Comparisons of the GlideScope and Macintosh Laryngoscope in Tracheal Intubation by Medical Students on Fresh Human Cadavers

AbstractObjectiveThe GlideScope Video Laryngoscope (GS) is an intubating device that provides equal or better glottic views than conventional laryngoscopes, but correct tube placement is more time-consuming, even when performed by experienced operators. The aim of this study was to investigate the use of the GS compared with the more conventional Macintosh laryngoscope in easy and difficult tracheal intubation when performed by inexperienced medical students on fresh human cadaversPatients and MethodsForty-one medical students were assigned to perform tracheal intubation using the direct Macintosh laryngoscope (DL) and the GS. Each student was given four attempts, with a maximum of 180 seconds for each attempt, to successfully intubate the trachea with a 6.5-mm tracheal tube in each of two scenarios, one with an easy airway and the other with a difficult airway cadaver.ResultsThe total time of intubation for the easy airway cadaver was significantly longer in the GS group (61.4 ± 4.8 seconds vs. 40.6 ± 5.3 seconds; p < 0.001) despite the modified Cormack-Lehane scores showing no difference between the two groups. In the difficult airway cadaver, total time of intubation was significant shorter in the GS group (64.3 ± 6.5 seconds vs. 98.7 ± 10.2 seconds; p < 0.001)ConclusionMost inexperienced operators found the GS to be more time-consuming for tracheal intubation than DL in the easy airway cadaver. However, an obvious advantage was demonstrated when the GS was used for the difficult airway

Melatonin acts synergistically with pazopanib against renal cell carcinoma cells through p38 mitogen-activated protein kinase-mediated mitochondrial and autophagic apoptosis

Background Mounting evidence indicates that melatonin has possible activity against different tumors. Pazopanib is an anticancer drug used to treat renal cell carcinoma (RCC). This study tested the anticancer activity of melatonin combined with pazopanib on RCC cells and explored the underlying mechanistic pathways of its action. Methods The 786-O and A-498 human RCC cell lines were used as cell models. Cell viability and tumorigenesis were detected with the MTT and colony formation assays, respectively. Apoptosis and autophagy were assessed using TUNEL, annexin V/propidium iodide, and acridine orange staining with flow cytometry. The expression of cellular signaling proteins was investigated with western blotting. The in vivo growth of tumors derived from RCC cells was evaluated using a xenograft mouse model. Results Together, melatonin and pazopanib reduced cell viability and colony formation and promoted the apoptosis of RCC cells. Furthermore, the combination of melatonin and pazopanib triggered more mitochondrial, caspase-mediated, and LC3-II-mediated autophagic apoptosis than melatonin or pazopanib alone. The combination also induced higher activation of the p38 mitogen-activated protein kinase (p38MAPK) in the promotion of autophagy and apoptosis by RCC cells than melatonin or pazopanib alone. Finally, tumor xenograft experiments confirmed that melatonin and pazopanib cooperatively inhibited RCC growth in vivo and predicted a possible interaction between melatonin/pazopanib and LC3-II. Conclusion The combination of melatonin and pazopanib inhibits the growth of RCC cells by inducing p38MAPK-mediated mitochondrial and autophagic apoptosis. Therefore, melatonin might be a potential adjuvant that could act synergistically with pazopanib for RCC treatment

Global, regional, and national incidence and mortality for HIV, tuberculosis, and malaria during 1990–2013: a systematic analysis for the Global Burden of Disease Study 2013

