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[A microbial growth study in parenteral nutrition].

Study on the behaviour of five microorganisms in different formulations of parenteral nutrition (PN) different from each other with regard to the presence or absence of lipids and the addition of vitamins or oligoelements. The bacteria investigated were Staphylococcus aureus (ATCC 12600), Bacillus subtilis (ATCC 6051), Pseudomonas aeruginosa (ATCC 9027) and Enterobacter cloacae (ATCC 13047), as well as Candida albicans (LSH 3156 D). It was observed that C. albicans grew well in all types of PN tested, S. aureus and E. cloacae showed growth in the formulations containing lipids, whereas in those lacking lipids, the number of microorganisms remained practically uniform. P. aeruginosa remained essentially constant throughout the study and in all mixtures and B. subtilis was reduced with regard to the number of feasible organisms, due to the formation of spores. Finally, the addition of vitamins or oligoelements did not appear to determine a particular model of evolution in any of the species studied.

Bacteria↗

[Evolution of Alu repeats. Imitation model].

At present, nucleotide sequences of 100 different Alu repeats are known, i.e. 0.01% of the total number of Alu repeats in the genome. It is clear that one can not refer the evolutionary characteristics of Alu repeats obtained from the analysis of the available limited sample to all Alu repeats comprised in the genome, without additional statistical estimations. For supplementary investigation of such average evolutionary characteristics as the extent of intraspecific divergence, the rate of Alu repeats transposition (insertion, excision), we used the method of imitation simulation of the process of Alu repeats transposition in the genome. As a result of simulation, phylogenetic relations were obtained among all Alu repeats. It was shown that the evolutionary characteristics evaluated for different samples of repeats were similar. It was proved that the extent of divergence of Alu repeats in the model is twice as small as that evaluated, according to the real data (0.15, instead of 0.3). Possible reasons for such discrepancy have been discussed.

Genome, Human↗

Evolution beyond the shared services model of consolidated hospital clinical laboratories.

OBJECTIVE: To compare the operational and financial outcomes of the transition from shared laboratory services to a recentralized model, in a consolidated hospital system. SETTING: United Health Services Hospitals (Binghamton General, Wilson Memorial, and Ideal hospitals, New York State). INTERVENTION: Consolidation of hospital services and recentralization of laboratory testing to a single site (Wilson Memorial Hospital). MAIN OUTCOME MEASURES: Laboratory workload, testing efficiency, personnel and nonpersonnel expenses, analytic error rate, turnaround time, and proficiency-testing scores. RESULTS: The postintervention period (1988 to 1992) was characterized by a 51% and a 10% increase in the out- and inpatient workloads, respectively, with a concomitant 24% increase in testing efficiency. The salary expenses were 26% lower, while the total true cost savings ranged from $1,544,000 (11.6%) to $2,500,000 (21.9%) compared with the shared services model. The recentralization produced decreased analytic error rates and improved testing turnaround time. CONCLUSIONS: The total costs per test have been lowered in the recentralized model. Recentralization may provide further true cost savings over the shared services model while maintaining high-quality service.

Cost Control↗

New data for AG haplotype frequencies in Caucasoid populations and selective neutrality of the AG polymorphism.

We present the results of AG antigen typings of three Caucasoid population samples: Lebanese, Tunisians, and Finns. AG haplotype frequencies estimated by maximum-likelihood methods are compared with the frequencies observed in 13 world populations previously tested for AG specificities by computing a genetic distance matrix used in a multivariate analysis. A high degree of polymorphism characterizes the three samples, with 10 haplotypes detected in the Lebanese and 11 haplotypes detected in the Tunisians and Finns; high heterozygosity levels are also present in the three populations. The genetic distance analysis shows that the three populations possess a genetic structure intermediate between those observed in sub-Saharan Africans and in Caucasoids from the Near East and India. This tight correspondence between AG differentiation and geography is confirmed by a highly significant correlation coefficient found between genetic and geographic distances computed worldwide, suggesting that an isolation by distance model of evolution applies to the AG system. The Ewens-Watterson test for selective neutrality on all world populations tested for AG specificities also supports the hypothesis that the AG system behaves like a neutral polymorphism. Overall, the AG differentiation pattern appears to be close to the patterns observed for other serological polymorphisms, such as RH, GM, and HLA, whose evolutionary mechanisms are also discussed.

Antigens, Differentiation↗

Melanocyte culture lines from Tyr-SV40E transgenic mice: models for the molecular genetic evolution of malignant melanoma.

