Cell-Growth Kinetics and Karyotype Analysis of Human Memory Lymphocytes Responding to Alloantigen and Mitogen

Peripheral-blood lymphocytes were primed in vitro with the mitogen phytohemagglutinin (PHA) or with allogeneic cells and their memory responses studied following sequential restimulation with either mitogen or alloantigen. Chromosome preparations were made every 12 hours following exposure to the stimulating agents. Cultures were labeled with BUdR for sister-chromatid staining of the chromosomes which provided information about the kinetics of cell growth and rates of sister chromatid exchange. Cultures containing no BUdR were used for the investigation of cell karyotypes after chromosome-banding.Following PHA as well as alloantigen restimulation, an earlier reaction of the responding cells was observed. The peak response after the first stimulation was found at 120 h with allogeneic stimulation and at 60 h with mitogen stimulation. In the second round of stimulation, the peak occurred after 48 h (allogeneic) and 36 h (PHA) and following the third stimulation after 36 h (allogeneic) and 24 h (PHA). The speed of cell growth was decreased following restimulation with either alloantigen and mitogen. In contrast to the allogeneic restimulation, the number of cells responding after PHA restimulation was decreased.No systematic numerical or structural aberration of the karyotype was detected following repeated stimulation with either alloantigen or mitogen. In this sense, the lymphocyte subpopulations selected by repeated stimulation did not differ from the starting material. On the other hand, the sister-chromatid exchange (SCE) frequency was increased following allogeneic restimulation, whereas it remained constant with PHA restimulation.     

Premenstrual symptomatology,locus of control,anxiety and depression in women with normal menstrual cycles

Summary The present study was designed to investigate the relationships between premenstrual symptomatology, locus of control, anxiety, and depression in women with normal menstrual cycles. Sixty-nine female participants completed a survey, comprised of the Menstrual Distress Questionnaire (MDQ; Moos, 1968), Levenson's (1981) locus of control scales, the Depression Anxiety Stress Scale (DASS; Lovibond and Lovibond, 1995), and a questionnaire constructed by the researchers based on the DSM-IV criteria for Premenstrual Dysphoric Disorder (PMDD). Both overall and specific subtypes of premenstrual symptomatology were found to correlate with external locus of control, anxiety, and depression. In addition, locus of control was found to moderate the relationship between premenstrual symptomatology, anxiety and depression. Finally, women who were in the premenstrual phase when completing the questionnaire scored significantly lower on the internal scale than those in either the follicular or early luteal phases. It was concluded that an external locus of control may be associated with a susceptibility to depression or anxiety when certain premenstrual or postmenstrual changes are experienced. Received August 10, 2002; accepted January 12, 2003 Published online February 19, 2003 Abbreviations · ANOVA · Analysis of variance · DASS · Depression anxiety stress scale · LOC · Locus of control · MANOVA · Multivariate analysis of variance · MDQ · Menstrual distress questionnaire · PMDD · Premenstrual dysphoric disorder · PMS · Premenstrual syndrome Acknowledgement The authors would like to thank John Reece, Department of Psychology and Disability Studies, RMIT University, Melbourne, Australia, for assistance with data analysis. Correspondence: Dr. Andrew Francis, Department of Psychology and Disability Studies, Faculty of Applied Science, RMIT University, P.O. Box 71, Bundoora, Victoria 3083, Australia; e-mail: andrew.francis@rmit.edu.au     

Diagnosing depression in primary care using self-completed instruments: UK validation of PHQ-9 and CORE-OM.

There is increased emphasis on routine assessment of depression in primary care. This report is the first UK validation of two self-completed measures: the Patient Health Questionnaire (PHQ-9) and the Clinical Outcomes in Routine Evaluation-Outcome Measure (CORE-OM). Optimum cut-off points were established against a diagnostic gold standard in 93 patients. PHQ-9 sensitivity = 91.7% (95% confidence interval [CI] = 77.5 to 98.3%) and specificity 78.3% (95% CI = 65.8 to 87.9%). CORE-OM sensitivity = 91.7% (95% CI = 77.5 to 98.2%) and specificity = 76.7% (95% CI = 64.0 to 86.6%). Brief self-rated questionnaires are as good as clinician-administered instruments in detecting depression in UK primary care.     

A history of personal violence and postpartum depression: is there a link?

Summary Background: A link between violence and depression has been shown, but not a link between violence and postpartum depression. This study sought to determine if there is an association between a history of abuse (physical, sexual, emotional as a child or adult) and postpartum depression (PPD). Method: 200 postpartum women were recruited from 6 hospitals. At 8–10 weeks postpartum, a telephone interviewer asked women about physical, emotional or sexual abuse as an adult or child and sociodemographic, obstetrical and personal medical history. PPD was assessed using the Edinburgh Postnatal Depression Scale (EPDS, score of ≥12). Abuse was determined by the Conflict Tactics Scale or the Abuse Assessment Screen. Chi-square and logistic regression were used to determine the relationship between violence and PPD. Results: 11% of women had EPDS scores of ≥12. Rates of childhood (6.5%), or adult (6.5%) physical abuse; and childhood (13%) or adult (14%) sexual abuse were reported by respondents. Emotional abuse in the current relationship (29.6%) exceeded that of childhood abuse (3.5%). Overall 43.2% of respondents had at least one form of abuse. Having a history of depression (OR = 3.3 (95% CI, 1.3–8.7)), panic attack during pregnancy (OR = 5.4 (1.6–19.0)), maternal complications (OR = 5.0 (1.7–15.1)), low social support (OR = 3.3 (1.3–8.7)) and emotional abuse (OR = 2.8 (1.1–7.4) were associated with PPD. Conclusion: Emotional abuse but not physical or sexual abuse was found to be associated with PPD. A possible explanation for this relationship may be that being in an abusive situation puts one at risk for depression and in turn, postpartum depression.     

