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The iterated continuous prisoner's dilemma game cannot explain the evolution of interspecific mutualism in unstructured populations.

The evolutionionary origin of inter- and intra-specific cooperation among non-related individuals has been a great challenge for biologists for decades. Recently, the continuous prisoner's dilemma game has been introduced to study this problem. In function of previous payoffs, individuals can change their cooperative investment iteratively in this model system. Killingback and Doebeli (Am. Nat. 160 (2002) 421-438) have shown analytically that intra-specific cooperation can emerge in this model system from originally non-cooperating individuals living in a non-structured population. However, it is also known from an earlier numerical work that inter-specific cooperation (mutualism) cannot evolve in a very similar model. The only difference here is that cooperation occurs among individuals of different species. Based on the model framework used by Killingback and Doebeli (2002), this Note proves analytically that mutualism indeed cannot emerge in this model system. Since numerical results have revealed that mutualism can evolve in this model system if individuals interact in a spatially structured manner, our work emphasizes indirectly the role of spatial structure of populations in the origin of mutualism.

Altruism↗

Epileptic encephalopathies in early infancy with suppression-burst.

Early infantile epileptic encephalopathy with suppression-burst, or Ohtahara syndrome (OS), and early myoclonic encephalopathy (EME) are epileptic encephalopathies with onset of frequent seizures in the neonatal and early infancy period and with a characteristic EEG pattern, namely, suppression-burst, in which higher-voltage bursts of slow waves mixed with multifocal spikes alternate with isoelectric suppression phase. Their nosologic independence is now widely accepted, although some controversy initially occurred because of their common characteristics such as age of onset, EEG features, seizure intractability, and poor prognosis. Major differences between the two syndromes include (1) tonic spasms in OS versus partial seizures and erratic myoclonias in EME, (2) continuous suppression-burst pattern in both waking and sleeping states in OS versus this EEG pattern almost limited to sleep in EME, and (3) static structural brain damage in OS versus genetic or metabolic disorders in EME. The most important differentiating point is their evolutional pattern with age, which may reflect their pathophysiologic difference. Ohtahara syndrome evolves to West syndrome and further to Lennox-Gastaut syndrome with age, but EME demonstrates no unique evolution; namely, it continues as such for a long time or changes into partial epilepsy or severe epilepsy with multiple independent spike foci.

Electroencephalography↗

[Populational speciation or chromosomal speciation? About the book of Jean de Grouchy "From the birth of species to the aberrations of life" (author's transl)].

According to Jean de Grouchy, the emergence of a new species is dependent on an "acceptable" chromosomic rearrangement, which passing from the heterozygous state (in the original bearer) to the homozygous state (in some of his enbred offspring) becomes definitively established and creates a population sexually isolated from its acestors. He is thus using the idea of karyotype to develop the typological theory put forward at the beginning of the century which postulates that a single mutant is at the origin of a new species. Although he gives an important place to chromosomic rearrangements in the sexual isolation of a new species, J. Ruffié demonstrates by arguments taken from population genetics and from the immunological polymorphism of wild populations that speciation is almost always the result of the evolution of an entire group, which, because of geographic isolation, drift, and differential selection, diverges from the ancestral branch and finally becomes totally incapable of breeding with it. He proposes a model of speciation which includes the two processes population and cytologic. At a first step, the group is isolated geographically and continues its independent evolution; the second step consists of chromosomic recombinations which render the sexual isolation complete. The modifications of the karyotype make the process of speciation irreversible.

Adaptation, Physiological↗

Effects of Temperature on Photosynthesis and CO(2) Evolution in Light and Darkness by Green Leaves.

