No Degree Required

[mvanwink5]

The new understanding is that the brain controls blood sugar through the liver with leptin.

[williatw]

The new understanding is that the brain controls blood sugar through the liver with leptin.

Found this:

Microbiota associated with type 2 diabetes and its related complications

Abstract

Recently, it has been established that the human resident microbiota plays key roles in health maintenance. Therefore, it has become an emerging prevention and treatment target for metabolic syndrome. The resident microbiota associated with chronic inflammation has been shown to contribute to the onset of type 2 diabetes mellitus (T2DM). Moreover, the microbiota is altered in the development of T2DM and its comorbid medical conditions/diseases, including diabetic retinopathy, kidney toxicity, atherosclerosis, hypertension, diabetic foot ulcers, cycstic fibrosis and Alzheimer's disease. Besides, some anti-T2DM regimens are also based microbiota metabolism-dependent mechanism. This review summarizes the current knowledge concerning the altered microbiota in the pathogenesis of T2DM and its related complications, which provides novel insights into these diseases and the potential intervention strategies from the microbiology point of view.

1.1. Gut microbiota in the pathogensis of type 2 diabetes

It is well established that the gut microbiota is involved in the process of energy harvest accounting for the development of obesity [2]. Some researches support the view that the gut microbiota is essential for the host immunity development [3]. As one of the most concerned obesity-related disorders, T2DM is associated with abnormal energy metabolism and low-level chronic inflammation in fat tissues [4] and [5]. Some hypotheses have proposed its relation with the presence of gut microbiota.

Principally, the gut microbiota plays an important role in the progression of prediabetes conditions, such as insulin resistance. Growing evidence in clinical studies suggested that obese people with insulin resistance were characterized by an altered composition of gut microbiota, particularly an elevated Firmicutes/Bacteroidetes ratio compared with healthy people [6] and [7]. Furthermore, transplantation of the obese gut microbiota in animals greatly affected the energy harvest of hosts [7]. Consequently, it is proposed that altered microbiota in obesity modulates intestinal permeability and increases metabolic endotoxin secretion that lead to chronic low-level inflammation, the pathogensis of insulin resistance and onset of T2DM. [8] and [9]. Recently, commensal bacterial species, such as Bacteroidetes thetaiotaomicron, Akkermansia muciniphila and Escherichia coli, were showed to have different influence on the intestinal mucus and glycocalyx layer, which may affect intestinal permeability [10]. Besides, microbiota-dependent changes in gut tight-junction proteins, endocannabinoid system and intestinal alkaline phosphatase activity may be also involved in altered intestinal permeability and the pathogensis of insulin resistance [9].

Moreover, the vicious circle between altered microbiota and the triggered low-level inflammation has also been considered as a deterioration factor in the development of T2DM. Accumulating evidence has revealed that T2DM patients exhibited an altered intestinal microbiota which was characterized by a decrease of Bacteroidetes/Firmicutes ratio and some functional bacteria (e.g. Bifidobacteria) with an increase of various opportunistic pathogens and some endotoxins-producing Gram-negative bacteria [11], [12] and [13]. Firstly, Bacteroidetes/Firmicutes alteration may modify the host energy metabolism through a specific polysaccharide utilization loci mechanism [14]. Moreover, the accumulation of gut-derived bacterial inflammatory molecules (e.g. LPS, peptidoglycans and flagellin) in intestine is thought to accelerate the inflammation in T2DM [15] and [16]. Besides, gastric bypass surgery, an effective way to normalize the blood glucose level to treat T2DM, could reduce body weight due to the alteration of the microbiome at the distal gut [17].

