemical control network based on glycyrrhizic acid in root of Glycyrrhiza uralensis

ABSTRACT One-year-old Glycyrrhiza uralensis Fisch. ex DC, Fabaceae, was treated with three exogenous phytohormones in June and July, namely gibberellin, auxin (indole-3-acetic acid), methyl jasmonate at different concentrations. Control plants were treated with water. Roots of controls and hormones-treated G. uralensis plants were harvested at different times, and the contents of seven main chemical components were determined. Root glycyrrhizic acid content of plants treated in June increased significantly compared with controls, and the difference was significant. As for plants treated in July, root glycyrrhizic acid content increased in which sprayed with appropriate concentrations of hormones, but the effects of hormones were more evident in plants treated in June coincided with the vigorous growth period than those treated in July. Gibberellin at 40 mg/l and auxin at 40 mg/l applied in the two treatment periods significantly promoted the accumulation of glycyrrhizic acid in G. uralensis root. Treatment with methyl jasmonate at 100 and 25 mg/l in June and July, respectively, also increased glycyrrhizic acid content significantly. The determination of major active compositions indicated that liquiritin, isoliquiritin, isoliquiritin apioside and liquiritin apioside contents were positively related to glycyrrhizic acid content. The study preliminarily found phytohormones and the main chemical components associated with glycyrrhizic acid content, and these discoveries could provide a basis for establishing a chemical control network with glycyrrhizic acid as the core, confirming the secondary product metabolic pathways in the network and completely uncovering synthesis mechanism underlying glycyrrhizic acid-combined functional gene polymorphism.

The analytical determination and electrochemiluminescence behavior of amoxicillin.

A novel electrochemiluminescence (ECL) luminophor of amoxicillin was studied and found to generate ECL following the oxidation or reduction of amoxicillin. The amoxicillin oxidation state was also found to eliminate the reduction state, generating ECL. When solutions of amoxicillin were scanned between +1.5 V and -1.0 V with a graphite electrode in the presence of cetyltrimethyl ammonium bromide using KC1 as the supporting electrolyte, ECL emissions were observed at potentials of -0.7 V and +0.5 V. The ECL intensity at -0.7 V was enhanced by H2O2. Based on these findings, an ECL method for the determination of the amoxicillin concentration is proposed. The ECL intensities were linear with amoxicillin concentrations in the range of 1.8 × 10-8 g/mL to 2.5 × 10-7 g/mL, and the limit of detection (signal/noise = 3) was 5 × 10-9 g/mL. The florescence of amoxicillin had the greatest emission intensity in a neutral medium, with the emission wavelength dependent on the excitation wavelength. The experiments on the ECL mechanism for amoxicillin found that the electrochemical oxidation products of dissolved oxygen and active oxygen species contributed to the ECL process. The data also suggest that the hydroxyl group of amoxicillin contributed to its ECL emission.

[The Emission Spectroscopy of Nitrogen Discharge under Low Voltage at Room Temperature].

A set of direct current (DC) discharge device of N2 plasma was developed, carbon nanotubes (CNT) modified ITO electrode was used as anode, aluminum plate as cathode, with -80 µm separation between them. Nitrogen emission spectra was observed at room temperature and low DC voltage (less than 150 V), and the emission spectrometry was used to diagnose the active species of the process of nitrogen discharge. Under DC discharge, the strongest energy band N2 (C3π(u)), the weak Gaydon's Green system N2 (H3 -Φ(u)-G3 Δ(g)) and the emission line of nitrogen atoms (4 p-4 p0) at 820 nm were observed. Found that metastable state of nitrogen molecules were the main factors leading to a series of excited state nitrogen atoms and nitrogen ionization. Compared the emission spectra under DC with that under alternating current (AC) (1.1 kV), and it can be seen that under DC the spectra band of nitrogen atoms can be obviously observed, and there was a molecular band in the range of 500 - 800 nm. The effect of oxygen and hydrogen on the emission spectra of nitrogen was investigated. The results showed that the oxygen inhibited the luminescence intensity of nitrogen, but the shape of spectra unchanged. All of the second positive system, Gaydon's Green system and atomic lines of nitrogen can be observed. The second positive system and Gaydon's Green system of nitrogen will be greatly affected when the volume ratio of nitrogen and hydrogen greatly affected is 1 : 1, which was due to the hydrogen. The hydrogen can depresse nitrogen plasma activation, and make the Gaydon's Green System disappeared. CNT modified ITO electrode can reduce the breakdown voltage, and the optical signal generated by the weakly ionized gas can be observed by the photo-multiplier tube at low voltage of 10 V.

Clinical characteristics and risk factors of an outbreak with scrub typhus in previously unrecognized areas, Jiangsu province, China 2013.

Scrub typhus, caused by Orientia tsutsugamushi, has emerged recently in Jingjiang City, China where the disease had not been known to exist. We analyzed epidemiological data, clinical characteristics and risk factors of scrub typhus outbreak in Jingjiang City, 2013. The 271 clinically diagnosed patients were predominantly farmers 50 to 69 years old and the peak of onset was early to mid-November. For the 187 laboratory-confirmed cases, the major clinical manifestations of the patients were fever (100%), eschar (88.2%), rash (87.7%), chills (87.7%), and headache (66.8%). A community-based case-control study was carried out to investigate the risk factors of the scrub typhus outbreak. Bundling or moving waste straw (OR=9.0, 95%CI 4.6-17.8) and living at the edge of village (OR=0.6, 95%CI 0.4-0.9) posed the highest risks through single- and multi-variable conditional logistic regression. Phylogenetic analysis of the 56-kDa TSA gene showed that the new cluster (GB-C2) and the previously reported cluster (GB-C1) of O. tsutsugamushi were associated with this outbreak. These findings are useful for the establishment of a detailed control strategy for scrub typhus infection in previously unrecognized areas of Jiangsu Province, China.

Systematic evaluation of bevacizumab in recurrent ovarian cancer treatment.

PURPOSE: This study aimed to evaluate the efficacy and safety of bevacizumab in the treatment of recurrent ovarian cancer. METHODS: The Cochrane Library, MEDLINE, and EMBASE were searched. Data regarding the use of bevacizumab in recurrent ovarian cancer were collected from randomized controlled trials (RCTs). Data were evaluated with the Cochrane systematic method, and statistical analysis was performed with the RevMan 5.2 software. Two RCTs comprising a total of 845 patients were included. RESULTS: Bevacizumab combined with conventional chemotherapy prolonged the progression-free survival (PFS) (hazard ratio [HR] 0.48; 95% confidence interval [CI], 0.41-0.56), without significantly altering the overall survival (OS) (HR 1.03; 95% CI 0.79-1.33). Adverse events (NCI-CTCAE v.4.0) associated with bevacizumab were ≥ grade 3 hypertension (relative risk [RR] 2.30; 95% CI 1.39-3.83) and bleeding (RR 4.76; 95% CI 1.38-16.37). CONCLUSIONS: Bevacizumab prolonged the PFS of patients with recurrent ovarian cancer. Additional high-quality randomized controlled trials are needed to verify these results.