Using an open and a closed system of gas analysis, it was found that CO(2) evolution in light and in darkness from plant leaves (sunflower, soybean, watermelon, eggplant, and jackbean) have a different response to temperature. While the rate of CO(2) evolution in light increased with increasing temperature from 17 to 35 degrees and then declined, the rate of CO(2) evolution in darkness increased continuously up to 40 degrees . The rate of CO(2) evolution in light was affected by light intensity. At 1800 ft-c and below 35 degrees the rate of CO(2) evolution in light was greater than in darkness, but above 35 degrees it became lower than in darkness. The Q(10) for CO(2) evolution in light was consistently lower than that in darkness.Apparent photosynthesis decreased with increasing temperature, from 20 to 40 degrees and its rate was affected by both light intensity and oxygen concentration. In leaves of dicotyledonous plants studied the decrease in apparent photosynthesis between 20 to 30 degrees at 21% O(2) was shown to be due primarily to an increase in CO(2) evolution in light with relatively little effect on photosynthesis.In corn which does not evolve CO(2) during illumination there was little effect of increasing temperature on the rate of apparent photosynthesis.The different response to temperature of CO(2) evolution in light and in darkness support the earlier conclusion that these are 2 different processes.

Journal Article↗

[Oddi's sphincterotomy in treatment of primary sclerous cholangitis].

In the paper are presented a total of 9 patients with primitive sclerous cholangitis that were hospitalized in the Surgical Department of the "Caritas" Hospital with this rare nosologic entity. The etiology of the disease is neither precise nor incontroversial. Primitive sclerous cholangitis raises particularly difficult problems, because of the high mortality rate (all patients die before the 6-th year after the diagnosis has been established. The ineluctable evolution of the disease toward secondary billiary cirrhosis has generated major difficulties in the choice of the treatment. Corticoid therapy and immunosuppressive drugs have been proven inefficient in improving the prognosis. The classical surgical therapy includes methods that are not followed by stable results since the icteric syndrome will show temporary remission, in spite of the fact that the chronic hepatopathy will continue its independent evolution. The authors have not achieved satisfactory results with the classical surgical techniques, which include external biliary draining and peri-hepatic artery neurectomia (either isolated or combined), not with the internal derivations. Since 1971 the authors have used oddian sphincterectomy in the treatment of sclerous cholangitis. The method was introduced following a long clinical and histopathologic study. The immediate and the late results obtained with this technique recommend it as a choice one because it will lead to disappearence of the jaundice and to stabilization of the hepatic lesions.

Adult↗

The origin of introns and their role in eukaryogenesis: a compromise solution to the introns-early versus introns-late debate?

BACKGROUND: Ever since the discovery of 'genes in pieces' and mRNA splicing in eukaryotes, origin and evolution of spliceosomal introns have been considered within the conceptual framework of the 'introns early' versus 'introns late' debate. The 'introns early' hypothesis, which is closely linked to the so-called exon theory of gene evolution, posits that protein-coding genes were interrupted by numerous introns even at the earliest stages of life's evolution and that introns played a major role in the origin of proteins by facilitating recombination of sequences coding for small protein/peptide modules. Under this scenario, the absence of spliceosomal introns in prokaryotes is considered to be a result of "genome streamlining". The 'introns late' hypothesis counters that spliceosomal introns emerged only in eukaryotes, and moreover, have been inserted into protein-coding genes continuously throughout the evolution of eukaryotes. Beyond the formal dilemma, the more substantial side of this debate has to do with possible roles of introns in the evolution of eukaryotes. RESULTS: I argue that several lines of evidence now suggest a coherent solution to the introns-early versus introns-late debate, and the emerging picture of intron evolution integrates aspects of both views although, formally, there seems to be no support for the original version of introns-early. Firstly, there is growing evidence that spliceosomal introns evolved from group II self-splicing introns which are present, usually, in small numbers, in many bacteria, and probably, moved into the evolving eukaryotic genome from the alpha-proteobacterial progenitor of the mitochondria. Secondly, the concept of a primordial pool of 'virus-like' genetic elements implies that self-splicing introns are among the most ancient genetic entities. Thirdly, reconstructions of the ancestral state of eukaryotic genes suggest that the last common ancestor of extant eukaryotes had an intron-rich genome. Thus, it appears that ancestors of spliceosomal introns, indeed, have existed since the earliest stages of life's evolution, in a formal agreement with the introns-early scenario. However, there is no evidence that these ancient introns ever became widespread before the emergence of eukaryotes, hence, the central tenet of introns-early, the role of introns in early evolution of proteins, has no support. However, the demonstration that numerous introns invaded eukaryotic genes at the outset of eukaryotic evolution and that subsequent intron gain has been limited in many eukaryotic lineages implicates introns as an ancestral feature of eukaryotic genomes and refutes radical versions of introns-late. Perhaps, most importantly, I argue that the intron invasion triggered other pivotal events of eukaryogenesis, including the emergence of the spliceosome, the nucleus, the linear chromosomes, the telomerase, and the ubiquitin signaling system. This concept of eukaryogenesis, in a sense, revives some tenets of the exon hypothesis, by assigning to introns crucial roles in eukaryotic evolutionary innovation. CONCLUSION: The scenario of the origin and evolution of introns that is best compatible with the results of comparative genomics and theoretical considerations goes as follows: self-splicing introns since the earliest stages of life's evolution--numerous spliceosomal introns invading genes of the emerging eukaryote during eukaryogenesis--subsequent lineage-specific loss and gain of introns. The intron invasion, probably, spawned by the mitochondrial endosymbiont, might have critically contributed to the emergence of the principal features of the eukaryotic cell. This scenario combines aspects of the introns-early and introns-late views. REVIEWERS: this article was reviewed by W. Ford Doolittle, James Darnell (nominated by W. Ford Doolittle), William Martin, and Anthony Poole.

