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Volume 47,
Issue 10,
1998
Volume 47, Issue 10, 1998
- Editorial
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- The 20Th C. L. Oakley Lecture
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Glycopeptide-resistant enterococci: a decade of experience
More LessSince their first description in 1988, glycopeptide-resistant enterococci (GRE) have emerged as a significant cause of nosocomial infections and colonisations, particularly in Europe and the USA. Two major genetically distinct forms of acquired resistance, designated VanA and VanB, are recognised, although intrinsic resistance occurs in some enterococcal species (VanC) and a third form of acquired resistance (VanD) has been reported recently. The biochemical basis of each resistance mechanism is similar; the resistant enterococci produce modified peptidoglycan precursors that show decreased binding affinity for glycopeptide antibiotics. Although VanA resistance is detected readily in the clinical laboratory, the variable levels of vancomycin resistance associated with the other phenotypes makes detection less reliable. Under-reporting of VanB resistance as a result of a lower detection rate may account, in part, for the difference in the numbers of enterococci displaying VanA and VanB resistance referred to the PHLS Laboratory of Hospital Infection. Since 1987, GRE have been referred from >1100 patients in almost 100 hospitals, but 88% of these isolates displayed the VanA phenotype. It is possible that, in addition to the problems of detection, there may be a real difference in the prevalence of VanA and VanB resistance reflecting different epidemiologies. Our present understanding of the genetic and biochemical basis of these acquired forms of glycopeptide resistance has been gained mainly in the last 5 years. However, these relatively new enterococcal resistances appear still to be evolving; there have now been reports of transferable VanB resistance associated with either large chromosomally borne transposons or plasmids, genetic linkage of glycopeptide resistance and genes conferring high-level resistance to aminoglycoside antibiotics, epidemic strains of glycopeptide-resistant Enterococcus faecium isolated from multiple patients in numerous hospitals, and of glycopeptide dependence (mutant enterococci that actually require these agents for growth). The gene clusters responsible for VanA and VanB resistance are located on transposable elements, and both transposition and plasmid transfer have resulted in the dissemination of these resistance genes into diverse strains of several species of enterococci. Despite extensive research, knowledge of the origins of these resistances remains poor. There is little homology between the resistance genes and DNA from either intrinsically resistant gram-positive genera or from the soil bacteria that produce glycopeptides, which argues against direct transfer to enterococci from these sources. However, recent data suggest a more distant, evolutionary relationship with genes found in glycopeptide-producing bacteria. In Europe, VanA resistance occurs in enterococci isolated in the community, from sewage, animal faeces and raw meat. This reservoir suggests that VanA may not have evolved in hospitals, and its existence has been attributed, controversially, to use of the glycopeptide avoparcin as a growth promoter, especially in pigs and poultry. However, as avoparcin has never been licensed for use in the USA and, to date, VanB resistance has not been confirmed in non-human enterococci, it is clear that the epidemiology of acquired glycopeptide resistance in enterococci is complex, with many factors contributing to its evolution and global dissemination.
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- Host Response To Infection
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Local cellular immune response in the acute phase of gastritis in mice induced chemically and by Helicobacter pylori
More LessGastritis was induced in mice by oral administration of acetic acid 5%, a cagA positive Helicobacter pylori strain, or both. The induction of a mild gastritis by acetic acid before inoculation with H. pylori resulted in a slight but not significantly decreased colonisation rate. To study the initial stage of inflammation, the presence of gastric lymphoid and non-lymphoid cells was studied by immunohistochemistry during the first 2 weeks after induction of gastritis. Treatment with acetic acid alone or in combination with H. pylori resulted in an increase in the number of neutrophils in the mucosa and submucosa, without evident epithelial damage. The influx of neutrophils was most prominent in the mice that received a combined treatment of acetic acid and H. pylori. Macrophages were also increased in both acetic acid and acetic acid plus H. pylori-treated groups, although a different kinetic pattern was present in these groups. In mice infected with H. pylori alone, only a slight but not significant increase in neutrophils and macrophages was observed. The early presence of lymphoid aggregates in the gastric mucosa of mice in which colonisation was shown with H. pylori was remarkable. This phenomenon was not seen in control mice, in mice that received acetic acid alone or when colonisation was not shown. These data suggest that gastritis induced by a chemical agent such as acetic acid occurs by a different mechanism than gastritis induced by H. pylori and that the continued presence of H. pylori is required for local lymphocyte activation.
