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Computers & Society/World Wide Web

Prehistory of the World Wide Web
Let us begin with a brief history of the World Wide Web (WWW). Now. Of what might a prehistory of the WWW consist?

Hypertext
From the history account we learn that the concept of hypertext plays a fundamental role. But it appears that there was a not unexpected pre-history to the emergence of the hypertext. In discussing the work of John Wilkins entitled An Essay towards a Real Character and a Philosophical Language, the author Umberto Eco makes the following interesting conclusion:

«What if we regarded the defect in Wilkins' system as its prophetic virtue? What if we treated Wilkins as if he were obscurely groping towards a notion for which we have only recently invented a name — hypertext? … If this were the case, many of [Wilkins'] system's contradictions would disappear, and Wilkins could be considered as a pioneer in the idea of a flexible and multiple organization of complex data … his [project] was instead the search for ways to articulate all that natural languages permit us to say.»

The X in XML
"XML is both a boon and a threat to the web dream."

The X in XML stands for eXtensible. This signifies that XML is open. It is open in the sense that it allows growth. Note that the abbreviation is XML and not EML. There is something daring, attractive, exciting about that X. X stands for many things, depending on the culture of the society in which it appears! The two most obvious things denoted are
 * X-rated stuff: films, books... intended for adults only!
 * X-roads: where choices in direction can be made.

Since the X in XML is pronounced "ex" and may sometimes even be written that way, then we have an opportunity of charting other potential meanings. For example, to say that "she is his ex" implies something in the past. This is not the intention of the X in XML. But we can make it so. We can think of XML poetically as X-ML to refer to the SGML that preceded it.

And we can use exactly the same interpretation for XHTML.

Xwords & partial understanding
We want to understand exactly how the XML-speaking machines influence the development of our societies. And yes! there is more than one society in the world. And yes! XML is language for the machines. "XML namespaces will allow documents to work in a mixture of globally standard terms and locally agreed-upon terms. The inference languages will allow computer to translate not all of a document, but enough of it to be able to act on it. Operating on such 'partial understanding' is fundamental, and we do it all the time in the nonelectronic world."

If you want to learn the technical details of XML then why not open the Wikibook on XML and start right away?

The X in Xword (or X-word) is usually taken to mean crossword (cross-word). But we will introduce the X meaning of XML and talk about extensible words. For example, "dossier" is a word which names a special kind of document. The bracketing pair ... is an Xword which extends "dossier". How does it extend dossier? Well, by filling in its meaning as structure, the structure of the document.

XLink
An XLink is a link belonging to the XML-world (or simply just the X-world). In other words an XLink is an "extensible" link. We can extend the concept and, hence the digital reality, as much as we can imagine. Much of the imagination is often dampened down by the technologies available, especially in general WWW use. It is important to recall, that XLink almost feels like "ancient history" in 2008. It precedes the arrival of Facebook (2004), Flickr (2004), YouTube (2005), and so on.

A good technical overview of XLink is available on Wikipedia.

But actual applications based on XLink are very few. Why is that? One major reason is undoubtedly the subsequent emergence of the Resource Description Framework (RDF). In the abstract, the essential component of RDF, called a triple, is simply represented by a directed arrow of the form • → • which connects something on the left (denoted abstractly by ‘•’) to something on the right (also abstractly by ‘•’). For example, the saying "faraway hills are green" is a simple statement connecting hills and the color green. In the arrow form, we might write "faraway hills" → "green" where the directed arrow is to be labelled with something like "hasColor". Sometimes the saying may be presented as "far away hills are green" where "faraway" is written as two separate words "far" and "away". Because of the focus or intent, the same triple would be used. And in the context of speech, rather than writing, there is no distinction between "faraway" and "far away". This remark is significant for the full richness of media in the WWW.

An XLink • → • is not a mere triple in the RDF sense. It is much much more.

XLink kinds
There are only two kinds of XLink: Although they are closely related conceptually, the simple-link is syntactically very different from the extended XLink. "Simple links offer shorthand syntax for a common kind of link, an outbound link with exactly two participating resources (into which category HTML-style A and IMG links fall). Because simple links offer less functionality than extended links, they have no special internal structure."
 * simple XLink
 * extended XLink

From this formal text we may deduce that the simple link has exactly the form • → • and it is an "outbound" link.

XForms
A good technical overview of Xforms is available on Wikipedia. Then if you wish to get into more detail, why not try out the XForms Wikibook?

Reading links

e-Links
There is a beautiful Wikibook on XML. Tim Berners-Lee: Weaving the Web.

title: Computers & Society/World Wide Web


text:
Talk:Computers & Society/World Wide Web

I want to use some "open source material" related to the WWW. Naturally, first port of call will be Wikipedia. Maybe there is also some good wikibook I can refer to?

I have begun to develop the section on XLink (Михал Орела 09:02, 12 July 2008 (UTC))

Hypertext
Added in a [surprising] text on hypertext:

«What if we regarded the defect in Wilkins' system as its prophetic virtue? What if we treated Wilkins as if he were obscurely groping towards a notion for which we have only recently invented a name — hypertext? … If this were the case, many of [Wilkins'] system's contradictions would disappear, and Wilkins could be considered as a pioneer in the idea of a flexible and multiple organization of complex data … his [project] was instead the search for ways to articulate all that natural languages permit us to say.» (Umberto Eco, The Search for the Perfect Language, p.258-9, FontanaPress: London, 1997.)

It appears that there was a not unexpected pre-history to the emergence of the hypertext. (Михал Орела)

History
It is clear that a preHistory of the WWW and the Hypertext is needed. :) (Михал Орела 08:26, 29 August 2008 (UTC))

Notes etc
Added in the usual Notes, Reading links, and e-Links sections. (Михал Орела 08:36, 29 August 2008 (UTC))

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Talk:Computers & Society/World Wide Web


text:
Talk:Computers & Society/Back Cover

It is hard to write a book in one day

I am trying to get the structure down with place holder text...

I am working on this is the little spare time I have...

--Михал Орела 11:15, 6 May 2008 (UTC)

title: Talk:Computers & Society/Back Cover


text:
User talk:Aniket ectech

hi

title: User talk:Aniket ectech


text: User talk:71.241.25.131

title: User talk:71.241.25.131


text: User talk:124.168.218.185

title: User talk:124.168.218.185


text:
Hebrew/Exercises/Aleph-Bet 9

Welcome to the exercises related to Aleph-Bet Lesson 9 of learning Hebrew.

Click "▼" to check your answers.

Letters & Niqqud
Assign each letter to the sound it stands for:

1.

2.

Assign each sound to the letter that makes it:

1.

2.

Vocabulary
How is each word pronounced?

Translate the following words from Hebrew to English:

Reading Without Vowels
How is each word pronounced?

Next Steps
Review lesson: Aleph-Bet 9 Next lesson: Aleph-Bet 10 >>>

title: Hebrew/Exercises/Aleph-Bet 9


text:
User:Dhtwatkins

David Watkins

An experienced mathematics teacher from the U.K.

