The goal of the Linux-Society (LS, dating back to the mid-90s as a professional club and tech-mentoring group) has been a purely-democratic Information Society; many of the articles are sociological in nature. The LS was merged with Perl/Unix of NY to form multi-layered group that included advocacy, project-oriented learning by talented high school students: textbook constructivism. Linux has severe limitations such that it is useless for any computer that will, say, print or scan. It is primarily used for webservers and embedded devices such as the Android. (Google is high-invested in it).

Technology is problematic. During the heyday of technology (1990s), it seemed it had the democratic direction Lewis Mumford said it should have in his seminal
Technics and Civilization.

Today, we are effectively stuck with Windows as Linux is poor on the desktop and has cultured a maladaptive following. Apple is prohibitive, and all other operating systems lack drivers, including Google's Android, an offshoot of linux.

In the late 90s there was hope for new kernels such as LibOS and ExoOS that would bare their hardware to programs, some of which would be virtual machines such as Java uses. Another important player was the L4 system that is a minor relation to the code underlying the Apple's systems. It was highly scientific but fell into the wrong hangs, apparently, and has suffered from having no progress on the desktop. There is a version, "SE" that is apparently running in many cell phones as specialized telecom chips, but is proprietary. SE's closed nature was only recently revealed, which is important because it is apparently built from publicly-owned code as it is not a "clean room" design it may violate public domain protections, and most certainly violates the widely-accepted social contract.

Recent attempts to enjoin into L4 development as an advocate for "the people" have been as frustrating (and demeaning) as previous attempts with the usual attacks to self-esteem by maladaptive "hacks" being reinforced by "leadership" (now mostly university professors).

In short, this leaves us with Windows, which is quite a reversal if you have read earlier posts here. But, upon Windows, we have free and open software development systems in the forms of GTK+ (the windows usually used on Linux) and the Minimal GNU Windows (MinGW and MSYS) systems. It is very likely this direction that development should go (that is, on Windows) such that s/w can then be ported to a currently-valid microkernel system that includes a driver system that can be adapted by hardware developers to reuse of their windows and apple drivers.

From a brief survey of L4, it appears that the last clean copy was the DROPS system of the early 2010s, was a German effort that used the Unix-like "OS kit" from an American University.

If we are going to be stuck on Windows, then it seems that a high level approach to free and open systems integration, such as creating fully transparent mouse communication between apps so that they can seamlessly work together as a single desktop (rather than deliberately conflicting). This would be very helpful for GIMP and Inkscape, both leading graphics programs that are strong in the special ways, but suffer from an inability to easily interrelate.

Another important issue is the nature, if you can call it that, of the "geek" or "hack." Technology is formed democratically but "harvested" authoritarian-ly --if I can coin a term that Mumford might use. Authority is plutarchy: a combination of aristocracy and oligarchy that is kept alive after all these millennia by using, or maligning, the information society as a part of the civilizing (or law-giving) process that embraces the dialectic as its method. Democratic restoration, that is to put humanity back on an evolutionary (and not de-evolutionary) track, I think, will require the exclusion of the "geek" from decision-making. As is, the free/open s/w culture attempts to give leadership to those who write the most lines of code --irrespective of their comprehension of the real world or relationship with normal users. We need normal people to somehow organize around common sense (rather than oligarchic rationalism) to bring to life useful and cohesive software and communications systems.

Interestingly, the most popular page on this site is about Carl Rogers' humanistic psychology, and has nothing to do with technology.

Friday, September 24, 2010

Comparing schizophrenia and bipolar (and also psychosis)

A review of recent material about schizophrenia and bipolar disorder confirms that the two diseases are genetically inherited.  One article suggests that families with a genetic tendency for one of these diseases also have a tendency for the other (McIntosh, 2009).  A search for genetic information about schizophrenia shows that a particular genetically expressed protein, NRG1, and its related receptors, ErbB3 and ErbB4, are central to schizophrenia.  Recent studies implicating NRG1 in schizophrenia also implicate it in bipolar disorder, giving oblique support to the idea that the two diseases are connected genetically, and in other ways.  But they focus on different areas, and hence have seemingly conflicting concepts: myelin and neurotransmitters.  Myelin implies neural speed, and neurotransmitters bring to mind, as an example, dopamine reactions to stress.

