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Only Mild (only + mild)
Selected AbstractsImpact of chemical elicitor applications on greenhouse tomato plants and population growth of the green peach aphid, Myzus persicaeENTOMOLOGIA EXPERIMENTALIS ET APPLICATA, Issue 3 2006Anthony J. Boughton Abstract Recent advances in the understanding of plant signaling pathways have opened the way for using elicitor-induced plant resistance as a tactic for protecting plants against arthropod pests. Four common elicitors of induced responses in tomato, Lycopersicon esculentum Mill. (Solanaceae), were evaluated with regard to phytotoxicity, induction of plant defensive proteins, and effects on population growth and fecundity of a common pest, the green peach aphid, Myzus persicae (Sulzer) (Homoptera: Aphididae). Ethephon and methyl jasmonate (MJ) treatments caused varying degrees of phytotoxicity. Ethephon caused pronounced changes in plant growth form and severe, dose-dependent negative impacts on plant growth and flowering. Effects with MJ were milder, but still caused temporary inhibition of development, leading to smaller plants and delayed flowering. The commercial elicitors benzothiadiazole (BTH) and harpin did not cause detectable phytotoxicity. The highest doses of ethephon and MJ significantly increased leaf peroxidase (POD) levels but only MJ treatments significantly increased polyphenol oxidase (PPO) levels. BTH and harpin had no detectable effects on POD and PPO. Populations of green peach aphids grew significantly more slowly on plants treated with BTH or MJ than on control plants or plants treated with harpin or ethephon. Slowed aphid population growth on BTH-treated plants was due to significant reductions in aphid fecundity, although this was independent of changes in time to onset of reproduction or time to death. Aphid fecundity was also reduced on MJ-treated plants relative to controls, but this difference was not statistically significant, suggesting that other mechanisms are involved in slowing aphid population growth on MJ-treated plants. Growth of aphid populations on plants treated with a MJ,BTH mixture was reduced almost as much as with treatments of MJ alone, suggesting that antagonism between JA-dependant and SA-dependent plant signaling pathways is only mild with regard to induced defenses against aphids. [source] Antiepileptogenic and antiictogenic effects of retigabine under conditions of rapid kindling: An ontogenic studyEPILEPSIA, Issue 10 2008Andréy Mazarati Summary Purpose:, To examine antiepileptogenic and antiictogenic potential of retigabine (RTG) under conditions of rapid kindling epileptogenesis during different stages of development. Methods:, The experiments were performed in postnatal day 14 (P14), P21, and P35 male Wistar rats. After stereotaxic implantation of hippocampal stimulating and recording electrodes, the effects of RTG on baseline afterdischarge (AD) properties were studied. Next, the animals underwent rapid kindling (sixty 10 s trains, bipolar 20 Hz square wave pulses delivered every 5 min). The progression of seizures (kindling acquisition), and responses to test stimulations after kindling (retention) were compared between RTG and vehicle-treated rats. Additionally, the effects of RTG on the severity of seizures in previously kindled animals were examined. Results:, When administered intraperitoneally in doses that induced only mild, or no motor deficits, RTG significantly dampened brain excitability, evident as the increase of AD threshold and shortening of AD duration. During kindling, RTG delayed the development of focal seizures in P14 rats, and prevented the occurrence of full limbic seizures at all three ages. At P14 and P21, but not at P35, pretreatment with RTG prevented the establishment of kindling-induced enhanced seizure susceptibility. Administration of RTG to kindled animals decreased the severity of seizures induced by test stimulation. The effect was most prominent at P14. Discussion:, RTG exerted both antiepileptogenic and antiictogenic effects under conditions of rapid kindling model. These effects were apparent during postneonatal, early childhood, and adolescent stages of development. [source] Clonally rearranged T-cell receptor , chain genes in HTLV-I carriers with abnormal, non-flower-like, lymphocytesEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 4 2005Maria M. Sales Abstract:,Background:,The diagnosis of Adult T-cell leukemia/lymphoma ATLL subtypes in