Improving Project Logistics by using IoT

This Bachelor´s thesis is made on behalf of Wärtsilä Energy Solutions, Project Logistics & Transport Management department whose main task is to coordinate and ensure that materials and products are transported to the right place and on time in Project Logistics. This thesis examines how you could improve Wärtsilä´s Project Logistics by using Internet of Things. By developing IoT, there has been an increased chance to get more information about transports than before and Wärtsilä is currently looking for new solutions to use that could improve their current logistics system. The purpose of this thesis is to review new, and used, solutions on the market, and then see what could work in practice at Wärtsilä. Material to this thesis are gathered from books, web pages and articles that reviewed interesting IoT solutions and which also gave examples on different solutions that are used by other companies in the same business. The Result is two different methods that could improve Wärtsilä´s Project Logistics in different occasions. These results are intended to give tips on how IoT could improve the department´s ways of coordinating and check transports and logistics within a project.Detta examensarbete är gjort i uppdrag av Wärtsilä Energy Solutions, Project logistics & Transport Management avdelningen vars huvuduppgift är att koordinera och se till att material och produkter transporteras till rätt plats i rätt tid inom projekt logistiken. Examensarbetet behandlar hur man kunde förbättra Wärtsiläs projekt logistik genom att använda Internet of Things. Genom att IoT har utvecklats har det uppstått möjligheter att få fram mer information om transporter än tidigare och Wärtsilä söker för tillfället nya lösningar som kunde användas för att förbättra deras nuvarande logistiksystem. Syftet med arbetet är att gå igenom nya, men även redan befintliga, lösningar som används på dagens marknad - för att sedan se vad som kunde fungera i praktiken hos Wärtsilä. Material till arbetet är samlat från böcker, webbsidor och artiklar som gick igenom intressanta IoT lösningar och som också gav exempel på hur olika system fungerar och används av andra företag inom samma bransch. Slutresultatet blev två olika metoder som kunde förbättra Wärtsiläs projekt logistik vid olika tillfällen. Dessa resultat är tänkta för att ge tips på hur IoT kunde förbättra avdelningens sätt hur man koordinerar och granskar transporter och logistiken inom ett projekt

Cortisol metabolic predictors of response to psychotherapy for symptoms of PTSD in survivors of the World Trade Center attacks on September 11, 2001

BACKGROUND: A proportion of subjects with symptoms of posttraumatic stress disorder (PTSD) are unresponsive to specialized psychotherapy, but a biological basis for this has not been described. To observe whether differences in cortisol or its metabolites predict or correlate with response to therapy for PTSD symptoms, cortisol and its metabolites were measured from urine samples at pre-treatment, at the conclusion of psychotherapy, and at 3-month follow-up. METHODS: 28 survivors of the World Trade Center attack on September 11, 2001 seeking psychological treatment for PTSD symptoms received four sessions of either exposure therapy or supportive counseling, followed by up to 10 sessions of prolonged exposure in a specialized PTSD treatment program at a private hospital serving the New York City metropolitan area. 24-hr mean integrated cortisol excretion was assessed by radioimmunoassay (RIA); urinary free cortisol and metabolites cortisone, 5α–tetrahydrocortisol (5α-THF), 5β–tetrahydrocortisol, and tetrahydrocortisone were assessed by gas chromatography-mass spectrometry (GCMS); and indices of enzyme activities for 5α–and 5β–reductase and for the 11β–hydroxysteroid dehydrogenases were derived from the metabolite and glucocorticoid measures. RESULTS: 5α-reductase activity was significantly lower at pre-treatment among non-responders, whereas there were no significant pre-treatment differences between responders and non-responders in any other hormone or metabolite level. In repeated-measures analyses across the three time points, 5α-reductase activity, as well as 5α-THF and total glucocorticoids, significantly differed between responders and non-responders. For urinary cortisol measured by RIA, there was a significant group × time interaction indicating that, although not different at pre-treatment, urinary cortisol levels declined over time in the non-responder group, such that by follow-up, lowered cortisol significantly distinguished non-responders from responders. Indices of 5α-reductase activity, including 5α-THF and total glucocorticoids, were significantly negatively correlated with avoidance symptom severity at pre-treatment. At follow-up, indices of 5α-reductase activity were significantly negatively correlated with severity of all three PTSD symptom clusters and with total PTSD severity scores. CONCLUSION: Lower 5α–reductase activity is associated with avoidance severity and predicts non-responsiveness to psychological treatment for PTSD symptomatology. Relatively diminished 5α–reductase activity may mark a state of primary vulnerability, perhaps via attenuated peripheral catabolism of cortisol resulting in the suppression of hypothalamic-pituitary-adrenal axis responsiveness. Lower cortisol levels appear later in the progression to chronic, treatment-resistant PTSD

