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PubMedDate not supplied

Neutralization epitope patterns of poliovirus strains isolated from cases of acute spinal paralysis and from healthy vaccinated children.

By using a battery of poliovirus neutralizing monoclonal antibodies received from the Pasteur Institute, Paris, we carried out the study of the patterns of neutralization epitopes of more than 300 poliovirus strains isolated from cases of acute spinal paralysis and from healthy vaccinated children. We tried to find out the utility of this test for establishing the origin (wild or Sabin) of a poliovirus strain and the possible evolution of the pattern of neutralization epitopes. The study of the neutralization epitopes was carried out by neutralization index assay (NI). The neutralization index represents the difference between the titers of poliovirus strain determined in parallel in the absence, as well as in the presence of constant concentration (predetermined) for each monoclonal antibody. An epitope was considered to be present for a NI > or = 2 and absent for a NI < or = 1.5. For types 1 and 3 polioviruses, Sabin-like epitopes have never been found to be present simultaneously with wild type epitopes on the same virus particle. Therefore, examination of the epitope pattern of these strains is very useful for intratypic differentiation. On the other hand, in type 2 poliovirus strains, Sabin and wild type epitopes sometimes coexist, in various combinations, thus rendering the interpretation of the results rather difficult.

Antibodies, Monoclonal↗
PubMed2006

Cheating can stabilize cooperation in mutualisms.

Mutualisms present a challenge for evolutionary theory. How is cooperation maintained in the face of selection for selfishness and cheating? Both theory and data suggest that partner choice, where one species preferentially directs aid to the more cooperative members of the other species, is central to cooperation in many mutualisms. However, the theory has only so far considered the evolutionary effects of partner choice on one of the species in a mutualism in isolation. Here, we investigate the co-evolution of cooperation and choice in a choosy host and its symbiont. Our model reveals that even though choice and cooperation may be initially selected, it will often be unstable. This is because choice reduces variation in the symbiont and, therefore, tends to remove the selective incentive for its own maintenance (a scenario paralleled in the lek paradox in female choice and policing in within-species cooperation). However, we also show that when variability is reintroduced into symbionts each generation, in the form of less cooperative individuals, choice is maintained. This suggests that the presence of cheaters and cheater species in many mutualisms is central to the maintenance of partner choice and, paradoxically, cooperation itself.

Animals↗
PubMed2025

Influence of genetic factors of humans, mosquitoes and parasites, on the evolution of Plasmodium falciparum infections, malaria transmission and genetic control methods: a review of the literature.

Despite significant progress, malaria remains a public health problem in many regions, particularly in sub-Saharan Africa. This situation is partly explained by the mosquito's resistance to insecticides and the emergence of parasite resistance to antimalarial drugs. Indeed, in spite of the various vectors' controls, insecticide resistance emerges from multi-generational selection and poses worldwide concern. In parallel, artemisinin resistance unfortunately emerged independently in multiple countries in eastern Africa. Since 2014, artemisinin resistance has been observed in 6 countries in Africa and, more concerningly, the evidence from longitudinal molecular surveys in these countries suggests that it is spreading. While phenotypic evidence of treatment failure is still limited, the increasing reports of validated artemisinin resistance mutations are alarming. Unlike the emergence of artemisinin resistance in South-East Asia, our understanding of the genetic determinants of artemisinin resistance and our ability to sequence and map the spread of resistance are significantly greater. In addition to mosquito and parasite genetics affecting malaria evolution, many human individual variants have been identified that are associated with malaria protection, but the most important of all relates to the structure or function of red blood cells, the classical polymorphisms that causes sickle cell trait, &#x3b1;-thalassaemia, G6PD deficiency, and the major red cell blood group variants. In that biological complex context, there is a need to characterize the various genetic factors in Plasmodium falciparum, humans and mosquitoes that are potentially associated with resistance to antimalarial drugs and insecticides, and their involvement in the evolution, severity and transmission of malaria. In this direction, A comprehensive literature review was conducted to capture the objectives highlighted above. The advances in genomic surveillance and emerging genetic control strategies, such as gene drive technology were also considered in this review. We used search engines such as PubMed and Google scholar to retrieve articles useful to the objective of this paper and information on the knowledge of genetic factors and methods that contributed to malaria control were synthesized.

Humans↗
PubMed2026

Evolution of virulence of a plant RNA virus in developmental stage-structured host populations.

