Die Siddhaṃ in der japanischen Kunst in Ritualen der Heilung

Siddhaṃ sind die Zeichen für Keimsilben aus den indischen Brahmi-Schriften, die besonders in den esoterischen Schulen des japanischen Buddhismus Verwendung finden. Der Fokus der Arbeit liegt auf der Erörterung der Siddhaṃ in der Kunst und ihrer Anwendung in Ritualen der Heilung. Als philologische Basis dient der japanische Schlüsseltext von dem Mönch Kakuban (1095-1143) über die kontemplative Meditation des Siddhaṃ A, kurz Ajikan. Dabei wird zunächst geprüft, ob und inwieweit das Siddhaṃ A und weitere Siddhaṃ in der Kunst auftreten und eine Funktion in Ritualen der Heilung haben. Darauf aufbauend wird auf die religionsgeschichtlichen und politischen Hintergründe eingegangen, bevor die Siddhaṃ in der japanischen Kunst und ihre Funktion in Ritualen beleuchtet wird. Dabei liegt der Schwerpunkt auf der Blüte der Siddhaṃ vom 11.-14. Jh.. Das Material wird systematisch in die Disziplinen Architektur, Malerei, Skulptur, Schriftkunst und Kunstgewerbe eingeteilt. Jedes Objekt wird auf seine rituellen Funktionen untersucht. Über die Kunst hinaus werden die Siddham in Meditationen und Ritualen der Heilung analysiert. Dabei zeigt sich, dass es in der Heilung mit den Siddhaṃ um einen geistigen Weg geht, der schließlich zur Buddhaschaft führen kann. Die Siddhaṃ bilden in Ritualen für Lebende und Verstorbene die Basis für eine Form der buddhistischen Heilkunst, die ebenso einen Einfluss auf die Entwicklung der japanischen Heilmethode Usui Reiki Ryôhô ausgeübt haben und darin als Schlüssel-Element zur Heilung des Geistes benutzt werden

MAINTENANCE ELECTROCONVULSIVE THERAPY IN SCHIZOPHRENIA

Background: The aim of our retrospective naturalistic observational study was to describe the use of maintenance electroconvulsive therapy (M-ECT) in chronic pharmacoresistant schizophrenia. Subjects and methods: We delineated 19 cases of chronic pharmacoresistant schizophrenia (females N=12) recently treated with maintenance electroconvulsive therapy at the Havlickuv Brod Psychiatric Hospital in the Czech Republic. Demographic, clinical and treatment variables were recorded. Results: M-ECT, when applied weekly to monthly mostly over a period of several years, was of no benefit in the treatment of chronic hallucinations and/or delusions. However, it did prove beneficial (p<0.001) in removing chronic serious symptoms like suicidal or violent behavior, automutilation, refusal of food or liquids, stupor or catatonia. Even though almost all of our patients remained hospitalized, we were nonetheless able to transfer them to an unlocked psychiatric ward and let them out for walks or occupational therapy with almost no need for using restraint. No serious adverse side effects of M-ECT were found. Conclusions: Our study is limited by using only one simple standardized measurement (Clinical Global Impression - Severity) that was retrospective. Another limitation of our retrospective study was that the subjects had not been regularly tested for their cognitive functions. According to our results, M-ECT mitigates the impact of the disease and improves social functioning of the patients. M-ECT does not treat chronic schizophrenia but does make the lives of patients more tolerable. We suggest further research into M-ECT and its clinical application in chronic pharmacoresistant schizophrenia

Pain and rheumatology: Thinking outside the joint

No abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/61864/1/24326_ftp.pd

Association of COMT genotypes with S-COMT promoter methylation in growth-discordant monozygotic twins and healthy adults

<p>Abstract</p> <p>Background</p> <p>Catechol-O-Methyltransferase (COMT) plays a key role in dopamine and estrogen metabolism. Recently, COMT haplotypes rather than the single polymorphism Val158Met have been reported to underlie differences in protein expression by modulating mRNA secondary structure. So far, studies investigating the epigenetic variability of the S-COMT (soluble COMT) promoter region mainly focused on phenotypical aspects, and results have been controversial.</p> <p>Methods</p> <p>We assessed S-COMT promoter methylation in saliva and blood derived DNA with regard to early pre- and postnatal growth as well as to genotype for polymorphisms rs6269, rs4633, and rs4680 (Val158Met) in 20 monozygotic twin pairs (mean age 4 years), who were discordant for intrauterine development due to severe feto-fetal-transfusion syndrome. Methylation levels of two previously reported partially methylated cytosines were determined by the quantitative SIRPH (SNuPE- IP RP HPLC) assay.</p> <p>Results</p> <p>Overall, we observed a high variability of S-COMT promoter methylation, which did not correlate with individual differences in the pre- or postnatal growth pattern. Within the twin pairs however we noted a distinct similarity that could be linked to underlying COMT genotypes. This association was subsequently confirmed in a cohort of 93 unrelated adult controls. Interestingly, 158Val-alleles were found at both ends of the epigenotypical range, which is in accordance with a recently proposed model of COMT haplotypes corresponding to a continuum of phenotypical variability.</p> <p>Conclusion</p> <p>The strong heritable component of S-COMT promoter methylation found in our study needs to be considered in future approaches that focus on interactions between COMT epigenotype and phenotype.</p

A Transposon in Comt Generates mRNA Variants and Causes Widespread Expression and Behavioral Differences among Mice

