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In today's modern world the manufacturing processes are designed in such a way as to ensure the desired quality of the end product. In this article are considered some aspects of desired quality in performance. The described quality management tools are based on Taguchi's theory Quality Engineering and Robust Engineering. In relation to this in the paper are presented a new application for assessing the losses of society from the irrational use of resources or their harmful impact in the transformation into a production process, the possibilities of Taguchi's theory in assessing the losses of the stakeholders in the functioning of the enterprise - in case of ineffective or inefficient use of the production process and proposal of the possibility for a complex assessment of the losses of the society and the stakeholders from the production of products and operation of production processes at quality indicators different from the desired nominal values

ICRH was extensively used in the 2015-16 JET-ILW (ITER like wall) experimental campaign; bulk heating together with high-Z impurity chase-out from plasma centre importantly contributed to the good DD fusion performance obtained recently in JET. Power up to 6 MW was launched in H-mode deuterium plasmas and 8 MW during the hydrogen campaign. The ILA was re-installed and contributed positively to the availability of ICRH power. The ILA produces slightly less high-Z impurities than the A2's and the PWI measured via Be line emission on limiters is in the same ballpark. Specific experiments were conducted to optimise ICRH scenarios in preparation for DT in particular the dual frequency scheme, (H)D and (He)D were tested. In addition, it was confirmed that the (D)H scenario is accessible in a ILW environment and the novel 3-ions ICRH scheme was validated experimentally.

Introduction Low-dose pancuronium is known to affect serum cholinesterase activity (BChE); however, the dose-response effect of clinical doses of pancuronium on BChE has not been investigated. Methods Thirteen ASA I-II patients scheduled for elective surgery requiring muscle relaxation were enrolled in this study. All patients had normal BChE before surgery. Incremental doses of pancuronium (10, 20, 50, and 100 µg/kg) were injected in accordance with surgical needs every 45 min. BChE was measured 3 min after injection by an automatic colorimetric method. Results BChE decreased significantly in all except one patient in comparison to the baseline ( P  < 0.05). However all values remained within normal clinical range. A dose of 100 µg/kg yielded significant decrease in comparison to 10 µg/kg but not to other dosages. Linear regression was not significant for the dose-response relationship ( P  = 0.05). Conclusion After clinical incremental doses of pancuronium, BChE remained within clinical range.

Potentiation of mivacurium by low-dose pancuronium is mostly due to an inhibition of plasma butyryl cholinesterase (BchE) resulting in a decreased rate of hydrolysis of mivacurium. Nevertheless, an interaction at the receptor site could not be ruled out. By changing the order of the muscle relaxant injections, we may lessen the pharmacokinetic interaction and assess the impact at the acetylcholine receptor level. Twenty patients scheduled for general anesthesia with propofol and fentanyl, and isoflurane were randomized into two groups receiving, mivacurium 100 microg kg-1 followed by pancuronium 15 microg kg-1 (group 1) or pancuronium 15 microg kg-1 followed by mivacurium 100 microg kg-1 (group 2). BchE before and after injection of each relaxant was measured. Neuromuscular block was assessed with a force transducer at the adductor pollicis measuring the elicited twitch to ulnar nerve stimulation. The neuromuscular block was greater when pancuronium was administered before mivacurium (100% versus 96+/-3%; P<0.05). Times to recovery of the elicited twitch response to 25% and 75% of control value were increased by 100% (P<0.05). After pancuronium, decreases in BchE of 11% and 14% in groups 1 and 2 were observed, respectively. Interaction between mivacurium and low dose pancuronium is significant only when mivacurium is injected after pancuronium.

STEP is a spherical tokamak prototype power plant that is being designed to demonstrate net electric power. The design phase involves the exploitation of plasma models to optimise fusion performance subject to satisfying various physics and engineering constraints. A modelling workflow, including integrated core plasma modelling, MHD stability analysis, SOL and pedestal modelling, coil set and free boundary equilibrium solvers, and whole plant design, has been developed to specify the design parameters and to develop viable scenarios. The integrated core plasma model JETTO is used to develop individual flat-top operating points that satisfy imposed criteria for fusion power performance within operational constraints. Key plasma parameters such as normalised beta, Greenwald density fraction, auxiliary power and radiated power have been scanned to scope the operational space and to derive a collection of candidate non-inductive flat-top points. The assumed auxiliary heating and current drive is either from electron cyclotron systems only or a combination of electron cyclotron and electron Bernstein waves. At present stages of transport modelling, there is a large uncertainty in overall confinement for relevant parameter regimes. For each of the two auxiliary heating and current drive systems scenarios, two candidate flat-top points have been developed based on different confinement assumptions, totalling to four operating points. A lower confinement assumption generally suggests operating points in high-density, high auxiliary power regimes, whereas higher confinement would allow access to a broader parameter regime in density and power while maintaining target fusion power performance.

