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Background: Outcomes of endovascular treatment of anterior cerebral artery (ACA) aneurysms are still not well-characterized., Objective: The study aimed to review the clinical effect, procedure-related complications and follow-up outcomes and to evaluate the safety and efficacy of endovascular treatment of ACA aneurysms in our center experience., Methods: From August 2014 to August 2018, a total of 75 consecutive patients with 77 ACA aneurysms were treated via the endovascular approach after providing informed consent. A retrospective review of the clinical, radiological, and endovascular details of these patients was conducted., Results: The mortality and the morbidity in this study were 4% and 9.3%, respectively. Compared with A1 and A2 aneurysms, intraoperative rupture was more common in A3 aneurysms (P = 0.029). Difference between the ruptured and unruptured aneurysms in the distribution of therapeutic strategy (P = 0.003) and immediate embolization degree (P = 0.004) was also significant. Statistical analysis demonstrated that the larger aneurysm (P = 0.031) was, the greater the ratio of aneurysm size to parent artery diameter (P = 0.029) was, the more likely the unruptured aneurysms were to occur ischemic events. Higher Hunt-Hess grade (P = 0.0066) was an independent risk factor for poor clinical outcome., Conclusion: Endovascular treatment is feasible and effective for ACA aneurysms., Competing Interests: Declaration of Competing Interest The authors declare that we have no conflict of interest., (Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.)

Objective: Systemic hypoperfusion is intricately involved in neurohormone secretion, vascular calcification (VC) related impaired vasodilation, and luminal stenosis. We aimed to conduct a joint evaluation of vasopressin-neurophysin II-copeptin peptide (VP) and advanced aortic arch calcification (AAC) on all-cause and cardiovascular (CV) mortality in maintenance hemodialysis (MHD) patients. Methods: Unadjusted and adjusted hazard ratios (aHRs) of mortality risks were analyzed for different groups of VP and AAC in 167 MHD patients. The modification effect between higher VP and advanced AAC on mortality risk was examined using an interaction product term. Results: Interactions between VP and AAC with respect to all-cause and CV mortality were statistically significant. In multivariable analysis, higher VP predicted all-cause and CV mortality [aHR: 2.2 (95% confidence interval (CI): 1.1-4.5)] and 2.6 (95% CI: 1.1-4.6), respectively. Advanced AAC was associated with incremental risks of all-cause and CV mortality [aHR: 2.1 (95% CI: 1.1-4.0)and 2.5 (95% CI: 1.0-4.3), respectively]. Patients with combined higher VP (>101.5 ng/mL) and advanced AAC were at the greatest risk of all-cause and CV mortality [aHR: 4.7 (95% CI: 1.2-16.2)and 4.9 (95% CI: 1.1-18.9), respectively]. Conclusion: Combined VP and advanced AAC predict not only all-cause but also CV death in MHD patients, and a joint evaluation is more comprehensive than single marker. In light of hypoperfusion and ischemic events in vital organs, VP and AAC could act as more robust dual marker for prognostic assessment., (Copyright © 2020 Chang, Chou, Wu, Chen, Ko, Liou, Hsieh, Lin, Wen, Chang, Tung and Wang.)

Background: Uremic vascular calcification (UVC) is reminiscent of osteogenesis and apoptosis in vascular smooth muscle cell (VSMC). We aimed to identify how circulating procalcific particles dramatically leak into VSMC layer in human tissue models of vascular rings. Methods: According to baseline estimated glomerular filtration rate (eGFR), patients following lower extremity amputation were divided into three groups: normal renal function (eGFR ≧ 60 ml/min), mild-to-moderate (15 ml/min < eGFR ≧ 60 ml/min) and severe chronic kidney disease (CKD) (eGFR ≦ 15 ml/min). Arterial specimens with immunohistochemistry stain were quantitatively analyzed for UVC, internal elastic lamina (EL) disruption, α-SMA, osteogenesis, apoptosis, and oxidative injury. Correlations among UVC severity, eGFR, EL disruption, osteogenesis, and oxidative injury were investigated. Results: CKD arteries were associated with eGFR-dependent EL disruption corresponding to UVC severity. CKD arteries exhibited lower α-SMA, higher expressions of caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), indicative of contractile VSMC loss, and apoptosis. Enhanced expressions of alkaline phosphatase and Runx2 were presented in VSMCs of CKD arteries, indicative of osteogenic differentiation. Above eGFR-dependent UVC and EL disruption correlated expressions of 8-hydroxy-2'-deoxyguanosine (8-OHdG), indicating oxidative EL injury promoted procalcific processes. Conclusions: Circulating uremic milieu triggers vascular oxidative stress, leading to progressive internal EL disruption as a key event in disabling VSMC defense mechanisms and catastrophic mineral ion influx into VSMC layer. Oxidative EL injury begins in early CKD, corresponding with active VSMC re-programming, apoptosis, and ultimately irremediable UVC. In light of this, therapeutic strategies targeting oxidative tissue injury might be of vital importance to hinder the progression of UVC related cardiovascular events., (Copyright © 2020 Chang, Liu, Lu, Ka, Hsieh, Ho, Lin, Wen, Liou, Chang, Wu, Wang and Li.)

