Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Mizushima, H. et al.

Mizushima, Nakamura, Matsumoto, Dohi, Matsumoto, Shioda, Banks,

The effect of cardiac arrest on the blood-testis barrier to albumin, tumor necrosis factor-alpha, pituitary adenylate cyclase activating polypeptide, sucrose, and verapamil in the mouse.

Impotence commonly occurs after events such as acute myocardial infarction, coronary bypass, head trauma, and cerebral bleeding, including subarachnoid hemorrhage. We hypothesize that the hypoxia accompanying these events could damage the blood-testis barrier (BTB) and so cause testicular dysfunction, a possible cause of impotence. We examined the effect of cardiac arrest in mice on testis weight and various aspects of BTB function. Testis weight was decreased by about 24% 12 hours after cardiac arrest but had recovered fully by day 7. The testis/serum ratio for albumin was increased 12 hours after arrest, showing a disruption in the vascular BTB with recovery by 24 hours. The testis/serum ratio for sucrose was not consistently elevated, showing that the Sertoli cell BTB remained intact. The testis/serum ratio for verapamil was increased on day 3 of cardiac arrest, suggesting impaired function of the BTB's p-glycoprotein efflux transporter. Transporters for pituitary adenylate cyclase activating polypeptide and tumor necrosis factor-alpha were not affected by cardiac arrest. These results show that cardiac arrest affects testis weight and some aspects of BTB function. Such changes might have long-term effects on testicular function.[1]

References

The effect of cardiac arrest on the blood-testis barrier to albumin, tumor necrosis factor-alpha, pituitary adenylate cyclase activating polypeptide, sucrose, and verapamil in the mouse. Mizushima, H., Nakamura, Y., Matsumoto, H., Dohi, K., Matsumoto, K., Shioda, S., Banks, W.A. J. Androl. (2001) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.