Journal Article↗

Interconnected patterns of biogeography and evolution.

Analysis of the fauna of the carabid beetles of New Guinea reveals both a broad dispersal pattern and a local turnover pattern that together fit into a world-wide pattern of successive dispersals and replacements that run from large to small areas and from more to less favorable climates. This pattern coincides broadly with a world-wide pattern of species numbers. Evolution by group selection, proceeding most rapidly and effectively where species are most numerous, connects the patterns and can supply the force that gives direction to the dispersal pattern. Directional change at any level of complexity involves movement that results in the formation of diverse groups of units (which are themselves groups of smaller units) and differential survival. This process-generalized group selection-has been continuous from chemical evolution on the earth's surface, through the origin of life, and into successive interacting levels of organic evolution. A corollary is that evolution should make situations favorable to itself, by group selection, and has probably done so in (for example) tropical rain forest, where new information about group evolution may be sought.

Journal Article↗

Evolutionary branching under asymmetric competition.

I investigate the evolution of a continuous trait, such as body size or arms level, which affects the outcome of competitive contests such that the contestant with the larger trait value has a higher probability of winning. I show that a polymorphism of distinctly different strategies can evolve in an initially monomorphic population even if mutations have only small phenotypic effect. In a simple Lotka-Volterra-type model of asymmetric competition, I derive the conditions under which two strategies can gradually evolve from a single ancestral strategy; the evolution of higher level polymorphisms is studied by numerical analysis and computer simulations of specific examples. High levels of polymorphism may build up during evolution. The coevolution of strategies in polymorphic populations, however, may also lead to extinction, which decreases the level of polymorphism. I discuss whether the evolution of several haploid strategies from a single initial strategy may correspond to the evolution of several sympatric species in a diploid outbreeding population.

Animals↗

Myelodysplastic syndromes: clinicopathologic features, pathobiology, and molecular pathogenesis.

