Evaluating the Correlation between Overjet and Skeletal Parameters Using DVT

Aim. To evaluate the degree of correlation between a dental parameter of immediate clinical relevance (overjet) with skeletal (ANB angle) and dentoskeletal parameters such as the IMPA angle and upper incisor-bispinal angle. Materials and Methods. A sample of 42 subjects, all in complete permanent dentition and without a history of orthodontic treatment or systemic pathologies, was subdivided into 2 groups: group 1 consisted of 25 subjects with ANB angle 0°–4° (skeletal class I), and group 2 was made up of 17 subjects with ANB angle >4° (skeletal class II). Each subject underwent cone-beam computed tomography (CBCT). For each right and left CBCT, the following parameters were measured: (1) ANB, (2) OJ (overjet), (3) IMPA angle, and (4) upper incisor-bispinal angle (U1/ANS-PNS). Results. Analysis of the entire sample revealed that both right and left overjets were correlated in a statistically significant fashion (<0.001) with ANB. No correlation between overjet and IMPA emerged, while a weak correlation between overjet and the left U1-bispinal plane was ascertained. Conclusions. Overjet may be a reliable predictor of ANB, and to a lesser extent the U1-bispinal plane, particularly in skeletal class II

Influenza virus and redox mediated cell signaling: a complex network of virus/host interaction

Several viruses, including influenza, induce an imbalance of intracellular redox state toward pro-oxidant conditions. Through different mechanisms these alterations contribute both to influenza virus replication and to the pathogene- sis of virus-induced disease. At the same time, influenza virus activates several intracellular signaling pathways involved in important physiological functions of the cell. Interestingly, many of these pathways are finely regulated by small changes in intracellular redox state, and the virus-induced redox imbalance might also control viral replication through this mechanism. Here we review the main intracellular redox-sensitive pathways activated upon influenza infection and involved in reg- ulating viral replication

Influenza virus and redox mediated cell signaling: a complex network of virus/host interaction

Several viruses, including influenza, induce an imbalance of intracellular redox state toward pro-oxidant conditions. Through different mechanisms these alterations contribute both to influenza virus replication and to the pathogenesis of virus-induced disease. At the same time, influenza virus activates several intracellular signaling pathways involved in important physiological functions of the cell. Interestingly, many of these pathways are finely regulated by small changes in intracellular redox state, and the virus-induced redox imbalance might also control viral replication through this mechanism. Here we review the main intracellular redox-sensitive pathways activated upon influenza infection and involved in regulating viral replication

HIV-1 Tat Recruits HDM2 E3 Ligase To Target IRF-1 for Ubiquitination and Proteasomal Degradation

In addition to its ability to regulate HIV-1 promoter activation, the viral transactivator Tat also functions as a determinant of pathogenesis and disease progression by directly and indirectly modulating the host anti-HIV response, largely through the capacity of Tat to interact with and modulate the activities of multiple host proteins. We previously demonstrated that Tat modulated both viral and host transcriptional machinery by interacting with the cellular transcription factor interferon regulatory factor 1 (IRF-1). In the present study, we investigated the mechanistic basis and functional significance of Tat−IRF-1 interaction and demonstrate that Tat dramatically decreased IRF-1 protein stability. To accomplish this, Tat exploited the cellular HDM2 (human double minute 2 protein) ubiquitin ligase to accelerate IRF-1 proteasome-mediated degradation, resulting in a quenching of IRF-1 transcriptional activity during HIV-1 infection. These data identify IRF-1 as a new target of Tat-induced modulation of the cellular protein machinery and reveal a new strategy developed by HIV-1 to evade host immune responses