Citations

This study assessed continuity of problematic sexualized behaviors (PSB) over a 1-year period. Ninety-seven 10-12-year-olds in either foster boarding homes or a residential treatment center participated at Time 1. Twelve months later, 78 youth were available for a second data collection assessment. At both data collection phases, researchers interviewed foster parents or primary therapists about the youths' sexual behavior. Findings revealed significant continuity in PSB over time, with children who at Time 1 exhibited PSB significantly more likely to exhibit PSB at Time 2. The reverse was also true in that the absence of PSB at Time 1 was associated with the absence of PSB at Time 2. In addition, a subset of specific PSB behaviors was noted to be most stable, although this varied across the groups. Youth with PSB exhibited several patterns of persistence in specific behaviors over time, including continuity, a mix of continuity and change, and complete discontinuity. The persistence of PSB over time was most true for the children living in a residential treatment center, the more disturbed group studied. We conclude that the persistence of PSB is more likely when the child has other problematic behaviors.

Two samples of adolescents were studied to assess the validity of several measures of dissociation. The first sample included 70 males from a residential treatment program for adolescent sex offenders (ASO). The second were 47 psychiatric inpatients. The measures included the DSM-IV field trial questionnaire for Dissociative Disorders of Childhood, Child Dissociative Checklist, Adolescent-Dissociative Experiences Schedule, Trauma Symptom Checklist for Children, and the Dissociation Research scale. Ten of the 70 adolescent sex offender subjects (14.3%) were identified as meeting DSM-IV criteria for a Dissociation-spectrum disorder diagnosis and two (4.2%) of the psychiatric patients. Between-groups analyses with the ASO revealed significant differences on the Child Dissociative Checklist and the Dissociation Research Scale. Cumulative trauma did not differ significantly between the dissociative and nondissociative groups of ASO, but physical abuse was related to a diagnosis of dissociation in this sample. The dissociation measures were highly intercorrelated for both groups, and suggest that they measure a similar construct.

Purpose Type 6 is an open fracture in which part of the physis is missing. It is the least common physeal fracture, but has the highest rate of complications, particularly the formation of a physeal bar. Without preemptive treatment, a physeal bar always forms, producing growth retardation and angular deformity, and excision of these physeal bars has been uniformly unsuccessful. The distal medial malleolus is a common site for the fracture. Methods Strategies for the treatment of two varieties of acute medial malleolar type-6 fractures and two types of late deformities following type-6 fracture are given. The acute fractures were treated with either fat or cartilage applied to the exposed physis. The late deformities were treated with corrective iliac bone grafting. Results The acute fractures were prevented from forming physeal bars and the two late deformities were fully corrected with good outcomes. Conclusion Fat applied to an acute type-6 physeal fracture has a good chance of preventing bar formation. Ankle deformities due to bars can be corrected by means of iliac bone grafting.

Abstract Early diagnosis of the onset of osteoporosis is key to the delivery of effective therapy. Biochemical markers of bone turnover provide a means of evaluating skeletal dynamics that complements static measurements of BMD by DXA. Conventional clinical measurements of bone turnover, primarily the estimation of collagen and its breakdown products in the blood or urine, lack both sensitivity and specificity as a reliable diagnostic tool. As a result, improved tests are needed to augment the use of BMD measurements as the principle diagnostic modality. In this study, the serum proteome of 58 postmenopausal women with high or low/normal bone turnover (training set) was analyzed by surface enhanced laser-desorption/ionization time-of-flight mass spectrometry, and a diagnostic fingerprint was identified using a variety of statistical and machine learning tools. The diagnostic fingerprint was validated in a separate distinct test set, consisting of serum samples from an additional 59 postmenopausal women obtained from the same Mayo cohort, with a gap of 2 yr. Specific protein peaks that discriminate between postmenopausal patients with high or low/normal bone turnover were identified and validated. Multiple supervised learning approaches were able to classify the level of bone turnover in the training set with 80% sensitivity and 100% specificity. In addition, the individual protein peaks were also significantly correlated with BMD measurements in these patients. Four of the major discriminatory peaks in the diagnostic profile were identified as fragments of interalpha-trypsin-inhibitor heavy chain H4 precursor (ITIH4), a plasma kallikrein-sensitive glycoprotein that is a component of the host response system. These data suggest that these serum protein fragments are the serum-borne reflection of the increased osteoclast activity, leading to the increased bone turnover that is associated with decreasing BMD and presumably an increased risk of fracture. In conjunction with the identification of the individual proteins, this protein fingerprint may provide a novel approach to evaluate high bone turnover states.

