bluuebunny/crossref_metadata_2025_split huggingface dataset:
Computer‐based multivariate economic analysis of neonatal‐intensive‐care‐unit‐based influenza vaccine administration to parents in a low‐socio‐economic, urban setting
Authors: Shah Shetal I. , Caprio Martha , Sen Alpana , Hendricks‐Munoz Karen 
Published: June 2007

AbstractOBJECTIVETrivalent inactivated influenza vaccine has been shown to reduce the number of influenza‐related outpatient visits and hospitalizations of children up to 24 months of age. The American Academy of Pediatrics, Centers for Disease Control, and Advisory Committee on Immunization Practices recommend that the influenza vaccine be administered to the first‐person contacts of infants less than 6 months of age. However, the economic implications of increasing immunization rates by using the neonatal intensive care unit (NICU) as an arena to capture the parents of these infants has not been fully evaluated. We sought to examine the direct and indirect costs of a program to administer the influenza vaccine to parents in the NICUs of a cohort of tertiary‐care units primarily serving a low socioeconomic population.METHODSThe probabilities of infants being hospitalized because of infection from contact and of the efficacy of prophylaxis used in the present study were based on published results where possible, with an estimated 10% reduction in hospitalization of patients whose parents had received the vaccine. Variables in the 3‐ and 4‐tiered analyses included chronic lung disease status, estimation if patients had siblings, vaccination status of siblings, seroconversion rate of vaccine, and parental vaccination status. Two thousand six hundred and thirty‐two patients were analyzed using 2003 admission data from the New York City Regional Perinatal Center, which encompasses 11 level III NICUs. Hospitalization costs, indirect costs, and outpatient costs were assessed using previously published standard calculations.RESULTSOn the basis of this computer model, costs were $188 per patient per influenza season, including $6.80 per patient in outpatient costs. Administration of an NICU‐based influenza vaccine increased costs to $200 per patient per influenza season, but decreased outpatient costs to $1.40 per patient. For cost savings to equal costs of vaccine administration, there must be either a 20% reduction in influenza hospitalizations of NICU patients or an increase in the sample size per influenza season to 4000 patients.CONCLUSIONSThe cost of administration of the influenza vaccine to parents of NICU patients is higher than the financial burden of influenza in this population as long as the sibling immunization rate remains low. Cost savings do not occur until the treated cohort increases to 4000 patients or the incidence of lung disease in this population increases. Further studies are needed to validate the cost savings of this mode and more accurately assess the financial savings. Journal of Hospital Medicine 2007;2:158–164. © 2007 Society of Hospital Medicine.
Synthesis of deuterium‐labelled standards of (±)‐DOM and (±)‐MMDA
Authors: Shaikh Ajam C. , Wang Yu‐Yun , Chen Chinpiao 
Published: June 2007

AbstractThis study describes the synthesis of deuterium‐labelled (±)‐4‐methyl‐2,5‐dimethoxyamphetamine (DOM) and (±)‐1‐(7‐methoxy‐1,3‐benzodioxol‐5‐yl)propan‐2‐amine (MMDA). The isotopically labelled compounds are potentially used as internal standards in gas chromatography–mass spectrometry (GC–MS) assays. Copyright © 2007 John Wiley & Sons, Ltd.
Progesterone increases brain‐derived neuroptrophic factor expression and protects against glutamate toxicity in a mitogen‐activated protein kinase‐ and phosphoinositide‐3 kinase‐dependent manner in cerebral cortical explants
Authors: Kaur Paramjit , Jodhka Parmeet K. , Underwood Wendy A. , Bowles Courtney A. , de Fiebre NancyEllen C. , de Fiebre Christopher M. , Singh Meharvan 
Published: June 2007

