Excerpt: A recent study published in Workplace Health & Safety concluded, “Morbidity burden level is an indicator of work limitations in employees with diabetes and can be used to identify employees who may benefit from specialized services aimed at addressing their work limitations associated with diabetes” (Sylvia et al., 2012, p. 425). This conclusion is not warranted by the findings of the study because of limitations to both internal and external validity.

The concepts of urban psychosis and urban trauma rarely appear in scholarly literature. This study explores what urban psychosis is from a health perspective and how it affects African Americans who have lived in urban environments. The study also explores in what ways the experiences of people from inner-city neighborhoods illustrate the tenets of urban trauma and urban psychosis. Through an exploratory qualitative study, the researcher seeks to discover how urban dwellers experience urban psychosis and/or urban trauma.

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The extant theories in PTSD describe significant initial symptom reactions, and these reactions may provide opportunities for clearer early identification and treatment of PTSD. There are empirically identified trajectories of PTSD, which indicates there is a critical starting point to those trajectories. Generally, theories and results suggest that the re-experiencing (Cluster B) and hyperarousal (Cluster E) symptoms are common reactions after traumatic events, while hyperarousal and negative cognitions and mood (Cluster D) clusters are generally identified as the most important and/or predictive. Thus, this dissertation utilized retrospective reports in order to identify initial symptom reactions and then subsequently predict PTSD severity over time. Participants included college women who experienced sexual and relationship violence within the past 2 years. Two primary hypotheses were investigated within the dissertation: 1) Cluster B and E symptoms were expected to be the most prevalent initial reactions reported, and 2) Clusters E and D were expected to significantly predict PTSD severity over time. The results indicated partial support for each hypothesis, such that Cluster B symptoms were among the most prevalent initial reactions and Cluster D was a significant predictor of PTSD severity over time. Specifically, earlier Cluster D ordering interacted with the presence of negative beliefs and loss of positive emotions to predict PTSD severity over time. / Doctor of Philosophy / There are ideas and theories about how posttraumatic stress disorder (PTSD) starts and gets worse. People develop PTSD in different ways; some develop it very quickly and it is very bad, while others develop it slowly and it may not affect them much at all. The first signs and symptoms may be the best place to look, much like when you first get a cough or a sore throat with a cold or the flu. Generally, research suggests that common reactions are re-living the trauma and having reactions like being on guard all the time. Being on guard all the time also may be one of those important symptoms that will help predict if someone will get PTSD, as well as experiencing things such as thinking harsh things about oneself. This dissertation included reports from people after they had experienced trauma in order to figure out those first symptoms. Then, it used those first symptoms to predict how bad their PTSD was in the weeks and months later. Participants included college women who experienced sexual assault and domestic violence within the past 2 years. The results showed that people often re-live the trauma, but it may not be the most important when predicting whether they will get PTSD or not. Negative thoughts and beliefs about oneself were the most important set of reactions when predicting who will get PTSD and how badly. More importantly, the earlier they had those negative thoughts, the worse their PTSD was in the coming weeks and months.

