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This review is based on a multiple database survey on published literature to determine the effects on health following voluntary exposure to cold-water immersion (CWI) in humans. After a filtering process 104 studies were regarded relevant. Many studies demonstrated significant effects of CWI on various physiological and biochemical parameters. Although some studies were based on established winter swimmers, many were performed on subjects with no previous winter swimming experience or in subjects not involving cold-water swimming, for example, CWI as a post-exercise treatment. Clear conclusions from most studies were hampered by the fact that they were carried out in small groups, often of one gender and with differences in exposure temperature and salt composition of the water. CWI seems to reduce and/or transform body adipose tissue, as well as reduce insulin resistance and improve insulin sensitivity. This may have a protective effect against cardiovascular, obesity and other metabolic diseases and could have prophylactic health effects. Whether winter swimmers as a group are naturally healthier is unclear. Some of the studies indicate that voluntary exposure to cold water has some beneficial health effects. However, without further conclusive studies, the topic will continue to be a subject of debate.

Childhood maltreatment is likely to influence fundamental biological processes and engrave long-lasting epigenetic marks, leading to adverse health outcomes in adulthood. We aimed to elucidate the impact of different early environment on disease-related genome-wide gene expression and DNA methylation in peripheral blood cells in patients with posttraumatic stress disorder (PTSD). Compared with the same trauma-exposed controls (n = 108), gene-expression profiles of PTSD patients with similar clinical symptoms and matched adult trauma exposure but different childhood adverse events (n = 32 and 29) were almost completely nonoverlapping (98%). These differences on the level of individual transcripts were paralleled by the enrichment of several distinct biological networks between the groups. Moreover, these gene-expression changes were accompanied and likely mediated by changes in DNA methylation in the same loci to a much larger proportion in the childhood abuse (69%) vs. the non-child abuse-only group (34%). This study is unique in providing genome-wide evidence of distinct biological modifications in PTSD in the presence or absence of exposure to childhood abuse. The findings that nonoverlapping biological pathways seem to be affected in the two PTSD groups and that changes in DNA methylation appear to have a much greater impact in the childhood-abuse group might reflect differences in the pathophysiology of PTSD, in dependence of exposure to childhood maltreatment. These results contribute to a better understanding of the extent of influence of differences in trauma exposure on pathophysiological processes in stress-related psychiatric disorders and may have implications for personalized medicine.

Background Individual genotypes at specific loci can result in different patterns of DNA methylation. These methylation quantitative trait loci (meQTLs) influence methylation across extended genomic regions and may underlie direct SNP associations or gene-environment interactions. We hypothesized that the detection of meQTLs varies with ancestral population, developmental stage, and tissue type. We explored this by analyzing seven datasets that varied by ancestry (African American vs. Caucasian), developmental stage (neonate vs. adult), and tissue type (blood vs. four regions of postmortem brain) with genome-wide DNA methylation and SNP data. We tested for meQTLs by constructing linear regression models of methylation levels at each CpG site on SNP genotypes within 50 kb under an additive model controlling for multiple tests. Results Most meQTLs mapped to intronic regions, although a limited number appeared to occur in synonymous or nonsynonymous coding SNPs. We saw significant overlap of meQTLs between ancestral groups, developmental stages, and tissue types, with the highest rates of overlap within the four brain regions. Compared with a random group of SNPs with comparable frequencies, meQTLs were more likely to be 1) represented among the most associated SNPs in the WTCCC bipolar disorder results and 2) located in microRNA binding sites. Conclusions These data give us insight into how SNPs impact gene regulation and support the notion that peripheral blood may be a reliable correlate of physiological processes in other tissues.

This is an executive summary of a workshop on the management and counseling issues of women anticipated to deliver at a periviable gestation (broadly defined as 20 0/7 through 25 6/7 weeks of gestation), and the treatment options for the newborn. Upon review of the available literature, the workshop panel noted that the rates of neonatal survival and neurodevelopmental disabilities among the survivors vary greatly across the periviable gestations and are significantly influenced by the obstetric and neonatal management practices (for example, antenatal steroid, tocolytic agents and antibiotic administration; cesarean birth; and local protocols for perinatal care, neonatal resuscitation and intensive care support). These are, in turn, influenced by the variations in local and regional definitions of limits of viability. Because of the complexities in making difficult management decisions, obstetric and neonatal teams should confer prior to meeting with the family, when feasible. Family counseling should be coordinated with the goal of creating mutual trust, respect and understanding, and should incorporate evidence-based counseling methods. Since clinical circumstances can change rapidly with increasing gestational age, counseling should include discussion of the benefits and risks of various maternal and neonatal interventions at the time of counseling. There should be a plan for follow-up counseling as clinical circumstances evolve. The panel proposed a research agenda and recommended developing educational curricula on the care and counseling of families facing the birth of a periviable infant.

