US climate policy yields water quality cobenefits in the Mississippi Basin and Gulf of Mexico.

We utilize a coupled economy-agroecology-hydrology modeling framework to capture the cascading impacts of climate change mitigation policy on agriculture and the resulting water quality cobenefits. We analyze a policy that assigns a range of United States government's social cost of carbon estimates ($51, $76, and $152/ton of CO2-equivalents) to fossil fuel-based CO2 emissions. This policy raises energy costs and, importantly for agriculture, boosts the price of nitrogen fertilizer production. At the highest carbon price, US carbon emissions are reduced by about 50%, and nitrogen fertilizer prices rise by about 90%, leading to an approximate 15% reduction in fertilizer applications for corn production across the Mississippi River Basin. Corn and soybean production declines by about 7%, increasing crop prices by 6%, while nitrate leaching declines by about 10%. Simulated nitrate export to the Gulf of Mexico decreases by 8%, ultimately shrinking the average midsummer area of the Gulf of Mexico hypoxic area by 3% and hypoxic volume by 4%. We also consider the additional benefits of restored wetlands to mitigate nitrogen loading to reduce hypoxia in the Gulf of Mexico and find a targeted wetland restoration scenario approximately doubles the effect of a low to moderate social cost of carbon. Wetland restoration alone exhibited spillover effects that increased nitrate leaching in other parts of the basin which were mitigated with the inclusion of the carbon policy. We conclude that a national climate policy aimed at reducing greenhouse gas emissions in the United States would have important water quality cobenefits.

Epigenetic Enzymes, Age, and Ancestry Regulate the Efficiency of Human iPSC Reprogramming.

Epigenetic enzymes regulate higher-order chromatin architecture and cell-type specific gene expression. The ATPase BRG1 and the SWI/SNF chromatin remodeling complex are epigenetic enzymes that regulate chromatin accessibility during steady and transitional cell states. Experiments in mice show that the loss of BRG1 inhibits cellular reprogramming, while studies using human cells demonstrate that the overexpression of BRG1 enhances reprogramming. We hypothesized that the variation of SWI/SNF subunit expression in the human population would contribute to variability in the efficiency of induced pluripotent stem cells (iPSC) reprogramming. To examine the impact of an individual's sex, ancestry, and age on iPSC reprogramming, we created a novel sex and ancestry balanced cohort of 240 iPSC lines derived from human dermal fibroblasts (DF) from 80 heathy donors. We methodically assessed the reprogramming efficiency of each DF line and then quantified the individual and demographic-specific variations in SWI/SNF chromatin remodeling proteins and mRNA expression. We identified BRG1, BAF155, and BAF60a expression as strongly correlating with iPSC reprogramming efficiency. Additionally, we discovered that high efficiency iPSC reprograming is negatively correlated with donor age, positively correlated with African American descent, and uncorrelated with donor sex. These results show the variations in chromatin remodeling protein expression have a strong impact on iPSC reprogramming. Additionally, our cohort is unique in its large size, diversity, and focus on healthy donors. Consequently, this cohort can be a vital tool for researchers seeking to validate observational results from human population studies and perform detailed mechanistic studies in a controlled cell culture environment. Stem Cells 2018;36:1697-1708.

Global market integration increases likelihood that a future African Green Revolution could increase crop land use and CO2 emissions.

There has been a resurgence of interest in the impacts of agricultural productivity on land use and the environment. At the center of this debate is the assertion that agricultural innovation is land sparing. However, numerous case studies and global empirical studies have found little evidence of higher yields being accompanied by reduced area. We find that these studies overlook two crucial factors: estimation of a true counterfactual scenario and a tendency to adopt a regional, rather than a global, perspective. This paper introduces a general framework for analyzing the impacts of regional and global innovation on long run crop output, prices, land rents, land use, and associated CO2 emissions. In so doing, it facilitates a reconciliation of the apparently conflicting views of the impacts of agricultural productivity growth on global land use and environmental quality. Our historical analysis demonstrates that the Green Revolution in Asia, Latin America, and the Middle East was unambiguously land and emissions sparing, compared with a counterfactual world without these innovations. In contrast, we find that the environmental impacts of a prospective African Green Revolution are potentially ambiguous. We trace these divergent outcomes to relative differences between the innovating region and the rest of the world in yields, emissions efficiencies, cropland supply response, and intensification potential. Globalization of agriculture raises the potential for adverse environmental consequences. However, if sustained for several decades, an African Green Revolution will eventually become land sparing.