It has been confirmed that some probiotic strains are able to modulate blood glucose homeostasis, and hence improve T2DM [18]. Several mechanisms have been proposed. Firstly, probiotic could acted as an effective immune system modulator against altered-microbiota induced chronic inflammation. It is well-established that obesity induced chronic low-level inflammation is a leading cause of the progression of T2D [19], [20] and [21]. Some probiotics have been confirmed to prevent onset of diabetes through down-regulating inflammatory IFN-γ and IL-2 or IL-1β or enhancing anti-inflammatory IL-10 production in diabetic animal studies [22], [23] and [24]. Recently, Lactobacillus reuteri GMNL-263 have been demonstrated to suppress serum glucose, insulin, leptin, C-peptide, glycated hemoglobin, GLP-1 level, inflammatory IL-6 and TNF-α in adipose tissues and PPAR-γ and GLUT4 gene expression in high fructose-fed rats [25]. Furthermore, human studies have revealed that probiotic yoghurt consumption could reduce hs-CRP level and improve HOMA-IR score in pregnancy which is also considered as metabolic syndrome [26] and [27]. In addition, some probiotic strains show favorable antioxidative effect which is one of the effects against chronic inflammation. They are apparently able to alleviate pancreatic oxidative stress which can lead to chronic inflammation and apoptosis of pancreatic β-cells [28] and [29].

Moreover, the supplementation of certain probiotic strains can potentially modulate the lipid metabolism and result in the reduction of the serum total cholesterol level and LDL-cholesterol, which will reduce the risk of T2DM [30]. Besides, endotoxemia has been identified as a triggering factor of insulin resistance in mice, making the suppression of endotoxemia by probiotic another potential protective mechanism [9]. An oral administration of Lactobacillus casei Shirota, was able to enhance the expression of plasma lipopolysaccharide-binding protein (LBP) and consequently reduce endotoxemia in murine models of obesity and T2DM [31]. In another study, the consumption of the probiotic strain, Bifidobacterium animalis subsp. lactis 420, suppressed the bacterial translocation process from intestine to tissues, which might lead to metabolic bacteremia in the early onset of T2DM [32]. From the perspective of nutrition, a novel probiotic strain, L. casei Zhang, was recently proven to exhibit osteocalcin-elevating effect leading to improvement of oral glucose tolerance in impaired glucose tolerance (IGT) rats. This was probably achieved via gut Bacteroides fragilis enriched vitamin K2 mechanism [33].

2. Microbiota and T2DM complications

2.1. Diabetic retinopathy

Diabetic retinopathy accounts for more than 60% incidence in T2DM [34]. As expected, a higher frequency of Gram-positive bacteria and a higher proportion of coagulase negative staphylococci was detected in diabetic patients, especially those with retinopathy [35] and [36]. This result was supported by Bilen et al., who found that Staphylococcus epidermidis and Staphylococcus aureus were the predominant conjunctival organisms in T2DM patients, and the frequency of S. aureus isolated from the patients’ eyes were higher than that of T1DM and healthy subjects [37]. Parkinson's disease is also one of complications with chronic diabetic neuropathy in T2DM [38]. Kusbeci et al. observed that the occurence of S. aureus was significantly higher in the conjunctival flora of Parkinson's patients than in healthy controls [39].

2.2. Renal toxicity and kidney stones

A high proportion of T2DM patients also suffer from clinical condition of chronic kidney toxicity, such as kidney stones. This is probably due to the disruption of colonic epithelial permeability which was implicated in the pathogenesis of T2DM and chronic kidney toxicity [40]. By phylogenetic microarray analysis, chronic kidney disease patients showed significant changes in 190 microbial operational taxonomic units (OTUs), particularly the high abundance of the Enterobacteriaceae compared to the healthy control group [40].



Moreover, Zheng et al. recently demonstrated that the bioconversion of melamine by gut microbiota, particularly Klebsiella, was essential for renal toxicity and the formation of crystal stones [41]. Oxalobacter formigenes, a commensal gut microbe, has been shown to improve the clinical condition of kidney stone patients [42]. However, commonly available probiotics, including Lactobacillus and Bifidobacterium species, were insufficient in degrading oxalate to treat kidney stones [43] and [44]. Besides, the extent of calcium oxalate stone formation may be dependent on the microbiota. This is evidenced by the low expression level of vitamin K epoxide reductase complex subunit 1 (VKORC1) in patients with calcium oxalate urolithiasis. The expression of VKORC1 could be influenced by vitamin K2 producing gut bacteria [45] and [46].

