Human Rhinovirus Types and Association with Respiratory Symptoms During the First Year of Life.

Human rhinoviruses (HRV) cause respiratory infections and are associated with asthma development. We assessed HRV prevalence, types and association with respiratory symptoms in the first year of life in 20 unselected infants. HRV was detected in 32% of 825 weekly nasal swabs. Seventy-four different types of all three species were identified. HRV presence and related respiratory symptoms are highly heterogeneous.

Rhinovirus Infections and Associated Respiratory Morbidity in Infants: A Prospective Cohort Study.

BACKGROUND Risk factors promoting rhinovirus (RV) infections are inadequately described in healthy populations, especially infants. OBJECTIVES To determine the frequency of symptomatic and asymptomatic RV infections and identify possible risk factors from host and environment among otherwise healthy infants. METHODS In a prospective birth cohort, respiratory health was assessed in 41 term-born infants by weekly telephone interviews during the first year of life, and weekly nasal swabs were collected to determine RV prevalence. In a multilevel logistic regression model, associations between prevalence and respiratory symptoms during RV infections and host/environmental factors were determined. RESULTS 27% of nasal swabs in 41 infants tested positive for RVs. Risk factors for RV prevalence were autumn months (OR=1.71, p=0.01, 95% CI 1.13-2.61), outdoor temperatures between 5-10 °C (OR=2.33, p=0.001, 95% CI 1.41-3.86), older siblings (OR=2.60, p=0.001, 95% CI 1.50-4.51) and childcare attendance (OR=1.53, p=0.07, 95% CI 0.96-2.44). 51% of RV-positive samples were asymptomatic. Respiratory symptoms during RV infections were less likely during the first three months of life (OR=0.34, p=0.003, 95% CI 0.17-0.69) and in infants with atopic mothers (OR=0.44, p=0.008, 95% CI 0.24-0.80). Increased tidal volume (OR=1.67, p=0.03, 95% CI 1.04-2.68) and outdoor temperatures between 2-5 °C (OR=2.79, p=0.02, 95% CI 1.17-6.61) were associated with more symptoms. CONCLUSIONS RVs are highly prevalent during the first year of life, and most infections are asymptomatic. Frequency of RV infections is associated with environmental factors, while respiratory symptoms during RV infections are linked to host determinants like infant age, maternal atopy, or premorbid lung function.

HETEROGENEITY IN VIRUS EXPRESSION, TUMORIGENICITY, AND IN VITRO GROWTH PROPERTIES OF DRUG-RESISTANT CLONES OF AN RIII MOUSE MAMMARY TUMOR CELL LINE

Four 8-azaguanine (AG)-resistant and 5-bromodeoxyuridine (BUdR)-resistant clones of a mouse mammary adenocarcinoma cell line, RIII 7387, were developed and analyzed for their tumorigenic properties, in vitro characteristics, and virus expression. These characteristics were analyzed for relationships of any of the cellular parameters and the ability of these lines to produce tumors in syngeneic animals.^ The results of this study demonstrated that the parental line consists of a heterogeneous population of cells. Doubling times, saturation densities, and 2-deoxy-D-glucose uptake varied between sublines. In addition, while all sublines were found to express both B-type and C-type viral antigenic markers, levels of the major B-type and C-type viral proteins varied in the subclones. The sublines also differed markedly in their response to the presence of dexamethasone, glutathione, and insulin in the tissue culture medium.^ Variations in retrovirus expression were convirmed by electron microscopy. Budding and extracellular virus particles were seen in the majority of the cell lines. Virus particles in one of the BUdR-resistant lines, BUD9, were found however, only in inclusions and vacuoles. The AG-resistant subline AGE11 was observed to be rich in intracytoplasmic A particles. The examination of these cell lines for the presence of retroviral RNA-dependent DNA polymerase (RT) activity revealed that some B-type RT activity could be found in the culture fluid of most of the cell lines but that little C-type RT activity could be found suggesting that the C-type virus particles expressed by these RIII clones contain a defective RT.^ Tumor clones also varied in their ability to form tumors in syngeneic RIII mice. Tumor incidence ranged from 50% to 100%. The majority of the tumors regressed within 30 days post infection.^ Statistical analysis indicated that while these clones varied in their characteristics, there was no correlation between the ability of these cell lines to form tumors in syngeneic mice and any of the other characteristics examined.^ These studies have confirmed and extended the growing evidence that tumors, regardless of their natural origin, consist of heterogeneous subpopulations of cells which may vary widely in their in vitro growth behavior, their antigenic expression, and their malignant properties. ^