Fear memory formation requires a coordination of molecular events, including protein synthesis, protein degradation, and epigenetic regulation of gene expression, throughout a circuit of brain regions. One mechanism highly studied for its involvement in protein degradation during fear memory is the ubiquitin-proteasome system (UPS), which utilizes the small protein ubiquitin to label proteins. Ubiquitin contains eight linkage sites that each lead to a unique outcome for the protein being labeled and a protein can gain one (monoubiquitination) or multiple (polyubiquitination) ubiquitins. The 26S proteasome is the catalytic component of the UPS and is comprised of a 20S catalytic core surrounded by two 19S regulatory caps. Phosphorylation of 19S cap regulatory subunit RPT6 at serine 120 (pRPT6-S120) has been widely implicated in controlling activity-dependent increases in proteasome activity. Interestingly, sex differences have been observed in proteasome-mediated protein degradation in the amygdala and hippocampus during fear memory formation. However, female subjects have only recently been regularly included in rodent behavioral studies so the majority of data on mechanisms of fear memory apply solely to the male brain. Considering post-traumatic stress disorder (PTSD) is two to three times more prevalent in females compared to males, understanding the mechanisms involved in fear memory in both sexes is important for understanding sex-specific development of fear-based disorders, such as PTSD. Importantly, the UPS also has non-proteolytic functions independent of proteasome-mediated protein degradation. For example, monoubiquitination and some forms of polyubiquitination do not lead to protein degradation. Additionally, 19S cap regulatory subunit RPT6 has been found to function independently of its role in the proteasome, where it has a transcription-like role in the hippocampus of male rats during fear memory formation. Unfortunately, proteasome-independent functions of the UPS have not been extensively studied in terms of different forms of ubiquitination. Additionally, it is unclear whether phosphorylation of RPT6 is necessary for its non-proteolytic roles in memory formation and the role of proteasome-independent RPT6 in general has not been investigated in female subjects. Here, we address these gaps in knowledge by 1) investigating sex-differences in the role of lysine 63 (K63-) polyubiquitination, a proteasome-independent ubiquitin linkage, in the amygdala during fear memory formation, 2) studying the role of proteasome-independent RPT6 in the hippocampus of female rats during fear memory formation, and 3) identifying proteasome-independent RPT6 target genes as well as the role of phosphorylation status of RPT6 at Serine-120 for its transcriptional activity during memory formation in the hippocampus of male rats. We first found that levels of K63-polyubiquitination targeting in the amygdala were increased in female, but not male, rats during fear memory formation. Interestingly, K63-polyubiquitination targeted proteins involved in ATP synthesis and proteasome functions in the amygdala of females and genetic manipulation of the K63 codon in the ubiquitin coding gene led to decreased ATP levels and proteasome activity. Additionally, this manipulation only led to impaired fear memory in females, suggesting that K63-polyubiquitination has a sex-selective role in the amygdala, where it regulates fear memory in females, but not males. We then investigated the role of proteasome-independent RPT6 in the hippocampus of females and males during fear memory formation. In females, we found RPT6 did not bind to DNA regions in the c-fos gene, a previously identified RPT6 target gene in males. However, RPT6 did bind to monoubiquitination of histone H2B at lysine-120 (H2BubiK120), an epigenetic modification identified as an RPT6 binding partner in males, suggesting a potential role for proteasome-independent RPT6 in transcriptional regulation in the hippocampus of female rats. In males, we identified RPT6 targets genes during memory formation, found that RPT6 DNA binding alone altered gene expression, and lastly observed that pRPT6-S120 was necessary for RPT6 to bind DNA and regulate transcription during memory formation. Collectively, these data reveal sex-differences in proteasome-independent roles of the UPS through ubiquitination and proteasomal subunits in both the amygdala and hippocampus during fear memory formation. Considering males and females have differences in PTSD prevalence, understanding proteasome-independent roles of the UPS in both sexes may lead to a better understanding of PTSD development as well as potential therapeutic targets in each sex. / Doctor of Philosophy / In order to remember a fear-provoking memory, or any memory, it must be stored in the brain after the event. To store a fear memory, cells in specific areas of the brain have to destroy some proteins and activate or shut off certain