Advanced 1.5-µm emitting materials that can be used to fabricate electrically driven light-emitting devices have the potential for developing cost-effective light sources for integrated silicon photonics. Sensitized erbium (Er 3+ ) in organic materials can give bright 1.5-µm luminescence and provide a route for realizing 1.5-µm organic light emitting diodes (OLEDs). However, the Er 3+ electroluminescence (EL) intensity needs to be further improved for device applications. Herein, an efficient 1.5-µm OLED made from a sensitized organic Er 3+ co-doped system is realized, where a "traditional" organic phosphorescent molecule with minimal triplet-triplet annihilation is used as a chromophore sensitizer. The chromophore provides efficient sensitization to a co-doped organic Er 3+ complex with a perfluorinated-ligand shell. The large volume can protect the Er 3+ 1.5-µm luminescence from vibrational quenching. The average lifetime of the sensitized Er 3+ 1.5-µm luminescence reaches ~0.86 ms, with a lifetime component of 2.65 ms, which is by far the longest Er 3+ lifetime in a hydrogen-abundant organic environment and can even compete with that obtained in the fully fluorinated organic Er 3+ system. The optimal sensitization enhances the Er 3+ luminescence by a factor of 1600 even with a high concentration of the phosphorescent molecule, and bright 1.5-µm OLEDs are obtained., Competing Interests: Conflict of interestThe authors declare that they have no conflict of interest., (© The Author(s) 2020.)

Astaxanthin (ATX) is a carotenoid that exerts strong anti-oxidant and anti-inflammatory property deriving from its highly unsaturated molecular structures. However, the low stability and solubility of ATX results in poor bioavailability, which markedly hampers its application as therapeutic agent in clinic advancement. This study investigated a promising way of transferrin conjugated to poly (ethylene glycol) (PEG)-encapsulated ATX nanoparticles (ATX-NPs) on targeted delivery and evaluated the possible mechanism underlying neuroprotection capability. As a result, the ATX integrated into nanocarrier presented both well water-dispersible and biocompatible, primely conquering its limitations. More than that, the transferrin-containing ATX-NPs exhibited enhanced cellular uptake efficiency than that of ATX-NPs without transferrin conjugated in primary cortical neurons. Additionally, compared to free ATX, transferrin-containing ATX-NPs with lower ATX concentration showed powerful neuroprotective effects on OxyHb-induced neuronal damage. Taken together, the improved bioavailability and enhanced neuroprotective effects enabled ATX-NPs as favorable candidates for targeted delivery and absorption of ATX. We believe that these in vitro findings will provide insights for advancement of subarachnoid hemorrhage therapy., (Copyright © 2019 You, Wu, Zhou, Zhang, Yuan, Wen, Xu, Cui, Tang and Zhang.)

