The frequency and duration of Salmonella–macrophage adhesion events determines infection efficiency

Salmonella enterica causes a range of important diseases in humans and a in a variety of animal species. The ability of bacteria to adhere to, invade and survive within host cells plays an important role in the pathogenesis of Salmonella infections. In systemic salmonellosis, macrophages constitute a niche for the proliferation of bacteria within the host organism. Salmonella enterica serovar Typhimurium is flagellated and the frequency with which this bacterium collides with a cell is important for infection efficiency. We investigated how bacterial motility affects infection efficiency, using a combination of population-level macrophage infection experiments and direct imaging of single-cell infection events, comparing wild-type and motility mutants. Non-motile and aflagellate bacterial strains, in contrast to wild-type bacteria, collide less frequently with macrophages, are in contact with the cell for less time and infect less frequently. Run-biased Salmonella also collide less frequently with macrophages but maintain contact with macrophages for a longer period of time than wild-type strains and infect the cells more readily. Our results suggest that uptake of S. Typhimurium by macrophages is dependent upon the duration of contact time of the bacterium with the cell, in addition to the frequency with which the bacteria collide with the cell.     

The morphological interpretation of epiascidiate leaves —An historical perspective—

Epiascidiate leaves are those foliar organs whose adaxial (ventral) side is the inside of a tube. Such tubular leaves are found in Nepenthaceae, Sarraceniaceae, Cephalotaceae, and Lentibulariaceae. Throughout botanical history these leaves have received considerable attention because of their bizarre morphology and problems of interpretation. This paper documents the attempts of the last 150 years to correctly understand their organographic nature. All epiascidiate foliar organs are structurally similar in their early ontogeny, each forms a distinctive adaxial outgrowth (Querzone), and the diverse morphologies of the mature organs seem to be modifications upon a similar primordial ground plan. Typologically these leaves are directly related to peltate leaves and phyllodes (non-petiolar,sensu Boke). Except for certain, highly speculative,de novo theories, such as the “foliar runner” theory of Croizat, all misinterpretations of the nature of epiascidiate leaves are directly attribuable to earlier errors in ascertaining the organography of typologically related leaf forms. Accordingly, the sympodial tubular leaf (Roth) is rejected, as is the petiolar nature of tubular leaves (de Candolle). The typological relationships of these leaves to unifacial foliar organs (Troll) seems well substantiated from both an organographic and a histogenetic viewpoint. The peltate carpel theory (?elakovský; Troll) is, in reality, an epiascidiate carpel theory. The idea of a fundamentally tubular carpel seems correct from both a typological and phylogenetic standpoint. To comprehend the various contradictory interpretations which have been used to explain morphologically complex problems, as well as to understand the genesis of morphological theories, it is necessary to acquire an accurate historical perspective of the subject.     

The disappearing CD4(+)T cells in HIV infection: a case of over-stimulation?

Infection with the human immunodeficiency virus (HIV) causes a gradual decline in essential immune-system cells called CD4(+)"helper" T cells. These cells are also principal viral targets, but, paradoxically, direct cell-killing does not explain their disappearance. HIV also induces a chronic and increasing state of immune activation. In a mathematical model of normal T-cell kinetics incorporating a cytokine growth factor, increased activation alone explains these T-cell losses, a switch from "na?ve" to "memory" phenotype, and certain other features of HIV disease.     

The mechanism of γ-Secretase dysfunction in familial Alzheimer disease

The mechanisms by which mutations in the presenilins (PSEN) or the amyloid precursor protein (APP) genes cause familial Alzheimer disease (FAD) are controversial. FAD mutations increase the release of amyloid β (Aβ)42 relative to Aβ40 by an unknown, possibly gain‐of‐toxic‐function, mechanism. However, many PSEN mutations paradoxically impair γ‐secretase and ‘loss‐of‐function’ mechanisms have also been postulated. Here, we use kinetic studies to demonstrate that FAD mutations affect Aβ generation via three different mechanisms, resulting in qualitative changes in the Aβ profiles, which are not limited to Aβ42. Loss of ε‐cleavage function is not generally observed among FAD mutants. On the other hand, γ‐secretase inhibitors used in the clinic appear to block the initial ε‐cleavage step, but unexpectedly affect more selectively Notch than APP processing, while modulators act as activators of the carboxypeptidase‐like (γ) activity. Overall, we provide a coherent explanation for the effect of different FAD mutations, demonstrating the importance of qualitative rather than quantitative changes in the Aβ products, and suggest fundamental improvements for current drug development efforts.     

