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Background Serotonin 1A receptors (5-HT 1A ) are implicated in major depressive disorder (MDD). We previously reported higher 5-HT 1A binding potential (BP F ) in antidepressant naive MDD subjects compared with control subjects, while other studies report lower BP ND . Discrepancies can be related to differences in study population or methodology. We sought to replicate our findings in a novel cohort and determine whether choice of reference region and outcome measure could explain discrepancies. Methods Nine new control subjects and 22 new not recently medicated (NRM) MDD subjects underwent positron emission tomography. BP F and BP ND were determined using a metabolite and free fraction corrected arterial input function. BP ND was also determined using cerebellar gray matter (CGM) and cerebellar white matter (CWM) reference regions as input functions. Results BP F was higher in the new NRM cohort ( p = .037) compared with new control subjects, comparable to the previous cohort ( p = .04). Cohorts were combined to examine the reference region and outcome measure. BP F was higher in the NRM compared with control subjects ( p = .0001). Neither BP ND using CWM ( p = .86) nor volume of distribution (V T ) ( p = .374) differed between groups. When CGM was used, the NRM group had lower 5-HT 1A BP ND compared with control subjects ( p = .03); CGM V T was higher in NRM compared with control subjects ( p = .007). Conclusions Choice of reference region and outcome measure can produce different 5-HT 1A findings. Higher 5-HT 1A BP F in MDD was found with the method with fewest assumptions about nonspecific binding and a reference region without receptors.

Posttraumatic stress disorder (PTSD) is a common psychiatric disorder in populations exposed to trauma, and it is among the most functionally-impairing, similar in scope to that observed in mood disorders. Recent years have seen many treatment studies assessing efficacy of diverse pharmacotherapies for PTSD. This article reviews the established, evidence-based pharmacotherapeutic treatments for PTSD and highlights current recommendations and controversial areas. The article primarily focuses on published randomized clinical trials that tested overall symptom reduction in PTSD compared to placebo. We also briefly review efforts to target particular symptoms commonly associated with PTSD (eg, sleep disturbance; psychotic symptoms) and at preventing PTSD among populations recently exposed to trauma. Where appropriate, recommendations are made for use of particular agents as first-line pharmacotherapies. To date, there are no validated sensitive and specific biomarkers of PTSD that can aid in diagnosis, treatment selection, or monitoring of clinical progress. Notable biological findings in PTSD1 include derangements in the two main branches of the stress response system, the noradrenergic/sympathetic brain systems and the hypothalamic-pituitary-adrenal (HPA) axis;2 increased cerebrospinal fluid concentrations of corticotropin-releasing factor (CRF);3,4 reduced volume of the hippocampus;5–7 functional differences in responding of fear system brain regions, such as hyperactivation of the amygdala and hypoactivation of the prefrontal cortex;8–10 sleep disturbances;11 measures of hyperarousal in response to stimuli and of delayed habituation to loud noises;12 and evidence for impaired conditioned fear extinction recall.13,14 Such findings have firmly grounded the psychopathology of PTSD in neurobiological dysfunctions, thereby suggesting routes of pharmacotherapeutic interventions.15 Agents that enhance serotonergic neurotransmission, such as serotonin selective reuptake inhibitors (SSRIs), appear to attenuate several of the prominent symptoms of the PTSD. However, randomized clinical trials (RCTs) published to date have, at best, demonstrated limited efficacy for the constellation of symptoms that make up PTSD.16,17 In fact, effect sizes (Cohen’s d statistic) from the best pharmacotherapy RCTs have been relatively small, prompting the United Kingdom’s National Institute for Clinical Excellence to recommend that medication treatments not be used as routine first-line treatments in preference to a trial of a trauma-focused psychological therapy.18 Yet the overall conclusion of a recent meta-analysis of existing RCTs in PTSD conducted by the Cochrane Collaboration was that medication treatments were superior to placebo in reducing the severity of PTSD symptom clusters as well as comorbid depression and disability.19 Therefore, both combination psychotherapy and pharmacotherapy and psychotherapy alone should be considered as first line approaches to PTSD while pharmacotherapy alone is generally not recommended, except in the circumstance when proven efficacious psychotherapies are not available.