2.3. Hypertension

Hypertension and T2DM are closely related to each other in clinical setting. Apart from being a complication to T2DM, it is also a major risk factor for cardiovascular disease and a symptom of metabolic syndrome. Recent evidence suggests that metabolic syndrome is partially regulated by the gut microbiota [6]. However, only very little is known about the role of the host gut microbiota in the case of hypertension. One experimental finding supporting the hypothesis of blood pressure regulation by the gut microbiota was provided by Pluznick et al. using a mouse model. Propionate is one of the end-products derived from the gut microbiota. It was revealed that, in response to propionate, the expression of renal olfactory receptor 78 (Olfr78) was increased, in turn mediating the secretion of rennin [47]. Consequently, the blood pressure was elevated. On the contrary, G protein-coupled receptor (GPR41), a short-chain fatty acid receptor, negatively regulated the blood pressure. Hence, it was concluded that these gut microbiota-derived short-chain fatty acids, in particular propionate, participated in the blood pressure regulation process via both receptors.

Furthermore, it has been reported that Lactobacillus johnsonii La1 ingestion could not only maintained low blood glucose level in streptozotocin (STZ)-induced diabetic rats, but also prevent rats from elevated blood pressure by reducing the renal sympathetic nerve activity and enhancing the parasympathetic nerve activity through the sympathoadrenal axis [48] and [49].

2.4. Atherosclerosis

Most T2DM patients tend to have higher levels of serum lipids, which predisposes them to atherosclerosis. Associations between microbiota and atherosclerosis have been proposed. Koren et al. analyzed the oral, gut and atherosclerotic plaque microbiota in atherosclerotic patients [50]. Good correlation was found between total abundances of Veillonella and Streptococcus in the oral cavity and the atherosclerotic plaque. Moreover, several oral and intestinal bacterial taxa, including Streptococcus, Neisseria and Fusobacterium, are correlated with the plasma cholesterol levels.

It is well established that probiotics with bile salt hydrolase activity could accelerate the bioconversion of cholesterol to primary bile, showing acids a serum lipids-reducing effect [30]. Moroti et al. reported that the administration of a synbiotic beverage called shake, which contained Lactobacillus acidophilus, Bifidobacterium bifidum and oligofructose, markedly increased the plasma HDL cholesterol and decreased the condition of fasting glycemia in elderly T2DM patients [51].

2.5. Cystic fibrosis

Patients with cystic fibrosis (CF) are also associated with high incidence of T2DM [52]. There is increasing evidence that an altered microbiota in CF respiratory tract plays an important role in its pathogenesis. The most commonly isolated bacterial species in airways of CF patients were Haemophilus influenzae, S. aureus, Pseudomonas aeruginosa and Burkholderia cepacia complex species [53]. Nowadays, high-throughput sequencing methods, such as 16S amplicon pyrosequencing, were applied to evaluate the whole composition of the airway microbiota. Goddard et al. found that CF lungs were typically dominated by only one to three species by direct sampling of explanted lungs [54]. They also observed that the microflora in the sputum and throat specimens could not represent the typical CF microflora.

A recent study monitoring the development of gut and respiratory microbiomes in CF infancy revealed that both compartments shared some common core microbes and the temporal fluctuation of microbiota over time was in concordance with each other. Moreover, a change in diet resulted in the alteration in the airway microbiota composition [55]. These together suggest that diet, gut microflora and the development of the respiratory tract microbiota are linked with one another. Because of this link, it is logical to hypothesize that the oral administration of probiotics may reduce symptoms caused by CF. At least two individual studies confirmed the probiotic effects of Lactobacillus GG in alleviating the intestinal inflammation and pulmonary exacerbations rate in CF patients [56] and [57]. Another common symptom of CF children is the malabsorption of bile acids. Roy et al. showed that antibiotic treatment reversed this condition, which was due to the reduction of gut anaerobes and their related enzymatic activities, such as bile salt hydrolase (BSH) [58]. Gut bile salt hydrolases deconjugate glycine or taurine from bile salts. The deconjugated bile salts are more efficient in lipid emulsification and absorption in the gut. Hence, the application of BSH-bearing probiotics may be another potential treatment for CF patients.