Natural host populations are age-structured, and developmental stages differ in susceptibility and within-host pathogen dynamics, potentially imposing distinct selective pressures on viruses. However, the evolutionary consequences of host age structure remain poorly understood. We experimentally evolved turnip mosaic potyvirus for 5 passages in Arabidopsis thaliana populations spanning 7 demographic regimes, from juvenile- to mature-dominated cohorts. We quantified disease progression, symptom severity, and viral load, cross-inoculated evolved lineages across host stages to construct infection matrices, and performed whole-population sequencing at passages 1 and 5. Disease traits changed markedly with passage, demography, and their interaction. Disease progression evolved faster in older populations, whereas symptom severity was independent of median age, indicating demographic reweighting of virulence components. Viral load increased across passages and positively correlated with severity, linking within-host fitness to symptoms. Cross-inoculation assays revealed a modular infection network: juvenile-evolved lineages specialized on juvenile hosts, whereas lineages from intermediate and older populations were more generalist. Genomically, we detected both parallel and demography-specific adaptations, including recurrent changes in the viral protein VPg (involved in translation, replication, and host interactions) as well as synonymous variants showing consistent or opposing selection across host population stage structures. Overall, host age structure emerges as a major ecological driver of virulence evolution, shaping tradeoffs between disease progression and severity and determining specialization versus generalism. These results integrate phenotypic and genomic responses and suggest that manipulating crop age structure could steer virus evolution toward less damaging outcomes.

Virulence↗
PubMed2003

Mode of selection and experimental evolution of antifungal drug resistance in Saccharomyces cerevisiae.

We show that mode of selection, degree of dominance of mutations, and ploidy are determining factors in the evolution of resistance to the antifungal drug fluconazole in yeast. In experiment 1, yeast populations were subjected to a stepwise increase in fluconazole concentration over 400 generations. Under this regimen, two mutations in the same two chromosomal regions rose to high frequency in parallel in three replicate populations. These mutations were semidominant and additive in their effect on resistance. The first of these mutations mapped to PDR1 and resulted in the overexpression of the ABC transporter genes PDR5 and SNQ2. These mutations had an unexpected pleiotropic effect of reducing the residual ability of the wild type to reproduce at the highest concentrations of fluconazole. In experiment 2, yeast populations were subjected to a single high concentration of fluconazole. Under this regimen, a single recessive mutation appeared in each of three replicate populations. In a genome-wide screen of approximately 4700 viable deletion strains, 13 were classified as resistant to fluconazole (ERG3, ERG6, YMR102C, YMR099C, YPL056C, ERG28, OSH1, SCS2, CKA2, SML1, YBR147W, YGR283C, and YLR407W). The mutations in experiment 2 all mapped to ERG3 and resulted in the overexpression of the gene encoding the drug target ERG11, but not PDR5 and SNQ2. Diploid hybrids from experiments 1 and 2 were less fit than the parents in the presence of fluconazole. In a variation of experiment 2, haploids showed a higher frequency of resistance than diploids, suggesting that degree of dominance and ploidy are important factors in the evolution of antifungal drug resistance.

Biological Evolution↗
PubMedDate not supplied

Genetic analysis of insulin signaling in Drosophila.

Studies in the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans have revealed that components of the insulin signaling pathway have been highly conserved during evolution. Genetic analysis in Drosophila suggests that structural conservation also extends to the functional level. Flies carrying mutations that reduce insulin signaling have a growth deficiency phenotype similar to that seen in mice with disruptions of genes encoding insulin-like growth factors (IGFs) or the IGF-I receptor. Recent studies in flies have demonstrated a role for the insulin signaling pathway in the regulation of metabolism, reproduction and lifespan via modulation of central neuroendocrine pathways. Similarly, mice with loss of brain insulin receptors or insulin receptor substrate 2 deficiency exhibit neuroendocrine defects and female infertility. These parallels suggest that the insulin system has multiple conserved roles, acting directly to modulate growth and indirectly, via the neuroendocrine system, to modulate peripheral physiology in response to changes in nutrient availability.

Animals↗
PubMed2005

Evolution and integration of innate immune systems from fruit flies to man: lessons and questions.

Despite broad differences in morphology, ecology and behavior, the fruit fly Drosophila melanogaster and humans show a remarkably high degree of conservation for many molecular, cellular, and developmental aspects of their biology. During the last decade, similarities have also been discovered in some of the mechanisms regulating their innate immune system. These parallels regard mainly the Toll-like receptor family and the intracellular signaling pathways involved in the control of the immune response. However, if the overall similarities are important, the detailed pathogen recognition mechanisms differ significantly between fly and humans, highlighting a complicated evolutionary history of the metazoan innate defenses. In this review, we will discuss the main similarities and differences between the two types of organisms. We hope that this current knowledge will be used as a starting point for a more comprehensive view of innate immunity within the broad variety of metazoan phyla.