Currently writing new entries for A-level Maths wikibooks

title: User:Dhtwatkins


text:
Talk:Metasploit/UsingMetasploit

This is a good page to start people with for metasploit usage. How about also some basic command line usuage information?

title: Talk:Metasploit/UsingMetasploit


text: User talk:208.67.140.121

title: User talk:208.67.140.121


text: User talk:198.209.35.250

title: User talk:198.209.35.250


text: User talk:75.144.167.141

title: User talk:75.144.167.141


text:
User:Hhayashi~enwikibooks/monobook.css

.code .input pre {padding:0; border: none; line-height: 1.5em; margin:0;} .code .result pre {border:0; padding:0.2em; margin: 0.3em; background-color: #DDDDFF;} .code .input pre:before {content: "\003E \0020";}

title: User:Hhayashi~enwikibooks/monobook.css


text: Category:Book:Adventist Youth Honors Answer Book/Zoology Master Award


text: User:B Fizz

title: User:B Fizz


text:
Template:AY limited availability

Limited availability

title: Template:AY limited availability


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User:Ines~enwikibooks

first of all hi to all! i'm a person who is so lucky to be alive and go through all terms of life, i love getting through all difficulties of life and really facing them with a brave and strong heart, i hate people who only care for shapes and people who are so very judjeful to others, i'm actully a gothic, but i believe in god.. i love deep stuff and personalities. nice to meet u all!

title: User:Ines~enwikibooks


text:
User talk:Ines~enwikibooks

Welcome!
Welcome, Ines!

Come introduce yourself at the new users page. If you have any questions, you can ask there or contact me personally.--Whiteknight (Page) (Talk) 17:22, 6 May 2008 (UTC)

Your account will be renamed
Hello,

The developer team at Wikimedia is making some changes to how accounts work, as part of our on-going efforts to provide new and better tools for our users like cross-wiki notifications. These changes will mean you have the same account name everywhere. This will let us give you new features that will help you edit and discuss better, and allow more flexible user permissions for tools. One of the side-effects of this is that user accounts will now have to be unique across all 900 Wikimedia wikis. See the announcement for more information.

Unfortunately, your account clashes with another account also called Ines. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Ines~enwikibooks that only you will have. If you like it, you don't have to do anything. If you do not like it, you can pick out a different name.

Your account will still work as before, and you will be credited for all your edits made so far, but you will have to use the new account name when you log in.

Sorry for the inconvenience.

Yours, Keegan Peterzell Community Liaison, Wikimedia Foundation 23:18, 17 March 2015 (UTC)

Renamed
 This account has been renamed as part of single-user login finalisation. If you own this account you can |log in using your previous username and password for more information. If you do not like this account's new name, you can choose your own using this form after logging in: . -- Keegan (WMF) (talk) 05:03, 19 April 2015 (UTC)

title: User talk:Ines~enwikibooks


text: Category:Book:Punjabi

title: Category:Book:Punjabi


text:
Category:Subject:Markup languages

fr:Catégorie:Langages balisés ja:カテゴリ:World_Wide_Web ko:분류:마크업 언어 ru:Категория:Языки разметки uk:Категорія:Мови розмітки

title: Category:Subject:Markup languages


text:
User:Vigilius

(See Vigilius on the English Wikipedia)

title: User:Vigilius


text:
User talk:Ryan.Wensmann

Welcome to Wikibooks, Ryan.Wensmann! – Mike.lifeguard  | talk 18:39, 6 May 2008 (UTC)

title: User talk:Ryan.Wensmann


text:
User talk:Graviphoton (usurped)

Welcome to Wikibooks, Graviphoton!

Mike, its Graviphoton

I am the author of the work published at BAUT forums. So there is no violation here.

Suggested reading
Have a look at: Consciousness_Studies/Table_Of_Theories RobinH (talk) 11:41, 16 May 2008 (UTC)

Relativity_-_Advanced
This book is likely to go the same way as the other one. Have you considered adding the content to the modern physics bookshelf? Take a look at Special relativity for instance. Again, all contributions would need to refer to published work by others. RobinH (talk) 11:46, 16 May 2008 (UTC)

title: User talk:Graviphoton (usurped)


text:
User talk:Itguru~enwikibooks

Welcome to Wikibooks, Itguru!

Your account will be renamed
Hello,

The developer team at Wikimedia is making some changes to how accounts work, as part of our on-going efforts to provide new and better tools for our users like cross-wiki notifications. These changes will mean you have the same account name everywhere. This will let us give you new features that will help you edit and discuss better, and allow more flexible user permissions for tools. One of the side-effects of this is that user accounts will now have to be unique across all 900 Wikimedia wikis. See the announcement for more information.

Unfortunately, your account clashes with another account also called Itguru. To make sure that both of you can use all Wikimedia projects in future, we have reserved the name Itguru~enwikibooks that only you will have. If you like it, you don't have to do anything. If you do not like it, you can pick out a different name.

Your account will still work as before, and you will be credited for all your edits made so far, but you will have to use the new account name when you log in.

Sorry for the inconvenience.

Yours, Keegan Peterzell Community Liaison, Wikimedia Foundation 23:14, 17 March 2015 (UTC)

Renamed
 This account has been renamed as part of single-user login finalisation. If you own this account you can |log in using your previous username and password for more information. If you do not like this account's new name, you can choose your own using this form after logging in: . -- Keegan (WMF) (talk) 05:03, 19 April 2015 (UTC)

title: User talk:Itguru~enwikibooks


text:
User talk:Etams

Thank you!
You're doinng a wonderful job with the Hebrew book. I worked on it earlier and hope to find time to help out again soon. But, since I'm just learning, it's slow going, and I probably make lots of mistakes. On the other hand, I can still help by knowing some of what may confuse a new learner or by letting you know what I'd like to learn. Thanks for the great job! -CocoaZen (talk) 14:41, 8 May 2008 (UTC)
 * Instead of redirecting pages to new locations, please move them. There is a move tab at the top of the page to do so. This will comply with the GFDL, while what you are currently doing doesn't and is messy. Thanks a bunch. – Mike.lifeguard  | talk 00:08, 10 May 2008 (UTC)
 * Yes, I was aware of that mistake. Sorry. Ētamš (Talk • Contribs) 07:49, 10 May 2008 (UTC)

Hi. Sorry I haven't been around much recently. Other parts of my life have been too busy and will continue to be for at least another month. After that I hope to be back more often again. --CocoaZen (talk) 18:17, 13 June 2008 (UTC)

title: User talk:Etams


text:
Hebrew/Exercises/Aleph-Bet 10

Welcome to the exercises related to Aleph-Bet Lesson 10 of learning Hebrew.

Click "▼" to check your answers.

Letters & Niqqud
Assign each letter to the sound it stands for:

1.

2.

Assign each sound to the letter that makes it: }}

Vocabulary
How is each word pronounced?

Translate the following words from Hebrew to English:

Reading Without Vowels
How is each word pronounced?

Numbers
What is the numerical value of the following numbers?

