A consistent individual pattern is seen. Attacks vary in frequency from more than 10 per day to less than 1 per month. Hypnagogic hallucinations (at sleep onset) or hypnapompic hallucinations (on waking) represent vivid dreamlike experiences of visual imagery (constant or changing colored forms), auditory hallucinations, or tactile sensations. Smell and taste are rarely affected. Some patients describe out-of-body experiences at sleep onset. Attacks usually last less than 10 min,

and the frequency varies from less than once a month Inhibitors,research,lifescience,medical to more than once a day. Sleep paralysis represents inability to move either at sleep onset or upon awakening; the episode can last up to 10 min. Patients can be frightened because they are unable to open their eyes or move their fingers Inhibitors,research,lifescience,medical and feel they have to struggle to move. Disturbed nocturnal sleep is the fifth component of the “tetrad” and is due to frequent awakenings. Although patients typically have short SOL, they may have trouble returning to sleep once awakened. Other reported symptoms include automatic behavior (PI3K inhibitor episodes of amnesia associated with semipurposeful activity), subjective memory impairment that is not validated during standard memory testing, tiredness or fatigue, blurry or double vision, and sexual dysfunction (which may be related to drug therapy).124 The PSG Inhibitors,research,lifescience,medical demonstrates SOL less than 10 min

and REM sleep latency less than 20 min.4 An MSLT demonstrates a mean sleep latency of less than 5 min with two or more sleep-onset REM (SOREM) episodes.4 Figure 2 depicts SOREM during an MSLT nap. Figure 2. Sleep-onset rapid Inhibitors,research,lifescience,medical eye movement (REM) during an mean sleep latency test (MSLT) nap in a patient with narcolepsy. Electroencephalogram (EEG) leads (C3-A2 and 02-A1) demonstrate low voltage mixed frequency theta activity. EMG-Chin shows atonia Inhibitors,research,lifescience,medical with phasic … HLA typing demonstrates an increased frequency of DQB1 *0602 or DR2 in patients with narcolepsy, especially with cataplexy. Low CSF levels of hypocretin-1

are highly associated with narcolepsy with cataplexy (89.5%), particularly in patients with cataplexy who are HLA DQBl*0602-positive (95.7%).129-132 Stimulant medications Cell press are the mainstay of treatment of EDS, with the objective of allowing the fullest possible return of normal function for patients at work, home, and school.118,122,123,125,133-135 The most common stimulants used, listed in incrementing order of relative efficacy are: pemoline, modafinil, dextroamphetamine, mcthamphetamine, and methylphenidate.133,135 The maximum recommended daily dosages of stimulants in adults are: dextroamphetamine sulfate, 100 mg; methamphetamine hydrochloride, 80 mg; and methylphenidate, 100 mg.133 Pemoline was utilized in the past, but is not currently recommended due to concerns about the risk of acute hepatic failure.

Lactate Dehydrogenase deficiency Lactate Dehydrogenase deficiency (LDH – GSD type XI) has been reported in few Caucasian and Japanese patients with myoglobinuria, myalgias and exercise intolerance. The gene has been assigned to chromosome 12. Only 5 mutations have been reported, so far, in LDH-deficient subjects (3). Aldolase A deficiency Aldolase A deficiency (GSD XII) has been described only in one patient (male), in 1996 (8), who complained of exercise intolerance, muscle weakness and hyperCKaemia. Muscle biopsy was unremarkable Inhibitors,research,lifescience,medical and the residual Selleckchem AZD0530 enzyme activity

was 11%. A missense mutation was considered pathogenic in this case. β-Enolase deficiency β-Enolase deficiency (GSD type XIII) has recently been described in an adult patient with easy muscle fatigability, myalgias and increased CK values after intense physical exertion. The gene involved in the disease maps to chromosome Inhibitors,research,lifescience,medical 17. Muscle biopsy was considered normal but residual enzyme activity was about 5%. The patient was heterozygous for two different missense mutations of ENO3 gene (9). Conclusions Despite the large amount of new

