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The role of long-term potentiation in persistent epileptiform burst-induced hyperexcitability following GABAA receptor blockade.

Persistent hyperexcitability follows synchronized bursting induced in the CA3 region of hippocampal slices by perfusion with high concentrations (2000 IU/ml) of the GABAA antagonist, penicillin. This hyperexcitable state is characterized by: i) slow recovery from bursting following penicillin washout; ii) persistent "post-burst" field potential oscillations and iii) increased probability of spontaneous bursting with ordinarily sub-convulsant doses of GABAA antagonists. An N-methyl-D-aspartate-independent type of long-term potentiation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate excitatory postsynaptic potentials occurred following bursting. However, similar increases in excitatory postsynaptic potential magnitude also occurred after a subconvulsant dose of penicillin (500 IU/ml) which did not produce the other features of persistent hyperexcitability. Furthermore, long-term potentiation either increased or remained stable after bursting stopped, whereas, post-burst oscillations gradually diminished with time. Low doses of the AMPA/kainate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, which restored the potentiated excitatory postsynaptic potentials to control levels, reduced but did not eliminate the post-burst oscillation. Tetanus-induced long-term potentiation did not reproduce the hyperexcitable state seen after bursting. These findings indicate that the epileptiform bursting caused by blocking GABAA-mediated inhibition induces long-term potentiation which is partially responsible for persistent burst-induced hyperexcitability but is not sufficient to entirely explain it. The hippocampus which is critical for normal memory is also frequently the generator of intractable epileptic seizures. Seizure-like discharges in the hippocampus induced long-lasting increases in synaptic efficacy similar to those thought to underlie normal memory. This form of long-term potentiation contributed to the network oscillations characteristics of the hyperexcitable state persisting after epileptiform activity but was not sufficient to entirely explain them. Epileptic seizures may engage normal memory mechanisms which increase neuronal excitability and predispose the hippocampal network to further seizures. This may, in part, account for the propensity for hippocampal seizure foci to become intractable.

Animals↗

A double dissociation within the hippocampus of dopamine D1/D5 receptor and beta-adrenergic receptor contributions to the persistence of long-term potentiation.

We compared the effects of the D1/D5 receptor antagonist SCH-23390 with the beta-adrenergic receptor antagonist propranolol on the persistence of long-term potentiation in the CA1 and dentate gyrus subregions of the hippocampus. In slices, SCH-23390 but not propranolol reduced the persistence of long-term potentiation in area CA1 without affecting its induction. The drugs exerted reverse effects in the dentate gyrus, although in this case the induction of long-term potentiation was also affected by propranolol. The lack of effect of SCH-23390 on the induction and maintenance of long-term potentiation in the dentate gyrus was confirmed in awake animals. The drug also had little or no effect on the expression of inducible transcription factors. In area CA1 of awake animals, SCH-23390 blocked persistence of long-term potentiation beyond 3 h, confirming the results in slices. To rule out a differential release of catecholamines induced by our stimulation protocols between brain areas, we compared the effects of the D1/D5 agonist SKF-38393 with the beta-adrenergic agonist isoproterenol on the persistence of a weakly induced, decremental long-term potentiation in CA1 slices. SKF-38393 but not isoproterenol promoted greater persistence of long-term potentiation over a 2-h period. In contrast, isoproterenol but not SKF-38392 facilitated the induction of long-term potentiation. These data demonstrate that there is a double dissociation of the catecholamine modulation of long-term potentiation between CA1 and the dentate gyrus, suggesting that long-term potentiation in these brain areas may be differentially consolidated according to the animal's behavioural state.

Adrenergic beta-Antagonists↗

Comparative studies of the persistence of animal mycoplasmas under different environmental conditions.