Transgenic Tyr-SV40E mice previously produced on the C57BL/6 inbred-strain background, with SV40 oncogenic sequences specifically expressed in pigment cells, are predisposed to melanoma [Bradl, M., Klein-Szanto, A., Porter, S. & Mintz, B. (1991). Proc. Natl. Acad. Sci. USA, 88, 164-168]. Separate lines of these animals differ genetically only in the number of copies and chromosomal site of integration of the transgene. Skin melanocytes from young mice with no apparent skin lesions were established in continuous culture from hemizygous donors with low, medium and high numbers of transgene copies, and from a homozygous offspring of the low-copy mouse line. The standard culture conditions enable C57BL/6 wild-type melanocytes to become stably immortalized without transformation. The transgenic cell lines all changed over time in an orderly progression. However, with greater numbers of transgene copies, the cells more rapidly displayed shorter doubling times, increased anchorage independence, reduced serum and growth factor requirements, decreased tyrosinase expression and melanin content, increased oncogene expression, and capacity to form malignant melanomas when tested by grafting. Melanocytes with the lowest number of transgene copies were of special interest. They grew more rapidly than the wild-type cells from the outset, but did not become tumorigenic until an apparently small number of still-unknown genetic changes had spontaneously occurred, or until the number of transgene copies was increased slightly by homozygosity. In contrast to the hemizygous low-copy cells, the homozygous counterparts underwent striking and rapid transformational changes and early conversion to malignancy. Thus such low-copy transgenic melanocyte lines afford an exceptional opportunity for molecular analysis of somatic genetic evolution toward malignant melanoma.

Animals↗

[Course and regression of HELLP syndrome].

The authors reported the outcome of a retrospective study of patients with HELLP syndrome to verify whether this pathology is a clinical entity with models of evolution, regression and well defined treatment. A total of 20 individual cases were reported at the Division of Obstetrics and Gynecology at the G. Gaslini Institute during the period from January 1990 to September 1995. All cases showed the normalisation of the various clinical and hematochemical parameters within a maximum of 8 days after birth. The rapid diagnosis, the immediate extraction of the fetus and appropriate medical treatment led to the prompt resolution of this severe pathology without the need for demolitive surgery frequently used in the past.

Adult↗

[Study of active myocardial damage in children with suspected myocarditis using antimyosin monoclonal antibodies (AMMoAb-111In)].

BACKGROUND: The study with monoclonal antimyosin antibody-111In has proved to be useful in the detection of the myocardial damage present in different processes. There is active myocardial damage and specific antimyosin uptake in myocarditis, as both experimental and clinical trials have shown. In experimental models the evolution of myocardial damage has been studied, where a parallelism between the histological changes of the myocardial damage and the evolution on the antimyosin uptake has been found. In clinical myocarditis it is difficult to do an histological follow up of the inflammatory process, and therefore the evolution of myocardial damage present in myocarditis is unknown. The antimyosin antibody images allow a non-invasive study of this evolution. OBJECTIVES: a) to study with monoclonal antimyosin antibody-111In, the myocardial damage present regarding the disease evolution in children with suspected clinical diagnosis of myocarditis; b) to evaluate the evolution of the active myocardial damage reflected on the changes on the monoclonal antimyosin antibody-111In uptake. METHODS: A study with monoclonal antimyosin antibody-111In was carried out on 43 children, 16 males and 27 females with a median age of 39 months (SD 48 m; range: 2-167) with suspected diagnosis of acute myocarditis defined as the presence of congestive cardiac failure or severe ventricular arrhythmia with less than 12 months of evolution. The image evaluation was done visually and through the heart to lung ratio. Twenty of these patients were also followed up with antimyosin antibody scan for a period of 19 +/- 9 months, and 3.8 +/- 1.7 studies were performed on them in this time. RESULTS: The prevalence of positive myocardial uptake was 83.72%. There is a negative correlation (r = -0.352; p < 0.02) between the evolution time of the process and the heart to lung ratio: patients studied before two months, have a higher heart to lung ratio and greater prevalence of positive studies than those studied later (heart to lung ratio 2.09 vs 1.74; p = 0.013; 90% vs 69.2%). Of the patients followed up with antimyosin antibody scans, 6 showed a clinical relapse which increased their heart to lung ratio. The other 14 showed an progressive decrease of the heart to lung ratio reaching normality in 14 +/- 6 months. CONCLUSIONS: a) the uptake intensity of monoclonal antimyosin antibody-111In, as a reflection of the myocardial damage, depends on the disease evolution time, as in the first two months is when the major damage happens; b) the uptake intensity slowly decreases, tending to normality around the 14th month, although this evolution may be altered by the appearance of relapses.

