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Research Article
seyed-Morteza Javadirad
University of Isfahan
Corresponding Author
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The necessity of PRM1/2 in male azoospermia has been approved, but the association of TXNDC2 deficiency with the phenotype, sperm retrieval and pathology has not been approved. Here we identified a joint cooperation of TXNDC2 and protamines in evaluating testis pathology and sperm retrieval. Extensive meta-analysis on human arrays of idiopathic, untreated and with unknown cause of azoospermia was done. After several steps of data quality controls, QC passed data were pooled and batch effect corrected. As Redox imbalance has been shown as a two edge sword toward fertility, wet lab studies began with candidated protamination and thioredoxin genes. Logistic regression model of TXNDC2 alongside PRM1 and PRM2 genes was built and collective ROC analysis indicated a sensitivity of 96.8% and specificity of 95.5% with the ROC value of 0.993 (SE=0.0075, 95% CI: 0.978-1.000). In conclusion, TXNDC2, PRM1 and PRM2 in joint, have a robust power to predict sperm retrieval and to correlate with severe pathology of azoospermia.
Keywords
Azoospermia, TXNDC2, PRM1, PRM2, Sperm retrieval
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No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
- SuppData.pdf
Supplementary data Supplementary data are available at Human Reproduction online.
- table1.pdf
- table2.pdf
- table3.pdf
- table4.pdf
- table5.pdf
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This preprint is under consideration at Scientific Reports. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
seyed-Morteza Javadirad
University of Isfahan
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 15 Mar, 2021
No community comments so far
Review #3 received
Received 31 Mar, 2021
Review #1 received
Received 31 Mar, 2021
Review #2 received
Received 31 Mar, 2021
Reviewer #8 agreed
On 26 Mar, 2021
Reviewer #6 agreed
On 26 Mar, 2021
Reviewer #4 agreed
On 26 Mar, 2021
Reviewer #7 agreed
On 26 Mar, 2021
Reviewer #3 agreed
On 26 Mar, 2021
Reviewer #1 agreed
On 26 Mar, 2021
Reviewer #5 agreed
On 26 Mar, 2021
Reviewer #2 agreed
On 26 Mar, 2021
Reviewers invited
Invitations sent on 23 Mar, 2021
Editor assigned
On 23 Mar, 2021
Editor invited
On 03 Mar, 2021
Submission checks complete
On 03 Mar, 2021
First submitted
On 27 Feb, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cellular & Molecular Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
The necessity of PRM1/2 in male azoospermia has been approved, but the association of TXNDC2 deficiency with the phenotype, sperm retrieval and pathology has not been approved. Here we identified a joint cooperation of TXNDC2 and protamines in evaluating testis pathology and sperm retrieval. Extensive meta-analysis on human arrays of idiopathic, untreated and with unknown cause of azoospermia was done. After several steps of data quality controls, QC passed data were pooled and batch effect corrected. As Redox imbalance has been shown as a two edge sword toward fertility, wet lab studies began with candidated protamination and thioredoxin genes. Logistic regression model of TXNDC2 alongside PRM1 and PRM2 genes was built and collective ROC analysis indicated a sensitivity of 96.8% and specificity of 95.5% with the ROC value of 0.993 (SE=0.0075, 95% CI: 0.978-1.000). In conclusion, TXNDC2, PRM1 and PRM2 in joint, have a robust power to predict sperm retrieval and to correlate with severe pathology of azoospermia.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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