A randomized, double-blind, placebo-controlled, crossover trial of mifepristone in Gulf War veterans with chronic multisymptom illness

No pharmacological treatments have been demonstrated to effectively treat chronic multisymptom illness (CMI) in Gulf War veterans (GWV). This study assessed the effect of the glucocorticoid receptor antagonist mifepristone in GWV with CMI. A randomized, double-blind, cross-over trial of mifepristone, with two six-week treatment phases separated by a one-month washout period, was conducted at a Veterans Affairs (VA) hospital between 2008 and 2011. Participants were randomized to receive either 200mg of mifepristone per day or matched placebo first. The primary clinical outcome measure was change in self-reported physical health. Neurocognitive functioning and self-reported measures of depression, PTSD, and fatigue were secondary outcomes. Sixty-five participants enrolled, of whom 36 were randomized and 32 (mean age, 49.1 (7.2) years) completed the study. Physical and mental health status and neurocognitive functioning were poor at baseline. Mifepristone treatment was not associated with improvement in self-reported physical health (p=0.838) or in other self-reported measures of mental health. Mifepristone treatment was significantly associated with improvements in verbal learning (p=0.008, d=0.508), in the absence of improvement in other cognitive measures (working memory (p=0.914), visual learning (p=0.643) and a global composite measure (p=0.937). Baseline morning cortisol levels and lysozyme IC50-DEX, a measure of peripheral glucocorticoid sensitivity, displayed a significant relationship with endpoint verbal learning scores (p=0.012 and p=0.007, respectively). The magnitude of cortisol change during treatment mediated the improvement in verbal learning. This study was negative for the primary and secondary clinical outcomes. However, the data suggest a moderate dose of mifepristone may have circumscribed cognitive-enhancing effects in CMI. Further study is warranted to determine whether and through which mechanisms mifepristone treatment can yield clinically meaningful improvement in cognitive function in CMI or other neuropsychiatric conditions associated with HPA axis dysregulation

Evidence for epigenetic alterations in PTSD

Rationale/statement of the problem : Neuropeptide Y (NPY) is a peptide with behaviorally relevant effects on the hippocampus and is thought to function as an endogenous anxiolytic. In prior work, we reported that veterans who had recovered from combat-related post-traumatic stress disorder (PTSD) had higher levels than those who were not combat exposed. NPY levels were significantly associated with the extent of symptom improvement, suggesting that plasma NPY levels may represent a biological correlate of resilience to, and/or recovery from, the adverse effects of trauma exposure. Cytosine methylation of the glucocorticoid gene (GR methylation) has been associated with PTSD risk and/or symptom expression. GR methylation is influenced by environmental factors that can result in enduring differences in function, including neuroendocrine regulation. As the NPY gene has glucocorticoid response elements, levels of circulating NPY represent a potential indicator of alterations in GR responsivity. Methods : The relationship of NPY to PTSD and GR methylation was examined in two samples. In the first sample, veterans who developed PTSD following combat exposure were compared to those who did not develop PTSD. In a second sample, veterans with combat-related PTSD were assessed prior to and following a course of prolonged exposure (PE). Results : In the cross-sectional study, veterans with PTSD had higher NPY levels than those who never developed PTSD (t (62) = − 1.99, p=0.05; 95.8±45.6 pm/l vs. 73.9±41.5 pm/l). NPY associated with number of GR methylated sites in the full sample (r=0.35, n=64, p=0.005), but not with average percent methylation (r= − 0.05). When the associations were examined separately by PTSD group status, results showed a positive association between NPY and number of methylated sites (r=0.36) as well as percent methylation (r=0.38) in veterans with PTSD. However, NPY was only associated with the number of methylated sites (r = 0.35) in the subjects who did not develop PTSD following combat exposure. In the treatment study, plasma NPY levels increased among veterans who responded to treatment (who no longer met diagnostic criteria for PTSD following PE), compared to treatment non-responders, as indicated by a significant group æ time interaction (F1,14 = 5.48, p=0.035). While plasma NPY was comparable in the two groups at pretreatment (responders: 71.4±20.3 pm/l, non-responders: 71.0±16.0 pm/l), responders had higher plasma NPY (84.0±24.2 pm/l) relative to non-responders (61.0±15.4 pm/l). Both pretreatment number of GR methylated sites (r=0.53, n=16, p=0.04) and average percent GR methylation (r=0.75, n=15, p=0.001) were associated with higher plasma NPY at post-treatment. Conclusion : To the extent that improvement from symptomatic PTSD may involve a mobilization of endogenous mechanisms to reduce hyperarousal and other post-trauma sequellae, the results of these studies are consistent in suggesting a role for NPY. NPY was elevated in a sample of combat veterans with PTSD, and increased in association with PTSD improvement in response to trauma-focused treatment. GR methylation was associated with combat-related PTSD in a cross-sectional study, and with treatment associated improvement in PTSD. These findings suggest that epigenetic modification of the GR gene may be associated with resilience in PTSD