A comparison of the persistence of mycoplasmas in animals was carried out. When inoculated into liquid media, strains of Mycoplasma bovis, M. arginini, Acholeplasma laidlawii, and A. axanthum persisted for 59-185 days post-inoculation. The survival periods were not significantly influenced by temperature (4, 30, 37 degrees C, and room temperature). The survival periods for M. bovigenitalium, M. gallisepticum, M. bovirhinis, and M. gateae ranged from <7 to 185 days depending on medium components and temperature. Further, it was determined that strains of M. bovigenitalium, M. bovis, M. bovirhinis, M. arginini, and A. laidlawii persisted in a dry paper disc for at most 28, 126, 154, 56 and over >168 days at 4 degrees C, respectively. At 4 degrees C, strains of M. gallisepticum, M. columborale, M. edwardii, M. felis, and M. gateae survived for at most 28, 21, 42, 28, 28 and 70 days, respectively. At 30 degrees C, strains of M. bovis, M. bovirhinis, M. arginini, A. laidlawii, and M. gallisepticum persisted for at most 28, 84, 56, >168 and 14 days, respectively, but strains of M. gallisepticum, M. columborale, M. edwardii, M. felis, M. gateae, and U. diversum did not survive for more than 14 days. In an outdoor environment, strains of M. bovirhinis and A. laidlawii survived for at most 28 and 14 days, respectively. Finally, it was found that 14 isolates of M. gallisepticum persisted for periods similar to those of the reference strains. The results under dry conditions at a variety of temperatures presented contribute to understanding the epizootiology of mycoplasmal infections in the field.

Animals↗

Histologic studies on normal and persistent ductus arteriosus in the dog.

The process of anatomic closure of the ductus arteriosus was studied at the ultrastructural level in 15 normal beagles (age 0 hour to 13 days) and in 18 specimens from a strain of dogs with hereditary persistent ductus arteriosus (age 4 hours to 27 days). Normal ductal closure takes place from the pulmonary artery to the aortic end. It is accompanied by a series of histologic changes: 1) separation of the endothelial cells from the internal elastic lamina resulting in a wide region of subendothelial edema; 2) ingrowth and infolding of endothelial cells and migration of undifferentiated smooth muscle cells from the inner media into the subendothelial region; 3) apposition of endothelial cells bordering the lumen; and 4) degenerative changes. In persistent ductus arteriosus, these changes do not occur. The endothelial cells remain closely adhered to the internal elastic lamina and the underlying media is abnormal in structure. In the case of partial persistent ductus arteriosus (ductus diverticulum), both the normal and the abnormal type of wall are found in a single ductus arteriosus. The histologic features of the normal and the persistent ductus arteriosus in the dog resemble those of the normal and the persistent ductus arteriosus in humans, suggesting a similar pathogenesis.

Animals↗

Use of amiodarone in the treatment of persistent and paroxysmal atrial fibrillation resistant to quinidine therapy.

The efficacy of amiodarone was assessed in 38 patients with atrial fibrillation resistant to quinidine and an effort made to identify factors correlated with amiodarone response. The study group included 29 patients with and 9 without organic heart disease and either persistent (n = 11) or paroxysmal (n = 27) atrial fibrillation. All patients were treated with amiodarone and followed up in a research clinic. Efficacy was classified as excellent (no recurrent symptomatic atrial fibrillation) in 15 (55%) of 27 patients with paroxysmal and 5 (45%) of 11 patients with persistent atrial fibrillation. Efficacy was poor (no effect on atrial fibrillation) in 5 (19%) of 27 patients with paroxysmal and 6 (55%) of 11 patients with persistent atrial fibrillation. Efficacy was good (amelioration but not total suppression) in 7 (26%) of 27 patients with paroxysmal atrial fibrillation. Efficacy was related to echocardiographic left atrial dimension, left ventricular ejection fraction and, in patients with persistent atrial fibrillation, the duration of the arrhythmia. During the follow-up period of 15 months (range 1 to 36), overall efficacy (considering response and toxicity) was 67% in the 27 patients with paroxysmal and 45% in the 11 patients with persistent atrial fibrillation. It is concluded that amiodarone offers an additional therapeutic alternative in quinidine-resistant atrial fibrillation and that certain clinical factors are correlated with amiodarone response.