genes using epigenetic mechanisms. Although the DNA itself never changes, epigenetic mechanisms recruit proteins to sit on the DNA to make it more (activate) or less (shut off) accessible. For protein destruction, it has been shown that brain cells use a mechanism called the ubiquitin-proteasome system (UPS) during fear memory storage. The UPS uses a small protein called ubiquitin to label proteins in the cell. Ubiquitin is versatile in its ability to label proteins due to it having eight different binding sites that can be used as a label. Some proteins only gain one ubiquitin (monoubiquitination), while other proteins can gain multiple ubiquitin proteins (polyubiquitination) and both the number of ubiquitins and the label used determines what happens to the protein. When a protein is labeled to be destroyed, the UPS uses a large complex of proteins called the 26S proteasome, which contains a section called the 20S catalytic core and two 19S regulatory caps that sit above and below the 20S core. It has been shown that when one of the proteins in the 19S regulatory cap called RPT6 gains a phosphate molecule at the 120th amino acid, which is a serine amino acid, it increases the number of proteins destroyed by the 26S proteasome. Interestingly, the UPS does not destroy proteins in the same way in male and female brains during storage of a fear memory. This is important because females are 2-3 times more likely to develop post-traumatic stress disorder (PTSD) than males, but it is unclear why, making the study of mechanisms involved in fear memory storage in both males and females important. The UPS also functions in ways that do not involve destroying proteins. For example, proteins with a monoubiquitination label are often not destroyed. Additionally, it has been observed that RPT6, a protein in the 19S regulatory cap, can work outside of the 19S regulatory cap of the 26S proteasome to activate genes in brain cells of male rats. Sadly, the ubiquitin labels that do not cause protein destruction have not been well studied. It is also unclear whether RPT6 must gain a phosphate group to activate genes and if it activates genes in both male and female brains during fear memory storage. In the present study, we investigated the role of a common ubiquitin linkage that does not cause protein destruction called lysine 63- (K63-) polyubiquitination during fear memory storage in the amygdala, the emotional control center of the brain, in male and female rats. We found that K63-polyubiquitination is increased in female, but not male, rats during fear memory storage. In females, K63-polyubiquitination was involved in making new ATP as well as controlling the number of proteins destroyed by the 26S proteasome. Lastly, we found that female, but not male, rats required K63-polyubiquitination in the amygdala for fear memory storage, suggesting a female-specific use of this ubiquitin label. In this study, we also studied the role of RPT6 in the hippocampus, another key area of the brain for memory storage, of male and female rats. In females, we found RPT6 did not activate the same gene we previously identified in male rats, but it did bind with a monoubiquitination label on a protein that DNA is wrapped around, known as a histone. Due to this finding, it appears that RPT6 may act freely of the 19S regulatory cap to alter accessibility of genes in the hippocampus of females. On the other hand, in males we found that RPT6 activates some genes and shuts off other genes and can do so by sitting on DNA by itself. We also found that the addition of phosphate to RPT6 was necessary for it to sit on a gene and activate it during fear memory storage. These results show differences in UPS mechanisms during fear memory storage between males and females, which will be important for understanding why females are more likely to develop PTSD than males and for identifying potential treatment options.

This research examined life events that affect the onset of delayed Post-Traumatic Stress Disorder in aging combat veterans. A common result from experiencing combat trauma is Post-Traumatic Stress Disorder. There is a rapidly growing veteran population experiencing delayed onset Post-Traumatic Stress Disorder. The occurrence of additional life stressors may increase the likelihood that someone will develop Post-Traumatic Stress Disorder in response to a prior traumatic event. Participants of the study were combat veterans over the age of 65. Qualitative data were gathered from interviewing participants on life events they have experienced since combat exposure as well as Post-Traumatic Stress Disorder symptoms. Findings suggested that life events contribute to the delayed onset of Post-Traumatic Stress Disorder in aging combat veterans. Understanding the development and causes of delayed Post-Traumatic Stress Disorder will help social work practice develop and move forward with programs to improve the quality of life for aging veterans.