Carbon monoxide and heme oxygenase-1 prevent intestinal inflammation in mice by promoting bacterial clearance.

BACKGROUND & AIMS: Heme oxygenase-1 (HO-1) and its metabolic by-product, carbon monoxide (CO), protect against intestinal inflammation in experimental models of colitis, but little is known about their intestinal immune mechanisms. We investigated the interactions among CO, HO-1, and the enteric microbiota in mice and zebrafish. METHODS: Germ-free, wild-type, and interleukin (Il)10(-/-) mice and germ-free zebrafish embryos were colonized with specific pathogen-free (SPF) microbiota. Germ-free or SPF-raised wild-type and Il10(-/-) mice were given intraperitoneal injections of cobalt(III) protoporphyrin IX chloride (CoPP), which up-regulates HO-1, the CO-releasing molecule Alfama-186, or saline (control). Colitis was induced in wild-type mice housed in SPF conditions by infection with Salmonella typhimurium. RESULTS: In colons of germ-free, wild-type mice, SPF microbiota induced production of HO-1 via activation of nuclear factor erythroid 2-related factor 2-, IL-10-, and Toll-like receptor-dependent pathways; similar observations were made in zebrafish. SPF microbiota did not induce HO-1 in colons of germ-free Il10(-/-) mice. Administration of CoPP to Il10(-/-) mice before transition from germ-free to SPF conditions reduced their development of colitis. In Il10(-/-) mice, CO and CoPP reduced levels of enteric bacterial genomic DNA in mesenteric lymph nodes. In mice with S typhimurium-induced enterocolitis, CoPP reduced the numbers of live S typhimurium recovered from the lamina propria, mesenteric lymph nodes, spleen, and liver. Knockdown of HO-1 in mouse macrophages impaired their bactericidal activity against E coli, E faecalis, and S typhimurium, whereas exposure to CO or overexpression of HO-1 increased their bactericidal activity. HO-1 induction and CO increased acidification of phagolysosomes. CONCLUSIONS: Colonic HO-1 prevents colonic inflammation in mice. HO-1 is induced by the enteric microbiota and its homeostatic function is mediated, in part, by promoting bactericidal activities of macrophages.

α(1,3)-Fucosyltransferases FUT4 and FUT7 control murine susceptibility to thrombosis.

The α(1,3)-fucosyltransferases, types IV and VII (FUT4 and FUT7, respectively), are required for the synthesis of functional selectin-type leukocyte adhesion molecule ligands. The selectins and their ligands modulate leukocyte trafficking, and P-selectin and its ligand, P-selectin glycoprotein ligand-1, can modulate hemostasis and thrombosis. Regulation of thrombosis by FUT4 and/or FUT7 activity was examined in mouse models of carotid artery thrombosis and collagen/epinephrine-induced thromboembolism. Mice lacking both FUT4 and FUT7 (Fut(-/-) mice) had a shorter time to occlusive thrombus formation in the injured carotid artery and a higher mortality due to collagen/epinephrine-induced pulmonary thromboemboli. Mice lacking P-selectin or P-selectin glycoprotein ligand-1 did not have a prothrombotic phenotype. Whole blood platelet aggregation was enhanced, and plasma fibrinogen content, clot weight, and clot strength were increased in Fut(-/-) mice, and in vitro clot lysis was reduced compared with wild type. Fut4(-/-), but not Fut7(-/-), mice had increased pulmonary thromboembolism-induced mortality and decreased thromboemboli dissolution in vivo. These data show that FUT4 and FUT7 activity regulates thrombosis in a P-selectin- and P-selectin glycoprotein ligand-1-independent manner and suggest that FUT4 activity is important for thrombolysis.

Expression and cellular localization of the classical progesterone receptor in healthy and amyotrophic lateral sclerosis affected spinal cord.