Early Brain Injury, rather than Cerebral Vasospasm, has been demonstrated to be more important for patients with Subarachnoid hemorrhage. It is considered that allicin can make sense in a wide range of pharmacological areas and can be taken as a therapeutic method in many pathologic situations. We have explored the potential effect of allicin and possible mechanisms in Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats. With therapy (70 mg/kg Allicin, rather than 30 mg/kg) 30 min post SAH, groups showed better neurological scores in 24 h. Significant differences could be found in body weight ratio between the SAH + vehicle groups and SAH + Allicin groups. Treatment with 70 mg/kg, not 30 mg/kg, Allicin significantly reduced brain edema and EB extravasation in 24 h after SAH. Assessments in 24 h after SAH showed that treatment with 70 mg/kg Allicin in 30 min after SAH significantly restrained the expression of cleaved caspase-3, mitigated the severity of neuronal degeneration, decreased the proportion of apoptotic neurons and the elevated MDA levels, and increased the suppressed GSH and SOD levels. We demonstrated for the first time that Allicin extenuated brain edema and blood-brain barrier dysfunction, improved neurological outcomes by the suppression of apoptosis and oxidative stress damage after SAH in experimental models, which may shade new light on the treatments of SAH., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: The increasing frequency of explosive injuries has increased interest in blast-induced traumatic brain injury (bTBI). Various shock tube models have been used to study bTBI. Mild-to-moderate explosions are often overlooked because of the slow onset or mildness of the symptoms. However, heavy gas cylinders and large volume chambers in the model may increase the complexity and danger. This study sought to design a modified model to explore the effect of moderate explosion on brain injury in mice., Methods: Pathology scoring system (PSS) was used to distinguish the graded intensity by the modified model. A total of 160 mice were randomly divided into control, sham, and bTBI groups with different time points. The clinical features, imaging features, neurobehavior, and neuropathology were detected after moderate explosion. One-way analysis of variance followed by Fisher's least significant difference posttest or Dunnett's t 3-test was performed for data analyses., Results: PSS of mild, moderate, and severe explosion was 13.4 ± 2.2, 32.6 ± 2.7 (t = 13.92, P < 0.001; vs. mild group), and 56.6 ± 2.8 (t = 31.37, P < 0.001; vs. mild group), respectively. After moderate explosion, mice showed varied symptoms of malaise, anorexia, incontinence, apnea, or seizure. After bTBI, brain edema reached the highest peak at day 3 (82.5% ± 2.1% vs. 73.8% ± 0.6%, t = 7.76, P < 0.001), while the most serious neurological outcomes occurred at day 1 (Y-maze: 8.25 ± 2.36 vs. 20.00 ± 4.55, t = -4.59, P = 0.048; 29.58% ± 2.84% vs. 49.09% ± 11.63%, t = -3.08, P = 0.008; neurologic severity score: 2.50 ± 0.58 vs. 0.00 ± 0.00, t = 8.65, P = 0.016). We also found that apoptotic neurons (52.76% ± 1.99% vs. 1.30% ± 0.11%, t = 57.20, P < 0.001) and gliosis (2.98 ± 0.24 vs. 1.00 ± 0.00, t = 14.42, P = 0.021) in the frontal were significantly higher at day 3 post-bTBI than sham bTBI., Conclusions: We provide a reliable, reproducible bTBI model in mice that can produce a graded explosive waveform similar to the free-field shock wave in a controlled laboratory environment. Moderate explosion can trigger mild-to-moderate blast damage of the brain., Competing Interests: There are no conflicts of interest

To develop B-O complementary-color white organic light-emitting diodes (WOLEDs) exhibiting high efficiency and low roll-off as well as color stability simultaneously, we have designed two orange iridium(III) complexes by simply controlling the position of the methoxyl group on the cyclometalated ligand. The obtained emitters mOMe-Ir-BQ and pOMe-Ir-BQ show good photophysical and electrochemical stabilities with a broadened full width at half-maximum close to 100 nm. The corresponding devices realize highly efficient electrophosphorescence with a maximum current efficiency (CE) and power efficiency (PE) of 24.4 cd A -1 and 15.3 lm W -1 at a high doping concentration of 15 wt %. Furthermore, the complementary-color all-phosphor WOLEDs based on these phosphors exhibit good performance with a maximum CE of 31.8 cd A -1 , PE of 25.0 lm W -1 , and external quantum efficiency of 15.5%. Particularly, the efficiency of this device is still as high as 29.3 cd A -1 and 14.2% at the practical brightness level of 1000 cd m -2 , giving a small roll-off. Meanwhile, extremely high color stability is achieved by these devices with insignificant chromaticity variation.

Perfluorinated chemicals (PFCs) have been used widely in consumer products manufacture. Recent in vitro as well as animal studies have found that there are different toxicity and pharmacokinetic profiles between isomers of perfluorooctanoic acid (PFOA) and/or perfluorooctane sulfonate (PFOS). However, the differential effects of linear or branched PFOA/PFOS isomers on human beings have never been reported. Herein, we examined 1871 adult subjects (age older than 18 years) from the National Health and Nutrition Examination Survey (NHANES) 2013-2014 to determine the association between the isomers of PFOA/PFOS and serum biochemistry profiles, including glucose, lipids, protein and components of metabolic syndrome (MS). The results showed that for PFOA, increased linear PFOA was associated with increases in total cholesterol, serum albumin and an enhancement of β cell function as well as a decrease in the serum globulin. Increased branched PFOA was significantly associated with increased fasting glucose. All isomers of PFOA were positively associated with high-density lipoprotein-cholesterol (HDL-C) and negatively associated with glycohemoglobin (HbA1C). The branched PFOS was positively associated with β cell function and inversely associated with serum globulin. Both linear and branched isomers of PFOS were positively associated with the total protein and albumin. The increased branched PFOA was associated with less HDL-C insufficiency defined by the National Cholesterol Education Program Third Adult Treatment Panel (NCEP-ATP III) MS criteria, whereas the increased concentrations of serum total and linear PFOS were associated with less hypertriglyceridemia by the NCEP-ATP III. In conclusion, serum isomers of PFOA and PFOS were associated with glucose homeostasis, serum protein as well as lipid profiles; they were also indicators of MS. This may suggest that there is a distinct difference in the toxicokinetics of the isomers of PFOA and PFOS. Further clinical and animal studies are warranted to clarify the putative causal relationships between isomers and biochemical alterations., (Copyright © 2017. Published by Elsevier Ltd.)

