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141.
142.
Dianne A.M. van der Kop Gerda Ruys Dianka Dees Chris van der Schoot A. Douwe de Boer Wouter G. van Doorn 《Physiologia plantarum》2003,117(2):256-263
The gene defender against apoptotic death ( DAD-1 ) prevents programmed cell death in animal cells. We investigated the expression pattern of DAD-1 in petals of iris ( Iris × hollandica cv. Blue Magic) and carnation ( Dianthus caryophyllus cv. Etarro). DAD-1 expression in Iris petals was strongly reduced by the time of visible senescence, which occurs 4 days after flower opening. Microscopic analysis showed that most mesophyll cells had died prior to a clear decrease in DAD-1 expression and that epidermis cells started to die by that time. In carnation petals DAD-1 expression also decreased by the time of massive cell death. After ethylene treatment, DAD-1 expression in carnation again decreased concomitant with the advance in massive cell death. In conclusion, DAD-1 is not an early regulator of petal cell death. Its expression may be required for the programmed dismantling of cells, as it ceases only just prior to, or concomitant with, cell death. 相似文献
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144.
Wouter A. Lotens 《European journal of applied physiology and occupational physiology》1992,65(1):59-65
A simple analytical model has been developed to simulate the cooling of the hands due to touching various types of cold material. The model consisted of a slab of tissue, covered on both sides with skin. The only active mechanism was the skin blood flow. The blood flow was controlled by body core temperature, mean skin temperature, and local hand temperature. The blood flowed along the palm before returning via the back of the hand. The control function was adapted from an earlier study, dealing with feet, but enhanced with a cold induced vasodilatation term. The palm of the hand was touching materials that were specified by conductivity and heat capacity. The hand was initially at a steady-state in a neutral environment and then suddenly grabbed the material. The resulting cooling curves have been compared to data from an experiment including six materials (foam, wood, nylon, steel, aluminium and metal at a constant temperature), three temperatures (-10, 0, and 10 degrees C), two thermal states of the body (neutral and 0.4 degrees C raised), and with and without gloves. There was a fair general agreement between the model and the experiment but the model failed to predict three specific effects: the unequal effect of equal 10 degrees C steps in cold surface temperature on the temperature of the palm of the hand, the cooling effect of nylon, and the rapid drop in back of the hand temperature. Nevertheless the overall regression was 0.88 with a standard deviation between model and experiment of about 2.5 degrees C. 相似文献
145.
Boerries Brandenburg Wouter Koudstaal Jaap Goudsmit Vincent Klaren Chan Tang Miriam V. Bujny Hans J. W. M. Korse Ted Kwaks Jason J. Otterstrom Jarek Juraszek Antoine M. van Oijen Ronald Vogels Robert H. E. Friesen 《PloS one》2013,8(12)
Human monoclonal antibodies have been identified which neutralize broad spectra of influenza A or B viruses. Here, we dissect the mechanisms by which such antibodies interfere with infectivity. We distinguish four mechanisms that link the conserved hemagglutinin (HA) epitopes of broadly neutralizing antibodies to critical processes in the viral life cycle. HA-stem binding antibodies can act intracellularly by blocking fusion between the viral and endosomal membranes and extracellularly by preventing the proteolytic activation of HA. HA-head binding antibodies prevent viral attachment and release. These insights into newly identified ways by which the human immune system can interfere with influenza virus infection may aid the development of novel universal vaccines and antivirals. 相似文献
146.
