Publications by authors named "Ahmad Sabra"

13 Publications

  • Page 1 of 1

Cardiovascular disease in the World Trade Center Health Program General Responder Cohort.

Am J Ind Med 2021 02 14;64(2):97-107. Epub 2020 Dec 14.

Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York, USA.

Background: Over 90,000 rescue and recovery responders to the September 2001 World Trade Center (WTC) attacks were exposed to toxic materials that can impair cardiac function and increase cardiovascular disease (CVD) risk. We examined WTC-related exposures association with annual and cumulative CVD incidence and risk over 17 years in the WTC Health Program (HP) General Responder Cohort (GRC).

Methods: Post 9/11 first occurrence of CVD was assessed in 37,725 responders from self-reported physician diagnosis of, or current treatment for, coronary artery disease, myocardial infarction, stroke and/or congestive heart failure from WTCHP GRC monitoring visits. Kaplan-Meier estimates of CVD incidence used the generalized Wilcoxon test statistic to account for censored data. Cox proportional hazards regression analyses estimated the CVD hazard ratio associated with 9/11/2001 arrival in responders with and without dust cloud exposure, compared with arrival on or after 9/12/2001. Additional analyses adjusted for comorbidities.

Results: To date, 6.3% reported new CVD. In covariate-adjusted analyses, men's CVD 9/11/2001 arrival risks were 1.40 (95% confidence interval [CI] = 1.26, 1.56) and 1.43 (95% CI = 1.29, 1.58) and women's were 2.16 (95% CI = 1.49, 3.11) and 1.59 (95% CI = 1.11, 2.27) with and without dust cloud exposure, respectively. Protective service employment on 9/11 had higher CVD risk.

Conclusions: WTCHP GRC members with 9/11/2001 exposures had substantially higher CVD risk than those initiating work afterward, consistent with observations among WTC-exposed New York City firefighters. Women's risk was greater than that of men's. GRC-elevated CVD risk may also be occurring at a younger age than in the general population.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/ajim.23207DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8215565PMC
February 2021

Genetic Diversity of Human Rotavirus A Among Hospitalized Children Under-5 Years in Lebanon.

Front Immunol 2020 26;11:317. Epub 2020 Feb 26.

Faculty of Medicine, Center for Infectious Diseases Research, American University of Beirut, Beirut, Lebanon.

Human rotavirus remains a major cause of gastroenteritis worldwide despite the availability of effective vaccines. In this study, we investigated the genetic diversity of rotaviruses circulating in Lebanon. We genetically characterized the VP4 and VP7 genes encoding the outer capsid proteins of 132 rotavirus-associated gastroenteritis specimens, previously identified in hospitalized children (<5 years) from 2011 to 2013 in Lebanon. These included 43 vaccine-breakthrough specimens and the remainder were from non-vaccinated subjects. Phylogenetic analysis of VP4 and VP7 genes revealed distinct clustering compared to the vaccine strains, and several substitutions were identified in the antigenic epitopes of Lebanese specimens. No unique changes were identified in the breakthrough specimens compared to non-breakthroughs that could explain the occurrence of infection in vaccinated children. Further, we report the emergence of a rare P[8] OP354-like strain with a G9 VP7 in Lebanon, possessing high genetic variability in their VP4 compared to vaccine strains. Therefore, human rotavirus strains circulating in Lebanon and globally have accumulated numerous substitutions in their antigenic sites compared to those currently used in the licensed vaccines. The successful spread and continued genetic drift of these strains over time might undermine the effectiveness of the vaccines. The effect of such changes in the antigenic sites on vaccine efficacy remains to be assessed.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fimmu.2020.00317DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7054381PMC
March 2021

Impairment of agonist-induced M muscarinic receptor activation by autoantibodies from chagasic patients with cardiovascular dysautonomia.

Clin Immunol 2020 03 16;212:108346. Epub 2020 Jan 16.

