Moving beyond Volatility Index (VIX): HARnessing the term structure of implied volatility

This paper considers how information from the implied volatility (IV) term structure can be harnessed to improve stock return volatility forecasting within the state-of-the-art HAR model. Factors are extracted from the IV term structure and included as exogenous variables in the HAR framework. We found that including slope and curvature factors leads to significant forecast improvements over the HAR benchmark at a range of forecast horizons, compared with the standard HAR model and HAR model with VIX as IV information set.     

Large contribution of sea surface warming to recent increase in Atlantic hurricane activity

Atlantic hurricane activity has increased significantly since 1995 (refs 1-4), but the underlying causes of this increase remain uncertain. It is widely thought that rising Atlantic sea surface temperatures have had a role in this, but the magnitude of this contribution is not known. Here we quantify this contribution for storms that formed in the tropical North Atlantic, Caribbean Sea and Gulf of Mexico; these regions together account for most of the hurricanes that make landfall in the United States. We show that a statistical model based on two environmental variables--local sea surface temperature and an atmospheric wind field--can replicate a large proportion of the variance in tropical Atlantic hurricane frequency and activity between 1965 and 2005. We then remove the influence of the atmospheric wind field to assess the contribution of sea surface temperature. Our results indicate that the sensitivity of tropical Atlantic hurricane activity to August-September sea surface temperature over the period we consider is such that a 0.5 degrees C increase in sea surface temperature is associated with a approximately 40% increase in hurricane frequency and activity. The results also indicate that local sea surface warming was responsible for approximately 40% of the increase in hurricane activity relative to the 1950-2000 average between 1996 and 2005. Our analysis does not identify whether warming induced by greenhouse gases contributed to the increase in hurricane activity, but the ability of climate models to reproduce the observed relationship between hurricanes and sea surface temperature will serve as a useful means of assessing whether they are likely to provide reliable projections of future changes in Atlantic hurricane activity.     

Global trends in emerging infectious diseases

Emerging infectious diseases (EIDs) are a significant burden on global economies and public health. Their emergence is thought to be driven largely by socio-economic, environmental and ecological factors, but no comparative study has explicitly analysed these linkages to understand global temporal and spatial patterns of EIDs. Here we analyse a database of 335 EID 'events' (origins of EIDs) between 1940 and 2004, and demonstrate non-random global patterns. EID events have risen significantly over time after controlling for reporting bias, with their peak incidence (in the 1980s) concomitant with the HIV pandemic. EID events are dominated by zoonoses (60.3% of EIDs): the majority of these (71.8%) originate in wildlife (for example, severe acute respiratory virus, Ebola virus), and are increasing significantly over time. We find that 54.3% of EID events are caused by bacteria or rickettsia, reflecting a large number of drug-resistant microbes in our database. Our results confirm that EID origins are significantly correlated with socio-economic, environmental and ecological factors, and provide a basis for identifying regions where new EIDs are most likely to originate (emerging disease 'hotspots'). They also reveal a substantial risk of wildlife zoonotic and vector-borne EIDs originating at lower latitudes where reporting effort is low. We conclude that global resources to counter disease emergence are poorly allocated, with the majority of the scientific and surveillance effort focused on countries from where the next important EID is least likely to originate.     

Diurnal change in stature: effects of sleep deprivation in young men and middle-aged men

Sleep deprivation was associated with decreased stature and it blunted the normal 24-h rhythm in young and in middle-aged men. Loss in stature was regained during the first recovery night of sleep. The 24-h rhythm in height is not an endogenous circadian rhythm but depends upon the periods of recumbency over the sleep/wake cycle.     

Fibrillation of tropoelastin induced by proteoglycan

Summary Electrostatic interaction between tropoelastin, the native precursor of elastin, and proteoglycan results in tropoelastin fibrillation. The finding suggests a possible involvement of proteoglycans in elastogenesis.     

Fibrillation of tropoelastin induced by proteoglycan.

Electrostatic interaction between tropoelastin, the native precursor of elastin, and proteoglycan results in tropoelastin fibrillation. The finding suggests a possible involvement of proteoglycans in elastogenesis.     

Pathogenic mutation in the ALS/FTD gene, <Emphasis Type="Italic">CCNF,</Emphasis> causes elevated Lys48-linked ubiquitylation and defective autophagy

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are fatal neurodegenerative disorders that have common molecular and pathogenic characteristics, such as aberrant accumulation and ubiquitylation of TDP-43; however, the mechanisms that drive this process remain poorly understood. We have recently identified CCNF mutations in familial and sporadic ALS and FTD patients. CCNF encodes cyclin F, a component of an E3 ubiquitin–protein ligase (SCF^{cyclin F}) complex that is responsible for ubiquitylating proteins for degradation by the ubiquitin–proteasome system. In this study, we examined the ALS/FTD-causing p.Ser621Gly (p.S621G) mutation in cyclin F and its effect upon downstream Lys48-specific ubiquitylation in transfected Neuro-2A and SH-SY5Y cells. Expression of mutant cyclin F^S621G caused increased Lys48-specific ubiquitylation of proteins in neuronal cells compared to cyclin F^WT. Proteomic analysis of immunoprecipitated Lys48-ubiquitylated proteins from mutant cyclin F^S621G-expressing cells identified proteins that clustered within the autophagy pathway, including sequestosome-1 (p62/SQSTM1), heat shock proteins, and chaperonin complex components. Examination of autophagy markers p62, LC3, and lysosome-associated membrane protein 2 (Lamp2) in cells expressing mutant cyclin F^S621G revealed defects in the autophagy pathway specifically resulting in impairment in autophagosomal–lysosome fusion. This finding highlights a potential mechanism by which cyclin F interacts with p62, the receptor responsible for transporting ubiquitylated substrates for autophagic degradation. These findings demonstrate that ALS/FTD-causing mutant cyclin F^S621G disrupts Lys48-specific ubiquitylation, leading to accumulation of substrates and defects in the autophagic machinery. This study also demonstrates that a single missense mutation in cyclin F causes hyper-ubiquitylation of proteins that can indirectly impair the autophagy degradation pathway, which is implicated in ALS pathogenesis.