OBJECTIVE: Only a few studies have examined whether a family history of suicide influences the severity of suicidal acts and the results have been inconsistent. The current study aimed to examine whether a family history of suicidal acts predicts severity of suicide attempts. METHOD: 190 suicide attempters aged 18-75 years with a lifetime history of major depression were assessed for first-degree family history of suicidality and severity of suicide attempts (number and lethality of prior suicide attempts and age at first attempt). RESULTS: Regression analyses indicate that a positive family history of suicidal behaviors predicts a greater number of suicide attempts. Reasons for living predict number and lethality of prior attempts. CONCLUSION: It is critical to assess for family history of suicidal behavior when treating depressed suicide attempters as it may serve as an indicator of the risk of repeat suicide attempt and as a guide for treatment. Language: en

This review discusses evidence-based pharmacotherapies for post-traumatic stress disorder (PTSD). The epidemiology of PTSD and its phenomenological characteristics are summarized. Focus is placed on the major classes of drugs for which at least a minimum of evidence-based outcome data are available from randomized controlled trials (RCTs). Drugs for the total symptom constellation of the disorder; specific PTSD symptoms, such as nightmares, and prevention of PTSD development post-trauma, are discussed. Where appropriate, RCT methodological problems that limit the conclusions drawn are discussed. In addition, recommendations for research to fill critical gaps in the knowledge of PTSD treatment are offered.

Ozman-Sullivan, Sebahat/0000-0001-5240-8110 WOS: 000261403300018 PubMed: 18483790 This study investigated Pseudomonas putida biotype B as a potential biological control agent of Tetranychus urticae. The bacteria were isolated from greenhouse soil from Carsamba, Turkey. The experiment was carried out in a completely randomized plot design under laboratory conditions. For this purpose, spraying and dipping applications of a suspension of P. putida biotype B (10(8)-10(9) colony forming units/ml) were applied to newly emerged, copulated females. Dead mite and egg counts were started on the 3rd day after treatments, and observations were continued daily until all the mites had died and egg hatching had finished. Both types of bacterial application significantly reduced total egg numbers and egg hatching, compared to their respective controls. Bacterial spraying was significantly more effective than dipping-the spray application demonstrated 100% efficacy and resulted in the fewest viable eggs. The results of this study indicated that P. putida biotype B has a strong efficacy in causing mortality in T. urticae.

This report, sponsored the Army's Energy Engineering Analysis Program, provides the Operations and Maintenance (O&M) Energy manager and practitioner with useful information about the top O&M opportunities consistently found across the DoD/Army sector. The target is to help the DoD/Army sector develop a well-structured and organized O&M program.

This updated market assessment for capturing water conservation opportunities in the Federal sector is based on a new analytical approach that utilizes newly available data and technologies. The new approach fine-tunes the original assessment by using actual Federal water use, which is now tracked by DOE (as compared to using estimated water use). Federal building inventory data is also used to disseminate water use by end-use technology in the Federal sector. In addition, this analysis also examines the current issues and obstacles that face performance contracting of water efficiency projects at Federal sites.

Measurements of ignition characteristics and emissions were made in a shock tube facility operating at engine-relevant conditions. Methane and methane/ethane fuels were injected down the centerline of the shock tube using an electronically controlled prototype gaseous fuel injector developed by Westport Innovations. Air was preheated and compressed using a reflected shock technique that produced run times of 4-5 ms. Particulate matter (PM) emissions were found to be highly intermittent. In only 6 out of 97 experiments was PM detected above background levels. In all of these 6 sooting experiments ignition kernels were located relatively close to the injector tip and ignition occurred prior to the end of fuel injection. Using the large orifice injector tip with pure methane fuel, PM was detected in 4 out of 28 experiments; using the small orifice with pure methane fuel, no PM was detected in any of 50 experiments. When 10% ethane was added to the fuel, PM was detected in 2 out of 20 experiments. Orifice size was found to significantly influence emissions of nitrogen oxides (NO x ). Emissions were reduced by over an order of magnitude when the orifice size was reduced by a factor of 4. Run-to-run variability in NO x emissions was relatively high at nominally constant operating conditions. NO x variability was associated with variability in ignition timing. At fixed operating conditions, NO x emissions were found to increase significantly with advancing ignition timing. Over the range of conditions studied, NO x emissions were found to be relatively insensitive to injection pressure ratio and injection duration.

Serotonin 1A receptors have been implicated in a variety of conditions including depression, suicidal behavior, and aggression. Dose estimates for current human studies are based on data from rat dosimetry studies. We report the biodistribution and dosimetry of the PET serotonin 1A antagonist 11C-WAY100,635 in humans.PET studies of 6 healthy human volunteers (3 male, 3 female) were acquired after a bolus injection of 11C-WAY100,635. Transmission scans of 3.5 min were obtained at each bed position before injection, and emission scans then were collected in 2-dimensional mode over 8 bed positions. Regions of interest were drawn around the brain, left and right lungs, heart, liver, stomach wall, gallbladder, left and right kidneys, spleen, and urinary bladder. Because no fluid was removed from the subjects, whole-body radioactivity was calculated using the injected dose and a calibration factor determined from a cylinder phantom. The area under the curve for each region of interest was determined by trapezoidal integration of the first 3 points, with subsequent points fit by a decreasing monoexponential. The area under the curve was then divided by counts in the whole body, and the resulting residence times were entered into the MIRDOSE3 program.Primary elimination was via kidneys to the urinary bladder. There were no sex differences in organ residence times. The urinary bladder wall was the organ with the highest estimated radiation dose (1.94 x 10(-1) +/- 3.57 x 10(-2) mGy/MBq). Except for the kidney and bladder wall, correlation was good between human dosimetry estimates and estimates reported previously from rats. The human dosimetry was 6.6 and 60.6 times higher in the kidneys and urinary bladder wall, respectively, than estimates from rats.The urinary bladder wall is the critical organ for 11C-WAY100,635 in humans. In the United States, according to Radioactive Drug Research Committee guidelines a single dose cannot exceed 300 MBq in a man and 227 MBq in a woman, with up to 3 such injections permitted per annum.