Laboratorio de Farmacología Molecular, Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET-UBA) and II Cátedra de Farmacología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, Piso 16, C1121ABG Buenos Aires, Argentina. Electronic address:

Previous studies showed that circulating autoantibodies against M muscarinic receptors (anti-MR Ab) are associated with decreased cardiac parasympathetic modulation in patients with chronic Chagas disease (CD). Here we investigated whether the exposure of MR to such antibodies could impair agonist-induced receptor activation, leading to the inhibition of associated signaling pathways. Preincubation of MR-expressing HEK 293T cells with serum IgG fractions from chagasic patients with cardiovascular dysautonomia, followed by the addition of carbachol, resulted in the attenuation of agonist-induced G protein activation and arrestin-2 recruitment. These effects were not mimicked by the corresponding Fab fractions, suggesting that they occur through receptor crosslinking. IgG autoantibodies did not enhance MR/arrestin interaction or promote MR internalization, suggesting that their inhibitory effects are not likely a result of short-term receptor regulation. Rather, these immunoglobulins could function as negative allosteric modulators of acetylcholine-mediated responses, thereby contributing to the development of parasympathetic dysfunction in patients with CD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.clim.2020.108346DOI Listing
March 2020

Prevalence and awareness of varicocele among athletes in Riyadh, Saudi Arabia.

Res Rep Urol 2019 13;11:21-27. Epub 2019 Feb 13.

Division of Urology, Department of Surgery, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia,

Purpose: To evaluate the prevalence and awareness about symptoms, and complications of varicocele among athletes (bodybuilding and aerobics exercises) in Riyadh, Saudi Arabia.

Patients And Methods: A cross-sectional study of male athletes aged between 18 and 48 years old was carried out in multiple branches of fitness centers over a period of 13 months in Riyadh, Saudi Arabia. A total of 382 face-to-face interviews using a predesigned questionnaire were conducted to identify the levels of knowledge, attitude, and practice. A randomly selected 48 subjects were examined. Varicocele was diagnosed and graded based on clinical examination and Doppler ultrasonography.

Results: Of the participants, 157 (41%) lacked knowledge and awareness regarding varicocele, its symptoms and complications. Of the examined participants, 22 (46%) were found to have varicocele. No difference in varicocele was found among bodybuilders and aerobic athletes (=0.249). Similarly, no difference was related to duration of exercise session whether for 1 hour or more (=0.131). However, our study revealed a higher rate of varicocele among athletes who exercised more than three times per week (=0.009). Testicular volume was neither significantly different among respondents with and without varicocele nor between the left or right sides within each group.

Conclusion: Knowledge about varicocele, its symptoms and complications is poor among male athletes in Riyadh, Saudi Arabia. Varicocele is more common in athletic men who are frequently exercising. Efforts to increase knowledge and enhance awareness of varicocele in young males, in general, are strongly warranted.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.2147/RRU.S195582DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386205PMC
February 2019

Rotavirus Genotypes and Vaccine Effectiveness from a Sentinel, Hospital-Based, Surveillance Study for Three Consecutive Rotavirus Seasons in Lebanon.

PLoS One 2016 29;11(8):e0161345. Epub 2016 Aug 29.

Department of Pediatrics and Adolescent Medicine, American University of Beirut, Faculty of Medicine, Beirut, Lebanon.

Introduction: Globally, rotavirus (RV) is the leading cause of gastroenteritis (GE) in children. Longitudinal data about changes in RV genotype distribution and vaccine effectiveness (VE) are scarce. This study was conducted in Lebanon over 3 consecutive RV seasons to estimate the rate of RVGE hospitalization, identify RV genotypes, determine the seasonal and geographical variations, and calculate RV VE.

Materials And Methods: This prospective, multicenter, hospital-based surveillance study was conducted between 2011 and 2013 and enrolled children (<5 years) admitted for GE. Socio-demographic and clinical data about the current episode of GE at admission were collected. Genotypes were determined from stool samples testing positive for RV by PCR.

