Impact of maternal trauma-related psychopathology and life stress on HPA axis stress response

To understand and curb intergenerational transmission of stress-related disorder, it is important to identify how trauma-related psychopathology in mothers impacts their psychophysiological stress regulation, particularly in the context of parenting their infants. In this study we investigated associations between mothers’ trauma-related psychopathology and life stress and HPA axis response to a personally relevant stressor (infant separation stress) in a non-clinical sample followed longitudinally postpartum. A community sample of low-income mothers (n = 73) and their infants completed laboratory sessions at 3, 6, 12, and 18 months postnatal, and salivary cortisol samples collected before and after dyadic stress tasks at the latter three sessions. These tasks were used to assess HPA function. A three-level hierarchical linear model of repeated cortisol measures nested within sessions within mother-infant dyads did not reveal significant main effects of trauma-related psychopathology on maternal cortisol response, but there was evidence that both a clinical interviewer-rated diagnosis of PTSD and ongoing self-reported trauma symptoms blunted effects of life events on cortisol reactivity. Region of significance analyses indicated that current life stress predicted more pronounced cortisol reactivity only among mothers without trauma-related psychopathology; for those with trauma-related psychopathology, life stress did not relate to cortisol response. Effects held when controlling for childhood trauma and previous (prenatal) maternal distress symptoms, suggesting they did not reflect ongoing impacts of past trauma exposure and/or psychopathology. Blunting effects of trauma-related psychopathology on maternal life stress responsiveness may help clarify how stress sensitivities and mental health are transmitted from parent to child.

     

Pregnancy during the COVID-19 pandemic: a qualitative examination of ways of coping

Archives of Women's Mental Health - The COVID-19 pandemic and related public health restrictions have impacted the mental health and coping strategies of many population groups, including...     

Analysis of the tyrosine phosphorylation and calcium fluxing of human CD6 isoforms with different cytoplasmatic domains

CD6 is a cell surface glycoprotein that functions both as a co-stimulatory and adhesion receptor on T cells. Recently we have described CD6 isoforms (CD6a, b, c, d, e) that arise via alternative splicing of exons encoding the cytoplasmic region of the molecule. CD6 becomes phosphorylated on tyrosine (Tyr) residues following stimulation through the T cell receptor (TCR) complex. Since the phosphorylation of Tyr residues renders some cell surface receptors competent for interactions with proteins of intracellular signaling pathways, we wanted to determine which region(s) and residues in the cytoplasmic domain of CD6 were important for phosphorylation on Tyr residues. We engineered and stably expressed chimeric receptors that consisted of the extracellular region of mouse CD6 and the cytoplasmic regions of either naturally occurring isoforms of human CD6, truncated proteins, or point mutants. We were able to demonstrate that of the nine Tyr residues in the cytoplasmic domain of the largest isoform CD6a, the two C-terminal Tyr residues (Tyr 629/662) are critical for the phosphorylation of CD6 following TCR cross-linking. Isoform CD6e, which is missing a region that contains two proline-rich motifs, is not phosphorylated. We further analyzed the ability of the different CD6 isoforms and truncated receptors to mobilize intracellular calcium after CD6/TCR co-ligation. All CD6 isoforms, including CD6e, as well as the truncation mutant Δ 555, which is missing approximately the C-terminal half of the cytoplasmic domain, are able to increase Ca²⁺ influx. Taken together, these results suggest that the region of CD6 which is critical for Ca²⁺ mobilization is located N-terminal from amino acid 555 and is therefore different from the region located at the C terminus of CD6, which is necessary for tyrosine phosphorylation.     

Clinical outcome of frequent exposure to Torque Teno virus (TTV) through blood transfusion in thalassemia patients with or without hepatitis C virus (HCV) infection

As a consequence of the high prevalence of TorqueTeno virus (TTV) in blood donors, thalassemia patients frequently acquire various genotypes of this virus through therapeutic blood transfusions. At present, the clinical consequences of TTV infection remain indeterminate for these patients. Here, several hundred thalassemia patients were tested for the presence of TTV and its genotypes using a combination of PCR and clone-based DNA sequencing. Approximately 10% (12/118) of the patients aged 2-20 years remained negative for TTV including eight genotypes of SENV. Ferritin, aspartate-aminotransferase (AST) and alanine-aminotransferase (ALT) levels were invariably lower in TTV-negative patients (P = 0.02, <0.01, and 0.06, respectively) than in TTV-positive patients. Patients with TTV-HCV co-infection showed elevated ferritin and ALT levels compared with patients with TTV infection alone (P < 0.02 and P < 0.01). AST and ALT levels were within the normal range for all TTV-negative patients, whereas abnormal levels of AST and ALT were seen in a significant proportion of TTV-positive patients (30.7% and 33.6%, respectively) and patients with TTV-HCV co-infections (70.0% and 56.6%, respectively). Only TTV-positive patients (28.0%) and patients with TTV-HCV co-infections (36.3%) had hyper-ferritin levels (> or =3,000 ng/ml). The genotype(s) of TTV responsible for the liver dysfunction could not be determined. However, high levels of AST and ALT were found to be correlated with detection of a higher number of TTV genotypes in the patients. The data suggests that frequent and persistent TTV infection through blood transfusion is associated with hepatic dysfunction and/or damage in transfusion dependent thalassemia patients.     

A new method for determining lumbar spine motion using Bayesian belief network

A Bayesian network dynamic model was developed to determine the kinematics of the intervertebral joints of the lumbar spine. Radiographic images in flexion and extension postures were used as input data for modeling, together with movement information from the skin surface using an electromagnetic motion tracking system. Intervertebral joint movements were then estimated by the graphic network. The validity of the model was tested by comparing the predicted position of the vertebrae in the neutral position with those obtained from the radiographic image in the neutral posture. The correlation between the measured and predicted movements was 0.99 (p < 0.01) with a mean error of less than 1.5°. The movement sequence of the various vertebrae was examined based on the model output, and wide variations in the kinematic patterns were observed. The technique is non-invasive and has potential to be used clinically to measure the kinematics of lumbar intervertebral movement. This work was supported by the Hong Kong Research Grant Council (Competitive Earmarked Research Grant CERG CUHK5251/04E).