H2S

All posts tagged H2S

Is Schizopherenia caused by a substance or lack of a substance?

Posted by gdnf on March 14, 2011
Posted in: CO2 Reactivity, Neuroscience, Schizophrenia, Science. Tagged: , , , , , , .

1

To little or to much of a substance?

Some of the theories of Schizophrenia etiology mention the drug induced hallucinations as a raw-model for Schizophrenia but there is a problem with that – Persons with Schizophrenia doesn’t have these substances in their blood while hallucinating. Some drugs and some medicines might create states that remind of Schizophrenia: Ketamine and Phencyclidine (PCP) are the most mentioned. But the substances are not identified in the blood of the persons having the problem.

Here will in show the signs of lacking Oxygen and that there actually is a substance that can cause some of the symptoms and that persons with schizophrenia have it in their exhaled breath.

2

Lacking essentials as cause of Schizophrenia?

Probably, as much as 50% of the genes involved in the disease could be changed due to hypoxia. And seeing the BOLD results really tells me that they don’t get the oxygen needed.  Can we really get a much stronger evidence of hypoxia?

The CO2 reactivity or the driving reaction to breath is also changed…

3

A substance that can give the symptoms is detected in the populations having the disease

We will show that there is in fact, a substance that by itself can create most of the symptomatology panorama and that this very substance also is detected in the individuals having disease. The substance is Carbon Sulfide or CS2. One of the most active metabolites are H2S (Hydrogen Sulfide) or more likely – H2S is the mother-substance and CS2 the metabolite.

BDNF – GDNF is Dead – Science and Nuts is here

Posted by gdnf on August 16, 2010
Posted in: General. Tagged: , , , , .

Long live GDNF – BDNF!

We have moved

Hopefully we can concentrate on what we do best write,  and nothing else. The new URL is a combination of H2S – Hydrogen sulfide and AMPK : 5′ AMP-activated protein kinase  or 5′ adenosine monophosphate-activated protein kinase or simply just AMPK, it mirrors what we  hopefully will write about in the in the time to come and possibly even a severe lack of fantasy.

Technorati, technorati tags, Thanks for al the links UrbotaInskränkthet. and al of you nice supporting ppl. Originals, Please be aware that we have changed the UR. And a word about wordpress.com to change URL with just a few click and most of the post and stuffs working right away -fantastic. Nice and very good, since moving can be quiet a job with al the redirect 301….

Schizophrenia H2S and Carbonic Anhydrase

Posted by gdnf on June 22, 2010
Posted in: Neuroscience, Schizophrenia. Tagged: , , , , , , , , , , .

After the updates of the new page: The Etiology of Schizophrenia – CS2. The work now continues by following the metabolism from CS2 to H2S in what could be and the reactive core in the etiology of Schizophrenia. Up next are the effects of H2S.

But first of all let us see that the CAC-hålet theory shows that the reactive substance CS2 which in itself can cause some of the symptoms in Schizophrenia and is metabolized to Hydrogen Sulfide – H2S in the body, by a new route.  CS2 is also detected in the exhaled air from persons with Schizophrenia.

Aspiration and Respiration

The core function in aspiration is gas exchange with the biosphere and to regulate the breathing to the needs of the cellular respiration. In schizophrenia the Carbonic Anhydrase Catalysis – CAC is slower than normally resulting in a prolonged hypoxia in the mitochondria after increases in the O2 consumption, part of these fundamentals are later shown in the BOLD fMRI where the blood oxygenation levels curve are steeper in persons with schizophrenia.

CS2 and the metabolites dithiocarbamates and H2S are potent inhibitors of CAC, this will result in a further decrease in the function of Carbonic Anhydrase and the CO2 reactivity will get even slower. Or the other way around, H2S is the mother-substance to the reaction.

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Refrenences
Carbonic anhydrase inhibitors. Inhibition of cytosolic isoforms I, II, III, VII and XIII with less investigated inorganic anions
Alessio Innocentia, Andrea Scozzafavaa and Claudiu T. SupuranCorresponding Author Contact Information, a, E-mail The Corresponding Author
Università degli Studi di Firenze, Laboratorio di Chimica Bioinorganica, Rm. 188, Via della Lastruccia 3, I-50019 Sesto Fiorentino, Firenze, Italy
2009.

Chengelis, C. P. and Neal, R. A., Studies of carbonyl sulfide toxicity: metabolism by carbonic anhydrase,
Towicol. Appl. Pharmacol., 55, 198, 1980

Baird, T.T., A. Waheed, T. Okuyama, W.S. Sly, & C.A. Fierke (1997) Catalysis and Inhibition
of Human Carbonic Anhydrase IV, Biochemistry, 36: 2669 – 2678.

The possible role of CO2 in producing a post-stimulus CBF
and BOLD undershoot
Meryem A. Yücel1,2, Anna Devor2,3, Ata Akın1 and David A. Boas2*
1 Institute of Biomedical Engineering, Bogˇ aziçi University, Istanbul, Turkey