Major depression comorbid with panic disorder has a more severe clinical picture and adverse course than either disorder alone, and both conditions are associated with abnormalities in the serotonin system. Therefore, we hypothesized that central serotonergic function in the patients with comorbid panic disorder would be more disturbed than in major depression alone. Concentrations of cerebrospinal fluid (CSF) monoamine metabolites of serotonin, norepinephrine, and dopamine were assayed by high-pressure liquid chromatography, and compared in female subjects with DSM-IV-diagnosed major depressive disorder and a lifetime diagnosis of panic disorder (MDD+PD, n=13), major depressive disorder and no lifetime panic disorder (MDD-, n=35), and a healthy volunteer (HV, n=15) group. All subjects were free of antidepressant medication for at least 14 d prior to the lumbar puncture procedure. CSF 5-hydroxylindoleacetic acid (5-HIAA) was higher in the MDD+PD group (124.0+/-43.0 nmol/l) compared with the MDD- group (100.1+/-28.8 nmol/l, p=0.03) and the HV group (93.3+/-33.6 nmol/l, p=0.02). The MDD- group and HV group did not differ in CSF 5-HIAA. There were no group differences in the CSF metabolites of norepinephrine and dopamine, 3-methoxy-4-hydroxyphenylglycol and homovanillic acid respectively. Higher CSF 5-HIAA in women with comorbid major depressive disorder and lifetime panic disorder is indicative of greater serotonin release, increased serotonin metabolism, and/or decreased 5-HIAA clearance in this group. This difference in pathophysiology is potentially related to the greater morbidity and poorer treatment response of this group.

This guide, sponsored by DOE's Federal Energy Management Program, highlights operations and maintenance (O&M) programs targeting energy efficiency that are estimated to save 5% to 20% on energy bills without a significant capital investment. The purpose of this guide is to provide the federal O&M energy manager and practitioner with useful information about O&M management, technologies, energy efficiency and cost-reduction approaches.

This document reports findings and recommendations as a result of a design assistance project with Fort Buchanan with the goals of developing a Water Management Plan (WMP). The WRMP developed during this task is an amalgam of the templates and guidelines from the Federal Energy Management Program and Army regulations.

Background Panic attacks, the hallmark of panic disorder, are often characterized by hyperventilation. Existing animal models of anxiety have not addressed the effects of the hyperventilation on anxiety-related behaviors. Doxapram is a respiratory stimulant that reliably evokes panic attacks in patients with panic disorder. We examined doxapram in four rodent models of anxiety and sought to identify brain regions involved in its behavioral effects. Methods The effects of doxapram were determined for cue and contextual fear conditioning, the open field test, and the social interaction test. The effect of doxapram on c-Fos–like immunoreactivity was examined in three brain regions. Results Doxapram at 4 mg/kg increased anxiety-related behaviors in all four anxiety models. An inverted U-shaped dose-response curve was identified for fear conditioning to cue. Doxapram induced c-Fos–like immunoreactivity in the central nucleus of the amygdala but not the lateral nucleus or the nucleus tractus solitarius. Conclusions Doxapram enhanced anxiety-related behaviors in four animal models of anxiety that involve conditioning or spontaneous avoidance. The effect of doxapram may result from activation of neurons in the amygdala. Doxapram, by inducing hyperventilation, may be a useful adjunct to existing animal anxiety models for improving validity for panic anxiety.

