Purpose Our goal was to examine the trajectory of bonding impairment across the first 6 months postpartum in the contexts of maternal risk, including maternal history of childhood abuse and neglect and postpartum psychopathology, and to test the association between self-reported bonding impairment and observed positive parenting behaviors. Method In a sample of women with childhood abuse and neglect (CA) histories (CA+, n=97) and a healthy control comparison group (CA-, n=53), participants completed questionnaires related to bonding with their infant at 6 weeks, 4 months, and 6 months postpartum and postpartum psychopathology at 6 months postpartum. In addition, during a 6 months postpartum home visit, mothers and infants participated in a dyadic play interaction subsequently coded for positive parenting behaviors by blinded coders. Results We found that all women independent of risk status increased in bonding to their infant over the first 6 months postpartum; however, women with postpartum psychopathology (depression and PTSD) showed consistently greater bonding impairment scores at all times points. Moreover, we found that at the 6 months assessment bonding impairment and observed parenting behaviors were significantly associated. Conclusion These results highlight the adverse effects of maternal postpartum depression and PTSD on mother-infant bonding in early postpartum in women with child abuse and neglect histories. These findings also shed light on the critical need for early detection and effective treatment of postpartum mental illness in order to prevent problematic parenting and the development of disturbed mother-infant relationships. Results support the use of the Parenting Bonding Questionnaire (PBQ) as a tool to assess parenting quality by its demonstrated association with observed parenting behaviors.

Chronic pain is a prevalent and persistent problem in middle childhood and adolescence. The biopsychosocial model of pain, which accounts for the complex interplay of the biological, psychological, social, and environmental factors that contribute to and maintain pain symptoms and related disability has guided our understanding and treatment of pediatric pain. Consequently, many interventions for chronic pain are within the realm of rehabilitation, based on the premise that behavior has a broad and central role in pain management. These treatments are typically delivered by one or more providers in medicine, nursing, psychology, physical therapy, and/or occupational therapy. Current data suggest that multidisciplinary treatment is important, with intensive interdisciplinary pain rehabilitation (IIPT) being effective at reducing disability for patients with high levels of functional disability. The following review describes the current state of the art of rehabilitation approaches to treat persistent pain in children and adolescents. Several emerging areas of interventions are also highlighted to guide future research and clinical practice.

Apolipoprotein B (apoB) is the major protein component of large lipoprotein particles that transport lipids and cholesterol. We have developed a detailed model of the first 1000 residues of apoB using standard sequence alignment programs (ClustalW and MACAW) and the MODELLER6 package for three-dimensional homology modeling. The validity of the apoB model was supported by conservation of disulfide bonds, location of all proline residues in turns and loops, and conservation of the hydrophobic faces of the two C-terminal amphipathic beta-sheets, betaA (residues 600-763) and betaB (residues 780-1000). This model suggests a lipid-pocket mechanism for initiation of lipoprotein particle assembly. In a previous model we suggested that microsomal triglyceride transfer protein might play a structural role in completion of the lipid pocket. We no longer think this likely, but instead propose a hairpin-bridge mechanism for lipid pocket completion. Salt-bridges between four tandem charged residues (717-720) in the turn of the hairpin-bridge and four tandem complementary residues (997-1000) at the C-terminus of the model lock the bridge in the closed position, enabling the deposition of an asymmetric bilayer within the lipid pocket.

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Protein translation is essential for all forms of life and is conducted by a macromolecular complex, the ribosome. Evolutionary changes in protein and RNA sequences can affect the three-dimensional organization of structural features in ribosomes in different species. The most dramatic changes occur in animal mitochondria, whose genomes have been significantly reduced and altered. The RNA component of the mitochondrial ribosome (mitoribosome) is reduced in size, with a compensatory increase in protein content. Until recently, it was unclear how these changes affect the three-dimensional structure of the mitoribosome. Here we present a structural model of the large subunit (LSU) of the mammalian mitoribosome developed by combining molecular modeling techniques with cryo-electron microscopic (cryo-EM) studies. The model contains 93% of the mitochondrial rRNA (mito-rRNA) sequence and 16 mitochondrial ribosomal proteins (MRPs) in the large subunit of the mitoribosome. Despite the smaller mitochondrial rRNA, the spatial positions of RNA domains known to be directly involved in protein synthesis are essentially the same as in Bacterial and Archaeal ribosomes. However, the dramatic reduction in rRNA content necessitates evolution of unique structural features to maintain connectivity between RNA domains. The smaller rRNA sequence also limits the likelihood of tRNA binding at E-site of the mitoribosome, and correlates with the reduced size of D-and T-loops in some animal mitochondrial tRNAs, suggesting co-evolution of mitochondrial rRNA and tRNA structures.

