Effect of Interferon-α Treatment of Chronic Hepatitis C on Health-Related Quality of Life

Studies of interferon- (IFN-)therapy for chronic hepatitis C have focused on viralclearance; however, few have evaluated patient'shealth-related quality of life during therapy. Thisstudy evaluates health-related quality of life and theprevalence of anxiety and depression in patients withchronic hepatitis C before, during, and followingIFN- therapy. Patients undergoing IFN-therapy for chronic hepatitis C were asked to completehealth status measures as well as anxiety and depressioninventories before, during, and following IFN-therapy. These measures were compared to the results of healthy adults in the general US population.Thirty-eight of forty-eight eligible patients (79%) withchronic hepatitis C completed the questionnaires.Respondents demonstrated a significant increase in depression during the sixth month ofinterferon therapy in comparison to pretreatmentresults. Anxiety scores improved significantly after onemonth of IFN- in comparison to pretreatmentresults. Scores on the health status measures did notvary with IFN- therapy. Patient responses wereanalyzed with respect to biochemical response(normalized transaminases) to IFN-. IFN-responders, who were aware of their transaminase results,exhibited lower scores on anxiety subscales during andafter therapy (P = 0.02-0.04). Scores on the healthstatus subscale, role emotional, improved in IFN- responders compared to nonresponders during thesixth month of therapy (P = 0.02). Response toIFN- therapy was not associated with any otherdifferences on subscale analysis. Patients with chronichepatitis C exhibited health perceptions similar to thegeneral US population, and these were unchanged duringIFN- therapy. However, the incidence ofdepression significantly increased during the sixthmonth of IFN- therapy. IFN- respondersexhibited fewer emotional problems as well as a lowerincidence of anxiety during and followingtherapy.     

A switch from inter‐ocular to inter‐hemispheric suppression following monocular deprivation in the rat visual cortex

Binocularity is a key property of primary visual cortex (V1) neurons that is widely used to study synaptic integration in the brain and plastic mechanisms following an altered visual experience. However, it is not clear how the inputs from the two eyes converge onto binocular neurons, and how their interaction is modified by an unbalanced visual drive. Here, using visual evoked potentials recorded in the juvenile rat V1, we report evidence for a suppressive mechanism by which contralateral eye activity inhibits responses from the ipsilateral eye. Accordingly, we found a lack of additivity of the responses evoked independently by the two eyes in the V1, and acute silencing of the contralateral eye resulted in the enhancement of ipsilateral eye responses in cortical neurons. We reverted the relative cortical strength of the two eyes by suturing the contralateral eye shut [monocular deprivation (MD)]. After 7 days of MD, there was a loss of interocular suppression mediated by the contralateral, deprived eye, and weak inputs from the closed eye were functionally inhibited by interhemispheric callosal pathways. We conclude that interocular suppressive mechanisms play a crucial role in shaping normal binocularity in visual cortical neurons, and a switch from interocular to interhemispheric suppression represents a key step in the ocular dominance changes induced by MD. These data have important implications for a deeper understanding of the key mechanisms that underlie activity‐dependent rearrangements of cortical circuits following alteration of sensory experience.     

Proteomic Analyses of Human Gingival and Periodontal Ligament Fibroblasts

Background: Although human gingival fibroblasts (hGFs) and human periodontal ligament fibroblasts (hPDLFs) exhibit numerous phenotypic similarities, it has been suggested that the secretory and behavioral differences, which exist between these cell types, are a result of the membrane protein composition of these cells. Methods: Four matched pairs of hGFs and hPDLFs were cultured. Before confluence, membrane‐bound and ‐associated proteins from cells of the fourth passage were extracted. The processed protein samples were evaluated using capillary‐liquid chromatography‐nanospray tandem mass spectrometry. Global protein identification was performed on an orbitrap mass spectrometer equipped with a microspray source operated in positive ion mode. Proteome software was used to validate protein identifications derived from tandem mass spectrometry sequencing results. Results: Four hundred fifty proteins were common to both hGFs and hPDLFs. Of the proteins identified, 214 were known membrane‐bound or ‐associated proteins, and 165 proteins were known nuclear‐associated proteins. Twenty‐seven proteins, identified from the 450 proteins, common to both hGFs and hPDLFs, were detected in statistically significant greater quantities in either hGFs or hPDLFs. More specifically, 13 proteins were detected in significantly greater quantities in hGFs, whereas 14 proteins were detected in significantly greater quantities in hPDLFs. Conclusions: Distinct differences in the cellular protein catalog may reflect the dynamic role and high energy requirements of hGFs in extracellular matrix remodeling and response to inflammatory challenge as well as the role of hPDLFs in monitoring mechanical stress and maintaining tissue homeostasis during regeneration and remineralization.