Animals↗
PubMed1976

Trapping at low temperature of oriented chloroplasts: application to the study of antenna pigments and of the trap of photosystem-1.

A technique is described for the preparation of oriented samples from spinach chloroplasts whose linear dichroism is then studied by (flash) absorption spectroscopy. The chloroplasts are suspended in a glycerol-containing medium, oriented in a magnetic field, and slowly cooled in the magnet until the medium is rigid enough to avoid disorientation effects. The absorption spectra in polarized light have been measured at -50 degrees and -170 degrees C. They allow the orientation of chlorophyll b to be resolved, and the red transition moment is found to be tilted out of the membrane plane. A study of the flash-induced absorption changes linked to Photosystem-1 activity reveals a progressive evolution of the difference spectra and of the linear dichroism with decreasing temperatures. At -170 degrees C, the difference spectrum of P700 in the red is well resolved. All transition moments are found to be largely parallel to the membrane plane. The potential use of the technique for other experiments by differential absorption spectroscopy and by EPR techniques is discussed.

Chlorophyll↗
PubMed2002

Magnetization structure contrast based on intermolecular multiple-quantum coherences.

In vivo and ex vivo MRI based on intermolecular multiple-quantum coherences (iMQC) is predicted to provide a fundamentally different source of contrast for MRI. This article investigates the dependence of image contrast upon the choice of correlation distance for a heterogeneous material. A closely packed array of parallel hollow cylinders was used to demonstrate signal intensity variations when the correlation distance becomes comparable to the gap size between the cylinders. The observed effects agree well with three-dimensional calculations of the time evolution of magnetization under the nonlinear Bloch equations.

Contrast Media↗
PubMed1994

Structure-function relationships in the neurotrophin family.

The study of structure-function relationships in the neurotrophin family has in recent years increased our understanding of several important aspects of neurotrophin function. Site-directed mutagenesis studies have localized amino acid residues important for binding to the low-affinity (p75LNGFR), as well as to the members of the Trk family of tyrosine kinase receptors. A cluster of positively charged residues has been shown to form a surface for binding to p75LNGFR in all four neurotrophins. Differences in the spatial distribution of these charges among the different neurotrophins may explain some of their distinct binding properties. Elimination of these positive charges drastically reduces binding to p75LNGFR but not to the Trk family members, and it does not impair the biological properties of the neurotrophins in vitro, arguing that binding to and activation of Trk receptors is sufficient to mediate the biological responses of neurotrophins. In contrast, the binding sites to Trk receptors appear to be formed by discontinuous stretches of amino acid residues distributed throughout the primary sequence of the molecule. These include the N-terminus, some of the variable loop regions and a beta-strand. Despite their apparent distribution, when viewed in the three-dimensional structure of NGF, these residues appear grouped on one side of the neurotrophin dimer, delineating a continuous surface extending approximately parallel to the twofold symmetry axis of the molecule. Two symmetrical surfaces are formed along the axis of the neurotrophin dimer providing a model for ligand-mediated receptor dimerization. In the neurotrophin family, co-evolution of cognate ligands and Trk receptors has developed specific contacts through different residues in the same variable regions of the neurotrophins. Thus, binding specificity is determined by the cooperation of distinct active and inhibitory binding determinants that restrict ligand-receptor interactions. Binding determinants to the Trk receptors can be manipulated independently in a rational fashion to create neurotrophin analogues with novel ligand-binding properties. In this way, second-generation chimeric neurotrophins with multiple specificities (pan-neurotrophins) have been engineered which may have valuable applications in the treatment of neurodegeneration and nerve damage.

Amino Acid Sequence↗
PubMed1996

The impact of polystyrene resins in solid-phase organic synthesis.

A major objective of the DIVERSOMER technology is to provide pure and characterized compounds for biological testing in order to prevent 'false negatives' in our libraries. On several occasions, analysis of the final products by 1H-NMR and MS, has revealed by-products from the polystyrene solid support. Subsequently, three alternative methods were studied to remove polystyrene by-products; (i) prewashing of the resin prior to execution of the synthesis; (ii) pretreatment of the resin with the cleavage conditions consistent with the solid-phase synthesis reaction scheme; and (iii) parallel purification.

Chemistry, Organic↗
PubMed2026

Defining and managing high-risk acute myeloid leukemia (AML) in 2026.