AbstractThe higher prevalence and risk for Alzheimer's disease in women relative to men has been partially attributed to the precipitous decline in gonadal hormone levels that occurs in women following the menopause. Although considerable attention has been focused on the consequence of estrogen loss, and thus estrogen's neuroprotective potential, it is important to recognize that the menopause results in a precipitous decline in progesterone levels as well. In fact, progesterone is neuroprotective, although the precise mechanisms involved remain unclear. Based on our previous observation that progesterone elicits the phosphorylation of ERK and Akt, key effectors of the neuroprotective mitogen‐activated protein kinase (MAPK) and phosphoinositide‐3 kinase (PI3‐K) pathways, respectively, we determined whether activation of either of these pathways was necessary for progesterone‐induced protection. With organotypic explants (slice culture) of the cerebral cortex, we found that progesterone protected against glutamate‐induced toxicity. Furthermore, these protective effects were inhibited by either the MEK1/2 inhibitor UO126 or the PI3‐K inhibitor LY294002, supporting the requirement for both the MAPK and PI3‐K pathways in progesterone‐induced protection. In addition, at a concentration and duration of treatment consistent with our neuroprotection data, progesterone also increased the expression of brain‐derived neurotrophic factor (BDNF), at the level of both protein and mRNA. This induction of BDNF may be relevant to the protective effects of progesterone, in that inhibition of Trk signaling, with K252a, inhibited the protective effects of progesterone. Collectively, these data suggest that progesterone is protective via multiple and potentially related mechanisms. © 2007 Wiley‐Liss, Inc.
Hepatocyte growth factor promotes endogenous repair and functional recovery after spinal cord injury
Authors: Kitamura Kazuya , Iwanami Akio , Nakamura Masaya , Yamane Junichi , Watanabe Kota , Suzuki Yoshinori , Miyazawa Daisuke , Shibata Shinsuke , Funakoshi Hiroshi , Miyatake Shinichi , Coffin Robert S. , Nakamura Toshikazu , Toyama Yoshiaki , Okano Hideyuki 
Published: June 2007

AbstractMany therapeutic interventions using neurotrophic factors or pharmacological agents have focused on secondary degeneration after spinal cord injury (SCI) to reduce damaged areas and promote axonal regeneration and functional recovery. Hepatocyte growth factor (HGF), which was identified as a potent mitogen for mature hepatocytes and a mediator of inflammatory responses to tissue injury, has recently been highlighted as a potent neurotrophic and angiogenic factor in the central nervous system (CNS). In the present study, we revealed that the extent of endogenous HGF up‐regulation was less than that of c‐Met, an HGF receptor, during the acute phase of SCI and administered exogenous HGF into injured spinal cord using a replication‐incompetent herpes simplex virous‐1 (HSV‐1) vector to determine whether HGF exerts beneficial effects and promotes functional recovery after SCI. This treatment resulted in the significant promotion of neuron and oligodendrocyte survival, angiogenesis, axonal regrowth, and functional recovery after SCI. These results suggest that HGF gene delivery to the injured spinal cord exerts multiple beneficial effects and enhances endogenous repair after SCI. This is the first study to demonstrate the efficacy of HGF for SCI. © 2007 Wiley‐Liss, Inc.
Myotonic dystrophy 1 in the nervous system: From the clinic to molecular mechanisms
Authors: de León Mario Bermúdez , Cisneros Bulmaro 
Published: June 2007

AbstractMyotonic dystrophy type 1 (DM1) is a dominant neuromuscular disorder caused by the expansion of trinucleotide CTG repeats in the 3′‐untranslated region (3′‐UTR) of the DMPK gene. Prominent features of classical DM1 are muscle wasting and myotonia, whereas mental retardation is distinctive for congenital DM1. The main nervous system symptoms of DM1 are cognitive impairment, neuroendocrine dysfunction, and personality and behavior abnormalities. It is thought that expansion of CTG repeats causes DM1 pathology through different molecular mechanisms; however, a growing body of evidence indicates that an RNA gain‐of‐function mechanism plays a major role in the disease development. At the skeletal muscle level, three main molecular events can be distinguished in this model: 1) formation of nuclear foci that are composed at least of mutant DMPK mRNA and recruited RNA‐binding proteins, such as splicing regulators and transcription factors; 2) disturbance of alternative splicing of specific genes; and 3) impairment of cell differentiation. Contrasting with the substantial advances in understanding DM1 muscle pathology, the molecular basis of DM1 in the nervous system has just started to be revealed. This review focuses in the DM1 nervous system pathology and provides an overview of the genetic and molecular studies analyzing the effects of the DMPK gene CUG expanded repeats on cell function in neuronal systems. A comparison between the molecular mechanisms of DM1 in the skeletal muscle and those identified in DM1 nervous system models is provided. Finally, future directions in the study of DM1 in the nervous system are discussed. © 2007 Wiley‐Liss, Inc.
Increased cerebral oxygen consumption in Eker rats and effects of N‐methyl‐D‐aspartate blockade: Implications for autism
Authors: Weiss Harvey R. , Liu Xia , Zhang Qihang , Chi Oak Z. 
Published: June 2007