Adult↗

Carbohydrate metabolism in temporal and persistent hypoglycemic chickens induced by insulin infusion.

In order to elucidate the regulatory mechanism of blood glucose concentrations specific to chickens, carbohydrate metabolism in the liver, muscle and kidney and metabolite concentrations in the blood were investigated in chickens with acute and persistent hypoglycemia. Acute and persistent hypoglycemia were experimentally induced by a single injection of insulin (8 U/kg BW) or by continuous infusion of insulin (22.5 U/kg BW/day) for 4 days. Non-esterified fatty acid (NEFA) concentration in plasma and D-3-hydroxybutyrate (3HB) concentrations in liver and muscle increased in the acute hypoglycemia. Plasma NEFA concentration and 3HB concentration in the blood and liver were not changed at day 3 of persistent hypoglycemia, while 3HB concentration in the muscle was decreased. Phosphofructokinase (PFK) activity in the liver tended to increase but PFK and pyruvate kinase (PK) activities were unchanged in acute hypoglycemia. In persistent hypoglycemia, increase of hepatic PFK activity at day 1 in which it was reversed at day 3, and a small increase of muscle PK activity were observed, while PK and phosphoenolpyruvate carboxykinase (PEPCK) activities in the liver and kidney were not significantly changed. These results show that in the persistent hypoglycemic chickens, hepatic glycolysis transiently increases, which is followed by a small decrease, while glycolysis in muscles and gluconeogenesis in the liver and kidney are not significantly changed.

3-Hydroxybutyric Acid↗

Persistent wound drainage after primary total knee arthroplasty.

A retrospective review of 597 total knee arthroplasties (TKAs) (546 primary and 51 revision cases) was undertaken to define the role and management of persistent postoperative wound drainage and its relationship to possible subsequent joint sepsis. Eight patients with persistent postoperative wound drainage were identified. The follow-up period averaged 4.3 years. These eight patients represent a 1.3% overall incidence of persistent drainage and only 0.5% with the "parent" group of primary TKAs. These very low incidences of wound drainage contrast markedly with the reported 17-50% incidence in the history of those patients who presented for treatment of established knee arthroplasty infections. Such high frequencies observed by the authors and published elsewhere suggested an important relationship between established knee arthroplasty infection and a history of previous prolonged wound drainage. Because of an initial suspicion that persistent drainage needs to be treated specifically, irrigation and debridement were undertaken in all of the eight cases reported. This secondary procedure occurred at an average of 12.5 days after the initial operation. Twenty-five percent of patients proved to have a positive joint culture at the time of irrigation and debridement, although all cases were treated successfully with adjuvant antibiotics. The success of reopening without introducing infection is of particular note. No morbidity from early irrigation and debridement was experienced, and the authors recommend this procedure for wounds that drain persistently after TKA. The authors hypothesize that recognizing this potential and acting upon it may prevent some chronic drainage problems from becoming true, established infections.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Neodymium:YAG laser capsulotomy in vitrectomized pseudophakic eyes with persistent endotamponade.