Wolbachia infection frequencies in insects: evidence of a global equilibrium?

Wolbachia are a group of cytoplasmically inherited bacteria that cause reproduction alterations in arthropods, including parthenogenesis, reproductive incompatibility, feminization of genetic males and male killing. Previous general surveys of insects in Panama and Britain found Wolbachia to be common, occurring in 16-22% of species. Here, using similar polymerase chain reaction methods, we report that 19.3% of a sample of temperate North American insects are infected with Wolbachia, a frequency strikingly similar to frequencies found in two other studies in widely separated locales. The results may indicate a widespread equilibrium of Wolbachia infection frequencies in insects whose maintenance remains to be explained. Alternatively, Wolbachia may be increasing in global insect communities. Within each of the three geographic regions surveyed, Hymenoptera are more frequently infected with A group Wolbachia and Lepidoptera more frequently infected with B group Wolbachia.     

Governmental policies on HIV infection in China

This article is a general review of the evolvement of HIV/AIDS-related public policies in China since 1980＇s. It tracks the important laws, regulations and other governmental documents in regard to HIV/AIDS prevention mainly at central level.     

The flocculation of wine yeasts: biochemical and morphological characteristics inZygosaccharomyces — flocculation inZygosaccharomyces

The floc-forming ability of flocculent strains ofZygosaccharomyces bailii andZ fermentati, isolated from musts, was tested for susceptibility to proteinase and sugar treatments.Z. fermentati was found highly resistant to the proteolytic enzymes tested, whereasZ. baili was only trypsin-resistant.The inhibition of flocculation by sugars distinguished two types: inZ. fermentati flocculation was completely inhibited by mannose, inZ. bailli by various sugars.By SEM observation, the cell surface ofZygosaccharomyces revealed the presence of a column structure, resulting from fusion of vesicles present on the cell surface.     

Some morphological observations concerning problems of endosporulation in Emmonsia crescens — Aetiological agent in adiaspiromycosis

Morphologic study dealing with problems of endosporulation in some spherules ofEmmonsia crescens.From the Departments of Pathology and Biology, Medical Faculty of Palacký University, Olomouc, Czechoslovakia.     

The HIV-poverty thesis re-examined: poverty, wealth or inequality as a social determinant of HIV infection in sub-Saharan Africa?

Although health is generally believed to improve with higher wealth, research on HIV in sub-Saharan Africa has shown otherwise. Whereas researchers and advocates have frequently advanced poverty as a social determinant that can help to explain sub-Saharan Africa's disproportionate burden of HIV infection, recent evidence from population surveys suggests that HIV infection is higher among wealthier individuals. Furthermore, wealthier countries in Africa have experienced the fastest growing epidemics. Some researchers have theorized that inequality in wealth may be more important than absolute wealth in explaining why some countries have higher rates of infection and rapidly increasing epidemics. Studies taking a longitudinal approach have further suggested a dynamic process whereby wealth initially increases risk for HIV acquisition and later becomes protective. Prior studies, conducted exclusively at either the individual or the country level, have neither attempted to disentangle the effects of absolute and relative wealth on HIV infection nor to look simultaneously at different levels of analysis within countries at different stages in their epidemics. The current study used micro-, meso- and macro-level data from Demographic and Health Surveys (DHS) across 170 regions within sixteen countries in sub-Saharan Africa to test the hypothesis that socioeconomic inequality, adjusted for absolute wealth, is associated with greater risk of HIV infection. These analyses reveal that inequality trumps wealth: living in a region with greater inequality in wealth was significantly associated with increased individual risk of HIV infection, net of absolute wealth. The findings also reveal a paradox that supports a dynamic interpretation of epidemic trends: in wealthier regions/countries, individuals with less wealth were more likely to be infected with HIV, whereas in poorer regions/countries, individuals with more wealth were more likely to be infected with HIV. These findings add additional nuance to existing literature on the relationship between HIV and socioeconomic status.     

Identity of `acid'' β-glucosidase and glucocerebrosidase in human spleen

1. Glucocerebrosidase, in association with a membrane-bound ;acid' beta-glucosidase, was separated from a soluble ;neutral' beta-glucosidase that had no activity towards glucocerebroside as substrate. 2. Glucocerebrosidase, as well as ;acid' beta-glucosidase activity depended upon the association of factor P (a heat-stable, soluble, acidic glycoprotein) with factor C (a heat-labile membrane-bound protein). 3. Factor C was solubilized under certain conditions. 4. Solubilized factor C, as well as membrane-bound factor C, could be alternatively stimulated by sodium taurocholate to give both glucocerebrosidase and ;acid' beta-glucosidase activities. 5. Membrane-bound factor C reacted optimally with factor P whereas solubilized factor C was preferentially stimulated by taurocholate. 6. Factor P-dependent glucocerebrosidase activity differed in kinetic properties from the taurocholate-stimulated enzyme activity. 7. The results are discussed in the light of (a) identity of glucocerebrosidase and ;acid' beta-glucosidase, (b) application in clinical diagnosis, (c) physiological significance of the enzyme system, and (d) polygenic inheritance in adult Gaucher's disease.     