2.6. Diabetic foot ulcers

Diabetic foot ulcers leading to infection and limb loss are both linked to an increasing risk of age-related diabetes. Several well-explored microorganisms, including Staphylococcus species, P. aeruginosa and E. coli, etc., were isolated from patients with infected diabetic foot ulcers [59]. The main plantar foot normal flora are coagulase-negative Staphylococcus species, which are recognized as strong competitors for the infection-associated S. aureus. Recently, Redel et al. found that the ratio of non-pathogenic Staphylococcus to pathogenic S. aureus on the feet of diabetic men was lower, compared to the normal subjects [60]. By bacterial 16S rRNA gene pyrosequencing, Gardner et al. analyzed the microbiomes in diabetic foot ulcers and revealed that the ulcer depth and duration were negatively correlated with the abundance of Staphylococcus, whereas the ulcer duration was positively correlated with that of Proteobacteria [61].

2.7. Alzheimer's disease

T2DM may result in an increase in risk in Alzheimer's disease (AD) and these may share common pathogenic mechanisms [62] and [63]. Vignini et al. summarized the recent experimental evidence and potential mechanisms that link the two medical conditions, including the possible roles of insulin deficiency or insulin resistance in facilitating cerebral β-amyloidogenesis, which accounts for the increased risk of diabetes patients to dementia [64]. In addition, AD had even been considered as the type 3 diabetes [65].

Currently, little data is available on the resident microflora of AD patients, thus how they are related to each other remains poorly understood. To date, only one study has directly compared the gut physiology and microbiota structure between wild type and AD transgenic mice. The gut alteration in AD transgenic mice was characterized by an increase of Gram-negative bacteria accompanied by mucosal disruption [66]. Moreover, the amyloid precursor protein (APP) expression level was significantly upregulated in the intestine of AD, but not in the control mice.

Even though the research area of the gut microbiota in AD is understudied, the possibility of preventing from or treating AD via enteria bacteria has been considered. Indole propionic acids (IPAs) are putative drugs for treating AD and T2DM [67] and [68]. The plasma amino acid metabolites, including the bioactive indole-containing metabolites, of germ-free mice were significantly affected as compared to the normal mice. Moreover, the bioconversion of indole to indole-3-propionic acid was found to be solely dependent on the gut microbiota [69]. Therefore, manipulations of gut microbiota seem to be a key to restore the plasma IPA level. Another metabolic characteristic of AD was the loss of GABA(A) receptors in the hippocampus of the brain [70]. The probiotic strain L. rhamnosus JB-1, an effective modulator of the gut microbiota, was proved to be able to increase GABA(Aα2) in the hippocampus of mice [71]. These are direct evidence showing the interaction between the residence flora and the host metabolism, which offers novel potential prophylaxis or treatment targets for AD.

3. Anti-T2D regimens concerning microbiota

In recent years, due to side-effects of anti-T2D drugs for glucose or insulin resistance control (e.g. metformin and pioglitazone) and anti-inflammatory drugs for T2D complications (e.g. NSAIDs), natural anti-T2D compounds extracted from plants potentially with less side effects have drawn more attention [4] and [72]. Particularly, these drugs with GI and cardiovascular side effects brought high risks for long-term use [73]. Berberine, a component from traditional Chinese herb Coptis chinensis, has been recently demonstrated to have anti-diabetic effect through modulating microbiota composition since it is mainly absorbed by gut [74]. The major bioactive constituents of Ginsing, another important anti-diabetic Chinese herb, were mainly from microbiota-mediated metabolism of ginsenosides [75]. Inhibition of intestinal α-glucosidase is another strategy to control the increase in blood glucose at early onset of T2D [76]. However, drugs for this target may lead to GI side effects [77]. A great deal of polyphenols, a series of natural compounds from tea, coffee, wine, fruit, vegetables, and chocolate, can inhibit glucose metabolism enzymes to exert anti-diabetic effect with no side effect [78] and [79]. Typically, wine polyphenols have been confirmed to significantly modulate some taxa of gut microbiota and reduce serum lipids and inflammatory C-reactive protein in humans [80]. Moreover, the microbiota is also important for the metabolism of polyphenols (e.g. catechin and gallocatechin from green tea) promoting their bioavailability in the small intestine [81].