Na 1 Nachlass Max Horkheimer, 529 - Korrespondenzen mit u.a. Henryk Grossmann (p. VI 10, 1 - 200)

24 Briefe und Abrechnugen von New York State Income Tax Resident Return (New York) an Henryk Grossmann, 1938 - 1948; 3 Briefe von Henryk Grossmann an das Department of Taxation and Finance, 1946; 5 Briefe zwischen C. Hartwig Inc. und der Social Studies Association (New York), 1949; 1 Brief an F. Pollock von A. P. Bersohn, 14.12.1948; 2 Briefe von Max Horkheimer an Henryk Grossmann, 1945/1947; 2 Briefe zwischen Henryk Grossmann und F. Pollock, 1948 - 1949; 1 Brief von American Scantic Line/Moore-McCormack Lines Inc (New York) an C. Hartwig Inc., 18.02.1949; 1 Brief an Collector of Internal Revenue (New York) von Max Horkheimer, 25.01.1949; 1 Brief von Frederick Wild an Herrn Edelman, 17.09.1946; 80 Briefe zwischen Julian und Lotte Gumperz und Max Horkheimer, 1934 - 1942; 4 Briefe zwischen dem Institut für Sozialforschung (Frankfurt a. M.) und Helen Mack, 1974 - 1975; 3 Briefe zwischen der Columbia University (New York) und Julian Gumperz, Juli 1934; 4 Briefe von Max Horkheimer an die Columbia University (New York), 1934/1938; 1 Brief von Julian Gumperz an A. E. Burns, 24.02.1938; 1 Brief an Louis H. Bean von Julian Gumperz, 24.02.1938; 1 Brief von Julian Gumperz an E. A. Goldenweiser, 24.02.1938; 1 Brief an F. H. Thomson von Julian Gumperz, 24.02.1938; 1 Brief von Julian Gumperz an Gardiner Means, 24.02.1938; 1 Brief an Hildegard Kneeland von Julian Gumperz, 24.02.1938; 1 Brief von Julian Gumperz an Mordecai Execiel, 24.02.1938; 1 Brief an Isador Lubin von Julian Gumperz, 24.02.1938; 1 Brief von Julian Gumperz an Boris Stern, 24.02.1938; 1 Brief an Lauchlin Currie von Julian Gumperz, 24.02.1938; 1 Brief von Julian Gumperz an B. H. Beckhart, 24.02.1938; 1 Brief von der Zeitschrift für Sozialforschung (New York) an Julian Gumperz, 08.10.1937;

Na 1 Nachlass Max Horkheimer, 600 - Korrespondenzen u.a. mit Friedrich Pollock (p. VI 42, 211-386)