Panic disorder is associated with an elevated risk of cardiovascular disease and sudden death. Individuals with panic disorder have been shown to have reduced variability in heart rate and increased variability in the QT interval on electrocardiogram (ECG), patterns predictive of sudden cardiac death in certain forms of cardiomyopathy. Given that panic disorder patients often hyperventilate during a panic attack, we assessed the effects of voluntary hyperventilation on the ECG utilizing linear analyses of heart rate and QT interval variability. Sixteen symptomatic, medication-free patients underwent hyperventilation challenge. A small subgroup of eight subjects underwent re-challenge after treatment. Pre-treatment, hyperventilation resulted in a decrease in a measure of heart rate variability and an increase in the QT variability index (QTVI; QT variance normalized for mean QT, divided by heart rate variance normalized for mean heart rate). In a remitted state, the QTVI was reduced both during rest and during hyperventilation compared with the respective pre-treatment levels. These findings suggest a possible mechanism explaining increased rates of cardiovascular morbidity and mortality in panic disorder. Moreover, the reduction in QTVI observed post-treatment raises the question of whether treatment might have cardioprotective effects, at least in panic disorder patients who have particular types of co-morbid cardiac disease. Yet these results must be interpreted cautiously; they are preliminary, exploratory and observed in a very small sample without a healthy comparison group.

This guide is designed to serve as a source for O&M management and technical staff. It does not try to represent the universe of O&M related material. Rather, it attempts to: (1) provide needed background information on why O&M is important and the potential for savings from good O&M, (2) define the major O&M program types and provide guidance on the structure of a good O&M program, (3) provide information on state-of-the-art maintenance technologies and procedures for key equipment, and (4) identify information sources and contacts to assist you in getting your job done.

This report assesses the potential impact of the U.S. Department of Energy?s (DOE?s) Federal Energy Management Program (FEMP) developing program offerings in support of Federal operations and maintenance activities.

The objective of this study was to develop, monitor, analyze, and report on an integrated resource-conservation program highlighting efficient residential appliances and fixtures. The sites of study were 50 homes in two water-constrained communities located in Oregon. The program was designed to maximize water savings to these communities and to serve as a model for other communities seeking an integrated approach to energy and water resource efficiency. The program included the installation and in-place evaluation of energy- and water-efficient devices including the following: horizontal axis clothes washers (and the matching clothes dryers), resource-efficient dishwashers, an innovative dual flush low-flow toilet, low-flow showerheads, and faucet aerators. The significance of this activity lies in its integrated approach and unique metering evaluation of individual end-use, aggregated residential total use, and system-wide energy and water benefits.

In a 1989 article, the authors provided a hypothesis for the neuroanatomical basis of panic disorder that attempted to explain why both medication and cognitive behavioral psychotherapy are effective treatments. Here they revise that hypothesis to consider developments in the preclinical understanding of the neurobiology of fear and avoidance.The authors review recent literature on the phenomenology, neurobiology, and treatment of panic disorder and impressive developments in documenting the neuroanatomy of conditioned fear in animals.There appears to be a remarkable similarity between the physiological and behavioral consequences of response to a conditioned fear stimulus and a panic attack. In animals, these responses are mediated by a "fear network" in the brain that is centered in the amygdala and involves its interaction with the hippocampus and medial prefrontal cortex. Projections from the amygdala to hypothalamic and brainstem sites explain many of the observed signs of conditioned fear responses. It is speculated that a similar network is involved in panic disorder. A convergence of evidence suggests that both heritable factors and stressful life events, particularly in early childhood, are responsible for the onset of panic disorder.Medications, particularly those that influence the serotonin system, are hypothesized to desensitize the fear network from the level of the amygdala through its projects to the hypothalamus and the brainstem. Effective psychosocial treatments may also reduce contextual fear and cognitive misattributions at the level of the prefrontal cortex and hippocampus. Neuroimaging studies should help clarify whether these hypotheses are correct.

Energy reduction goals for Federal agencies were first established in the National Energy Conservation Policy Act of 1988, and directed 10{percent} reduction in facility energy use based on a 1985 baseline. Since that time, Federal sites have been actively seeking and implementing a wide variety of energy-efficiency measures in facilities across the Federal sector. In the intervening years this energy reduction goal has been progressively increased to 20{percent} through legislation (Public Law 102-486, The Energy Policy Act of 1992) and a number of Executive Orders. Executive Order 13123, Greening the Government Through Efficient Energy management (signed June 3, 1999), further increased the facility energy-efficiency improvement goal from 30{percent} in 2005 to 35{percent} by 2010 relative to the 1985 baseline.