An initial event in atherosclerosis is the retention of lipoproteins within the intima of the vessel wall. Previously we identified Site B (residues 3359 -3369) in apolipoprotein (apo) B100 as the proteoglycan binding sequence in low density lipoproteins (LDLs) and showed that the atherogenicity of apoB-containing lipoproteins is linked to their affinity for artery wall proteoglycans. However, both apoB100-and apoB48-containing lipoproteins are equally atherogenic even though Site B lies in the carboxyl-terminal half of apoB100 and is absent in apoB48. If binding to proteoglycans is a key step in atherogenesis, apoB48-containing lipoproteins must bind to proteoglycans via other proteoglycan binding sites in the amino-terminal 48% of apoB. In vitro studies have identified five clusters of basic amino acids in delipidated apoB48 that bind negatively charged glycosaminoglycans. To determine which of these sites is functional on LDL particles, we analyzed the proteoglycan binding activity of recombinant human LDLs from transgenic mice or rat hepatoma cells. Substitution of neutral amino acids for the basic amino acids in Site B-Ib (residues 84 -94) abolished the proteoglycan binding activity of recombinant apoB53. Carboxyl-truncated apoB80 bound biglycan with higher affinity than apoB100 and apoB48. ApoB80 in which Site B was mutated had the same affinity for proteoglycans as apoB48. These data support the hypothesis that the carboxyl terminus of apoB100 "masks" Site B-Ib, the aminoterminal proteoglycan binding site, and that this site is exposed in carboxyl-truncated forms of apoB. The presence of a proteoglycan binding site in the aminoterminal region of apoB may explain why apoB48-and apoB100-containing lipoproteins are equally atherogenic.

Objective Somatic symptoms (e.g., pain, fatigue) are common after childhood cancer and are associated with greater fear of cancer recurrence and poorer health‐related quality of life (HRQoL). Qualitative studies indicate that survivors of childhood cancer (SCCs) worry about somatic symptoms as indicating cancer recurrence, which could in part explain associations between symptoms and poorer psychosocial outcomes. However, the prevalence, characteristics, and impact of symptom worry has not been quantitatively studied. Methods SCCs (N = 111; 52% female; Mage at study = 17.67 years, range = 8–25 years; Mage at diagnosis = 6.70 years) across a variety of diagnoses were recruited from a pediatric cancer center in Canada and completed self‐report measures of symptom worry, symptom frequency, general anxiety, fear of cancer recurrence, and HRQoL. Results A majority (62%) of SCCs worried about at least one symptom as a sign of recurrence. Pain was the most worrisome symptom, but SCCs also reported worrying about symptoms that are rarely associated with cancer recurrence such as hunger, dizziness, and feeling cold. Symptom worry was more strongly associated with fear of cancer recurrence than the mere frequency of those symptoms, and this relationship held while controlling for treatment factors and general anxiety. Symptom worry and frequency each explained unique variance in HRQoL. Conclusions Worry about somatic symptoms as a sign of cancer recurrence is common and may be impactful after childhood cancer. Excessive worry about somatic symptoms could be an important target to reduce fear of recurrence and increase HRQoL in SCCs.

Phytophthora pini was named by Leonian in 1925, but this species was largely ignored until 1956 and then merged with P. citricola by Waterhouse in 1963. This study compared the ex-type and exauthentic cultures of these two species with isolates of P. plurivora and the P. citricola subgroups Cil I and III reported previously. Examination of these isolates revealed that the ex-type culture of P. pini is identical to P. citricola I. Phytophthora pini Leonian therefore is resurrected to distinct species status and redescribed here with a Latin description, replacing P. citricola I. Molecular, physiological and morphological descriptions of this species are presented. The molecular description includes DNA sequences of five nuclear and mitochondrial regions as well as PCR-SSCP fingerprints. The relationship among the above species and other species recently segregated from the P. citricola complex also is discussed.