information concerning PFK deficiencies and Distal Glycogenoses reported in the last 15 years, a variety of problems remain unsolved. In fact, genotype-phenotype Inhibitors,research,lifescience,medical correlation is still weak and no therapy is available at present. More patients and extensive studies in this field are necessary to better understand the pathophysiology of these disorders and to suggest appropriate treatment options, as recently obtained in Inhibitors,research,lifescience,medical Pompe disease or Acid Maltase deficiency (GSD type II) (10).
Lafora bodies (LBs) are carbohydrate storage products that characterize LD and underlie the epileptic disorder. They are composed of polyglucosans, which are abnormally formed glycogen molecules resembling starch. The polyglucosans in LD consist of long chains of glucose units that are infrequently branched. This makes them insoluble,

leading to their accumulation and formation of the LBs (3, 5). LBs stain strongly with periodic Inhibitors,research,lifescience,medical acid-Schiff due to their polysaccharide composition, and they are resistant to amylase digestion owing to dense packing (6). Ultrastructural analysis suggests a physical association between newly formed polyglucosans and endoplasmic Metalloexopeptidase reticulum (ER) or ER ribosomes (7). LBs are found in brain, skin, liver, cardiac and skeletal muscle. However, despite this distribution, patients usually do not have extra-neurological manifestations. In skin, LBs are seen in either eccrine sweat gland duct cells or in apocrine sweat gland myoepithelial cells. Skin biopsy can be used for diagnosis if genetic testing is not possible (8). In the central nervous system, LBs are found in the perikarya or dendrites, but not in axons. Perikaryal LBs can grow very large, outgrowing the neuronal body and destroying the cell.

, 2007). And in an environmentally induced model of circadian rhythm disruption, mice that were housed on a shortened 20-h light–dark cycle exhibited learning and structural connectivity deficits comparable to those seen in chronic stress states, including apical dendritic atrophy in mPFC pyramidal cells and PFC-dependent Libraries cognitive deficits ( Karatsoreos et al.,

2011). Studies like this also highlight implications for patients outside the psychiatric realm. For example, mice that were housed on a shortened 20-h light–dark cycle also developed metabolic problems, including obesity, increased leptin levels, and signs of insulin resistance. Shift workers and frequent travelers who suffer from chronic jet lag may experience analogous cognitive and metabolic changes (Sack et al., 2007, Lupien et al., 2009 and McEwen, 2012), and in susceptible click here Pazopanib cost individuals, travel across time zones may even trigger severe mood episodes requiring psychiatric hospitalization (Jauhar and Weller, 1982). An increasing

awareness of the importance of circadian and ultradian glucocorticoid oscillations in learning-related synaptic remodeling may also have implications for efforts to optimize training regimens for promoting motor skill learning, which is known to vary with the time of day in both adolescents and adults (Atkinson and Reilly, 1996 and Miller et al., 2012). Similarly, disruptions in circadian glucocorticoid oscillations may be an important factor to consider in patients undergoing treatment with corticosteroids, which are frequently used in the management of a variety of common autoimmune disorders. Cognitive complaints and mood symptoms are extremely common but poorly understood side effects of treatment (Brown and Suppes, 1998, Otte et al., 2007 and Cornelisse et al., 2011), which could potentially be mitigated by designing treatment regimens to preserve

naturally occurring oscillations whenever possible. Converging evidence from animal models next and human neuroimaging studies indicates that stress-associated functional connectivity changes are a common feature of depression, PTSD, and other neuropsychiatric conditions and are associated with correlated structural changes in the prefrontal cortex, hippocampus, and other vulnerable brain regions. These, in turn, may be caused in part by circadian disturbances in glucocorticoid activity. Circadian glucocorticoid peaks and troughs are critical for generating and stabilizing new synapses after learning and pruning a corresponding subset of pre-existing synapses. Chronic stress disrupts this balance, interfering with glucocorticoid signaling during the circadian trough and leading to widespread synapse loss, dendritic remodeling, and behavioral consequences.

Jerse (Uniformed Services University of the Health Sciences, USA); Christine Johnston (University of Washington, USA); Nicola Low (University of Bern, Switzerland); David Mabey (Libraries London School of Hygiene and Tropical Medicine, UK); Noni MacDonald (Dalhousie University, Canada); Fred Mhalu (Muhimbili University of Health and Allied Sciences, Tanzania); André Meheus (University of Antwerpen, Belgium); Lori Newman (World Health Organization, Switzerland); Jacques Ravel (University of Maryland

School of Medicine, USA); Helen Rees, Consultation FXR agonist Chairperson (Wits Reproductive Health and HIV Institute, University of the Witwatersrand, South Africa); Anne M. Rompalo (Johns Hopkins University School of Medicine, USA); Kenneth L. Rosenthal (McMaster University, Canada);