CONTEXT: Myelodysplastic syndromes (MDSs) are clonal stem cell diseases characterized by ineffective hematopoiesis, multilineage dysplasia, and peripheral cytopenias with normocellular or hypercellular marrow. They represent a heterogeneous group of disorders with a varied spectrum of clinical, morphologic, biologic, and genetic characteristics. This heterogeneity in disease characterization has led to evolving classification systems, developing prognostic models, and continuing research efforts to elucidate its pathobiology and pathogenesis. OBJECTIVE: To summarize updated information and provide a general overview of the clinicopathologic features, pathobiology, and cytogenetic and molecular pathogenesis of MDSs. DATA SOURCES: Relevant articles indexed in PubMed (National Library of Medicine) between 1982 and 2005 and reference medical texts. CONCLUSIONS: Although MDSs remain a relatively poorly defined disease entity, recent advancements in cytogenetic and molecular studies have significantly contributed to our present knowledge of MDSs. Novel strategies for studying the pathogenesis and evolution of MDSs continue to shape our understanding of this disease and guide our approaches to diagnosis and treatment.

Cytogenetics↗

Trans gene regulation in adaptive evolution: a genetic algorithm model.

This is a continuation of earlier studies on the evolution of infinite populations of haploid genotypes within a genetic algorithm framework. We had previously explored the evolutionary consequences of the existence of indeterminate-"plastic"-loci, where a plastic locus had a finite probability in each generation of functioning (being switched "on") or not functioning (being switched "off"). The relative probabilities of the two outcomes were assigned on a stochastic basis. The present paper examines what happens when the transition probabilities are biased by the presence of regulatory genes. We find that under certain conditions regulatory genes can improve the adaptation of the population and speed up the rate of evolution (on occasion at the cost of lowering the degree of adaptation). Also, the existence of regulatory loci potentiates selection in favour of plasticity. There is a synergistic effect of regulatory genes on plastic alleles: the frequency of such alleles increases when regulatory loci are present. Thus, phenotypic selection alone can be a potentiating factor in a favour of better adaptation.

Adaptation, Physiological↗

[Child mortality in francophone Europe: the state of the matter].

The interest of a comparative approach at a supranational level is to identify and to underscore the trends that sometimes overcome regional characteristics. Therefore among the great variety of parameters likely to influence mortality, the factors acting on levels and the factors acting on trends must be strictly distinguished. What is more striking where comparisons are possible, is the conformity of trends and the fact that evolution is not continuous but moves forward in stages. This is the reason why socio-economic explanations must be excluded. A whole part of Western Europe knew an important decline of infants' mortality at the turn of the XIXth and XXth centuries and probably also of the XVIIIth century. It was such a rapid, simultaneous extensive decline that the interference of very general factors must be acknowledged. Then the question is raised of the effect that a modification in the pathological balance can produce on the chances of infants to survive. The hypothesis considered here is a minor incidence of infectious diseases connected to changing bio-meteorological conditions (a drop in the temperature gap between winter and summer) which would have acted as a transforming mass along with cumulatiave effects because of the interactive synergy between ill-nourishment and infections. The evolution in the XIXth century and the contrasted profiles or mortality according to age confirm the hypothesis of a modification in the nosological context unrelated to the economic conditions.

Child↗

Detection and typing of human papillomavirus DNA in uterine cervices with coexistent grade I and grade III intraepithelial neoplasia: biologic progression or independent lesions?

OBJECTIVE: To examine the HPV type infection of cervical cone specimens with coexistent CIN1 and CIN3 lesions, in order to define if coexistence of low- and high-grade lesions in the same cervix represent different stages of evolution in a continuing process that is caused by a single viral type or independent lesions induced by different HPV types. STUDY DESIGN: The examined material included 43 cases with coexistent CIN1 and CIN3 in the cone biopsy specimen. Detection and typing of HPV was made by RFLP-PCR. RESULTS: All CIN1 lesions were HPV positive, while three CIN3 lesions were HPV-negative. The proportion of agreement of the HPV type in the two lesions, excluding negative cases (n = 40), was 60% (95% confidence interval: 43.3-75.1). HPV 16 was the most common type in both CIN3 (56.8%) and CIN1 (46.5%). CONCLUSIONS: The so-called morphologic progression of CIN is not always synonymous with biologic progression, since many coexistent CIN lesions are caused by different HPV types, and so represent different cell clones. Clonality of coexistent CIN lesions may be implicated in the evolution of CIN as other recent studies have shown.