Briefwechsel zwischen Max Horkheimer, Frederick Pollock und Karl August und Olga Wittfogel; 2 Briefe zwischen Edith B. Bernett und Max Horkheimer, April 1940; 2 Briefe zwischen Max Horkheimer und Philip Vaudrin, Juli 1939; 3 Briefe an David H. Stevens von Max Horkheimer, 26.03.1938; 1 Brief von A. Radcliffe an Frederick Pollock, 18.11.1937; 3 Briefe an Max Horkheimer von der Columbia University Faculty of Political Science (New York), November 1937; 2 Briefe von der Columbia University Department of History (New York) an Max Horkheimer, November 1937; 1 Brief an Max Horkheimer von Sharon Beard, 27.11.1937; 1 Brief von Ruth Benedict an Max Horkheimer, 19.11.1937; 1 Brief an Max Horkheimer von Franz Boas, 19.11.1937; 1 Brief von R. E. Chaddock an Max Horkheimer, 21.11.1937; 1 Brief an Max Horkheimer von Ch'ao-ting Chi, 19.11.1937; 1 Brief von J. M. Clark an Max Horkheimer, 22.11.1937; 1 Brief an Dr. Wertheimer von Morris R. Cohen, 29.11.1937; 1 Brief von Alfred E. Cohn an Max Horkheimer, 26.11.1937; 1 Brief an Max Horkheimer von John J. Coss, 22.11.1937; 1 Brief von George S. Counts an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von A. P. Evans, 22.11.1937; 3 Briefe von Gertrude Stewart an Max Horkheimer, 20. - 24.11.1937; 1 Brief an Max Horkheimer von L. C. Goodrich, 22.11.1937; 1 Brief von John W. Innes an Max Horkheimer, 20.11.1937; 1 Brief an Max Horkheimer von Philip C. Jessup, 24.11.1937; 1 Brief von John A. Krout an Max Horkheimer, 23.11.1937; 1 Brief an Max Horkheimer von Bruno Lasker, 20.11.1937; 1 Brief von Samuel McCune Lindsay an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von K. N. Llewellyn, 26.11.1937; 1 Brief von R. S. Lynd an Max Horkheimer, [November 1937]; 1 Brief an Max Horkheimer von R. M. MacIver, 19.11.1937; 1 Brief von Julian W. Mack an Max Horkheimer, 24.11.1937; 1 Brief an Max Horkheimer von Arthur Maxmahon, 20.11.1937; 1 Brief von Jerome Michael an Max Horkheimer, 26.11.1937; 1 Brief an Max Horkheimer von Wesley C. Mitchell, 22.11.1937; 1 Brief von der Columbia University School of Business (New York) an Max Horkheimer, 22.11.1937; 2 Briefe zwischen Max Horkheimer und der John Simon Guggenheim Memorial Foundation (New York), November 1937; 2 Briefe von der Columbia University Department of Psychology (New York) an Max Horkheimer, November 1937; 1 Brief an Max Horkheimer von Goodwin Watson, 23.11.1937; 1 Brief von Otto Nathan an Max Horkheimer, 26.11.937; 1 Brief an Max Horkheimer von John K. Norton, 23.11.1937; 1 Brief von der Columbia University Department of Chinese (New York) an Max Horkheimer, 23.11.1937; 1 Brief an Max Horkheimer von Gerold Tanquary Robinson, 19.11.1937; 1 Brief von der Columbia University Department of Public Law and Government (New York) an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von R. C. Sailer, 20.11.1937; 1 Brief von Herbert W. Schneider an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von R. L. Schuyler, 20.11.1937; 1 Brief von Pauline Steorns an Max Horkheimer, 22.11.1937; 1 Brief an Max Horkheimer von Frank Tannenbaum, 19.11.1937; 1 Brief von Alfred Vagés an Max Horkheimer, 26.11.1937;

BIOCHEMICAL CHARACTERIZATION AND CLINICAL SIGNIFICANCE OF COAGULASE-NEGATIVE STAPHYLOCOCCI

Although coagulase-negative staphylococci (C-NS) have been implicated in certain human infections, they are generally regarded as contaminants and their clinical significance is questioned. To assess their role as pathogens, 205 isolates of C-NS from wounds, and body fluids (blood, urine, pleural and peritoneal fluids, etc.) were studied. Patient's charts were reviewed and using strict criteria a determination was made regarding the clinical significance of these isolates. The organisms were then identified using the scheme of Kloos and Schleifer to determine if certain species of C-NS were associated with specific infections. S. epidermidis sensu stricto accounted for 81% of the C-NS isolated; the frequency of other species was S. haemolyticus (6%), S. hominis (5%), S. capitis (4%), S. warneri (3%), and others (1%). Only two isolates were novobiocin resistant; neither was identified as S. saprophyticus. Using these criteria, 22% of C-NS were considered to be clinically significant and the majority of these (93%) were due to S. epidermidis. The most common source of the clinically relevant C-NS isolates was from wounds. These data suggest that identifying C-NS species other than S. epidermidis may be of limited value in predicting clinical significance.^ In addition, selected pathogenic and non-pathogenic strains of C-NS were compared for their ability to adhere to human cells in vitro. Although the results were not conclusive, it appeared that pathogenic C-NS adhered more avidly than non-pathogenic C-NS to buccal cells. Experiments with HeLa cells showed no difference between pathogenic and non-pathogenic C-NS in adherence abilities. ^

The effects of DNA cytosine methylation on H -ras promoter structure and function

