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At least 19 recordsLinked to original sources
PubMed1979

Y chromosome duplication: a minor route evolutive pattern in CML.

2 patients have been investigated, in which Y chromosome duplication occurred during blastic transformation of chronic myelocytic leukaemia. Comparison of cytogenetic findings and survival data in our cases and in previously reported individuals, suggests preliminary conclusions about the prognostic significance of this aneuploidy. Y chromosome gain does not seem to represent per se an unfavourable event, unless it is associated with additional chromosome change.

Aneuploidy↗
PubMed2025

Large future genetic diversity losses are predicted even with habitat protection.

Genetic diversity within species is the basis for evolutionary adaptive capacity and has recently been included as a target for protection in the United Nations' Global Biodiversity Framework (GBF). However, we lack large-scale mathematical frameworks to quantify how much genetic diversity has already been lost, let alone to predict future losses under 21st century conservation scenarios. To fill this gap, we developed an area-based spatio-temporal predictive framework of genetic diversity calibrated with population-scale genomic data of 29 plant and animal species. To estimate present genetic diversity loss with our framework, we used species' habitat area and population sizes losses reported in the Living Planet Index, the Red List, and new GBF indicators across 13,808 species for the last 5 decades. Applying our evolutionary framework across these species, we estimate genetic diversity loss lags behind population and habitat area declines, with an estimated current 13-22% π genetic diversity loss. However, we forecast future genetic diversity losses will reach 41-76% even if populations are not further contracted. These results highlight that safeguarding existing habitats is insufficient to maintain the genetic health of species and relying solely on continuous genetic monitoring underestimates lagging long term impacts.

Genetic diversity↗
PubMed1979

Histopathologic sequence of events in adult mice undergoing lethal graft-versus-host reaction developed across H-2 and/or non-H-2 histocompatibility barriers.

The sequence of histologic events in graft-versus-host reaction (GVHR) caused by major and/or minor histoincompatibilities was studied. It was discovered that GVHR may manifest itself in the form of two distinct multiphasic disease entities, depending on whether the donor cells are incompatible with the host for both major and minor histocompatibility antigens ("major GVHR") or for minor histocompatibility antigens alone ("minor GVHR"). The acute or major GVHR has four phases: 1) a transient phase of aplasia, 2) a repopulation phase, 3) a proliferative phase involving lymphoid, presumably immunocompetent, cells, and 4) a phase of acute organ rejection (terminal). The chronic or minor GVHR is characterized by six phases, namely: 1) a transient phase of aplasia, 2) a repopulation phase, 3) a phase of proliferation and tissue infiltration by lymphoid, presumably immunocompetent cells, 4) a phase of major immunologic injuries, 5) a phase of repair, and 6)a terminal phase with advanced sclerosis and proliferative glomerulonephritis. In acute or major GVHR the disease was manifested by the tissue reactions characteristic of acute organ rejection. Lesions were seen in the kidney, liver, bone marrow, lymph nodes, spleen, thymus, intestine, and skin. In the chronic or minor GVHR, tissue injuries were more widespread, affecting the collagen, vessel walls, adipose tissue, renal glomeruli, heart muscle, fascias of skeletal muscles, lymph nodes, spleen, thymus, bone marrow, intestine, skin, esophageal mucosa, and urinary tract. A pronounced plasma cell proliferation was a striking feature in the minor GVHR. Its evolution coincided with advanced thymic epithelial atrophy. It is suggested that the destruction of thymic epithelium resulted in depletion of suppressor T cells and, consequently, in an unopposed proliferation of plasma cells.

Animals↗
PubMed2026

Selective context, rather than persister cycling alone, drives resistance fixation in Escherichia coli.