4. Conclusion

In summary, great progress has been made in the field of the resident microbiota in T2DM in recent years. Microbiota contributes not only to low-level inflammation in the onset of T2D, but also to the further development of T2D through inflammatory components. It has also been extended to various T2DM related complications, including diabetic retinopathy, kidney toxicity, atherosclerosis, hypertension, diabetic foot ulcers, cycstic fibrosis and Alzheimer's disease. These studies together support the crucial role of microbiota in maintaining the intestinal barrier integrity, sustaining a normal metabolic homeostasis, protecting the host from infection by pathogens, enhancing host defense system and even influencing the nervous system in T2DM. Microbiota-mediated mechanism is also involved in some anti-T2D regimens using natural compounds from plants. However, the potential mechanisms linking the microbiota to T2DM have not been fully elucidated and continuing research efforts are needed.

Anything that outnumbers the cells in our bodies by 10-100 to one probably has a profound affect on many aspects of our health, hard to see how it wouldn't; they must be doing something inside our bodies.

http://www.sciencedirect.com/science/ar ... 3013000451

[mvanwink5]

Another issue is how these nasties evade the innate immune system, combined with the ability to pass capabilities from one bacteria type to another very different type via plasmid transfer.

The understanding of the human Microbiota, what it is doing, and its relation to chronic disease is not even on the medical profession's radar. 'Autoimmune' disease was terminology that came from the ancient era before the dawning of the human Microbiome, and it will be 50 years before that changes thanks to its protective monopoly.

Like a handyman that sees doors sticking, windows sticking, toilet leaking, roof sagging, etc as the house has 'door' disease, 'window' disease, 'leaky wax seal' disease, 'roof sag' disease and all normal for an aging house, instead of 'you got a problem with termites,' these medical professionals have a thousand names for differing chronic diseases, with palliation as their solution (a good coat of paint).

That is what you get with a government monopoly on 'health care.' Stand in line for the feel good pain medication. And that doesn't even touch the psychiatric effects of the Microbiome on the brain ( take a lie down on the couch for $XXX / 45 minute 'hour' + prescription for some pills )

A good medical college education based on last century knowledge - EE's don't have a monopoly - imagine if we were still stuck with relays and vacuum tubes.

[GIThruster]

Saw this one documentary on education, it made the claim that the two countries tied for top spot in math and science education were S. Korea and Finland. In S. Korea the kids spent every awake moment of their lives doing homework and studying, in Finland there is no homework. For Finland, they start the kids education one year later than anywhere else, and to work as a teacher requires a seven year Masters degree in Education.

One of the mistakes people make when looking at the whole question of education is to presume there is a single answer to all needs, which is certainly not true. When Dewey formed what became the modern progressive educational paradigm, he hand picked the kids in his test cases, and those kids would have succeeded no matter what educational program was used. What is really needed, is both a program that inspires kids who are not highly motivated to learn, and that nurtures those who already are bright or motivated or both, to do their best work. And yeah, there is some truth in every statement above, but the fact that you can do a job with just the skill for that job, and that you improve in your skills by doing the job, has no bearing on what a good education is all about.

IMHO, a good education has to include some familiarity with the classics. It has to include some history. It has to leave you with a since of humility concerning what you don't know, and motivate you to become a life long learner--and not just in your chosen field. It needs to cram some stuff in by rote to be sure, and I for one hate that part, but it also needs to carefully nurture the eternity in our hearts that loves truth, and learning just for its own sake.

[Tom Ligon]

The push to get everyone 2 years in community college has this trap in it. Not everybody should go.

I recall, back in the late 60's, a couple of my friends got welder training. The government had decided that welding was a good trade and that they could encourage young men to learn the trade. So we cranked them out, using statistics to assure them that this would produce a good income. And, of course, they saturated the market with young men who could stick two pieces of metal together but who had zero experience and were all scrambling for a few entry level jobs. There was no program to actually encourage an industry to need all those welders.

And had there been such an industry created, it would have needed more than just welders.

Encouraging everyone to get some basic CoCo certificate ignores a lot of valuable trades. It also does not do much for the kids who really could benefit from top quality 4-year degrees, washed down with grad school.