How do you write in Hebrew the following numbers:

Next Steps
Review lesson: Aleph-Bet 10 Aleph-Bet review >>>

title: Hebrew/Exercises/Aleph-Bet 10


text: User talk:87.252.227.42

title: User talk:87.252.227.42


text:
User:Logictheo

cookbook. I would maybe add a salad to We just made a salad. It had cabbage, celery and carrot. We put lemon juice and olive oil in it.

= Books I'm interested in =
 * Gtk
 * Cookbook

= more userboxes = user templates

el:User:Logictheo

title: User:Logictheo


text:
Metabolomics/Hormones/Insulin

 * Previous chapter: Metabolites
 * Next chapter: Analytical Methods
 * Next section: Glucagon

The three dimensional dtructure of insulin
Insulin is a small protein with two polypeptide chains joined by two disulfide bonds. It is synthesized in the pancreas as an inactive single chain precursor, preproinsulin, with an maison terminal signal sequence that directs its passage into secretory vesicles.

Insulin (Latin insula, "island", as it is produced in the Islets of Langerhans in the pancreas) is a polypeptide hormone that regulates carbohydrate metabolism. Apart from being the primary effector in carbohydrate homeostasis, it also has a substantial effect on small vessel muscle tone, controls storage and release of fat (triglycerides) and cellular uptake of both amino acids and some electrolytes. In this last sense, it has anabolic properties. Its concentration (more or less, presence or absence) has extremely widespread effects throughout the body.

Insulin is used medically in some forms of diabetes mellitus. Patients with Type 1 diabetes mellitus depend on exogenous insulin (injected subcutaneously) for their survival because of an absolute deficiency of the hormone; patients with Type 2 diabetes mellitus have either relatively low insulin production or insulin resistance or both, and a non-trivial fraction of Type 2 diabetics eventually require insulin administration when other medications become inadequate in controlling blood glucose levels. Insulin structure varies slightly between species. Its carbohydrate metabolism regulatory function strength in humans also varies. Pig insulin is particularly close to the human one.

The exact sequence of amino acids comprising the insulin molecule, the so-called primary structure, was determined by British molecular biologist Frederick Sanger. It was the first protein the structure of which was completely determined. For this he was awarded the Nobel Prize in Chemistry in 1958. In 1967, after decades of work, Dorothy Crowfoot Hodgkin determined the spatial conformation of the molecule, by means of X-ray diffraction studies. She also was awarded a Nobel Prize.

Control of insulin secretion
Insulin is secreted in primarily in response to elevated blood concentrations of glucose. This makes sense because insulin is "in charge" of facilitating glucose entry into cells. Some neural stimuli (e.g. sight and taste of food) and increased blood concentrations of other fuel molecules, including amino acids and fatty acids, also promote insulin secretion.

Glucose is transported into the beta cell by facilitated diffusion through a glucose transporter; elevated concentrations of glucose in extracellular fluid lead to elevated concentrations of glucose within the beta cell. Elevated concentrations of glucose within the beta cell ultimately leads to membrane depolarization and an influx of extracellular calcium. The resulting increase in intracellular calcium is thought to be one of the primary triggers for exocytosis of insulin-containing secretory granules. The mechanisms by which elevated glucose levels within the beta cell cause depolarization is not clearly established, but seems to result from metabolism of glucose and other fuel molecules within the cell, perhaps sensed as an alteration of ATP:ADP ratio and transduced into alterations in membrane conductance. Increased levels of glucose within beta cells also appears to activate calcium-independent pathways that participate in insulin secretion.

General overview
Throughout body it regulates blood glucose levels, increases storage of glycogen, and facilitates glucose intake by body cells. Proteolytic removal of the signal sequence and formation of three disulfide bonds produces proinsulin, which is stored in secretory granules in pancreatic beta cells. When elevated blood glucose triggers insulin secretion, proinsulin is converted to active insulin by specific proteases, which cleave two peptide bonds to form the mature insulin molecule.

Insulin process from precursor
The effect of insulin is to favor the conversion of excess blood glucose to two storage forms glycogen (in the liver and muscle), and triacylglycerol (in adipose tissue)

Proinsulin is synthesized in the pancreatic beta cells as a 9390 mw polypeptide of 86 amino acids.

Proinsulin is subsequently cleaved enzymatically, releasing insulin into the circulation along with a residual 3000 mw fragment called C-peptide, so-named because it connects the A and B chains of insulin within the proinsulin molecule.

Proinsulin, which has relatively low biological activity (approximately 10% of insulin potency), is the major storage form of insulin. Normally, only small amounts (~3% of the amount of insulin, on a molar basis) of proinsulin enter the circulation. Because the hepatic clearance of proinsulin is only 25% of insulin clearance, the half-life of proinsulin is two- to threefold longer and concentrations in the fasting state are approximately 10% to 15% of insulin concentrations.

Website sources
Association of Adiposity, Cardiorespiratory Fitness and Exercise Practice with the Prevalence of Type 2 Diabetes in Brazilian Elderly Women

http://www.medsci.org/v04p0288.htm

General overview
The incidences of diabetes in age increasing women are substantially growing in alarming rate. Therefore it is important to keep close research on this topic to reduce the growing communities in type 2 diabetes. In order to analyze the effects, adiposity, cardio respiratory fitness, and exercise practice in T2D in Brazilian elderly women are put to several exercises to measure their health conditions.

The general and central adiposity were directly associated with T2D, whereas cardio respiratory fitness was inversely related with T2D. The joint effect of exercise practice and central adiposity showed that inactive women had higher rate of odd in facing T2D when compared with active women.

The researchers were able to determine the association of general and central adiposity as well as an inverse relation with CRF (cardio respiratory fitness) and exercise practice side by side with T2D. Elderly women practicing regular exercise had lower odds of acquiring T2D than the inactive group of women. By having proper exercise, the exercise will reduce the body fatness and possibly benefiting from reducing the prevalence of T2D in old aging group.

New terms

 * Adiposity: loose connective tissue composed of adipocyte, which is derived from lipoblasts and their maine role is to store energy in the form of fat
 * CRF (Cardio respiratory fitness): refers to the ability of the circulatory and respiratory systems to supply oxygen to skeletal muscles during sustained physical activity.
 * Type 2 diabetes (T2D): common form of diabetes. In type 2 diabetes, either the body does not produce enough insulin or the cells ignore the insulin.

Course relevance

 * Analysis of prevalence of diabetes and poor glycemic control
 * Metabolic control; this was measured by reduced insulin resistance and inflammation in study subjects
 * Biochemical measure method

Website #2
Insulin secretion location http://www.clarian.org/ADAM/doc/graphics/images/en/19200.jpg

General Overview

 * Throughout body it regulates blood glucose levels, increases storage of glycogen, and facilitates glucose intake by body cells. Proteolytic removal of the signal sequence and formation of three disulfide bonds produces proinsulin, which is stored in secretory granules in pancreatic beta cells. When elevated blood glucose triggers insulin secretion, proinsulin is converted to active insulin by specific proteases, which cleave two peptide bonds to form the mature insulin molecule.

