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Findings from these studies are somewhat difficult to interpret, however, because ratings may be subject to mood-related biases due to their subjective and retrospective nature and because studies differ in terms of the specific memory attributes rated. Such fragmentation is thought to result from disorganized initial encoding of the traumatic event, which leads to inconsistent consolidation and poorly regulated retrieval. Van der Kolk (63,64), for example, proposed that the lack of narrative coherence of trauma memories is a reflection of emotionally induced dissociative states at the time of trauma, which result in routing of the memories through distinct neurochemical pathways. According to this model, trauma memories are preserved in an implicit memory system as vivid sensory and perceptual experiences but are not accessible as explicit verbal narratives. Brewin (66,67) proposed a dual-representation model according to which trauma memories are based on two separate representations: (1) a hippocampally mediated narrative representation that supports verbally accessible memories that are integrated with the rest of the autobiographical memory base and can be retrieved either automatically or strategically, and (2) an image-based represen tation mediated by the amygdala that does not interact with the autobiographi cal memory base and can only be retrieved automatically by trauma cues. According to this model, the two systems may be differentially impacted by neurohormonal responses to stress, leading to enhanced encoding of situationally accessible trauma memories and reduced encoding of verbally accessible trauma memories. Most memory fragmentation theories of trauma memory assert that some combination of heightened arousal, emotional distress, and dissociation at the time of the event lead to disorganized encoding of trauma memories. Consistent with the view that extreme distress during trauma affects the manner in which an event is encoded, studies of emotional memory encoding in nonclinical sam ples suggest that intensely negative and arousing memories lead to enhanced memory for the information central to the event but impoverished memory of peripheral details (for a review, see 69), a phenomenon referred to as tunnel memory (70). However, tunnel memory is a common source of memory distor tion for emotionally significant events and can equally be explained with refer ence to general principles of autobiographical memory (71). More important, perhaps, the phenomenon of tunnel memory fails to explain the enhanced clarity of peripheral trauma details thought to be associ ated with intense reliving phenomena (72). The empirical basis for memory fragmentation models has largely been based on narrative recall paradigms and metamemory studies. In narrative recall para digms, participants are asked to describe the trauma event, and the narratives are then coded for their cohesiveness and semantic structure. In metamemory studies, participants are asked to make a subjective appraisal of the coherence of their own memory. Some studies have found that traumatic memories are more fragmented in individuals with acute stress disorder. Of special note in the literature on trauma memory is the subgroup of stud ies that have attempted to link other symptoms to autobiographical memories of the trauma. This has led some theorists to maintain that those memories manifested in the form of reexperi encing symptoms, in particular, may differ qualitatively from other trauma and nontrauma autobiographical memories (17,66,74). Brewin (75), for example, has suggested that flashbacks are clearer than other trauma memories, albeit more 114 Verfaellie and Vasterling fragmented and less easy to retrieve in a well-regulated manner. In examining non flashback intrusions, Rubin, Feldman, and Beckham (61), however, found no evidence that trauma memories differed from nontrauma memories in coher ence, although reliving phenomena increased as memories were more related to the trauma. Indeed, recurrent involuntary trauma memories appear to share many of the same characteristics. Characterizing the New Learning Impairments the results of neuropsychological studies examining the presence and nature of difficulties in new learning remain unclear. These studies raise the question of whether impaired memory, when observed, may be due to comorbid conditions such as substance abuse or depression (95). A meta-analysis by Brewin, Kleiner, Vasterling, and Field (78) helps to clar ify the role of several of these variables. Although the magnitude of memory impairment is greater when the comparison group consists of individuals without trauma expo sure, a significant impairment remains when a trauma-matched control group is used, which is on the order of one-third of a standard deviation. To the extent that continued stress expo sure may lead to a progressive course of the disorder, cognitive deficits might be more obvious over time; indeed, in at least one study, memory impairment was absent on most measures of memory in recent adult trauma survivors with post-traumatic stress symptoms (98).
