Mapping loci for chlorosis associated with chlorophyII b deficiency in potato

About 30% of the potato plants from a (Solanum tuberosum × S. berthaultii) × S. tuberosum backcross population had chlorotic, malformed leaves; but a gradation in symptom severity suggested regulation by more than one gene. The study was undertaken to determine whether this was the case, whether any genes previously reported to control chlorosis in potato were involved, and to see how symptoms were related to effects on chlorophyll content. Testing for quantitative trait loci indicated major control by a single recessive gene on chromosome 1, close to one or more loci that have been reported to produce chlorosis in tomato, but distinct from similar genes previously identified in potato. The proposed symbol for the potato gene that confers phenotype with chlorotic and malformed leaves is cml (chlorotic and malformed leaves). The effects of this gene appeared to be accentuated by a second gene, located on chromosome 12. Chlorotic plants showed a 50% decrease in chlorophyll b level in the affected parts of leaves. It is concluded that cml is different from previously reported genes for chlorosis in potato, that at least one other gene modifies the intensity of symptom expression, and that the observed chlorosis is produced through effects on chlorophyll b level

Effects of perinatal exposure to PCBs and dioxins on play behavior in Dutch children at school age.

Polychlorinated biphenyls (PCBs) and dioxins are known as neurotoxic compounds that may modulate sex steroid hormones. Steroid hormones play a mediating role in brain development and may influence behaviors that show sex differences, such as childhood play behavior. In this study we evaluated the effects of perinatal exposure to environmental levels of PCBs and dioxins on childhood play behavior and whether the effects showed sex differences. As part of the follow-up to the Dutch PCB/dioxin study at school age, we used the Pre-School Activity Inventory (PSAI) to assess play behavior in the Rotterdam cohort (n = 207). The PSAI assesses masculine or feminine play behavior scored on three subscales: masculine, feminine, and composite. Prenatal exposure to PCBs was defined as the sum of PCB 118, 138, 153, and 180 in maternal and cord plasma and breast milk. For breast milk we measured additional PCBs as well as 17 dioxins. Respondents returned 160 questionnaires (age 7.5 years +/- 0.4). Effects of prenatal exposure to PCBs, measured in maternal and cord plasma, on the masculine and composite scales were different for boys and girls (p <.05). In boys, higher prenatal PCB levels were related with less masculinized play, assessed by the masculine scale (p(maternal) =.042; p(cord) =.001) and composite scale (p(cord) =.011), whereas in girls higher PCB levels were associated with more masculinized play, assessed by the composite scale (p(PCBmilk) =.028). Higher prenatal dioxin levels were associated with more feminized play in boys as well as girls, assessed by the feminine scale (p =.048). These effects suggest prenatal steroid hormone imbalances caused by prenatal exposure to environmental levels of PCBs, dioxins, and other related organochlorine compounds

Phytochrome A Protects Tomato Plants From Injuries Induced by Continuous Light

Plants perceive and transduce information about light quantity, quality, direction and photoperiod via several photoreceptors and use it to adjust their growth and development. A role for photoreceptors has been hypothesized in the injuries that tomato plants develop when exposed to continuous light as the light spectral distribution influences the injury severity. Up to now, however, only indirect clues suggested that phytochromes (PHY), red/far-red photoreceptors, are involved in the continuous-light-induced injuries in tomato. In this study, therefore, we exposed mutant and transgenic tomato plants lacking or over-expressing phytochromes to continuous light, with and without far-red light enrichment. The results show that PHYA over-expression confers complete tolerance to continuous light regardless the light spectrum. Under continuous light with low far-red content, PHYB1 and PHYB2 diminished and enhanced the injury, respectively, yet the effects were small. These results confirm that phytochrome signaling networks are involved in the induction of injury under continuous light.HIGHLIGHTS- PHYA over-expression confers tolerance to continuous light regardless the light spectrum.- In the absence of far-red light, PHYB1 slightly diminishes the continuous light-induced injury.- Continuous light down-regulates photosynthesis genes in sensitive tomato lines

Coastal engineers embrace nature: characterizing the metamorphosis in hydraulic engineering in terms of Four Continua

Hydraulic engineering infrastructures, such as reservoirs, dikes, breakwaters, and inlet closures, have significantly impacted ecosystem functioning over the last two centuries. Currently, nature-based solutions are receiving increasing attention in hydraulic engineering projects and research programs. However, there is a lack of reflection on the concomitant, fundamental changes occurring in the field of hydraulic engineering, and coastal engineering in particular, and what this could mean for sustainability. In this article, we signal the shift from conventional to ecosystem-based hydraulic engineering design and characterize this in terms of four continua: (i) the degree of inclusion of ecological knowledge, (ii) the extent to which the full infrastructural lifecycle is addressed, (iii) the complexity of the actor arena taken into account, and (iv) the resulting form of the infrastructural artefact. We support our arguments with two carefully selected, iconic examples from the Netherlands and indicate how the stretching ideals of ecosystem-based engineering could engender further shifts towards sustainability