Adult↗

Evolution of vertebrate IgM: complete amino acid sequence of the constant region of Ambystoma mexicanum mu chain deduced from cDNA sequence.

cDNA clones coding for the constant region of the Mexican axolotl (Ambystoma mexicanum) mu heavy immunoglobulin chain were selected from total spleen RNA, using a cDNA polymerase chain reaction technique. The specific 5'-end primer was an oligonucleotide homologous to the JH segment of Xenopus laevis mu chain. One of the clones, JHA/3, corresponded to the complete constant region of the axolotl mu chain, consisting of a 1362-nucleotide sequence coding for a polypeptide of 454 amino acids followed in 3' direction by a 179-nucleotide untranslated region and a polyA+ tail. The axolotl C mu is divided into four typical domains (C mu 1-C mu 4) and can be aligned with the Xenopus C mu with an overall identity of 56% at the nucleotide level. Percent identities were particularly high between C mu 1 (59%) and C mu 4 (71%). The C-terminal 20-amino acid segment which constitutes the secretory part of the mu chain is strongly homologous to the equivalent sequences of chondrichthyans and of other tetrapods, including a conserved N-linked oligosaccharide, the penultimate cysteine and the C-terminal lysine. The four C mu domains of 13 vertebrate species ranging from chondrichthyans to mammals were aligned and compared at the amino acid level. The significant number of mu-specific residues which are conserved into each of the four C mu domains argues for a continuous line of evolution of the vertebrate mu chain. This notion was confirmed by the ability to reconstitute a consistent vertebrate evolution tree based on the phylogenic parsimony analysis of the C mu 4 sequences.

Ambystoma↗

Molecular evidence of a common clonal origin and subsequent divergent clonal evolution in vulval intraepithelial neoplasia, vulval squamous cell carcinoma and lymph node metastases.

VIN is thought to be the precursor of some VSCCs because it is monoclonal, frequently occurs contiguously with VSCC and shares similar risk factors with a subgroup of VSCC. There has been no conclusive molecular evidence supporting this assumption. We performed X-chromosome inactivation analysis on 9 cases of lone VIN, 10 cases of VSCC and associated contiguous VIN and 11 cases of VSCC and associated noncontiguous VIN. Eight of the 9 cases of lone VIN appeared to be monoclonal. All 7 informative and monoclonal cases of VIN with contiguous VSCC and 6/9 informative cases of VIN with noncontiguous VSCC showed patterns of X-chromosome inactivation consistent with a common monoclonal origin for both VIN and VSCC. Two of the 9 cases of VIN with noncontiguous VSCC showed X-chromosome inactivation patterns consistent with a separate clonal origin. We performed LOH analysis at 6 chromosomal loci on these samples and 7 cases with lymph node metastases. Identical losses occurred 7 times in VIN and contiguous VSCC (random probability 1.2 x 10(-9)), twice in VIN and noncontiguous VSCC (random probability 1.5 x 10(-3)) and 3 times in VSCC and associated metastases (random probability 1.8 x 10(-5)). Some losses occurring in VSCC did not appear in the contiguous VIN or associated metastases and vice versa. These data provide molecular evidence that VIN is the precursor of VIN-associated VSCC, that multifocal disease may arise via either different clones or a single clone and that continued divergent clonal evolution may occur in vulval neoplasia.

Carcinoma, Squamous Cell↗

Isolation of an Escherichia coli K-12 mutant strain able to form biofilms on inert surfaces: involvement of a new ompR allele that increases curli expression.