AbstractBecause there is a strong correlation between tuberous sclerosis and autism, we used a tuberous sclerosis model (Eker rat) to test the hypothesis that these animals would have an altered regional cerebral O2 consumption that might be associated with autism. We also examined whether the altered cerebral O2 consumption was related to changes in the importance of N‐methyl‐D‐aspartate (NMDA) receptors. Young (4 weeks) male control Long Evans (N = 14) and Eker (N = 14) rats (70–100 g) were divided into control and CGS‐19755 (10 mg/kg, competitive NMDA antagonist)‐treated animals. Cerebral regional blood flow (14C‐iodoantipyrine) and O2 consumption (cryomicrospectrophotometry) were determined in isoflurane‐anesthetized rats. NMDA receptor protein levels were determined by Western immunoblotting. We found significantly increased basal O2 consumption in the cortex (6.2 ± 0.6 ml O2/min/100 g Eker vs. 4.7 ± 0.4 Long Evans), hippocampus, cerebellum, and pons. Regional cerebral blood flow was also elevated in Eker rats at baseline, but cerebral O2 extraction was similar. CGS‐19755 significantly lowered O2 consumption in the cortex (2.8 ± 0.3), hippocampus, and pons of the Long Evans rats but had no effect on cortex (5.8 ± 0.8) or other regions of the Eker rats. Cerebral blood flow followed a similar pattern. NMDA receptor protein levels (NR1 subunit) were similar between groups. In conclusion, Eker rats had significantly elevated cerebral O2 consumption and blood flow, but this was not related to NMDA receptor activation. In fact, the importance of NMDA receptors in the control of basal cerebral O2 consumption was reduced. This might have important implications in the treatment of autism. © 2007 Wiley‐Liss, Inc.
Spinal AMPA receptor inhibition attenuates mechanical allodynia and neuronal hyperexcitability following spinal cord injury in rats
Authors: Gwak Young Seob , Kang Jonghoon , Leem Joong Woo , Hulsebosch Claire E. 
Published: June 2007

AbstractIn this study, we examined whether a competitive AMPA receptor antagonist, NBQX, attenuates mechanical allodynia and hyperexcitability of spinal neurons in remote, caudal regions in persistent central neuropathic pain following spinal cord injury in rats. Spinal cord injury was produced by unilateral T13 transverse spinal hemisection, from dorsal to ventral, in male Sprague Dawley rats (200–250 g). Mechanical thresholds were measured behaviorally, and the excitability of wide‐dynamic‐range (WDR) dorsal horn neurons in the lumbar cord (L4–L5) was measured to assess central neuropathicpain. On postoperation day (POD) 28 after spinalhemisection, mechanical thresholds were significantly decreased in both injured (ipsilateral) and noninjured (contralateral) hindpaws compared with preinjury and sham control, respectively (P< 0.05). Intrathecal administration of NBQX (0.25, 0.5, 1 mM) significantly reversed the decreased mechanical thresholds in both hindpaws, dose dependently (P< 0.05). The excitability of WDR neurons was significantly enhanced on both sides of the lumbar dorsal horn 28 days following spinal hemisection (P< 0.05). The hyperexcitability of WDR neurons was attenuated by topical administration of NBQX (0.125, 0.25, 0.5, 1 mM), dose dependently (P< 0.05). Regression analysis indicated that at least three molecules of NBQX bond per receptor complex, and are needed to achieve inhibition of WDR hyperexcitability. In conclusion, our study demonstrates that the AMPA receptor plays an important role in behaviors related to the maintenance of central neuropathic pain below the level of spinal cord injury. © 2007 Wiley‐Liss, Inc.
Torsional strength estimates of femoral diaphyses with endosteal lytic lesions: Dual‐energy x‐ray absorptiometry study
Authors: Robertson Douglas D. , Beck Thomas J. , Chan Brandon W. , Scott William W. , Sharma Gulshan B. , Maloney William J. 
Published: June 2007