Understanding the experience of social housing pathways

This report is part of an Australian Housing and Urban Research Institute (AHURI) Inquiry examining how social housing pathways could be reimagined to provide more effective assistance for low-income households in Australia. This research sets out to understand the ways in which individuals and households experience pathways into, within and out of the Australian social housing system

De invloed van orthografie op verleden tijdsvorming door zwakke lezers

In dit onderzoek werden morfofonologische vaardigheden van normale en zwakke lezers vergeleken. Specifiek werd de invloed van orthografie op de vervoeging van de verleden tijd bekeken bij 8- tot 11-jarige normale en zwakke lezers. Deze groepen lezers kregen bestaande werkwoorden en pseudo-werkwoorden gepresenteerd in de infiniefvorm (bijvoorbeeld blaffen of taven), waarna hen gevraagd werd de verleden tijdsvorm te produceren. Er is onderzocht of kinderen de juiste vorm van het suffix (-te of -de) selecteerden, op basis van de stemhebbendheid van de mediale obstruent. Ook is onderzocht of kinderen gevoelig waren voor de relatie tussen klinkerlengte en stemhebbendheid in het Nederlands, door pseudo-woorden aan te bieden die verschillen in de mate waarin ze het Nederlandse patroon volgen. Tot slot werd bekeken of auditieve presentatie van de werkwoorden mét het bijbehorende schriftbeeld (waarbij dus ook letters als ‘f’ of ‘v’ zichtbaar waren) leidde tot meer correcte verleden tijdsvormen dan alleen auditieve presentatie van de werkwoorden. De resultaten laten geen verschillen zien tussen de normale en zwakke lezers in het aantal correct vervoegde werkwoorden. Beide groepen zijn beter in staat correcte verleden tijden te maken van bestaande dan van pseudo-werkwoorden. Daarnaast zijn beide groepen gevoelig voor subtiele fonotactische patronen: kinderen maken meer correcte verleden tijdsvormen als de pseudo-werkwoorden het Nederlandse patroon volgen. Ook maakten beide groepen meer fouten met stemloze dan stemhebbende mediale obstruenten (zoals in blaffen - *blafde). De normale lezers presteerden echter beter in de vervoeging van bestaande werkwoorden wanneer het schriftbeeld werd toegevoegd, in tegenstelling tot de zwakke lezers die hier niet van profiteerden. Deze resultaten laten zien dat de (morfo-)fonologie van de zwakke lezers (op deze leeftijd en taak) niet verschilt van de normale lezers, maar dat ze minder gebruik kunnen maken van de orthografie. Dit wijst erop dat niet de fonologische verwerving als zodanig aangetast is bij slechte lezers in deze leeftijdsgroep, maar dat de integratie tussen (morfo-)fonologie en orthografie anders verloopt

R-h-erythropoietin counteracts the inhibition of in vitro erythropoiesis by tumour necrosis factor alpha in patients with rheumatoid arthritis

Anaemia of chronic disease (ACD) is a common extra-articular manifestation of rheumatoid arthritis (RA). Tumour necrosis factor alpha (TNFα) plays an important role in the development of ACD. The objective of the present study was to assess inhibition of in vitro colony-forming unit erythrocyte (CFUe) and blast-forming unit erythrocyte (BFUe) growth by TNFα and to examine whether this suppression could be counteracted by adding increasing concentrations of recombinant human erythropoietin (EPO) (r-h-EPO) to bone marrow cultures of RA patients with ACD and without anaemia (controls). Bone marrow cells of RA patients with ACD and control patients were cultured. The cultures were incubated with increasing concentrations of r-h-EPO (0.25; 0.5; 1; 2 U/ml), each in combination with increasing quantities of TFNα (0; 50; 100; 200; 400 U/ml). CFUe and BFUe were assessed after 7 and 14 days, respectively. Dose-dependent inhibition of BFUe and CFUc by increasing concentrations of TNFα was observed in ACD and controls. Regarding CFUe (ACD patients) incubated with 0.25 U/ml EPO, 50 U/ml TNFα caused 28% suppression compared to cultures without TNFα. Increasing the concentration of r-h-EPO from 0.25 U/ml to 2 U/ml completely restored the number of CFUe. A similar pattern was observed in BFUe growth in both groups. These data demonstrated the suppressive effects of TNFα on erythropoiesis in vitro and that the suppresed erythropoiesis could be partly corrected by the addition of excess r-h-EPO to the cultures. No significant differences were observed between ACD and control RA patients. This in vitro model may help explain the clinical response to r-h-EPO therapy as documented in RA patients with ACD