The ability to effectively regulate emotions and a secure attachment style are critical for maintaining mental health across the life span. The experience of childhood maltreatment interferes with normal development of emotional regulation and dramatically increases risk for a wide range of psychiatric disorders in adulthood. The central nervous system oxytocin systems are critically involved in mediating social attachment and buffering psychophysiological responses to stress. We therefore investigated the impact of childhood maltreatment and an oxytocin receptor (OXTR) single nucleotide polymorphism (rs53576) and their interaction on emotional dysregulation and attachment style in adulthood in a sample of low-income, African American men and women recruited from primary care clinics of an urban, public hospital. Consistent with prior research, we found that the severity of childhood maltreatment was associated with increased levels of emotional dysregulation in adulthood. Childhood maltreatment was also positively associated with ratings of disorganized/unresolved adult attachment style and negatively associated with ratings of secure adult attachment style. There was no direct association between rs53576 and emotional dysregulation or ratings of adult attachment style. However, there were significant interactions between rs53576 and childhood maltreatment in predicting level of adult emotional dysregulation and attachment style. Specifically, G/G genotype carriers were at risk for increased emotional dysregulation when exposed to three or more categories of childhood abuse. In addition, G/G genotype carriers exhibited enhanced disorganized adult attachment style when exposed to severe childhood abuse compared to A/A and A/G carriers. Our findings suggest that A allele carriers of OXTR rs53576 are resilient against the effects of severe childhood adversity, by protection against emotional dysregulation and disorganized attachment.

Posttraumatic stress disorder (PTSD) affects 5–10% percent of the US adult population with a higher prevalence among women compared with men. Although it remains unclear how biological sex associates with susceptibility to PTSD, one mechanism may involve a role for estrogen in a gene by environment interaction. We previously demonstrated a sex-dependent association between the pituitary adenylate cyclase-activating polypeptide type 1 receptor (PAC1) and PTSD, where carriers of a C allele at single-nucleotide polymorphism (SNP) rs2267735 within the PAC1 receptor gene ( ADCYAP1R1 ) have increased symptoms of PTSD. This SNP is located within a predicted estrogen response element (ERE), which regulates gene transcription when bound to estradiol (E2) activated estrogen receptor alpha (ERα). In the current study, we examined E2 regulation of ADCYAP1R1 in vitro , in cell culture, and in vivo in mice and humans. We find in mice that fear conditioning and E2 additively increase ADCYAP1R1 expression. In vitro , we show that E2/ERα binds to the ADCYAP1R1 ERE, with less efficient binding to an ERE containing the C allele of rs2267735. In women with low serum E2, the CC genotype associates with lower ADCYAP1R1 expression, which further associates with higher PTSD symptoms. These findings lead to a model in which E2 induces the expression of ADCYAP1R1 through binding of ERα at the ERE as an adaptive response to stress. Inhibition of E2/ERα binding to the ERE containing the rs2267735 risk allele results in reduced expression of ADCYAP1R1 , diminishing estrogen regulation as an adaptive stress response and increasing risk for PTSD.

The study aimed to investigate factors contributing to heat development during light curing of a flowable bulk-fill resin-based composite (SDR , Lot # 602000876, Dentsply Sirona, Konstanz, Germany) (RBC). Temperatures were measured with calibrated thermocouples. A multi-wave light-emitting diode (LED) light curing unit (LCU) was used (Ivoclar Vivadent, Schaan, Lichtenstein). In all experiments, the RBC was first cured (cured) for 30 s and, after 5 min of recovery time, received a second LCU irradiation (post-cured) for 30 s. The exothermic reaction was measured by calculating the Δ temperature between cured and post-cured RBC. In a cylinder-shaped polymer mold, temperature was recorded inside of RBC during curing (part 1) and light transmission through RBC during curing was investigated (part 2). Pulpal temperatures were assessed in an extracted third molar during light curing (part 3). Data were statistically analyzed using one-way ANOVA (α=0.05). Increased thickness of RBC led to decreased pulp chamber temperatures. Inside RBC, there was a large variation in heat development between the cured and post-cured groups (p<0.05). The cured group absorbed more LCU irradiation than the post-cured group. The irradiance of the LCU seemed to be a more important factor than exothermic reaction of RBCs for pulp chamber heat development. Flowable bulk-fill RBCs can act as a pulpal insulator against LCU irradiation, despite their exothermic curing reaction.

This short review will summarize the current knowledge on the uptake, storage, and export of copper ions by astrocytes and will address the potential roles of astrocytes in copper homeostasis in the normal and diseased brain. Astrocytes in culture efficiently accumulate copper by processes that include both the copper transporter Ctr1 and Ctr1-independent mechanisms. Exposure of astrocytes to copper induces an increase in cellular glutathione (GSH) content as well as synthesis of metallothioneins, suggesting that excess of copper is stored as complex with GSH and in metallothioneins. Furthermore, exposure of astrocytes to copper accelerates the release of GSH and glycolytically generated lactate. Astrocytes are able to export copper and express the Menkes protein ATP7A. This protein undergoes reversible, copper-dependent trafficking between the trans-Golgi network and vesicular structures. The ability of astrocytes to efficiently take up, store and export copper suggests that astrocytes play a key role in the supply of neurons with copper and that astrocytes should be considered as target for therapeutic interventions that aim to correct disturbances in brain copper homeostasis.

Existential theory and previous qualitative research have suggested that a lack of life meaning and purpose causes boredom, as well as other types of negative affect such as depression or anxiety. Although these variables have been shown to be correlated at one point in time, the relationships among these constructs have not been investigated using a controlled, quantitative research design. In Study 1a (N = 131), boredom was shown to be related to, yet psychometrically distinct from, life meaning, depression, and anxiety. In Study 1b (N = 88), life meaning significantly predicted changes in boredom across time while depression and anxiety did not. In addition, boredom was a significant predictor of changes in life meaning across time, while depression and anxiety were not. Finally, in Study 2 (N = 102), manipulating perceptions of life meaning significantly changed boredom, while a manipulation of mood did not. The nature of the relationship between life meaning and boredom, as well as some clinical implications, are discussed. [PUBLICATION ABSTRACT]