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The aim of the present study was to examine the effects of academic examination stress on leukocyte subset distribution in university students. Thirty-eight university students had repeated blood collections for white blood cell differentiation and flow cytometric assay of lymphocytic subsets a few weeks before and after (i.e. two baseline conditions) as well as the day before a difficult academic examination (i.e. stress condition). Flow cytometry was used to determine the number of peripheral blood mononuclear cells (PBMC). In students, who were reactors to psychological stress (criterion based on changes in the Perceived Stress Scale, PSS), but not in stress non-reactors, a significant increase in the number of neutrophils, monocytes, CD8⁺, CD2⁺CD26⁺, and CD2⁺HLA-DR⁺ T cells and CD19⁺ B cells, and significant reductions in the CD4⁺/CD8⁺ T cell ratio were observed in the stress condition. There were significant and positive relationships between the stress-induced changes in perceived stress (PSS scale) and number of leukocytes, neutrophils, CD2⁺, CD2⁺CD26⁺ and CD2⁺HLADR⁺ T cells, and CD19⁺ B cells. There were significant and negative relationships between the stress-induced changes in the CD4⁺/CD8⁺ ratio and the stress-induced changes in the PSS scale. Female students taking oral contraceptives showed significantly higher stress-induced responses in number of leukocytes, neutrophils and CD19⁺ B cells than male and female students without use of oral contraceptives. The results suggest that academic examination stress induces changes in the distribution of PBMC, which indicate immune activation and which are probably orchestrated by a stress-induced production of cytokines.

Effective treatment of severe or chronic unipolar depression requires the combination of pharmacological and psychotherapeutic interventions, and demands a theoretical paradigm integrating biological and psychosocial aspects of depression. Supported by recent research, we propose in our article a biopsychosocial diathesis-stress model of depression. Its basic aim is psychoeducational: to provide therapists, patients, and their environment a constructive conceptual framework to understand depressive complaints, vulnerability, and stress. The core of the model consists of the concept of psychobiological vulnerability, which is determined by risk factors-of a biogenetic, psychological, somatic, and societal nature-and by protective factors. Life events with an idiosyncratic, stress-inducing value interact with this vulnerability, triggering severe or chronic distress that affects the individual's resilience and leads to symptoms of depression. The pathogenesis of depression is symbolized by a negative downward loop, in which interactions among symptoms, vulnerability, and stressors drive the patient toward a depressive condition. Moreover, experiencing recurrent depression influences psychobiological vulnerability, the occurrence of stressors, and tremendously increases the risk of further relapse. The model stresses the self-evident integration of biological and psychological therapeutic interventions that need to focus on symptom reduction and on relapse prevention. Moreover, it offers the patient and therapist a psychoeducational context in which the individual's vulnerability and depressive symptoms can be treated. Finally, applications of the depression model as a therapeutic approach to severe depression in the phases of remoralization, symptom reduction, and relapse prevention are presented.

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Mononuclear phagocytes originate in the bone marrow, where dividing promonocytes form monocytes . The monocytes leave the bone marrow and are transported via the circulation to the tissues, in which they become macrophages . This pathway is followed by the mononuclear phagocytes in the normal steady state (1, 2) as well as in acute and chronic inflammations (1, 3-10), although in some forms of chronic inflammation local proliferation may occur in the tissues (11, 12) .The promonocyte is the most immature cell of the mononuclear phagocyte system to have been fully characterized so far (2, 13, 14), but it is unlikely that this cell is the direct descendant of the stem cell . The available evidence suggests that at least one other type of cell occurs between the stem cell and the promonocyte (2, 15) . It is not yet known whether this precursor of the promonocyte is also a mononuclear phagocyte . Some authors think that the mononuclear phagocytes in the bone marrow derive from immature granulocytes at some stage (16-18), but direct proof is lacking . This problem led us to investigate the origin of the bone marrow promonocytes .Since promonocytes constitute only about 0 .25% of the nucleated bone marrow cells (13), promonocyte precursors can be expected to occur in low numbers and therefore cytological preparations will not be very informative . The available methods for the study of the bone marrow monocyte and promonocyte (2, 13), which are based on the common property of mononuclear phagocytes to adhere to glass (19,20), have not led to the identification of any type of cell preceding the promonocyte .Another way to study immature bone marrow cells is the recently described technique by which in the presence of a colony-stimulating factor mononuclear phagocyte and granulocyte colonies are grown in vitro (21-23) . This kind of culture, in which each colony develops from a single immature bone marrow cell (18,21,(24)(25)(26), would be suitable for the investigation of the immature proliferating mononuclear phagocytes, but study of the characteristics of the cells in these colonies is hampered by the agar or methyl cellulose used as support for the cells .For the present study, therefore, this method was modified such that leukocyte colonies develop in a liquid medium on a glass surface. The cells adhering to the glass surface (e .g., mononuclear phagocytes) are then directly accessible for observation and characterization .The aim of the present study was to identify and characterize the promonocyte precursor in the mononuclear phagocyte colony . The findings concerning the morphology, cytochemistry, functional characteristics, and proliferative capac-

