Forecasting House Prices in the United States with Multiple Structural Breaks

The boom-bust cycle in U.S. house prices has been a fundamental determinant of the recent financial crisis leading up to the Great Recession. The risky financial innovations in the housing market prior to the recent crisis fueled the speculative housing boom. In this backdrop, the main objectives of this empirical study are to i) detect the possibility of multiple structural breaks in the US house price data during 1995-2010, exhibiting very sharp upturns and downturns; ii) endogenously determine the break points and iii) conduct house price forecasting exercises to see how models with structural breaks fare with competing time series models – linear and nonlinear. Using a very general methodology (Bai-Perron, 1998, 2003), we found four break points in the trend in the S&P/Case-Shiller 10 city aggregate house-price index series. Next, we compared the forecasting performance of the model with structural breaks to four competing models – namely, Random Acceleration (RA), Autoregressive Moving Average (ARMA), SelfExciting Threshold Autoregressive (SETAR), and Smooth Transition Autoregressive (STAR). Our findings suggest that house price series not only has undergone structural changes but also regime shifts. Hence, forecasting models that assume constant coefficients such as ARMA may not accurately capture house price dynamics

Reemergence of Epidemic Vibrio cholerae O139, Bangladesh

During March and April 2002, a resurgence of Vibrio cholerae O139 occurred in Dhaka and adjoining areas of Bangladesh with an estimated 30,000 cases of cholera. Patients infected with O139 strains were much older than those infected with O1 strains (p<0.001). The reemerged O139 strains belong to a single ribotype corresponding to one of two ribotypes that caused the initial O139 outbreak in 1993. Unlike the strains of 1993, the recent strains are susceptible to trimethoprim, sulphamethoxazole, and streptomycin but resistant to nalidixic acid. The new O139 strains carry a copy of the Calcutta type CTXCalc prophage in addition to the CTXET prophage carried by the previous strains. Thus, the O139 strains continue to evolve, and the adult population continues to be more susceptible to O139 cholera, which suggests a lack of adequate immunity against this serogroup. These findings emphasize the need for continuous monitoring of the new epidemic strains

Accessing dual toroidal modes in terahertz plasmonic metasurfaces through polarization-sensitive resonance hybridization

Plasmonic metasurfaces have been quite a fascinating framework to invoke transformation of incident electromagnetic waves for a while now. Oftentimes, the building block of these metasurfaces or the unit cells consists of two or more meta-resonators. As a consequence, near-field coupling amongst these constituents may occur depending upon the spatial and spectral separation of the individual elements (meta-resonators). In such coupled structures resonance mode-hybridization can help in explaining the formation and energy re-distribution among the resonance modes. However, the coupling of these plasmonic modes is extremely sensitive to the polarization of the incident probe beam and offers ample amount of scope to harness newer physics. A qualitative understanding of the same can be attained through mode-hybridization phenomena. In this context, here, we have proposed a multi-element metastructure unit cell consisting of split ring and dipole resonators aiming to explore the intricate effects of the polarization dependency of these hybridized modes. Multi-resonator systems with varied inter-resonator spacing ( sp = 3.0, 5.0, and 7.0 μ m) are fabricated and characterized in the terahertz domain, showing a decrement in the frequency detuning ( δ ) by 30% (approx.) for a particular polarization orientation of THz probe beam. However, no such detuning is observed for the other orthogonal polarization configuration. Therefore, modulation of the resonance-hybridization is strongly dependent on the terahertz beam polarization. Further, as an outcome of the strong near-field coupling, the emergence of dual toroidal modes is observed. Excitation of toroidal modes demands thoughtful mode engineering to amplify the response of these otherwise feeble modes. Such modes are capable of strongly confining electromagnetic fields due to higher Quality (Q-) factor. Our experimental studies have shown significant signature of the presence of these modes in the Terahertz (THz) domain, backed up by rigorous numerical investigations along with multipole analysis. The calculated multipole decomposition demonstrates stronger scattering amplitude enhancements (∼7 times) at both the toroidal modes compared to off-resonant values. Such dual toroidal resonances are capable of superior field confinements as compared to single toroidal mode, and therefore, can potentially serve as an ideal testbed in developing next-generation multi-mode bio-sensors as well as realization of high Q-factor lasing cavities, electromagnetically induced transparency, non-radiating anapole modes, novel ultrafast switching, and several other applications

Human Primary Epithelial Cells Acquire an Epithelial-Mesenchymal-Transition Phenotype during Long-Term Infection by the Oral Opportunistic Pathogen, Porphyromonas gingivalis

Porphyromonas gingivalis is a host-adapted oral pathogen associated with chronic periodontitis that successfully survives and persists in the oral epithelium. Recent studies have positively correlated periodontitis with increased risk and severity of oral squamous cell carcinoma (OSCC). Intriguingly, the presence of P. gingivalis enhances tumorigenic properties independently of periodontitis and has therefore been proposed as a potential etiological agent for OSCC. However, the initial host molecular changes induced by P. gingivalis infection which promote predisposition to cancerous transformation through EMT (epithelial-mesenchymal-transition), has never been studied in human primary cells which more closely mimic the physiological state of cells in vivo. In this study, we examine for the first time in primary oral epithelial cells (OECs) the expression and activation of key EMT mediators during long-term P. gingivalis infection in vitro. We examined the inactive phosphorylated state of glycogen synthase kinase-3 beta (p-GSK3β) over 120 h P. gingivalis infection and found p-GSK3β, an important EMT regulator, significantly increases over the course of infection (p &lt; 0.01). Furthermore, we examined the expression of EMT-associated transcription factors, Slug, Snail, and Zeb1 and found significant increases (p &lt; 0.01) over long-term P. gingivalis infection in protein and mRNA expression. Additionally, the protein expression of mesenchymal intermediate filament, Vimentin, was substantially increased over 120 h of P. gingivalis infection. Analysis of adhesion molecule E-cadherin showed a significant decrease (p &lt; 0.05) in expression and a loss of membrane localization along with β-catenin in OECs. Matrix metalloproteinases (MMPs) 2, 7, and 9 are all markedly increased with long-term P. gingivalis infection. Finally, migration of P. gingivalis infected cells was evaluated using scratch assay in which primary OEC monolayers were wounded and treated with proliferation inhibitor, Mitomycin C. The cellular movement was determined by microscopy. Results displayed P. gingivalis infection promoted cell migration which was slightly enhanced by co-infection with Fusobacterium nucleatum, another oral opportunistic pathogen. Therefore, this study demonstrates human primary OECs acquire initial molecular/cellular changes that are consistent with EMT induction during long-term infection by P. gingivalis and provides a critically novel framework for future mechanistic studies