Susan Rosenthal (Columbia INK1197 ic50 University Medical Center, USA); Michael W. Russell (University of Buffalo, USA); Robin Shattock (Imperial College London, UK); Lawrence Stanberry (Columbia University Medical Center, USA); Yot Teerawattananon (Department of Health Ministry of Public Health, Thailand); Peter Timms (Queensland University of Technology, Australia); Daisy Vanrompay (Ghent University, Belgium); Andrea Vicari (World Health Organization/Pan American Health Organization, Costa Rica); Teodora Wi (World Health Organization, Switzerland). Special thanks

to Gail Bolan, Nicola Low, Anne M. Rompalo, and Lawrence Stanberry for serving as working group chairs during the Technical Consultation, and to the authors of the papers included in this special issue of Vaccine. “
“The name herpes comes from the Greek meaning to ‘Creep and Crawl’, and centuries later Shakespeare referred to herpes as the ‘blister plague’. In the Middle Ages syphilis was treated with Mercury, leading to the expression that “a night in the arms of Venus means a lifetime spent almost on Mercury”. In the 19th century the symptoms of gonorrhoea were treated with silver nitrate and, early in the 20th century, syphilis with arsenicals. These were replaced by antibiotics that were so powerful that it was anticipated that the fight against syphilis, as well as against chlamydia, gonorrhoea and trichomoniasis was finally won. In the 21st century, resistance of Neisseria gonorrhoeae to all first line antimicrobials is now being encountered. Despite effective diagnostics and treatment, little progress is being made today in controlling chlamydial infection, and syphilis is again epidemic among men who have sex with men.

76 The observation that baseline corticosterone levels were undetectable throughout the

circadian cycle revealed a role of CRHR1 in the development of the adrenal medulla and adrenocortical sensitivity to ACTH.32 In the PVH, only low levels of CRHR1 mRNA can be found, but levels are induced in response to stress22,77-80 or ICV CRH Epacadostat order administration.81 This induction of CRHR1 mRNA may be implemented in the positive feedback action of CRH on paraventricular neurons, but the evidence Inhibitors,research,lifescience,medical needs to be further solidified. Exposure of the CRHR2-deficient and wildtype mice to restraint stress revealed changes in HPA axis regulation at different levels in two out of three mutant lines.51-53 Presumably, due to single-time

-point Inhibitors,research,lifescience,medical analysis, Kishimoto et al53 did not observe any changes in stressinduced HPA activity. The other two CRHR2 mutant mouse lines showed increased responses in plasma ACTH and corticosterone levels to restraint stress.51,52 The plasma ACTH levels in the mutant mice decreased within just 10 min of onset of stress, which is in sharp contrast to the wildtype animals, whereas corticosterone levels continued to rise reaching higher levels than the wildtypes.51,52 At 90 min poststress, corticosterone levels were still higher in the mutant mice. It is clear from these data that there is an array of changes in the HPA axis of CRHR2 mutant Inhibitors,research,lifescience,medical mice that may explain the different hormonal responses: (i) hypersensitivity of the corticotrophs to hypothalamic secretogogues; (ii) higher glucocorticoid Inhibitors,research,lifescience,medical levels cause ACTH levels to fall earlier due to higher negative

feedback inhibition; and (iii) the adrenal cortex of the mutant mice is possibly hypersensitive to ACTH.51,52 In summary, these changes in HPA responses to stress suggest that Inhibitors,research,lifescience,medical CRHR1 and CRHR2 arc acting in an antagonistic manner with CRHR1 acting proactively and CRHR2 acting attenuatively. The sites of these antagonistic actions are currently unknown, but may include the pituitary gland, the PVH, brain areas providing afferent input to the PVH such as the amygdala, BNST, and the lateral septum, and the sympathetic motor nuclei driving the sympathoadrenomedullary pathway. Studies on the HPA axis of recently created CRHR1- and CRHR2-double mutant mice confirm the data obtained with the Thiamine-diphosphate kinase single gene mutants, with the CRHR1 mutation nevertheless having a dominating influence, presumably due to its “key” position on the anterior pituitary corticotrophs.82 Beside the CRH receptors, corticosteroid receptors are also key elements in the regulation of the HPA axis.72,73 They can be distinguished in two types of glucocorticoid-binding receptors: the mineralocorticoid receptor (MR or type I) and the glucocorticoid receptor (GR or type II).83 MRs are mainly localized in the hippocampus, whereas GRs have a widespread distribution in the CNS.