BACKGROUND AND PURPOSE: Previous studies have suggested that elevated progesterone levels are associated with a slower disease course in amyotrophic lateral sclerosis (ALS). Given that the effects of progesterone are mediated in part by the classical progesterone receptor (PR), the expression and cellular localization of the A and B isoforms (PR-A and PR-B, respectively) of the PR in control (neuropathologically normal) and ALS-affected spinal cord (SC) were examined. METHODS: Semi-quantitative RT-PCR, immunohistochemistry and immunofluorescence analyses of the cervical and lumbar SC of post-mortem ALS patients (n = 19) and control subjects (n = 10) were performed. Primers and antibodies used allowed the detection of both PR-A and PR-B isoforms together (PR-A+B) or PR-B isoform alone. RESULTS: Lumbar PR-A+B and cervical PR-B mRNA expression were significantly higher in ALS than controls. In both ALS and controls, PR-A+B immunoreactivity (IR) was occasionally detected in motor neurons. In contrast, PR-A+B IR was prominent in axonal processes and vessels. This was more evident in nerve roots and large arteries in ALS compared with controls. Colocalization of PR-A+B with markers of neurons, axonal processes and vascular endothelium was also observed. CONCLUSIONS: Evidence that both PR-A and PR-B isoforms are expressed in the human SC is provided, with some regional variation in isoform expression between ALS and controls. The IR was more prominent in nerve roots and large arteries in ALS, suggesting a potential role in the degenerative process.

Projecting global oil palm expansion under zero-deforestation commitments: Direct and indirect land use change impacts.

In the last three decades, global production of oil palm has boomed, which has partly come at the expense of tropical rainforests. Recognizing this, many companies operating in the palm oil industry have committed to eliminate deforestation from their operations, often referred to as zero-deforestation commitments (ZDCs). Here, we estimate that if ZDCs are fully adopted and enforced across all sectors and geographies, the global extent of oil palm plantations may be 11 M ha or 40% smaller in 2030 than in a business-as-usual (BAU) scenario that assumes no compliance with ZDCs. As a result of such land-sparing effects, we estimate that 96 M ha of forests are saved from conversion, of which, 17% would otherwise have been converted (directly or indirectly) due to expanding oil palm plantations. Overall, these figures suggest that ZDCs have the potential to deliver major environmental benefits if they are fully adopted and enforced.

Microbial colonization induces dynamic temporal and spatial patterns of NF-κB activation in the zebrafish digestive tract.

BACKGROUND & AIMS: The nuclear factor κ-light-chain enhancer of activated B cells (NF-κB) transcription factor pathway is activated in response to diverse microbial stimuli to regulate expression of genes involved in immune responses and tissue homeostasis. However, the temporal and spatial activation of NF-κB in response to microbial signals have not been determined in whole living organisms, and the molecular and cellular details of these responses are not well understood. We used in vivo imaging and molecular approaches to analyze NF-κB activation in response to the commensal microbiota in transparent gnotobiotic zebrafish. METHODS: We used DNA microarrays, in situ hybridization, and quantitative reverse transcription polymerase chain reaction analyses to study the effects of the commensal microbiota on gene expression in gnotobiotic zebrafish. Zebrafish PAC2 and ZFL cells were used to study the NF-κB signaling pathway in response to bacterial stimuli. We generated transgenic zebrafish that express enhanced green fluorescent protein under transcriptional control of NF-κB, and used them to study patterns of NF-κB activation during development and microbial colonization. RESULTS: Bacterial stimulation induced canonical activation of the NF-κB pathway in zebrafish cells. Colonization of germ-free transgenic zebrafish with a commensal microbiota activated NF-κB and led to up-regulation of its target genes in intestinal and extraintestinal tissues of the digestive tract. Colonization with the bacterium Pseudomonas aeruginosa was sufficient to activate NF-κB, and this activation required a functional flagellar apparatus. CONCLUSIONS: In zebrafish, transcriptional activity of NF-κB is spatially and temporally regulated by specific microbial factors. The observed patterns of NF-κB-dependent responses to microbial colonization indicate that cells in the gastrointestinal tract respond robustly to the microbial environment.

IgE enhances mouse mast cell Fc(epsilon)RI expression in vitro and in vivo: evidence for a novel amplification mechanism in IgE-dependent reactions.