PURPOSE: To evaluate the feasibility and limits of neodymium:YAG (Nd:YAG) laser capsulotomy in eyes with persistent endotamponade. SETTING: Department of Ophthalmology, University Cologne, Cologne, Germany. METHODS: In this consecutive series, an Nd:YAG laser capsulotomy was performed by 1 surgeon in 6 eyes with posterior capsule opacification (PCO) and persistent endotamponade caused by proliferative vitreoretinopathy. The endotamponade was with silicone oil (5000 centistokes) in 5 eyes and with perfluorohexyloctane (F(6)H(8)) in 1 eye. Also evaluated were 6 vitrectomized eyes without endotamponade that had an Nd:YAG laser capsulotomy for PCO by the same surgeon. All 12 eyes were pseudophakic. The mean follow-up after capsulotomy was approximately 6 months (range 2 to 12 months). Follow-up examinations included visual acuity, intraocular pressure measurement, and IOL centration and capsule reopacification evaluation. RESULTS: The total energy required was higher in eyes with persistent endotamponade. In 3 of these eyes, the laser capsulotomy could not be successfully completed and was surgically enhanced. The laser capsulotomy in eyes without endotamponade was successful in all cases. Complete reopacification occurred in 2 eyes with persistent endotamponade within 2 months and in no eye without endotamponade. Improvement in visual acuity was limited in all eyes because of retinal pathology. CONCLUSIONS: Neodymium:YAG laser capsulotomy in pseudophakic eyes with persistent endotamponade was successful but had a relatively high reintervention rate. The visual prognosis was limited in all cases because of retinal pathology.

Adult↗

Persistent sciatic artery: case report, anatomy, and review of the literature.

We report the case of a 64-year-old woman with an aneurysm of a left persistent sciatic artery presenting with arterial insufficiency from distal embolization. Treatment was exclusion of the aneurysm and femoropopliteal bypass after distal embolectomy with a Fogarty balloon catheter. We reviewed 71 cases in the literature to define characteristics of this anomaly which has many synonyms: including persistent sciatic artery, persistent axial artery, ischiopopliteal trunk. The persistence of the sciatic portion of the embryonic dorsal axial artery and failure of development of anastomoses with the ventral femoral network results in the anomaly. The persistent sciatic artery was "complete" in 75% of cases. In this configuration, it arises from the internal iliac artery, leaves the pelvic cavity through the lower part of the greater sciatic foramen caudad to the pyriformis muscle, reaches the posterior compartment of the thigh and continues as the popliteal artery. In 35% of cases, the artery is aneurysmal with a pulsatile mass in the buttock or a complication of the aneurysm. Arteriography required for diagnosis of the mass leads to discovery of the anomaly in many cases. The treatment of choice is exclusion followed by femoropopliteal vein bypass.

Aneurysm↗

Prenatal diagnosis of abnormal persistence of the right or left umbilical vein: report of 4 cases and literature review.

Four cases of prenatally diagnosed abnormal persistence of an umbilical vein are presented. Of the 4 cases, 2 are in association with congenital heart disease, 2 are in the setting of abdominal visceral situs inversus, and 1 is with extrahepatic persistence of an umbilical vein. Whereas persistent right umbilical vein may occur in 0.2% to 0.4% of fetuses undergoing screening prenatal ultrasonography, reports of an extrahepatic course are rare. A review of the 62 reported cases of prenatally diagnosed abnormally persistent umbilical vein revealed 9 fetuses (15%) with a congenital cardiovascular malformation, of which 6 were significant enough to likely require surgery. Other organ system malformations were present in 9 patients (15%). The prevalence of congenital cardiovascular malformations was 3 (7%) of 42 when combining 2 large series that were relatively unbiased for referrals for possible heart disease. Detailed evaluation by ultrasonography and fetal echocardiography should be used for prenatally diagnosed cases of abnormal persistence of an umbilical vein.

Adolescent↗

Relation of echocardiographic left ventricular mass and hypertrophy to persistent electrocardiographic left ventricular hypertrophy in hypertensive patients: the LIFE Study.

