Isocitrate dehydrogenase gene duplication and fixed heterophenotype in the cultivated soybeanGlycine max

Summary Isocitrate dehydrogenase (E.C. 1.1.1.42) gene duplication was demonstrated in the self-pollinated soybean (Glycine max) by means of starch-gel electrophoresis. This finding explains the heterogeneity and/or fixed heterophenotype observed in some soybean cultivars.     

A physical map of the mouse genome

A physical map of a genome is an essential guide for navigation, allowing the location of any gene or other landmark in the chromosomal DNA. We have constructed a physical map of the mouse genome that contains 296 contigs of overlapping bacterial clones and 16,992 unique markers. The mouse contigs were aligned to the human genome sequence on the basis of 51,486 homology matches, thus enabling use of the conserved synteny (correspondence between chromosome blocks) of the two genomes to accelerate construction of the mouse map. The map provides a framework for assembly of whole-genome shotgun sequence data, and a tile path of clones for generation of the reference sequence. Definition of the human-mouse alignment at this level of resolution enables identification of a mouse clone that corresponds to almost any position in the human genome. The human sequence may be used to facilitate construction of other mammalian genome maps using the same strategy.     

Dominant effector genetics in mammalian cells

We have expressed libraries of peptides in mammalian cells to select for trans-dominant effects on intracellular signaling systems. As an example-and to reveal pharmacologically relevant points in pathways that lead to Taxol resistance-we selected for peptide motifs that confer resistance to Taxol-induced cell death. Of several peptides selected, one, termed RGP8.5, was linked to upregulation of expression of the gene ABCB1 (also known as MDR1, for multiple drug resistance) in HeLa cells. Our data indicate that trans-dominant effector peptides can point to potential mechanisms by which signaling systems operate. Such tools may be useful in functional genomic analysis of signaling pathways in mammalian disease processes.     

Effect of Splice Marking on Fabric Roll Planning

Minimising the fabric loss during spreading can reduce the total production costs of garment manufacturing. Although marker planning is a major determinant of material utilisation, considerable savings on materials also will be made from the area of spreading loss. In the spreading process, it is general to have variance on the fabric yardage between each fabric roll, and the number of splice markings on each cutting lay is also varied. This paper aim to study how the fabric roll planning and the number of splice marks of a cutting lay will affect the material usage in the spreading process. By using a genetic algorithm approach, the amount of fabric to be saved by optimising the fabric roll sequence was derived by comparing the best arrangement and the worst arrangement of the fabric roll sequences of a cutting lay. The result of the study showed that both fabric roll planning and the number of splice marking have effect on the fabric loss. The findings could help the apparel manufacturer to reduce the     

面的并区域与三正则图的Ham ilton圈

Sachs. Kozyrev和 Grinbery指出了平面图具有 Hamilton圈的一个必要条件是 ∑ni=3 ( i-2 )i=∑ni=3 ( i-2 ) ′i=n-2 ,其中 i 和 ′i 分别为 Hamilton圈内 ,外度为 i的面数 ,在这个必要条件的基础上 ,给出了三正则平面图 Hamilton圈的一个算法     

TNF-induced necroptosis and PARP-1-mediated necrosis represent distinct routes to programmed necrotic cell death