I'm hardly against education. I am quite worried if the government thinks that giving people community college, by itself, steers the nation to prosperity. The jobs have to be there. Not just jobs, but new opportunities. There is no way at all that government knows how to do this. Government looks at what was, picks a few things that used to work, and gives kids a route to become, say, welders. Or IP specialists (with an education that will be obsolete in 5 years or less). The idea of education as a machine for stamping out standardized pieces of machinery to supply existing "needs" is a strategy for getting more of what you already have, feeding these standardized commodities into HR intake bins that categorize their skills according to some enterprise database template.

Anybody tried applying to a large corporation lately? Did they even look at your resume? Or did they have you fill in an online form with the information in your resume, such of it that fit the form? Did the form actually ask the right questions?

Has anybody here (I raise my hand) recently quit a large corporation when it became obvious that said institution had no idea of what your actual talents were?

Education must be custom for every person, and I want to see a broad array of choices out there. Careers should be as well. Systems that try to stamp out standardized cogs don't do a good job of creating new industries.

So I do appreciate a well rounded education that opens your eyes to a world beyond some narrow specialty. What I don't appreciate is that the cost of education has exploded, with this concept that one needs to get an expensive specialty in order to get a job, and that you need to pay so much for it that you will spend the first half of your career trying to pay it back.

I personally think that most people should not go for a college degree until they've spent at least one summer flipping burgers or cleaning toilets. Too many people go to college to "find themselves", and pick a career after two years of college not because they've found their calling but because they've been warned that they have to pick a "track." One should go to college with at least a strong conviction as to what they don't want to be doing the rest of their lives.

[Tom Ligon]

Getting back to the original premise about some jobs not needing a degree ...

There is a specialized field called Project Management. People get degrees and specialty certificate in it. They are in big demand. The cream of the crop are the Program Managers, handling programs with lots of projects.

Sara was the first Project Manager we hired at my last job. I had no idea what her background was, but she was easy to work with and seemed to make problems go away. She tracked the projects and made sure we had the resources we needed and we never had to worry much about wasting time tracking milestones, etc. She did a lot more of asking us what WE needed and a lot less of telling us what SHE needed.

Then we started hiring other PMs. Some of these were high-pressure types, and each of them felt a need to defend their little kingdom. The problem was, most of us doing anything useful were working on 2-3 projects at a time, but each PM figured their job was the most important one at the company, and demanded our full attention, so we typically had 2-3 jobs, each of which were priority number 1. They all spent a lot of time telling us what THEY needed and thought the other way around was whining, not to mention putting demands on their precious resources.

On top of which, the PMs always wanted us to work for them but to shift expenses to overhead, or put hours in that were not recorded, in order to make their numbers look better. This was, of course, totally contrary to both company policy and the terms of the government contracts we worked under.

Turnover of PMs was always very high, except for Sara, who hung in there for years. Most were gone in about 6 months. Usually this was because they missed their targets, but they always found another job quickly.

At one point I noticed, while we had only 3 women engineers (out of about 40), we all of our PMs were women, without any technical field behind them. Just a curious detail ... they did seem to be able to sweet talk the guys into working harder.

One day I stumbled onto Sara's background. She had a high school diploma, and was a mom. And when you get right down to it, being a mom may be the best qualification there is for program management. She was always the best of the lot.

[JoeP]

Tom, I enjoyed that post.

I used to work in a large org that utilized PMs like that. Oh, and FWIW, usually the best PMs were female, running projects that were mostly staffed by males. So I saw the same thing. Hmmm.

It is amazing how much value a good PM can provide. And how much HARM a bad one can inflict. The bad ones cause everyone to burn cycles and muck around with spreadsheets, charts, data and rules without enough progress to the solution.

[GIThruster]

One day I stumbled onto Sara's background. She had a high school diploma, and was a mom. And when you get right down to it, being a mom may be the best qualification there is for program management. She was always the best of the lot.

Project Management is not difficult, and though you can get a professional degree called a masters in it, it is not an academic degree, since it does not require an academic degree to get into such a program. This is the distinction between a professional and an academic degree.