The binding of immunoglobulin E (IgE) to high affinity IgE receptors (Fc(epsilon)RI) expressed on the surface of mast cells primes these cells to secrete, upon subsequent exposure to specific antigen, a panel of proinflammatory mediators, which includes cytokines that can also have immunoregulatory activities. This IgE- and antigen-specific mast cell activation and mediator production is thought to be critical to the pathogenesis of allergic disorders, such as anaphylaxis and asthma, and also contributes to host defense against parasites. We now report that exposure to IgE results in a striking (up to 32-fold) upregulation of surface expression of Fc(epsilon)RI on mouse mast cells in vitro or in vivo. Moreover, baseline levels of Fc(epsilon)RI expression on peritoneal mast cells from genetically IgE-deficient (IgE -/-) mice are dramatically reduced (by approximately 83%) compared with those on cells from the corresponding normal mice. In vitro studies indicate that the IgE-dependent upregulation of mouse mast cell Fc(epsilon)RI expression has two components: an early cycloheximide-insensitive phase, followed by a later and more sustained component that is highly sensitive to inhibition by cycloheximide. In turn, IgE-dependent upregulation of Fc(epsilon)RI expression significantly enhances the ability of mouse mast cells to release serotonin, interleukin-6 (IL-6), and IL-4 in response to challenge with IgE and specific antigen. The demonstration that IgE-dependent enhancement of mast cell Fc(epsilon)RI expression permits mast cells to respond to antigen challenge with increased production of proinflammatory and immunoregulatory mediators provides new insights into both the pathogenesis of allergic diseases and the regulation of protective host responses to parasites.

Involvement of Bruton's tyrosine kinase in FcepsilonRI-dependent mast cell degranulation and cytokine production.

We investigated the role of Bruton's tyrosine kinase (Btk) in FcepsilonRI-dependent activation of mouse mast cells, using xid and btk null mutant mice. Unlike B cell development, mast cell development is apparently normal in these btk mutant mice. However, mast cells derived from these mice exhibited significant abnormalities in FcepsilonRI-dependent function. xid mice primed with anti-dinitrophenyl monoclonal IgE antibody exhibited mildly diminished early-phase and severely blunted late-phase anaphylactic reactions in response to antigen challenge in vivo. Consistent with this finding, cultured mast cells derived from the bone marrow cells of xid or btk null mice exhibited mild impairments in degranulation, and more profound defects in the production of several cytokines, upon FcepsilonRI cross-linking. Moreover, the transcriptional activities of these cytokine genes were severely reduced in FcepsilonRI-stimulated btk mutant mast cells. The specificity of these effects of btk mutations was confirmed by the improvement in the ability of btk mutant mast cells to degranulate and to secrete cytokines after the retroviral transfer of wild-type btk cDNA, but not of vector or kinase-dead btk cDNA. Retroviral transfer of Emt (= Itk/Tsk), Btk's closest relative, also partially improved the ability of btk mutant mast cells to secrete mediators. Taken together, these results demonstrate an important role for Btk in the full expression of FcepsilonRI signal transduction in mast cells.

Ancestry-dependent gene expression correlates with reprogramming to pluripotency and multiple dynamic biological processes.

Induced pluripotent stem cells (iPSCs) can be derived from differentiated cells, enabling the generation of personalized disease models by differentiating patient-derived iPSCs into disease-relevant cell lines. While genetic variability between different iPSC lines affects differentiation potential, how this variability in somatic cells affects pluripotent potential is less understood. We generated and compared transcriptomic data from 72 dermal fibroblast-iPSC pairs with consistent variation in reprogramming efficiency. By considering equal numbers of samples from self-reported African Americans and White Americans, we identified both ancestry-dependent and ancestry-independent transcripts associated with reprogramming efficiency, suggesting that transcriptomic heterogeneity can substantially affect reprogramming. Moreover, reprogramming efficiency-associated genes are involved in diverse dynamic biological processes, including cancer and wound healing, and are predictive of 5-year breast cancer survival in an independent cohort. Candidate genes may provide insight into mechanisms of ancestry-dependent regulation of cell fate transitions and motivate additional studies for improvement of reprogramming.

Quinacrine: mechanisms of antimalarial action.

Two new interesting modes of action of quinacrine have been discovered. The first concerns a dose-related inhibition of uptake of [8-(3)H] adenosine into host cells of parasitized blood. Second, the drug inhibits the incorporation of tritiated adenosine triphosphate primarily into RNA but also into DNA of the erythrocyte-free malarial parasite Plasmodium berghei.

Evidence for widespread hydrated minerals on asteroid (101955) Bennu.