Programmed necrosis is important in many (patho)physiological settings. For specific therapeutic intervention, however, a better knowledge is required whether necrosis occurs through one single “core program” or through several independent pathways. Previously, the poly(ADP-ribose) polymerase (PARP) pathway has been suggested as a crucial element of tumor necrosis factor (TNF)-mediated necroptosis. Here, we show that TNF-induced necroptosis and the PARP pathway represent distinct and independent routes to programmed necrosis. First, DNA-alkylating agents such as 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) or methyl methanesulfonate rapidly activate the PARP pathway, whereas this is a late and secondary event in TNF-induced necroptosis. Second, inhibition of the PARP pathway does not protect against TNF-induced necroptosis, e.g., the PARP-1 inhibitor 3-AB prevented MNNG- but not TNF-induced adenosine-5′-triposphate depletion, translocation of apoptosis-inducing factor, and necrosis. Likewise, olaparib, a more potent and selective PARP-1 inhibitor failed to block TNF-induced necroptosis, identical to knockdown/knockout of PARP-1, pharmacologic and genetic interference with c-Jun N-terminal kinases and calpain/cathepsin proteases as further components of the PARP pathway. Third, interruption of TNF-induced necroptosis by interference with ceramide generation, RIP1 or RIP3 function or by the radical scavenger butylated hydroxyanisole did not prevent programmed necrosis through the PARP pathway. In summary, our results suggest that the currently established role of the PARP pathway in TNF-induced necroptosis needs to be revised, with consequences for the design of future therapeutic strategies.     

Which neurological abnormalities and neuropsychological impairments share the same substrate in psychosis?

Approximately 60% of subjects with schizophrenia present minor neurological signs (neurological soft signs, NSS), which include abnormalities in sensory and motor performance indicative of a non-specific cerebral dysfunction. These are also present in healthy individuals and relatives of patients with psychosis, at significantly lower rates. The excess of NSS in psychosis may be a potential endophenotype for this disorder, and reflect the same neurodevelopmental brain dysfunction that also underlies the cognitive deficits consistently reported in psychosis. To establish whether neurological and cognitive dysfunction meet the essential criterion required for a refined endophenotype for psychosis, the association with the illness, we explored evidence that certain neurological and cognitive deficits co-occur in affected individuals. This evidence suggests that signs of motor dysfunctions may be specific to patients with psychosis, in whom they are associated with dysfunction in cognitive tasks requiring motor skills. Thus, they may form a promising candidate endophenotype for psychosis.     

First episode psychosis with extrapyramidal signs prior to antipsychotic drug treatment

Extrapyramidal movement disorders are common in chronic schizophrenia, and may be an intrinsic feature of the illness as well as related to antipsychotic drug treatment. Similar dysfunctions at illness onset may have implications for outcome, and for under- standing the mechanisms of illness. The objectives were to examine the clinical correlates of pre-treatment movement disorders at first episode of psychosis, and determine associations with neuropsychological function and striatal structure. Never medicated subjects were recruited from consecutive admissions to Early Psychosis Programs with defined catchment areas in Hong Kong, China, and Halifax, Canada. Standardized clinical, neuropsychological and brain imaging assessments were carried out at baseline and following acute and long term treatment with typical or atypical antipsychotic drugs. At the Hong Kong site, we studied 84 subjects with first episode psychosis (n = 10 with EPS). At the Halifax site, we studied 40 subjects with first episode psychosis (n = 17 with EPS), and 23 healthy comparison subjects. Subjects with movement disorders prior to treatment (EPS+) had higher total PANSS scores at baseline (mean elevation 19.9% Hong Kong, P = 0.016; 14.7% Halifax, P = 0.049). In subjects treated with atypical antipsychotics (all Halifax), EPS+ status at baseline predicted more movement disorders at long term follow up (P = 0.0005). In both cohorts, EPS+ subjects had poorer acute symptomatic treatment response assessed with the PANSS (Hong Kong P = 0.005; Halifax P = 0.017). Neuropsychological impairment related to executive dysfunction appeared greater in a small sam- ple of EPS+ subjects (Hong Kong, effect size 0.26-0.27, P < 0.05). Caudate volumes were 4.5% larger in EPS+ compared with EPS-subjects (Halifax P = 0.042), and correlations between striatal volumes and age were different in the EPS+ group. In conclu- sion, pre-treatment EPS is present in a substantial minority of subjects with first episode psychosis, appears to persist at long term follow up, and is associated with poorer response of symptoms to treatment. Selective impairment of executive function and stria- tal enlargement provides evidence of abnormalities of brain function and structure associated with this aspect of early psychosis.