With stratification by APOE allele status, we examined the effect of plasma apoE/lipids on longitudinal change in the cognitive function of community-dwelling

elderly using the data from a 3-year follow-up study. Three-year follow-up examinations of the effect of plasma apoE/lipids on cognitive function in the elderly Participants were recruited in the present study from the “Tone Project” in Tone town, Ibaraki, Japan.10 A total of 1395 volunteers Inhibitors,research,lifescience,medical participated in the first baseline study INK 128 order between December 2001 and April 2002. Three years later, 622 of them who had no history of stroke during follow-up were able to be evaluated again between December Inhibitors,research,lifescience,medical 2004 and April 2005, and we used the results from those subjects tested twice. At the initial examination, all of the eligible subjects provided written informed consent for

their participation in the study. This study was approved by the ethics committee of Tsukuba University. All participants underwent the same cognitive assessment at the baseline and 3-year examinations using a set of four tests to measure the following cognitive domains: attention, Inhibitors,research,lifescience,medical memory, language, and reasoning. We evaluated attention by using the Japanese version of a Set-dependent activity,11 memory ability using the Category Cued Recall test,12 and language ability with a category fluency test.13 Abstract reasoning ability was evaluated with the Similarities subtest of the Wechsler Adult Intelligence Scale-Revised (WAIS-R).14 The assessment procedures have been described elsewhere.8,9 A composite cognitive score was computed from the four scores using the first component of the scores of principal component Inhibitors,research,lifescience,medical analysis. Blood samples were Inhibitors,research,lifescience,medical collected from the subjects at fasting visits at the initial examination. Plasma levels of lowdensity lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides (TG), and total cholesterol (TC) were measured using standard enzymatic methods on routine automated chemistry systems. Plasma

apoE levels were determined by turbidimetric immunoassay. Genomic DNA was used for APOE typing. Subjects were divided into two APOE groups by E4 status with E4-(n=509) (genotypes ε2/ε3 [n=52], ε3/ε3 [n=457]) and E4+ (n=113) (genotypes [ε2/ε4 Linifanib (ABT-869) n=6], ε3/ε4 [n=99] and ε4/ε4 [n=8]) to test for the influence of genotype on the association between lipids and cognitive function. The subjects in each category were divided into three strata according to the plasma concentrations of lipids. To examine the influence of plasma lipids on cognitive function, composite cognitive scores of the three strata of plasma concentrations were compared in E4- and E4+ groups separately by ANCOVA, with age, sex, years of education, Geriatric Depression Scale score, cigarette smoking, and medical history of diseases as covariates.

Cardiac disease among children ranges from unaffected to moderate cardiac hypertrophy and cardiac dysfunction while adult patients usually have no clinically identifiable heart disease. A less frequent complication of late onset Pompe disease is vascular involvement of intracranial blood vessels; glycogen accumulation in vasculare

smooth muscle, results in aneyeurysm and rupture of basilar artery, internal carotid artery and medial cerebral arteries Inhibitors,research,lifescience,medical (1). In a review of 225 published cases of late onset Pompe disease the median age at the onset was 24 years (0-68), at the start of ventilation 34 years, at the start of wheelchair use 16 years, at the death 24.5 years. Patients with a later onset of symptoms have a better prognosis (2). Emerging clinical features Natural history Inhibitors,research,lifescience,medical of infantile Pompe disease reflects the predominant involvement of cardiac and ABT-199 in vivo respiratory systems. However glycogen storage is autoptically present also in the brain, brainstem and anterior horns (8). It is expected that enzyme replacement therapy will have a tremendous beneficial impact upon systemic manifestations of Pompe disease, but enzyme does Inhibitors,research,lifescience,medical not cross blood brain barrier and cannot cure central nerve system disease. Therefore neurological manifestations may be uncovered during long-term enzyme replacement therapy. The hearing loss was discovered in patients with infantile Pompe disease treated by enzyme replacement therapy.