AbstractPathologic fracture is a significant problem for individuals with metastatic bone disease. Current guidelines for prophylactic internal fixation are neither reliable nor easily applied. The purpose of this study was to validate dual‐energy X‐ray absorptiometry (DXA) as an accurate method for estimating torsional bone strength of diaphyseal bone with endosteal lytic lesions. Endosteal lesions of varying sizes were simulated in the diaphyses of 12 adult cadaveric femurs. Unaltered contralateral femurs served as matched controls. Machined lesions ranged from 3 to 6.5 cm in length, 1 to 3 cm in width, 15 to 48 cm2 in elliptical area, with 10% to 100% removal of the cortical thickness. Morphology and density data obtained from DXA images were used to estimate torsional strength. All femora were mechanically tested to failure in torsion. Physically measured torsional strength was not significantly correlated to lesion elliptical area (r = 0.542, p > 0.05) or percentage cortical thickness removed (r = 0.257, p > 0.05). Measured torsional strength was significantly correlated to DXA‐based torsional strength estimates (r = 0.855, p < 0.01). Lesion size alone did not correlate with the strength of bones with simulated endosteal lytic lesions. In contrast, calculations based on DXA (morphology, density) did correlate with torsional strength. This is the first step in the development of a DXA‐based tool for objectively estimating bone strength in the presence of endosteal lytic lesions. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1343–1350, 2007
Trauma and anxiety: The cognitive approach
Authors: Kreitler Shulamith , Kreitler Hans 
Published: June 2007

AbstractThe purpose was to show how anxiety, the perception of the input and predisposing personality factors are interrelated in the generation of the posttraumatic stress disorder (PTSD). After a review of the role of each of these elements in regard to the PTSD, a new conception of anxiety, the core element of trauma, is introduced, grounded in an innovative system of meaning assessment. Two experiments are summarized demonstrating that anxiety is a pattern of meaning assignment tendencies of the individual and that changing these tendencies brings about the expected changes in the level of anxiety and of cognitive performance. The findings are applied to the treatment and prevention of the PTSD by showing how changing the meaning of specific inputs and of the relevant meaning assignment tendencies of individuals suffering from PTSD or at risk may help to reduce anxiety and increase coping abilities.
Traumatic stress as an area for research
Authors: Hartsough Don M. 
Published: June 2007

AbstractTraumatic stress as a research area draws attention from several disciplines, each contributing its own unique tradition to the field. Three research backgrounds are described, including strengths and weaknesses. Research issues currently focus on the psychophysiological basis for stress reactions, the role of personality in stress response patterns, and the trauma stimulus as an independent variable. An overview of this issue's contributions is provided.
Proving cause and effect in traumatic stress: The draft lottery as a natural experiment
Authors: Hearst Norman , Newman Thomas B. 
Published: June 2007

AbstractA dozen years after the end of U.S. involvement in the Vietnam war, considerable evidence suggests that some Vietnam veterans have suffered longterm mental health problems as a result of their experiences while in the military. Published reports began with the first descriptions of post‐traumatic stress disorder, which is now a recognized psychiatric diagnosis. Recently, we have added to this literature by using a new technique based on the military draft lottery of 1970–1972. This article discusses the rationale behind the approach that we used, summarizes our results, which have been published in detail elsewhere, discusses how our results complement those of previous studies, and suggests ways in which similar techniques might be used to further investigate delayed effects of the Vietnam‐era military draft.
Post‐traumatic stress disorder in victims of rape
Authors: Burge Sandra K. 
Published: June 2007

AbstractRape is a stressor that legitimately can be included in experiences that cause post‐traumatic stress. A review of the professional literature on rape shows evidence for each of the criteria for PTSD. A sample of convenience of 29 rape victims showed a range of PTSD patterns, but 25 (86%) were either moderately or severely stressed. Victims consistently scored higher on standard stress measures than normal or out‐patient samples. Implications of the study are discussed in terms of reframing the rape victim's experience as a response to traumatic stress.
The trauma spectrum: The interaction of biological and social events in the genesis of the trauma response
Authors: van der Kolk Bessel A. 
Published: June 2007