Although daytime emotional stressful events are often presumed to cause sleep disturbances, the few studies of stressful life events on sleep physiology have resulted in various and contradictory findings. As research has focused in particular on stress in itself, the present study is the first to investigate the effect using polysomnography (PSG). Results indicate a significant increase in sleep fragmentation, as expressed by decreased sleep efficiency, total sleep time, percentage of rapid eye movement (REM) sleep, and an increased wake after sleep onset latency, total time awake, latency to SWS, number of awakenings and number of awakenings from REM sleep. The results demonstrate that negative emotion correlates with enhanced sleep fragmentation helping us to understand why sleep patterns change and how sleep disturbances may develop.

As it stands now, the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; American Psychiatric Association, in press) will maintain the categorical model and criteria distinguishing the 10 personality disorders (PDs) described in the fourth edition of the manual (DSM-IV; American Psychiatric Association, 1994). An alternative diagnostic proposal based on two criteria, being impaired personality functioning and the presence of maladaptive traits, will be referred to a special section for further research and clinical evaluation. Two issues pertaining to this alternative diagnostic approach need further clarification. First, more insight is required in the specific nature of personality dysfunction, its underlying structure, and optimal operationalization. Second, confusion still exists about how personality dysfunction and traits are interconnected and how they both contribute to the PD diagnosis. The current study addresses both issues empirically in a sample of 159 psychiatric patients by (a) investigating the structure of personality functioning as assessed by the Severity Indices of Personality Problems (SIPP-118), and (b) determining the incremental validity of the resulting dysfunction factors vis-à-vis trait domains (measured by the NEO Personality Inventory-Revised [NEO-PI-R]) in explaining DSM-IV PD variance. Trait and dysfunction dimensions were strongly correlated but showed significant, though limited, incremental validity above each other. Implications for the conceptualization of personality pathology are discussed.

The aim of the present study was to examine the relationships between suicidal ideation or suicidal attempts and severity of depression, presence of personality disorders, and sociodemographic factors in a population of depressed in-patients. A total of 338 adult depressed psychiatric in-patients were examined and classified according to DSM-III criteria as having major depression with or without melancholic or psychotic features, adjustment disorder with depressed mood or dysthymic disorder. Scores on the Hamilton Depression Rating Scale (HDRS), Beck Depression Inventory (BDI) and Zung Self-Rating Depression and Anxiety Scales (SDS and SAS) were measured. We found that suicidal ideation was significantly related to severity of depression (according to the HDRS and all self-rating scales), a lower global assessment of functioning the year before hospitalization, and previous psychiatric hospitalizations. The items with the strongest predictive value for suicidal ideation were hopelessness, depressed mood, feelings of guilt, loss of interest and low self-esteem. These symptoms predicted 43% of the variance in suicidal ideation. None of the above predictors of suicidal ideation was related to suicidal attempts. Depressed patients with a personality disorder attempted significantly more suicidal attempts and showed more suicidal ideation than depressed patients without personality disorder. No significant correlations were found between suicidal ideation or suicide attempts and gender, marital status, employment status or psychosocial stressors during the previous 6 months.