Immunopathologic differences of Sjögren's syndrome versus sicca syndrome in HCV and HIV infection

A clinical picture of dry eye and dry mouth with the histological counterpart of focal lymphocytic sialoadenitis, usually detected in minor salivary glands, is considered the hallmark of Sjögren's syndrome. The association of sicca complaints and focal sialoadenitis can be also found in a number of other diseases, including some systemic viral infections. Among these conditions, chronic hepatitis C virus infection, associated with mixed cryoglobulinaemia and extra-hepatic manifestations, and HIV infection, particularly in the phase of diffuse interstitial lymphocytic infiltration, may mimic the clinical and histological aspects of Sjögren's syndrome. However, each disorder is characterised by specific, disease-related immunopathological aspects. Besides sicca complaints, the various disorders may also share a number of systemic extra-glandular features and the possible development of mucosa-associated lymphoid tissue lymphomas. This latter event represents in all of these diseases the final result of an antigen-driven chronic stimulation of B lymphocytes.     

The ‘requirement of total evidence’ and its role in phylogenetic systematics

The question of whether or not to partition data for the purposes of inferring phylogenetic hypotheses remains controversial. Opinions have been especially divided since Kluge's (1989, Systematic Zoology 38, 7–25) claim that data partitioning violates the requirement of total evidence (RTE). Unfortunately, advocacy for or against the RTE has not been based on accurate portrayals of the requirement. The RTE is a basic maxim for non-deductive inference, stipulating that evidence must be considered if it has relevance to an inference. Evidence is relevant if it has a positive or negative effect on a given conclusion. In the case of ℈partitioned’ phylogenetic inferences, the RTE is violated, and the basis for rational belief in any conclusion is compromised, unless it is shown that the partitions are evidentially irrelevant to one another. The goal of phylogenetic systematics is to hypothesize past causal conditions to account for observed shared similarities among two or more species. Such inferences are non-deductive, necessitating consideration of the RTE. Some phylogeneticists claim the parsimony criterion as justification for the RTE. There is no relation between the two – parsimony is a relation between a hypothesis and causal question(s). Parsimony does not dictate the content of premises prior to an inference. ℈Taxonomic congruence,’ ℈supertrees,’ and ℈conditional combination’ methods violate the RTE. Taxonomic congruence and supertree methods also fail to achieve the intended goal of phylogenetic inference, such that ℈consensus trees’ and ℈supertrees’ lack an empirical basis. ℈Conditional combination’ is problematic because hypotheses derived from partitioned data cannot be compared – a causal hypothesis inferred to account for a set of effects only has relevance to those effects, not any comparative relevance to other causal hypotheses. A similar problem arises in the comparisons of hypotheses derived from different causal theories.     

Low heritability in morphological characters of Tengmalm's owls: The role of cyclic food and laying date?

Summary In parent—offspring regressions, high heritability estimates of characters may simply be due to common environment: the resemblance between the living conditions of parents and their offspring in species showing restricted natal dispersal. In vole-eating Tengmalm's owls (Aegolius funereus), the natal dispersal and breeding dispersal of adult females are wide (up to > 1000 km and > 500 km, respectively), whereas adult males are resident. We found that body measurements of 183 recruits born in western Finland were independent of parental age and vole abundance in the birth year. Early-laid eggs produced longer winged recruits than late-laid eggs. The wing lengths of the daughters showed a significant positive regression on the wing length of their mothers, but the removal of the maternal effect via laying date lowered this relationship. The development time of offspring to the first autumn might also be crucial for morphological characters of females in their later life. Significant regressions were not found between the wing length of the son and his father. The mother—daughter regression was small for laying date, but positive (p = 0.08) for clutch size. These results suggest low heritability in breeding and morphological characters of owls and this low heritability may enable plastic adjustment to optimize fitness at any stage in a fluctuating environment. Nonadditive genetic variance also creates variation between offspring characters that are not genetically correlated with the parents and may explain these low heritability estimates.