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Birth parents with trauma histories and the child welfare system: A guide for resource parents. Twelve months ago, John and Elaina had their three children (boys 8 and 14, and a daughter aged 9) removed from their care for chronic neglect. The children had been left alone in their apartment for three days while John and Elaina went on a drug binge. The three children have been living in the current resource family home for the past 10 months and are doing well overall except for a few incidents of sexualized behavior on the part of the younger children. When the resource family tried to talk with the children about the observed behavior, the children seemed confused and not able to understand the concerns. The social worker wants to reunify John and Elaina with their children, but thinks that their one bedroom apartment is not adequate. John and Elaina have successfully completed their substance use treatment and parenting program, and they visit their children as often as possible. They have made positive behavioral changes that show they can provide safety, and they continue to look for jobs. Convene a family team meeting to develop a safety plan with their support network to identify support for the parents so they can reunify with the children. Continue services for parents and add counseling recommendation for children and parents. Two teenage parents (Sarah, mother, 15 and Steve, father, 16) leave the hospital with their newborn without completing discharge paperwork after Sarah overhears that nurses suspect she was using drugs while pregnant. Sarah agrees to work with the social worker through a plan of family maintenance so that she can get child care while she is in school. She also agrees to attend a parenting class but denies a substance use problem of any kind and refuses a drug and alcohol assessment. When the fighting escalated to the father shoving Sarah and hitting her with his fist, Mary called the police and Steve was arrested. Mary says Sarah is not committed to the baby and she wants her grandchild placed with her and will adopt if necessary. What is the most important next step that the social worker should take in deciding whether the infant can be protected without removalfi Meet with Sarah privately, discuss how things are going with Mary, and ask her to discuss her plans for raising her child with Steve. Explain to Sarah the consequences of failing to comply with the terms of the family maintenance agreement and the possibility that the baby could be removed from her care. Case records show that at the initial family meeting, it was decided that the safety goal would consist of keeping Keesha in her home on the condition that the parents agree to call maternal grandma (Karen) when Frank starts drinking.
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Score 2: diffuse mucosal infltrates without sub mucosal spreading and intact epithelial layer; D. Score 3: moderate infltration of infammatory cells into mucosa and submucosa with epithelial hyperplasia and goblet cell loss; E. Score 4: marked infammatory cell infltrates in mucosa and submucosa accompanied by crypt abscesses and loss of goblet cells and crypts; F. Score 5: marked infammatory cell infltrates within the mucosa spreading to the submucosa going along with crypt loss and hemor rhage. Scoring scheme 6 for infammation of the small intestine mediated by luminal antigens Infammatory cell infltrate: Intestinal architecture: Score 1 Score 2 Severity Extent Epithelial changes Mucosal architecture Mild Mucosa and sometimes submucosal 1 Mild villous blunting 1 Moderate Mucosa and sometimes submucosal 2 Mild hyperplasia Moderate villous blunting 2 Marked Mucosa and submucosa, sometimes 3 Moderate hyperplasia and goblet cell loss Moderate villous blunting 3 transmural and broadening, sometimes villous atrophy Marked Transmural 4 Marked hyperplasia and goblet cell loss Villous atrophy, ulcerations 4 Sum of scores 1 and 2: 0-8 described the level of leukocyte infltration and tion necessitated a separate scoring system the intestinal architecture and acknowledged that we adapted to our general outline with a the severity with maximum combined rates of 8 maximum of 4 (Table 9, Figure 12). The use of this scheme is exemplifed by duodenal tissue from the model of oral infec Discussion tion with Heligmosomoides polygyrus (Figure 11) but it also worked for the jejunum upon Comparing intestinal histomorphology as asse infection with Nippostrongylus brasiliensis (not ssed from H&E stained tissue sections from shown). The obligate intracellular parasite different mouse models or from the same Toxoplasma gondii causes an acute small model in the hands of different researchers bowel infammation due to T helper (Th)-1 cell requires consistent criteria. Score 1: minimal infammatory cell infltrates in the mucosa with intact epithelium; B. Score 2: mild infammatory cell infltrates in the mucosa with mild hyperplasia and mild goblet cell loss; C. Score 3: moderate infammatory cell infltrates in mucosa and submucosa with moderate goblet cell loss; D. Score 4: marked infammatory cell infltration into mucosa and submucosa with marked hyperplasia and marked goblet cell loss, multiple crypt abscesses and crypt loss. Overall increase of epithelial cell each other but distinguishable from those mod numbers visible as crypt elongation in longitu els resulting from imbalanced immune disposi dinal crypts is also referred to as crypt hyper tions (inside events). Epithelial cytes and lymphocytes were common in all hyperplasia is typical for transfer colitis, the models and parts of the infamed intestine. So best characterized model of colitis induced by all models ftted the defnitions evaluating disruption of the T-cell homeostasis . Score 3: moderate infammatory cell infltrates in mucosa and submucosa with villous blunting; E. Score 4: marked mucosal, submucosal and transmural infammatory cell infltration with lymphoid ag gregates predominantely in the submucosa accompanied by villous broadening; F. Score 5: marked transmural in fammatory cell infltration and villous atrophy (insert: submucosal granuloma; fi400). Histomorphology of duodenal tissue in mice infected with Heligmosomoides polygyrus representing scores according to scheme 6 referring to Table 8. Sum score 2: mild mucosal and submucosal infammation (score 1: 1) with normal crypts and villi (score 2: 0); C. Sum score 4: moderate infltra tion of mucosa (score 1: 2) with mild villous blunting and mild hyperplasia (score 2: 2); D. Sum score 5: transmural infammation (score 1: 3) with moderate villous blunting and mild hyperplasia (score 2: 2); E. Sum score 6: mucosal infammatory cell infltration (score 1: 2) with moderate villous blunting and marked hyperplasia (score 2: 4); F. Sum score 7: marked transmural infammation (score 1: 4) with moderate blunting and moderate hyperplasia (score 1: 3). Score for small intestinal infammation upon infection with Toxoplasma gondii Infammatory cell infltrate Epithelial changes Mucosal architecture Score Severity Extent Minimal, focal Mucosa Intact epithelium 1 Mild, focal to diffuse Mucosa and submucosa Sometimes associated with erosions 2 Moderate, diffuse Mucosa and submucosa Erosions and/or ulcerations; cryptitis Distortion of villous structure 3 and/or crypt abscesses Severe, diffuse Mucosa and submucosa, Ulcerations associated with necroses Distortion of villous structure 4 sometimes transmural and fbroses Figure 12. Histomorphology of ileal tissue in mice infected with Toxoplasma gondii at day 7 representing scores referring to Table 9. Score 1: minimal and focal infammatory cell infltrates in the mucosa with an intact epithelial layer; B. Score 2: mild, diffuse infammatory cell infltrates in mucosa and submucosa with fattened epithelium and villous blunting; C.