Isolated torsion of the fallopian tube is a rare cause of lower abdominal pain and commonly occurs after menarche. Prompt identification of this entity can prevent irreversible vascular damage, but the diagnosis is rarely made before surgery due to nonspecific clinical and imaging features. We report a case of isolated tubal torsion with specific imaging features on preoperative computed tomography and magnetic resonance imaging.

Allosteric regulation of heteromultimeric ATP-sensitive potassium (KATP) channels is unique among protein systems as it implies transmission of ligand-induced structural adaptation at the regulatory SUR subunit, a member of ATP-binding cassette ABCC family, to the distinct pore-forming K+ (Kir6.x) channel module. Cooperative interaction between nucleotide binding domains (NBDs) of SUR is a prerequisite for KATP channel gating, yet pathways of allosteric intersubunit communication remain uncertain. Here, we analyzed the role of the ED domain, a stretch of 15 negatively charged aspartate/glutamate amino acid residues (948–962) of the SUR2A isoform, in the regulation of cardiac KATP channels. Disruption of the ED domain impeded cooperative NBDs interaction and interrupted the regulation of KATP channel complexes by MgADP, potassium channel openers, and sulfonylurea drugs. Thus, the ED domain is a structural component of the allosteric pathway within the KATP channel complex integrating transduction of diverse nucleotide-dependent states in the regulatory SUR subunit to the open/closed states of the K+-conducting channel pore.

The cardiac neural crest is a subpopulation of neural crest cells (NCCs) that originates from the dorsal neural tube and later migrates to the heart and pharyngeal arch (PA), where they contribute to distinct aspects of cardiogenesis and PA patterning. Wnt family members have been implicated in general neural crest induction; however, the molecular mechanisms underlying the specification of distinct cell types such as cardiac NCCs remain unclear. Here, we have identified cysteine-rich intestinal protein 2 ( crip2 ), a gene encoding for a LIM domain–containing protein, as a novel marker for cardiac NCCs in zebrafish. We observed a dynamic expression pattern for crip2 , with expression being detected in the premigratory NCCs in rhombomere 6 (r6), migrating NCCs, ventricular cardiomyocytes, and aortic vessels in PAs 3 to 6. Interestingly, expression of wnt3a was detected in regions of the dorsal neural tube encompassing r6, and reduction of wnt3a led to disrupted expression of crip2 in r6, abnormal migration of NCCs, and defective cardiac function, as well as PA development. Furthermore, these phenotypes could be recapitulated by reduction of crip2 and rescued by overexpression of crip2 . In summary, our data suggest a specific role for Wnt3a in the development of cardiac NCCs. We propose that this function of wnt3a in r6 is partially mediated by crip2 expression in the premigratory cardiac NCCs, which subsequently affects cardiac function and PA patterning.

Activation of complement stimulates inflammation and provides an initial vigorous defense against infection. Insertion of the membrane attack complex in cell membranes of vascular endothelial cells induces changes in cell differentiation that promote coagulation, thrombosis, inflammation, and immunity. These changes are mediated by production of interleukin (IL)-1α by endothelial cells, which acts locally on endothelial cells to contain infection and promote healing of the affected site. In healthy tissues, however, promoting coagulation and inflammation would be dysphysiologic. Accordingly, endothelial cell activation by the membrane attack complex depends on both transcriptional regulation of IL-1α and availability of that cytokine to broadly modify endothelial cell physiology. Here, we report that the IL-1α gene contains a suppressor sequence that cooperates with histone modification to regulate production of IL-1α by endothelial cells. The suppressor sequence binds C/EBP (CCAAT enhancer–binding protein) family DNA-binding proteins isolated from the nucleus of quiescent endothelial cells. These results suggest constitutive suppression of IL-1α maintains quiescence of endothelium and that terminal complement complexes remove that suppression, allowing IL-1α transcription and, ultimately, activation of endothelium to proceed.