It was not reported before because the medical attention was drawn to the cardiopulmonary Inhibitors,research,lifescience,medical complications that lead to death in the first year of life. Hearing deficits are due to conductive apparatus and cochlea involvement and seem not to be present in patients with late onset form (9). Furthermore in some patients with infantile onset form delay myelination was shown by brain MRI (10). Finally some children experienced fever of central origin, causing death despite Inhibitors,research,lifescience,medical having had a good cardiac and muscular response to enzyme replacement therapy (11). Diagnostic tests In the first evaluation

of a patient suspected of having Pompe disease laboratory testing should include serum creatine kinase, AST, ALT, LDH and tetrasaccharides in blood and urine. However, adult patients are reported to have normal creatine kinase (2). Due to variability of glycogen accumulation between different muscles and muscle fiber types within muscle, lack of muscle glycogen storage demonstration does not Farnesyltransferase exclude Pompe disease: actually 20% of late onset patients have a normal glycogen muscle content (2). GAA assay on skin fibroblasts or muscle biopsy is the diagnostic gold standard for diagnosis (12). White cells are unreliable tissue for measurement of enzyme activity because of interfering alternate isoenzyme activities: GAA assay in leukocyte can give false negative results in 10% of the patients (13), except for using inhibitors of interfering maltase, like acarbose.

Focusing on what is known

as “the prodromal period” will also make it possible to characterize a subset of individuals who are at risk and go on to develop schizophrenia, versus another subset of individuals who are at risk but who do not go on to develop schizophrenia. A focus on this group of subjects will also make it possible to learn more about the timing of brain abnormalities in schizophrenia, and to begin to develop putative brain markers or brain signatures that predispose an individual to develop schizophrenia. Another approach is to study family members of schizophrenic Inhibitors,research,lifescience,medical patients in order to discern brain abnormalities that are associated with genetically regulated Inhibitors,research,lifescience,medical variations in brain structure, but which are neither necessary nor sufficient for the development of psychosis. Some of these strategies, along with recent findings, are reviewed, below. High-risk studies To address the question of “what is the timing of brain abnormalities in schizophrenia?” it is useful to study individuals who are at high risk for developing schizophrenia, but who have not yet developed the disorder, ie, before psychosis begins. As noted above, this can be addressed to some extent with longitudinal studies, but can also be addressed Inhibitors,research,lifescience,medical by studying individuals who are at high risk for developing

schizophrenia, as one can observe whether or not there are brain abnormalities present prior to Inhibitors,research,lifescience,medical onset of schizophrenia. This approach is quite appealing

given that there is evidence to suggest that as many as 35% of individuals defined as being at ultra high-risk for Ku-0059436 supplier schizophrenia convert to schizophrenia within the first year of being indentified17 (see also discussion below). With respect to high-risk studies, two of the largest and best known research programs come to mind. The first Inhibitors,research,lifescience,medical is the Edinburgh High-Risk Study (EHRS),47 which evaluates individuals at risk for developing schizophrenia. The EHRS defines “at-risk” based on cognitive impairment measures from the Structural Interview for Schizotypy (SIS). Findings thus far indicate that indi viduals who are at risk and who also have schizotypal too features tend to have increased right prefrontal cortical folding, which further predicts those individuals who develop schizophrenia. These investigators speculate that abnormalities in cortical folding reflect disordered connectivity in the right prefrontal lobe. The second large research program to evaluate individuals at risk for psychosis is the Melbourne Ultra HighRisk Studies, in collaboration with the Personal Assessment and Crisis Evaluation (PACE) clinic. This study investigates individuals at risk for developing psychosis.

We would also like to thank Mr Xiaowe Su for assistance

with literature PI3K Inhibitor Library price research, and Drs G. Aghajanian and R-J. Li for providing images of PFC dendrites in Figure 2. Selected abbreviations and acronyms ADT antidepressant treatment AMPA α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid BDNF brain derived neurotrophic factor IDO indoleamine 2,3-dioxygenase MDD major depressive Inhibitors,research,lifescience,medical disorder NMDA N-methyl-D-aspartic acid PFC prefrontal cortex TNF tumor necrosis factor
Family history is one of the greatest risk factors for psychiatric disorders, yet their genetic basis remains poorly understood despite substantial advances in whole genome sequencing techniques. While the search for Inhibitors,research,lifescience,medical genetic mutations continues at a rapid pace, the field is also investigating the environmental component of family history,