Acute myeloid leukemia (AML) remains a highly heterogeneous malignancy in which outcomes are particularly poor for patients classified as having high-risk disease. Traditionally, high-risk AML has been defined by adverse baseline genetic features, including complex cytogenetics, TP53 alterations, and mutations associated with secondary or therapy-related disease. However, this static, genetics-centered definition is increasingly insufficient in the modern therapeutic era. Emerging evidence supports a more dynamic and context-dependent model in which risk is shaped not only by molecular architecture but also by treatment intensity, patient fitness, measurable residual disease (MRD), and evolving resistance mechanisms. Advances in genomic profiling have refined risk stratification frameworks, including ELN 2022 for intensively treated patients and the ELN 2024 classification for those receiving less-intensive therapies. In parallel, MRD has emerged as a powerful biomarker that reclassifies patients during treatment, identifying those with persistent, therapy-resistant disease despite morphologic remission. Biologically, high-risk AML is driven by the interplay of clonal evolution, epigenetic plasticity, leukemic stem cell persistence, and protective microenvironmental and immune interactions, all of which contribute to relapse. Therapeutically, the landscape has expanded to include targeted agents, venetoclax-based combinations, and transplantation strategies, yet outcomes remain limited in key high-risk subsets, particularly TP53-mutated disease and post-venetoclax relapse. Accordingly, current strategies emphasize rational combination therapies, MRD-guided treatment adaptation, and approaches targeting both leukemic cells and their supportive niches. In 2026, high-risk AML is best understood as a dynamic, treatment-context-dependent state. Improving outcomes will require integration of precision diagnostics, biologically informed therapy, and adaptive strategies designed to anticipate and overcome resistance.

Humans↗
PubMedDate not supplied

[Generic drugs in Spain: first stage].

OBJECTIVES: To analyse the evolution of the consumption of generic medicines in the first months of their existence in our country, and the additional savings that could have been achieved if they had been used to their full potential. In parallel, to analyse the supply of these products. DESIGN: Observational, retrospective study. SETTING: The entire National Health Service. PARTICIPANTS: All medical prescriptions officially issued under the National Health System in Spain between October 1997 and December 1998. MEASUREMENTS AND MAIN RESULTS: During this period generic medicines to the value of 1727 million pesetas (10.4 million euros) were consumed in our country. This was equivalent to 22.8 millions DDD of 18 different active principles. This figure represented 0.15% of the total consumption of pharmaceutical products in retail amount paid, and 0.17% in number of packages. The potential additional saving that could have been achieved was calculated at 13,227 million pesetas (79.5 million euros). The number of different kinds of generic medicines on sale in May 1999 was 67. CONCLUSIONS: The consumption of generic medicines in Spain is increasing steadily in absolute figures in this first stage of their existence. However, there is a long way to go before they reach their maximum potential. As such, the saving not achieved is still very substantial. Supply is also increasing steadily.

Drug Prescriptions↗
PubMed2000

Cochlear mechanisms from a phylogenetic viewpoint.

The hearing organ of the inner ear was the last of the paired sense organs of amniotes to undergo formative evolution. As a mechanical sensory organ, the inner-ear hearing organ's function depends highly on its physical structure. Comparative studies suggest that the hearing organ of the earliest amniote vertebrates was small and simple, but possessed hair cells with a cochlear amplifier mechanism, electrical frequency tuning, and incipient micromechanical tuning. The separation of the different groups of amniotes from the stem reptiles occurred relatively early, with the ancestors of the mammals branching off first, approximately 320 million years ago. The evolution of the hearing organ in the three major lines of the descendents of the stem reptiles (e.g., mammals, birds-crocodiles, and lizards-snakes) thus occurred independently over long periods of time. Dramatic and parallel improvements in the middle ear initiated papillar elongation in all lineages, accompanied by increased numbers of sensory cells with enhanced micromechanical tuning and group-specific hair-cell specializations that resulted in unique morphological configurations. This review aims not only to compare structure and function across classification boundaries (the comparative approach), but also to assess how and to what extent fundamental mechanisms were influenced by selection pressures in times past (the phylogenetic viewpoint).

Animals↗
PubMed1998

Dependencies of substitution steps number on Hamming distance are identical for one-parameter discrete models of both direct and parallel genetic diversity.

With the help of previously introduced enumeration procedure (M.Yu. Shchelkanov, A.N. Yudin, A.V Antonov, N.S. Starikov, A.A. Vedenov, E.V. Karamov, J. Biomol. Struct. Dyn. 15, 217-229 (1997)) and probability distribution function for the enumeration after some substitution steps (M.Yu. Shchelkanov, L.A. Soinov, V.V. Zalunin, D.A. Gumennyi, A.N. Yudin, A.A. Natan, V.B. Kireev, E.V. Karamov, J. Biomol. Struct. Dyn. 15, N 4, (1998)) we have demonstrated that dependencies of replication acts number on Hamming distance are identical for one-parameter discrete models of both direct and parallel genetic diversity.

