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The etiologic basis for sporadic forms of neurodegenerative diseases has been elusive but likely represents the product of genetic predisposition and various environmental factors. Specific gene-environment interactions have become more salient owing, in part, to the elucidation of epigenetic mechanisms and their impact on health and disease. The linkage between traumatic brain injury (TBI) and Parkinson's disease (PD) is one such association that currently lacks a mechanistic basis. Herein, we present preliminary blood-based metabolomic evidence in support of potential association between TBI and PD. Using untargeted and targeted high-performance liquid chromatography-mass spectrometry we identified metabolomic biomarker profiles in a cohort of symptomatic mild TBI (mTBI) subjects (n = 75) 3⁻12 months following injury (subacute) and TBI controls (n = 20), and a PD cohort with known PD (n = 20) or PD dementia (PDD) (n = 20) and PD controls (n = 20). Surprisingly, blood glutamic acid levels in both the subacute mTBI (increased) and PD/PDD (decreased) groups were notably altered from control levels. The observed changes in blood glutamic acid levels in mTBI and PD/PDD are discussed in relation to other metabolite profiling studies. Should our preliminary results be replicated in comparable metabolomic investigations of TBI and PD cohorts, they may contribute to an "excitotoxic" linkage between TBI and PD/PDD.

Biostimulation to induce reduction of soluble U(VI) to relatively immobile U(IV) is an effective strategy for decreasing aqueous U(VI) concentrations in contaminated groundwater systems. If oxidation of U(IV) occurs following the biostimulation phase, U(VI) concentrations increase, challenging the long-term effectiveness of this technique. However, detecting U(IV) oxidation through dissolved U concentrations alone can prove difficult in locations with few groundwater wells to track the addition of U to a mass of groundwater. We propose the 238U/235U ratio of aqueous U as an independent, reliable tracer of U(IV) remobilization via oxidation or mobilization of colloids. Reduction of U(VI) produces 238U-enriched U(IV), whereas remobilization of solid U(IV) should not induce isotopic fractionation. The incorporation of remobilized U(IV) with a high 238U/235U ratio into the aqueous U(VI) pool produces an increase in 238U/235U of aqueous U(VI). During several injections of nitrate to induce U(IV) oxidation, 238U/235U consistently increased, suggesting 238U/235U is broadly applicable for detecting mobilization of U(IV).

One of the major ecological concerns associated with the in situ recovery (ISR) of uranium (U) is the environmental release of soluble, toxic selenium (Se) oxyanions generated by mining. Post-mining natural attenuation by the residual reductants in the ore body and reduced down-gradient sediments should mitigate the risk of Se contamination in groundwater. In this work, we investigate the Se concentrations and Se isotope systematics of groundwater and of U ore bearing sediments from an ISR site at Rosita, TX, USA. Our results show that selenate (Se(VI)) is the dominant Se species in Rosita groundwater, and while several up-gradient wells have elevated Se(VI), the majority of the ore zone and down-gradient wells have little or no Se oxyanions. In addition, the δ82SeVI of Rosita groundwater is generally elevated relative to the U ore up to +6.14‰, with the most enriched values observed in the ore-zone wells. Increasing δ82Se with decreasing Se(VI) conforms to a Rayleigh type distillation model with an ε of -2.25‰ ± 0.61‰, suggesting natural Se(VI) reduction occurring along the hydraulic gradient at the Rosita ISR site. Furthermore, our results show that Se isotopes are excellent sensors for detecting and monitoring post-mining natural attenuation of Se oxyanions at ISR sites.

Purpose/objectives: The objectives of this study were to assess the influence of learner‐ and education‐related factors on standardized in‐service examination performance and determine whether in‐service examination scores predict residency outcomes. Methods: American Academy of Periodontology (AAP) In‐service Examination (AIE) scores from 10 periodontics residency classes at a single center were recorded and compared against a panel of learner‐ and education‐related variables using multiple linear regression models. Defined residency outcome measures were analyzed against AIE scores using binomial logistic regression. Results: No evaluated learner‐ or education‐related variable was a statistically significant predictor of AIE score in this study sample. Likewise, AIE score was not a statistically significant predictor of any assessed residency outcome. Conclusions: The AAP has performed a tremendous service to periodontics residents and programs by marshaling the leadership and expertise necessary to offer a professionally constructed assessment instrument. However, in the current study, no relationship could be identified between AIE score and any outcome, including first‐attempt board certification. The AAP In‐service Committee appears well situated to provide additional leadership focusing on exam implementation, which may enhance AIE value in competency decision making. [ABSTRACT FROM AUTHOR]

Background: The physiologic bone remodeling accompanying tooth extraction is a phenomenon well described in the dental literature. Extraction sockets severely compromised by local infection, trauma, iatrogenesis, or other factors may exhibit enhanced reduction in alveolar dimensions during healing. The purpose of this report is to present an alveolar ridge preservation (ARP) protocol specifically intended for use at severely compromised sites. Methods: Seven patients presented to the Department of Periodontics, Army Postgraduate Dental School, Fort Gordon, Georgia, requiring extraction of teeth with partial or near‐complete loss of the facial/buccal cortex. At each site, a cross‐linked bovine collagen membrane was used to prevent collapse of the facial/buccal soft tissue and maintain space, a freeze‐dried bone allograft was applied in the socket, and a dense polytetrafluoroethylene membrane covered the occlusal aspect. Results: All sites healed uneventfully and resulted in favorable alveolar ridge dimensions for implant placement. Conclusion: Few authors have proposed specific ARP methods for managing severely deficient extraction sockets. The predominant recommendation has been staged reconstruction of the site applying hard and soft tissue augmentation. Observations reported herein suggest that staged reconstruction is avoidable at some extraction sockets exhibiting severe alveolar compromise. Controlled clinical investigation of this protocol appears warranted. Key points: Few authors have proposed alveolar ridge preservation (ARP) methods specifically intended for use at severely compromised extraction sockets.The prevailing recommendation at such sites is a staged protocol involving tooth extraction with delayed hard and soft tissue augmentation.The presented bilaminar ARP technique may eliminate the need for staged reconstruction at some severely compromised extraction sockets. [ABSTRACT FROM AUTHOR]