which has remained more difficult to explain mechanistically. One hypothesis is that environmental stimuli alter gene expression patterns in certain brain regions that ultimately change neural function and behavior. Support for this hypothesis Inhibitors,research,lifescience,medical has been observed in animal models of psychiatric illness, as well as in human patients. The interactions between the environment and the genes that give rise to specific phenotypes are termed “epigenetic.”1 An example of this process is observed in cellular differentiation, where unique chemical signals induce totipotent stem cells to differentiate into genetically identical cell types with vastly different functions. This is due in part to the vastly different sets of genes expressed between Inhibitors,research,lifescience,medical distinct cell types (eg, neurons vs hepatocytes),

despite their identical DNA templates. Mechanistic insight into this process has recently been uncovered, and involves the transduction of unique environmental signals into precise and highly stable alterations in chromatin structure that ultimately gate access of transcriptional Inhibitors,research,lifescience,medical machinery to specific gene programs, thereby providing unique gene expression profiles in response to specific environmental cues.2 Importantly, many of these chromatin remodeling mechanisms are highly stable, contributing to the maintenance of specific gene expression programs in the correct tissues throughout Rutecarpine the life of an individual. The strong control exerted by chromatin remodeling on gene expression, and the potential stability of chromatin mechanisms, make chromatin regulation a prime candidate for mediating aspects of the long-lasting neural plasticity that ultimately results in psychiatric syndromes. It is also interesting to note that certain neurological and psychiatric diseases are caused by rare genetic mutations in chromatin remodeling enzymes (Table I). While these mutations are rare, they directly illustrate how disruption of chromatin regulation can profoundly affect neural function and lead to complex behavioral abnormalities.

She is also responsible study review, IRB submission. Dr. Ogedegbe is responsible for the overall coordination of the study, preparation of abstracts and manuscripts from data on this project. WC, PhD, a quantitative psychologist, was the biostatiscian on the study. He was responsible for the power analysis, and the data analysis plan. JF, MD, a practicing Emergency Physician and Chair of Department of Emergency Medicine, was very involved in selection of the specific project, ensuring that specific

study design and goals remained aligned with the goals of the study sponsors. Also reviewed and endorsed all aspects of manuscript creation. Authors’ information Inhibitors,research,lifescience,medical Herman Morchel, MD a practicing Board Certified Emergency Medicine Physician holds Bachelors and Masters Inhibitors,research,lifescience,medical degrees in Electrical Engineering as well as two United States Patents. He has decades of experience in advanced technology research and development. Areas of concentration

include electronics, computers, and communications systems. Adjunct Clinical Professor of Biomedical Engineering at Stevens Institute of Technology, Hoboken, New Jersey. Vikki Hazelwood, PhD a Biomedical Engineering Professor currently at Stevens Institute, works part time with the team, has experience in RAD001 development of biomedical devices in the lab, as well as translating them to commercial products for use in the Inhibitors,research,lifescience,medical clinic. Chinwe Ogedegbe, MD, MPH, FACEP a practicing Board Certified Emergency Physician and Director for research in Emergency Department, member of the Institution’s IRB committee, and Associate Professor of St Georges University Department of Emergency Medicine. William Chaplin, PhD, a quantitative psychologist, was the biostatiscian on the study. He has worked collaboratively on prior Inhibitors,research,lifescience,medical projects with our team.

He works primarily in the Department of Psychology, at St. Johns University, Queens NY. Joseph Feldman, MD, FACEP a practicing Board Certified Emergency Physician and Chair of Department Inhibitors,research,lifescience,medical of Emergency Medicine and Emergency Services at the 775-bed institution, Director of Medical Education for the St. Georges University School of Medicine program at Hackensack University Medical Center. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1471-227X/12/19/prepub Acknowledgements Would like to acknowledge 17-DMAG (Alvespimycin) HCl Drs. Steve Vets, and Betty Chang, who assisted with initial protocol development; as well as Marissa Gray, Mark Butler, Cindy Hassler, Bertha Lake, Chris Winckler and Deborah Brahee; who all assisted in various aspects of study preparation, subject testing and image editing. Also thanks to DTRA, Suzanne Lutwick, Grant’s officer; Cipher systems LLC.; as well as John Locurto, MD, Sanjeev Kaul, MD and colleagues (Trauma Service, HUMC). Abstract was presented at the Annual Applied Technologies for Advanced Combat Casualty Care (ATACCC), Aug.