TH-Marker for Diabetic Neuropathy

New Pub Referencing our Tyrosine Hydroxylase.

Blount, Andrew L. B.A.; Peled, Ziv M. M.D.; Dexter, Erica L. B.S.; Nagle, Raymond B. M.D., Ph.D.; Maloney, Christopher T. M.D.; Dellon, A Lee M.D., Ph.D. Sympathetic Nerves in the Tarsal Tunnel: Implications for Blood Flow in the Diabetic Foot. Plastic & Reconstructive Surgery. 122(1):188-191, July 2008.

...Specimens were fixed in 10% neutral buffered formalin for 3 to 4 hours and then embedded in paraffin. Three-micron sections were obtained from the block and used for immunohistochemistry, which was performed using a mouse monoclonal antibody against tyrosine hydroxylase (MO20001; Neuromics, Edina, Minn.) diluted 1:50 in Discovery Diluent (Ventana Medical Systems, Inc., Tucson, Ariz.) on a Discovery XT Automated Immunostainer (Ventana Medical Systems)...
Images: (A) Tyrosine hydroxylase immunohistochemical staining of tibial epineurium from the tarsal tunnel. Positively staining sympathetic fibers (arrows) are seen within a larger nerve bundle. (B) Tyrosine hydroxylase immunohistochemical staining of connective tissue from the tarsal tunnel. Several positively staining sympathetic fibers (arrows) are seen innervating the media of a local venule.

SP is Back and Better than Ever

We have successfully re-made our widely used Guinea Pig Substance P antibody. It has been tested both internally and by an interested customer. The results exceeded expectations.

This antibody has proven useful for Pain/Inflammation and Diabete/Obesity Research.

Image: Immuofluorescent detection of Substance P in rat spinal cord dorsal horn (red fluorescence). DAPI (blue) was used as counter stain.

Here're are related publications:

P . Tsai , A . Alonso , M . Pinto , D . Leigh , E . Weiler , J . Fricton , M . Erickson , L . Stone , L . Kehl. Substance P is co-localized with protein gene product 9.5-immunoreactive nerve fibers in intervertebral discs from patients with painful degenerative disc disease. doi:10.1016/j.jpain.2006.01.096
...guinea pig anti-substance P (1:500; Neuromics, Edina, MN) ...
Mei Bigliardi-Qi, Claire Gaveriaux-Ruff, Katrin Pfaltz, Pierre Bady, Tommy Bauman, Theo Rufli, Brigitte L Kieffer and Paul L Bigliardi. Deletion of - and -Opioid Receptors in Mice Changes Epidermal Hypertrophy, Density of Peripheral Nerve Endings, and Itch Behavior. Journal of Investigative Dermatology (2007) 127, 1479–1488. doi:10.1038/sj.jid.5700661; published online 21 December 2006.
.. substance P (Neuromics 1:200) staining, the sections were incubated at 4°C over night in Zamboni buffer. ...

Related Reagents:
Neurokinin-1 (NK 1) Receptor
Neurokinin-1 (NK 1) Human Receptor
Neurokinin-3 (NK 3) Receptor
proNeurokinin B (proNKB or P2)
All Neuropeptides
Pain and Inflammation Antibodies
Diabetes and Obesity Antibodies
Substance P Customer Data

ELISPOT

We will be releasing soon a website dedicated to ELISA and ELISpot.

Here are excellent "how to" videos.

Molecular Pathways and Heart Development

Owen WJ Prall, Mary K Menon, Mark J Solloway, Yusuke Watanabe, Stéphane Zaffran, Fanny Bajolle, Christine Biben, Jim J McBride, Bronwyn R Robertson, Hervé Chaulet, Fiona A Stennard, Natalie Wise, Daniel Schaft, Orit Wolstein, Milena B Furtado, Hidetaka Shiratori,6 Kenneth R Chien, Hiroshi Hamada,6 Brian L Black, Yumiko Saga, Elizabeth J Robertson, Margaret E Buckingham, and Richard P Harvey. An Nkx2-5/Bmp2/Smad1 negative feedback loop controls second heart field progenitor specification and proliferation. Cell. 2007 March 9; 128(5): 947–959. doi: 10.1016/j.cell.2007.01.042.

Summary: During heart development the second heart field (SHF) provides progenitor cells for most cardiomyocytes and expresses the homeodomain factor Nkx2-5. We now show that feedback repression of Bmp2/Smad1 signaling by Nkx2-5 critically regulates SHF proliferation and outflow tract (OFT) morphology. In the cardiac fields of Nkx2-5 mutants, genes controlling cardiac specification (including Bmp2) and maintenance of the progenitor state were up-regulated, leading initially to progenitor over-specification, but subsequently to failed SHF proliferation and OFT truncation. In Smad1 mutants, SHF proliferation and deployment to the OFT were increased, while Smad1 deletion in Nkx2-5 mutants rescued SHF proliferation and OFT development. In Nkx2-5 hypomorphic mice, which recapitulate human congenital heart disease (CHD), OFT anomalies were also rescued by Smad1 deletion. Our findings demonstrate that Nkx2-5 orchestrates the transition between periods of cardiac induction, progenitor proliferation and OFT morphogenesis via a Smad1-dependent negative feedback loop, which may be a frequent molecular target in CHD.

...goat anti-Isl1, raised against full length human Isl1, GT15051, Neuromics)...