BACKGROUND: The Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) trial used left ventricular hypertrophy (LVH) on a screening ECG to identify patients at high risk for morbid events. Because of regression to the mean, not all patients who met screening criteria had persistent ECG LVH on the ECG performed at study baseline. METHODS: The relationship of echocardiographic LV mass and LVH to persistence or loss of ECG LVH between screening and baseline evaluation was examined in 906 hypertensive patients in the LIFE study, who had echocardiograms and additional ECG performed at study baseline. Patients were categorized according to the presence or absence of ECG LVH by Cornell voltage-duration product criteria or Sokolow-Lyon voltage criteria; echocardiographic LVH was defined by LV mass index (LVMI) > 104 g/m2 in women and > 116 g/m2 in men. RESULTS: A total of 678 patients (75%) had persistent ECG LVH at baseline evaluation. Compared with the 228 patients without ECG LVH on the second ECG by either criterion, the 106 patients with LVH by both Cornell product and Sokolow-Lyon criteria had significantly higher LVMI (140+/-31 v 114+/-21 g/m2, P < .001) and a higher prevalence of echocardiographic LVH (86% v 55%, P < .001). Patients with ECG LVH on the baseline ECG by either Cornell product criteria (n = 410) or Sokolow-Lyon voltage criteria (n = 162) had intermediate values of LVMI (125+/-25 and 121+/-21 g/m2) and prevalences of echocardiographic LVH (78% and 62%). After controlling for possible effects of age, sex, ethnicity, systolic blood pressure, and body mass index, persistence of ECG LVH on the baseline ECG was associated with an increased risk of echocardiographic LVH: compared with patients with neither ECG criteria for LVH, patients with only Sokolow-Lyon voltage criteria had a 1.2-fold increased risk of echocardiographic LVH, those with only Cornell product criteria had a 2.7-fold increased risk, and patients with both ECG criteria had a 4.1-fold increased risk of echocardiographic LVH (P < .001). CONCLUSIONS: Persistent ECG LVH between screening and LIFE study baseline identified patients with greater LV mass and a higher prevalence of echocardiographic LVH, suggesting that these patients may be at higher risk for subsequent morbid and mortal events.

Aged↗

Functional impairment of CD8(+) T cells by regulatory T cells during persistent retroviral infection.

The establishment of viral persistence generally requires evasion of the host CD8(+) T cell response. Here we describe a form of evasion wherein the CD8(+) T cells are fully capable of recognizing their cognate antigen but their effector functions are suppressed by regulatory T cells. Virus-specific CD8(+) T cells adoptively transferred into mice persistently infected with Friend virus proliferated and appeared activated, but failed to produce IFNgamma or reduce virus loads. Cotransfer experiments revealed that a subpopulation of CD4(+) T cells from persistently infected mice suppressed IFNgamma production by the CD8(+) T cells. Treatment of persistently infected mice with anti-GITR antibody to ameliorate suppression by regulatory T cells significantly improved IFNgamma production by transferred CD8(+) T cells and allowed a significant reduction in viral loads. The results indicate that CD4(+) regulatory T cells contribute to viral persistence and demonstrate an immunotherapy for treating chronic retroviral infections.

Acute Disease↗

Minimal persistent inflammation, an emerging concept in the nature and treatment of allergic rhinitis: the possible role of leukotrienes.

OBJECTIVE: To review the emerging concept of minimal persistent inflammation in allergic rhinitis and its implications for therapy. DATA SOURCES: Relevant clinical studies in the English language were reviewed. STUDY SELECTION: Material was taken from academic/scholarly journals. RESULTS: Accumulating evidence suggests that allergic rhinitis is a chronic inflammatory disease instead of a disease of acute symptoms. An approach to the therapy for allergic rhinitis should consider that even when symptoms are absent, a minimal level of persistent inflammation may persist. To prevent unexpected exacerbations, the treatment strategy may need to include managing subclinical persistent inflammation. Therapeutic options addressing the major inflammatory elements in allergic rhinitis, including eosinophils, the cysteinyl leukotrienes, and histamine, must be evaluated as management strategies that can achieve effective control. Traditional medications include intranasal corticosteroids, antihistamines, and immunotherapy. Recently, a leukotriene receptor antagonist has been approved for major rhinitis symptoms (congestion, rhinorrhea, sneezing, and pruritus), suggesting a new option for the treatment of allergic rhinitis. CONCLUSIONS: Because of the possible presence of a minimal persistent inflammation during rhinitis patients' asymptomatic periods, it is important to consider a prophylactic approach to treating allergic rhinitis to prevent or reduce exacerbations during an acute increase in allergen. In light of the advances in the understanding of the pathogenesis of allergic rhinitis, agents must be considered based on their safety, efficacy, and ability to deal with underlying inflammation as well as symptom relief.