Classical laboratory strains of Escherichia coli do not spontaneously colonize inert surfaces. However, when maintained in continuous culture for evolution studies or industrial processes, these strains usually generate adherent mutants which form a thick biofilm, visible with the naked eye, on the wall of the culture apparatus. Such a mutant was isolated to identify the genes and morphological structures involved in biofilm formation in the very well characterized E. coli K-12 context. This mutant acquired the ability to colonize hydrophilic (glass) and hydrophobic (polystyrene) surfaces and to form aggregation clumps. A single point mutation, resulting in the replacement of a leucine by an arginine residue at position 43 in the regulatory protein OmpR, was responsible for this phenotype. Observations by electron microscopy revealed the presence at the surfaces of the mutant bacteria of fibrillar structures looking like the particular fimbriae described by the Olsén group and designated curli (A. Olsén, A. Jonsson, and S. Normark, Nature 338:652-655, 1989). The production of curli (visualized by Congo red binding) and the expression of the csgA gene encoding curlin synthesis (monitored by coupling a reporter gene to its promoter) were significantly increased in the presence of the ompR allele described in this work. Transduction of knockout mutations in either csgA or ompR caused the loss of the adherence properties of several biofilm-forming E. coli strains, including all those which were isolated in this work from the wall of a continuous culture apparatus and two clinical strains isolated from patients with catheter-related infections. These results indicate that curli are morphological structures of major importance for inert surface colonization and biofilm formation and demonstrate that their synthesis is under the control of the EnvZ-OmpR two-component regulatory system.

Alleles↗

Review of immunosuppressive usage in pancreas transplantation.

Throughout 1997, nearly 10,000 pancreas transplants have been performed worldwide, with 88% being simultaneous kidney transplants (SKPT). The current 1 yr patient survival rate exceeds 90% and pancreas graft survival (complete insulin independence) rate exceeds 80% for SKPT, 70% for sequential pancreas after kidney transplant (PAKT), and 65% for pancreas transplant alone (PTA). According to registry data, rejection accounts for 32% of graft failures in the first year after pancreas transplantation. However, improvements are expected to continue with the evolution of treatment protocols. Most pancreas transplant centers employ quadruple drug immunosuppression with anti-lymphocyte induction with either a monoclonal or polyclonal antibody agent. In recent years, there has been an overall decline in the use of antibody induction therapy from 90% during the period 1987-1993 to 83% of pancreas transplants performed during 1994-1997. Maintenance immunosuppression is triple therapy consisting of a calcineurin inhibitor (cyclosporine or tacrolimus), corticosteroids, and an anti-metabolite (AZA or MMF). Prior to 1995, nearly all pancreas transplant recipients were managed with Sandimmune. In the last 2 yr, tacrolimus-based therapy has been used in approximately 20% of cases and a new microemulsion formulation of cyclosporine (Neoral) has replaced Sandimmune in contemporary post-transplant immunosuppression. In addition, MMF is replacing AZA as part of the standard immunosuppressive regimen after pancreas transplantation. At present, a number of centers are conducting various trials with new drug combinations including either Neoral or tacrolimus in combination with steroids and MMF with or without antibody induction therapy. From 1994 to 1997, the 1 yr rates of immunologic graft loss have decreased to 2% after SKPT, 9% after PAKT, and 16% after PTA. The current array of new immunosuppressive agents are providing more effective control of rejection and permitting solitary pancreas transplantation to become an accepted treatment option in diabetic patients without advanced complications. The apparent potency of new drug combinations has also resulted in a resurgence of interest in steroid withdrawal. Immunosuppressive strategies will continue to evolve in order to achieve effective control of rejection while minimizing injury to the allograft and risk to the patient. In addition, new regimens must not only address the issue of specific drug toxicities but also long-term economic, metabolic, and quality of life outcomes. Pancreas transplantation will remain an important alternative in the treatment of diabetic patients until other strategies are developed that can provide equal glycemic control with less immunosuppression and overall morbidity.

Antilymphocyte Serum↗

Immunosuppression in pancreas transplantation: progress, problems and perspective.