The effect of DNA cytosine methylation on H-ras promoter activity was assessed using a transient expression system employing the plasmid H-rasCAT (NaeI H-ras promoter linked to the chloramphenicol acetyltransferase (CAT) gene). This 551 bp promoter is 80% GC rich, enriched with 168 CpG dinucleotides, and contains six functional GC box elements which represent major DNA methylation target sites. Prokaryotic methyltransferases HhaI (CGm$\sp5$CG) and HpaII (Cm$\sp5$CGG) alone or in combination with a human placental methyltransferase (HP MTase) were used to introduce methyl groups at different CpG sites within the promoter. To test for functional promoter activity, the methylated plasmids were introduced into CV-1 cells and CAT activity assessed 48 h post-transfection. Methylation at specific HhaI and HpaII sites reduced CAT expression by 70%, whereas more extensive methylation at generalized CpG sites with HP MTase inactivated the promoter $>$95%. The inhibition of H-ras promoter activity was not attributable to methylation-induced differences in DNA uptake or stability in the cell, topological form of the plasmid, or methylation effects in nonpromoter regions. We also observed that DNA cytosine methylation of a 360 bp promoter fragment by HP MTase induced a local change in DNA conformation. Using three independent methodologies (nitrocellulose filter binding assays, gel mobility shifts, and Southwestern blots), we determined that this change in promoter conformation affected the interaction of nuclear proteins with cis-regulatory sequences residing in the promoter region. The results provide evidence to suggest that DNA methylation may regulate gene expression by inducing changes in local promoter conformation which in turn alters the interactions between DNA and protein factors required for transcription. The results provide supportive evidence for the hypothesis of Cedar and Riggs, who postulated that DNA methylation may regulate gene expression by altering the binding affinities of proteins for DNA. ^

AS RELAÇÕES ENTRE GESTÃO DA DIVERSIDADE E CULTURA ORGANIZACIONAL EM UMA EMPRESA DO SETOR PORTUÁRIO DO RIO DE JANEIRO

A cultura de uma organização é importante para que seus colaboradores possuam mesmos objetivos e valores. Porém, em busca de manter uma estratégia competitiva e agir de forma responsável na comunidade em que se encontra, a empresa precisa inovar e adaptar-se. A gestão da diversidade apresenta-se como uma válida forma de enfrentar estes novos desafios e exigências. Contudo, há muitos obstáculos para que uma gestão da diversidade seja bem-sucedida. Este estudo propõe-se em entender como a diversidade pode afetar a cultura de uma organização. Além disso, como a cultura pode afetar a estratégia de gestão da diversidade. Foi utilizado para este objetivo um estudo de caso em profundidade com seis entrevistas. As entrevistas foram apoiadas em um roteiro semi estruturado. A análise dos dados obtidos foi feita pela análise de conteúdo. De acordo com a pesquisa realizada, sugere que a cultura organizacional e a gestão da diversidade estão diretamente conectadas e que podem influenciar positivamente uma a outra, porém precisam manter um equilíbrio em suas ações para que não causem prejuízos à organização.

Cell autonomous regulation of multiple Dishevelled-dependent pathways by mammalian Nkd

Genetic studies have identified Drosophila Naked Cuticle (Nkd) as an antagonist of the canonical Wnt/β-catenin signaling pathway, but its mechanism of action remains obscure [Zeng, W., Wharton, K. A., Jr., Mack, J. A., Wang, K., Gadbaw, M., et al. (2000) Nature (London) 403, 789–795]. Here we have cloned a cDNA encoding a mammalian homolog of Drosophila Nkd, mNkd, and demonstrated that mNkd interacts directly with Dishevelled. Dishevelled is an intracellular mediator of both the canonical Wnt pathway and planar cell polarity (PCP) pathway. Activation of the c-Jun-N-terminal kinase has been implicated in the PCP pathway. We showed that mNkd acts in a cell-autonomous manner not only to inhibit the canonical Wnt pathway but also to stimulate c-Jun-N-terminal kinase activity. Expression of mNkd disrupted convergent extension in Xenopus, consistent with a role for mNkd in the PCP pathway. These data suggest that mNkd may act as a switch to direct Dishevelled activity toward the PCP pathway, and away from the canonical Wnt pathway.