Bouncing back: remission from depression in a 12-year panel study of a representative Canadian community sample

Purpose

This study sought to investigate time to remission from depression in a community-based sample of adults followed for 12 years.

Methods

Data were derived from the National Population Health Survey (1994/5–2006/7 and 1996/7–2008/9). Fully 1,128 adults were included who were depressed at baseline according to DSM-III/CIDI-SF criteria. Kaplan–Meier and Cox proportional hazards procedures were used to determine time to remission and the demographic (e.g., gender and marital status), psychosocial (e.g., social support and adverse childhood experience) and health-related (e.g., pain, health conditions and alcohol use) factors with which it is associated.

Results

More than three quarters of the sample (77 %) no longer screened positive for depression at 2 years, and nearly the entire sample (94 %) had remitted by 12 years. Adverse childhood experiences (i.e., childhood abuse and parental additions), lack of social support, the presence of pain and health conditions (i.e., migraines, arthritis and back pain) each predicted more time to remission. The only factor associated with time to remission in the multivariate analysis was a history of childhood physical abuse.

Conclusions

Most community members with depression get better after 2 years and nearly all will have remitted, at least once, by 12 years. The results of this study may help guide the development of interventions for chronic depression that focus on early prevention of childhood abuse.     

Challenges and strategies of children and adolescents with inflammatory bowel disease: a qualitative examination

Background  

The aims of this study were to understand the lived experience and elements of quality of life as depicted by children and adolescents with inflammatory bowel disease (IBD).     

Intrinsic and extrinsic regulation of the proliferation and differentiation of cells in the rodent rostral migratory stream

An overriding principle of development is that neurons become permanently postmitotic once they initiate differentiation. Work in our laboratory, however, has provided evidence for a population of progenitor cells in mammalian forebrain that express properties of differentiated neurons, even though they continue to divide. These neuronal progenitor cells are situated in the rostral migratory stream (RMS), which extends from a specialized portion of the subventricular zone surrounding the anterior tip of the lateral ventricle, referred to as the SVZa, to the middle of the olfactory bulb. As SVZa-derived cells migrate to the olfactory bulb, they undergo cell division, and they never deviate from the RMS. Once they reach their final destinations, they become terminally postmitotic interneurons. This Mini-Review concerns findings from our recent experiments designed to reveal the intrinsic and extrinsic mechanisms governing the proliferation and differentiation of the unique SVZa neuronal progenitor cells. We have investigated the role(s) of cell cycle regulatory proteins, in particular, the cell cycle inhibitor p19(INK4d), in the control of SVZa cell proliferation. Several studies have indicated that cells withdraw from the cell cycle once they express p19(INK4d). To begin to investigate whether p19(INK4d)(+) SVZa-derived cells are postmitotic, we analyzed the pattern of p19(INK4d) expression by the cells of the RMS. A pronounced gradient of p19(INK4d) expression was demonstrated; progressively more cells are p19(INK4d) immunoreactive as the olfactory bulb is approached. In addition, the capacity of p19(INK4d)(+) cells to incorporate bromodeoxyuridine was investigated. From the results of these studies, we conclude that SVZa cells in the RMS can successively down-regulate their expression of p19(INK4d) as they migrate and that they repeatedly exit and reenter the cell cycle while en route to the olfactory bulb. These studies led us to investigate whether bone morphogenetic proteins (BMPs) are involved in the regulation of SVZa cell proliferation and p19(INK4d) expression, because, elsewhere in the CNS, BMPs modulate cell proliferation and influence cell fate decisions. To determine the effects of BMP signaling on SVZa cell proliferation and differentiation, we altered the expression of the BMP receptor Ia (BMPR-Ia) using retrovirally mediated gene transfer. The cells in the SVZa encoding the wild-type BMPR-Ia exit the cell cycle and do not appear to migrate through the RMS. Conversely, both within the SVZa and along the RMS, the majority of SVZa-derived cells encoding a dominant-negative BMPR-Ia gene do not express p19(INK4d). These findings indicate that p19(INK4d) expression is suppressed when BMP signaling is inhibited. Furthermore, SVZa-derived cells with both augmented and inhibited BMP signaling retain their neuronal commitment. Collectively, these studies have revealed that SVZa cell proliferation and differentiation is under the control of several interacting intrinsic and extrinsic factors.     

Estrogen-induced gonadotropin surge in rhesus monkeys is not inhibited by cortisol synthesis inhibition or hypoglycemia

Acute administration of corticotrophin-releasing hormone (CRH) has been shown to inhibit gonadotropin secretion in several species including rodents, sheep, humans, and nonhuman primates. Similarly, a variety of acute stressors have been shown to inhibit tonic gonadotropin secretion and may do so through a CRH mechanism. Stress-induced inhibition of tonic gonadotropin secretion below levels required for follicular maturation would be expected to inhibit ovulation. An additional mechanism whereby acute stressors could interfere with ovulation is through inhibition of the preovulatory gonadotropin surge. In the present study, we determined the effect of acute activation of the hypothalamic-pituitary-adrenal (HPA) axis on phasic gonadotropin secretion in female rhesus monkeys. Activation of the HPA axis was achieved by either a hypoglycemic challenge or blockage of cortisol synthesis with metyrapone, 24h after an estradiol benzoate challenge. Neither metyrapone nor insulin-induced hypoglycemia inhibited gonadotropin secretion. In fact, the initiation of the luteinizing hormone and folliclestimulating hormone surge was advanced by 7.4±0.4 h (p<0.001) and 4.8±1.4 h (p=0.04) respectively, in metyrapone-treated monkeys compared with saline controls. By contrast, hypoglycemia did not affect the gonadotropin surge. The gonadotropin surge was preceded by increased progesterone secretion in metyraponetreated but not insulin-treated monkeys. This difference in progesterone secretion likely explains the advancement of the gonadotropin surge in the metyraponetreated animals.     

