scholarly journals Trimethoprim resistance gene inShigella dysenteriae1 isolates obtained from widely scattered locations of Asia

1990 ◽  
Vol 104 (2) ◽  
pp. 219-228 ◽  
Author(s):  
K. Haider ◽  
A. Chatkaeomorakot ◽  
B. A. Kay ◽  
K. A. Talukder ◽  
D. N. Taylor ◽  
...  

SUMMARYTrimethoprim-resistance genes ofShigella dysenteriae1 strains, isolated from a different location of six different countries of Asia over a 5-year period were characterized by using three different dihydrofolate reductase (DHFR) gene probes. The trimethoprim-resistant (TMPR) strains hybridized only with the type I DHFR gene probe by colony hybridization. None of the strains hybridized with types II and III DHFR gene probes. Southern blot experiments using plasmid DNA extracted from these resistant strains indicated that the type I DHFR genes were either on a 20 MDa plasmid or might be located on the chromosome. None of the other plasmids present inS. dyysenteriae1 strains hybridized with the probe. This indicates that the TMP resistance in theseS. dysenteriae1 strains are mediated by type I DHFR enzyme, and there may be transposition of this type I DHFR gene occurs between the 20 MDa plasmid and the chromosome in this serotype of shigella.

1992 ◽  
Vol 109 (3) ◽  
pp. 453-462 ◽  
Author(s):  
Lin-Li Chang ◽  
Shui-Feng Chang ◽  
Teh-Yuan Chow ◽  
Wen-Jeng Wu ◽  
Jong-Chou Chang

SUMMARYBetween July 1987 and June 1989, 1054 urinary isolates of enterobacteria from Kaohsiung, Taiwan were studied for their trimethoprim resistance. Trimethoprim resistance was defined as MIC greater than 4 μg/ml and high-level resistance by MIC greater than 1000 μg/ml. The incidence of trimethoprim resistance increased from 33·6% in 1987 to 42·1% in 1989. Among the resistant strains studied, 90% were resistant to high levels of trimethoprim. An increase in the proportion of resistant strains (33·9–46·3%) exhibiting high-level non-transferable trimethoprim resistance was noted. The distribution of the dihydrofolate reductase (DHFR) genes by colony hybridization in 374 trimethoprim-resistant isolates revealed the presence of type I and type V DHFR genes in most of these isolates (45·4% and 10·4% respectively). Type I was predominant inEscherichia coliwhereas type V was frequently seen inEnterobacterspp. None showed homology with the type II and type III DHFR probe DNA. In addition, transposon Tn7 was present in 7·8% of 374 trimethoprim-resistant enterobacteria.


1994 ◽  
Vol 57 (2) ◽  
pp. 163-165 ◽  
Author(s):  
CHARLES A. KAYSNER ◽  
CARLOS ABEYTA ◽  
KAREN C. JINNEMAN ◽  
WALTER E. HILL

We have developed a means of differentiating and enumerating Vibrio parahaemolyticus and Vibrio vuinificus by DNA-DNA colony hybridization directly on HGMF filters. V. parahaemolyticus can be detected by a tdh-3-radiolabeled gene probe and V. vuinificus detected by a specific cytotoxin-hemolysin-radiolabeled probe with enumeration directly from autoradiograms. This procedure is more rapid than current techniques allowing enumeration and identification of these two species in samples as diverse as seawater, oyster (Crassostrea gigas), and shrimp (Pandalidae family) within 4 d. Our method is based on a rapid technique (18 h) for isolation and enumeration of V. parahaemolyticus from food using a membrane filtration technique with hydrophobic grid filters (HGMF). With the HGMF method, however, it is not possible to differentiate V. parahaemolyticus from V. vuinificus since on the HGMF-sucrose-based agar used, the two species are indistinguishable as both species are unable to ferment sucrose. Using a combination of the HGMF and selective gene probes, these two species can be differentiated.


1995 ◽  
Vol 31 (5-6) ◽  
pp. 345-350 ◽  
Author(s):  
B. Genthe ◽  
M. Gericke ◽  
B. Bateman ◽  
N. Mjoli ◽  
R. Kfir

Gene probes developed locally for both enteric Adenoviruses 40 and 41 were used to determine whether these viruses were present in both raw and treated waters. Approximately sixty water samples were concentrated by ultrafiltration and analysed directly for the presence of enteric adenoviruses. Three pretreatment techniques, namely sephadex columns, cellulose fibre and GenecleanTM were tested for the removal of inhibitory substances from concentrated water samples. The effect of chlorine treatment on viral detection using gene probe hybridization was also examined by exposing adenoviruses to chlorine concentrations of up to 20mg/l for 1 hour. Enteric adenoviruses were detected in up to 59% of both raw and treated waters analysed. Cellulose fibre and GenecleanTM were found to successfully remove inhibitory substances from concentrated raw waters. Viral DNA was detected after exposure to a range of chlorine concentrations indicating that the viruses detected in the treated waters may have been inactivated virus particles.