Liability of a Surgeon for the Extension of an Authorized Operation

Polyunsaturated fatty acids modulate the voltage dependence of several voltage-gated ion channels, thereby being potent modifiers of cellular excitability. Detailed knowledge of this molecular mechanism can be used in designing a new class of small-molecule compounds against hyperexcitability diseases. Here, we show that arginines on one side of the helical K-channel voltage sensor S4 increased the sensitivity to docosahexaenoic acid (DHA), whereas arginines on the opposing side decreased this sensitivity. Glutamates had opposite effects. In addition, a positively charged DHA-like molecule, arachidonyl amine, had opposite effects to the negatively charged DHA. This suggests that S4 rotates to open the channel and that DHA electrostatically affects this rotation. A channel with arginines in positions 356, 359, and 362 was extremely sensitive to DHA: 70 mu M DHA at pH 9.0 increased the current greater than500 times at negative voltages compared with wild type (WT). The small-molecule compound pimaric acid, a novel Shaker channel opener, opened the WT channel. The 356R/359R/362R channel drastically increased this effect, suggesting it to be instrumental in future drug screening

Interaction of inflammatory cytokines and erythropoeitin in iron metabolism and erythropoiesis in anaemia of chronic disease

In chronic inflammatory conditions increased endogenous release of specific cytokines (TNFα, IL-1, IL-6, IFNγ and others) is presumed. It has been shown that those of monocyte lineage play a key role in cytokine expression and synthesis. This may be associated with changes in iron metabolism and impaired erythropoiesis and may lead to development of anaemia in patients with rheumatoid arthritis. Firstly, increased synthesis of acute phase proteins, like ferritin, during chronic inflammation is proposed as the way by which the toxic effect of iron and thereby the synthesis of free oxy-radicals causing the damage on the affected joints, may be reduced. This is associated with a shift of iron towards the mononuclear phagocyte system which may participate in the development of anaemia of chronic disease. Secondly, an inhibitory action of inflammatory cytokines (TNFα, IL-1), on proliferation and differentiation of erythroid progenitors as well as on synthesis of erythropoietin has been shown, thereby also contributing to anaemia. Finally, chronic inflammation causes multiple, complex disturbances in the delicate physiologic equilibrium of interaction between cytokines and cells (erythroid progenitors, cells of mononuclear phagocyte system and erythropoietin producing cells) leading to development of anaemia of chronic disease (Fig. 1)

Variants in MARC1 and HSD17B13 reduce severity of NAFLD in children, perturb phospholipid metabolism, and suppress fibrotic pathways

Background & aims: Genome-wide association studies in adults have identified variants in HSD17B13 and MARC1 as protective against NAFLD. It is not known if they are similarly protective in children and, more generally, whether the peri-portal inflammation of pediatric NAFLD and lobular inflammation seen in adults share common genetic influences. Therefore, we aimed to: establish if these variants are associated with NAFLD in children, and to investigate the function of these variants in hepatic metabolism using metabolomics. Methods: 960 children (590 with NAFLD, 394 with liver histology) were genotyped for rs72613567T>TA in HSD17B13, rs2642438G>A in MARC1. Genotype-histology associations were tested using ordinal regression. Untargeted hepatic proteomics and plasma lipidomics were performed in a subset of samples. In silico tools were used to model the effect of rs2642438G>A (p.Ala165Thr) on MARC1. Results: rs72613567T>TA in HSD17B13 was associated with lower odds of NAFLD diagnosis (OR 0.7 (95%CI 0.6-0.9) and lower grade of portal inflammation (PA in MARC1 was associated with lower grade of hepatic steatosis (P=0.02). Proteomics found reduced expression of HSD17B13 in carriers of the protective allele, whereas MARC1 levels were not affected by genotype. Both variants showed downregulation of hepatic fibrotic pathways, upregulation of retinol metabolism and perturbation of phospholipid species. Modelling suggests that p.Ala165Thr would disrupt the stability and metal-binding of MARC1. Conclusions: There are shared genetic mechanisms between pediatric and adult NAFLD, despite their differences in histology. MARC1 and HSD17B13 are involved in phospholipid metabolism and suppress fibrosis in NAFLD