Motor control alteration in posturography in learning-disabled children

BACKGROUND: Some authors have mentioned that intersensory integration is damaged in children with learning disabilities (LDs), and other investigators point to motor control alterations in the same patients. Thus, we decided to study these hypotheses by means of posturographic recordings. METHODS: A highly selected group of 27 children with LDs was compared with 27 children of control group without LDs. Patients and controls were placed on the Equitest equipment platform. Sensory organization tests evaluated different test conditions that systematically vary visual, vestibular, and foot somatosensory cues available to subjects while they attempt to maintain a stable, quiet stance. Movement coordination test involved sudden posterior and anterior translations of the patient support surface. RESULTS: No significant correlations between scholastics and posturographic performance were observed. No difference in the six conditions and in sensory organization ratios or in visual preference between both groups was disclosed. Motor control test on children with LDs showed significant higher values in latencies in averages of large translations. CONCLUSIONS: Our data suggest that vestibular-visual-somatosensory organization for posture control are not abnormal in children with LDs; instead, motor controls show higher latencies with large translation movements, which suggest abnormal rate and timing precision motor coordination.     

Circulating soluble adhesion molecules E-cadherin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in patients with gastric cancer.

The concentrations of the soluble adhesion molecules E-cadherin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were investigated in 45 patients with gastric cancer before treatment and their correlation with clinical, histological and routine laboratory parameters was examined. Data were collected on tumour stage at presentation, presence and sites of metastatic disease, tumour pathology, survival and results of routine laboratory tests. Serum concentrations of ICAM-1 and VCAM-1 were significantly elevated in the patients with gastric cancer in comparison with the group of healthy subjects (P < 0.00001 and P < 0.0001 respectively). Increased serum concentrations of VCAM-1 were associated with locally advanced and metastatic disease whereas ICAM-1 was significantly elevated both in local and in advanced/metastatic disease. Soluble E-cadherin and E-selectin concentrations did not show any significant elevation in gastric cancer patients. Concentrations of soluble adhesion molecules showed significant correlation with each other (except E-selectin and VCAM-1) and with alkaline phosphatase. Soluble ICAM-1 and VCAM-1 were significantly associated with an elevated total white cell count. Patients with elevated VCAM-1 had significantly poorer survival in comparison with patients with normal serum levels (P = 0.0361).     

The effects of eticlopride on Morris water task performance in male and female rats neonatally treated with quinpirole

Rationale Previous studies have shown that neonatal quinpirole treatment which results in long-term dopamine D2 receptor supersensitization (D2 receptor priming) produces cognitive deficits in preweanling and adult rats behaviorally tested on the Morris water task (MWT).Objective This study was designed to analyze whether pretraining administration of the D2 antagonist eticlopride alleviates cognitive deficits produced by neonatal quinpirole treatment.Methods Both male and female Sprague–Dawley rats were treated with quinpirole HCl (1 mg/kg) or saline from postnatal days 1 to 21. From P22 to P24, rats were tested on the place version of the MWT in which a hidden platform remains stationary throughout training. From P25 to P28, rats were tested on the match-to-place version of the MWT, and rats are given a pair of daily training trials to locate the hidden platform that was moved to a new location each day. Fifteen minutes before each training session, rats were intraperitoneally administered with eticlopride (0.01 or 0.02 mg/kg) or saline.Results Pretraining eticlopride treatment alleviated cognitive deficits produced by neonatal quinpirole treatment in both male and female rats on the place version of the MWT, as well as in males tested on the match-to-place version of the MWT. However, there were no significant deficits produced by neonatal quinpirole treatment in females tested on the match-to-place version of the MWT, and control males demonstrated superiority over control females on this version of the task.Conclusions Pretraining administration of the dopamine D2 antagonist eticlopride alleviated cognitive deficits produced by neonatal quinpirole treatment. However, it appears that the dopamine D2 receptor may have a more important influence on cognitive performance in males than in females, which may be related to increased sensitivity of the D2 receptor in males.     

Bilateral bispectral index monitoring during suppression of unilateral hemispheric function

Bispectral Index (BIS) has been used to monitor level of "sedation" based on the electroencephalogram (EEG). Patients evaluated for surgery to control a seizure disorder undergo Wada testing, during which one hemisphere is rendered functionally inactive after injecting a short-acting barbiturate. We surmised that the BIS values would reflect these functional changes. Eight epileptic patients were enrolled. A full array of 21 EEG electrodes and 2 BIS XP (Quatro) strips over each frontal region of the scalp were applied. The EEG was continuously recorded. BIS values from each hemisphere were recorded every minute. Angiography was performed by advancing a catheter into each internal carotid artery. Amobarbital or methohexital was injected until the patient developed a hemiparesis. The EEG confirmed a significant lateralized cortical effect of the barbiturate. Repeated measures analysis of variance was used to analyze the differences between the BIS values from monitor electrode strips placed on the left (left BIS) and the right (right BIS) sides of the head as well as the differences in the left and right BIS values before and after each injection of the barbiturate. Injection of barbiturate into either the left or right internal carotid artery produced a significant change on the 21-electrode EEG. However, there was no difference between left BIS to right BIS values (P = 0.84). With repeated injections of barbiturates, some patients became sedated. At these times, both left BIS and right BIS values decreased together before and after injection of barbiturate. The BIS monitor was unable to distinguish significant hemispheric EEG and clinical functional changes except when the patient became sedated.