Toxins ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 329
Author(s):  
Andrew Holmes ◽  
Jessie Sadlon ◽  
Keith Weaver

A majority of toxins produced by type I toxin–antitoxin (TA-1) systems are small membrane-localized proteins that were initially proposed to kill cells by forming non-specific pores in the cytoplasmic membrane. The examination of the effects of numerous TA-1 systems indicates that this is not the mechanism of action of many of these proteins. Enterococcus faecalis produces two toxins of the Fst/Ldr family, one encoded on pheromone-responsive conjugative plasmids (FstpAD1) and the other on the chromosome, FstEF0409. Previous results demonstrated that overexpression of the toxins produced a differential transcriptomic response in E. faecalis cells. In this report, we identify the specific amino acid differences between the two toxins responsible for the differential response of a gene highly induced by FstpAD1 but not FstEF0409. In addition, we demonstrate that a transporter protein that is genetically linked to the chromosomal version of the TA-1 system functions to limit the toxicity of the protein.


2001 ◽  
Vol 38 (02) ◽  
pp. 542-553 ◽  
Author(s):  
Ji Hwan Cha

In this paper two burn-in procedures for a general failure model are considered. There are two types of failure in the general failure model. One is Type I failure (minor failure) which can be removed by a minimal repair or a complete repair and the other is Type II failure (catastrophic failure) which can be removed only by a complete repair. During a burn-in process, with burn-in Procedure I, the failed component is repaired completely regardless of the type of failure, whereas, with burn-in Procedure II, only minimal repair is done for the Type I failure and a complete repair is performed for the Type II failure. In field use, the component is replaced by a new burned-in component at the ‘field use age’ T or at the time of the first Type II failure, whichever occurs first. Under the model, the problems of determining optimal burn-in time and optimal replacement policy are considered. The two burn-in procedures are compared in cases when both the procedures are applicable.


1979 ◽  
Vol 4 (1) ◽  
pp. 14-23 ◽  
Author(s):  
Juliet Popper Shaffer

If used only when a preliminary F test yields significance, the usual multiple range procedures can be modified to increase the probability of detecting differences without changing the control of Type I error. The modification consists of a reduction in the critical value when comparing the largest and smallest means. Equivalence of modified and unmodified procedures in error control is demonstrated. The modified procedure is also compared with the alternative of using the unmodified range test without a preliminary F test, and it is shown that each has advantages over the other under some circumstances.


1995 ◽  
Vol 89 (1) ◽  
pp. 69-73 ◽  
Author(s):  
Andrew E. Pocock ◽  
Martin J. O. Francis ◽  
Roger Smith

1. Skin fibroblast lines were cultured from nine patients who had the features of idiopathic juvenile osteoporosis, six relatives, five unrelated control subjects and three unrelated patients with osteogenesis imperfecta type I. Some patients with idiopathic juvenile osteoporosis were adults whose previous osteoporosis was in remission. Two patients with idiopathic juvenile osteoporosis were siblings and one patient with idiopathic juvenile osteoporosis had a daughter with severe osteogenesis imperfecta (type III). 2. The ratio of type III to type I collagen, synthesized by fibroblasts, was increased in two of the patients with osteogenesis imperfecta type I and in the daughter with osteogenesis imperfecta type III, but was normal in all the other patients with idiopathic juvenile osteoporosis and the other relatives. 3. Radiolabelled collagen was digested by cyanogen bromide and separated on SDS-PAGE. Unreduced collagen peptides migrated normally, except those from both the two siblings with idiopathic juvenile osteoporosis. In these two lines, abnormal migration suggested the presence of collagen I mutations. 4. The secretion of synthesized collagen by these two idiopathic juvenile osteoporosis lines and two others was reduced to only 43–45% as compared with a line from a 13-year-old control subject, which was defined as 100%. The three osteogenesis imperfecta type I lines secreted 18–37%, the other five idiopathic juvenile osteoporosis lines secreted 57–75%, the relatives (including the daughter with severe osteogenesis imperfecta) secreted 49–115% and the controls secreted 69–102%. 5. We conclude that qualitative abnormalities of type I collagen associated with a reduction in total secreted collagen synthesis may occur in a minority of patients with idiopathic juvenile osteoporosis; these patients could represent a subset of patients with this disorder.


