China
Africa
Explore chapters and articles related to this topic
The Molecular Basis of Action of Abused Substances
Published in Frank Lynn Iber, Alcohol and Drug Abuse as Encountered in Office Practice, 2020
This is the mode of action of the volatile anesthetic agents and of ethanol at concentrations greater than 400 mg/dl. Of great interest is animal experimentation showing that prolonged and chronic exposure to ethanol results in host adaptation to these plasma membrane changes such that the impairment is less in the chronically exposed animal; this host adaptation is associated with specific changes in the composition of the cellular membranes. Such changes appear after 2 to 3 weeks of chronic ethanol exposure and disappear about 1 week after cessation of such treatment. During withdrawal this compensation is unbalanced, producing symptoms. These results, however, do not explain the clear fact that alcohol produces effects on behavior at a level well below that needed to alter plasma membrane function.
The Acute Phase Response: An Overview
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Irving Kushner, Andrzej Mackiewicz
The known biological functions of APP can be divided into three major categories: participation in host adaptation or defense, inhibition of serine proteinases, and transport of proteins with antioxidant activity, as recently reveiwed by Volanakis.10 His review serves as the basis for portions of this section. These categories, however, do not include all of the APP, since biological functions of some others, notably SAA, are not known.
The Treatment of Advanced Prostatic Cancer with Drugs and Hormones
Published in Nicholas Bruchovsky, James H. Goldie, Drug and Hormone Resistance in Neoplasia, 2019
Two main theories have been entertained to explain the relapse of patients initially responding to orchiectomy or estrogen therapy. Historically, the first was host adaptation and partial compensatory rise of circulating androgens which might be overcome by increased surgical or medical efforts to reduce them. The adrenal cortex was suspected as the putative source, and a twofold rise of androstenedione has been noted in the first month after orchiectomy in 10/27 patients.210 This was accompanied by fivefold higher residual testosterone levels, and both could be suppressed to low levels by dexamethasone. Sanford et al.216 demonstrated testosterone secretion from the adrenal cortex by measuring an arteriovenous gradient; however, they did not find any difference in adrenal testosterone secretion before and after orchiectomy. In long-term studies, cortisol continues to rise after orchiectomy over a 5-year period,217 implying increased ACTH drive, and injected ACTH is known to raise serum testosterone after prolonged estrogen therapy compared to the testosterone supression produced prior to treatment.178 Compensatory adrenal hypertrophy is well-known in the rat, but has had rare mention in man.218 Although some have found sustained low levels of testosterone,173 there may be a delayed rise which can be suppressed by pituitary ablation or aminoglutethimide.160
Genetic heterogeneity of group A rotaviruses: a review of the evolutionary dynamics and implication on vaccination
Published in Expert Review of Anti-infective Therapy, 2022
Cornelius A. Omatola, Ademola O. Olaniran
In intragenotypic recombination, the effects of change are usually long-lasting on the new strain and the emerging genotype could be maintained in the population and disseminated widely [73]. Recombination events taking place in regions of genes that encode conserved antigenic determinants, particularly in the sequence coding for proteins needed for cellular attachment and entry afford rotavirus a selective advantage by allowing the virus to escape the immune-mediated attack. However, mutants that evaded host immunological attacks may not be as adapted to the host as wild-type viruses but are more likely to have a fitness advantage in the hosts as they are no longer recognized by the host immune system. Succeeding intra-host adaptation may then select for compensatory fitness through an increase in mutations, thereby enabling these strains to be competitive with circulating rotavirus strains [73].
The Sporobiota of the Human Gut
Published in Gut Microbes, 2021
Muireann Egan, Eugene Dempsey, C. Anthony Ryan, R. Paul Ross, Catherine Stanton
On the other hand, a recent publication by Browne et al. investigated the loss of sporulation in the Firmicutes of the adult gut microbiome.50 Genomes with a low sporulation signature score were designated as Former Spore-Formers (FSF), based on the belief that sporulation evolved just once in Firmicutes, while those with a high score were designated Spore-Formers (SF).5,7,46 Genomes from the Lactobacillales order were entirely FSF, while in the Lachnospiraceae (described in more detail below), just 18% were FSF. FSF genomes were associated with broader genome decay, not just in sporulation genes, indicative of host adaptation. However, while the FSF genomes were more abundant in the gut, they were less prevalent across samples, indicating that a loss of sporulation ability limits the transmission of FSF bacteria.50
“I will survive”: A tale of bacteriophage-bacteria coevolution in the gut
Published in Gut Microbes, 2019
Luisa De Sordi, Marta Lourenço, Laurent Debarbieux
Reductionist approaches using E. coli and its bacteriophages have successfully deciphered major mechanisms of molecular biology.21-23 By lifting the reductionist approach to the next level of complexity, namely the study of the intestinal microbiota, we recently described the coevolution of one bacteriophage with multiple host strains within the mouse gut.24 We studied P10, a virulent bacteriophage from the Myoviridae family, infecting the E coli strain LF82, and we assessed its ability to adapt to E. coli strain MG1655, to which it was initially unable to bind and therefore could not infect. Such host-range expansion was observed, but only occurred during coevolution in the gut of conventional mice hosting E. coli strains LF82 and MG1655 within their microbiota. In planktonic in vitro cultures or in the gut of dixenic mice colonized solely by the two E. coli strains, this event was never detected. Based on these findings, we hypothesized that the mouse microbiota played a crucial role in promoting adaptation. Indeed, we showed that this adaptation was initiated by the infection of an intermediate host, E. coli strain MEc1, which we isolated from the murine microbiota. Mixing bacteriophage P10 in vitro with the three E. coli strains also promoted viral host-range expansion. This adaptation was accompanied by genomic differentiation in the bacteriophage population: a single point mutation in a tail fibre-encoding gene was found to be sufficient to promote host adaptation, but additional mutations were required to optimise the infectious cycle.