 * Insulin process from precursor

 * The effect of insulin is to favor the conversion of excess blood glucose to two storage forms: glycogen (in the liver and muscle), and triacylglycerol (in adipose tissue)

References
 * Elaine Marieb, Anatomy & Physiology 3rd Ed. McGraw Hill, 2007
 * Nelson, David L. and Cox, Micheal M. Lehninger Principles of Biochemistry, 4th Ed. New York: W. H. Freeman and Company, 2005.

Website #3
Strength training improves muscle quality and insulin sensitivity in Hispanic older adults with type 2 diabetes

http://www.medsci.org/v04p0019.htm

General overview

 * Type 2 diabetes is a chronic disease characterized by hyperglycemia and disturbances of carbohydrate,fat and protein metabolism. Diet, exercise and weight loss are cornerstones of diabetes management to improve glycemic control, reduce muscle wasting and mortality. Targeted interventions are needed to improve long-term diabetes control in high risk groups,like Hispanic older adults for whom diabetes and poor glycemic control are prevalent.
 * The inflammatory response is correlated with multiple metabolic markers of insulin resistance. We measured CRP, a systemic marker of low-grade systemic inflammation. It has recently been shown that ten months of aerobic exercise reduced CRP levels in elderly subjects and aerobic exercise training combined with a dietary intervention in diabetic men reduced their CRP levels. The decrease in CRP levels we observed in the present study suggests that the reduction in the inflammatory state of diabetes may be an important factor leading to improved insulin sensitivity and better metabolic control. Furthermore, since adiponectin has anti-inflammatory actions and we showed a significant increase in this adipokine, the reduction in inflammation may be related to this increase.
 * In conclusion, the findings of the present study suggest that 16 weeks of strength training results in improved muscle quality, skeletal muscle fiber hypertrophy, accompanied by concomitant changes in biochemical markers known that contribute to whole-body insulin sensitivity; namely, reduced HOMA-IR, increased adiponectin levels and decreased FFA and CRP levels. Further studies are needed to establish the mechanisms associated with these relationships. However, these data show that strength training is an exercise modality worth considering as an adjunct of standard of care for high risk populations with diabetes.

New terms
involved in insulin resistance and inflammation reduced risk of type 2 diabetes in healthy individuals
 * Type 2 diabetes: a chronic disease characterized by hyperglycemia and disturbances of carbohydrate, fat, and protein metabolism
 * Muscle quality: maximal force prodection per unit of muscle mass, better indicator of muscle function
 * Adipokines: soluble proteins released from adipocytes in response to metabolic signals and are
 * Adiponectin levels:decrease with increasing fat mass and higher levels of plasma adiponectin are independently associated with
 * CRP: carbon reactive protein
 * ST: strength training with standard care group
 * CON: control group standard care alone
 * FFA: free fatty acid
 * HOMA IR: metabolic control including insulin resistance (Homeostasis Model Assessment)

Grb14
Interactions between the Grb14 molecular adapter and the autophosphorylated insulin receptor (IR) have been identified. As an IR interacting partner, Grb14 has been identified in insulin sensitive tissues as a selective inhibitor for IR catalytic activity. Enhanced insulin signaling has been identified in adult male Grb14 knockout (KO) mice. However, researchers had been unsure if this phenotype was a result of compensatory action that occurred during growth development. Therefore, in order to determine the exact physiological role of Grb14, small interfering RNAs (siRNA) were used in primary cultured hepatocytes. Grb14 knock-down resulted in improvement of insulin signaling pathways. However, results from another RNA sequence indicated that these observations could not be a consequence of unspecific siRNA action. The resultant Grb14 depletion suggested that Grb14 activity had a second role, in addition to its function as an IR catalytic inhibitor. Experimental results indicated that, under acute modulation of its level of expression, the prevailing effect of Grb14 was more distal.

The assumed inhibitory role of Grb14 was supported by a sustained increase in Akt phosphorylation of Grb14-depleted hepatocytes. This was observed to be in direct response to insulin stimulation. Increased phosphorylation of Akt substrates resulted in an increase of downstream kinases, which accompanied the Grb14 insulin stimulation response. Grb14 knock-down has also been discovered to reduce the impact of insulin. Specifically, Grb14 has been observed to decrease the expression of SREBP-1c, Insig1, GK and FAS, in addition to inhibiting glycogen synthesis.

Link to article:

http://www.ncbi.nlm.nih.gov/pubmed/18339716?ordinalpos=157&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Synaptotagmin
Synaptotagmin-7 mutant mice have been proven to undergo a reduction in insulin secretion, which in turn results in higher glucose tolerance. The reduction of insulin secretion had been believed to be a result of a Ca2+ defect in insulin-containing granule exocytosis, because there had been no observed abnormalities in steps that lead to increased [Ca2+]I, or peripheral insulin sensitivity. These observations also supported the capacity of the synaptotagmin-7 calcium sensor as an insulin secretion regulator.

There have been a minimum of fifteen synaptotagmin isoforms identified in brain and peripheral tissues. However, synaptotagmin-1, -2, and -9 are the only established Ca2+ sensors for fast neurotransmitter release. Synaptotagmin-7 is one of the most proliferate Ca2+ sensors with different affinities, and has been proven to have an exceedingly higher Ca2+ affinity than synaptotagmin-1 and -2, in addition to having insulin secretion regulatory capabilities. When compared with a control, synaptotagmin-7 mutant mice had reduced insulin secretion and impaired glucose tolerance.

As a major anabolic hormone, insulin promotes lipid synthesis while inhibiting lipolysis. In support of this activity, lower plasma insulin levels in synaptotagmin-7 mutant mice were discovered to experience significant reductions of body fat content. Furthermore, exogenous insulin administration was proven to suppress plasma glucose more effectively in synaptotagmin-7 mutant mice than in the controls. It was speculated that, under usual conditions and with high insulin sensitivity, a low level of insulin would be sufficient to maintain blood glucose homeostasis.

It was discovered that synaptotagmin-7 mutant mice had lower insulin levels from birth. Research has indicated that liver insulin receptor mRNA regulation was increased, in these mice. This implied an adaptation to insulin sensitivity. Furthermore, glucose intolerance in the synaptotagmin-7 mice was believed to be a result of insulin secretion dysfunction in beta-cells, instead of peripheral insulin resistance.

Link to article:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18308938#id2619994

title: Metabolomics/Hormones/Insulin


text: Wikibooks:Requests for deletion/Ancient Civilizations 6


text: Wikibooks:Requests for deletion/Xetsa

title: Wikibooks:Requests for deletion/Xetsa


text: Wikibooks:Requests for deletion/Authoring Webpages


text: User talk:74.167.171.141

title: User talk:74.167.171.141


text: User talk:98.192.164.184

title: User talk:98.192.164.184


text:
User talk:209.232.145.1

{{mbox|type=serious|msg=Please help improve Wikibooks.