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Induction of granulomas in interferon-γ gene-disrupted mice by avirulent but not by virulent strains of Mycobacterium tuberculosis
To gain a better understanding of the pathological role of interferon-γ (IFN-γ) in specific granuloma formation, IFN-γ gene-deficient mice (BALB/c and C57BL/6) were produced. The IFN-γ gene in embryonic stem (ES) cells was disrupted by inserting the β-galactosidase gene (lacZ) and the neomycin resistance gene (neo) at the translation initiation site in exon 1 by homologous recombination. Six-week-old IFN-γ-deficient and wild-type mice were inoculated with 103-107 bacilli of various strains of Mycobacterium tuberculosis (Kurono, H37Rv, H37Ra and BCG Pasteur) through their tail veins. The mice were examined 7 weeks later for granuloma formation. The avirulent BCG Pasteur and H37Ra strains (103-104 bacilli/ml) induced granulomas in the spleen, liver and lungs of IFN-γ-deficient mice. The granulomas consisted of epithelioid macrophages and Langhans multinucleate giant cells, but lacked caseous necrosis. The virulent Kurono and H37Rv strains induced disseminated abscesses but not granulomas in various organs of IFN-γ-deficient mice and Mac-3-positive macrophages were not detected in the abscess lesions. These results suggest that IFN-γ may be primarily responsible for macrophage activation and that other factor(s) may be involved in the granuloma formation mechanism.
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Binding of Clostridium difficile toxin A to human milk secretory component
More LessToxigenic Clostridium difficile is isolated from a majority of healthy human infants. The exact mechanism of asymptomatic colonisation is unclear; however, previous studies in this laboratory have shown that components of both the immunoglobulin and non-immunoglobulin fractions of human milk bind to toxin A and prevent its interaction with hamster intestinal brush border membranes (BBMs). Secretory IgA (sIgA) is the primary immunoglobulin found in human milk. As sIgA resists digestion in the infant stomach and passes at high levels into the colon, its ability to bind toxin A was the subject of this investigation. Purified sIgA in concentrations at and below those found in human milk inhibited the binding of toxin A to purified BBM receptors. Heating sIgA to 100° for 5 min did not affect its inhibitory activity. IgM, IgG and serum IgA did not appreciably inhibit the binding of toxin A to BBM receptors. SDS-PAGE separated sIgA into three major bands: secretory component, heavy chains and light chains. Autoradiography with radiolabelled toxin A revealed that toxin A bound to the secretory component (SC) of sIgA. When the three purified subunits of sIgA were coated on to microtitration wells, SC bound significantly more toxin A than the heavy or light chains of sIgA. Purified SC also inhibited toxin binding to receptors in a dose-dependent fashion similar to sIgA. The heavy and light chains of sIgA did not inhibit toxin A receptor binding. Removing carbohydrates from sIgA and SC by enzymic digestion showed that toxin A binds much less to deglycosylated SC than to glycosylated SC. These data suggest that SC in human milk binds to toxin A and may function as a receptor analogue, protecting human infants against C. difficile-associated disease.
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- Diagnostic Microbiology
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Speciation of presumptive viridans streptococci from early onset neonatal sepsis
More LessTwenty isolates resembling viridans streptococci, 16 from blood and four from gastric aspirates, from 17 cases of early onset neonatal sepsis were identified by the AP120 Strep, Rapid ID 32 Strep and conventional tests plus hydrolysis of methylumbelliferyl glycoside substrates. Nineteen of the isolates were identified as species of viridans streptococci and one as a Leuconostoc sp. Ten of the isolates were Streptococcus oralis, three S. mitis biotype 1, two S. mitis biotype 2 and one each of S. sanguis, S. vestibularis, S. salivarius and S. intermedius. The Rapid ID 32 Strep and conventional plus methylumbelliferyl tests gave the same species identity for 17 of the isolates. S. intermedius was identified by the Rapid ID 32 Strep as S. constellatus and S. salivarius as S. equinus, with S. salivarius at lower probability. The AP120 Strep failed to identify S. vestibularis and identified S. salivarius as S. defectivus. The absence of certain critical tests, including urea hydrolysis, does not allow the AP120 Strep to identify all the currently recognised species of viridans steptococci. The species distribution was unexpected and the incidence of S. oralis and other viridans streptococci in vaginal swabs from prenatal patients is being investigated further.
