Longitudinal comparisons of a whole-mouth taste test to clinician-rated and patient-reported outcomes of dysgeusia postradiotherapy in patients with head and neck cancer and associations with oral intake.

BACKGROUND: After head and neck cancer (HNC) treatment, dysgeusia may be a barrier to oral intake. In this exploratory study, we prospectively examined taste perception, clinician-rated (CRO) and patient-reported (PRO) taste changes and their effect on oral intake postradiotherapy. METHODS: Twenty-eight patients were assessed at baseline, treatment weeks 2 and 4, and 1, 3, and 6 months post-treatment using a whole-mouth taste test and associated CRO and subjective PRO measures. RESULTS: Greater taste impairment was reflected by subjective than by a whole-mouth taste test. The most significant and consistent decline occurred mid-treatment. The Chemotherapy-Induced Taste Alteration Scale (PRO) discomfort subscale correlated significantly with maintaining an oral diet, percent of oral intake, and appetite level from mid-treatment to 6 months post-treatment. CONCLUSIONS: PRO results indicated ongoing oral intake issues. Whole-mouth taste tests may fail to fully reflect functional taste-loss. Dysgeusia prevention and treatment methods are needed to improve patient outcomes.

Identifying Needs for Advancing the Profession and Workforce in Environmental Health.

An ever-changing landscape for environmental health (EH) requires in-depth assessment and analysis of the current challenges and emerging issues faced by EH professionals. The Understanding the Needs, Challenges, Opportunities, Vision, and Emerging Roles in Environmental Health initiative addressed this need.After receiving responses from more than 1700 practitioners, during an in-person workshop, focus groups identified and described priority problems and supplied context on addressing the significant challenges facing EH professionals with state health agencies and local health departments. The focus groups developed specific problem statements detailing the EH profession and workforce's prevailing challenges and needs according to 6 themes, including effective leadership, workforce development, equipment and technology, information systems and data, garnering support, and partnerships and collaboration.We describe the identified priority problems and needs and provide recommendations for ensuring a strong and robust EH profession and workforce ready to address tomorrow's challenges.

Survey of Radon Testing and Mitigation by Wisconsin Residents, Landlords, and School Districts.

INTRODUCTION: Radon is the second-leading cause of lung cancer in the United States, the leading cause of lung cancer in nonsmokers, and is estimated to cause 21,000 deaths every year. Radon is especially prevalent in the upper Midwest. This study aimed to assess radon testing and mitigation practices among residential homeowners, landlords, and school districts in Wisconsin. METHODS: Two survey sample datasets were used to assess radon testing and mitigation in residential homes: the Survey of the Health of Wisconsin (SHOW) and Wisconsin Behavioral Risk Factor Surveillance System (BRFSS) survey. Wisconsin landlords and school administrators were surveyed to assess radon testing and mitigation in rental properties and schools, respectively. RESULTS: Approximately 30% of Wisconsin homeowners (22.1% from SHOW and 39.9% from BRFSS) have tested their properties for radon. Similarly, 31.0% of Wisconsin landlords (40/129) and 35.1% of Wisconsin school districts (78/222) have tested their schools for radon. Of homeowners with elevated radon, about 60% mitigated. School districts whose radon levels tested high most commonly did not mitigate, with costs and/or lack of funding cited as the most common barrier. DISCUSSION/CONCLUSION: Radon testing and mitigation practices are inadequate in Wisconsin, and future work will seek to determine the best methods to increase testing and mitigation and reduce radon-induced lung cancer deaths in Wisconsin.

Microglial activation is required for Abeta clearance after intracranial injection of lipopolysaccharide in APP transgenic mice.

Inflammation has been argued to play a fundamental role in the pathogenesis of Alzheimer's disease. Mice transgenic for mutant human amyloid precursor protein (APP) develop progressive amyloid deposition, gliosis, and cognitive impairment. Paradoxically, intracranial administration of lipopolysaccharide (LPS) to promote neuroinflammation results in a reduction in amyloid-beta peptide (Abeta) burden concurrent with the inflammatory response. To determine whether microglia mediate Abeta clearance after LPS, we used dexamethasone to inhibit the microglial response. Amyloid precursor protein mice were injected intrahippocampally with either LPS or saline and were allowed to survive for 7 days with or without dexamethasone cotreatment. Brain tissue was then analyzed by immunohistochemistry. Hippocampal Abeta burden was reduced 7 days after LPS injection, and this was prevented by cotreatment with dexamethasone. Markers of microglial activation [CD45, complement receptor 3 (CR3), and macrosialin (CD68)] were increased by LPS, and these increases were attenuated by dexamethasone. Dexamethasone failed to block LPS-induced increases in all microglial markers, and Fcgamma receptors II/III and scavenger receptor A were increased by LPS but were unaffected by dexamethasone cotreatment. These results indicate a complex response by microglia to acute LPS treatment, with only some responses sensitive to steroidal anti-inflammatory drug treatment. Nonetheless, microglial activation was necessary to remove Abeta in this model of neuroinflammation.

Diverse microglial responses after intrahippocampal administration of lipopolysaccharide.

Inflammation has been argued to play a primary role in the pathogenesis of Alzheimer's disease by contributing to the development of neuropathology and clinical symptoms. However, the mechanisms underlying these effects remain obscure. Lipopolysaccharide (LPS) activates the innate immune response and triggers gliosis when injected into the central nervous system. In the studies described in the present work, we evaluated the time course of microgliosis after a single intrahippocampal injection of LPS. Mice were injected bilaterally with 4 mug of LPS. Post-injection survival times were 1, 6, and 24 h, as well as 3, 7, 14, and 28 days. Protein and RNA analyses were performed for inflammatory markers. Significant elevations of cluster differentiation marker CD45, glial fibrillary acidic protein (GFAP), scavenger receptor A (SRA), and Fcgamma receptor mRNA were seen after 24 h. Immunohistochemistry revealed a complex pattern of protein expression by microglia, as well as changes in cell morphologies. RNA and protein for Fcgamma receptor and SRA were transiently elevated, peaked at 3 days, and returned to basal levels after 1 week. In contrast, microglia remained significantly activated through the 28-day time point, as determined by CD45 and complement receptor 3 levels. These findings indicate a multivariate response to LPS, and evaluation of microglial phenotypes may lead to a better understanding of neuroinflammatory diseases.