Naomi Wray and colleagues report an analysis of genome-wide association data sets from the Psychiatric Genomics Consortium for five psychiatric disorders. They find that common variation explains 17–29% of the variance in liability and provide further support for a shared genetic etiology for these related psychiatric disorders. Most psychiatric disorders are moderately to highly heritable. The degree to which genetic variation is unique to individual disorders or shared across disorders is unclear. To examine shared genetic etiology, we use genome-wide genotype data from the Psychiatric Genomics Consortium (PGC) for cases and controls in schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD). We apply univariate and bivariate methods for the estimation of genetic variation within and covariation between disorders. SNPs explained 17–29% of the variance in liability. The genetic correlation calculated using common SNPs was high between schizophrenia and bipolar disorder (0.68 ± 0.04 s.e.), moderate between schizophrenia and major depressive disorder (0.43 ± 0.06 s.e.), bipolar disorder and major depressive disorder (0.47 ± 0.06 s.e.), and ADHD and major depressive disorder (0.32 ± 0.07 s.e.), low between schizophrenia and ASD (0.16 ± 0.06 s.e.) and non-significant for other pairs of disorders as well as between psychiatric disorders and the negative control of Crohn's disease. This empirical evidence of shared genetic etiology for psychiatric disorders can inform nosology and encourages the investigation of common pathophysiologies for related disorders.

Better analytical methods are needed to extract biological meaning from genome-wide association studies (GWAS) of psychiatric disorders. Here the authors take GWAS data from over 60,000 subjects, including patients with schizophrenia, bipolar disorder and major depression, and identify common etiological pathways shared amongst them. Genome-wide association studies (GWAS) of psychiatric disorders have identified multiple genetic associations with such disorders, but better methods are needed to derive the underlying biological mechanisms that these signals indicate. We sought to identify biological pathways in GWAS data from over 60,000 participants from the Psychiatric Genomics Consortium. We developed an analysis framework to rank pathways that requires only summary statistics. We combined this score across disorders to find common pathways across three adult psychiatric disorders: schizophrenia, major depression and bipolar disorder. Histone methylation processes showed the strongest association, and we also found statistically significant evidence for associations with multiple immune and neuronal signaling pathways and with the postsynaptic density. Our study indicates that risk variants for psychiatric disorders aggregate in particular biological pathways and that these pathways are frequently shared between disorders. Our results confirm known mechanisms and suggest several novel insights into the etiology of psychiatric disorders.

The Schizophrenia Psychiatric Genome-Wide Association Study Consortium reports five genetic loci newly associated with risk of schizophrenia, involving 17,836 cases of schizophrenia and 33,859 healthy controls. The new locus with the strongest support of association was located within an intron for microRNA 137, a known regulator of neuronal development. Four other genome-wide significant loci for schizophrenia contain predicted targets of MIR137 , suggesting that disruption to pathways involving MIR137 may be an etiologic mechanism in schizophrenia. We examined the role of common genetic variation in schizophrenia in a genome-wide association study of substantial size: a stage 1 discovery sample of 21,856 individuals of European ancestry and a stage 2 replication sample of 29,839 independent subjects. The combined stage 1 and 2 analysis yielded genome-wide significant associations with schizophrenia for seven loci, five of which are new (1p21.3, 2q32.3, 8p23.2, 8q21.3 and 10q24.32-q24.33) and two of which have been previously implicated (6p21.32-p22.1 and 18q21.2). The strongest new finding ( P = 1.6 × 10 −11 ) was with rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development. Four other schizophrenia loci achieving genome-wide significance contain predicted targets of MIR137 , suggesting MIR137 -mediated dysregulation as a previously unknown etiologic mechanism in schizophrenia. In a joint analysis with a bipolar disorder sample (16,374 affected individuals and 14,044 controls), three loci reached genome-wide significance: CACNA1C (rs4765905, P = 7.0 × 10 −9 ), ANK3 (rs10994359, P = 2.5 × 10 −8 ) and the ITIH3-ITIH4 region (rs2239547, P = 7.8 × 10 −9 ).

Schizophrenia risk: overlap with bipolar disorder A genome-wide association study using the International Schizophrenia Consortium (ISC) data set revealed that common genetic variation underlies risk of schizophrenia. The study identified common variants within the major histocompatibility complex (MHC) locus and provided molecular genetic evidence for a substantial polygenic component to risk of schizophrenia that involved thousands of common alleles of very small effect. These alleles of small effect also contribute to risk of bipolar disorder (BPD). In the second of three papers on the genetics of schizophrenia, a large genome-wide association study looking at common genetic variants underlying the risk of schizophrenia implicates the major histocompatibility complex — and thus, immunity — and provides molecular genetic evidence for a substantial polygenic component to the risk of schizophrenia. The latter involves thousands of common alleles of very small effect that also contribute to the risk of bipolar disorder. Schizophrenia is a severe mental disorder with a lifetime risk of about 1%, characterized by hallucinations, delusions and cognitive deficits, with heritability estimated at up to 80% 1 , 2 . We performed a genome-wide association study of 3,322 European individuals with schizophrenia and 3,587 controls. Here we show, using two analytic approaches, the extent to which common genetic variation underlies the risk of schizophrenia. First, we implicate the major histocompatibility complex. Second, we provide molecular genetic evidence for a substantial polygenic component to the risk of schizophrenia involving thousands of common alleles of very small effect. We show that this component also contributes to the risk of bipolar disorder, but not to several non-psychiatric diseases.