<h1>Abstract <em></em></h1><p>This essay will present actual research around the concept of Post- Traumatic Stress Disorder, how it can reveal itself in school children and how it can influence young people’s learning ability and capacity to retain knowledge.</p><p>The purpose is, above all, to clearly diagnose PTSD so that children with this complex of problems can receive good possibilities in learning and understanding.</p><p>The question at hand is responded to by interviewees with an expertise on the subject and one “story”, collectively with literary studies.</p><p>The results illustrate that there can be neurological and biological, as well as social explanations for PTSD but it is seldom a permanent diagnosis. It is though something to take very seriously. PTSD can lead to severe psychobiological consequences, mostly by causing damage in one particular part of the brain, known as hippocampus. The hippocampus is essential in terms of memory and concentration. Other negative effects caused by PTSD might be a disturbed cognition, difficulties in the ability to store information or a deterioration of language. All of these consequences affect the child’s ability to learn in a negative way.</p><p>The essay demonstrates how educators can simplify a PTSD diagnosed child’s difficulties and how school time can be adjusted to fit their needs. The importance of educator’s getting deep knowledge of the diagnosis is emphasized. Children with this diagnosis need an individual designed study plan and one must take much consideration with the learning difficulty that hinder these young people.<em></em></p>

Abstract This essay will present actual research around the concept of Post- Traumatic Stress Disorder, how it can reveal itself in school children and how it can influence young people’s learning ability and capacity to retain knowledge. The purpose is, above all, to clearly diagnose PTSD so that children with this complex of problems can receive good possibilities in learning and understanding. The question at hand is responded to by interviewees with an expertise on the subject and one “story”, collectively with literary studies. The results illustrate that there can be neurological and biological, as well as social explanations for PTSD but it is seldom a permanent diagnosis. It is though something to take very seriously. PTSD can lead to severe psychobiological consequences, mostly by causing damage in one particular part of the brain, known as hippocampus. The hippocampus is essential in terms of memory and concentration. Other negative effects caused by PTSD might be a disturbed cognition, difficulties in the ability to store information or a deterioration of language. All of these consequences affect the child’s ability to learn in a negative way. The essay demonstrates how educators can simplify a PTSD diagnosed child’s difficulties and how school time can be adjusted to fit their needs. The importance of educator’s getting deep knowledge of the diagnosis is emphasized. Children with this diagnosis need an individual designed study plan and one must take much consideration with the learning difficulty that hinder these young people.

Posttraumatiskt stressyndrom (PTSD) är en sjukdom som är traumarelaterad och svår att få en övergripande bild av då statistiken för antalet drabbade är bristfällig framför allt av ett stort mörkertal. Symtombilden vid denna sjukdom är mycket individuell och de upplevda symtomen är många, vilket skapar en svårighet i att diagnostisera sjukdomen. Vem som helst kan drabbas när som helst under sin livstid och att få en behandling som fungerar är problematisk då ingen exakt bot finns. Under ett trauma påverkas vårt alarmsystem i kroppen för att varna om fara och då har hjärnstrukturen amygdala en övergripande roll. Eftersom amygdala har stor betydelse för vår uppfattning om faror har därför denna studie valt att se om dessa traumatiska händelser orsakar symtomen vid PTSD. Mer specifikt var syftet med denna litteraturstudie att se om förändringar i amygdala och närliggande regioner kan vara bidragande till symtomen som upplevs av individer med PTSD samt vilka neurologiska förändringar som skett/finns i dessa hjärnregioner som kan ha en bidragande faktor till uppkomsten av sjukdomen. Av sex utvalda orginalartiklar kunde det sammantaget konstateras att vissa neurologiska förändringar som amygdala aktivitet och kortikal volym möjligtvis kan ha en koppling till vissa upplevda symtom som bland annat förhöjd vaksamhet och känsloregleringsförmåga. Artikel 1 visade på minskad volym av grå substans i premotorcortex och i främre cingulate cortex (p&lt;0.05)samt att de med PTSD hade svårare att hantera vardagliga utmaningar, var mindre positiva och mer negativa (p&lt;0.0001).Artikel 2 visade på att volymen av grå substans hade korrelationer med svårighetsgraden av PTSD samt symtombilden. Artikel 3 visade att individer med PTSD hade en minskad aktivitet i högra och vänstra amygdala och ventrala striatum (p&lt;0.005). Där emotionellt avtrubbande hade korrelationer med högra ventrala striatum(p&lt;0.05).Artikel 4 såg att de med PTSD hade förändrad cortex, i högra hemisfären var det åttaregioner och i den vänstra sex regionersom antagligen hade samband med totala CAPS poäng. Artikel 5visade att PTSD gruppen