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11.
Genetic susceptibility to keloid disease and hypertrophic scarring: transforming growth factor beta1 common polymorphisms and plasma levels 总被引:10,自引:0,他引:10
Bayat A Bock O Mrowietz U Ollier WE Ferguson MW 《Plastic and reconstructive surgery》2003,111(2):535-43; discussion 544-6
Keloid disease and hypertrophic scars are dermal tumors that are often familial and typically occur in certain races. Their exact etiology is still unknown. Transforming growth factor beta1 (TGF-beta1) plays a central role in wound healing and fibrosis and has been implicated in the pathogenesis of keloid disease and hypertrophic scar. The aims of this study were to measure the plasma level of TGF-beta1 in patients compared with controls, and to investigate the association of five common single nucleotide polymorphisms in TGF-beta1 with the risk of keloid disease and hypertrophic scar formation. Platelet-poor plasma levels of TGF-beta1 in 60 patients (15 with hypertrophic scar and 45 with keloid disease) and 18 controls were measured using an enzyme-linked immunoabsorbent assay technique. A polymerase chain reaction-restriction fragment length polymorphism method was used for genotyping TGF-beta1 polymorphisms. DNA samples from 133 patients (101 with keloid disease and 32 with hypertrophic scar) and 200 controls were examined. All patients and controls were Caucasians of Northern European extraction. There was no statistically significant difference in TGF-beta1 plasma levels between patients with keloid disease and hypertrophic scar and controls. There was also no statistically significant difference in genotype or allele frequency distributions between patients and controls for codons 10, 25, and 263 and for -509 and -800 single nucleotide polymorphisms of the TGF-beta1 gene. These results suggest that TGF-beta1 plasma levels and common polymorphisms are not associated with a risk of keloid disease and hypertrophic scar formation. This lack of association may be significant in view of the importance attached to the role of TGF-beta1 in dermal scarring. To the authors' knowledge, this is the first report of a case-control association study in keloid disease and hypertrophic scars using any single nucleotide polymorphisms. 相似文献
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Mohammadi RS Samih MA Rezvani A Talebi AA 《Communications in agricultural and applied biological sciences》2007,72(3):475-485
Wrinkling aphid of pistachio leaf, Forda hirsuta Mordv. (Hem.:Pemphigidae) is one of the pests of pistachio trees. This aphid caused the shrinkage, thickening, and changing the color of the pistachio leaves. Since insect feeds from leave edges, the thick and rolled upward wrinkles were formed, which its green color turned into red. Therefore, its economical damages are out of direct feeding from plant extraction, twisting pistachio leaves, and the decrease of photosynthesis. In this research two orchards and 10 trees that each of them were selected in Rafsanjan region and 58 fundatrix galls, 120 nymphal galls were marked and the demographic parameters for apterus parthenogenesis female of this aphid were calculated via daily observations. The results indicated that intrinsic rates of increase (r) for 1, 2 and 3 generations were 0.01, 0.0638 and 0.0575 femal/femal/days respectively, Doubling time (DT) were 69.31, 10.52 and 12.04 days, respectively, net fecundity rates were 1.71, 11.5 and 7.37 femal/femal/days, respectively, Net fertility rates were 1.11, 8.87 and 5.01 days, respectively, and mean generation times (Tc) were calculated to be 31.5, 32.2 and 31.87 days, respectively. Other reproductive parameters such as gross hatch rate, gross fecundity rate, gross fertility rate, mean age gross fecundity and fertility, mean age net fecundity and fertility, mean age hatch, finite rate of increase (lambda), intrinsic birth rate (b) intrinsic death rate (d) and daily reproductive rate were also calculated. The results revealed that population parameters especially r in the first and second generations were lowest and highest, respectively and mean longevity of fundatrix was 30 days and the born nymphs made separate galls in the edge of pistachio leaves. 相似文献
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Hajibarat Zahra Saidi Abbas Hajibarat Zohreh Talebi Reza 《Physiology and Molecular Biology of Plants》2015,21(3):365-373
Physiology and Molecular Biology of Plants - To evaluate the genetic diversity among 48 genotypes of chickpea comprising cultivars, landraces and internationally developed improved lines genetic... 相似文献
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Dupuytren's disease (DD) is an ill-defined fibroproliferative disorder of the palm of the hands leading to digital contracture.
DD commonly occurs in individuals of northern European extraction. Cellular components and processes associated with DD pathogenesis
include altered gene and protein expression of cytokines, growth factors, adhesion molecules, and extracellular matrix components.