1984 ◽  
Vol 4 (10) ◽  
pp. 2010-2016 ◽  
Author(s):  
V L Funanage ◽  
T T Myoda ◽  
P A Moses ◽  
H R Cowell

Cells from a dihydrofolate reductase-deficient Chinese hamster ovary cell line were hybridized to human fetal skin fibroblast cells. Nineteen dihydrofolate reductase-positive hybrid clones were isolated and characterized. Cytogenetic and biochemical analyses of these clones have shown that the human dihydrofolate reductase (DHFR) gene is located on chromosome 5. Three of these hybrid cell lines contained different terminal deletions of chromosome 5. An analysis of the breakpoints of these deletions has demonstrated that the DHFR gene resides in the q11----q22 region.


2021 ◽  
Vol 34 (1) ◽  
pp. 79-88
Author(s):  
Dean Radin ◽  
Helané Wahbeh ◽  
Leena Michel ◽  
Arnaud Delorme

An experiment we conducted from 2012 to 2013, which had not been previously reported, was designed to explore possible psychophysical effects resulting from the interaction of a human mind with a quantum system. Participants focused their attention toward or away from the slits in a double-slit optical system to see if the interference pattern would be affected. Data were collected from 25 people in individual half-hour sessions; each person repeated the test ten times for a total of 250 planned sessions. “Sham” sessions designed to mimic the experimental sessions without observers present were run immediately before and after as controls. Based on the planned analysis, no evidence for a psychophysical effect was found. Because this experiment differed in two essential ways from similar, previously reported double-slit experiments, two exploratory analyses were developed, one based on a simple spectral analysis of the interference pattern and the other based on fringe visibility. For the experimental data, the outcome supported a pattern of results predicted by a causal psychophysical effect, with the spectral metric resulting in a 3.4 sigma effect (p = 0.0003), and the fringe visibility metric resulting in 7 of 22 fringes tested above 2.3 sigma after adjustment for type I error inflation, with one of those fringes at 4.3 sigma above chance (p = 0.00001). The same analyses applied to the sham data showed uniformly null outcomes. Other analyses exploring the potential that these results were due to mundane artifacts, such as fluctuations in temperature or vibration, showed no evidence of such influences. Future studies using the same protocols and analytical methods will be required to determine if these exploratory results are idiosyncratic or reflect a genuine psychophysical influence.


2019 ◽  
Vol 26 (6) ◽  
pp. 782-786 ◽  
Author(s):  
Ahmed Eleshra ◽  
Tilo Kölbel ◽  
Nikolaos Tsilimparis ◽  
Giuseppe Panuccio ◽  
Martin Scheerbaum ◽  
...  

Purpose: To present the early results of false lumen (FL) occlusion in chronic aortic dissection using the Candy-Plug generation II (CP II), which has a self-closing fabric channel that obviates the need for separate occlusion of its center. Materials and Methods: Fourteen consecutive patients (mean age 60±11 years; 10 men) with persistent FL backflow and aneurysm formation at the thoracic segment in chronic aortic dissection underwent thoracic endovascular aortic repair (TEVAR) with FL occlusion using the refined CP II. Primary endpoints were technical success (successful deployment) and clinical success (no FL backflow at the CP II level). Secondary endpoints included 30-day mortality and morbidity and aortic remodeling during follow-up. Results: Technical success was 100%. One patient required additional intraprocedural FL embolization at the CP II level due to persistent FL backflow on final angiography (clinical success 93%), though there was no flow through the CP II center. There were no intraprocedural complications. Immediate complete FL occlusion was achieved in 12 patients; the other 2 required reintervention. One had contrast enhancement in the distal FL proximal to the CP II and was treated with coil embolization. The other patient had persistent type I endoleak at the level of the left subclavian artery (LSA) and underwent left carotid–LSA bypass and proximal stent-graft extension. One patient died due to retrograde type A aortic dissection that was not related to CP II placement. Over a mean 8-month follow-up (range 3–12), 9 patients had computed tomography angiography; 8 patients had evidence of aortic remodeling, while 1 aneurysm sac was stable. Conclusion: The CP II reduces the number of procedural steps and offers good seal, with minimal morbidity and mortality and a high rate of aortic remodeling.


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