Hydrocortisone responsiveness in Gulf War veterans with PTSD: Effects on ACTH, declarative memory hippocampal [ 18F]FDG uptake on PET

Neuroendocrine, cognitive and hippocampal alterations have been described in Gulf War (GW) veterans, but their inter-relationships and significance for posttraumatic stress disorder (PTSD) have not been described. Hydrocortisone (Hcort) was administered to GW veterans with (PTSD+ n = 12) and without (PTSD− n = 8) chronic PTSD in a randomized, placebo-controlled, double-blind challenge. Changes in plasma ACTH, memory, and hippocampal [ 18F]FDG uptake on positron emission tomography were assessed. The low-dose dexamethasone suppression test was also administered. The PTSD+ group showed greater cortisol and ACTH suppression, reflecting greater peripheral glucocorticoid receptor (GR) responsiveness, and did not show an Hcort–induced decrement in delayed recall or retention. The groups had comparable relative regional hippocampal [ 18F]FDG uptake at baseline, but only the PTSD− group had an Hcort–associated decrease in hippocampal [ 18F]FDG uptake. Asymmetry in hippocampal hemispheric volumes differed between PTSD+ and PTSD− groups. This asymmetry was associated with cortisol, ACTH, retention and functional hippocampal asymmetry before, but not after, Hcort administration. Differences in brain metabolic responses between GW veterans with and without PTSD may reflect differences in peripheral and central GR responsiveness

Epigenetic age in male combat-exposed war veterans. associations with posttraumatic stress disorder status

DNA methylation patterns change with age and can be used to derive an estimate of "epigenetic age," an indicator of biological age. Several studies have shown associations of posttraumatic stress disorder (PTSD) with worse somatic health and early mortality, raising the possibility of accelerated biological aging. This study examined associations between estimated epigenetic age and various variables in 160 male combat-exposed war veterans with (n = 79) and without PTSD (n = 81). DNA methylation was assessed in leukocyte genomic DNA using the Illumina 450K DNA methylation arrays. Epigenetic age was estimated using Horvath's epigenetic clock algorithm and Δage (epigenetic age-chronological age) was calculated. In veterans with PTSD (Δage = 3.2), Δage was on average lower compared to those without PTSD (Δage = 5.0; p = 0.02; Cohen's d = 0.42). This between-group difference was not explained by race/ethnicity, lifestyle factors or childhood trauma. Antidepressant use, however, explained part of the association. In the PTSD positive group, telomerase activity was negatively related to Δage (β = -0.35; p = 0.007). In conclusion, veterans with PTSD had significantly lower epigenetic age profiles than those without PTSD. Further, current antidepressant use and higher telomerase activity were related to relatively less epigenetic aging in veterans with PTSD, speculative of a mechanistic pathway that might attenuate biological aging-related processes in the context of PTSD

Association of dimensional psychological health measures with telomere length in male war veterans.

BackgroundSeveral psychiatric disorders may be characterized by peripheral telomere shortening. However, it is unclear whether telomere shortening is associated with these psychiatric disorders per se or, rather, with underlying dimensional parameters that are often, but not necessarily, associated with them. We explored the association between dimensional psychopathological measures and telomere length (TL) in granulocytes among veterans independent of psychiatric diagnosis.MethodsSeventy-six combat-exposed male veterans (41 psychiatrically healthy, 18 with Posttraumatic Stress Disorder [PTSD] and 17 with concomitant PTSD and Major Depressive Disorder [MDD]) had TL assayed. Assessments included Clinician-Administered PTSD Scale (CAPS), Beck Depression Inventory-II (BDI-II), Early Trauma Inventory (ETI), Symptom Checklist-90-R Global Severity Index (SCL-90-GSI), Perceived Stress Scale (PSS) and Positive and Negative Affect Schedule (PANAS). Correlations were corrected for age, BMI, antidepressants and ethnicity.ResultsAcross subjects, TL was negatively correlated with early trauma (p<0.001), global psychopathological severity (p=0.044) and perceived stress (p=0.019), positively correlated with positive affect (p=0.026), not significantly correlated with symptom severity of PTSD, depression or negative affect. Across these dimensions, early trauma and positive affect were associated with TL after excluding subjects with somatic illnesses.LimitationsThe study was cross-sectional with a moderate sample size and only male combat-exposed subjects.ConclusionsThese preliminary findings suggest that early trauma, severity of perceived stress and general psychopathological symptoms are more closely associated with shorter TL than is the severity of core diagnostic symptoms of PTSD or MDD, whereas positive affect is associated with longer TL. Larger-scale studies should assess TL associated with specific psychiatric dimensions, apart from only categorical psychiatric diagnoses, to develop more specific biologically-relevant endophenotypes