A myelin, or ErbB3, study (McIntosh, 2009), shows that mutations resulting in NRG1/ErbB3 signaling failures causes oligodendrocyte activity to be impaired so that less "white matter" is produced resulting in a diminished "anterior internal capsule in subjects with both disorders" (p. 2) including unaffected directly-related family members of the bipolar disorder and schizophrenia subjects.  This effect is assumed to be developmental, and myelin formation in "frontal lobes, continues into late adolescence and beyond" (p. 3), giving optimism that new drugs could reinforce myelination for those at risk. 

This study also says that plasticity relates to myelination, and that there is myelination in adults, and hence plasticity, that may relate to schizophrenia and bipolar disorder in terms of both development and maturity.

    Genetic loading for psychosis and the internal capsule (McIntosh, 2009)

Neurotransmitter, or  ErbB4, studies have a brain-wide view with a focus on neuron and transmitter activity such glutamatergic hypofunction (Li, 2007), failures in the formation of inhibitory synapses (Fazzari, 2010), and neural development such as the "wiring" of GABA-mediated circuits (Fazzari, 2010), all in the context of schizophrenia.  While a bipolar disorder can be linked to schizophrenia in the context of ErbB4 (Chong, 2007), the more detailed material on neural activity focuses on schizophrenia. 

As dopamine hyperactivity is part of the schizophrenia pharmacological model (Stone, 2007), and methamphetamine is used to simulate it experimentally (Homayoun, 2008), studies concentrating on stimulants may give clues about the neural activity of schizophrenia and bipolar disorder.

The "white matter" study links myelination to plasticity, and is optimistic that new drugs may reinforce myelination (p. 4), and so raises an idea about myelination and plasticity with respect to maturity: could such drugs help the elderly retain plasticity?

These studies show similar diseases apparently caused by the same mutations, creating a causal relationship that should point to a common location for both diseases.  But we find the expressions on completely different levels--the causal relationship is misleading!  Still, the "neurotransmitter" studies show causal relationships linking the neural functions of bipolar disorder and schizophrenia to glutamatergic, GABAergic, and dopaminergic responses to stimulants, such as methamphetamine.  These relations may help show us how the disordered neurons may affect behavior. 


Chong, V.,  Thompson, M., Beltaifa, S., Webster, M., Law A., and Weickertad, S. (2007). Elevated Neuregulin-1 and ErbB4 protein in the prefrontal cortex of schizophrenic patients: Schizophr Res. 2008 March ; 100(1-3): 270–280. doi:10.1016/j.schres.2007.12.474.

Fazzari, P., Paternain, A., Valiente, M., Pla, R., Luján, R., Lloyd, K., et al. (2010). Control of cortical GABA circuitry development by Nrg1 and ErbB4 signalling. Nature, 464(7293), 1376-1380. doi:10.1038/nature08928.

Gever, J. (2009, January 15). Bipolar disorder and schizophrenia have overlapping genetic roots. MedPage Today

Homayoun, H., & Moghaddam, B. (2008). Orbitofrontal cortex neurons as a common target for classic and glutamatergic antipsychotic drugs. Proceedings of the National Academy of Sciences of the United States of America, 105(46), 18041-18046. doi:10.1073/pnas0806669105.

Li, B., Woo, R., Mei L., Malinow, R., (2007, May 24). The neuregulin-1 receptor ErbB4 controls glutamatergic synapse maturation and plasticity. Neuron, 54(4), 583-597.

McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009). Genetic risk for white matter abnormalities in bipolar disorder. International Review of Psychiatry, 21(4), 387-393. doi:10.1080/09540260902962180.

McIntosh, A., Hall, J., Lymer, G., Sussmann, J., and Lawrie, S. (2009).
Genetic loading for psychosis and the internal capsule disorder. International Review of Psychiatry, 21(4), 387-393. doi:10.1080/09540260902962180.

tone, J., Morrison, P., and Pilowski, L. (2007, January 26). Review: Glutamate and dopamine dysregulation in schizophrenia — a synthesis and selective review. Journal of Psychopharmacology June 2007 vol. 21 no. 4 440-452

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