We have previously reported that perfluorooctanesulfonate (PFOS) causes cell apoptosis in renal tubular epithelial cells (RTCs). Here, we extend our findings and provide evidence of epithelial-mesenchymal transition (EMT)-associated renal fibrosis caused by PFOS and the protection by l-carnitine. Our results demonstrate that PFOS increased the expression of EMT and renal injury biomarkers (eg, N-cadherin, vimentin, Snail, Kim1, and Lcn2). In addition, PFOS caused EMT induction through Sirt1-mediated PPARγ deacetylation and inactivation. l-carnitine reversed the EMT induction caused by PFOS and alleviated PFOS-mediated increases in cell migration by reactivating PPARγ through the inhibition of Sirt1 activity. The critical role of Sirt1 in this process was validated by using Sirt1 overexpression, resveratrol (a pharmacologic activator of Sirt1), nicotinamide (a Sirt1 inhibitor) and siSirt1. Nicotinamide and siSirt1, but not Sirt1 overexpression and resveratrol, alleviated PFOS-mediated EMT induction, suggesting that increased Sirt1 activity contributed to the alterations. Furthermore, through PPARγ overexpression and pharmacologic interventions, we validated the crucial role of increased PPARγ deacetylation caused by aberrant increased Sirt1 activity in RTC transformation. Similar to PPARγ overexpression, rosiglitazone (a PPARγ agonist) alleviated the effects of PFOS on the EMT-related features, whereas GW9662 (a PPARγ antagonist) mimicked the effects. The protective effect of l-carnitine was also verified in a mouse model of chronic PFOS exposure, in which decreased EMT biomarker levels and renal fibrosis by l-carnitine were observed in Western blot and histological analyses. Accordingly, l-carnitine alleviated EMT-associated renal fibrosis caused by PFOS through a Sirt1- and PPARγ-dependent mechanism., (© The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.)

Background: Preoperative embolization of hypervascular brain tumors is frequently used to minimize intraoperative bleeding., Objective: To explore the efficacy of embolization using flat-detector CT (FDCT) parenchymal blood volume (PBV) maps before and after the intervention., Materials and Methods: Twenty-five patients with hypervascular brain tumors prospectively received pre- and postprocedural FDCT PBV scans using a biplane system under a protocol approved by the institutional research ethics committee. Semiquantitative analysis, based on region of interest measurements of the pre- and post-embolization PBV maps, operating time, and blood loss, was performed to assess the feasibility of PBV maps in detecting the perfusion deficit and to evaluate the efficacy of embolization., Results: Preoperative embolization was successful in 18 patients. The relative PBV decreased significantly from 3.98±1.41 before embolization to 2.10±2.00 after embolization. Seventeen patients underwent surgical removal of tumors 24 hours after embolization. The post-embolic tumor perfusion index correlated significantly with blood loss (ρ=0.55) and operating time (ρ=0.60)., Conclusions: FDCT PBV mapping is a useful method for evaluating the perfusion of hypervascular brain tumors and the efficacy of embolization. It can be used as a supplement to CT perfusion, MRI, and DSA in the evaluation of tumor embolization., Competing Interests: Competing interests: None declared., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.)

Background: The aging rate in Taiwan is the second highest in the world. As the population ages quickly, the prevalence of dementia increases rapidly. There are some studies that have explored the association between air pollution and cognitive decline, but the association between air pollution and dementia has not been directly evaluated., Methods: This was a case-control study comprising 249 Alzheimer's disease (AD) patients, 125 vascular dementia (VaD) patients, and 497 controls from three teaching hospitals in northern Taiwan from 2007 to 2010. Data of particulate matter <10 μm in diameter (PM10) and ozone were obtained from the Taiwan Environmental Protection Administration for 12 and 14 years, respectively. Blood samples were collected to determine the apolipoprotein E (APOE) ɛ4 haplotype. Bayesian maximum entropy was used to estimate the individual exposure level of air pollutants, which was then tertiled for analysis. Conditional logistic regression models were used to estimate adjusted odds ratios (AORs) and 95% confidence intervals between the association of PM10 and ozone exposure with AD and VaD risk., Results: The highest tertile of PM10 (≥49.23 μg/m(3)) or ozone (≥21.56 ppb) exposure was associated with increased AD risk (highest vs. lowest tertile of PM10: AOR = 4.17; highest vs. lowest tertile of ozone: AOR = 2.00). Similar finding was observed for VaD. The association with AD and VaD risk remained for the highest tertile PM10 exposure after stratification by APOE ɛ4 status and gender., Conclusions: Long-term exposure to the highest tertile of PM10 or ozone was significantly associated with an increased risk of AD and VaD.