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- Epidemiology Of Infection
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A case-control study of diarrhoea in children caused by Escherichia coli producing heat-stable enterotoxin (EAST-1)
More LessEscherichia coli strains associated with diarrhoeal disease have been classified into several types according to the pathogenic mechanism. Among these, enteroaggregative E. coli strains (EAggEC) have been associated with persistent childhood diarrhoea. Some strains of EAggEC produce a heat-stable toxin (EAST-1) that differs from others described previously. The main goal of this case-control study was to determine the prevalence of EAggEC and EAST-1-producing E. coli strains as a cause of diarrhoea in children in Spain and to study their in-vitro susceptibility to 21 antimicrobial agents. In the case group (115 children) 22 (19%) isolates and four (3.5%) isolates were EAST-1-producing E. coli and EAggEC, respectively, whereas in the control group (79 children) four (5%) isolates produced EAST-1 (p = 0.005) and three (3.8%) isolates were EAggEC. The present study suggests that EAST-1-producing E. coli strains are associated with diarrhoeal diseases in Spanish children, whereas EAggEC strains are not. Moreover, EAST-1-producing E. coli strains showed a high susceptibility to all the antimicrobial agents tested except for ampicillin.
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Streptococcal emm types associated with T-agglutination types and the use of conserved emm gene restriction fragment patterns for subtyping group A streptococci
The T-agglutination types were determined for a diverse collection of 1531 group A streptococci for which the 5′ M protein gene (emm) sequences had been analysed. The majority of the T-agglutination types correlated with previously seen M/emm/T-type associations; however, several new associations were found. Analysis of a subset of this collection – which included 1157 clinical isolates with multiply encountered emm types – found that emm amplicon restriction profiles of isolates sharing identical T types and opacity factor phenotypes are useful for detecting groups of isolates with identical emm genes. Many emm genes of known 5′ sequence display a highly conserved restriction pattern amongst clinical isolates widely separated both geographically and temporally.
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- Technical Notes
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Growth temperature ranges of Borrelia burgdorferi sensu lato strains
More LessThree strains of Borrelia burgdorferi sensu lato, representing three human pathogenic genomospecies (B31, B. burgdorferi sensu stricto; BR14, B. garinii; BR75, B. afzelii) were grown in BSK-H medium at different temperatures and the spirochaetal cells were counted by dark-field microscopy after 0, 4, 8, 16 and 48 days. Approximate optimum (minimum-maximum) temperatures for the in-vitro growth were found to be 33°C (22-39°C) in strain B31, 35°C (20-40°C) in strain BR75 and 37°C (20-41°C) in strain BR14. Maximum, optimum and minimum growth temperatures seem to be important characteristics of B. burgdorferi s.l. strains, with relevance for the symptomatology, epidemiology and epizoology of Lyme borreliosis.
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Development of a rapid method for quantitative evaluation of Mycobacterium tuberculosis growth based on competitive polymerase chain reaction
More LessA competitive polymerase chain reaction (cPCR) assay for the quantitative evaluation of Mycobacterium tuberculosis growth was developed based on co-amplification of genomic DNA and a modified DNA fragment derived from a well-conserved region of the 16S rRNA gene. There was a good correlation between the number of DNA copies in the sample, indicated by competitive PCR, and the number of colony forming units determined by conventional culture methods.
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- Correspondence
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- Microbial Pathogenicity
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Ability of clinical isolates of group A streptococci to adhere to and invade HEp-2 epithelial cells
More LessIndividual strains of group A streptococci (GAS) differ in virulence, but the reasons for these differences are incompletely understood. To determine if the ability of GAS to cause invasive disease corresponded with their capacity to adhere to or invade epithelial cells, 63 clinical isolates of GAS (40 from patients with systemic infection and 23 from superficial disease) were examined in quantitative assays of bacterial adhesion to and invasion of HEp-2 cells, a continuous line of human pharyngeal epithelial cells. The results showed that individual isolates of GAS varied considerably in their ability to adhere to and penetrate HEp-2 cells. However, on the whole, strains from patients with invasive disease adhered to cells in numbers c.1.5 greater than those from superficial infection. Paradoxically, strains from patients with invasive disease invaded HEp-2 cells to a significantly lesser extent than those from superficial sites, with a two-fold difference in invasion index (defined as the percentage of cell-associated bacteria located intracellularly). To determine if these differences were caused by differences in the production of hyaluronic acid capsule or M protein by the two groups of bacteria, the adherence and invasive capacities of bacteria carrying defined mutations in the genes for these factors were examined. Although M18-protein-deficient bacteria were less adherent to HEp-2 cells than the wild-type, neither the hyaluronic acid capsule nor the M protein had a significant influence on the ability of GAS to adhere to or invade HEp-2 cells. The results of this study demonstrate that there are biological differences between GAS isolates associated with invasive and superficial diseases and that these differences can be demonstrated by an assay of bacterial adherence to and invasion of HEp-2 epithelial cells.