Transthyretin plays an important role in the transport and distribution of thyroid hormone in the central nervous system (CNS). This study replicated and extended to patients with nonrefractory depressive illness a pilot study indicating that patients with refractory major depression have significantly lower levels of CSF transthyretin than do healthy comparison subjects.Lumbar punctures were performed in drug-free subjects with DSM-III-R major depression (N = 18), DSM-III-R bipolar disorder, depressed phase (N = 1), and healthy comparison subjects (N = 24). CSF concentrations of transthyretin, determined by a quantitative dot-immunobinding assay, of the depressed patients and comparison subjects were compared by analysis of covariance (ANCOVA). The relationship between CSF transthyretin levels and Hamilton Depression Rating Scale scores was determined in a subset of the depressed patients.CSF concentrations of transthyretin were significantly lower in the depressed patients than in the comparison subjects by ANCOVA. Within the depressed group there was no significant overall correlation between CSF transthyretin levels and Hamilton depression scale scores, but there was a significant inverse correlation in male depressed patients (N = 8) between CSF transthyretin concentrations and Hamilton depression scores.Lower CSF transthyretin concentrations in depressed patients may reflect either a stable trait in this population or a state change secondary to depression or other factors. Lower CSF transthyretin concentrations may result in altered CNS thyroid hormone homeostasis. Such alteration could account for certain mood and neurovegetative symptoms of depression and might contribute to failure of standard antidepressant treatment.

The current understanding of the neurobiology of anxiety disorders is generally based on symptomatologic data for diagnostic classification, empirically effective psychopharmacologic agents, chemical and naturalistic challenge paradigms, and psychoneuroendocrinologic assessments. The field of anxiety disorder research is at an exciting stage in which these approaches, along with functional and anatomic data from neuroimaging and cognitive neuroscience, are converging toward a unified conceptualization of pathophysiology. This article focuses on neuroendocrine measures in anxiety states and their relationships to neurotransmitter and neuroendocrine function. Further, a hypothetical link to the findings of cognitive neuroscience fear research will be made. Particular emphasis will be placed on panic disorder (PD) because of both the discreet symptomatology engendering ease of experimental design and the large accumulation of data using various pharmacologic probes. It should be noted that some of the challenge paradigms that will be reviewed demonstrate biologic abnormalities that cut across DSM–IV diagnostic categories of mood and anxiety disorders, and will likely point the way to effective treatment in spectrums of conditions. Indeed, clinical overlap among these disorders are increasingly demonstrated to be extensive, 114 and such biologic studies may eventually prove more relevant to the treatment of the individual patient than phenomenologic categorization.

Many multidrug-resistant (MDR) cell lines overexpress the epidermal growth factor receptor (EGFR) as well as P-glycoprotein (P-gp). However, the role of the increased EGFR in P-gp-mediated drug resistance remains unclear. Since recent studies suggest that activation of phospholipase C (PLC) could increase the phosphorylation of P-gp, and activation of the EGFR would also activate PLC, we investigated whether the effect of epidermal growth factor (EGF) on the phosphorylation of P-gp was mediated through PLC. Treatment of the human MDR breast cancer cell line, MCF-7/AdrR, with EGF increased the phosphorylation of P-gp by 20-50%. The increased phosphorylation of P-gp was accompanied by stimulation of PLC activity, as measured by the production of inositol, 1,4,5-trisphosphate and diacylglycerol, products of phosphatidylinositol-4,5-bisphosphate hydrolysis. Treatment of MDR cells with EGF also had detectable effects on P-gp function. For example, following incubation of MCF-7/AdrR cells with ECF, we observed a consistent decrease in total vinblastine (VBL) accumulation. Kinetic analysis revealed this change to be due to an increase in membrane efflux. The latter was measured by the initial uptake velocity, which was inhibited by EGF. VBL uptake measured at 0-320 sec was inhibited by 20-40%, which was associated with a similar increase in VBL efflux. EGF had no effect on drug accumulation, uptake, or efflux in sensitive MCF-7 cells. These data indicate that EGF can modulate the phosphorylation and function of P-gp, and suggest that this effect may be initiated by the activation of PLC.

“T-cell B-cell Activating Molecule” (T-BAM) is an activation-induced surface protein on CD4 + T cells that mediates a contact-dependent signal for B cell differentiation and immunoglobulin (Ig) secretion. The T-BAM protein on a helper clone of Jurkat (D1.1) was affinity purified using the anti-T-BAM mAb, 5c8. The NH 2 -terminal amino acid sequence of purified T-BAM was determined and found to be highly homologous to the predicted NH 2 -terminal sequence of a T cell ligand to the B cell CD40 molecule (CD40-L). From a D1.1 cDNA library, a clone was isolated that encodes CD40-L by sequence and drives expression of T-BAM protein on transfected cells, demonstrating that the T-BAM and CD40-L genes and proteins are identical. Moreover, transfection of T-BAM was shown to confer to non-lymphoid cells, the ability to induce B cells to upregulate the expression of surface CD23 molecules. In previous studies we showed that T-BAM was expressed predominantly on activated CD4 + and on few if any CD8 + cells. Although the current work confirms that T-BAM is largely restricted to activated CD4 + T cells, we now provide definitive evidence that T-BAM can be expressed by a small population of CD8 + T cells after activation. Importantly, a subset of CD8 + T cells do not express T-BAM after activation and this T-BAM − phenotype is maintained on certain CD8 + T cell clones. Taken together, these data unify the biology and structure of T-BAM and CD40-L and this synthesis has implications for understanding the T cell regulation of the humoral immune response.