Objective: To study the apoptosis inducing effects of bufalin on various human osteosarcoma cells and the concerning molecular mechanisms., Method: MTT assay was used to detect the growth inhibition rates of osteosarcoma cells U-20S, U-20S/MTX300, SaOS-2, IOR/OS9 treated with bufalin in different concentrations and times. The apoptosis of cells was observed flow cytometry 48 h following bufalin treatment. The proteomic techniques were used to separate and compare the treated and control groups 48 h after bufalin-incubation. Then, the proteomic results were validated by western blot., Result: Bufalin inhibited the growth of human osteosarcoma cells U20S, U20S/MTX300 (methotrexate resistant cells), SAOS2, IOR/OS9 in a dose- and time-dependent manner. The 72 h IC50 were (37.43 +/- 4.1), (32.24 +/- 5.3) nmol x L(-1) in U20S,U20S/MTX300 cells,respectivly. Flow cytometry showed that the apoptosis cells were increased following bufalin treatment. The protein expression profile showed 24 differentiated expression proteins. Among these proteins, the level of an anti-apoptotic protein, heat shock protein 27 (Hsp27) decreased significantly and the result was then validated by western blot. Ectopic expression of Hsp27 could reduce the bufalin-induced apoptosis remarkably in U20S and U20S/MTX300 cells., Conclusion: Bufalin could inhibit the cell growth and induce apoptosis on human osteosarcoma cells. The effect of bufalin may be related to the joint intervention with multiple protein targets. Among them, downregulation of Hsp27 plays a critical role in the bufalin-induced apoptosis in human osteosarcoma cells.

Context: Perfluorooctanoic acid (PFOA) and perfluorooctane sulfate (PFOS) are used in a variety of products worldwide. However, the relationship among serum PFOA, PFOS concentration, bone mineral density (BMD), and the risk of fractures has never been addressed., Objectives: The study examined the association among serum PFOA, PFOS concentration, and lumbar spine and total hip BMD in the general US population., Design and Participants: We analyzed data on 2339 adults (aged ≧20 y) from the National Health and Nutrition Examination Survey conducted in 2005-2006 and 2007-2008 to determine the relationship among serum PFOA, PFOS concentration, and total lumbar spine and total hip BMD measured by dual-energy x-ray absorptiometry and history of fractures cross-sectionally., Results: After weighting for sampling strategy, a 1-U increase in the natural log-transformed serum PFOS level was associated with a decrease in total lumbar spine BMD by 0.022 g/cm(2) (95% confidence interval -0.038, -0.007; P = .006) in women not in menopause. There was no association among PFOA, PFOS concentration, and self-reported fracture in adults., Conclusion: Serum PFOS concentration is associated with decreased total lumbar spine BMD in women not in menopause. However, the potential biological significance of this effect is marginal and subclinical in the general US population. Further studies are warranted to clarify the causal relationship between perfluorinated chemical exposure and BMD.

Context: Perfluorinated chemicals (PFCs) have been widely used in a variety of products worldwide for years. The relationship between serum PFCs and thyroid function has never been addressed in a nationally representative survey., Objectives: The study examined the association between serum PFCs and thyroid function in the general U.S. population., Design and Participants: We selected 1181 subjects (aged >20 years) from a National Health and Nutrition Examination Survey (NHANES) in 2007 through 2008 and 2009 through 2010 to determine the relationship between serum PFCs and thyroid function. Data were adjusted for confounding variables., Results: The geometric means and 95% confidence interval (CI) concentrations of perfluorooctanoate (PFOA), perfluorooctane sulfonate, perfluorononanoic acid, and perfluorohexane sulfonate (PFHxS) were 4.15 (4.02-4.29), 14.2 (13.59-14.86), 1.54 (1.48-1.59), and 2.00 (1.89-2.11) ng/mL, respectively. After weighting for sampling strategy, we determined a 1-U increase in natural log-serum PFOA increased serum total T3 concentration by 6.628 ng/dL (95% CI = 0.545-12.712, P = .035) in women. A 1-U increase in natural log-PFHxS was associated with an increase of total T4 by 0.26 μg/mL (95% CI = 0.108-0.413, P = .002) and total T3 by 4.074 ng/dL (95% CI = 2.232-5.916, P < .001) in women and a decrease of natural log-free T4 by 0.016 (ng/dL) (95% CI = -0.029 to 0.003, P = .019) in men., Conclusion: Higher serum concentrations of PFOA and PFHxS are associated with total T3, total T4, and free T4 in the U.S. general population. More studies are warranted to clarify the causal relationship between PFCs and thyroid function.