Results: Of 1,414 cases included in the final analysis, 83% were <2 years old and 55.6% were boys. Median duration of hospitalization was 4 days and 91.6% of GE cases were severe (Vesikari score ≥11). PCR testing showed that 30.3% of subjects were RV-positive of which 62.1% had fever versus 71.1% of RV-negative subjects (P = 0.001). RV was predominantly detected in the cold season from November till March (69.9%). G and P genotype pairs for all RV-positive stool specimens showed a predominance of G1P[8] in 36% (n = 154) of specimens, G9P[8] in 26.4% (n = 113), and G2P[4] in 17.8% (n = 76). RV-negative subjects were more likely to be RV-vaccinated (21%) compared to the RV-positive subjects (11.3%) (P<0.001), with a vaccine breakthrough rate of 18.8%. The ratio of RV1-vaccinated for each RV5-vaccinated subject was 7.8 and VE against RV disease was 68.4% (95%CI, 49.6%-80.2%).

Conclusion: RV is a major cause of GE requiring hospitalization of children under 5 years of age in Lebanon. A few genotypes predominated over the three RV seasons studied. Mass RV vaccination will likely decrease the burden of hospitalization due to RV. VE is similar to what has been observed for other middle-income countries.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161345PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5003350PMC
August 2017

Effect of rifampicin and gentamicin on Shiga toxin 2 expression level and the SOS response in Escherichia coli O104:H4.

Foodborne Pathog Dis 2015 Jan 10;12(1):47-55. Epub 2014 Nov 10.

Department of Experimental Pathology, Immunology, & Microbiology, Faculty of Medicine, American University of Beirut , Beirut, Lebanon .

Background: A novel pathotype, Shiga toxin-producing Escherichia coli O104:H4, was the cause of a severe outbreak that affected European countries, mainly Germany, in 2011. The effect of different regimens of rifampicin and gentamicin were evaluated to determine possible treatment modes for the novel strain, and to evaluate the SOS response and its effect on toxin release.

Materials And Methods: Pulsed-field gel electrophoresis (PFGE) was performed on the novel E. coli O104:H4 pathotype and two pre-outbreak E. coli O104:H4 CDC strains. Transcript levels of the stx2 and recA gene (SOS response inducer) were evaluated using quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) in the novel E. coli O104:H4 samples subjected to different regimens of rifampicin and gentamicin. Consequently, reverse passive latex agglutination (RPLA) was used to determine the Stx2 titers in these samples. Western blot was performed to determine the LexA levels (SOS response repressor) in E. coli O104:H4. The efficacy of treatment with antimicrobial agents was assessed in BALB/c mice.

Results: The outbreak and pre-outbreak strains are closely related as shown by PFGE, which demonstrated slight genomic differences between the three strains. The transcription level of the stx2 gene in the new pathotype was 1.41- and 1.75-fold that of the 2009 EL-2050 and 2009 EL-2071 pre-outbreak strains, respectively. Moreover, the transcription level of the stx2 gene in the new pathotype was substantially decreased as a result of treatment with the different concentrations of the antimicrobial agents, but was enhanced when the antibiotics were administered at two subinhibitory levels. RPLA data were in accordance with the qRT-PCR results. E. coli O104:H4 exposed to gentamicin at both sub-minimum inhibitory concentration (MIC) levels led to high transcription levels of the recA gene and lack of expression of the LexA protein, implying that the SOS response was activated. Rifampicin at both sub-MIC levels resulted in low transcript levels of the recA gene, indicating that the SOS response was not induced. In vivo, the highest survival rate in BALB/c mice was observed in the group that was treated with the minimum bactericidal concentration (MBC) of gentamicin.

Conclusion: The use of antimicrobial agents in E. coli O104:H4 infection seems to be effective at the MIC and MBC levels. This provides a promising ground for treatment of E. coli O104:H4.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/fpd.2014.1824DOI Listing
January 2015

Design of pairs of reflectors.

