Are Current or Future Mesothelioma Epidemics in Hong Kong the Tragic Legacy of Uncontrolled Use of Asbestos in the Past?

BACKGROUND: Because of the long latent period of asbestos-related mesothelioma, investigators suggest that the high incidence of this disease will continue in the coming decades. OBJECTIVES: We describe the time trends of mesothelioma incidence and its relationship to historical consumption of asbestos in Hong Kong and project future trends of mesothelioma incidence. METHODS: We obtained local annual consumption of total asbestos for 1960-2006 (converted to kilograms per person per year). Age-standardized incidence rates (ASIRs) of mesothelioma were computed and depicted on graphs using the centered moving average method. Indirectly standardized rates were regressed on a transformation of consumption data that assumed that the latency between asbestos exposure and mesothelioma diagnosis followed a normal distribution with a mean ± SD of 42 ± 10.5 years. RESULTS: ASIRs for males started to increase substantially in 1994 and were highest in 2004; for females, ASIRs climbed in the 1980s and in the early 1990s but have fluctuated without obvious trends in recent years. The highest asbestos consumption level in Hong Kong was in 1960-1963 and then decreased sharply afterward. Using past asbestos consumption patterns, we predict that the mesothelioma incidence rate for males will peak in 2009, with the number of cases peaking in 2014, and then slowly decline in the coming decades. CONCLUSIONS: Hong Kong experienced an epidemic of mesothelioma from 2000 to 2006 that corresponded with the peak of local asbestos consumption in the early 1960s assuming an average latent period of 42 years. The incidence is anticipated to decline in the coming decades but may not decrease back to the background risk level (the risk unrelated to asbestos exposure)

Au Nanoparticles as Interfacial Layer for CdS Quantum Dot-sensitized Solar Cells

Quantum dot-sensitized solar cells based on fluorine-doped tin oxide (FTO)/Au/TiO2/CdS photoanode and polysulfide electrolyte are fabricated. Au nanoparticles (NPs) as interfacial layer between FTO and TiO2 layer are dip-coated on FTO surface. The structure, morphology and impedance of the photoanodes and the photovoltaic performance of the cells are investigated. A power conversion efficiency of 1.62% has been obtained for FTO/Au/TiO2/CdS cell, which is about 88% higher than that for FTO/TiO2/CdS cell (0.86%). The easier transport of excited electron and the suppression of charge recombination in the photoanode due to the introduction of Au NP layer should be responsible for the performance enhancement of the cell

Pancreatic β-Cell Death in Response to Pro-Inflammatory Cytokines Is Distinct from Genuine Apoptosis

A reduction in functional β-cell mass leads to both major forms of diabetes; pro-inflammatory cytokines, such as interleukin-1beta (IL-1β) and gamma-interferon (γ-IFN), activate signaling pathways that direct pancreatic β-cell death and dysfunction. However, the molecular mechanism of β-cell death in this context is not well understood. In this report, we tested the hypothesis that individual cellular death pathways display characteristic phenotypes that allow them to be distinguished by the precise biochemical and metabolic responses that occur during stimulus-specific initiation. Using 832/13 and INS-1E rat insulinoma cells and isolated rat islets, we provide evidence that apoptosis is unlikely to be the primary pathway underlying β-cell death in response to IL-1β+γ-IFN. This conclusion was reached via the experimental results of several different interdisciplinary strategies, which included: 1) tandem mass spectrometry to delineate the metabolic differences between IL-1β+γ-IFN exposure versus apoptotic induction by camptothecin and 2) pharmacological and molecular interference with either NF-κB activity or apoptosome formation. These approaches provided clear distinctions in cell death pathways initiated by pro-inflammatory cytokines and bona fide inducers of apoptosis. Collectively, the results reported herein demonstrate that pancreatic β-cells undergo apoptosis in response to camptothecin or staurosporine, but not pro-inflammatory cytokines

A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (me/cfs) and sickness behavior

