Early Adolescent Depressive Symptoms: Prediction from Clique Isolation, Loneliness, and Perceived Social Acceptance

This study examined whether clique isolation predicted an increase in depressive symptoms and whether this association was mediated by loneliness and perceived social acceptance in 310 children followed from age 11–14 years. Clique isolation was identified through social network analysis, whereas depressive symptoms, loneliness, and perceived social acceptance were assessed using self ratings. While accounting for initial levels of depressive symptoms, peer rejection, and friendlessness at age 11 years, a high probability of being isolated from cliques from age 11 to 13 years predicted depressive symptoms at age 14 years. The link between clique isolation and depressive symptoms was mediated by loneliness, but not by perceived social acceptance. No sex differences were found in the associations between clique isolation and depressive symptoms. These results suggest that clique isolation is a social risk factor for the escalation of depressive symptoms in early adolescence. Implications for research and prevention are discussed

Schwann cell myelination requires Dynein function

<p>Abstract</p> <p>Background</p> <p>Interaction of Schwann cells with axons triggers signal transduction that drives expression of Pou3f1 and Egr2 transcription factors, which in turn promote myelination. Signal transduction appears to be mediated, at least in part, by cyclic adenosine monophosphate (cAMP) because elevation of cAMP levels can stimulate myelination in the absence of axon contact. The mechanisms by which the myelinating signal is conveyed remain unclear.</p> <p>Results</p> <p>By analyzing mutations that disrupt myelination in zebrafish, we learned that Dynein cytoplasmic 1 heavy chain 1 (Dync1h1), which functions as a motor for intracellular molecular trafficking, is required for peripheral myelination. In <it>dync1h1</it> mutants, Schwann cell progenitors migrated to peripheral nerves but then failed to express Pou3f1 and Egr2 or make myelin membrane. Genetic mosaic experiments revealed that robust Myelin Basic Protein expression required Dync1h1 function within both Schwann cells and axons. Finally, treatment of <it>dync1h1</it> mutants with a drug to elevate cAMP levels stimulated myelin gene expression.</p> <p>Conclusion</p> <p>Dync1h1 is required for retrograde transport in axons and mutations of Dync1h1 have been implicated in axon disease. Our data now provide evidence that Dync1h1 is also required for efficient myelination of peripheral axons by Schwann cells, perhaps by facilitating signal transduction necessary for myelination.</p

Renal artery stenosis and abdominal aorta aneurysm in patients with pseudoexfoliation syndrome

PURPOSE: To evaluate the renal arteries and abdominal aorta in patients with pseudoexfoliation syndrome (PEX). DESIGN: Prospective, case–control study. METHODS: The study involved 49 patients with PEX and 42 control subjects. Abdominal aorta and renal arteries were examined by Doppler ultrasonography. In both renal arteries (proximal and distal portions) and abdominal aorta, the peak systolic velocity (PSV) was measured. Renal artery stenosis (RAS) was defined as the renal artery PSV >150 cm/s or renal-to-aortic ratio (RAR) >3.0. Patients who had an abdominal aortic diameter >3 cm were recorded. Computed tomographic angiography was performed to confirm these findings in patients with RAS and/or abdominal aorta aneurysm. RESULTS: The mean PSV in the proximal renal artery was 88.3 cm/s in PEX group and 79.5 cm/s in control group (P=0.314); in distal renal artery was 91.7 cm/s in PEX group and 93.0 cm/s in control group (P=0.794); in abdominal aorta was 76.0 cm/s in PEX group and 65.2 cm/s in control group (P=0.046). RAS was observed in nine patients with PEX and in only one patient without PEX (P=0.017). Seven out of 10 patients with RAS (six patients in PEX group; one patient in control group) had hypertension. Abdominal aorta aneurysm was observed in four patients in PEX group but not in control group (P=0.061). CONCLUSIONS: Our study has demonstrated that there is a significant association between PEX and RAS. The abdominal aorta aneurysm may be seen in patients with PEX

NF-κB regulates neuronal ankyrin-G via a negative feedback loop

The axon initial segment (AIS) is a neuronal compartment defined by ankyrin-G expression. We here demonstrate that the IKK-complex co-localizes and interacts with the cytoskeletal anchor protein ankyrin-G in immunoprecipitation and proximity-ligation experiments in cortical neurons. Overexpression of the 270 kDa variant of ankyrin-G suppressed, while gene-silencing of ankyrin-G expression increased nuclear factor-κB (NF-κB) activity in primary neurons, suggesting that ankyrin-G sequesters the transcription factor in the AIS. We also found that p65 bound to the ank3 (ankyrin-G) promoter sequence in chromatin immunoprecipitation analyses thereby increasing ank3 expression and ankyrin-G levels at the AIS. Gene-silencing of p65 or ankyrin-G overexpression suppressed ank3 reporter activity. Collectively these data demonstrate that p65/NF-κB controls ankyrin-G levels via a negative feedback loop, thereby linking NF-κB signaling with neuronal polarity and axonal plasticity