Exposure to mass trauma is common. In the United States, 15% of women and 19% of men have reported lifetime exposure to natural disasters alone.1 Since the advent of 24-hour television news, exposure to mass violence and natural disasters through the media is even more widespread. Although exposure to trauma has a wide range of psychopathological consequences, posttraumatic stress disorder (PTSD) has been shown to be the most common.2 PTSD is unique among psychiatric disorders because it requires exposure and fearful response to traumatic events as the proximate precipitants of the syndrome. The clinical presentation of PTSD includes a diverse array of distressing and disabling ongoing symptoms in the realms of reexperiencing phenomena (eg, nightmares), hyperarousal (eg, startle response), avoidance of reminders of the exposure, and general affective numbing. Yet community surveys have consistently demonstrated that most adults exhibit resilience following exposure to trauma, even among those who develop symptoms consistent with PTSD in the immediate aftermath, with many recovering over time without clinical intervention. A significant minority, however, will develop PTSD, which is the posttrauma clinical trajectory associated with a considerable health burden, including psychiatric comorbidities, severe psychosocial dysfunction, and increased rates of suicidal behaviors. The neuroscience model of pavlovian fear conditioning and extinction has been proposed to have direct relevance to PTSD pathophysiology. This heuristic model explains how fear learning may be involved in the emergence of PTSD symptoms and how the persistence of symptoms over time potentially involves a failure of basic extinction processes of learned fear memory.3 In a neurobiological study, a fear learning and extinction task with psychophysiological and functional brain imaging assessments revealed significant biological differences between patients exposed to trauma who had developed PTSD and controls exposed to trauma who had not.3 Moreover, increased efforts to develop and test extinction-based psychotherapeutic approaches for treatment of PTSD, such as prolonged exposure (a type of therapy that encourages reexperience of trauma through recalling and reengaging with it), have proven these interventions to be efficacious for many, and these approaches have become first-line interventions for PTSD.4 However, the fear-learning and extinction model has yet to be fully applied for understanding the trajectories of PTSD over time among populations indirectly exposed to mass trauma, disasters, and terrorism. The attacks of September 11, 2001, unprecedented in the United States in their magnitude and aftermath, were followed by a surge of research on their mental health consequences over the last decade. Longitudinal studies suggest that the mental health burden among directly exposed populations, such as evacuees, first responders, and bereaved persons, is substantial and frequently enduring. For example, a 2-wave study among individuals directly exposed to the World Trade Center attacks found prevalence of PTSD symptoms among rescue/recovery workers to increase from 12.1% at 2 to 3 years after the attacks to 19.5% at 5 to 6 years after the attacks.5 In contrast, the burden of PTSD symptoms in the general population, who were for the most part indirectly exposed to the trauma through media, was found to be lower in severity and substantially diminished over time. In New York City, the initial estimates of prevalence of probable PTSD declined from 7.5% at 1 month after the September 11 attacks to 1.7% and 0.6% at 4 and 6 months, respectively, after the attacks.6 Some of the general population studies following September 11 have also examined the association between exposure to the attacks via television and development of PTSD. In a national survey, exposure to televised live broadcasting during the attacks was found to be associated with increased risk for short-term PTSD symptoms 1 to 2 months after the attacks.7 Those findings raised the question of whether indirect exposure in general, and via the media in particular, is indeed traumatic, with effects similar to those of direct exposure, and whether the PTSD symptoms related to indirect exposure persist over a long period. The New York City data regarding persons indirectly exposed to the September 11 attacks are comparable to data from the 2008–2009 military conflict in southern Israel. A 3-wave, longitudinal study of young adults evacuated from the Israel-Gaza border to distant areas with minimal exposure to missile attacks found that probable PTSD symptoms spiked to 20% during the conflict, followed by a rapid and sharp decline to 3.0% and 2.0%, 2 and 4 months, respectively, after the conflict had ceased.8 The findings in these 2 populations, characterized by acute emergence of PTSD-like symptoms that rapidly decline over several months to a lower, more stable rate with ongoing PTSD, raise a number of possible explanations about the effects of indirect exposure to mass violence. For example, the more transient symptoms in the majority of persons with PTSD symptoms who present initially may be due to activation of the fear/stress response system in a setting of actual ongoing threat of war or terrorism; once the immediacy of the actual threat abates, appropriate deactivation occurs, with learned fear responses mostly extinguished when the situation is “safe” and “aversive” events no longer appear imminent. Another possibility is that indirect exposure to mass trauma acts as a low-impact trauma that may result in rapidly resolving symptoms of PTSD in low-vulnerability populations and that only a small portion of individuals exposed—those with preexisting vulnerability mediated through genetic factors, prior exposure to trauma, or preexposure psychiatric history—remain with a clinical diagnosis of PTSD months to years after indirect exposure.9 An analysis of a subset of New York City residents indirectly exposed to trauma during the September 11 attacks (those not in the vicinity of the World Trade Center, experiencing no September 11 loss, or not taking part in recovery and cleaning efforts) from a sample of primary care patients studied after the attacks supports this hypothesis. At 1 year after the attacks, indirect exposure alone was not associated with PTSD among individuals without a history of pre–September 11 trauma, family psychiatric history, or both.10 These findings, if supported by future studies, may suggest that even though exposure severity is similar among persons indirectly exposed to terrorist attacks or disasters (and might be considered a lower-severity exposure despite exposure to graphic images on television, because the danger is not imminent), development of longer-term PTSD to such exposure may have more to do with the preexisting vulnerability than with the indirect exposure severity per se. Thus, such lower-severity exposure may be expected to result in low rates of PTSD over time, such as 1% to 2% after September 11 in New York City6 or 2% to 3% after war in the Israel study.8 Moreover, the initial elevated rates of PTSD symptoms may be an artifact of measurement too soon after the exposures, when extinction mechanisms have not had sufficient time to aid in recovery of the majority of indirectly exposed individuals. Future research evaluating the putative role of fear conditioning in the development of PTSD and fear extinction in recovery processes, whether spontaneous or attributable to treatment, should address these questions and could aid in the triage of individuals exposed to mass trauma to identify those most likely to develop ongoing psychopathology. In sum, evidence from epidemiologic studies indicates initial but not extended increases in rates of PTSD symptoms among individuals indirectly exposed to mass trauma through sources such as mass media. This raises questions about the trajectory of clinical course in these individuals and the possibility of preexisting vulnerability among those with enduring symptoms. Importantly, these questions may be directly addressed by research using fear conditioning and extinction models, ultimately aiding in the identification of high-risk individuals for triage of clinical interventions that prevent development of, or enhance recovery from, PTSD through enhancement of basic extinction processes.