There are fewer reports of brain infection by Klebsiella pneumoniae than there are in other organs, but an increase incidence and morbidity has been noted. We have previously developed a rat model of K. pneumoniae meningoencephalitis. Cortistatin (CST) is a recently discovered neuropeptide with endocrine activities in humans. In this study, we found that brain infection by K. pneumoniae increased endogenous prepro-CST messenger RNA expression, which occurred earlier than did leukocyte infiltration in vivo and also occurred in cultured neuron-glia. Postinfection treatment with CST (either intracerebroventricularly or intraperitoneally), but not somatostatin, reduced leukocyte recruitment and clinical illness as revealed by fever and clinical score in vivo. Postinfection increases of proinflammatory cytokine messenger RNA levels were attenuated by CST in neuron-glia cultures, further confirming a direct effect on neuroinflammation. Administration of CST resulted in less postinfection neuronal loss in vitro, suggesting a direct neuroprotective effect and potential as an adjuvant for treating bacterial meningoencephalitis.

To establish an early-warning system for source water pollution accident, a membrane inlet/time-of-flight mass spectrometry technology was applied to a series of pollution scenarios as an online monitoring method for typical volatile organic compounds such as BTEX (benzene, toluene, ethylbenzene and xylene), substituted benzenes, and halogenated aliphatic hydrocarbons. It was shown that this technology can adequately meet the requirements of realtime analysis with short response time to the target organic pollutants (30-70 s for BTEX and 30 s for halogenated aliphatic hydrocarbons) in a linear detecting range of 3-4 magnitudes; the detection limits of BTEX and chlorobenzene were less than 10 microg x L(-1). The results of 52 simulated water pollution accidents in a 30-days' continuous monitoring indicated that the monitoring system was stable with the relative standard deviation less than 5%; the accuracy was acceptable and could be reduced to within 10% by periodical calibrations. Membrane inlet/time-of-flight mass spectrometry technology was proven to be available for the remote monitoring and early-warning of source water pollution accident.

Objective: To compare the effects of sevoflurane and propofol-remifentanil anesthesia on neuromuscular blockade produced by continuous cisatracurium infusion., Methods: Forty ASA I or II patients undergoing selective surgery were randomly divided into sevoflurane and propofol-remifentanil anesthesia groups (n=20). Neuromuscular blockade was monitored using train-of-four (TOF) stimulation by recording the contraction force of the adductor pollicis muscle with a muscle relaxation monitor. A bolus dose of cisatracurium of 0.15 mg/kg was administered to facilitate endotracheal intubation, followed by continuous infusion adjusted manually to maintain the first twitch (T1) < or = 5% of the control level. The following variables were recorded including the infusion rate, total amount of cisatracurium, spontaneous recovery index (RI), and the time interval from termination of infusion cisatracurium to recovery of TOF ratio (TOFR) to 0.9., Results: With the maintenance of a 95%-99% neuromuscular blockade, the infusion rate was significantly lower in sevoflurane group than in propofol-remifentanil group (P<0.05), and stabilized in both groups after 120 min. No significant differences were found in RI or the time to TOFR of 0.9 between the two groups (P>0.05)., Conclusion: During the maintenance of stable neuromuscular blockade by continuous cisatracurium infusion, both sevoflurane and propofol-remifentanil anesthesia can time-dependently enhance the effect of cisatracurium without producing significant differences in the recovery properties.