J Opt Soc Am A Opt Image Sci Vis 2014 Apr;31(4):891-9

Given a 3D reflecting surface G, which is not necessarily rotationally symmetric, away from a point source, and a direction e, we design a reflecting surface F so that the system (G,F) reflects all rays into the direction e. We also solve the near-field problem when the direction e is replaced by a given point R. The surface F satisfies a system of first-order partial differential equations that can be explicitly solved in terms of G and e. We also apply the same ideas to designing refracting plates, of which the Schmidt corrector plate is an example.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1364/JOSAA.31.000891DOI Listing
April 2014

The inhibitory effect of micafungin on biofilm formation by Pseudomonas aeruginosa.

Biofouling 2013 Sep 23;29(8):909-15. Epub 2013 Jul 23.

Department of Experimental Pathology, Immunology and Microbiology, American University of Beirut, Beirut, Lebanon.

This study assesses the potential effect of micafungin, an antifungal agent known to inhibit 1,3-β-D-glucan synthesis in Candida albicans, on biofilm formation of selected Pseudomonas aeruginosa isolates by decreasing the synthesis of extracellular matrix β-D-glucan forming units. The effect of an optimal therapeutic dose of 10 mg ml(-1) micafungin on the production of biofilm was monitored in vitro using a microtiter plate assay. Phenotypic reduction in the formation of biofilm was significant (based on average optical density; p < 0.05) in most of the isolates. Moreover, the relative gene expression of biofilm encoding genes for alginate and pellicles (algC and pelC, respectively), and the cell wall 1,3-β-D-glucan encoding gene (ndvB) was evaluated using quantitative reverse transcription PCR. For all the genes tested, the levels of mRNA transcription were also decreased significantly (p < 0.05) in micafungin-treated samples cf. their untreated counterparts. In conclusion, this study presents micafungin as a potential agent for disrupting the structure of a biofilm of P. aeruginosa allowing the possible exposure and treatment of core-planktonic cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/08927014.2013.816299DOI Listing
September 2013

Effects of subinhibitory concentrations of antimicrobial agents on Escherichia coli O157:H7 Shiga toxin release and role of the SOS response.

Foodborne Pathog Dis 2013 Sep 28;10(9):805-12. Epub 2013 Jun 28.

Department of Experimental Pathology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

Treatment of Escherichia coli O157:H7 by certain antimicrobial agents often exacerbates the patient's condition by increasing either the release of preformed Shiga toxins (Stx) upon cell lysis or their production through the SOS response-triggered induction of Stx-producing prophages. Recommended subinhibitory concentrations (sub-MICs) of azithromycin (AZI), gentamicin (GEN), imipenem (IMI), and rifampicin (RIF) were evaluated in comparison to norfloxacin (NOR), an SOS-inducer, to assess the role of the SOS response in Stx release. Relative expression of recA (SOS-inducer), Q (late antitermination gene of Stx-producing prophage), stx1, and stx2 genes was assessed at two sub-MICs of the antimicrobials for two different strains of E. coli O157:H7 using reverse transcription-real-time polymerase chain reaction. Both strains at the two sub-MICs were also subjected to Western blotting for LexA protein expression and to reverse passive latex agglutination for Stx detection. For both strains at both sub-MICs, NOR and AZI caused SOS-induced Stx production (high recA, Q, and stx2 gene expression and high Stx2 production), so they should be avoided in E. coli O157:H7 treatment; however, sub-MICs of RIF and IMI induced Stx2 production in an SOS-independent manner except for one strain at the first twofold dilution below MIC of RIF where Stx2 production decreased. Moreover, GEN caused somewhat increased Stx2 production due to its mode of action rather than any effect on gene expression. The choice of antimicrobial therapy should rely on the antimicrobial mode of action, its concentration, and on the nature of the strain.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/fpd.2013.1510DOI Listing
September 2013

Genotypes and serotype distribution of macrolide resistant invasive and non-invasive Streptococcus pneumoniae isolates from Lebanon.