And you can just get a certification online in PM if you like. It is pretty much just learning the lingo and concepts and keeping on top of a Gantt chart.

Or you can just learn how to make a Gantt chart with one of the free online programs. Not so complex as you'd imagine but relies first of all upon good common sense and an emotionally mature ability to work with others. Sounds like that's what you're describing.

[GIThruster]

It is amazing how much value a good PM can provide. And how much HARM a bad one can inflict.

One of the big breakthroughs Kelly Johnson made when he formed Skunkworks was he essentially removed all middle management by working directly and shoulder to shoulder with his engineers, so they all knew what each other were doing. I think Ben Rich said they all worked at the same table at times. No time wasted with engineers writing reports instead of doing the engineering, which is what a layer of middle management normally requires. Removing that waste was intrinsic to Skunkwork's ability to arrive on budget and on schedule in record time, with the U2, and the SR-71. Word is though, that ability is all gone now that Skunkworks has institutionalized--it's just like the rest of Lock-Mart--back to forcing engineers off task to write reports so middle management can justify their position by making these reports to upper management.

[krenshala]

But ... but ... I'm a people person! I'm good with people!

[Tom Ligon]

I had the delightful chance to work with the Skunk Works a few years back. I was to build a Hardware In Loop simulator for a new aircraft control system we were going to build for a really innovative project they had going on. They sent me a bunch of servos for it. I looked at this cardboard box full of servos marked with bits of masking tape with very little information, and wondered what kind of amateurs these were. In aviation, you use a colored tag system to mark aircraft parts pulled from service, which should identify the provenance of the part and just what is wrong with it. Green tags don't mean what you would expect. Masking tape just is not allowed.

I proceed to test the servos, and most were screwed up beyond use. I contacted them, and they admitted those had come from a crashed project.

Then I remembered just how little the Skunk Works cares for the rules other aviation outfits work under.

Alas, before we could move on with the project, they went suddenly very quiet and dropped the project. I think maybe some rumors came out about a new secret project about then.

Cheer up ... they're still pretty informal.

[paperburn1]

Green tags just mean they were following the 4790

[palladin9479]

So I do appreciate a well rounded education that opens your eyes to a world beyond some narrow specialty. What I don't appreciate is that the cost of education has exploded, with this concept that one needs to get an expensive specialty in order to get a job, and that you need to pay so much for it that you will spend the first half of your career trying to pay it back.

This is on purpose, it's no accident that realized costs go up at rates higher then inflation. Universities does the same thing the medical field does, raise prices based on inflation instead of on costs. This practically guarantees maximized profit, as long as you have a captive audience. Because the mantra "you must have a degree to get a good job" was drilled into so many children's head, they feel they have no choice but to pay those rates at some university institution. The universities then seek to lock in upper class individuals by raising tuition until only those from that class can attend. It successfully turned "education" into a branding system that is then encouraged in the hiring system which only further empowers those who control the brand. This is why online and distance learning is so threatening to those who prescribe to the institutional system of education.

[GIThruster]

Universities does the same thing the medical field does, raise prices based on inflation instead of on costs. This practically guarantees maximized profit, as long as you have a captive audience.

This is again nonsense. You need to stop posting stuff that you make up and have no way to know. Universities set their rates the same way every other institution and mom and pop shop sets their rates in Western civilization: they charge whatever the market will bear. This is the way capitalism works. Why didn't you learn this in high school?

Just after OBama took office, he raised the funds going to student loans because this makes him a fan of all the students who will then vote Democrat. What he knew when he did this, and what the stupid students did not know, was that all the universities would then immediately raise their rates, because they are based upon supply and demand and the demand and funds for students had suddenly skyrocketed while the numbers of chairs in the schools had essentially stayed the same. What this debacle ends in is thus the schools get paid more and can afford that new gym, or sculptures, or rose gardens--certainly not classrooms and teachers as there are no more students coming in! The students who do come pay more, the school makes more, the students go into more debt. The end result is the students get a far worse situation than they had before USG artificially inflated the market. This is just one example of why governments should not in general tinker with the market--it almost always goes wrong.