Rumination in Early Adolescent Girls: Interactive Contributions of Mother–Adolescent Relationship Quality and Maternal Coping Suggestions

Research suggests that rumination places adolescents at risk for psychopathology. However, little is known about the association between parenting and rumination. Moreover, relevant theoretical models suggest that parents contribute to the development of rumination both explicitly through their suggestions about how to cope and implicitly through the context of the mother–adolescent relationship. However, prior work has not examined implicit and explicit factors within the same investigation, precluding exploration of their unique and interactive effects. To address these gaps, the present study examined links between mother–adolescent relationship quality, maternal coping suggestions, and adolescent rumination. Participants were early adolescent girls (M age = 12.41 years) and their primary female caregivers. Findings suggested that maternal disengagement suggestions and mother–adolescent relationship quality were each uniquely associated with adolescent rumination. Moreover, the effect of maternal disengagement suggestions depended on the level of maternal engagement suggestions and mother–adolescent relationship quality. Follow-up analyses revealed that these findings were specific to the maladaptive ruminative brooding component of rumination. Future directions for research were elaborated.     

Absence of IFNγ expression induces neuronal degeneration in the spinal cord of adult mice

Background  

Interferon gamma (IFNγ) is a pro-inflammatory cytokine, which may be up-regulated after trauma to the peripheral or central nervous system. Such changes include reactive gliosis and synaptic plasticity that are considered important responses to the proper regenerative response after injury. Also, IFNγ is involved in the upregulation of the major histocompatibility complex class I (MHC class I), which has recently been shown to play an important role in the synaptic plasticity process following axotomy. There is also evidence that IFNγ may interfere in the differentiation and survival of neuronal cells. However, little is known about the effects of IFNγ absence on spinal cord neurons after injury.     

Elastomechanical properties of bovine veins

Veins have historically been discussed in qualitative, relative terms: “more compliant” than arteries, subject to “lower pressures”. The structural and compositional differences between arteries and veins are directly related to the different functions of these vessels. Veins are often used as grafts to reroute flow from atherosclerotic arteries, and venous elasticity plays a role in the development of conditions such as varicose veins and valvular insufficiency. It is therefore of clinical interest to determine the elastomechanical properties of veins. In the current study, both tensile and vibration testing are used to obtain elastic moduli of bovine veins. Representative stress–strain data are shown, and the mechanical and failure properties reported. Nonlinear and viscoelastic behavior is observed, though most properties show little strain rate dependence. These data suggest parameters for constitutive modeling of veins and may inform the design and testing of prosthetic venous valves as well as vein grafts.     

Comparison of Calcaneal Ultrasound and DXA to Assess the Risk of Corticosteroid-Induced Osteoporosis: A Cross-sectional Study

Patients on long-term oral corticosteroids have an increased risk of low bone mass and fragility fractures. Fracture risk rises soon after commencement of corticosteroid therapy and it is possible that these agents adversely influence bone architecture disproportionately to their effect on bone mass. The best means of assessing bone status in patients using corticosteroids remains uncertain, but quantitative ultrasound of the calcaneus may provide evidence of microarchitectural changes not detected by dual-energy X-ray absorptiometry (DXA). Patients with Crohn’s disease have an increased risk of low bone mineral density (BMD), the etiology of which is multifactorial but includes corticosteroid use. We studied 118 consecutive patients with Crohn’s disease, 21 of whom used continuous oral corticosteroids, 70 of whom were intermittent users, and 27 who had never used the drug. All patients received DXA of the lumbar spine, hip and calcaneus and quantitative ultrasound (QUS) of the calcaneus. The different techniques were compared using a femoral neck T-score ≤−1.5 as the threshold of corticosteroid-induced osteoporosis. When compared with the femoral neck T-score, there were no significant differences between the predictive values of lumbar spine DXA, calcaneal DXA or calcaneal QUS to identify low femoral neck BMD. However, the absolute T-score required to give similar discriminatory capacity to femoral neck T-score varied substantially (T=−0.81 to −1.5) between the different measurement techniques and sites. Received: 29 July 2000 / Accepted: 9 April 2001     

Crystal structure of the HIV-1 integrase catalytic core and C-terminal domains: a model for viral DNA binding

Insolubility of full-length HIV-1 integrase (IN) limited previous structure analyses to individual domains. By introducing five point mutations, we engineered a more soluble IN that allowed us to generate multidomain HIV-1 IN crystals. The first multidomain HIV-1 IN structure is reported. It incorporates the catalytic core and C-terminal domains (residues 52-288). The structure resolved to 2.8 A is a Y-shaped dimer. Within the dimer, the catalytic core domains form the only dimer interface, and the C-terminal domains are located 55 A apart. A 26-aa alpha-helix, alpha6, links the C-terminal domain to the catalytic core. A kink in one of the two alpha6 helices occurs near a known proteolytic site, suggesting that it may act as a flexible elbow to reorient the domains during the integration process. Two proteins that bind DNA in a sequence-independent manner are structurally homologous to the HIV-1 IN C-terminal domain, suggesting a similar protein-DNA interaction in which the IN C-terminal domain may serve to bind, bend, and orient viral DNA during integration. A strip of positively charged amino acids contributed by both monomers emerges from each active site of the dimer, suggesting a minimally dimeric platform for binding each viral DNA end. The crystal structure of the isolated catalytic core domain (residues 52-210), independently determined at 1.6-A resolution, is identical to the core domain within the two-domain 52-288 structure.     

On the mechanism of sensing unfolded protein in the endoplasmic reticulum

Unfolded proteins in the endoplasmic reticulum (ER) activate the ER transmembrane sensor Ire1 to trigger the unfolded protein response (UPR), a homeostatic signaling pathway that adjusts ER protein folding capacity according to need. Ire1 is a bifunctional enzyme, containing cytoplasmic kinase and RNase domains whose roles in signal transduction downstream of Ire1 are understood in some detail. By contrast, the question of how its ER-luminal domain (LD) senses unfolded proteins has remained an enigma. The 3.0-A crystal structure and consequent structure-guided functional analyses of the conserved core region of the LD (cLD) leads us to a proposal for the mechanism of response. cLD exhibits a unique protein fold and is sufficient to control Ire1 activation by unfolded proteins. Dimerization of cLD monomers across a large interface creates a shared central groove formed by alpha-helices that are situated on a beta-sheet floor. This groove is reminiscent of the peptide binding domains of major histocompatibility complexes (MHCs) in its gross architecture. Conserved amino acid side chains in Ire1 that face into the groove are shown to be important for UPR activation in that their mutation reduces the response. Mutational analyses suggest that further interaction between cLD dimers is required to form higher-order oligomers necessary for UPR activation. We propose that cLD directly binds unfolded proteins, which changes the quaternary association of the monomers in the membrane plane. The changes in the ER lumen in turn position Ire1 kinase domains in the cytoplasm optimally for autophosphorylation to initiate the UPR.