AbstractWhen Kardiner first described the full syndrome of what is now called PTSD in 1941, he called the trauma response a “physioneurosis,” that is, a mental disorder which affects both the soma and the psyche. Now, more than 40 years later much knowledge has been gained about the biological effects of traumatization. Based on the studies of disruptions of attachment bonds in non‐human primates, the animal model of inescapable shock, and numerous studies of traumatized children and adults, we are beginning to understand the nature of the biological changes which underlie the psychological response to trauma. This paper will explore (1) the nature of the biological alterations in response to traumatization, (2) how these biological shifts depend on the maturation of the central nervous system (CNS), cognitive processes, and the social matrix in which they occur, (3) and how these alterations can influence psychopathological and interpersonal processes.
A critical survey of hypotheses regarding post‐traumatic stress disorders in light of recent research findings
Authors: Kolb Lawrence C. 
Published: June 2007

AbstractThis paper reviews briefly recent findings from psychobiological research upon Post‐traumatic Stress Disorders. A critical assay is provided of the various hypotheses advanced as the result of this research data. The author suggests neuropsychological theory provides the best explanation for understanding and classifying both the clinical phenomenology and the biological abnormalities discovered in the chronic forms of PTSD.
Psychosocial aspects of parental response patterns to the death of a child by Homicide
Authors: Rinear Eileen E. 
Published: June 2007

AbstractHomicide is a major cause of mortality in contemporary American society, affecting all age groups, but showing a special predilection for members of the adolescent and young adult populations. Surviving parents of murder victims face a complex bereavement which derives not only from the sudden and traumatic nature of their child's death but also from the shattering of their own previously held personal assumptions about themselves and the world. In an effort to understand better the unique stresses and psychological processes which accompany the death of a child by homicide, a survey of more than 200 parents of murdered children was conducted, which forms the central framework upon which the ideas set forth in this paper are based. Emphasis is placed primarily upon the legitimization of such bereft individuals as covictims of these homicide crimes; the occurrence of symptoms of Posttraumatic Stress Disorder (APA, 1980) with sufficient frequency and duration to warrant its chronic subtype diagnosis, the presence of disordered variants of mourning deriving from the coexistence of such traumatic stress symptomatology, and the impact that the destruction of previously held personal beliefs about oneself and the world has upon postmurder reactions and subsequent adjustment.
Long‐term coping with combat stress
Authors: Green Bonnie L. , Lindy Jacob D. , Grace Mary C. 
Published: June 2007

AbstractThe present report examined ongoing patterns of coping in Vietnam combat veterans from community, outreach, and treatment samples. After reviewing various schemas for conceptualizing coping which exist in the literature, seven coping strategies empirically derived from the Horowitz Coping Inventory were described. Results indicated that the modes of coping most associated with combat intensity were the same as those associated with more symptomatology and a clinical diagnosis of PTSD in the present: event processing, time out for reflection, religion, and denial. Veterans who improved in short‐term therapy for PTSD, on the other hand, used emotional expression and sublimation strategies. The findings were discussed in terms of the disorder of PTSD, the recovery process, and conceptual models of adapation to stress.
Post‐traumatic symptoms in abused children
Authors: Goodwin Jean 
Published: June 2007

AbstractA variety of symptoms have been described as sequelae of physical and sexual abuse in childhood. This review suggests that some of these symptoms can be understood as developmentally mediated manifestations of posttraumatic disorders. Like traumatized combat or concentration camp survivors, severely abused children develop anxiety, compulsive repetitions, sleep disturbances and depression, ego constriction, and disturbed expressions of anger. The example of incest trauma illustrates how developmental transformations of childhood post‐traumatic symptoms can produce the varying patterns of presenting psychopathology seen in adult survivors.
Therapeutic approaches to traumatized Cambodian refugees
Authors: David Kinzie J. 
Published: June 2007

AbstractThe treatment of severely traumatized Cambodian refugees is a difficult task. Through an understanding of the patient's culture and the posttraumatic stress disorder, the author recommends several treatment approaches. These include: supportive long‐term therapy, case management, reinforcing traditional values, socialization group therapy, and specific medication. Through a sensitive, flexible approach, the Western practitioner can greatly reduce the suffering of these patients.