Whether persister cells contribute to the evolution of antibiotic resistance and, if so, under what selective conditions this occurs, remain unresolved. Here, we examined whether repeated persister cycling itself promotes resistance evolution and how persister-associated minor variants are retained, lost, or fixed under distinct selective contexts. We compared five Escherichia coli cellular states: mutation-induced cells (M), persister-Amp cycling cells (A), persister cycling cells without selection (R), stationary-phase cells (S), and NaCl-stored persisters (P), using state-resolved whole-genome sequencing and phenotypic assays. Persister cycling without selection, stationary-phase cells, and NaCl-stored persisters maintained baseline MICs and showed no detectable high-frequency variant fixation. In contrast, mutation-induced cells fixed efflux-regulatory mutations in marR, acrR, and acrB, increasing MIC to 32 μg/mL. Persister-Amp cycling cells showed an intermediate MIC increase to 16 μg/mL without detectable quality-filtered genetic fixation, distinguishing this state from mutation-induced resistance. The stfE/stfP prophage background further shaped adaptive routes under mutation-inducing conditions. Exploratory analysis revealed sub-threshold low-frequency variant signals during persister cycling, but lineage tracking showed that these variants were not stage-specifically fixed and were instead stochastically retained or lost. These findings support a model in which persister cycling can reveal low-frequency genetic heterogeneity, but fixed resistance evolution requires selection that promotes variant retention and clonal expansion. Thus, resistance fixation was governed primarily by selective context during regrowth rather than by the persister state itself.

Journal Article↗
PubMed2026

Pathogen local adaptation shapes Pierce's disease of grapevines outcomes under field conditions.

Climate change is broadly expected to increase the range of many plant diseases, yet the current status of local thermal adaptation in many pathogens is poorly understood. Xylella fastidiosa (Xf) is a global bacterial plant pathogen that causes Pierce's disease (PD) of grapevines and infects over 700 other host plant species, impacting both agricultural and natural ecosystems. In a common garden experiment with 477 vines in the field, we compared PD outcomes from a local (colder climate in CA) vs non-local (warmer climate in CA) bacterial strain in 13 Mediterranean grapevine varieties over 3 years. Relative to the local strain, there was 77% lower overwinter survival in the non-local strain from a warmer climate, strongly indicating local adaptation in these CA Xf populations. Host genotype also had a significant effect on pathogen winter survival, and grapevine varieties differed in PD susceptibility. Additionally, we assessed in planta evolution of the two pathogen strains over 3 years by whole-genome sequencing 58 field-derived isolates. There were convergent loss-of-function mutations in genes encoding minor Type IV pilin (T4P) proteins, which control twitching motility and other virulence phenotypes, suggesting rapid adaptive evolution. Our results suggest local adaptation to cold temperatures in a bacterial plant pathogen and a possible role for minor Type IV pilins in thermal adaptation. These findings demonstrate the urgent need to incorporate X. fastidiosa evolution and local thermal adaptation into global models of PD spread. Differentiating pathotypes with distinct thermal adaptations will improve disease forecasting and inform quarantine decisions.IMPORTANCEForecasting the movement of plant pathogens is a critical issue under global warming to effectively manage future plant disease outbreaks. Yet, current plant pathogen local thermal adaptation is often unaccounted for, especially in bacterial pathogens. Our study examines local adaptation to temperature in a bacterial plant pathogen, Xylella fastidiosa, that causes disease in grapevines in addition to infecting 700 other plant species. In a large-scale field experiment across 13 grapevine varieties, we demonstrate local adaptation in pathogen winter survival in distinct Xylella fastidiosa strains. Additionally, we found evidence of adaptive evolution in just 3 years, as we observed convergent mutations after resequencing strains that evolved in the field. Our results suggest that X. fastidiosa populations-even within a small geographic area-have distinct adaptations to winter temperatures and may exhibit differential responses to warming winters.

Type IV pili↗
PubMed2026

Late acquisition of BCR::ABL1 during clonal evolution of SAMD9-associated MDS with phenotypic shift from AML to B-ALL.

We describe a unique case of SAMD9-associated myelodysplastic syndrome (MDS) with monosomy 7 that evolved over 16 years into BCR::ABL1-positive acute myeloid leukemia (AML) and subsequently manifested as B-cell acute lymphoblastic leukemia (B-ALL). Genomic analysis at AML diagnosis revealed a germline SAMD9 mutation together with somatic RUNX1 and PPM1D mutations, supporting stepwise clonal evolution, with BCR::ABL1 emerging as a late leukemogenic event. The dominant leukemic population at AML onset showed myeloid morphology and immunophenotype, whereas a minor CD19+CD10+ population was already detectable. Following venetoclax and azacitidine therapy, the dominant leukemic phenotype shifted to B-ALL while retaining BCR::ABL1 positivity. Detection of the Philadelphia chromosome in mature neutrophils at both AML onset and ALL relapse supported multilineage involvement of a multipotent BCR::ABL1-positive clone. Ponatinib achieved disease control. This case highlights late acquisition of BCR::ABL1 during SAMD9-associated clonal evolution and therapy-driven phenotypic shift within a shared Ph-positive leukemic stem-cell hierarchy.