The categorical and dimensional models of endogenous depression

We calculated a Research Diagnostic Criteria (RDC) endogenous score for 257 depressed inpatients based on the number of endogenous criteria present. The distribution of RDC endogenous scores was unimodal. There was no association between endogenous scores and results of the Dexamethasone Suppression Test, or morbid risk for depression in the patients' first-degree relatives. The morbid risk for a family history of alcoholism tended to decrease with increasing endogenous scores, although a consistent steady decline was not observed. The results suggest that the RDC criteria do not fit either the categorical or dimensional model of endogenous classification. Potential sources of difficulty with the RDC endogenous criteria are discussed.     

A randomised controlled trial to test the feasibility of a collaborative care model for the management of depression in older people

BACKGROUND: Depression is the most common mental health disorder in people aged over 65 years. Late-life depression is associated with chronic illness and disability. AIM: To investigate the feasibility of a collaborative care model for depression in older people in a primary care setting. DESIGN OF STUDY: Randomised controlled trial with 16-weeks follow up. SETTING: A primary care trust in Manchester. METHOD: Participants were 105 people aged 60 years or older who scored 5 or more on the Geriatric Depression Scale; 53 were randomly allocated to an intervention group and 52 to a usual care group. The intervention group received care managed by a community psychiatric nurse who delivered an intervention comprising a facilitated self-help programme with close liaison with primary care professionals and old-age psychiatry according to a defined protocol. The usual care group received usual GP care. A nested qualitative study explored the views of the health professionals and patients regarding the acceptability and effectiveness of the intervention. RESULTS: The main outcome measure was recovery from depression. Patients in the intervention group were less likely to suffer from major depressive disorder at follow up compared with usual care (0.32, 95% confidence = interval = 0.11 to 0.93, P = 0.036). The qualitative component of the study demonstrated the acceptability of the intervention to patients. CONCLUSION: A model of collaborative care for older people with depression, used in a primary care setting with a facilitated self-help intervention is more effective than usual GP care. This study demonstrates that the implementation of a collaborative care model is feasible in UK primary care and that the intervention is effective and acceptable to patients.     

LHRH messenger RNA in neurons in the intact and castrate male rat forebrain,studied by in situ hybridization

Summary The slow potential change (spc) accompanying spreading depression (SD) was studied in rats and in a seizure-sensitive strain of Mongolian gerbil under three different experimental paradigms, each involving the use of naloxone. Gerbils undergoing electroconvulsive shock treatment displayed SD during the post-ictal phase, which was blocked by the intraperitoneal (i.p.) administration of naloxone (20–50 mg kg^-1). Topical application of naloxone to the exposed cortex of the anaesthetized gerbil and rat blocked the spc of SD evoked by KCl. Microiontophoretic ejection of naloxone during extracellular recordings reversed cell refractoriness following the spc, demonstrated by the observation of a maintained sensitivity to iontophoretic pulses of glutamate. The results suggest a possible involvement of naloxone-sensitive processes in the mechanism responsible for cortical SD.     

Coping strategies,hostility, and depressive symptoms: A path model

Previous studies of coping, hostility, and depressive symptoms have highlighted the significant relations between all possible pairs of these 3 variables. To more completely explore the nature of depressive symptoms, we link them all together in this study by testing a coping→hostility→depressive symptoms path model. One hundred forty participants completed psychological questionnaires measuring coping strategies, hostility, and depressive symptoms. While controlling age and social class as covariates, SPSS stepwise regression analyses were used to examine relations among these 3 constructs. Results suggest that coping has a direct relation with depressive symptoms as well as an indirect relation mediated by hostility. Passive coping may lead to increased hostility, resulting in depressive symptoms. Active coping may have the opposite effect. These findings suggest that the inclusion of measures of both coping strategies and hostility yields a more thorough understanding of concomitants of depressive symptoms. From a clinical perspective, knowing what coping strategies a person uses and how much anger they experience and express may be useful in guiding the management of depressive symptoms.     

Testing genetic models for multiple symptoms: An application to the genetic analysis of liability to depression

A model is presented which allows for the contribution of genes and environment to categorical data on multiple symptoms. The model distinguishes between parameters needed to express the relationship between a latent trait and observed responses and the parameters required to represent the causes of variation in the latent trait. The regression of the latent trait on covariates may also be specified. The model is applied to symptoms of depression in 1983 pairs of adult female monozygotic and dizygotic twins. A model which allows only for polygenic variation in the latent trait is supported as well as the mixed model, which also allows for the effects of a major gene. The likelihood is significantly lower when all genetic effects are ascribed to a single gene. Practical limitations of the method are discussed.This research is supported by Grants AG04954, AA06781, GM32782, GM30250, and MH40828 from the National Institutes of Health. We are indebted to Dr. Greg Carey for his incisive discussion.