Evolution, Molecular↗
PubMed1993

The SLT2 (MPK1) MAP kinase homolog is involved in polarized cell growth in Saccharomyces cerevisiae.

Bud emergence, spindle pole body duplication and DNA replication are all dependent on the activation of the CDC28 protein kinase at the Start point in the G1 phase of the cell cycle. Bud emergence requires polarization of the cytoskeleton and secretory vesicles to a specific site on the cell surface. Cdc28p activated by G1-cyclins triggers polarization of actin to the site of bud emergence and favors apical bud growth (Lew, D. J., and S. I. Reed. 1993. J. Cell Biol. 120:1305-1320). We isolated slt2-1 as a mutation that enhances the division defect of cdc28 mutants with defects at Start. Slt2p(Mpk1p) is a member of the MAP kinase family (Lee, K. S., K. Irie, Y. Gotoh, Y. Watanabe, H. Araki, E. Nishida, K. Matsumoto, and D. E. Levin. 1993. Mol. Cell. Biol. 13:3067-3075). We show that slt2 mutants exhibit phenotypes similar to those shown by mutants of the yeast actin cytoskeleton, including delocalization of chitin deposition and of actin cortical spots and the accumulation of secretory pathway membranes and vesicles. Furthermore, slt2::HIS3 act1-1 and slt2::HIS3 myo2-66 double mutants are inviable. We suggest that Slt2p functions downstream or in parallel with Cdc28p in promoting bud formation and apical growth.

Actins↗
PubMed2006

A therapeutic dose of the lipophilic statin pitavastatin enhances oxidant-induced apoptosis in human vascular smooth muscle cells.

We examined effects of a physiologic concentration of pitavastatin (0.01 micromol/L) on oxidant-induced apoptosis in cultured human vascular smooth muscle cells (VSMCs). Apoptosis was induced in VSMCs by hydrogen peroxide (H2O2, 300 micromol/L), as evidenced by in situ nick end-labeling and scanning electron microscopy. This apoptotic response was accompanied by increased activation of mitogen-activated protein kinases (MAPKs--ie, increases in the phosphorylated forms of extracellular signal-regulated kinase (p-ERK), c-Jun N-terminal kinase (p-JNK), and p38 MAPK (p-p38 MAPK). Although pitavastatin alone did not induce VSMC death, pretreatment with pitavastatin significantly enhanced H2O2-induced apoptosis and prolonged activation of JNK and p38 MAPK (for up to 24 h) but not ERK. Expression of MAPK phosphatase-1 (MKP-1) also was upregulated by H2O2, but this was not affected by pitavastatin. The apoptosis accelerating effect was observed also in simvastatin but not in pravastatin. Treating VSMCs with mevalonate, farnesyl pyrophosphate, or geranylgeranyl pyrophosphate completely blocked the statin-induced enhancement of VSMC apoptosis, suggesting that protein prenylation is critically involved. It thus appears that pitavastatin enhances H2O2-induced VSMC apoptosis, at least in part, via increases in MAPK activation and protein prenylation, but independently of MKP-1 expression, which consequently results in reduction of VSMC population.

Apoptosis↗
PubMed1997

The parallels between Asclepian and Hippocratic medicine on the island of Kos.

At the end of the 20th century, Hippocratic medicine--which developed at the cross-roads between the occidental and oriental civilisations--acts as a link, a bridge and a symbol for the need to combine both the experience of traditional (Eastern) and the trends of modern (Western) medicine. Hippocratic medicine is one vital pathway to the proper study of the evolution of the medical art. Not only is it the beginning of the art and science of medicine, but modern medicine can still learn from the Hellenic medicine of ancient Greece. Hippocratic medicine is both an antidote to an overconcentration and overemphasis on medical technology and a stimulus to more humane technical achievements. Hippocratic bedside examination has not died, but is merely pushed aside temporarily by modern technology. The fact that ancient Hellenic medicine was based on the coexistence of both Asclepian (traditional) and Hippocratic (rational) medicine on the island of Kos reveals and symbolises the necessary coexistence and cooperation of both systems, a synthesis of their concepts being essential to solve the problems threatening the future of humankind. Hellenic medicine serves to highlight that the parallels between Asclepian and Hippocratic medicine are closer than medical historians usually realise, and that alternative medicine may function in a complementary way to conventional primary medical care.

Greece↗