Early spectral data from the Origins, Spectral Interpretation, Resource Identification, and Security-Regolith Explorer (OSIRIS-REx) mission reveal evidence for abundant hydrated minerals on the surface of near-Earth asteroid (101955) Bennu in the form of a near-infrared absorption near 2.7 µm and thermal infrared spectral features that are most similar to those of aqueously altered CM carbonaceous chondrites. We observe these spectral features across the surface of Bennu, and there is no evidence of substantial rotational variability at the spatial scales of tens to hundreds of meters observed to date. In the visible and near-infrared (0.4 to 2.4 µm) Bennu's spectrum appears featureless and with a blue (negative) slope, confirming previous ground-based observations. Bennu may represent a class of objects that could have brought volatiles and organic chemistry to Earth.

Mast cells as sentinels of innate immunity.

Mast cells are widely regarded as important effector cells in immune responses associated with Th2 cells and IgE. Recent work shows that they can also contribute significantly to the expression of innate immunity; furthermore, survival in a model of acute bacterial infection that is dependent on complement and mast cells can be greatly enhanced by long-term treatment of mice with the kit ligand (stem cell factor) at least in part because of the effects of such treatment on mast cell numbers and/or function. These findings not only indicate that mast cells can represent a critical component of host defense in natural immunity but also suggest that mast cell function in this setting can be manipulated for therapeutic ends.

The increasing use of polypharmacotherapy for refractory mood disorders: 22 years of study.

BACKGROUND: Few studies have approached the subject of polypharmacotherapy systematically. This retrospective review of 178 patients with refractory bipolar disorder or unipolar depression (Research Diagnostic Criteria or DSM-III-R criteria) discharged from the National Institute of Mental Health (NIMH) Biological Psychiatry Branch between 1974 and 1996 was conducted to assess the degree and efficacy of "add-on" pharmacotherapy. METHOD: Following completion of formal structured blinded research protocols, patients entered a treatment phase (often again on a blind basis) in which all agents available in the community could be utilized. Each patient's retrospective life chart and all prospective double-blind nurse- and self-rated NIMH data were reviewed. The overall degree of improvement at discharge was assessed by rating on the Clinical Global Impressions scale (CGI) as modified for bipolar illness (CGI-BP). RESULTS: A 78% improvement rate (moderate or marked on the CGI) was achieved at the time of discharge. There was a significant relationship between number of medications utilized at discharge as a function of discharge date (r = 0.45, p < .0001). The percentages of patients discharged on treatment with 3 or more medications were 3.3% (1974-1979), 9.3% (1980-1984), 34.9% (1985-1989), and 43.8% (1990-1995). No correlation was found between polypharmacy and age (r = -0.03, p = .66). Patients more recently discharged from the NIMH had an earlier age at illness onset, more lifetime weeks depressed, and a higher rate of rapid cycling than patients in the earlier cohorts. CONCLUSION: Increasing numbers of medications in more recent NIMH cohorts were required to achieve the same degree of improvement at hospital discharge. More systematic approaches to the complex regimens required for treatment of patients with refractory mood disorder are clearly needed.

Behavior and interpretation of the kappa statistic: resolution of the two paradoxes.

Two apparent paradoxes have been identified for the kappa (kappa) statistic: (1) high levels of observer agreement with low kappa values; (2) lack of predictability of changes in kappa with changing marginals. The first paradox is a function of prevalence of the trait in the sample, while the second is related to symmetry of observations in the disagreement categories. While examining the behavior of kappa as a function of the distribution of responses in a contingency table, it was discovered that for any measured level of observer agreement (Po) there are three characteristic values of kappa: kappa max, kappa min, and kappa nor, each of which is a function only of Po. The characteristic values allow an observed kappa (kappa o) to be placed into perspective. By observing symmetry in agreement and disagreement categories, the behavior of kappa is readily understood and predictable. We define symmetry expressions for agreement (SA) and disagreement (SD) in order to represent and quantify these effects. Kappa alone has little interpretive value and we recommend that studies reporting kappa also report Po, SD, and P++ (agreement on the presence of the trait).

Clinical validity and stability of active and passive cervical range of motion with regard to total and unilateral uniplanar motion.