hade en ökad respons i högra amygdala vid syn av skrämmande ansikten (p&lt;0.05) samt att högra amygdala aktiviteten hade samband med symtomet förhöjd vaksamhet. Artikel 6 visade att förmågan att reglera känslor var förändrad hos individer med PTSD. Både vid intensifiering av en känsla (amygdala (p&lt;0.04), bakre cingulate cortex (p&lt;0.01), främre cingulate cortex (p&lt;0.04), middle cingulate cortex (p&lt;0.02), vänstra inferior frontal cortex (p&lt;0.04), vänstra putamen (p&lt;0.04), bilaterala inferior parietal loben (p&lt;0.03)) samt vid minskning av känsla (inferior frontal cortex (p&lt;0.01), vänstra putamen (p&lt;0.02), bilaterala inferior parietal loben (p&lt;0.01), insula (p&lt;0.03)).Denna studie kunde alltså inte påvisa tydliga hjärnområden, kopplade till amygdala, vilka hade förändringar som kan ha orsakat uppkomsten av ångestrelaterade besvär vid PTSD. Eftersom hjärnan är mycket komplex och kan bearbeta intryck på väldigt olika sätt kan dessa resultat kanske förklaras med hjälp av att de olika typer av trauman som individerna utsattes för i stor utsträckning påverkade skilda hjärnregioner. Det är alltså därför viktigt att fler studier, med större deltagarantal och likartade traumatiska händelser, fortsätter belysa PTSD symtom och deras koppling mot amygdala och närliggande hjärnregioner för att öka förståelsen för uppkomsten av PTSD. Eftersom kunskapen idag är begränsad vid behandling av PTSD-relaterad symtom behövs dessa frågeställningar klarläggas för att snabbare kunna ställa diagnos och kunna ge tidigbehandling till individer med PTSD. / Post-traumatic stress disorder (PTSD) is a trauma-related disorder that is difficult to get an overall picture of because of lack of statistics regarding affected individuals, most likely due to a large number of unrecorded cases. The symptoms of this disease are very individual and the perceived symptoms are many, which create a difficulty in diagnosing the disease. Anyone can be affected at any time during his or her lifetime, where effective treatment still needs to be developed. During a trauma our alarm systems in the body warns us of danger and then the brain structure amygdala has a central role. Because the amygdala is of great importance for our understanding of dangers, this study set out to examineif these traumatic events cause the symptoms of PTSD. More specifically, the purpose of this study was to examine if changes in the amygdala and nearby regions may contribute to the symptoms experienced by individuals with PTSD, as well as if the neurological changes that occurred in these brain regions may be a contributing factor to the onset of the disease. Of the six selected original articles it could be noted that certain neurological changes, including amygdala activity and cortical volume, could be linked to certain perceived symptoms together with heightened alertness and emotional regulation skills. Article 1 showed reduced volume of gray matter in the premotor cortex and the anterior cingulate cortex (p &lt;0.05), and those individuals with PTSD had more difficulties handling everyday challenges together with less positive attitudes (p &lt;0.0001). Article 2 showed that the volume of gray matter had correlations with the severity of PTSD and symptoms. Article 3 showed that individuals with PTSD had a decreased activity in the right and left amygdala and ventral striatum (p &lt;0.005). There, emotional numbing had correlations with right ventral striatum (p &lt;0.05). Article 4 showed that those with PTSD had altered cortex in the right hemisphere was the eight regions and in the left six regions that probably was associated with total CAPS score. Article 5 indicated that PTSD group had a higher response in the right amygdala at sight of the faces daunting (p &lt;0.05) and the right amygdala activity was associated with elevated symptom vigilance. Article 6 showed that the ability to regulate emotions was altered in individuals with PTSD. Both the intensification of a sense (amygdala (p &lt;0:04), the posterior cingulate cortex (p &lt;0:01), anterior cingulate cortex (p &lt;0:04), middle cingulate cortex (p &lt;0:02), left inferior frontal cortex (p &lt;0:04) left putamen (p &lt;0.04), bilateral inferior parietal lobe (p &lt;0.03)) and the reduction of sensation (the inferior frontal cortex (p &lt;0.01), the left putamen (p&lt;0.02), bilateral inferior parietal lobe (p &lt;0.01 ), insula (p &lt;0:03)). This study could thus not demonstrate distinct brain areas, linked to amygdala, which had changes that may have caused the onset of anxiety-related disorders in PTSD. Since the brain is very complex and can process impressions in very different ways, these results may be explained by the different types of trauma that the individuals were exposed to,which in turn could affect different brain regions. It is thus important that more studies with larger number of participants, and similar traumatic events, continues highlighting PTSD symptoms and their relationship to amygdala and related brain regions to increase understanding of the onset of PTSD. As knowledge today is limited in the treatment of PTSD-related symptoms, these issues must be continuously examined to develop earlier diagnosecriterias and finally propose proper treatments for individuals with PTSD.