Objective: a To observe the analgesic effect of fentanyl combined with flurbiprofen axetil for postoperative analgesia after gynecologic surgery., Methods: One hundred and forty patients undergoing gynecologic surgery were randomized equally into two groups to receive postoperative patient controlled intravenous analgesia (PCIA) with fentanyl (1.6-1.8 mg) plus tropisetron (5 mg/100 ml) (group I), or with fentanyl (0.8-1.0 mg) and flurbiprofen axetil (200 mg) plus tropisetron (5 mg/100 ml) (group II), at the PCIA rate of 2 ml/h, bolus dose of 1 ml, and lock time of 15 min. At 6 h (T1), 12 h (T2), 24 h (T3), and 48 h (T4) after the operation, the analgesic effect was evaluated with the Prine-Henry score (PHS), and the side effects were recorded. The coagulation function of the patients was assessed with thrombelastography before (T0) and 48 h (T4) after the operation, and the time of gastrointestinal function recovery was recorded., Results: The fentanyl dose was significantly less in group II than in group I (P<0.05). At the time points of T1 and T2, the PHS in group II was significantly lower than that in group I (P<0.05), but comparable between the two groups at T3 and T4 (P>0.05). Significant higher incidences of the adverse effects such as nausea, dizziness and lethargy was noted in group I than in group II (P<0.05). Compared with that at T0, the parameter K was significantly delayed at T4 in both groups (P<0.05). The two groups showed similar time of gastrointestinal function recovery after the operation (P>0.05)., Conclusion: Flurbiprofen axetil combined with fentanyl for postoperative analgesia can significantly reduce fentanyl dose and the incidence of adverse effects associated with fentanyl without obviously affecting the coagulation and gastrointestinal functions.

Background & Objective: A prolonged period of one-lung ventilation(OLV) is required during thoracic surgery and this may activate cytokine release and cause lung inflammatory response. The lung protective ventilatory strategy has reduced lung and systemic cytokine release and achieved remarkable curative effect in patients with acute respiratory distress syndrome (ARDS). This study was to investigate the effect of the lung protective ventilatory strategy on proinflammatory cytokine release during OLV in patients underwent thoracic surgery., Methods: Forty patients underwent esophagectomy were randomly divided into conventional ventilation (CV) group (n=20) and protective ventilation (PV) group (n=20). In CV group, all patients received two-lung ventilation (TLV) and OLV with a tidal volume (VT) of 10 mL/kg and an inspiration/expiration ratio (I/E) of 1:1.5. In PV group, all patients received TLV with a VT of 10 mL/kg and an I/E ratio of 1:1.5, and received OLV with a VT of 5-6 mL/kg and an I/E ratio of 1:1, along with positive end-expiratory pressure (PEEP) preset at 3-5 cm H2O. Blood samples of 3 mL were extracted at three time courses, which were after tracheal intubation (T1), 120 min after OLV (T2) and 24 h after operation (T3), to analyze concentrations of interleukin (IL)-6 and IL-8 in the two groups. Values of airway peak pressure (Ppeak), airway plateau pressure (Pplat), and airway resistance(Raw)were also recorded using side stream spirometry., Results: In CV group, concentrations of IL-6 and IL-8 at T2 [(269.4+/-57.2) ng/L, (180.8+/-35.0) ng/L] and T3[(335.8+/-98.7) ng/L,(178.5+/-18.3) ng/L] were significantly increased as compared with those at T1 [(17.0+/-5.4) ng/L,(18.2+/-2.8) ng/L](P<0.05). In PV group, concentrations of IL-6 and IL-8 at T2 [(209.3+/-55.7) ng/L], (115.3+/-71.5) ng/L] and T3 [(278.2+/-100.8) ng/L,(124.2+/-40.1) ng/L] were significantly increased as compared with those at T1[(20.0+/-7.1) ng/L,(15.3+/-3.6) ng/L] (P<0.05). Concentrations of IL-6 and IL-8 at T2 and T3 were significantly higher in CV group than in PV group (P<0.05). Ppeak, Pplat and Raw at T2 were significantly higher in CV group [(33.6+/-4.6 cmH2O,(21.5+/-3.1) cmH2O, (26.3+/-2.1) cmH2O.L(-1).S(-1)] than in PV group [(26.7+/-3.5) cmH2O, (12.4+/-2.1) cmH2O, (18.3+/-2.3) cmH2O.L(-1).S(-1)](P<0.05)., Conclusions: Concentrations of IL-6 and IL-8 are increased during and after OLV in thoracic surgery. The lung protective ventilatory strategy can reduce the airway pressure and airway resistance during OLV, decrease the release of IL-6 and IL-8, and inhibit lung inflammatory responses during OLV and postoperatively.