Recent edits you made have not been considered constructive by your fellow contributors. You have been previously warned about this. (Red4tribe (talk) 22:04, 20 May 2008 (UTC))

title: User talk:209.232.145.1


text: User talk:79.102.78.187

title: User talk:79.102.78.187


text: User talk:66.217.128.4

title: User talk:66.217.128.4


text:
C++ Programming/Code/Standard C Library/Functions/frexp

frexp
The function frexp is used to decompose num into two parts: a mantissa between 0.5 and 1 (returned by the function) and an exponent returned as exp. Scientific notation works like this:

 * Related topics: ldexp - modf


text:
C++ Programming/Code/Standard C Library/Functions/ldexp

ldexp
The ldexp function returns num * (2 ^ exp). And get this: if an overflow occurs, HUGE_VAL is returned.

 * Related topics: frexp - modf


text:
C++ Programming/Code/Standard C Library/Functions/modf

modf
The function modf splits num into its integer and fraction parts. It returns the fractional part and loads the integer part into i.

 * Related topics: frexp - ldexp


text:
User talk:64.231.251.27

If you have a real reason for deleting large amounts of material from a book (such as Accounting/Principle of Accounting, it is generally a good idea to explain your actions either in the edit summary or on that module's talk page. Otherwise, your edits are very likely to be rolled back. --Jomegat (talk) 00:55, 7 May 2008 (UTC)

title: User talk:64.231.251.27


text:
Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. Nc3/3...dxe4/4. Nxe4/4...Bf5/5. Bd3

= Caro-Kann Defence:Burris Gambit =

Accepting the gambit seems particularly risky for black, where White gets very good development and an open game.


text:
Chess Opening Theory/1. e4/1...c6/2. d4/2...d5/3. Nc3/3...dxe4/4. Nxe4/4...Bf5/5. Bd3/5...Qxd4

= Caro-Kann Defence:Burris Gambit accepted =


text:
User:Ryan52

Hi.

title: User:Ryan52


text: Talk:Video Game Design/Print version

title: Talk:Video Game Design/Print version


text: Talk:Video Game Design/Chapters/Getting Started


text: Talk:Video Game Design/Chapters/Getting Started/Print Version


text:
User:Robert Daeley

Robert Daeley is a writer and programmer in California. He can be found at Celsius1414.

title: User:Robert Daeley


text:
Parrot Virtual Machine/Licensing

Licensing
The text of this book is released under the following license:

Parrot, it's source code, and the tools required to build it are released under the terms of the Artistic License 2.0.

Compatibility with Artistic 2.0
Parrot and most of it's documentation library is released under the terms of the Artistic 2.0 license. For maximum compatibility, and for the ability to reuse content developed here on Wikibooks in other places in the Parrot ecosystem, some users have opted to have their contributions to this book explicitly dual-licensed GFDL and Artistic 2.0:

 * Whiteknight
 * Andrew Whitworth

Contributions to this book by users who are listed above may be reused under the Artistic 2.0 license where necessary. This is not a condition to editing this book, and edits made by users who have not listed themselves above are to be considered GFDL-only.

title: Parrot Virtual Machine/Licensing


text: User talk:75.4.28.17

title: User talk:75.4.28.17


text:
User:Derek Ross

See My home page

title: User:Derek Ross


title: File:Web1000.png


text:
Metabolomics/Hormones/Glucagon

Back to Previous Chapter: Metabolites Next chapter: Analytical Methods Go to: Somatostatin Go back to: Insulin

Glucagon is a peptide hormone that works in conjunction with insulin to maintain a stable blood glucose level. In situations of high blood glucose, or hyperglycemia, insulin takes over, stimulating the storage of excess blood glucose in the form of glycogen for later use. However, when blood glucose levels fall, it is the duty of glucagon to stimulate gluconeogenesis and glycogen breakdown, whereby replenishing glucose levels in the blood, and inhibit glycolysis. In doing so, glucagon plays a key role in regulating blood glucose levels, providing the fuel necessary for our cells to function even when our bodies are experiencing a low sugar or starved state.

=Discovery= Physiologists C.P. Kimball and John Murlin from the University of Rochester in Rochester, NY, published a paper in 1923 discussing their attempts to find an inexpensive method of concentrating insulin for medicinal use as well as begin experimenting on methods to isolate the pure substance. The paper explains their efforts to test a variety of inorganic and organic materials on rabbits and test pancreatic synthesis by measuring blood sugar. First observed in December 1922, addition of acetone would throw down an unknown substance that had a distinctly hyperglycemic effect. Purifying this substance and injecting it into a depancreatized dog raised its blood sugar, and the duo named the material glucagon (Kimball, 1923).

=Physiology=

Purpose
The objective of glucagon is to increase the amount of glucose in the blood for use by cells of the body. When there is a lack of glucose in the blood, the islets of langerhans on the pancreas are stimulated to create and release glucagon into the bloodstream. Once glucagon has been released, it travels through the bloodstream until it reaches the liver where it binds to specific glucagon binding sites. Although the liver is the main target of glucagon, receptors for this hormone have also been found in the kidney, intestinal smooth muscle, brain and adipose tissue as well as on insulin producing beta cells where it acts as a feedback mechanism to stimulate the creation of insulin. Because its effects on the liver are extremely important and well understood, however, this will be our main focus. Once bound, the glucagon activates adenylyl cyclase which is the first step in a cascade reaction which ultimately lowers the levels of fructose 2,6-bisphosphate. Fructose 2,6-bisphosphate is an important regulatory molecule in glycolysis/gluconeogenesis. At high levels, this molecule stimulates glycolysis by allosterically binding to phosphofructokinase-1, which increases its ability to function and so stimulates glycolysis. In this case, by lowering the concentration of fructose 2,6-bisphosphate the opposite occurs. Glycolysis is disengaged and gluconeogenesis is stimulated to help restore glucose levels in the body.

Another very important function of glucagon is its stimulation of glycogen breakdown. Activation of glycogen breakdown hinges on the same cascade reaction described in the previous paragraph. When glucagon binds to receptors in the liver it activates the adenylyl cyclase which increases cyclic AMP. The end result is an activation of glycogen phosphorylase which begins the glycogen breakdown process leading to increased blood sugar levels.

Function
Glucagon is an important regulatory hormone and is integral to our ability to properly regulate the amount of glucose in our bodies. Composed of 29 amino acids, the endocrine producing cells known as the Islets of Langerhans on the pancreas are responsible for the synthesis and excretion of this hormone. The specialized cells that produce this molecule are known as alpha cells but several others, including beta cells which produce glucagon's sister hormone insulin, are also located here.

Regulation
Although we know of several molecules other than glucose that are important in the regulation of glucagon, many of the exact mechanisms by which this is done are still not fully understood. For example, presence of the hormone insulin down regulates the production of glucagon by alpha cells but details of this process are still being worked out by researchers. Other molecules known to regulate glucagon include somatostatin and GLP-1. Because understanding such processes have the potential to further enhance our ability to treat metabolic diseases such as diabetes, much current research is being put towards understanding these mechanisms.