Histamine↗

Spinal mechanisms of acute and persistent pain.

Although there is considerable information about the mechanisms through which injury stimuli produce acute pain, recent studies indicate that there are significant long-term consequences of persistent injury. Pain is exacerbated, in part, because of a reorganization of spinal cord circuitry in the setting of persistent injury. This review describes our studies of the contribution of the primary afferent neurotransmitter, substance P (SP), to these changes. By following internalization of the SP receptor in spinal cord dorsal horn neurons, we have identified the stimuli that evoke SP release and the neurons that respond to these stimuli. Importantly, based on the intensities of stimuli required to evoke internalization, we conclude that SP is only released under conditions in which severe pain would be produced, that the release can be evoked by intense stimulation of somatic and visceral tissue, and that multiple stimulus modalities are effective. We also found that the numbers of neurons that are influenced increases dramatically in the setting of inflammation. Using a knockout strategy, we have also raised mice with a deletion of the preprotachykinin-A (PPT-A) gene, which encodes for SP and neurokinin A (NKA), and have identified a specific behavioral phenotype in which the animals do not detect a window of "pain" intensities; this window cuts across stimulus modalities. These results provide an important behavioral correlate of the receptor internalization studies. On the other hand, the allodynia (lowered pain threshold) that occurs in the setting of injury was not altered in these animals. Among the factors that could underlie injury-induced allodynia are the second messenger systems that are activated in dorsal horn neurons. Our studies have recently implicated the gamma isoform of protein kinase C (PKCgamma) in the development of nerve injury-induced neuropathic pain. Specifically, we found that although acute pain responses of mice with a deletion of PKCgamma are not altered, partial injury to the sciatic nerve (which induces a severe thermal and mechanical allodynia in the wild type mouse) is without effect in the knockout. Furthermore, the anatomical/neurochemical reorganization that typically follows sciatic nerve section does not occur in the PKCgamma mutant mice. Because the spinal cord distribution of interneurons that express PKCgamma is concentrated almost exclusively in the inner part of lamina II, we believe that changes in the properties of these neurons are key to the development of nerve injury-induced neuropathic pain conditions. Taken together, these studies emphasize that persistent pain should be considered a disease state of the nervous system, not merely a symptom of some other disease conditions. In the setting of persistent injury, the nervous system undergoes dramatic changes that exacerbate and prolong the pain condition. Our studies underscore the importance of preventing the long-term changes that result from persistent injury.

Acute Disease↗

Persistence and transmission of tick-borne viruses: Ixodes ricinus and louping-ill virus in red grouse populations.

The population dynamics of tick-borne disease agents and in particular the mechanisms which influence their persistence are examined with reference to the flavivirus that causes louping-ill in red grouse and sheep. Pockets of infection cause heavy mortality and the infection probably persists as a consequence of immigration of susceptible hosts. Seroprevalence is positively associated with temporal variations in vectors per host, although variation between areas is associated with the abundance of mountain hares. The presence of alternative tick hosts, particularly large mammals, provides additional hosts for increasing tick abundance. Grouse alone can not support the vectors and the pathogen but both can persist when a non-viraemic mammalian host supports the tick population and a sufficiently high number of nymphs bite grouse. These alternative hosts may also amplify virus through non-viraemic transmission by the process of co-feeding, although the relative significance of this has yet to be determined. Another possible route of infection is through the ingestion of vectors when feeding or preening. Trans-ovarial transmission is a potentially important mechanism for virus persistence but has not been recorded with louping-ill and Ixodes ricinus. The influence of non-viraemic hosts, both in the multiplication of vectors and the amplification of virus through non-viraemic transmission are considered significant for virus persistence.