Ann Clin Microbiol Antimicrob 2012 Jan 16;11. Epub 2012 Jan 16.

Department of Experimental Pathology, Immunology & Microbiology, Faculty of Medicine, American University of Beirut, Riad El-Solh, Beirut, Lebanon.

Background: This study determined macrolide resistance genotypes in clinical isolates of Streptococcus pneumoniae from multiple medical centers in Lebanon and assessed the serotype distribution in relation to these mechanism(s) of resistance and the source of isolate recovery.

Methods: Forty four macrolide resistant and 21 macrolide susceptible S. pneumoniae clinical isolates were tested for antimicrobial susceptibility according to CLSI guidelines (2008) and underwent molecular characterization. Serotyping of these isolates was performed by Multiplex PCR-based serotype deduction using CDC protocols. PCR amplification of macrolide resistant erm (encoding methylase) and mef (encoding macrolide efflux pump protein) genes was carried out.

Results: Among 44 isolates resistant to erythromycin, 35 were resistant to penicillin and 18 to ceftriaxone. Examination of 44 macrolide resistant isolates by PCR showed that 16 isolates harbored the erm(B) gene, 8 isolates harbored the mef gene, and 14 isolates harbored both the erm(B) and mef genes. There was no amplification by PCR of the erm(B) or mef genes in 6 isolates. Seven different capsular serotypes 2, 9V/9A,12F, 14,19A, 19F, and 23, were detected by multiplex PCR serotype deduction in 35 of 44 macrolide resistant isolates, with 19F being the most prevalent serotype. With the exception of serotype 2, all serotypes were invasive. Isolates belonging to the invasive serotypes 14 and 19F harbored both erm(B) and mef genes. Nine of the 44 macrolide resistant isolates were non-serotypable by our protocols.

Conclusion: Macrolide resistance in S. pneumoniae in Lebanon is mainly through target site modification but is also mediated through efflux pumps, with serotype 19F having dual resistance and being the most prevalent and invasive.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1476-0711-11-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3371826PMC
January 2012

Decrease in Shiga toxin expression using a minimal inhibitory concentration of rifampicin followed by bactericidal gentamicin treatment enhances survival of Escherichia coli O157:H7-infected BALB/c mice.

Ann Clin Microbiol Antimicrob 2011 Sep 12;10:34. Epub 2011 Sep 12.

Department of Microbiology and Immunology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

Background: Treatment of Escherichia coli O157:H7 infections with antimicrobial agents is controversial due to an association with potentially fatal sequelae. The production of Shiga toxins is believed to be central to the pathogenesis of this organism. Therefore, decreasing the expression of these toxins prior to bacterial eradication may provide a safer course of therapy.

Methods: The utility of decreasing Shiga toxin gene expression in E. coli O157:H7 with rifampicin prior to bacterial eradication with gentamicin was evaluated in vitro using real-time reverse-transcription polymerase chain reaction. Toxin release from treated bacterial cells was assayed for with reverse passive latex agglutination. The effect of this treatment on the survival of E. coli O157:H7-infected BALB/c mice was also monitored.

Results: Transcription of Shiga toxin-encoding genes was considerably decreased as an effect of treating E. coli O157:H7 in vitro with the minimum inhibitory concentration (MIC) of rifampicin followed by the minimum bactericidal concentration (MBC) of gentamicin (> 99% decrease) compared to treatment with gentamicin alone (50-75% decrease). The release of Shiga toxins from E. coli O157:H7 incubated with the MIC of rifampicin followed by addition of the MBC of gentamicin was decreased as well. On the other hand, the highest survival rate in BALB/c mice infected with E. coli O157:H7 was observed in those treated with the in vivo MIC equivalent dose of rifampicin followed by the in vivo MBC equivalent dose of gentamicin compared to mice treated with gentamicin or rifampicin alone.

