Peer Smoking, Other Peer Attributes, and Adolescent Cigarette Smoking: A Social Network Analysis

Peer attributes other than smoking have received little attention in the research on adolescent smoking, even though the developmental literature suggests the importance of multiple dimensions of adolescent friendships and peer relations. Social network analysis was used to measure the structure of peer relations (i.e., indicators of having friends, friendship quality, and status among peers) and peer smoking (i.e., friend and school smoking). We used three-level hierarchical growth models to examine the contribution of each time-varying peer variable to individual trajectories of smoking from age 11 to 17 while controlling for the other variables, and we tested interactions between the peer structure and peer smoking variables. Data were collected over five waves of assessment from a longitudinal sample of 6,579 students in three school districts. Findings suggest a greater complexity in the peer context of smoking than previously recognized.     

Further refining the stress-coping model of alcohol involvement

Informed by the optimal match hypothesis, the current study examined whether coping styles differentially moderate the relation between stress and alcohol use depending on the type of stressor experienced and coping style under consideration. Gender differences in these moderated relations were also examined. A sample of 83 college students completed surveys repeatedly administered over 1 month. Specificity in the roles of coping and stress in predicting heavy alcohol use was found. As compared to women, men were at greater risk for alcohol involvement associated with social adjustment and school problems given a limited active coping style. Men also showed greater alcohol involvement associated with relationship stress given a limited support seeking style but less heavy alcohol use was associated with relationship stress given a limited active coping style.     

The role of Janus Kinase 2 V617F mutation in extramedullary hematopoiesis of the spleen in neoplastic myeloid disorders.

Extramedullary hematopoiesis (EMH) in the spleen is a characteristic feature of the chronic myeloproliferative disorders (CMPDs) and various other neoplastic or reactive myeloid conditions. However, the origin of these hematopoietic precursor cells and the molecular mechanisms underlying their development in the spleen is uncertain. The V617F mutation in the Janus Kinase 2 gene (JAK2(V617F)) was recently shown to be frequently and preferentially present in the peripheral blood and bone marrow cells of CMPD patients, and the resulting dysregulation of its downstream targets is important to CMPD pathogenesis. To determine the occurrence and potential role of JAK2(V617F) in splenic EMH cells, we studied splenectomy specimens from 47 patients with significant EMH. JAK2(V617F) was detected by real-time PCR melting curve analysis in 22 specimens, including 11/17 chronic idiopathic myelofibrosis, 7/7 polycythemia vera, 1/1 essential thrombocythemia, 1/3 CMPD unclassifiable, 1/5 chronic myelomonocytic leukemia, 0/5 chronic myelogenous leukemia, 1/3 myelodysplastic syndrome and 0/6 acute myeloblastic leukemia cases, whereas only the JAK2 wild-type allele was detected in the other 25. Nineteen of 20 cases with adequate bone marrow samples available for molecular examination demonstrated concordant JAK2 genotypes. Laser-capture microdissection was then used to enrich the EMH and non-EMH splenic cell fractions, confirming that the mutant alleles specifically originated from the EMH cells. Furthermore, megakaryocytes in the JAK2(V617F)-positive splenectomy specimens expressed higher levels of Bcl-xL, an antiapoptotic protein and downstream target of the JAK2/STAT5 pathway. Thus, JAK2(V617F) is frequently present in splenic EMH cells associated with CMPD, but it is rarely identified in splenic EMH cells associated with other myeloid disorders. Our results indicate that the precursor cells leading to extramedullary hematopoietic expansion in CMPD most likely originate from the transformed bone marrow clone. Also, dysregulation of downstream pathways such as Bcl-xL may be important to CMPD disease pathogenesis in the spleen.     

Atypical acinar cell foci in human pancreas

Summary Conclusion The morphological and quantitative findings of the present study suggest that atypical acinar cell foci are not neoplastic in nature. Background Atypical acinar cell foci (AACF) are rare and unusual lesions in the human pancreas. The biological nature of AACF is poorly understood, and is not clear whether they represent neoplastic or degenerative changes in the acinar cells. Methods To further characterize and understand the significance of AACF in relation to acinar cell tumor development, we have examined these lesions by light and electron microscopy and evaluated the growth pattern by measuring cell proliferation and the size of the foci in the pancreas of a 16-yr-old male. Results The pancreas was grossly unremarkable. AACF were randomly distributed throughout the pancreas, well delineated, and showed minimal variation in sizes. The constituent, cells contained uniform nuclei, pale vacuolated cytoplasm, and exhibited low nuclear-cytoplasmic ratio. Electron microscopic examination showed a few zymogen granules and markedly dilated rough endoplasmic reticulum. Proliferative index in AACF (13%) was less than in adjacent uninvolved acinar tissue (19%). Quantitative stereological analysis showed the pancreas to contain approximately 1800 AACF/cm³ with a mean focal diameter of 360 μm.     

Defining risk heterogeneity for internalizing symptoms among children of alcoholic parents

Adopting a developmental epidemiology perspective, the current study examines sources of risk heterogeneity for internalizing symptomatology among children of alcoholic parents (COAs). Parent-based factors, including comorbid diagnoses and the number of alcoholic parents in the family, as well as child-based factors, namely child gender, formed the indicators of heterogeneity. Following a novel approach to cross-study methods, we present a three-stage analysis involving measurement development using item response theory, examination of study effects on latent trajectories over time using latent curve modeling, and prediction of these latent trajectories testing our theoretically derived hypotheses in two longitudinal investigations across both mother- and self-reported symptomatology. Specifically, we replicated previous findings that parent alcoholism has a unique effect on child internalizing symptoms, above and beyond those of both parent depression and antisocial personality disorder. However, we also found important subgroup differences, explaining heterogeneity within COAs' risk profile in terms of the number of alcoholic parents in the family, comorbid diagnoses for the alcoholic parent and, for self-reported symptoms, child gender. Such factors serve to refine the definition of risk among COAs, suggesting a more severely impaired target group for preventive interventions, identifying the significance of familial alcoholism in individual differences underlying internalizing symptoms over time, and further specifying the distal risk matrix for an internalizing pathway to alcohol involvement.