Inledning: Trauma påverkar drömmar och dess bearbetningsförmåga av innehåll. En viktig punkt är att etiologin av PTSD anses vara en traumatisk upplevelse som kan leda till återkommande mardrömmar. Idag finns det många personer i samhället som lider av trauma och traumarelaterade problem vilket gör att utveckling av traumateorin får en central betydelse för att erbjuda bra behandlingsmetoder. Syftet med studien är att bidra med kunskap om hur traumatiska upplevelser bearbetas i drömmarna med fokus på affekter och interaktioner med andra människor som kan leda till vidareutveckling av psykodynamisk traumateori. Frågeställningar:  Vad finns det för skillnader i drömmarna mellan grupperna i avseende på affekter?  Vilka centrala teman förekommer i båda gruppernas drömmar och hur ser det ut i jämförelse mellan grupperna? Metod: Den metod som använts är en kombinerad kvantitativ och kvalitativ ansats där 60 drömmar från tidigare krigsveteraner studeras och jämförs i två grupper. Resultat: Studiens resultat visar traumats negativa effekter på affektregleringsförmåga och relationer. Det lyfter också fram drömmens betydelse som en ingång till det psykiska livet för att få inblick i hur traumatiska händelser och affekter hanteras, samt drömmandets funktion i affektreglering som är en viktig bearbetande faktor för trauma. Diskussion: Studiens resultat är i många avseenden i linje med tidigare forskning och teoribildning, men särskilt två aspekter av resultatet förtjänar att lyftas fram: Drömmen som en scen för det psykiska livet: 1. hur traumatiska händelser och affekter hanteras; 2. vilka faktorer kan tänkas vara bearbetande för trauma. / Introduction: Trauma affects dreams and its processing skills of content. An important point is that the etiology of PTSD is considered to be a traumatic experience that can lead to recurrent nightmares. Today there are many people in the community who suffer from trauma and trauma-related problems making the development of trauma theory be of central importance for providing good treatment. The aim of this study is to contribute knowledge about how traumatic experiences are processed in dreams with a focus on affects and interactions with other people that can lead to further development of psychodynamic trauma theory. Research questions:  What are the differencesindreamsbetween thegroupsin terms of emotions ?  What are thekey themespresent inboth groupsdreams andhowdoes it lookincomparisonbetween the groups? Method: The used method is a combined quantitative and qualitative approach where 60 dreams from former war veterans studied and compared in two groups. Results: Results of the study demonstrate traumas negative effects on affect regulation skills and relationships. It also highlights both the dream's meaning as an entrance to the psychic life to gain insight into how traumatic events and affects handled, and the function of dreaming in affect regulation as an important processing factor for trauma. Discussion: The study results are in many aspects in line with previous research and theory, but in particular, two aspects of the results deserve to be highlighted: The dream as an entrance for the psychic life: 1. how traumatic events and affects handled; 2. Which factors could be of importance in the processing of trauma.