There are two conditions that are known to trigger glucagon secretion. The first is elevated blood levels of amino acids. Persistat after a protein-rich meal, glucagon is utilized to convert the excess amino acids to glucose by gluconeogenesis. Worth noting is that this is one of the rare situations where both insulin and glucagon are active, as high levels of amino acids in the blood stream triggers its release as well. The second condition of significant glucagon increase is during exercise, although at the time of the latest update(2002), it was unknown whether exercise was a stimulus or if the increased synthesis was due to the induced depletion of glucose.

Postabsorptive plasma glucose concentration has been discovered to be physiologically maintained within the range of 70 mg/dl [3.9 mmol/l] to 110 mg/dl [6.1 mmol/l] in humans. This is accomplished via increased glucose levels from glucagon and decreased glucose levels from insulin. However, there has not yet been any convincing evidence of the involvement of glucagon in postabsorptive plasma glucose concentration maintenance.

Combined deficiency of insulin and glucagon results in an initial drop in plasma glucose levels, but is followed by an increase in plasma glucose levels. This indicates that there is support of postabsorptive plasma glucose concentrations from glucagon, when in concert with insulin. Changes in plasma glucose concentrations also result from changes in glucose production but not from glucose utilization. Furthermore, during insulin and partial glucagon deficiency, and the exclusive partial deficiency glucagon, the rate of glucose appearance increases to a point greater than the rate of glucose disappearance. This rate increase seems to be even larger than during insulin and glucagon deficiency, as well as when glucagon is made exclusively deficient. Both scenarios result in much higher plasma glucose concentrations.

Increases in plasma glucose levels are ultimately followed by plateaus. These plateaus occur within a postabsorptive physiological range, and after octreotide-induced suppression of insulin and glucagon secretion. It has been determined that hormones and additional factors are involved in postabsorptive glucose level maintenance, after short periods of time. However, chronic insulin and glucagon deficiencies still remain victims of diabetes. Therefore, insulin has been proven to contribute to the maintenance of postabsorptive plasma glucose concentrations, while high levels of glucagon are not required to onset diabetes.

These findings do not distinguish the individual roles of insulin and of glucagon. However, chronic insulin and glucagon deficiencies have been proven to cause hyperglycemia and, therefore, strongly suggest that insulin is the predominant factor of postabsorptive glucose levels.

Link to article:

http://diabetes.diabetesjournals.org/cgi/content/full/56/10/2442#SEC3

Pathology
While there are many Americans affected by an inbalance of insulin (diabetes types I and II ), there are only very specific and very uncommon situations in which glucagon has been shown to cause disease in humans.

Excessive glucagon secretion
Diseases associated with excessively high or low secretion of glucagon are bad. Cancers of alpha cells (glucagonomas) are one situation known to cause excessive glucagon secretion. These tumors typically lead to a wasting syndrome and, interestingly, rash and other skin lesions.

Hyperglycemia
Hyper glycemia occurs when blood glucose levels are too high, usually over 11 mmol/L, and occurs most often an hour or so after a large meal, especially one heavily laced with sugars. Hyperglycaemia occurs when there is too little insulin in the blood, or in the rare situation of an overabundance of glucagon. Thanks to fairly dependable regulation of glucagon, our body typically prevents an overabundance of glucagon when it senses high blood glucose levels.

=Resources=

1. glucagon.com

This website can be located at:  http://www.glucagon.com/index.html

This webpage was a very useful and informative description of not only the hormone glucagon but of all relating molecules, pathways, regulators, and diseases associated with the molecule. It contains effective descriptions of all information known about glucagon and related molecules up to this point in time. Because this topic has so much research dedicated to it, the site also provides useful links to primary articles most of which demonstrate the most recent discoveries linked to glucagon and related pathways.

Proglucagon - Precursor of glucagon which is also secreted by alpha cells of the islets of Langerhans.

Prohormone - A molecule produced as a precursor to the actual hormone.

Hyperplasia - The overproduction of cells within an organ or tissue.

Exocytotic - The process by which a cell excretes vesicles containing the desired molecule or protein.

Polymorphism - Multiple alleles of a gene within a population.

The information found on this website is extremely relevant to topics learned in class. It fully explains factors involved in the regulation of blood glucose levels which we studied in detail in chapter 15 this quarter. It goes beyond just the functions of insulin and glucagon, however, and describes other mechanisms and molecules which are or are thought to be involved in this important metabolic process.

2. Relationship of Glucagon Suppression by Insulin and Somatostatin to the Ambient Glucose Concentration

This journal can be found in full text for free at:  http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=423975&blobtype=pdf

The main point of this article was to determine the amount of glucagon suppression exhibited by the molecules insulin and somatostatin. Although both are known to regulate this hormone, the exact effects they have on glucagon regulation are not yet confirmed.

Hyperglucagonemia - Abnormally high levels of glucagon in the blood.

Phloridzin - A dihydrochalcone occurring in many parts of the apple tree which is used experimentally to produce glycosuria in animals.

Glycosuria - An abnormal condition of osmotic diuresis due to excretion of glucose by the kidneys.

Diuresis - The increased production of urine by the kidney.

Normoglycemic - The presence of normal concentrations of glucose in the blood.

This is an important and relevant article because it delves further into the mechanisms used by the body to keep levels of glucagon regulated. This study is also important to further understand how to control diabetes and other abnormalities in this metabolic pathway.

3. Aquaeous Extracts of Pancreas

This journal can be found in full text for free at: http://www.jbc.org/cgi/reprint/58/1/337

As mentioned above in the Discovery section, this paper was the first to identify and name the compound glucagon, making it very relevant to this article, as well as our text. At the time of publication, 1923, the researchers were looking to synthesize insulin for medical purposes, by adding various compounds to the pancreas. The subjects involved were rabbits and dogs, and the paper hints at the difficulty of science publication during the era. Because the paper uses terminology from almost a century ago and the paper's main focus was on insulin, not glucagon, it seems only right to include only the terms that would appear relevant to this wikibook entry.

glucagon - a substance that exhibits a highly hyperglycemic effect. When given to a depancreatized dog by subcutaneous injection, blood sugar was reported to rise significantly in 3 hours.

4. Colorado State Hypertexts of Biomedical Sciences

This website can be found at: http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/glucagon.html

In an effort similar to this wikibook, Colorado State University created an online textbook pertaining to the Endocrine Pancreas in 2000. Focusing on the page that deals with glucagon, this article lists many new definitions that pertain to biochemistry and enhance the reading. If the images were available, the source offers several simple but effective images and diagrams that show the pathway and function of not only glucagon but insulin as well. Information from this source is used in several locations within the 'Physiology' section of this article.

Secretin - a hormone that is structurally similar to glucagon, secretin is released in response to acid in the small intestine and stimulates the pancreas and bile ducts to release a flood of bicarbonate base, which neutralizes the acid.

Enteroglucagon - the precursor of glucagon, the proglucagon gene, can also expressed in the terminal small intestine and large intestine, where it is cleaved into a number of peptides other than glucagon. Also known as enteroglucagon or glucagon-like peptides, this alternative pathway for processing of proglucagon occurs in gut endocrinocytes called L cells.