Through 1997, over 10,000 pancreas transplants have been performed world-wide, with 88% being simultaneous kidney-pancreas transplants (SKPTs). Current 1-year patient survival exceeds 90% and pancreas graft survival (complete insulin independence) exceeds 80% for SKPT, 70% for sequential pancreas after kidney transplant (PAKT), and 65% for pancreas transplant alone (PTA). According to Registry data, rejection accounts for 32% of graft failures in the first year after pancreas transplantation. However, improving outcomes are expected to continue with the evolution of treatment protocols. Most pancreas transplant centres employ quadruple drug immunosuppression with anti-lymphocyte induction, using either a monoclonal or polyclonal antibody agent. In recent years, there has been an overall decline in the use of antibody-induction therapy from 90% during 1987-93, to 83% of pancreas transplants performed during 1994-97. Maintenance immunosuppression is triple therapy consisting of a calcineurin inhibitor (cyclosporine or tacrolimus), corticosteroids, and an anti-metabolite such as azathioprine (AZA) or mycophenolate mofetil (MMF). Prior to 1995, nearly all pancreas transplant recipients were managed with Sandimmune. Since 1986, tacrolimus-based therapy has been used in approximately 20% of cases, and a new microemulsion formulation of cyclosporine (Neoral) has replaced Sandimmune in contemporary post-transplant immunosuppression. In addition, MMF is replacing AZA as part of the standard immunosuppressive regimen following pancreas transplantation. At present, a number of centres are conducting various trials with new drug combinations including either Neoral or tacrolimus in combination with steroids and MMF, with or without antibody-induction therapy. From 1994 to 1997, the 1-year rates of immunologic graft loss have decreased to 2% after SKPT, 9% after PAKT, and 16% after PTA. The current array of new immunosuppressive agents are providing more effective control of rejection and permitting solitary pancreas transplantation to become an accepted treatment option in diabetic patients without advanced complications. The apparent potency of new drug combinations has also resulted in a resurgence of interest in steroid withdrawal. Immunosuppressive strategies will continue to evolve to achieve effective control of rejection while minimizing injury to the allograft and risk to the patient. In addition, new regimens must not only address the issue of specific drug toxicities, but also long-term economic, metabolic, and quality of life outcomes. Pancreas transplantation will remain an important alternative in the treatment of diabetic patients until other strategies are developed that can provide equal glycaemic control with less immunosuppression and overall morbidity.

Humans↗

Effects of branch length errors on the performance of phylogenetically independent contrasts.

We examined Type I error rates of Felsenstein's (1985; Am. Nat. 125:1-15) comparative method of phylogenetically independent contrasts when branch lengths are in error and the model of evolution is not Brownian motion. We used seven evolutionary models, six of which depart strongly from Brownian motion, to simulate the evolution of two continuously valued characters along two different phylogenies (15 and 49 species). First, we examined the performance of independent contrasts when branch lengths are distorted systematically, for example, by taking the square root of each branch segment. These distortions often caused inflated Type I error rates, but performance was almost always restored when branch length transformations were used. Next, we investigated effects of random errors in branch lengths. After the data were simulated, we added errors to the branch lengths and then used the altered phylogenies to estimate character correlations. Errors in the branches could be of two types: fixed, where branch lengths are either shortened or lengthened by a fixed fraction; or variable, where the error is a normal variate with mean zero and the variance is scaled to the length of the branch (so that expected error relative to branch length is constant for the whole tree). Thus, the error added is unrelated to the microevolutionary model. Without branch length checks and transformations, independent contrasts tended to yield extremely inflated and highly variable Type I error rates. Type I error rates were reduced, however, when branch lengths were checked and transformed as proposed by Garland et al. (1992; Syst. Biol. 41:18-32), and almost never exceeded twice the nominal P-value at alpha = 0.05. Our results also indicate that, if branch length transformations are applied, then the appropriate degrees of freedom for testing the significance of a correlation coefficient should, in general, be reduced to account for estimation of the best branch length transformation. These results extend those reported in Díaz-Uriarte and Garland (1996; Syst. Biol. 45:27-47), and show that, even with errors in branch lengths and evolutionary models different from Brownian motion, independent contrasts are a robust method for testing hypotheses of correlated evolution.

Computer Simulation↗