Humans↗
PubMedDate not supplied

Allotypes of the a series and their variants in rabbit immunoglobulins.

Six allotypic specificities of the a series are found on rabbit immunoglobulins: a1, a2 and a3 are found both in domestic and wild rabbits Oryctolagus cuniculus; a100, a101 and a102 seem to be present only in wild rabbits. Each of these specificities is a family of variants always present together in a given serum. These variants can be studied through the cross-reactivities detected between the patterns of the a series. The results of studies of cross-reactivities between a1, a3 and the two specificities a100, and a102 and also the cross-reactivity between a2 and a minor variant of the a1 specificity suggested a hypothetical scheme. This hypothesis attempts to take into account the evolution of the specificities of the a series and their variants. This hypothesis also postulates the existence of a set of closely linked genes which control the synthesis of the variants of a given specificity. One could suppose that primordial allelic genes might have appeared from an ancestor gene. By duplication each allele would have led to the appearance of a set of genes coding for a given specificity. These genes might have evolved through mutations and recombinations. In wild rabbits, the observation of an allotype which seems to result from a recombination between the group of genes coding for the a2 variants and the group of genes coding for a3 variants argues in favors of the genetic recombination mechanism.

Animals↗
PubMed2025

Deep Sequencing Reveals Dual Evolution of SARS-CoV-2: Insights Into Defective Genomes From Wuhan-Hu-1 Variants to Omicron Subvariants.

SARS-CoV-2 has evolved from early variants dominating the first (B.1.5, B.1.1) and second (B.1.177) pandemic waves, which exhibited a higher frequency of minority mutants with deletions leading to Defective Viral Genomes (DVGs) in the spike region near the S1/S2 cleavage site than the Alpha, Beta, and Delta variants. The emergence of Omicron has significantly altered the dominant variant profile, with Omicron subvariants now representing 100% of circulating viruses. To monitor the evolution and adaptation of Omicron in the human population, a deep-sequencing study was performed in RNA samples of BA.1, BA.1.1, BA.2, BA.5, BQ.1.1, XBB.1.5 and BA.2.86 Omicron subvariants. The findings reveal two occurrences of similar evolutionary patterns within SARS-CoV-2 characterized by a shift from a significant to a very low production of DVGs. This event suggests that DVGs might play a role in the virus's spread and adaptation for persistence in infected humans.

SARS-CoV-2↗
PubMed1978

Lung function in alpha-1-antitrypsin deficient sisters.

Two sisters were found to homozygous for alpha-1-antitrypsin deficiency. One was disabled by breathlessness and had advanced clinical and radiological emphysema which was confirmed on lung function testing. The other, of similar age and smoking history, was symptom-free with a normal chest radiograph. She had a slightly increased airways resistance, a reduced gas transfer, a bilaterally reduced apex--base perfusion gradient and a small but generalized increase in physiological dead space in all zones. The minor pulmonary and vascular abnormalities present in the younger sibling suggest that we are witnessing early changes in the evolution of the panacinar emphysema characteristic of alpha-1-antitrypsin deficiency. The reason for the different rates of progress of the disease in these two sisters is not understood.

Adult↗
PubMed1978

Comparison of cloned mouse alpha- and beta-globin genes: conservation of intervening sequence locations and extragenic homology.

We have cloned and characterized a 9.7-kilobase EcoRI fragment of mouse DNA that contains an alpha-globin gene. The gene is encoded in at least three discontinous segments of DNA interrupted by two small intervening sequences that can be visualized as R-loop structures in the electron miscroscope. The size of the gene and its small intervening sequences fits well with the known size of the alpha-globin mRNA precursor, suggesting that these intervening sequences, like those of beta-globin, are transcribed. Partial sequence analysis indicates that the larger intervening sequence interrupts the alpha-globin gene at a site exactly corresponding to that interrupted by the larger intervening sequences in both the beta-globin major and minor genes. This observation suggests that these sequences were present when the alpha- and beta-globin genes diverged in early vertebrate evolution, more than 500 million years ago. Furthermore, though alpha and betamaj genes are encoded on different chromosomes, when their sequences are compared directly by visualization of heteroduplex structures, only one 150- to 200-base-pair segment of homology is recognized. These homologous sequences are located on the 3'-flanking segments of both genes, about 1.5 kilobases from each.