Background: Catechol-O-methyltransferase (COMT) is a key enzyme responsible for the degradation of dopamine and norepinephrine. COMT activity influences cognitive and emotional states in humans and aggression and drug responses in mice. This study identifies the key sequence variant that leads to differences in Comt mRNA and protein levels among mice, and that modulates synaptic function and pharmacological and behavioral traits. Methodology/Principal Findings: We examined Comt expression in multiple tissues in over 100 diverse strains and several genetic crosses. Differences in expression map back to Comt and are generated by a 230 nt insertion of a B2 short interspersed element (B2 SINE) in the proximal 39 UTR of Comt in C57BL/6J. This transposon introduces a premature polyadenylation signal and creates a short 39 UTR isoform. The B2 SINE is shared by a subset of strains, including C57BL/6J

Role of Novelty Seeking Personality Traits as Mediator of the Association between COMT and Onset Age of Drug Use in Chinese Heroin Dependent Patients

Personality traits such as novelty seeking (NS) are associated with substance dependence but the mechanism underlying this association remains uncertain. Previous studies have focused on the role of the dopamine pathway.Examine the relationships between allelic variants of the catechol-O-methyltransferase (COMT) gene, NS personality traits, and age of onset of drug use in heroin-dependent subjects in China.The 478 heroin dependent subjects from four drug rehabilitation centers in Shanghai who were genotyped for eight tagging single nucleotide polymorphisms (SNP) on the COMT gene completed the NS subscale from the Temperament and Character Inventory. Multivariate analyses were used to assess the potential mediating role of NS personality traits in the association between COMT gene variants and the age of onset of heroin use.In the univariate analysis the COMT rs737866 gene variants were independently associated with both NS and age of onset of drug use: those with the TT genotype had higher NS subscale scores and an earlier onset age of heroin use than individuals with CT or CC genotypes. In the multivariate analysis the inclusion of the NS subscore variable weakened the relationship between the COMT rs737866 TT genotype and an earlier age of onset of drug use. Our findings that COMT is associated with both NS personality traits and with the age of onset of heroin use helps to clarify the complex relationship between genetic and psychological factors in the development of substance abuse

Contributions of Dopamine-Related Genes and Environmental Factors to Highly Sensitive Personality: A Multi-Step Neuronal System-Level Approach

Traditional behavioral genetic studies (e.g., twin, adoption studies) have shown that human personality has moderate to high heritability, but recent molecular behavioral genetic studies have failed to identify quantitative trait loci (QTL) with consistent effects. The current study adopted a multi-step approach (ANOVA followed by multiple regression and permutation) to assess the cumulative effects of multiple QTLs. Using a system-level (dopamine system) genetic approach, we investigated a personality trait deeply rooted in the nervous system (the Highly Sensitive Personality, HSP). 480 healthy Chinese college students were given the HSP scale and genotyped for 98 representative polymorphisms in all major dopamine neurotransmitter genes. In addition, two environment factors (stressful life events and parental warmth) that have been implicated for their contributions to personality development were included to investigate their relative contributions as compared to genetic factors. In Step 1, using ANOVA, we identified 10 polymorphisms that made statistically significant contributions to HSP. In Step 2, these polymorphism's main effects and interactions were assessed using multiple regression. This model accounted for 15% of the variance of HSP (p<0.001). Recent stressful life events accounted for an additional 2% of the variance. Finally, permutation analyses ascertained the probability of obtaining these findings by chance to be very low, p ranging from 0.001 to 0.006. Dividing these loci by the subsystems of dopamine synthesis, degradation/transport, receptor and modulation, we found that the modulation and receptor subsystems made the most significant contribution to HSP. The results of this study demonstrate the utility of a multi-step neuronal system-level approach in assessing genetic contributions to individual differences in human behavior. It can potentially bridge the gap between the high heritability estimates based on traditional behavioral genetics and the lack of reproducible genetic effects observed currently from molecular genetic studies

Multivariate Analysis of Dopaminergic Gene Variants as Risk Factors of Heroin Dependence

BACKGROUND: Heroin dependence is a debilitating psychiatric disorder with complex inheritance. Since the dopaminergic system has a key role in rewarding mechanism of the brain, which is directly or indirectly targeted by most drugs of abuse, we focus on the effects and interactions among dopaminergic gene variants. OBJECTIVE: To study the potential association between allelic variants of dopamine D2 receptor (DRD2), ANKK1 (ankyrin repeat and kinase domain containing 1), dopamine D4 receptor (DRD4), catechol-O-methyl transferase (COMT) and dopamine transporter (SLC6A3) genes and heroin dependence in Hungarian patients. METHODS: 303 heroin dependent subjects and 555 healthy controls were genotyped for 7 single nucleotide polymorphisms (SNPs) rs4680 of the COMT gene; rs1079597 and rs1800498 of the DRD2 gene; rs1800497 of the ANKK1 gene; rs1800955, rs936462 and rs747302 of the DRD4 gene. Four variable number of tandem repeats (VNTRs) were also genotyped: 120 bp duplication and 48 bp VNTR in exon 3 of DRD4 and 40 bp VNTR and intron 8 VNTR of SLC6A3. We also perform a multivariate analysis of associations using Bayesian networks in Bayesian multilevel analysis (BN-BMLA). FINDINGS AND CONCLUSIONS: In single marker analysis the TaqIA (rs1800497) and TaqIB (rs1079597) variants were associated with heroin dependence. Moreover, -521 C/T SNP (rs1800955) of the DRD4 gene showed nominal association with a possible protective effect of the C allele. After applying the Bonferroni correction TaqIB was still significant suggesting that the minor (A) allele of the TaqIB SNP is a risk component in the genetic background of heroin dependence. The findings of the additional multiple marker analysis are consistent with the results of the single marker analysis, but this method was able to reveal an indirect effect of a promoter polymorphism (rs936462) of the DRD4 gene and this effect is mediated through the -521 C/T (rs1800955) polymorphism in the promoter