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[
Ann Parasitol Hum Comp
]
In lactating females of many animal species infested by Nematoda, the self-cure is, if not suppressed, at least very distinctly delayed. It does not appear that an immunological deficiency is the cause of this. We show that this phenomenon also exists in lactating female rats with Strongyloides ratti parasites. In fact, for Strongyloides ratti, the maintenance of the worms is not the only notable modification determined by lactation; much more important is the decrease in the intensity of the parasitism. This aspect is not mentioned by writers who have only studied the different parasitic states in their final phase. Parallel to these alterations in the parasitism, the evolution of the corticosteronemy differs, from two points of view, from that described in infested virgin rats: --Suppression of the hypercorticosteronemy which normally appears 48 hours after infestation; --Attenuation of the hypocorticosteronemy which usually sets in from the tenth day of infestation. This opposition of lactation to the variations in the corticosteronemy induced by the worms is explained by the effect of lactation on the secretion of gluco-cortico-steroids, described under the term of "buffer effect of lactation". The decrease in the intensity of the parasitism may be explained by the fact that lactation, by preventing the hypercorticosteronemy normally caused by larval migration, permits the intervention of aspecific defences. As for the prolongation of the parasitism, it would seem to result on one hand, from a reduced solicitation of the means of defence owing to a smaller number of worms and, on another hand, from the slowing down of the hypocorticosteronemy through the buffer effect of lactation with all the consequences flowing from this at the level of the specific and aspecific defence reactions.
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[
Ann Parasitol Hum Comp
]
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[
Ann Parasitol Hum Comp,
1986]
In order to assess the role of inflammation and its components in spontaneous cure of Strongyloides ratti infestation, rats were treated with non-steroid anti-inflammatory agents (indometacin; sodium salicylate) or with antagonists of certain mediators (dexchlorpheniramin; cyproheptadin, promethazin). Results were compared with those obtained in similar treatments of rats infested by other Nematoda which also give rise to spontaneous cure: especially Trichinella spiralis, and Nippostrongylus brasiliensis. Coordinating the various findings made it possible to devise a pattern accounting for the chain of reactions that lead to rejection of the parasite.
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[
Ann Parasitol Hum Comp
]
Repeated injections of corticosterone acetate, physiological hormone of the Rat, in rats carrying Strongyloides ratti, oppose the deparasiting which normally takes place spontaneously. The secretion induced by this hormone by impregnating the organism through the corticotropic factor administered in the form of tetracosactide-zinc, achieves the same result. During all these treatments, an important hypercorticosteronemy is established. Stopping the injections is quickly followed by the worms-being rejected and the corticosteronemy returning to normal. The relations between the corticosteronemy and the parasitism are analysed and lead to the conclusion that the parasite induces an aspecific hypocorticosteronemiant reaction which, through its aspecific and specific repercussions, participates in the self-cure phenomenon.
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[
Ann Parasitol Hum Comp
]
The variations in corticosteronemy induced by the development of Stronglyoides ratti in the Rat can be detected both in the afternoon, when corticosteronemy reaches its maximum, and in the morning when it is at its lowest rate. Nevertheless, hypercorticosteronemy, which is at its maximum 48 hours after infestation, is more sensible in the morning, whereas on the contrary hypocorticosteronemy is more significant in the afternoon and then shows a sudden and very important drop which seems to coincide with the beginning of the expulsion of the adult worms. According to previous results, inhibition of the secretion of gluco-cortico-steroids is caused by the worms; furthermore, Ogilvie and Jones show the determinant role of sensitized lymphocytes, for the expulsion of antibody-damaged worms, whereas some authors suggest that eosinophils act as cytotoxic cells on sensitized helminths; the hypothesis may therefore be put forward that hypocorticosteronemy liberates the intervention of active lymphocytes and eosinophils, triggering so the phenomenon of spontaneous deparasiting.