human T-lymphotropic virus type I (HTLV-I) carriers based in morphology and immunophenotype of lymphocytes can be challenger. We propose that polymerase chain reaction (PCR) amplification of the rearranged TCR gene in HTLV-I healthy carriers would be a convenient method for establishing the nature of the circulating T lymphocytes in asymptomatic HTLV-I carriers, presenting only mild and inconclusive signals of deviation from normality. Methods:,Using PCR, we analyzed the genetic recombination pattern of the T-cell , -chain receptor gene (TCR - ,) in order to identify clonal expansion of peripheral blood T lymphocytes in 17 HTLV-I-positive healthy carriers and in nine normal HTLV-I-negative blood donors. To evaluate the performance of PCR in detection of clonality, we also analyzed 18 patients with post-thymic/mature T-cell malignancies presenting circulating abnormal lymphocytes. Results:,Seven of the 17 HTLV-I positive individuals presented circulating abnormal lymphocytes; monoclonal or oligoclonal expansion of T-cells was detected in five of the 17 HTLV-I-positive individuals, all of them presenting abnormal lymphocytes. Clonal expansion was not detected in any of the negative controls or in any of the 12 remaining healthy carriers. All patients in the positive control group tested positive by PCR and Southern blots. Southern blots were negative for all 17 healthy carriers. Conclusions:,PCR amplification of segments of rearranged TCR- , is reliable for allowing early detection of small populations of clonal T cells in blood samples from asymptomatic HTLV-I carriers, providing an additional alert in the follow-up of carriers with abnormal circulating lymphocytes. [source] Co-expression of C-terminal truncated alpha-synuclein enhances full-length alpha-synuclein-induced pathologyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2010Ayse Ulusoy Abstract Lewy bodies, which are a pathological hallmark of Parkinson's disease, contain insoluble polymers of alpha-synuclein (,syn). Among the different modifications that can promote the formation of toxic ,syn species, C-terminal truncation is among the most abundant alterations in patients with Parkinson's disease. In vitro, C-terminal truncated ,syn aggregates faster and sub-stoichiometric amounts of C-terminal truncated ,syn promote aggregation of the full-length ,syn (,synFL) and induce neuronal toxicity. To address in vivo the putative stimulation of ,syn-induced pathology by the presence of truncated ,syn, we used recombinant adeno-associated virus to express either ,synFL or a C-terminal truncated ,syn (1-110) in rats. We adjusted the recombinant adeno-associated virus vector concentrations so that either protein alone led to only mild to moderate axonal pathology in the terminals of nigrostriatal dopamine neurons without frank cell loss. When these two forms of ,syn were co-expressed at these pre-determined levels, it resulted in a more aggressive pathology in fiber terminals as well as dopaminergic cell loss in the substantia nigra. Using an antibody that did not detect the C-terminal truncated ,syn (1-110) but only ,synFL, we demonstrated that the co-expressed truncated protein promoted the progressive accumulation of ,synFL and formation of larger pathological accumulations. Moreover, in the co-expression group, three of the eight animals showed apomorphine-induced turning, suggesting prominent post-synaptic alterations due to impairments in the dopamine release, whereas the mild pathology induced by either form alone did not cause motor abnormalities. Taken together these data suggest that C-terminal truncated ,syn can interact with and exacerbate the formation of pathological accumulations containing ,synFL in vivo. [source] Relationship between presence of basidiomes, above-ground symptoms and root infection by Collybia fusipes in oaksFOREST PATHOLOGY, Issue 1 2000B. Marçis Summary Collybia fusipes is a common cause of root rot on oak in the north of France. Collybia fusipes basidiomes can be as frequent on oaks in stands where no decline of the trees occurs compared with stands where the decline is chronic. This might be explained by differences in the amount of roots damaged by the parasite. To test that hypothesis, 430 oak trees, Quercus petraea, Quercus robur and Quercus rubra, located in six forests were selected. Half of them showed C. fusipes basidiomes at the trunk base. The association between presence of basidiomes and decline of affected trees depended on the