It is of importance whether myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a variant of sickness behavior. The latter is induced by acute infections/injury being principally mediated through proinflammatory cytokines. Sickness is a beneficial behavioral response that serves to enhance recovery, conserves energy and plays a role in the resolution of inflammation. There are behavioral/symptomatic similarities (for example, fatigue, malaise, hyperalgesia) and dissimilarities (gastrointestinal symptoms, anorexia and weight loss) between sickness and ME/CFS. While sickness is an adaptive response induced by proinflammatory cytokines, ME/CFS is a chronic, disabling disorder, where the pathophysiology is related to activation of immunoinflammatory and oxidative pathways and autoimmune responses. While sickness behavior is a state of energy conservation, which plays a role in combating pathogens, ME/CFS is a chronic disease underpinned by a state of energy depletion. While sickness is an acute response to infection/injury, the trigger factors in ME/CFS are less well defined and encompass acute and chronic infections, as well as inflammatory or autoimmune diseases. It is concluded that sickness behavior and ME/CFS are two different conditions

Efficient electron injection in organic light emitting diodes with Al-Mg alloy cathode

We report the enhancement of electron injection using an Al-Mg alloy cathode in organic light emitting diodes (OLEDs). The luminescence value at 15 V drastically increased from 800 to 5800 cd/m(2) as the Al cathode was replaced by an Al-Mg alloy with a 1:1 ratio of Al to Mg in weight percent. Synchrotron radiation photoelectron spectroscopy results showed that the work function of the Al-Mg alloy is lower by 0.2 eV than that of Al. Thus, the energy barrier for electron injection was lowered, reducing the turn-on voltage and increasing the quantum efficiency of OLEDs. (c) 2005 The Electrochemical Society. [DOI: 10.1149/1.2135426] All rights reserved.X11159sciescopu

Uric acid and xanthine oxidoreductase in wound healing

Chronic wounds are an important health problem because they are difficult to heal and treatment is often complicated, lengthy and expensive. For a majority of sufferers the most common outcomes are long-term immobility, infection and prolonged hospitalisation. There is therefore an urgent need for effective therapeutics that will enhance ulcer healing and patient quality of life, and will reduce healthcare costs. Studies in our laboratory have revealed elevated levels of purine catabolites in wound fluid from patients with venous leg ulcers. In particular, we have discovered that uric acid is elevated in wound fluid, with higher concentrations correlating with increased wound severity. We have also revealed a corresponding depletion in uric acid precursors, including adenosine. Further, we have revealed that xanthine oxidoreductase, the enzyme that catalyses the production of uric acid, is present at elevated levels in wound fluid. Taken together, these findings provide evidence that xanthine oxidoreductase may have a function in the formation or persistence of chronic wounds. Here we describe the potential function of xanthine oxidoreductase and uric acid accumulation in the wound site, and the effect of xanthine oxidoreductase in potentiating the inflammatory response

Modulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki disease

Systemic arterial stiffness is increased in patients after Kawasaki disease (KD). Recently, associations between mannose-binding lectin (MBL) gene mutation and coronary complications in infants with KD and atherosclerosis in adults have been reported. We tested the hypothesis that MBL genotype modulates arterial stiffness in children after KD. Seventy-one KD patients (42 with and 29 without coronary aneurysms), aged 9.5 ± 3.7 y, and 41 age-matched controls were studied. We determined and compared their blood pressure, brachioradial arterial stiffness as determined by pulse wave velocity (PWV), fasting total cholesterol, serum MBL level, and MBL genotype. Additionally, the modulating effects of different MBL expression genotypes [high level (HL) versus intermediate or low level (IL/LL)] on arterial stiffness in different groups were assessed. The MBL genotype distributions did not differ between patients and controls (p = 0.41) or between patients with and without coronary aneurysms (p = 0.42). Patients with IL/LL expression genotypes had significantly faster PWV than those with HL expression genotypes (7.93 ± 1.38 m/s versus 6.67 ± 2.28 m/s, p = 0.027). This genotype-modulating effect is more pronounced in patients without (HL 8.86 ± 0.77 m/s versus IL/LL 6.48 ± 2.32 m/s, p = 0.02) than those with (HL 7.50 ± 1.41 m/s versus IL/LL 6.80 ± 2.28 m/s, p = 0.32) coronary aneurysms. Multiple linear regresion analysis identified age (β = 0.26, p = 0.012), being a Kawasaki patient (β = 0.22, p = 0.015), and MBL IL/LL genotype subgroup (β = 0.20, p = 0.03) as significant determinants of arterial stiffness in the entire cohort. In conclusion, MBL genotype modulates arterial stiffness, an important cardiovascular risk factor, in children after KD.link_to_subscribed_fulltex