Histology has shown increased but varying levels of particular types of collagen, myofibroblasts and myoglobin proteins in
DD tissue. Free radicals and localised ischaemia have been suggested to trigger the proliferation of DD tissue. Although the
existing available biological information on DD may contain potentially valuable (though largely uninterpreted) information,
the precise aetiology of DD remains unknown. Systems biology combines mechanistic modelling with quantitative experimentation
in studies of networks and better understanding of the interaction of multiple components in disease processes. Adopting systems
biology may be the ideal approach for future research in order to improve understanding of complex diseases of multifactorial
origin. In this review, we propose that DD is a disease of several networks rather than of a single gene, and show that this
accounts for the experimental observations obtained to date from a variety of sources. We outline how DD may be investigated
more effectively by employing a systems biology approach that considers the disease network as a whole rather than focusing
on any specific single molecule. 相似文献
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Palmfeldt J Vang S Stenbroen V Pavlou E Baycheva M Buchal G Monavari AA Augoustides-Savvopoulou P Mandel H Gregersen N 《Journal of proteome research》2011,10(5):2389-2396
Deficiency of the sulfide metabolizing protein ETHE1 is the cause of ethylmalonic encephalopathy (EE), an inherited and severe metabolic disorder. To study the molecular effects of EE, we performed a proteomics study on mitochondria from cultured patient fibroblast cells. Samples from six patients were analyzed and revealed seven differentially regulated proteins compared with healthy controls. Two proteins involved in pathways of detoxification and oxidative/reductive stress were underrepresented in EE patient samples: mitochondrial superoxide dismutase (SOD2) and aldehyde dehydrogenase X (ALDH1B). Sulfide:quinone oxidoreductase (SQRDL), which takes part in the same sulfide pathway as ETHE1, was also underrepresented in EE patients. The other differentially regulated proteins were apoptosis inducing factor (AIFM1), lactate dehydrogenase (LDHB), chloride intracellular channel (CLIC4) and dimethylarginine dimethylaminohydrolase 1 (DDAH1). These proteins have been reported to be involved in encephalopathy, energy metabolism, ion transport, and nitric oxide regulation, respectively. Interestingly, oxidoreductase activity was overrepresented among the regulated proteins indicating that redox perturbation plays an important role in the molecular mechanism of EE. This observation may explain the wide range of symptoms associated with the disease, and highlights the potency of the novel gaseous mediator sulfide. 相似文献
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Nafisi S Sobhanmanesh A Alimoghaddam K Ghavamzadeh A Tajmir-Riahi HA 《DNA and cell biology》2005,24(10):634-640
Arsenic salts have been used for centuries to treat a variety of medical conditions ranging from infectious disease to cancer. More recently, trivalent arsenic trioxide was found to exhibit high antitumor activity towards hematological malignancies. Even though much is known about antitumor activity and DNA damage by As2O3, there has been no report on the interaction of arsenic trioxide with isolated DNA or RNA. Therefore, it was of interest to examine the interaction of As2O3 with DNA and RNA in aqueous solution at physiological pH. FTIR and UV-visible difference spectroscopic methods were used to characterize the nature of drug-DNA and drug-RNA interactions and to determine the As binding site, the binding constant, the sequence selectivity, the helix stability, and the biopolymer secondary structure in the As2O3-polynucleotide complexes in vitro. The FTIR spectroscopic studies were conducted with As2O3-polynucleotide (phosphate) ratios of 1/40, 1/20, 1/10, and 1/5, with a final DNA (P) or RNA (P) concentration of 6.25 mmol/l. Spectroscopic results showed As2O3 binds to DNA and RNA at G-C, A-T, and A-U bases, and no interaction with the backbone PO2 group. As2O3-DNA and -RNA adducts showed one type of binding with overall binding constant of K(As2O3-DNA) = 1.24 x 10(5) M(-1) and K(As2O3-RNA) = 2.60 x 10(5) M(-1). The As2O3-polynucleotide complexation is associated with a partial biopolymer aggregation and no major alterations of B-DNA or A-RNA structure. 相似文献
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Payabvash S Ghahremani MH Goliaei A Mandegary A Shafaroodi H Amanlou M Dehpour AR 《Free radical biology & medicine》2006,41(12):1817-1828
Nitric oxide is known to modulate intracellular glutathione levels, but the relationship between nitric oxide synthesis and glutathione metabolism during endotoxemia is unknown. The present study was designed to examine the effects of increased nitric oxide formation on hepatic glutathione synthesis and antioxidant defense in endotoxemic mice. Our results demonstrate that hepatic glutathione synthesis is decreased for 24 h following injection of lipopolysaccharide (LPS). Administration of the cysteine precursor, L-2-oxothiazolidine-4-carboxylic acid (OTZ), failed to normalize hepatic glutathione concentration, and suggests that decreased γ-glutamylcysteine ligase activity is primarily responsible for the decrease in hepatic glutathione levels during endotoxemia. Inhibition of nitric oxide synthesis prevented the endotoxin-induced changes in hepatic and plasma glutathione status and up-regulated liver glutathione and cysteine synthesis pathways at the level of gene expression. Furthermore, whereas the activity of glutathione peroxidase and glutathione S-transferase decreased during endotoxemia, both of these changes were prevented by inhibition of nitric oxide synthesis. In conclusion, increased nitric oxide synthesis during endotoxemia causes marked changes in glutathione flux and defenses against oxidative stress in the liver. 相似文献
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Mohammad Hossein Soleimani Majid Talebi Badraldin Ebrahim Sayed-Tabatabaei 《Plant Systematics and Evolution》2012,298(6):1141-1149
Sequence-related amplified polymorphism (SRAP) was used to assess the genetic diversity of 63 cultivated, wild, and ornamental pomegranate genotypes from five different geographical regions of Iran. A total of 250 fragments were amplified using 13 primer combinations; among these, 133 bands (53?%) were polymorphic. The average PIC value was 0.28 over all PCs. The genetic distance among genotypes ranged from 0.10 to 0.37 with an average of 0.24. Cluster analysis using the neighbor-joining (NJ) method suggested there are close relationships between ornamental and some wild genotypes. Although AMOVA results revealed significant differences in the genetic diversity among the regions (P?=?0.0048), the genetic variation was mainly caused by variation of intra regions. The results indicated low genetic differentiation (Fst?=?0.025) and high gene flow (Nm?=?2.28) among regions. These results confirmed that SRAP markers could be powerful tools and an effective marker system for determining the genetic diversity and population genetic structure of the pomegranate. 相似文献