Ozman-Sullivan, Sebahat/0000-0001-5240-8110 WOS: 000281671600005 Overwintering pupae of the phytophagous lepidopteran pest Hyphantria cunea (Drury) (Lepidoptera: Arctiidae) were collected from 38 hazelnut (Corylus avellana L.) plantations in Samsun province, Turkey. Five species of ichneumonids, Virgichneumon dumeticola (Gravenhorst), V. albilineatus (Gravenhorst), Enicospilus ramidulus (L.), Pimpla rufipes(Miller) and one Gelis sp. were reared. Average parasitism was 0.13% and 2.33% for 2008 and 2009, respectively. Highest site parasitism was 14.9% and highest site diversity was 4 species. Virgichneumon dumeticola was the commonest species, with 73% of the total speciments. Virgichneumon albilineatus and E. ramidulus are reported for the first time from H. cunea, and V. albilineatus is also reported for the first time from Turkey. Gelis sp. is reported for the first time as a parasitoid of H. cunea in Turkey. Suleyman Demirel UniversitySuleyman Demirel University The authors are grateful to Suleyman Demirel University for financial support, to hazelnut growers for access to their properties, and to Murat Bostan and Unal Budak for their assistance on field trips.

This paper discusses the key theoretical concepts related to staff development strategies for the experienced adult learner. These concepts would include adult learning and transformative learning theories. The focus of this article is on coaching education, but it should be noted that the key concepts discussed are transferable to any staff development strategy where adult education is needed. Furthermore, specific practical strategies are outlined and discussed for the facilitating and conducting of a workshop for adult learners.

Noradrenergic antidepressants and treatment response Kar1RickeIqM.D.; NicholasDcMsrtiM MoiraRynn,MD. Departmeat of Psj’cbiatty, University of Pennsylvania 3600 Market Street Suite 803 Philadelphia, PA 19104 USA The role that scvcral third generation antidepressants with noradrenergic properties have for the treatment of depression will be reviewed in terms of chnical efticacy and tolerabiJity. Seroronia and neradrtnalia rC-u@C inh%itOsS C.g. VW, selective noradmnn will be reviewed and compared to selective serotenin m-uptake inhibitors aad the older tricychc aatidepressants. Advantages and disadvaatages of these various gmups of antidcprcssaats will bc rcviewcd and su&cstioas wiJJ be tiered as to whether or not differences in terms of efficacy and tolerability exist between noradrencrgic and serotenqic antidepressants, and whether or not data c&t that allow the &i&n to choose one mcdicadon above the other for the treatment of his depressed patients, including scvcrcly depressed and tmaanent resistant patients. Finally, rhe role that these antidePressants, e.g. im&aminc, VW, have for the treatment ef anxiety and particularly GAD wiJI be discussed