Background: Serum amyloid A (SAA) is a useful biomarker for gastric cancer in an animal model. We investigated the potential of SAA as a biomarker for gastric cancer in humans., Methods: Serum levels of SAA from 96 gastric cancer patients were measured before and after curative gastrectomy; 32 patients with gastric ulcers and 52 healthy subjects were the control groups. The immunohistochemical study was performed to evaluate the protein expression over gastric cancer tissue slides., Results: The mean SAA concentration was higher in gastric cancer patients (88.54 +/- 50.44 mg/l) than in healthy subjects (3.36 +/- 2.29 mg/l) and gastric ulcer patients (10.48 +/- 8.97 mg/l) (P < .05). The SAA concentration was associated with tumor stage (P = .0244) and location (P = .0016) but not with Lauren's histological type (P = .839). In the multivariate analysis, SAA level was correlated with tumor location (P < .0001) and lymph node status (P < .05). During follow-up, the mean SAA concentration increased significantly in 24 patients with tumor recurrence (P < .05) but did not change in 77 patients without recurrence. In the survival analysis, patients with SAA levels > 97 mg/l had a nearly fourfold increase in risk of death. Immunoreactivity was most prominent in blood vessel regions but not within cancer cells., Conclusions: These data not only demonstrated SAA was useful in predicting survival of patients with gastric cancer, but they also showed that SAA was a valuable tool for postoperative follow-up.

Oxidative stress, in which production of highly reactive oxygen species (ROS) and reactive nitrogen species (RNS) overwhelms antioxidant defenses, is a feature of many neurological diseases and neurodegeneration. ROS and RNS generated extracellularly and intracellularly by various processes initiate and promote neurodegeneration in CNS. ROS and RNS can directly oxidize and damage macromolecules such as DNA, proteins, and lipids, culminating in neurodegeneration in the CNS. Neurons are most susceptible to direct oxidative injury by ROS and RNS. ROS and RNS can also indirectly contribute to tissue damage by activating a number of cellular pathways resulting in the expression of stress-sensitive genes and proteins to cause oxidative injury. Moreover, oxidative stress also activates mechanisms that result in a glia-mediated inflammation that also causes secondary neuronal damage. Associated with neuronal injuries caused by many CNS insults is an activation of glial cells (particularly astrocytes and microglia) at the sites of injury. Activated glial cells are thus histopathological hallmarks of neurodegenerative diseases. Even though direct contact of activated glia with neurons per se may not necessarily be toxic, the immune mediators (e.g. nitric oxide and reactive oxygen species, pro-inflammatory cytokines and chemokines) released by activated glial cells are currently considered to be candidate neurotoxins. Therefore, study of the protective role of antioxidant compounds on inhibition of the inflammatory response and correcting the fundamental oxidant/antioxidant imbalance in patients suffering from neurodegenerative diseases are important vistas for further research. The purpose of this review is to summarize the current evidence in support of this critical role played by oxidative stress of neuronal and glial origin in neurodegenerative diseases. The mechanistic basis of the neuroprotective activity of antioxidants does not only rely on the general free radical trapping or antioxidant activity per se in neurons, but also the suppression of genes induced by pro-inflammatory cytokines and other mediators released by glial cells. We propose that combinations of agents which act at sequential steps in the neurodegenerative process can produce additive neuroprotective effects. A cocktail of multiple antioxidants with anti-inflammatory agents may be more beneficial in the prevention of neurodegenerative disease. A clearer appreciation of the potential therapeutic utility of antioxidants would emerge only when the complexity of their effects on mechanisms that interact to determine the extent of oxidative damage in vivo are more fully defined and understood.

Five novel interesting d(10) metal coordination polymers, [Zn(PDCO)(H2O)2]n (PDCO = pyridine-2,6-dicarboxylic acid N-oxide) (1), [Zn2(PDCO)2(4,4'-bpy)2(H2O)2.3H2O]n (bpy = bipyridine) (2), [Zn(PDCO)(bix)]n (bix = 1,4-bis(imidazol-1-ylmethyl)benzene) (3), [Zn(PDCO)(bbi).0.5H2O]n (bbi = 1,1'-(1,4-butanediyl)bis(imidazole)) (4), and [Cd(PDCO)(bix)(1.5).1.5H2O]n (5), have been synthesized under hydrothermal conditions and structurally characterized. Polymer 1 possesses a one-dimensional (1D) helical chainlike structure with 4(1) helices running along the c-axis with a pitch of 10.090 Angstroms. Polymer 2 has an infinite chiral two-dimensional (2D) brick-wall-like layer structure in the ac plane built from achiral components, while both 3 and 4 exhibit an infinite 2D herringbone architecture, respectively extended in the ac and ab plane. Polymer 5 features a most remarkable and unique three-dimensional (3D) porous framework with 2-fold interpenetration related by symmetry, which contains channels in the b and c directions, both distributed in a rectangular grid fashion. Compounds 1-5, with systematic variation in dimensionality from 1D to 2D to 3D, are the first examples of d(10) metal coordination polymers into which pyridinedicarboxylic acid N-oxide has been introduced. In addition, polymers 1, 4, and 5 display strong blue fluorescent emissions in the solid state. Polymer 3 exhibits a strong SHG response, estimated to be approximately 0.9 times that of urea.