genetic technique
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2020 ◽  
Vol 34 (4) ◽  
pp. 1-21
Author(s):  
A. El-Ansary ◽  
Abd El-Razek Zeidan ◽  
Mahmoud Mohamed Ahmed El-Gamal ◽  
Hamdy Ahmed El-Ghandour

2020 ◽  
Vol 80 (4) ◽  
Author(s):  
Kelly E. Williams ◽  
Richard E. Sherwin ◽  
Kaci K. Vandalen ◽  
Antoinette J. Piaggio

2020 ◽  
Author(s):  
Anna Duckworth ◽  
Michael A. Gibbons ◽  
Robin N Beaumont ◽  
Andrew R Wood ◽  
Howard Almond ◽  
...  

AbstractIn a normal year, the fatal lung disease Idiopathic Pulmonary Fibrosis (IPF) accounts for ∼1% of UK deaths. Smoking is a recognised risk factor for IPF but the question of causality remains unanswered. Here, we used data from the UK Biobank (UKBB) and the well-established genetic technique of Mendelian randomisation (MR) methods to investigate whether smoking is causal for IPF compared with COPD, where causality is established.We looked at observational associations in unrelated Europeans, with 871 IPF cases, 11,413 COPD cases and 366,942 controls. We performed analyses using one-sample MR to test for inferred smoking causality in ever smokers using genetic variants that have a previously demonstrated association with smoking heaviness.Strong associations between disease status and ever having smoked were found in both IPF (OR = 1.52; 95%CI:1.32-1.74; P=2.4×10−8) and COPD (OR= 5.77; 95%CI:5.48-6.07; P<1×10−15). Using MR, a one allele increase in smoking volume genetic risk score was associated with higher odds of COPD in ever smokers, (OR = 4.32; 95%CI:3.37-5.54; P<1×10−15), but no association was seen in IPF (OR=0.55; 95%CI: 0.17-1.81; P=0.33). No association was found between the genetic risk score and disease prevalence in never smokers with IPF (OR = 1.00; 95%CI:0.98-1.02; P=1.00) or COPD (OR = 1.00; 95%CI:0.99-1.01; P=0.53).Although both IPF and COPD are observationally associated with smoking, our analysis provides evidence inferring that the association is causal in COPD but there is no such evidence in IPF. This suggests that other environmental exposures also need consideration in IPF.


QJM ◽  
2020 ◽  
Vol 113 (Supplement_1) ◽  
Author(s):  
G M Tawfeek

Abstract Schistosomiasis remains the most important tropical snail-borne trematodiasis that threatens many millions of human lives. In achieving schistosomiasis elimination targets, sustainable control of the snail vectors represents a logical approach. Nonetheless, the ineffectiveness of the present snail control interventions emphasizes the need to develop new complementary strategies to ensure more effective control outcomes. Accordingly, the use of genetic techniques aimed at driving resistance traits into natural vector populations has been put forward as a promising tool for integrated snail control. The use of CRISPR/Cas9 based snail modification strategy appears fascinating and potentially effective. However, this approach is currently still underdeveloped in snail molecular research. This review provides knowledge related to this genetic technique without neglecting the current existing gaps and trying to identify ways to bypass potential future challenges, all are requisites for achieving this promising snail control strategy.


2019 ◽  
Vol 20 (3) ◽  
pp. 914-921
Author(s):  
YANTI ARIYANTI ◽  
ACHMAD FARAJALLAH

Abstract. Ariyanti Y, Farajallah A. 2019. Species confirmation of juvenile cloudy grouper, Epinephelus erythrurus (Valenciennes, 1828), based on a morphologic analysis and partial CO1 gene sequencing. Biodiversitas 20: 914-921. The genus Epinephelus is the most species among the genera within the subfamily Epinephelinae. Species identification techniques for groupers, especially in the Epinephelus, are commonly based on color patterns and a suite of morphological characters, including body shape and the size and number of fins, scales and gill rakers. In some species, juveniles are morphologically distinct from adults of the same species, making morphological identification highly problematic. This present work will provide some morphological description or variations of juveniles that have been identified as Epinephelus erythrurus based on CO1 sequences. Further, the present study demonstrates that a molecular genetic technique, based on partial sequencing of the mitochondrial CO1 gene, may be used for the rapid species confirmation of every developmental stage and phase of an organism (juvenile E. erythrurus). Two DNA sequences of E. erythrurus from the Pangandaran District (7o43’8.31”S 108o30’11.59”E) have been submitted to GenBank under accession numbers KP998441 and KP998442.


2018 ◽  
Vol 63 (No. 12) ◽  
pp. 561-570
Author(s):  
X.K. Wei ◽  
Y.Z. Zhong ◽  
Y. Pan ◽  
X.N. Li ◽  
J.J. Liang ◽  
...  

To explore the effects of different gene combinations on the pathogenicity of the rabies virus (RABV), six chimeric RABV mutants, rRC-HL(G), rRC-HL(NG), rRC-HL(PG), rRC-HL(NP), rRC-HL(NM) and rRC-HL(NPG), were constructed using a reverse genetic technique based on an avirulent parental rRC-HL strain and a virulent parental GX074 isolate. These mutants were intracerebrally inoculated into adult mice. The results indicated that 10<sup>2</sup> ffu and 10<sup>6</sup> ffu of rRC-HL(G), rRC-HL(NG), rRC-HL(PG) and rRC-HL(NPG) were 100% lethal. In the case of intramuscular viral infection, none of the mice inoculated with 10<sup>2 </sup>ffu of any of the RABV mutants, including GX074, died; at 10<sup>6 </sup>ffu, rRC-HL(G) was lethal in 2/5 cases, rRC-HL(NG) was lethal in 1/5 cases and rRC-HL(PG) was lethal for 2/5 mice. The rRC-HL(NPG) mutant was fatal for 3/5 mice, as was the parental GX074. Furthermore, the LD<sub>50</sub> values of the chimeric RABV mutants were measured, with the results showing that the LD<sub>50</sub> values of both rRC-HL(NG) and rRC-HL(PG) were lower than that of rRC-HL(G), but higher than that of rRC-HL(NPG). Thus, the action of N + G, or P + G, or N + P + G gene combinations may be more pronounced than that of the G gene alone. Body weight changes and the clinical symptoms of the tested mice were consistent with pathogenicity. These data indicate that the N and P genes are involved in and facilitate the pathogenicity of the RABV G gene. These experiments provide further evidence that multi-gene cooperation is responsible for the virulence of RABV.


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