Background: Delivery of a high‐quality provisional restoration at a maxillary anterior immediate implant site enhances patient‐centered outcomes and promotes development of favorable hard and soft tissue architecture. The purpose of this report is to present a protocol relying upon compatible guided surgery and laboratory systems for fabrication of a custom provisional crown prior to immediate implant surgery in the esthetic zone. Methods and Results: A female patient, aged 33 years, presented to the Army Postgraduate Dental School, Fort Gordon, Georgia, with an unfavorable prognosis for tooth #9. The patient elected extraction with immediate implant placement. Prior to the surgery, we utilized a cone‐beam computed tomography volume, stone models, implant planning software, and an implant indexing system to fabricate a custom provisional crown. Following extraction of tooth #9 and immediate implant placement, the provisional crown exhibited excellent fit and finish, requiring virtually no chairside adjustment. We noted minimal change in baseline mucosal contours throughout the healing phase. Conclusion: The clinical/restorative protocol described in this report assured accurate three‐dimensional implant positioning and permitted indirect fabrication of a high‐quality custom provisional crown in advance of surgery. The laboratory workflow—which dental technicians/auxiliaries can master—has the potential to shorten surgery, enhance treatment outcomes, and increase patient satisfaction. Key points: Why is this case new information? This report provides a stepwise workflow guiding indirect fabrication of a custom provisional crown prior to immediate implant placement. What are the keys to successful management of this case? The described technique requires compatible laboratory and guided surgery systems to assure that the restoration accounts for the three‐dimensional position and timing of the implant. What are the primary limitations to success in this case? Dental technicians/auxiliaries can master this protocol and independently produce high‐quality provisional implant restorations under supervision, potentially enhancing practice efficiency. However, practitioners should provide adequate staff training to optimize reliability and quality. [ABSTRACT FROM AUTHOR]

Focused Clinical Question: Under what circumstances may a clinician consider dental implant placement at a site exhibiting a focal high or mixed density (HMD) osseous lesion radiologically? Summary: Some conditions and pathologic entities exhibiting high and mixed density radiological appearance pose low risk for dental implant failure or complications following implant surgery. However, other lesions represent contraindications to implant placement, and implant surgery at such sites can result in severe morbidity. Conclusion: Potential implant sites exhibiting focal HMD osseous lesions/conditions present varying levels of risk. In most cases, optimal management will include advanced imaging of the site, multidisciplinary consultations, and detailed informed consent to assure full understanding of procedural risks, benefits, and complications. Currently, clinical recommendations rely on case reports, opinion, and usual practice (level 3 evidence). The strength of each recommendation provided in this report is categorized as level C. [ABSTRACT FROM AUTHOR]

CHARGE syndrome is a multiple anomaly disorder in which patients present with a variety of phenotypes, including ocular coloboma, heart defects, choanal atresia, retarded growth and development, genitourinary hypoplasia and earabnormalities (1). Despite 70-90% of CHARGE syndrome cases resulting from mutations in the gene CHD7, which encodes an ATP-dependent chromatin remodeller, the pathways underlying the diverse phenotypes remain poorly understood (2). Surprisingly, our studies of a knock-in mutant mouse strain that expresses a stabilized and transcriptionally dead variant of the tumour-suppressor protein p53 (p[53.sup.25,26,53,54]) (3), along with a wild-type allele of p53 (also known as Trp53), revealed late-gestational embryonic lethality associated with a host of phenotypes that are characteristic of CHARGE syndrome, including coloboma, inner and outer ear malformations, heart outflow tract defects and craniofacial defects. We found that the p[53.sup.25,26,53,54/-] mutant protein stabilized and hyperactivated wild-type p53, which then inappropriately induced its target genes and triggered cell-cycle arrest or apoptosis during development. Importantly, these phenotypes were only observed with a wild-type p53 allele, as p[53.sup.25,26,53,54/-] embryos were fully viable. Furthermore, we found that CHD7 can bind to the p53promoter, thereby negatively regulating p53 expression, and that CHD7 loss in mouse neural crest cells or samples from patients with CHARGE syndrome results in p53 activation. Strikingly, we found that p53 heterozygosity partially rescued the phenotypes in Chd7-null mouse embryos, demonstrating that p53 contributes to the phenotypes that result from CHD7 loss. Thus, inappropriate p53 activation during development can promote CHARGE phenotypes, supporting the idea that p53 has a critical role in developmental syndromes and providing important insight into the mechanisms underlying CHARGE syndrome., Unrestrained p53 activity induced by loss of the negative regulators MDM2 or MDM4 causes early embryonic lethality (4). To explore the role of transcriptional activation by p53 in promoting developmental [...]

Focused Clinical Question: In generally healthy patients receiving third molar, periodontal, or dental implant surgery, do postoperative oral corticosteroids effectively limit pain and swelling compared with placebo or alternative medications? [ABSTRACT FROM AUTHOR]