Genetic diversity and virulence potential of environmental Vibrio cholerae population in a cholera-endemic area

To understand the evolutionary events and possible selection mechanisms involved in the emergence of pathogenic Vibrio cholerae, we analyzed diverse strains of V. cholerae isolated from environmental waters in Bangladesh by direct enrichment in the intestines of adult rabbits and by conventional laboratory culture. Strains isolated by conventional culture were mostly (99.2%) negative for the major virulence gene clusters encoding toxin-coregulated pilus (TCP) and cholera toxin (CT) and were nonpathogenic in animal models. In contrast, all strains selected in rabbits were competent for colonizing infant mice, and 56.8% of these strains carried genes encoding TCP alone or both TCP and CT. Ribotypes of toxigenic O1 and O139 strains from the environment were similar to pandemic strains, whereas ribotypes of non-O1 non-O139 strains and TCP(-) nontoxigenic O1 strains diverged widely from the seventh pandemic O1 and the O139 strains. Results of this study suggest that (i) the environmental V. cholerae population in a cholera-endemic area is highly heterogeneous, (ii) selection in the mammalian intestine can cause enrichment of environmental strains with virulence potential, (iii) pathogenicity of V. cholerae involves more virulence genes than currently appreciated, and (iv) most environmental V. cholerae strains are unlikely to attain a pandemic potential by acquisition of TCP and CT genes alone. Because most of the recorded cholera pandemics originated in the Ganges Delta region, this ecological setting presumably favors extensive genetic exchange among V. cholerae strains and thus promotes the rare, multiple-gene transfer events needed to assemble the critical combination of genes required for pandemic spread

Pathogenic Potential of Environmental Vibrio cholerae Strains Carrying Genetic Variants of the Toxin-Coregulated Pilus Pathogenicity Island

The major virulence factors of toxigenic Vibrio cholerae are cholera toxin (CT), which is encoded by a lysogenic bacteriophage (CTXΦ), and toxin-coregulated pilus (TCP), an essential colonization factor which is also the receptor for CTXΦ. The genes for the biosynthesis of TCP are part of a larger genetic element known as the TCP pathogenicity island. To assess their pathogenic potential, we analyzed environmental strains of V. cholerae carrying genetic variants of the TCP pathogenicity island for colonization of infant mice, susceptibility to CTXΦ, and diarrheagenicity in adult rabbits. Analysis of 14 environmental strains, including 3 strains carrying a new allele of the tcpA gene, 9 strains carrying a new allele of the toxT gene, and 2 strains carrying conventional tcpA and toxT genes, showed that all strains colonized infant mice with various efficiencies in competition with a control El Tor biotype strain of V. cholerae O1. Five of the 14 strains were susceptible to CTXΦ, and these transductants produced CT and caused diarrhea in adult rabbits. These results suggested that the new alleles of the tcpA and toxT genes found in environmental strains of V. cholerae encode biologically active gene products. Detection of functional homologs of the TCP island genes in environmental strains may have implications for understanding the origin and evolution of virulence genes of V. cholerae

Genomic analysis of the Mozambique strain of Vibrio cholerae O1 reveals the origin of El Tor strains carrying classical CTX prophage

Cholera outbreaks in subSaharan African countries are caused by strains of the El Tor biotype of toxigenic Vibrio cholerae O1. The El Tor biotype is the causative agent of the current seventh cholera pandemic, whereas the classical biotype, which was associated with the sixth pandemic, is now extinct. Besides other genetic differences the CTX prophages encoding cholera toxin in the two biotypes of V. cholerae O1 have distinct repressor (rstR) genes. However, recent incidences of cholera in Mozambique were caused by an El Tor biotype V. cholerae O1 strain that, unusually, carries a classical type (CTX<SUP>class</SUP>) prophage. We conducted genomic analysis of the Mozambique strain and its CTX prophage together with chromosomal phage integration sites to understand the origin of this atypical strain and its evolutionary relationship with the true seventh pandemic strain. These analyses showed that the Mozambique strain carries two copies of CTXclass prophage located on the small chromosome in a tandem array that allows excision of the prophage, but the excised phage genome was deficient in replication and did not produce CTX<SUP>class</SUP> virion. Comparative genomic microarray analysis revealed that the strain shares most of its genes with the typical El Tor strain N16961 but did not carry the TLC gene cluster, and RS1 sequence, adjacent to the CTX prophage. Our data are consistent with the Mozambique strain's having evolved from a progenitor similar to the seventh pandemic strain, involving multiple recombination events and suggest a model for origination of El Tor strains carrying the classical CTX prophage