Animals↗
PubMedDate not supplied

[Salmonellosis in children in Ivory Coast, (A study on 69 cases) (author's transl)].

Salmonellosis are still endemic in Ivory Coast. In 1975 they were responsible for 1,75 p. 100 of the admittances in the pediatric department of Treichville University Hospital. In children, the conventional distinction between major and minor salmonellosis is not always obvious. Interpretation of Widal sero-diagnosis is often difficult and awkward. Chloramphenicol generally leads to satisfactory evolution. Salmonellosis are still a problem for Public Health Service. Immunization, is the only effective prophylaxis, but is not carried out yet in Ivory Coast.

Adolescent↗
PubMed2026

Case Report: Immune-driven clonal selection underlying lineage switch from B-Precursor acute lymphoblastic leukemia to acute myeloid leukemia following inotuzumab ozogamicin.

Lineage switch (LS), defined as a change in leukemic lineage during the disease course, is a rare but clinically significant event in acute leukemia and is typically associated with poor prognosis. Although LS has been increasingly reported following targeted immunotherapies, the clonal mechanisms underlying this phenomenon remain incompletely understood, particularly in cases without KMT2A rearrangement. We report a case of LS from B-precursor acute lymphoblastic leukemia (BCP-ALL) to acute myeloid leukemia (AML) following treatment with the CD22-targeted antibody-drug conjugate inotuzumab ozogamicin. To elucidate the clonal architecture underlying LS, targeted next-generation sequencing was performed on bone marrow samples obtained at multiple time points throughout the disease course. Genomic analysis demonstrated that the lymphoid and myeloid disease phases shared ancestral genetic alterations but displayed distinct mutational profiles. At the time of LS, TP53 and SMC1A mutations newly emerged, whereas only a subset of mutations detected at ALL relapse was retained. These findings suggest that the AML phase most likely resulted from the selective expansion of a genetically distinct subclone derived from a common progenitor, rather than the direct transdifferentiation of the dominant ALL clone, consistent with immunotherapy-driven clonal selection. Longitudinal genomic profiling revealed stepwise clonal evolution during disease progression, supporting a model of immunotherapy-driven clonal selection leading to LS. This case provides molecular evidence suggesting that immune-targeted therapy can promote expansion of minor pre-existing subclones with alternative lineage potential within a common progenitor even in non-KMT2A-rearranged leukemia. Our findings highlight the importance of comprehensive genomic monitoring during immunotherapy to identify therapy-resistant subclones and better understand mechanisms of lineage plasticity in acute leukemia.

Humans↗
PubMed1977

[Cerebral arterial embolism during extracorporeal circulation].

From October 1st 1970 to October 1st 1975, electrical and clinical post-operative observation of 1.700 operations under E.C.C. allowed record of E.E.G. and thus study incidents depending of cerebral embolism during their formation. 18 cases have been seen during E.C.C. and 2 at the stop of E.C.C. In 9 cases, it was an air embolus, in 4 others an atheromatous embolus. In the 7 remaining cases, origin of the embolus is uncertain, but probably gaseous. Semiology of the accident is first only E.E.G. In 10 cases, signs were minor, and moderate in 10 others, preceding a late but hard clinical symptomatology, frequently characterized by a delayed advent of epilepsy crisis. Later on, an annoying evolution of the accident was seen in 4 cases (1 death, 3 lasting neurologic deficiency). For the treatment, many observations confirm the highly beneficient part of early hyperbaric oxygen.

Adolescent↗
PubMed1978

Kinetic factors and form determination of the head of bacteriophage T4.