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[
Ann Parasitol Hum Comp,
1985]
The plasma corticosterone induced in the rat by the development of Strongyloides ratti or Trichinella spiralis reaches a sufficient level of intensity to determine reticulocytopenia. The latter is linked chronologically to the inhibition of parasitemia in Plasmodium berghei, which occurs when this protozoa develops at the same time as the Nematodes, and seems to be the causal factor. This hypothesis may be verified by replacing the helminths with the corticotropic action of A.C.T.H. which causes a decrease in the number of reticulocytes.
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[
Biochemistry,
1987]
The major intestinal esterase from the nematode Caenorhabditis elegans has been purified to essential homogeneity. Starting from whole worms, the overall purification is 9000-fold with a 10% recovery of activity. The esterase is a single polypeptide chain of Mr 60,000 and is stoichiometrically inhibited by organophosphates. Substrate preferences and inhibition patterns classify the enzyme as a carboxylesterase (EC 3.1.1.1), but the physiological function is unknown. The sequence of 13 amino acid residues at the esterase N- terminus has been determined. This partial sequence shows a surprisingly high degree of similarity to the N-terminal sequence of two carboxylesterases recently isolated from Drosophila mojavensis [Pen, J., van Beeumen, J., & Beintema, J. J. (1986) Biochem. J. 238, 691-699].
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[
Curr Biol,
1999]
In this Brief Communication, which appeared in the 14 September 1998 issue of Current Biology, the UV dose was reported erroneously. The dose reported was 20 J/m2 but the actual dose used was 0.4 J/cm2. Also, the gene formally referred to as
tkr-1 has since been renamed
old-1 (overexpression longevity determination).
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[
J Bacteriol,
2014]
Volume 195, no. 16, p. 35143523, 2013. A number of problems related to images published in this paper have been brought to our attention. Figure 1D contains duplicated images in lanes S and LE, and Fig. 4D and 6B contain images previously published in articles in this journal and in Microbiology and Microbial Pathogenesis, i.e., the following: C. G. Ramos, S. A. Sousa, A. M. Grilo, J. R. Feliciano, and J. H. Leitao, J. Bacteriol. 193:15151526, 2011. doi:10.1128/JB.01374-11. S. A. Sousa, C. G. Ramos, L. M. Moreira, and J. H. Leitao, Microbiology 156:896908, 2010. doi:10.1099/mic.0.035139-0. C. G. Ramos, S. A. Sousa, A. M. Grilo, L. Eberl, and J. H. Leitao, Microb. Pathog. 48:168177, 2010. doi: 10.1016/j.micpath.2010.02.006. Therefore, we retract the paper. We deeply regret this situation and apologize for any inconvenience to the editors and readers of Journal of Bacteriology, Microbial Pathogenesis, and Microbiology.
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Berynskyy M, Morimoto RI, Bukau B, Stengel F, Kirstein J, Szlachcic A, Arnsburg K, Stank A, Scior A, Nillegoda NB, Gao X, Guilbride DL, Aebersold R, Wade RC, Mayer MP
[
Nature,
2015]
Protein aggregates are the hallmark of stressed and ageing cells, and characterize several pathophysiological states. Healthy metazoan cells effectively eliminate intracellular protein aggregates, indicating that efficient disaggregation and/or degradation mechanisms exist. However, metazoans lack the key heat-shock protein disaggregase HSP100 of non-metazoan HSP70-dependent protein disaggregation systems, and the human HSP70 system alone, even with the crucial HSP110 nucleotide exchange factor, has poor disaggregation activity in vitro. This unresolved conundrum is central to protein quality control biology. Here we show that synergic cooperation between complexed J-protein co-chaperones of classes A and B unleashes highly efficient protein disaggregation activity in human and nematode HSP70 systems. Metazoan mixed-class J-protein complexes are transient, involve complementary charged regions conserved in the J-domains and carboxy-terminal domains of each J-protein class, and are flexible with respect to subunit composition. Complex formation allows J-proteins to initiate transient higher order chaperone structures involving HSP70 and interacting nucleotide exchange factors. A network of cooperative class A and B J-protein interactions therefore provides the metazoan HSP70 machinery with powerful, flexible, and finely regulatable disaggregase activity and a further level of regulation crucial for cellular protein quality control.