Severe drug-induced gingival enlargement and periodontitis: A case series with clinical presentation and management

Gingival enlargement (GE) is a condition in which the size of the gingiva increases in response to inflammation, systemic disease, or certain medications including anticonvulsants, calcium-channel blockers, and immunosuppressants. This report describes the management of two cases involving severe gingival enlargement related to the use of an anti-hypertensive calcium-channel blocker and an immunosuppressant. Besides taking amlodipine, one patient had undergone a heart transplantation seven years prior and has been taking two immunosuppressant drugs, mycophenolate and tacrolimus. The extent of the destruction of periodontal support, aggravated by gingival enlargement, resulted in extensive tooth loss. Periodontitis and gingival enlargement exacerbate and accelerate one another and can result in loss of the entire dentition, severely affecting function and esthetics. The pharmacologic etiology sometimes cannot be altered and the patient has to be carefully managed and maintained with periodontal therapy. Physicians and dentists should be aware of these medications and be able to identify early changes in the oral cavity and to prevent, diagnose, and successfully manage the unwanted side effects of these drugs in patients

Specific Soluble Oligomers of Amyloid-β Peptide Undergo Replication and Form Non-Fibrillar Aggregates in Interfacial Environments

Aggregates of amyloid-β (Aβ) peptides have been implicated in the etiology of Alzheimer disease. Among the different forms of Aβ aggregates, low molecular weight species ranging between ∼2- and 50-mers, also called “soluble oligomers,” have emerged as the species responsible for early synaptic dysfunction and neuronal loss. Emerging evidence suggests that the neurotoxic oligomers need not be formed along the obligatory nucleation-dependant fibril formation pathway. In our earlier work, we reported the isolation of one such “off-pathway” 12–18-mer species of Aβ42 generated from fatty acids called large fatty acid-derived oligomers (LFAOs) (Kumar, A., Bullard, R. L., Patel, P., Paslay, L. C., Singh, D., Bienkiewicz, E. A., Morgan, S. E., and Rangachari, V. (2011) PLoS One 6, e18759). Here, we report the physiochemical aspects of LFAO-monomer interactions as well as LFAO-LFAO associations in the presence of interfaces. We discovered that LFAOs are a replicating strain of oligomers that recruit Aβ42 monomers and quantitatively convert them into LFAO assemblies at the expense of fibrils, a mechanism similar to prion propagation. We also found that in the presence of hexane-buffer or chloroform-buffer interfaces LFAOs are able to associate with themselves to form larger but non-fibrillar aggregates. These results further support the hypothesis that low molecular weight oligomers can be generated via non-fibril formation pathways. Furthermore, the unique replicating property of off-pathway oligomers may hold profound significance for Alzheimer disease pathology

Childhood Adversity is Associated with Left Basal Ganglia Dysfunction During Reward Anticipation in Adulthood

Background: Childhood adversity increases the risk of psychopathology, but the neurobiological mechanisms underlying this vulnerability are not well-understood. In animal models, early adversity is associated with dysfunction in basal ganglia regions involved in reward processing, but this relationship has not been established in humans. Methods: Functional magnetic resonance imaging was used to examine basal ganglia responses to (a) cues signaling possible monetary rewards and losses, and (b) delivery of monetary gains and penalties, in 13 young adults who experienced maltreatment before age 14 and 31 non-maltreated controls. Results: Relative to controls, individuals exposed to childhood adversity reported elevated symptoms of anhedonia and depression, rated reward cues less positively, and displayed a weaker response to reward cues in the left globus pallidus. There were no group differences in right hemisphere basal ganglia response to reward cues, or in basal ganglia response to loss cues, no-incentive cues, gains, or penalties. Conclusions: Results indicate that childhood adversity in humans is associated with blunted subjective responses to reward-predicting cues as well as dysfunction in left basal ganglia regions implicated in reward-related learning and motivation. This dysfunction may serve as a diathesis that contributes to the multiple negative outcomes and psychopathologies associated with childhood adversity. The findings suggest that interventions that target motivation and goal-directed action may be useful for reducing the negative consequences of childhood adversity.Psycholog

Electrical Anomalies Observed During DC3

The primary scientific goals of DC3 involved improving our understanding of the chemical impacts of thunderstorms and their anvils. However, the Colorado domain provided opportunities to study other interesting phenomena, including the potential impacts of smoke ingestion on convection and thunderstorms, electrification processes in smoke plumes and pyrocumulonimbus clouds, and the production of sprites by unconventional thunderstorm

Underdiagnosis of mild cognitive impairment: A consequence of ignoring practice effects

INTRODUCTION: Longitudinal testing is necessary to accurately measure cognitive change. However, repeated testing is susceptible to practice effects, which may obscure true cognitive decline and delay detection of mild cognitive impairment (MCI). METHODS: We retested 995 late-middle-aged men in a ∼6-year follow-up of the Vietnam Era Twin Study of Aging. In addition, 170 age-matched replacements were tested for the first time at study wave 2. Group differences were used to calculate practice effects after controlling for attrition effects. MCI diagnoses were generated from practice-adjusted scores. RESULTS: There were significant practice effects on most cognitive domains. Conversion to MCI doubled after correcting for practice effects, from 4.5% to 9%. Importantly, practice effects were present although there were declines in uncorrected scores. DISCUSSION: Accounting for practice effects is critical to early detection of MCI. Declines, when lower than expected, can still indicate practice effects. Replacement participants are needed for accurately assessing disease progression.Published versio

Response to Questions in the First White Paper, \u27Modernizing the Communications Act\u27

The House Energy and Commerce Committee has begun a process to review and update the Communications Act of 1934, last revised in any material way in 1996. As the Committee begins the review process, this paper responds to questions posed by the Committee that all relate, in fundamental ways, to the question: What should a modern Communications Act look like? The Response advocates a clean slate approach under which the regulatory silos that characterize the current statute would be eliminated, along with almost all of the ubiquitous \u27public interest\u27 delegation of authority found throughout the Communications Act. The replacement regime would have at its core a new competition-based standard that, except in limited circumstances, would require that the FCC\u27s regulatory activities be tied to findings of consumer harm resulting from lack of sufficient competition. The FCC\u27s authority to adopt broad anticipatory rules on an ex ante basis would be substantially circumscribed, and the agency would be required to rely more heavily than is presently the case on ex post adjudication of individual complaints alleging specific abuses of market power and consumer harm. Some aspects of the FCC\u27s current jurisdiction, such as privacy and data security regulation, might be transferred to the FTC in light of the FTC\u27s institutional competence in these areas