Antibodies, Monoclonal↗

Retaliatory cuckoos and the evolution of host resistance to brood parasites.

We present a dynamic model of the evolution of host resistance to avian brood parasites, when the latter can retaliate against hosts that reject parasitic eggs. In a verbal model, Zahavi (1979, American Naturalist, 113, 157-159) suggested that retaliatory cuckoos might prevent the evolution of host resistance by reducing the reproductive success of rejecter hosts (i.e. by destroying their eggs or nestlings). Here we develop a model based on the association between the great spotted cuckoo, Clamator glandarius, and its main host, the European magpie, Pica pica, because this is the only system that has provided supportive evidence, to date, for the existence of retaliatory behaviour. Our aims were (1) to derive the conditions for invasion of the retaliation strategy in a nonretaliatory parasite population and (2) to investigate the consequences of retaliation for the evolution of host defence. If we assume a cost of discrimination for rejecter hosts in the absence of parasitism, and a cost paid by a retaliator for monitoring nests, our model shows cyclical dynamics. There is no evolutionarily stable strategy, and populations of both hosts and parasites will cycle indefinitely, the period of the cycles depending on mutation and/or migration rate. A stable polymorphism of acceptors and rejecters occurs only when parasites are nonretaliators. The spread of retaliator parasites drives rejecter hosts to extinction. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗

Evolution of migration under kin selection and local adaptation.

We present here a stochastic two-locus, two-habitat model for the evolution of migration with local adaptation and kin selection. One locus determines the migration rate while the other causes local adaptation. We show that the opposing forces of kin competition and local adaptation can lead to the existence of one or two convergence stable migration rates, notably depending on the recombination rate between the two loci. We show that linkage between migration and local adaptation loci has two antagonist effects: when linkage is tight, cost of local adaptation increases, leading to smaller equilibrium migration rates. However, when linkage is tighter, the population structure at the migration locus tends to be very high because of the indirect selection, and thus equilibrium migration rates increases. This result, qualitatively different from results obtained with other models of migration evolution, indicates that ignoring drift or the detail of the genetic architecture may lead to incorrect conclusions.

Adaptation, Biological↗

Understanding the overdispersed molecular clock.

Rates of molecular evolution at some protein-encoding loci are more irregular than expected under a simple neutral model of molecular evolution. This pattern of excessive irregularity in protein substitutions is often called the "overdispersed molecular clock" and is characterized by an index of dispersion, R(T) > 1. Assuming infinite sites, no recombination model of the gene R(T) is given for a general stationary model of molecular evolution. R(T) is shown to be affected by only three things: fluctuations that occur on a very slow time scale, advantageous or deleterious mutations, and interactions between mutations. In the absence of interactions, advantageous mutations are shown to lower R(T); deleterious mutations are shown to raise it. Previously described models for the overdispersed molecular clock are analyzed in terms of this work as are a few very simple new models. A model of deleterious mutations is shown to be sufficient to explain the observed values of R(T). Our current best estimates of R(T) suggest that either most mutations are deleterious or some key population parameter changes on a very slow time scale. No other interpretations seem plausible. Finally, a comment is made on how R(T) might be used to distinguish selective sweeps from background selection.

Alleles↗

Evolution of virulence: a unified framework for coinfection and superinfection.

Models of the evolution of parasite virulence have focused on computing the evolutionarily stable level of virulence favored by tradeoffs within a host and by competition for hosts, and deriving conditions under which strains with different virulence levels can coexist. The results depend on the type of interaction between disease strains, such as single infection (immunity of infected individuals to other strains), coinfection (simultaneous infection by two strains), and superinfection (instantaneous takeover of host by the more virulent strain). We present a coinfection model with two strains and derive the superinfection model as the limit where individuals are rapidly removed from the doubly-infectious class. When derived in this way, the superinfection model includes not only the takeover of hosts infected by the less virulent strain, but new terms which take into account the possibility of increased mortality of doubly-infected individuals. Coinfection tends to favor higher virulence and support more coexistence than the single infection model, but the detailed results depend sensitively on two factors: (1) whether and how the model is near the superinfection limit, and (2) the shape of the coinfection function (the function describing the rate at which a more virulent strain can infect a host). If the superinfection limit arises due to rapid mortality of doubly-infected hosts, there is a region of uninvadable virulence levels rather than coexistence. When the coinfection function is discontinuous, as in many previous models, neither the coinfection model nor the superinfection limit can support an evolutionarily stable virulence level. Piecewise differentiable and differentiable coinfection functions produce qualitatively different results, and we propose that these more general cases should be used to study evolution of virulence when other mechanisms like space, population dynamics, and stochasticity interact.

Animals↗