Quality Appraisal of Research Reporting for Aromatherapy and Essential Oil Studies in Humans: Proposed Checklist for "Transparent Reporting for Essential oil and Aroma Therapeutic Studies".

Introduction: Reporting of aromatherapy-focused research often lacks sufficient quality and detail for replication and subsequent application of results. To our knowledge currently, no quality appraisal tool exists for aromatherapy research reporting. To address this gap, the Aromatic Research Quality Appraisal Taskforce (ARQAT) composed of aromatherapy professionals with varied expert backgrounds came together. Presented here is the Transparent Reporting for Essential oil and Aroma Therapeutic Studies (TREATS) checklist, which is a result of this collaborative effort. Methods: Creation of TREATS followed a three-stage process, including determination of interest/need, development, and dissemination. The shortcomings of existing aromatherapy research reporting quality were evaluated and responses to address these shortcomings were used to create checklist items that were then grouped into sections. Items for each section were brain-stormed with reference to the aromatherapy literature and ARQAT's expert knowledge, and the development of each section followed an iterative process until agreement was reached. An explanatory document was also created to assist more accurate use of the tool; it and the checklist were reviewed by a group of aromatherapy experts. Results: The TREATS checklist with 38 items in four sections was developed along with the explanatory document. The ARQAT and a global group of aromatherapy experts reviewed the TREATS. Their results and comments assisted development of the current version. The TREATS identifies key components of research involving essential oils, their application, and olfactory considerations that ARQAT considers the minimum necessary for high-quality aromatherapy research. Conclusion: The TREATS, explanatory document, and associated website (www.arqat.org) contribute to thorough aromatherapy research critique. The TREATS checklist aids appraisal of quality and can be used with any study design. It lays the foundation for the future development of aromatic research reporting guidelines.

Differential distribution of cholesterol pools across arteries under high-cholesterol diet.

Excessive cholesterol constitutes a major risk factor for vascular disease. Within cells, cholesterol is distributed in detergent-sensitive and detergent-resistant fractions, with the largest amount of cholesterol residing in cellular membranes. We set out to determine whether various arteries differ in their ability to accumulate esterified and non-esterified cholesterol in detergent-sensitive versus detergent-resistant fractions throughout the course of a high-cholesterol diet. Male Sprague-Dawley rats were placed on 2 % cholesterol diet while a control group was receiving iso-caloric standard chow. Liver, aorta, and pulmonary, mesenteric, and cerebral arteries were collected at 2-6, 8-12, 14-18, and 20-24 weeks from the start of high-cholesterol diet. After fraction separation, esterified and free non-esterified cholesterol levels were measured. In all arteries, largest cholesterol amounts were present in detergent-sensitive fractions in the non-esterified form. Overall, cholesterol in aorta and cerebral arteries was elevated during 14-18 weeks of high-cholesterol diet. Cerebral arteries also exhibited increase in esterified cholesterol within detergent-sensitive domains, as well as increase in cholesterol level in the detergent-resistant fraction at earlier time-points of diet. Pulmonary artery and mesenteric artery were largely resistant to cholesterol accumulation. Quantitative polymerase chain reaction (qPCR) analysis revealed up-regulation of low-density lipoprotein receptor (Ldlr) and low-density lipoprotein receptor-related protein 1 (Lrp1) gene expression in cerebral arteries when compared to mesenteric and pulmonary arteries, respectively. In summary, we unveiled the differential ability of arteries to accumulate cholesterol over the course of a high-cholesterol diet. The differential accumulation of cholesterol seems to correlate with the up-regulated gene expression of proteins responsible for cholesterol uptake.

Bisphenol A and Related Alkylphenols Exert Nongenomic Estrogenic Actions Through a G Protein-Coupled Estrogen Receptor 1 (Gper)/Epidermal Growth Factor Receptor (Egfr) Pathway to Inhibit Meiotic Maturation of Zebrafish Oocytes.

Xenobiotic estrogens, such as bisphenol A (BPA), disrupt a wide variety of genomic estrogen actions, but their nongenomic estrogen actions remain poorly understood. We investigated nongenomic estrogenic effects of low concentrations of BPA and three related alkylphenols on the inhibition of zebrafish oocye maturation (OM) mediated through a G protein-coupled estrogen receptor 1 (Gper)-dependent epidermal growth factor receptor (Egfr) pathway. BPA (10-100 nM) treatment for 3 h mimicked the effects of estradiol-17beta (E2) and EGF, decreasing spontaneous maturation of defolliculated zebrafish oocytes, an effect not blocked by coincubation with actinomycin D, but blocked by coincubation with a Gper antibody. BPA displayed relatively high binding affinity (15.8% that of E2) for recombinant zebrafish Gper. The inhibitory effects of BPA were attenuated by inhibition of upstream regulators of Egfr, intracellular tyrosine kinase (Src) with PP2, and matrix metalloproteinase with ilomastat. Treatment with an inhibitor of Egfr transactivation, AG1478, and an inhibitor of the mitogen-activated protein kinase (MAPK) 3/1 pathway, U0126, increased spontaneous OM and blocked the inhibitory effects of BPA, E2, and the selective GPER agonist, G-1. Western blot analysis showed that BPA (10-200 nM) mimicked the stimulatory effects of E2 and EGF on Mapk3/1 phosphorylation. Tetrabromobisphenol A, 4-nonylphenol, and tetrachlorobisphenol A (5-100 nM) also inhibited OM, an effect blocked by cotreatment with AG1478, as well as with the GPER antagonist, G-15, and displayed similar binding affinities as BPA to zebrafish Gper. The results suggest that BPA and related alkylphenols disrupt zebrafish OM by a novel nongenomic estrogenic mechanism involving activation of the Gper/Egfr/Mapk3/1 pathway.

The behavioral pharmacology of zolpidem: evidence for the functional significance of α1-containing GABA(A) receptors.

RATIONALE: Zolpidem is a positive allosteric modulator of γ-aminobutyric acid (GABA) with preferential binding affinity and efficacy for α1-subunit containing GABA(A) receptors (α1-GABA(A)Rs). Over the last three decades, a variety of animal models and experimental procedures have been used in an attempt to relate the behavioral profile of zolpidem and classic benzodiazepines (BZs) to their interaction with α1-GABA(A)Rs. OBJECTIVES: This paper reviews the results of rodent and non-human primate studies that have evaluated the effects of zolpidem on motor behaviors, anxiety, memory, food and fluid intake, and electroencephalogram (EEG) sleep patterns. Also included are studies that examined zolpidem's discriminative, reinforcing, and anticonvulsant effects as well as behavioral signs of tolerance and withdrawal. RESULTS: The literature reviewed indicates that α1-GABA(A)Rs play a principle role in mediating the hypothermic, ataxic-like, locomotor- and memory-impairing effects of zolpidem and BZs. Evidence also suggests that α1-GABA(A)Rs play partial roles in the hypnotic, EEG sleep, anticonvulsant effects, and anxiolytic-like of zolpidem and diazepam. These studies also indicate that α1-GABA(A)Rs play a more prominent role in mediating the discriminative stimulus, reinforcing, hyperphagic, and withdrawal effects of zolpidem and BZs in primates than in rodents. CONCLUSIONS: The psychopharmacological data from both rodents and non-human primates suggest that zolpidem has a unique pharmacological profile when compared with classic BZs. The literature reviewed here provides an important framework for studying the role of different GABA(A)R subtypes in the behavioral effects of BZ-type drugs and helps guide the development of new pharmaceutical agents for disorders currently treated with BZ-type drugs.