Attachment insecurities, emotion dynamics and stress in intimate relationships during the transition to parenthood.

BACKGROUND: In intimate relationships, which are characterized by emotional interdependence, partners act as attachment figures which serve emotion regulation functions. The experience of emotions as well as the strategies that partners use to regulate them and to respond to relational experiences, especially during stressful periods, differ greatly according to their attachment orientation. An important aspect in emotion dynamics is emotional inertia, which reflects the degree to which a person's current affective state is resistant to change on a moment-to-moment basis. Inertia has been related to maladaptive emotion regulation strategies, like suppression and rumination, preferentially used by highly anxious and avoidant individuals. The aim of this study is to examine associations between attachment orientations and reports on the experience of positive and negative affect, and their dynamics in daily life across the transition to parenthood. METHODS: Longitudinal data from a sample of 152 mixed-gender couples collected across the transition to parenthood was analyzed. We predicted that individuals with a more insecure attachment would report more negative and less positive affect, and that their emotional experience would be more resistant to change over time. We explored effects when participants reported feeling stressed. RESULTS: The data suggested that attachment anxiety was associated with less positive and more negative affect and that attachment avoidance was associated with more positive affect. Anxious individuals showed lower emotional inertia and not higher as we expected. Reported stress for anxious and avoidant individuals was significantly associated with more negative but not less positive affect. CONCLUSIONS: Results are discussed in the light of their impact on couples during stressful periods. Differences between anxiety and avoidance are found, emphasizing the importance of attachment insecurities on the experience of emotion. Furthermore, our findings on momentary fluctuating affect offer complementary insight into the emotional functioning of individuals with different attachment orientations.

ER stress and SREBP-1 activation are implicated in beta-cell glucolipotoxicity.

The reduction in insulin secretory capacity and beta-cell mass observed in type 2 diabetes is thought to be caused by glucolipotoxicity secondary to hyperglycemia and hyperlipidemia. Our aim in this study was to elucidate the underlying molecular mechanisms. We found a strong correlation between chronic high-glucose treatment and SREBP-1c activation in INS-1 cells and rat islets. Both high-glucose treatment and SREBP-1c activation in INS-1 cells resulted in lipid accumulation, impaired glucose-stimulated insulin secretion, apoptosis, and strikingly similar gene expression patterns, including upregulation of lipogenic and pro-apoptotic genes and downregulation of IRS2, Bclxl and Pdx1. These lipotoxic effects of high glucose were largely prevented by induction of a dominant-negative mutant of SREBP-1c, suggesting SREBP-1c is a major factor responsible for beta cell glucolipotoxicity. Moreover, overexpression of another lipogenic transcription factor, ChREBP, in INS-1 cells did not cause lipotoxicity. Intriguingly, chronic high glucose treatment in INS-1 cells led to pronounced induction of the ER stress marker genes, BIP and Chop10. Treatment of rat islets with both chronic high glucose and two ER stress inducers, thapsigargin and tunicamycin, enhanced SREBP-1 binding to the human IRS2 promoter. These results suggest that SREBP-1 activation caused by ER stress is implicated in beta-cell glucolipotoxicity.

Synaptotagmin V and IX isoforms control Ca2+ -dependent insulin exocytosis.

Synaptotagmin (Syt) is involved in Ca2+ -regulated secretion and has been suggested to serve as a general Ca2+ sensor on the membrane of secretory vesicles in neuronal cells. Insulin exocytosis from the pancreatic beta-cell is an example of a Ca2+ -dependent secretory process. Previous studies have yielded conflicting results as to which Syt isoform is present on the secretory granules in the native beta-cell. Here we show by western blotting and RT-PCR analysis, the presence of both Syt V and Syt IX in rat pancreatic islets and in the clonal beta-cell line INS-1E. The subcellular distribution of the two Syt isoforms was assessed by confocal microscopy and by sedimentation in a continuous sucrose density gradient in INS-1E cells. These experiments show that both proteins colocalize with insulin-containing secretory granules but are absent from synaptic-like microvesicles. Further immunofluorescence studies performed in primary pancreatic endocrine cells revealed that Syt V is present in glucagon-secreting alpha-cells, whereas Syt IX is associated with insulin granules in beta-cells. Transient overexpression of Syt V and Syt IX did not alter exocytosis in INS-1E cells. Finally, reduction of the expression of both Syt isoforms by RNA interference did not change basal secretion. Remarkably, hormone release in response to glucose was selectively and strongly reduced, indicating that Syt V and Syt IX are directly involved in the Ca2+ -dependent stimulation of exocytosis.

Double trisomy (48,XXY,+21) in monozygotic twins: case report and review of the literature.

The occurrence of double aneuploidy in the same individual is a relatively rare phenomenon. We describe twin newborns with typical clinical features of Down's syndrome, of which one revealed 48,XXY,+21 GTG-band karyotype. The second newborn died 2 days after its birth, and was clinically diagnosed having Down syndrome. Due to the same clinical features of the twins, the common placenta and amniotic sac, we speculate that they were monozygotics and as a result the second newborn should also be a Klinefelter. The purpose of this report is to present a rare case of possible coincidence of double aneuploidy in newborn twins. A review of the literature showed that double trisomy (48,XXY,+21) in a twin newborn infant has never occurred.