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Chlamydia pneumoniae in coronary and iliac arteries of Japanese patients with atherosclerotic cardiovascular diseases
More LessRecent studies suggest the association of atherosclerotic cardiovascular diseases with Chlamydia pneumoniae infection in western populations. It is of great interest whether such an association exists in Asians with their distinct genetic background. Symptomatic patients with coronary heart disease (29) or arteriosclerosis obliterans (10) who underwent directional endo-atherectomy were studied. Atherectomy specimens of coronary and iliac arteries were examined for C. pneumoniae by culture, nested PCR and immunohistochemical stain (IHC) with one Chlamydia genus-specific, two C. pneumoniae species-specific, and two C. trachomatis species-specific monoclonal antibodies. Among the 29 patients with coronary artery disease, C. pneumoniae was detected in the coronary arteries of 13 by IHC, 16 by PCR and 20 by IHC or PCR, or both. C. pneumoniae was also found in the iliac arteries of four patients by IHC, three by PCR and five by IHC or PCR, or both, of the 10 patients with arteriosclerosis obliterans. Attempts to isolate C. pneumoniae by culture were unsuccessful. The re-stenotic rate after atherectomy was higher in the C. pneumoniae-positive group than in the negative group, but not significantly so. These findings support the high incidence of C. pneumoniae in atherosclerotic lesions of symptomatic patients with coronary heart disease and arteriosclerosis obliterans in Asians.
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Protein kinase C activation and vacuolation in HeLa cells invaded by Mycoplasma penetrans
More LessThe AIDS-associated Mycoplasma penetrans is capable of inducing its own uptake by non-phagocytic cells. This study investigated the invasion of HeLa cells and its consequences by confocal laser scanning microscopy. Invasion was dependent on the duration of infection and temperature, diminished by inhibiting microfilament assembly with cytochalasin D and almost completely abolished by disorganising microtubules with vinblastine or taxol. After a short infection period (≤ 20 min), pronounced activation of protein kinase C was detected in host cells, whereas prolonged infection resulted in intensive vacuolation of the host cells and a pronounced increment in intracellular organic peroxide levels. A marked decrease in the extent of vacuolation was observed when peroxide accumulation was partially prevented by α-tocopherol. The possibility that M. penetrans entry into HeLa cells involves the activation of protein kinases and the recruitment of cytoskeleton components is discussed.
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Volumes and issues
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Volume 74 (2025)
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Volume 73 (2024)
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Volume 72 (2023 - 2024)
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Volume 71 (2022)
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Volume 70 (2021)
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Volume 69 (2020)
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Volume 68 (2019)
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Volume 67 (2018)
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Volume 66 (2017)
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Volume 65 (2016)
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Volume 64 (2015)
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Volume 63 (2014)
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Volume 62 (2013)
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Volume 61 (2012)
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Volume 60 (2011)
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Volume 59 (2010)
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Volume 58 (2009)
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Volume 57 (2008)
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Volume 56 (2007)
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Volume 55 (2006)
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Volume 54 (2005)
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Volume 53 (2004)
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Volume 52 (2003)
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Volume 51 (2002)
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Volume 50 (2001)
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Volume 49 (2000)
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Volume 48 (1999)
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Volume 47 (1998)
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Volume 46 (1997)
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Volume 45 (1996)
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Volume 44 (1996)
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Volume 43 (1995)
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Volume 42 (1995)
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Volume 41 (1994)
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Volume 40 (1994)
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Volume 39 (1993)
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Volume 38 (1993)
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Volume 37 (1992)
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Volume 36 (1992)
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Volume 35 (1991)
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Volume 34 (1991)
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Volume 33 (1990)
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Volume 32 (1990)
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Volume 31 (1990)
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Volume 30 (1989)
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Volume 29 (1989)
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Volume 28 (1989)
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Volume 27 (1988)
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Volume 26 (1988)
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Volume 25 (1988)
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Volume 24 (1987)
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Volume 23 (1987)
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Volume 22 (1986)
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Volume 21 (1986)
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Volume 20 (1985)
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Volume 19 (1985)
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Volume 18 (1984)
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Volume 17 (1984)
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Volume 16 (1983)
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Volume 15 (1982)
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Volume 14 (1981)
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Volume 13 (1980)
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Volume 12 (1979)
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Volume 11 (1978)
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Volume 10 (1977)
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Volume 9 (1976)
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Volume 8 (1975)
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Volume 7 (1974)
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Volume 6 (1973)
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Volume 5 (1972)
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Volume 4 (1971)
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Volume 3 (1970)
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Volume 2 (1969)
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Volume 1 (1968)
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