BACKGROUND: The Millennium Declaration in 2000 brought special global attention to HIV, tuberculosis, and malaria through the formulation of Millennium Development Goal (MDG) 6. The Global Burden of Disease 2013 study provides a consistent and comprehensive approach to disease estimation for between 1990 and 2013, and an opportunity to assess whether accelerated progress has occured since the Millennium Declaration. METHODS: To estimate incidence and mortality for HIV, we used the UNAIDS Spectrum model appropriately modified based on a systematic review of available studies of mortality with and without antiretroviral therapy (ART). For concentrated epidemics, we calibrated Spectrum models to fit vital registration data corrected for misclassification of HIV deaths. In generalised epidemics, we minimised a loss function to select epidemic curves most consistent with prevalence data and demographic data for all-cause mortality. We analysed counterfactual scenarios for HIV to assess years of life saved through prevention of mother-to-child transmission (PMTCT) and ART. For tuberculosis, we analysed vital registration and verbal autopsy data to estimate mortality using cause of death ensemble modelling. We analysed data for corrected case-notifications, expert opinions on the case-detection rate, prevalence surveys, and estimated cause-specific mortality using Bayesian meta-regression to generate consistent trends in all parameters. We analysed malaria mortality and incidence using an updated cause of death database, a systematic analysis of verbal autopsy validation studies for malaria, and recent studies (2010-13) of incidence, drug resistance, and coverage of insecticide-treated bednets. FINDINGS: Globally in 2013, there were 1·8 million new HIV infections (95% uncertainty interval 1·7 million to 2·1 million), 29·2 million prevalent HIV cases (28·1 to 31·7), and 1·3 million HIV deaths (1·3 to 1·5). At the peak of the epidemic in 2005, HIV caused 1·7 million deaths (1·6 million to 1·9 million). Concentrated epidemics in Latin America and eastern Europe are substantially smaller than previously estimated. Through interventions including PMTCT and ART, 19·1 million life-years (16·6 million to 21·5 million) have been saved, 70·3% (65·4 to 76·1) in developing countries. From 2000 to 2011, the ratio of development assistance for health for HIV to years of life saved through intervention was US$4498 in developing countries. Including in HIV-positive individuals, all-form tuberculosis incidence was 7·5 million (7·4 million to 7·7 million), prevalence was 11·9 million (11·6 million to 12·2 million), and number of deaths was 1·4 million (1·3 million to 1·5 million) in 2013. In the same year and in only individuals who were HIV-negative, all-form tuberculosis incidence was 7·1 million (6·9 million to 7·3 million), prevalence was 11·2 million (10·8 million to 11·6 million), and number of deaths was 1·3 million (1·2 million to 1·4 million). Annualised rates of change (ARC) for incidence, prevalence, and death became negative after 2000. Tuberculosis in HIV-negative individuals disproportionately occurs in men and boys (versus women and girls); 64·0% of cases (63·6 to 64·3) and 64·7% of deaths (60·8 to 70·3). Globally, malaria cases and deaths grew rapidly from 1990 reaching a peak of 232 million cases (143 million to 387 million) in 2003 and 1·2 million deaths (1·1 million to 1·4 million) in 2004. Since 2004, child deaths from malaria in sub-Saharan Africa have decreased by 31·5% (15·7 to 44·1). Outside of Africa, malaria mortality has been steadily decreasing since 1990. INTERPRETATION: Our estimates of the number of people living with HIV are 18·7% smaller than UNAIDS's estimates in 2012. The number of people living with malaria is larger than estimated by WHO. The number of people living with HIV, tuberculosis, or malaria have all decreased since 2000. At the global level, upward trends for malaria and HIV deaths have been reversed and declines in tuberculosis deaths have accelerated. 101 countries (74 of which are developing) still have increasing HIV incidence. Substantial progress since the Millennium Declaration is an encouraging sign of the effect of global action. FUNDING: Bill & Melinda Gates Foundation

Determination of Spread of Injectate After Ultrasound-guided Interscalene and Supraclavicular Brachial Plexus Block: A Fresh Cadaveric Study

AbstractObjectiveThe aim of this anatomical study was to establish the likely spread of local anesthetics in vivo and the segmental nerve involvement resulting from ultrasound-guided interscalene brachial plexus blocks and supraclavicular brachial plexus blocks.Materials and MethodsWe performed ultrasound-guided injections of different alinine dyes into the right brachial plexus at the interscalene and supraclavicular levels in seven fresh human cadavers. We then dissected the cadavers to determine the extent of dye spread and the nerve that was dyed.ResultsThe cadavers provided excellent sonographic images during nerve blocks. After excluding one pilot specimen, six right brachial plexus blocks were successfully performed and dissected. The extent of dye spread and nerve involvement were different in the interscalene brachial plexus blocks and supraclavicular brachial plexus blocks. The phrenic nerve with dye was identified in the interscalene brachial plexus block.ConclusionThis study showed that the extent of dye spread and nerve involvement differs in interscalene and supraclavicular brachial plexus blocks. Phrenic nerve involvement in the interscalene block was confirmed through dissection. Fresh human cadavers, by providing excellent sono-graphic images, are potential learning and practice models in ultrasound-guided brachial plexus blocks