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Baldev Kumar A Conceptual and Clinical Study of Sadhyata-Asadhyata of Associate Professor Prameha. Nisha Gupta An Evaluation of Dhumpana Therapy in Anurjatajanya Firoda Associate Professor Tamaka Svasa A Comparative Study. Shailja A Conceptual Study on Role of Rasayana Therapy in Verma Bhatnagar Womens Health. Kedar Lal Meena A conceptual, clinical and comparative study of Meena Professor alambushadi churna and rasnadwadashaka kwatha in Dr. Kedar Lal Meena A comparative clinical study of yavanyadi peya and Gupta Professor kantakari avelaha in vatika kasa w. Kedar Lal Meena A survey study of diabetic patients (type i and ii) with Verma Professor special reference to different types of prameha 15. Kedar Lal Meena Conceptual and clinical study of prameha in the purview Sikandar Professor of fififififififififi fi fififififififififififi fififififififififififififififififififififififififififi fififififi fifififififififififi fifififififififi(fi. Kedar Lal Meena A Comprehensive Review on the Role of Vegadharana on Tamrakar Professor Pranavahasrotogata Vyadhi and their Chikitsa Siddhanta. Govind Pareek Observational and Analytical Study of Dengue and Sharma Assistant Professor Chikungunyain Purview of Ayurveda. Shailza Clinical Evaluation of Rasayana Effect of Guduchi Swarasa Manki Mita Bhatnagar in Apparently Healthy Individuals. Kedar Lal Meena A Clinical and Comparative Study of Madhu Pippalyadi Sthitaprajna Professor Yoga And Gudadyo Modaka on Amlapitta. Meena A Clinical and Comparative Study of Guduchyadi Yoga and Associate Professor Madhumehari Churna on Prameha. Kedar Lal Meena A Survey Based Conceptual Study on Prognosis of Kushta Professor Roga in the Purview of Vikara Vighata Bhava and Abhava. Panja A Comprehensive Review of Dosha Gati and its Assistant Professor Implementation in Vata Rakta and Kustha. Nisha Gupta Fundamental Study of various Nyaya in Associate Professor Brhattrayi: Intervening Therapeutics. Baldev Kumar A Comprehensive Study of Prameha in relevance Associate Professor with its Ayurvedic Management and Prognosis. Kedar Lal Meena fifififififi fifi fififififi fififififi fififififi fififififififi fifi Kumawat Professor fififififififififififi fififififi Allergic Clinic: An Allergic Clinic runs by the Department wherein patients suffering from allergy etc. Clinical: the Teachers of the Department provided their duties to patients in Indoor as well as Outdoor hospitals. Govind Pareek Supplementation of previously Assistant Professor published book Ayurveda Samgrah. Kedar Lal Meena Efficacy of Satavari Curna and Kaparda Punarnav Professor Bhasma in Management of Postmenopausal Vol. Kedar Lal Meena A Review on Sadvritta and Its Clinical Pezzottaite journals Professor Importance. Kedar Lal Meena the Concept of Prajnaparadha in relation Journal of ayurveda Professor with Bhutvidhya A Review. Nisha Gupta A Critical Study of Viruddhaahara with Journal of Ayurveda Associate Professor special reference to Food Allergy. Nisha Gupta A Review of Preventive Health Care in International Journal of Associate Professor Geriatrics Through Ayurveda.
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