STUDY DESIGN: A study of inter- and intra-examiner reliability and clinical validity using two instruments for assessment of spinal range of motion in healthy individuals. OBJECTIVE: To assess the clinical validity, stability, and normative values for active and passive cervical range of motion as measured by the CA-6000 (Orthopedic Systems Inc., Union City, CA), an electrogoniometer. SUMMARY OF BACKGROUND DATA: The authors' early trials with the electrogoniometer yielded values that differed substantially from those in other reports. The authors sought to resolve those discrepancies and understand their sources. METHODS: Axial rotations along the transverse, coronal, and frontal planes were measured as half-cycles (i.e., left-right or flexion-extension) that were repeated seven times per trial. Test-retest data were collected on the same healthy individuals for active and passive motion using men and women aged 20-39 years. For validity, simultaneous digital dual inclinometry and electrogoniometry were performed twice over a 1-week interval. In addition, a bench test was performed for validation of axial rotation. RESULTS: Clinical reliability of the CA-6000 was high for inter- and intra-examiner studies of total active motion, and validity was high when compared with that obtained with dual inclinometry. Total range of motion had less between-trial variability than half-cycles, axial rotation and lateral bending measurements had greater reliability than did flexion-extension measurements, and active motion was more reliable than passive motion. CONCLUSION: The CA-6000 provides valid and reliable measures of cervical range of motion. Discrepancies reported elsewhere appear to have arisen from several sources, as discussed in this article.

Meta-analysis of normative cervical motion.

STUDY DESIGN: Meta-analysis of normative cervical range of motion literature performed by applying summary statistics to range of motion and reliability values reported among studies. OBJECTIVES: To identify reliable and valid methods for measuring active and passive cervical range of motion and to estimate normative values. SUMMARY OF BACKGROUND DATA: Range of motion studies use a variety of measuring instruments and statistical analyses, making it difficult to select the most suitable instruments, procedures, and normative values for clinical application. Reviews of the literature, being limited in scope, have not quantitatively synthesized the literature. METHODS: Range of motion and reliability data were grouped by technology and types of motion, then summarized by deriving means and variabilities. Clinical validity was assessed by examining discrepancies, variabilities, and correlations. Change in range of motion as a function of age was determined by comparing range of motion ratios (fourth:third and seventh:third decades). RESULTS: Nine technologies were identified. Overall, passive motion was greater than active motion, and range of motion decreased as age increased, with women exhibiting greater range of motion than men. Variations within each technology were as large as or larger than those between technologies, indicating that clinical procedures are as important as the accuracy and precision of the technology itself. Reliability has not been adequately tested for the majority of technologies. CONCLUSIONS: Clinical procedures appear to be as important as accuracy and precision in determining the reported range of motion values. Further research is needed to establish a gold standard for normative values and to identify an instrument that is reliable for all motions.

Development of the Muscle Dysmorphia Inventory (MDI).

AIM: The development of the 6-factor, 27-item Muscle Dysmorphia Inventory (MDI) was based on Lantz et al. proposed model of characteristics associated with Muscle Dysmorphia. EXPERIMENTAL DESIGN: quantitative procedures including item-to-total correlations, exploratory and confirmatory factor analyses, and structure equation modeling confirmed the construct validity of the scale. Convergent validity was also tested. SETTING: bodybuilding and powerlifting competition venues, weight training facilities, and university athletic venues. PARTICIPANTS: the 1(st) study consisted of 77 experienced male free weight lifters. The 2(nd) study consisted of 156 male non-competitive bodybuilders and weight lifters and 168 elite level powerlifters and bodybuilders. The 3(rd) study consisted of 151 male and female bodybuilders and weight lifters. MEASURES: each participant completed demographic information, the MDI, Drive for Thinness subscale of the Eating Disorder Inventory, and the Training Dependency subscale of the Bodybuilding Dependence Scale. RESULTS: Reliability estimates (Cronbach's a) ranged from 0.72 to 0.94. Factor loadings in all 3 studies supported the 6-factor structure (size/symmetry, supplement use, exercise dependence, pharmacological use, dietary behavior, and physique protection). Much of the scale validation was focused on construct validity, however, correlations with the MDI's subscales and the Training Dependency subscale of the Bodybuilding Dependence Scale and the Drive for Thinness subscale of the Eating Disorder Inventory provided evidence of convergent validity also. CONCLUSIONS: From these preliminary results, the MDI appears to contribute to the identification of a newly formed disorder by offering a multi-dimensional measure of factors related to Muscle Dysmorphia.