(USDA, 1982 and 1985). Farm revenues obtained from sales of the fish to commercial sIncregasing tconcentration in food pro- processing plants have increased steadily since cessing has important economic implications 1976 exceeding $100 million in 1984 for agricultural producers and consumers., i This paper addresses the issue by focusing (USDA, 1985). In early 1985, a national fast This paper addresses the issue by focusing chain contracted with the industry to on a case where pure monopsony conditions food chain contracted with the industry to appear to hold-catfish processing in West purchase 54 million pounds of processed fish appear to hold-catfish processing in West Alabama. Farm-level impacts of the market over a 15-month period (Jensen). Based on power imbalance are described via a six equa- a 1984 industry base of 154 million pounds tion theoretical model. Results show price (USDA, 1985), this action alone represented elasticity of farm supply governing the eco- a-28 percent increase in annual processor nomic incentive to the processor for ex- purchases. ploiting its market power: less (more) elastic A potential problem facing this emerging supply implies greater (lesser) divergence industry is an apparent imbalance of market between competitive and monopsony price. power between catfish producers and the The theoretical model is operationalized us- processing sector. Currently, some 14 coming an indirect procedure recently suggested mercial sized processors service the indusby Houck for estimating farm level supply try's 1,000 producers (USDA, 1982 and elasticities. Based on these supply elasticities 1985). A 1981 study of catfish processors and historical prices, the model predicts a concluded that the industry "is characterized 12-35 percent potential reduction in prices structurally by a high degree of market conreceived by West Alabama producers as a centration" (p. v) with five of the nine reresult of market power imbalance. porting firms handling 98 percent of the total pounds processed (Miller et al.). Further evi

Soluble fragments of elastin are frequently present in biological tissue in small amounts. Because of their hydrophobic character, these peptides are not well resolved by a number of conventional techniques. However, their separation should be possible by reversed-phase chromatography. A wide range of columns, gradients and solvents were evaluated. Two systems are described. One was a C18 liganded silica column eluted isocratically by gravity flow. Some degree of size fractionation was achieved with larger peptides being eluted with methanol and smaller ones with isopropanol. The second system uses a pressurized elution from another C18 ligand column. A concave gradient of trifluoroacetic acid-acetonitrile with a decreasing acetonitrile concentration was optimal. Similar resolution of peptides produced by a variety of digestion methods was obtained with the lower-molecular-mass peptides eluting in the middle of the gradient.

The marketing system for cattle in the United States has evolved with shifts from delivery to large terminal centers, to more decentralized markets. Because of innovations in transportation and processing technology, these structural changes have created a need for greater vertical coordination between different stages in the cattle marketing channels (Rhodes, p. 174; Sporleder, p. 101). Improved coordination requires appropriate market information about product supplies and the form of cattle preferred by buyers (Purcell, 1973, 1980).

Attempts to increase food productivity, make the agricultural sector more cost efficient, improve diets of lower income people, and increase net incomes of farmers and livestock owners are receiving considerable interest on a worldwide basis. In many areas, however, these goals are not being met. In particular, livestock development programs in arid and semi-arid pastoral and sedentary regions in Africa have been especially discouraging. The general problem confronted in this article is to determine why the livestock industry is not developing, and to analyze alternatives related to one major source of concern: communally grazed areas. Africa warrants a special place in development planning due to a multitude of non-economic factors. Political instability, language differences, and tribal and racial tensions have often tended to overshadow economic considerations (Bates, 1981). Perhaps most striking has been the heavy emphasis on equity considerations, possibly because many nations have recently emerged from colonial rule. The relatively short post emergence period (two to three decades in most cases) combined with the continent's economic and natural resource diversity, and a host of other factors such as trade policies, make analysis of economic development potential very difficult (World Bank, 1981). It is evident that there is no one problem and no unique solution in defining policies related to Sub-Saharan Africa's livestock sector.' Perhaps most important is to recognize that the various kinds of livestock systems themselves, as well as associated social institutions, are dynamic forces. Furthermore, it is crucial that the industry and associated problems be understood in the context of human population growth and pressure which has only recently emerged as a source of concern (Development Forum, 1984). In fact, it is population growth which is bringing about a shift in emphasis from livestock production as a primarily ethical or sociological problem to one of determining the role which livestock can play in meeting basic food needs. In this article, a perspective of Sub-Saharan Africa's livestock industry is developed by explaining the dynamic setting in which it is now found. Discussion then turns to communal grazing, a topic we feel has not been properly