Hypoglycemia - in Greek the term literally means "under-sweet blood", hypoglycemia is the term for lower than normal blood glucose levels. Treatment is typically oral or inject glucose.

Hyperglycemia -"over sweetened blood", the polar opposite of hypoglycemia, this is the term for higher than normal blood glucose levels, and is typically treated with additional insulin. And as mentioned in the wikibook entry, this is the more likely scenario to be created by an irregular level of glucagon, that is, too much in the blood.

Somatostatin - Metabolomics/Hormones/Somatostatin is another hormone discussed in this Wikibook, but does play some role with glucagon, in which somatostatin is known to inhibit glucagon when it prevents all pancreatic hormones from being distributed in an effort to regulate the endocrine system,

Glucagonoma - Cancer of α-cells of the pancreas, which has been known to cause excessive glucagon secretion.

title: Metabolomics/Hormones/Glucagon


text:
Trainz/AM&C/Removing Unwanted Assets

Beginner Steps in Trainz
For those new to Trainz, a typical starting point involves selecting an existing route and beginning to modify it. This method is not only highly recommended but also utilized in our tutorials. It serves as an effective way for beginners to learn about terrain matching, coloring, and modifying routes. Often, new users start by choosing a route with an appealing name, only to find it underwhelming yet full of potential. This process is vital for gaining experience and understanding the nuances of route modification.

Route Upgrading and Exploration
A key phase in the Trainz journey is upgrading older, less interactive routes into dynamic, engaging environments. This involves adding functional passenger stations, industries that interact with products, and creating portals. Such enhancements are crucial for understanding the capabilities of your Trainz installation and serve as an introduction to exploring the Content Manager (CM) and the Download Station (DLS). The goal is often to transform older routes from mere visual attractions into fully interactive and enjoyable experiences. This section aims to guide users through this process intelligently, avoiding common pitfalls.

Thinking Like a Programmer in Trainz
It's important in Trainz to adopt a mindset similar to that of a programmer: be cautious and always plan for the possibility of reverting changes. Before implementing major additions or radical changes, it is advisable to save the route. Cloning the route for significant modifications is considered a best practice, enabling users to experiment while preserving the original state of their work. This approach helps in advancing with new insights and avoids repeating past mistakes.

How to Manage Unwanted Assets
When you're new to Trainz and start modifying routes, you might end up with too many assets from the Download Station (DLS). You may not need all these extra items at first. But as you get more experience, you'll learn which ones are useful for your projects. Here, we'll talk about ways to handle these extra assets without having to delete them.

Often, when you download a route from the DLS, it comes with many other assets. These are called dependencies. At first, this might seem overwhelming, but these routes can actually have some really good stuff in them. Sometimes, you might not want to use certain assets, like catenary wiring or trolley-style rail lines. Here's what you can do instead of deleting them:

1. Disable Unused Assets: In the Content Manager (CM), you can choose assets you don't want and disable them. This means they won't show up in Surveyor anymore. To do this, select the asset and use the right mouse button. You can manage many assets at once or select them one by one. If you're managing a lot of assets, it's easier to work with a few at a time. You can use keyboard shortcuts like CTRL and SHIFT with your mouse to make selecting easier.

2. Archive Assets: Another option is to archive assets. This is like putting them in storage. You do this the same way as disabling, but instead, you're moving them to a special folder. They won't appear in Surveyor, but they're still there if you need them later. When you archive assets, remember where you put them. You can't move the folder later, but the assets are still usable for driving sessions or other routes.

3. Uncluttering Surveyor: Both disabling and archiving help make Surveyor less crowded. This lets you focus on the assets that are really useful for your current project. These methods don't hide the assets in the Content Manager, so you can still find them if you need to. In the Content Manager, you can set up filters to show or hide certain assets. This way, you have control over what you see.

With large hard drives being common now, you might not need to delete assets often. But if you decide to delete, especially if you want to improve a route you're not happy with, this page has tips to help you do that. Remember, managing assets well can make your Trainz experience more enjoyable and less cluttered.

Backing up, in case
As a safety precaution, you may wish to backup assets that you have created and/or downloaded before removing any of them. Do as you will with routes, but good scenery assets, trackside signals and boxes, and different track and bridge types make the rounds to many a route, so you may need such assets again for some other route. />  to  or   to  )
 * 1) The obvious method for that is to export them to CDP, so you need to scheme out a naming and tracking system for yourself, if nothing else, cut and paste kuids into a text file listing the cdp contents using the same name and folder.
 * 2)  — Capture that 'name' before saving the first file (recommend the text file first— when you save as,  to the extension selection line, then  to back-TAB to the Save As title line, this will then be fully highlighted,  to copy the name for the cdp file operation.)
 * 3) If CDPing a single asset, one 'Good Practice is to systematically append the KUID as part of the title in a standard never-varying method (to aid searching).  format syntax  . That's a valid format for base initial KUID codes expressed in Windows compatible file notations— and it allows you to search for just the   when needing something.
 * 4) If you sort your List after applying selection criteria filters by KUID (: Click on the column header, it will sort to that column)
 * 5) This dual save by same name gives you a Near Instant way to find them, going forwar. Many text search utilities (including the built-in Notepad++  ability) can see into many files to Search (Find) a kuid then. Details on how-to see into files is covered elsewhere, but being systematic and organized about the prospect will speed success in finding them later.
 * 6) For another method, this one giving you a stash of things you can examine at your leisure to see how content is put together:
 * 7) Open them for edit, Run PEV-tools from a batch file in the folder,
 * 8) Copy them all to another temporary directory,
 * 9) edit their kuid to a Kuid2 suffixed ':+1', pseudo-improvement. (for example:<br
 * 1) re-import the 'pseudo-fixed' asset to verify it is all in that folder (Textures, meshes in particular might be missing)
 * 2) recommit both of them (Note: Trainz will have made a new local folder in ..\editing when you import the changed one, so best to also change the asset name when promoting the kuid and/or version. I suffix a '-a' meaning adjusted, and can search THAT in CM→Names search to find all non-stock assets immediately.)
 * 3) afterwards, copy or move the error tested one in the temp folder (That can just be dragged into your archive directory once you know it's gestalt--next step), then after committing the +1-kuid test version and the original, delete both of them.
 * 4) Recommitting before deleting is in some cases an necessary step, so form the habit and make it a 'good practice' of yours from the start.
 * 5) If successful, move the folder to the 'manually managed' archive directory you manage without Trainz knowledge, freeing up the temp folder for 2-3 new assets to pillage.
 * 6) Trainz will promptly forget they were around, especially after quitting out and reloading it, which is recommended every couple hours as a good practice.

