Lack of Association Between Dendritic Cell Nuclear Protein-1 Gene and Major Depressive Disorder in the Han Chinese Population.
Lack of association between dendritic cell nuclear protein-1 gene and major depressive disorder in the Han Chinese population.
Prog Neuropsychopharmacol Biol Psychiatry. 2013 Apr 22;
Li H, Wang YJ, Hua L, Yang YT, Zhang M, Zhang D, Wang C, Xu ZQ
OBJECTIVES: Dendritic cell nuclear protein-1(DCNP1) has been associated with major depressive disorder (MDD) based on analysis of a population of patients in the United Kingdom. In the present study we have investigated a possible role of DCNP in MDD in the Han Chinese population, including a meta-analysis of different ethnic populations. METHODS: Eight single nucleotide polymorphisms (SNPs) spanning the entire DCNP1 were carefully selected, genotyped and used for the SNP and haplotype analyses in 574 patients with MDD and 642 healthy controls. Considering the potential genetic association difference across different ethnic populations, we further conducted a meta-analysis for Chinese and European populations. RESULTS: rs10061623 showed initial association with MDD in females in the allele analysis (p-value: 0.043). However, this association did not remain significant after Bonferroni correction to adjust for multiple comparisons (corrected p-value: 0.344). Other single-marker and haplotype analyses did not reveal any significant differences between patients and controls. The SNP (rs12520799), positive in the original UK study, gave negative results in all our analyses. The meta-analysis results of rs12520799 also suggested possible negative association between this SNP and MDD in the Han Chinese population. CONCLUSIONS: In the Han Chinese population, common DCNP1 polymorphisms are unlikely to be important in the genetic susceptibility to MDD. HubMed – depression
BDNF and CREB1 genetic variants interact to affect antidepressant treatment outcomes in geriatric depression.
Pharmacogenet Genomics. 2013 Jun; 23(6): 301-13
Murphy GM, Sarginson JE, Ryan HS, O’Hara R, Schatzberg AF, Lazzeroni LC
Brain-derived neurotrophic factor (BDNF) is associated with antidepressant response on the cellular level, in animal models, and in clinical studies. A common variant in the BDNF gene results in a substitution of a methionine (Met) for a valine at the amino acid position 66. Previous studies reported that the Met variant results in enhanced response to antidepressant medications. These findings may be at odds with studies indicating that on a cellular level the Met variant impairs the secretion of BDNF.We examined the effects of BDNF single nucleotide polymorphisms (SNPs) in response to the antidepressants paroxetine and mirtazapine in a sample of 246 geriatric patients with major depression, treated in a double-blind, randomized, 8-week clinical trial. We also examined the effects of genetic variation at the BDNF-related loci neurotrophic tyrosine kinase receptor 2, cyclic AMP responsive element binding protein 1 (CREB1), and CREB binding protein. A total of 53 SNPs were genotyped.BDNF genetic variation had a significant effect on the efficacy of paroxetine, with patients carrying the Met allele showing impaired response. SNPs at the CREB1 locus, which encodes a transcription factor important in BDNF signaling, also predicted response to paroxetine. Furthermore, we found a significant gene-gene interaction between BDNF and CREB1 that affected response to paroxetine. Because BDNF has been associated with cognitive function, we tested the effects of BDNF SNPs on change in a wide variety of cognitive tests over the 8-week trial, but there were no significant effects of genotype on cognition.These results provide new evidence for the importance of the BDNF pathway in antidepressant response in geriatric patients. The negative effect of the Met66 allele on antidepressant outcomes is consistent with basic science findings indicating a negative effect of this variant on BDNF activity in the brain. Further, the effect of BDNF genetic variation on antidepressant treatment is modified by variation in the gene encoding the downstream effector CREB1. HubMed – depression
Jumping mechanisms in gum treehopper insects (Hemiptera, Eurymelinae).
J Exp Biol. 2013 Apr 25;
Burrows M
Jumping in a species of Australian gum treehopper was analysed from high speed images. Adults and nymphs of Pauroeurymela amplicincta lived together in groups that were tended by ants, but only adults jumped. The winged adults with a body mass of 23 mg and a body length of 7 mm had some morphological characteristics intermediate between those of their close relatives the leafhoppers (Cicadellidae) and the treehoppers (Membracidae). They, like leafhoppers, lacked the prominent prothoracic helmets of membracid treehoppers, but their large hind coxae were linked by press studs (poppers), that are present in leafhoppers but not treehoppers. The hind legs were only 30-40% longer than the other legs and 67% of body length. They are thus of similar proportions to the hind legs of treehoppers but much shorter than those of most leafhoppers. Jumping was propelled by the hind legs, that moved in the same plane as each other beneath and almost parallel to the longitudinal axis of the body. A jump was preceded by full levation of the coxo-trochanteral joints of the hind legs. In its best jumps, the rapid depression of these joints then accelerated the insect in 1.4 ms to a take-off velocity of 3.8 m s(-1) so that it experienced a force of almost 280 g. In 22% of jumps, the wings opened before take-off but did not flap until airborne when the body rotated little in any plane. The energy expended was 170 µJ, the power output was 122 mW, and the force exerted was 64 mN. Such jumps are predicted to propel the insect forwards 1450 mm (200 times body length) and to a height of 430 mm if there is no effect of wind resistance. The power output per mass of jumping muscle far exceeded the maximum active contractile limit of muscle and indicates that a catapult-like action must be used. This eurymelid therefore outperforms both leafhoppers and treehoppers in its faster acceleration and in its higher take-off velocity. HubMed – depression
Stressors, Stress Response, and Cancer Recurrence: A Systematic Review.
Cancer Nurs. 2013 Apr 24;
Todd BL, Moskowitz MC, Ottati A, Feuerstein M
BACKGROUND:: Cancer survivors assume that stress plays an important role in cancer recurrence. However, the role of stress in the etiology of cancer recurrence remains unclear. OBJECTIVE:: A systematic review examining the causal role of exposure to stressors and/or stress response and cancer recurrence was conducted. METHODS:: The authors screened the scientific literature published from December 1979 through April 2012. Prospective studies and randomized control trials that examined the link between exposure to stressors and/or stress response and cancer recurrence were included in the review. RESULTS:: Fifteen studies examined exposures to stressors (life event questionnaires) and/or multiple indices of the stress response (mood, anxiety, depression, biological, and immune measures). The relationships between stressors and/or stress response and recurrence were observed as no relationship (80%), positive relationship (33%), and inverse relationship (27%). One of 3 randomized control trials reported a positive relationship between stress reduction and reduced risk of recurrence. CONCLUSIONS:: The scientific literature to date indicates no clear evidence for a causal relationship between stress (measured as stressor exposure and/or stress response) and cancer recurrence. Although additional high-quality research is needed to provide a more definitive answer, the evidence to date does not support this hypothesis. IMPLICATIONS FOR PRACTICE:: Although at present, there is no evidence indicating a causal relationship between stress and cancer recurrence, attending to the reduction in a cancer survivor’s stress response can improve emotional well-being and quality of life. HubMed – depression