The form of the bacteriophage T4 prehead is described by its icosahedral symmetry, its diameter, and its length. We show how each of these parameters is regulated during prehead formation and ascribe specific form-determining functions to the prehead proteins. The major protein of the head shell can assemble in several different forms. The structure produced in vivo depends on the rate of synthesis of the major protein relative to the rates of synthesis of minor shell proteins and the major core protein. From our observations, we propose a model for form determination of the prehead and suggest a pathway for the evolution of its prolate shape.

Biological Evolution↗
PubMedDate not supplied

[Supra trochlear femoral erosions. Their relations with gonarthrosis and chondrocalcinosis (author's transl)].

Studying one hundred cases of simple gonarthrosis we found only one supra trochlear femoral erosion (STFE). Such a lesion was discovered in 14 cases among 150 chondrocalcinosis with arthrosic lesions. The cases involving STFE trend to a commun marked chondro-osteolytic evolution. The caracteristic patella sizes show clearly that STFE is not in relation with en anomaly of patella (patella alta...). The upper osteophyte of the patella presents only a minor importance in the formation of STFE. This STFE formation begins probably with a progressive chondro-osteolysis of patella and trochlea. Then, appears a progressive nipping between the upper point of patella and the supra trochlear femoral bone.

Aged↗
PubMed1975

[Mixed tumors and cylindromas].

The lacrimals glands may be the focus of the pleomorphic tumours with the same property as the major and minor salivary glands. Their localisation causes different clinical and therapeutic consequences. The cylindromes or Adenoid Cystic Carcinoma are to be put on a parallel with the pleomorphic tumours, though the issue of the clinical evolution is very different for each of them.

Adenoma, Pleomorphic↗
PubMed1976

[Treatment of disseminated oro-pharyngo-laryngeal epidermoid carcinomas with a combination of methotrexate and bleomycine in small doses].

In the previously published series of patients with generalized head and neck epidermoid carcinoma, a high dose combination of methotrexate (MTX) (0.4 mg/kg biw. i.v.) and bleomycin (BLM) (30 mg biw. iv) produced an objective remission rate of 60% with a median duration of 9 weeks. The disappointingly short duration of the remissions was tentatively related to the short period of treatment, which was limited to 5 weeks in order to keep the cumulative dosage of BLM below 300 mg. In the present study, covering 26 patients, a lower weekly dose was adopted (BLM 15 mg, MTX 0.6 mg/kg). 13 partial remissions were obtained with a median duration of 26 weeks; in 7 cases there was no evolution, in 6 cases progression of the tumor was registered, and there was one death from hematological toxicity. The major toxicity was leuko- and thrombopenia with one toxic death. Digestive and cutaneous side effects and fever were minor. There were 2 cases of major pulmonary toxicity, one of which was lethal. In conclusion, a combination of MTX and BLM at a relatively low dosage is active in disseminated head and neck carcinoma and appears to be compatible with longer maintenance of palliation in comparison with results obtained at a high dose level.

Bleomycin↗
PubMed1978

Intracellular serine protease of Bacillus subtilis: sequence homology with extracellular subtilisins.

Intracellular serine protease was isolated from stationary-grown Bacillus subtilis A-50 cells and purified to homogeneity. The molecular weight of the enzyme is 31,000 +/- 1,000, with an isoelectric point of 4.3. Its amino acid composition is characteristically enriched in glutamic acid content, differing from that of extra-cellular subtilisins. The enzyme is completely inhibited with phenylmethylsulfonyl fluoride and ethylenediaminetetraacetic acid. Intracellular protease possesses negligible activity towards bovine serum albumin and hemoglobin, but has 5- to 20-fold higher specific activity against p-nitroanilides of benzyloxycarbonyl tripeptides than subtilisin BPN'. Esterolytic activity of the enzyme is also higher than that of subtilisin BPN'. The enzyme is sequence homologous with secretory subtilisins throughout 50 determined NH2-terminal residues, indicating the presence of duplicated structural genes for serine proteases in the B. subtilis genome. The occurrence of two homologous genes in the cell might accelerate the evolution of serine protease not only by the loosening of selective constrainst, but also by creation of sequence variants by means of intragenic recombination. Three molecular forms of intracellular protease were found, two of them with NH2-terminal glutamic acid and one minor form, three residues longer, with asparagine as NH2 terminus. These data indicate the possible presence of an enzyme precursor proteolytically modified during cell growth.

Amino Acid Sequence↗