forest. The level of infection of each tree by C. fusipes, as well as the crown appearance, the tree height : diameter at breast height ratio, age and sapwood width were determined. The presence of C. fusipes basidiomes was always associated with significant root infections. The crowns of the trees deteriorated with increasing level of root infection and the decline was severe only when the root damage was heavy. Although the decline of trees that were heavily damaged by C. fusipes was severe in some of the stands, in others, it was only mild, and so the differences in tree decline between the stands could not be attributed solely to differences in root infection severity. Trees damaged by C. fusipes seemed not to be subjected to more competition than their undamaged neighbour as reflected by a similar tree height: diameter at breast height ratio. [source] Novel, single-dose, topical treatment of tinea pedis using terbinafine: results of a dose-finding clinical trialMYCOSES, Issue 1 2008Martine Feuilhade De Chauvin Summary Tinea pedis is the most common dermatophytosis requiring topical antifungals for at least 1,4 weeks. To determine the effectiveness of a novel topical single dose formulation of terbinafine (film forming solution-FFS) in the treatment of tinea pedis, 344 outpatients from 43 dermatological centres in France and Bulgaria suffering from tinea pedis with possible extension to soles confirmed by mycological examination (direct and culture) were evaluated for efficacy of terbinafine 1%, 5%, 10% FFS in a randomised double blind vehicle controlled parallel group dose finding study. Evaluations were carried out at baseline, 1 and 6 weeks after a single application of FFS. Effective treatment rate based on negative mycology (direct and culture) and minimal signs and symptoms (two or less with only mild recorded) was measured at week 6. Effective treatment rates at week 6 with terbinafine 1%, 5% and 10% FFS were 66%, 70%, 61% compared with 18% with placebo. All three active preparations were shown to be significantly superior to placebo (P < 0.001). Terbinafine 1% and 5% FFS were shown to be non-inferior to terbinafine 10% FFS. Terbinafine 1% FFS is an effective, safe dose for the treatment of tinea pedis. This novel product represents a significant advance with the enhanced compliance and convenience that it offers. [source] Absence of neuronal nitric oxide synthase (nNOS) as a pathological marker for the diagnosis of Becker muscular dystrophy with rod domain deletionsNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2004S. Torelli Immunohistochemistry using antibodies to dystrophin is the pathological basis for the diagnosis of Duchenne and Becker muscular dystrophy (DMD and BMD). While the sarcolemma of DMD muscle is negative, BMD muscle generally shows variable labelling because of the translation of a partially functional dystrophin that is localized to the sarcolemma. In rare cases, however, this labelling is equivocal and similar to that observed in controls making diagnosis difficult. We report here that in such instances immunolabelling with antibodies to the neuronal form of nitric oxide synthase (nNOS) can be useful in suspecting a dystrophinopathy with a mutation in the ,hot-spot' rod domain and help to direct molecular analysis. nNOS localizes to the sarcolemma of mature muscle fibres via several components of the dystrophin-associated protein complex (DAPC) including dystrophin but sarcolemmal nNOS is lost when dystrophin levels are very low or absent because of deletions in critical regions of the rod domain. We report three cases who presented with only mild or no muscle weakness but had elevated serum creatine kinase activity and dystrophin immunolabelling indistinguishable from normal, making a pathological diagnosis difficult. All three cases had a complete absence of sarcolemmal nNOS and were subsequently found to have an in-frame deletion in the common rod domain exons (in these cases 48, 45,51, 47,53) compatible with a BMD. In addition, we observed that nNOS appears to be developmentally regulated with the antibody used and was often absent from the sarcolemma of immature fibres. These findings demonstrate the value of including antibodies to nNOS in routine immunohistochemical studies and that absence of nNOS can be a more sensitive marker than up-regulation of utrophin for diagnosis of BMD. Immaturity of fibres, however, needs to be taken into account, especially in neonates. [source] | |||||||||||||