Animals↗

Lifetime risk and persistence of psychiatric disorders across ethnic groups in the United States.

BACKGROUND: Recent research in the United States has demonstrated striking health disparities across ethnic groups. Despite a longstanding interest in ethnic disadvantage in psychiatric epidemiology, patterns of psychiatric morbidity across ethnic groups have never been examined in a nationally representative sample. METHOD: Ethnic differences in psychiatric morbidity are analyzed using data from the National Comorbidity Survey (NCS). The three largest ethnic groups in the United States--Hispanics, Non-Hispanic Blacks and Non-Hispanic Whites were compared with respect to lifetime risk and persistence of three categories of psychiatric disorder: mood disorder, anxiety disorder, and substance use disorder. RESULTS: Where differences across ethnic groups were found in lifetime risk, socially disadvantaged groups had lower risk. Relative to Non-Hispanic Whites, Hispanics had lower lifetime risk of substance use disorder and Non-Hispanic Blacks had lower lifetime risk of mood, anxiety and substance use disorders. Where differences were found in persistence of disorders, disadvantaged groups had higher risk. Hispanics with mood disorders were more likely to be persistently ill as were Non-Hispanic Blacks with respect to both mood disorders and anxiety disorders. Closer examination found these differences to be generally consistent across population subgroups. CONCLUSIONS: Members of disadvantaged ethnic groups in the United States do not have an increased risk for psychiatric disorders. Members of these groups, however, do tend to have more persistent disorders. Future research should focus on explanations for these findings, including the possibility that these comparisons are biased, and on potential means of reducing the disparity in persistence of disorders across ethnic groups.

Adolescent↗

Self-devaluative dysphoric experience and the prediction of persistent first-episode major depressive disorder in adolescents.

BACKGROUND: The quality of subjective experience of dysphoria may predict persistence of depression, independently of severity. This is tested in a clinic sample of adolescents with first episode of major depression using the Depressed States Checklist adapted for adolescents. METHOD: Ninety-four adolescents with DSM-IV major depressive disorder (MDD) were followed up at 12 months. Self-devaluative components of dysphoric experience, ruminative style, over-general autobiographical memory, and self-reported and observer-rated measures of depression severity were assessed at presentation and evaluated as predictors of persistent MDD. RESULTS: Persistent MDD was predicted by the independent additive effects of the higher self-devaluative component of dysphoria, lower general intelligence and greater observer-rated severity of depression at presentation. Neither self-reported depression score, overgeneral memory retrieval nor ruminative style contributed. CONCLUSIONS: High levels of self-devaluative dysphoric experience increase the liability for persistence of first-episode MDD. Other affective-cognitive components also contribute. The adolescent version of the Depressed States Checklist is a useful brief measure of cognitive vulnerability for persistence in currently depressed young people.

Adolescent↗

Parent participation in community activities and the persistence of criminality.

This study assessed whether the lack of parental participation in community activities during late childhood is significantly related to the persistence of criminal activity from adolescence to adulthood. A prospective, longitudinal investigation of a representative cohort of 548 boys from a middle-sized Swedish community was employed. A pattern-oriented analysis identified five configurations of boys who showed different profiles of social and academic competence at the age of 13 years. The configurations were compared with respect to persistent criminality among the boys for parents who did, and who did not, show stable participation in a community activity when their sons were in late childhood. Fathers engaged in a community activity had sons with significantly lower rates of persistent criminality. This result was most marked for youth with low school achievement, and multiple problem profiles of social and academic disadvantage. The findings held after controlling for family socioeconomic status. Mother's participation in community activities was statistically dependent on father participation but was not related to persistent offending among multiple problem boys. Results are discussed in terms of the different impact associated with mother and father community activity participation on persistent offending, and the holistic perspective to development guiding this research.

Adolescent↗