Conclusions: The use of non-lethal expression-inhibitory doses of antimicrobial agents prior to bactericidal ones in treating E. coli O157:H7 infection is effective and may be potentially useful in human infections with this agent in addition to other Shiga toxin producing E. coli strains.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1476-0711-10-34DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3180354PMC
September 2011

Correlation between Group B Streptococcal Genotypes, Their Antimicrobial Resistance Profiles, and Virulence Genes among Pregnant Women in Lebanon.

Int J Microbiol 2009 2;2009:796512. Epub 2010 Feb 2.

Department of Obstetrics and Gynecology, Faculty of Medicine, American University of Beirut, 11072020 Beirut, Lebanon.

The antimicrobial susceptibility profiles of 76 Streptococcus agalactiae (Group B Streptococci [GBS]) isolates from vaginal specimens of pregnant women near term were correlated to their genotypes generated by Random Amplified Polymorphic DNA analysis and their virulence factors encoding genes cylE, lmb, scpB, rib, and bca by PCR. Based on the distribution of the susceptibility patterns, six profiles were generated. RAPD analysis detected 7 clusters of genotypes. The cylE gene was present in 99% of the isolates, the lmb in 96%, scpB in 94.7%, rib in 33%, and bca in 56.5% of isolates. The isolates demonstrated a significant correlation between antimicrobial resistance and genotype clusters denoting the distribution of particular clones with different antimicrobial resistance profiles, entailing the practice of caution in therapeutic options. All virulence factors encoding genes were detected in all seven genotypic clusters with rib and bca not coexisting in the same genome.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2009/796512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817894PMC
July 2011

Molecular characterization of ESBL-producing Shigella sonnei isolates from patients with bacilliary dysentery in Lebanon.

J Infect Dev Ctries 2009 May 1;3(4):300-5. Epub 2009 May 1.

Department of Microbiology and Immunology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.

Background: Emergence of extended-spectrum beta-lactamases (ESBLs) in Shigella species imparting resistance to third-generation cephalosporins is a growing concern worldwide. The aim of this study is to molecularly characterize the newly emerging beta-lactam resistant Shigella sonnei, specifically ESBLs in Lebanon, and compare them to beta-lactam sensitive isolates.

Methodology: We compared five beta-lactam-resistant S. sonnei isolates to six isolates susceptible to beta-lactams. Presence of ESBLs was established by the combination disk method. PCR amplification and sequence analysis of the beta-lactamase-encoding genes, along with other antimicrobial resistance genes, were performed. The localization of beta-lactamase genes was established by conjugation experiments. Beta-lactamase gene transcription levels were determined by real-time RT-PCR. Molecular typing was performed by pulsed-field gel electrophoresis (PFGE).

Results: Four of five beta-lactam resistant isolates were extended spectrum beta-lactamase producers. These harbored the bla-CTX-M-15 gene borne on a 70 Kb plasmid and class 2 integron genes on their chromosomes. The bla-CTX-M-15 gene was flanked by an insertion element ISEcp1. A chromosomal bla-TEM-1 gene was detected in one beta-lactam resistant Shigella isolate and two of the ESBL producing isolates. The bla-CTX-M-15 gene transcription levels were increased in EBSL isolates exposed to subinhibitory concentrations of ceftazidime. PFGE analysis revealed that the four bla-CTX-M-15 positive isolates were nonclonal but two of them shared genotypes with -lactam susceptible isolates.

Conclusion: Dissemination of broad-spectrum beta-lactam resistance in Shigella sonnei is mediated by bla-CTX-M-15 through horizontal plasmid transfer rather than by clonal spread of the resistant isolates. Expression of this gene is further induced in the presence of ceftazidime.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3855/jidc.128DOI Listing
May 2009
-->