Pruning Routes and Sessions
Layouts that you have created yourself can be deleted in Surveyor Main Menu where the Table of Contents of Routes, Sessions and Scenarios is displayed.
 * This section also covers a process to try and move a session onto a newer version of the layout.
 * 1) First delete any related sessions, for if kept, their referencing the Route asset KUID as a dependency, so will create a  or a problem to be dealt with by deleting in CM.
 * 2) The second option has two forks, start by doing a author name search for yourself, this can be your Trainz Kuid pre-fix preceded by the  key: '#497853' for example. Refine that if you wish by filtering for just Routes and Sessions.
 * 3) Now with your target(s) in sight you have a choice, providing you have done as many of us do routinely and saved major change versions with a suffixed version number (Mod XXX, or V15-7) AND you want to try to put some of those old sessions on the new version, before deleting the route, Hand Edit the Session Config.txt for the Route and change it's KUIDs by searching for the old route, and replacing each place the kuid appears. In pre-2009-SP4, their will be one in the body near the English  data or above the English, and if later versions hold true, as the last item in the  container.
 * 4) This gives you better than even chances the old session will work on the new route. It's a crap shoot if you have positioned train consists somewhere where you have adjusted track heights and/or moved the track a bit.
 * 5) One reason to hang onto that old Route until testing is it can possibly be recovered by moving back to the old kuids (Reverse the above), Edit the old route & Session, relocate the cars missing the tracks to a place you didn't molest, then repeat starting above. Loop a couple of times through such attempts before giving up.
 * 6) If the consist has just been a little off it's 3D co-ordinates, using the  tool can allow you to grab the engine or cars from the minimap. Best to rotate the camera straight down, do a  (Find) on one of the cars, then without moving the mouse try to grab and move it. If successful, the entire consist will move too, per normal, and you will see it snaps to the track at the new height. All is well... if you can grab them. If not, delete the session and forget it.
 * 7) Did you record the session rules settings as you went on a card-file or spreadsheet? If you did a thorough job documenting it (Easiest way to write a complicated session) you can just refer to that and re-enter it.
 * 8) In all the CM versions, all assets can be deleted from inside the Content Manager screen. Once you've done so, it's gone. Hopefully to bit heaven. Other older Trainz are more basic. TRS2004 and earlier Trainz assets can be removed by manually deleting their kuid folder in Windows Explorer. Alternatively, for this older generation, TrainzObjectz can be used to delete unwanted assets.

TRS2006
(The following information is kindly supplied by ColPrice2002)

Routes that have been created by you can be deleted in Surveyor.

Also you can delete any asset that is not built-in with CMP.

To delete a layout and its dependencies:

Open CMP, search form "Location = Local" + "Category = Routes" and select the layout to be deleted.

Right-click and select "show dependencies" from the menu. This lists the dependencies in a pop-up window.

Now click the "view in main screen" button, and all of the dependencies are listed. Press CTRL/A (or use the Select All menu option), then "Delete" to actually delete the assets.

Then return to the CMP list of layouts, select the relevant layout and delete that.

You will receive error messages if you try to delete built-in content and these can be ignored.

The only problem is that you may delete a dependency that's used by another route. You won't find out until you look at all the routes you have installed and look for the missing dependency flag (or try to load the route).

One way of reducing the impact is to archive the route and its dependencies (create a new archive for deleted routes). Carry on as before - deleting everything - if you need a deleted asset CMP will pull it from the archive. Once you're happy that the archive isn't needed you can delete it - this saves you re-downloading.

title: Trainz/AM&C/Removing Unwanted Assets


text:
Talk:IB Computer Science/Further System Fundamentals

Mistake
Navid: Who can correct the typo, it is Fundamental not Fundemental! I corrected this on the main page of the book, but do not know how to change it in here... I think to correct the typo we should make a whole new page and move everything... So never mind.

Voting on DMA
Josh: I think the first definition is the more clear and understandable one.


text:
Talk:False Friends of the Slavist/Map chrvn

Untitled
in polish there is also word "czerwień" pronounciated [červěŋ] (or somehow in IPA) meaning "redness"

In Czech language there's also word "červen" which means "June".--Kovtun (talk) 22:38, 26 January 2009 (UTC)

In Ukrainian there is also word "червінь" wich means: 1. "redness", "red paint", 2. blush. See: http://sum.in.ua/s/chervinj


text:
Computers & Society/Social Web/Global village

We begin with a short text: "The new electronic interdependence recreates the world in the image of a global village." The quotation is from Marshall McLuhan's Gutenberg Galaxy (1962), p. 31. This "global village" is like living "in a single constricted space resonant resonant with tribal drums."

Such a concept of tribal drums brings to mind almost immediately the Indian tribal traditions of North America.

Drums are like bells.

They call to meeting.

They call to prayer.

They call to war.

Without their sound...

...there is no community at all.

Let us imagine that the concept of global village used by Marshall McLuhan in his Gutenberg Galaxy is wrong! What could we possibly mean by this?

And what about the earlier use of the global village by Wyndham Lewis?

Instead of us giving the answer here we invite you to find it for yourself. How would you do that? It seems obvious that you will search using something like "global village" + "Wyndham Lewis"? Try it out!

On a google search there are around 811 hits {2008-05-08}.

Now the challenge is find the text in which it appears.

=the medium is the MASSAGE= Later on (1967) in his book "The Medium is the Massage — An inventory of effects" with Quentin Fiore and produced by Jerome Agel, Gingko Press, "We now live in a global village...a simultaneous happening. We are back in acoustic space." p. 63.

And for good measure, a picture of some of the tribe in action is shown p. 66-67. This is a photo by N. R. Farbman, for Time, Inc.

=The Village= So! How many people here reading this stuff come from a village? Hands up!

Ha! I thought as much! No-one!

Walled Gardens
Although the Internet offers global communications, it is still heavily divided by the varieties of language. For example, "Far Eastern" countries have sites in Korean/Chinese/Japanese, which are unreadable and therefore inaccessible to those who don't know the language. Furthermore there are sites on the site that actively block users from that don't have a 'correct' address. As addresses are typically doled out to ISP who tend to have a strong regional presence this creates essentially walled gardens.

Global Village pump
The concept of the Internet as "Global Village" might be considered erroneous, because communication via electronic means is not entirely analogous to that of real-life interpersonal communication. The methods of communication via electronic means such as Internet fora, IRC, instant messaging etc. (excluding video conferencing) remove the somatic component from conversation. It is believed that the content of language in conversation accounts for merely 30% of global communication — the remaining 70% is due to body language and tone. The removal of these vital components from the act of communication do not lend themselves to real, meaningful conversation. Also, the extreme cultural and linguistic diversity of the Internet does not correspond well with the definition of a Village, obtained from Wikipedia: This would imply that the nodes of communication on the Internet are fixed and unchanging. However it is a widely regarded fact that web sites and links are mostly transient; Indeed, using the Internet as a reference in academia is often frowned upon for this very reason. Perhaps the concept of a "Global Village Pump", à la Wikipedia is more semantically accurate.
 * "Villages are normally permanent, with fixed dwellings;"

The view from India
Mohandas Gandi declared that "The soul of India lives in its villages". What this implies is that villages themselves have their own character and ambience. However, the Internet as a whole does not conform to this idea; In fact, the chimeric nature of the Internet makes this nearly impossible, as the depth of complexity could never permit such a declaration.