AgNWs@TiO₂ and AgNPs@TiO₂ Double-Layer Photoanode Film Improving Light Capture and Application under Low Illumination

In this article, silver nanowires (AgNWs) were prepared and introduced into the double-layer photoanode of dye-sensitized solar cells (DSSCs). Silver nanowires with a diameter of about 50–60 nm and a length of 1–2 mm were prepared by the polyol method. The power conversion efficiency of the double-layer photoanode DSSC made of AgNWs@TiO2 and AgNPs@TiO2 composite materials is 6.38%. Compared with the unmodified DSSC, the composite double-layer photoanode combined with AgNWs and AgNPs increased the efficiency of DSSC by 58.7%. This increased efficiency was mainly due to the localized surface plasmon resonance effect caused by AgNPs and AgNWs. The increased light collection was caused by the plasma effect of AgNPs, and it increased the short-circuit photocurrent density (JSC). The conductive properties of AgNWs improved interface charge transfer and delay charge recombination. The effect of a low light environment on DSSC efficiency was also investigated, and the best photovoltaic conversion efficiency under an irradiance of 10 mW/cm2 was found to be 8.78%

AgNWs@TiO2 and AgNPs@TiO2 Double-Layer Photoanode Film Improving Light Capture and Application under Low Illumination

In this article, silver nanowires (AgNWs) were prepared and introduced into the double-layer photoanode of dye-sensitized solar cells (DSSCs). Silver nanowires with a diameter of about 50–60 nm and a length of 1–2 mm were prepared by the polyol method. The power conversion efficiency of the double-layer photoanode DSSC made of AgNWs@TiO2 and AgNPs@TiO2 composite materials is 6.38%. Compared with the unmodified DSSC, the composite double-layer photoanode combined with AgNWs and AgNPs increased the efficiency of DSSC by 58.7%. This increased efficiency was mainly due to the localized surface plasmon resonance effect caused by AgNPs and AgNWs. The increased light collection was caused by the plasma effect of AgNPs, and it increased the short-circuit photocurrent density (JSC). The conductive properties of AgNWs improved interface charge transfer and delay charge recombination. The effect of a low light environment on DSSC efficiency was also investigated, and the best photovoltaic conversion efficiency under an irradiance of 10 mW/cm2 was found to be 8.78%

Synthesis of Oxygen-Free [2]Rotaxanes: Recognition of Diaryl­guanidinium Ions by Tetraazacyclophanes

Simple cyclophanes containing four distant amino N atoms or ether O atoms behave as hosts for the threading of guest diarylguanidinium ions. The recognition system exhibits high synthetic flexibility, allowing unique O-free [2]­rotaxanes to be synthesized efficiently (yields of up to 80%) through both “threading-followed-by-stoppering” and “clipping” approaches

Temporal Genetic Modifications after Controlled Cortical Impact—Understanding Traumatic Brain Injury through a Systematic Network Approach

Traumatic brain injury (TBI) is a primary injury caused by external physical force and also a secondary injury caused by biological processes such as metabolic, cellular, and other molecular events that eventually lead to brain cell death, tissue and nerve damage, and atrophy. It is a common disease process (as opposed to an event) that causes disabilities and high death rates. In order to treat all the repercussions of this injury, treatment becomes increasingly complex and difficult throughout the evolution of a TBI. Using high-throughput microarray data, we developed a systems biology approach to explore potential molecular mechanisms at four time points post-TBI (4, 8, 24, and 72 h), using a controlled cortical impact (CCI) model. We identified 27, 50, 48, and 59 significant proteins as network biomarkers at these four time points, respectively. We present their network structures to illustrate the protein–protein interactions (PPIs). We also identified UBC (Ubiquitin C), SUMO1, CDKN1A (cyclindependent kinase inhibitor 1A), and MYC as the core network biomarkers at the four time points, respectively. Using the functional analytical tool MetaCore™, we explored regulatory mechanisms and biological processes and conducted a statistical analysis of the four networks. The analytical results support some recent findings regarding TBI and provide additional guidance and directions for future research