Dorina Ibi Manon Boot Martijn E.T. Dollé J. Wouter Jukema Frits R. Rosendaal Constantinos Christodoulides Matt J. Neville Robert Koivula Patrick C.N. Rensen Fredrik Karpe Raymond Noordam Ko Willems van Dijk 《Journal of lipid research》2022,63(5):100193
Triglyceride (TG)-lowering LPL variants in combination with genetic LDL-C-lowering variants are associated with reduced risk of coronary artery disease (CAD). Genetic variation in the APOA5 gene encoding apolipoprotein A-V also strongly affects TG levels, but the potential clinical impact and underlying mechanisms are yet to be resolved. Here, we aimed to study the effects of APOA5 genetic variation on CAD risk and plasma lipoproteins through factorial genetic association analyses. Using data from 309,780 European-ancestry participants from the UK Biobank, we evaluated the effects of lower TG levels as a result of genetic variation in APOA5 and/or LPL on CAD risk with or without a background of reduced LDL-C. Next, we compared lower TG levels via APOA5 and LPL variation with over 100 lipoprotein measurements in a combined sample from the Netherlands Epidemiology of Obesity study (N = 4,838) and the Oxford Biobank (N = 6,999). We found that lower TG levels due to combined APOA5 and LPL variation and genetically-influenced lower LDL-C levels afforded the largest reduction in CAD risk (odds ratio: 0.78 (0.73–0.82)). Compared to patients with genetically-influenced lower TG via LPL, genetically-influenced lower TG via APOA5 had similar and independent, but notably larger, effects on the lipoprotein profile. Our results suggest that lower TG levels as a result of APOA5 variation have strong beneficial effects on CAD risk and the lipoprotein profile, which suggest apo A-V may be a potential novel therapeutic target for CAD prevention. 相似文献
147.
Maria Tsamou Karen Vrijens Narjes Madhloum Wouter Lefebvre Charlotte Vanpoucke 《Epigenetics》2018,13(2):135-146
Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM2.5 over various time windows during pregnancy. The placental expression of miR-21 (?33.7%, 95% CI: ?53.2 to ?6.2, P = 0.022), miR-146a (?30.9%, 95% CI: ?48.0 to ?8.1, P = 0.012) and miR-222 (?25.4%, 95% CI: ?43.0 to ?2.4, P = 0.034) was inversely associated with PM2.5 exposure during the 2nd trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1st trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 µg/m³ increment, 95% CI: 26.9 to 100.7, P < 0.0001) with 3rd trimester PM2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM2.5 exposure affects miRNAs expression as well as its downstream target PTEN. 相似文献
148.
Aude Nicolas Kevin P. Kenna Alan E. Renton Nicola Ticozzi Faraz Faghri Ruth Chia Janice A. Dominov Brendan J. Kenna Mike A. Nalls Pamela Keagle Alberto M. Rivera Wouter van Rheenen Natalie A. Murphy Joke J.F.A. van Vugt Joshua T. Geiger Rick A. Van der Spek Hannah A. Pliner John E. Landers 《Neuron》2018,97(6):1268-1283.e6
149.
150.
Identification of a Novel, Putative Rho-specific
GDP/GTP Exchange Factor and a RhoA-binding Protein:
Control of Neuronal Morphology 总被引:14,自引:2,他引:12 下载免费PDF全文
Martijn F.B.G. Gebbink Onno Kranenburg Mieke Poland Francis P.G. van Horck Brahim Houssa Wouter H. Moolenaar 《The Journal of cell biology》1997,137(7):1603-1613
The small GTP-binding protein Rho has been implicated in the control of neuronal morphology. In N1E-115 neuronal cells, the Rho-inactivating C3 toxin stimulates neurite outgrowth and prevents actomyosin-based neurite retraction and cell rounding induced by lysophosphatidic acid (LPA), sphingosine-1-phosphate, or thrombin acting on their cognate G protein–coupled receptors. We have identified a novel putative GDP/GTP exchange factor, RhoGEF (190 kD), that interacts with both wild-type and activated RhoA, but not with Rac or Cdc42. RhoGEF, like activated RhoA, mimics receptor stimulation in inducing cell rounding and in preventing neurite outgrowth. Furthermore, we have identified a 116-kD protein, p116Rip, that interacts with both the GDP- and GTP-bound forms of RhoA in N1E-115 cells. Overexpression of p116Rip stimulates cell flattening and neurite outgrowth in a similar way to dominant-negative RhoA and C3 toxin. Cells overexpressing p116Rip fail to change their shape in response to LPA, as is observed after Rho inactivation. Our results indicate that (a) RhoGEF may link G protein–coupled receptors to RhoA activation and ensuing neurite retraction and cell rounding; and (b) p116Rip inhibits RhoA-stimulated contractility and promotes neurite outgrowth. 相似文献