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Venn Diagram

A rapid post today.... just because I was thinking about Venn Diagrams when I woke up this morning. I was having the strangest dream. In the dream, I was on campus sewing Venn Diagram patches over all my clothes and putting Venn Diagram stickers on my office door, my rat cages, my pipes, my computer, etc. I do not know why I was doing this, but it seemed in my mind that I was so enamored with the shape of these images that I was trying to make an artistic statement. The second aspect of my dream was that there was a campus wide series of calculator thefts. People had started to walk around on campus (faculty, staff, & students) with their calculators hanging from their necks via lanyards or using carbiners to secure their calculators to their belt loops.

The odd part about this dream is that, while I find Venn Diagrams interesting, I do not widely use them or teach about them as an neuroendocrinologist. Additionally, calculators are not of huge importance to me either. It is strange what the mind thinks up when dreaming. I keep trying to see if there is a "meaning" behind this dream.

A rather humorous Venn Diagram cartoon for you to examine.

PipeTobacco

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Day 373 (Day 8)

Today is my 373rd day of walking 4-5 miles in a row. I have now lost 100 pounds total from my highest weight (My highest weight was in 1999 when I weighed 282 pounds.). I have lost 60 pounds in the last year due to the walking.

My wife has decided to begin her own consistency quest with exercise. Today is her 8th day in a row.

PipeTobacco

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Damn!

Today's science information hit too damn close to home. I hope I am not setting myself up for Alzheimer's.

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Alzheimer's Linked to Lack of Zzzzs:
Sleep Deprivation Leads to More Plaques in Genetically Susceptible Mice

By Tina Hesman Saey

Web edition : Thursday, September 24th, 2009

Levels of amyloid-beta protein fluctuate over the day and night/sleep-wake cycle in the brain of a mouse genetically engineered to express the human amyloid precursor protein. The brain of a sleep-restricted mouse (bottom left) shows more amyloid plaques compared with the brain from a mouse that did not undergo sleep restriction. Dark deposits represent amyloid plaques, which are associated with Alzheimer's disease in humans.

Losing sleep could lead to losing brain cells, a new study suggests.

Levels of a protein that forms the hallmark plaques of Alzheimer’s disease increase in the brains of mice and in the spinal fluid of people during wakefulness and fall during sleep, researchers report online September 24 in Science. Mice that didn’t get enough sleep for three weeks also had more plaques in their brains than well-rested mice, the team found.

Scientists already knew that having Alzheimer’s disease was associated with poor sleep, but they had thought that Alzheimer’s disease caused the sleep disruption.

“This is the first experimental study that clearly shows that disrupted sleep may contribute to the disease process,” says Peter Meerlo, a neuroscientist at the University of Groningen in the Netherlands. “What makes it exciting for me is that it shows that chronic sleep loss, in the long run, changes the brain in ways that may contribute to disease.” A vicious cycle could result if sleep loss leads to Alzheimer’s disease and the disease leads to more sleep loss, he says.

Researchers led by David Holtzman, a neurologist and neuroscientist at Washington University in St. Louis, used a method called microdialysis to measure the levels of a protein known as amyloid-beta in the fluid between brain cells of mice. Amyloid-beta sometimes twists into a sticky form and clumps together, forming such plaques. Scientists don’t yet understand how, but they think that clumping of amyloid-beta eventually leads to the death of neurons and the symptoms of Alzheimer’s disease (SN: 8/16/08, p. 20).

Although levels of amyloid-beta in the brain tissue of the mice didn’t seem to change, Holtzman’s group found that levels of the protein released into brain fluid did rise and fall throughout the day. “We didn’t know it would coordinate with sleep and wakefulness,” Holtzman says. “We just knew the levels fluctuated.”

Levels of the protein increased in mice during the night — when mice are mostly awake — and fell during the day when mice sleep. The longer the mice stayed awake, the more amyloid-beta levels increased, the team found. The team also measured amyloid-beta levels in the cerebral spinal fluid of some healthy young people and found the same pattern observed in the mice — amyloid-beta levels increase when people are awake and fall during sleep.

Giving mice a shot of a hormone called orexin, which promotes wakefulness, also caused amyloid-beta levels to increase. And blocking orexin’s activity led to a decrease in the amount of protein released into the brain fluid. The researchers don’t yet know whether orexin is directly responsible for helping release amyloid-beta into brain fluid or if orexin keeps animals awake, allowing more time for levels of the protein to build up.

For three weeks, Holtzman’s team studied mice that were genetically predisposed to build Alzheimer’s plaques, allowing some of the animals to sleep only four hours a day while others slept normally. Sleep-deprived mice made more plaques than well-rested mice, but a drug that blocks orexin’s action was also able to stop plaque buildup, the researchers discovered.

Studies in people haven’t shown a link between Alzheimer’s disease and chronic sleep loss, but Holtzman speculates that lack of sleep, particularly in mid-life when plaques begin to form, could hasten onset of the disease in genetically susceptible individuals. Drugs that block orexin might also be used as a potential therapy for halting plaque development, he says.

Other researchers aren’t so sure that’s a good idea. “Treating patients chronically with orexin inhibitors is really not an option,” says Masashi Yanagisawa, a Howard Hughes Medical Institute investigator at the University of Texas Southwestern Medical Center at Dallas. The drugs would likely make patients sleepy unless used at extremely low doses, he says. One such drug is in clinical testing as a treatment for insomnia.

It is also unclear whether orexin or some other aspect of the sleep and wake cycle regulates amyloid-beta levels, researchers say.

“Mechanistically we don’t understand why [sleep] is manipulating amyloid-beta rhythms,” says Sangram Sisodia, a molecular neurobiologist at the University of Chicago, “but we do know it’s doing something good for the brain.… There’s a clear message here about why it is so important to sleep.”

* * * * *

The one saving grace is that this may simply indicate that if a person HAS the gene for Alzheimer's that it can be more easily coaxed into expressing if a person has significant sleep deprivation. Hopefully, I do not have this gene.

PipeTobacco

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Disruption of Routine

I am a man who likes routines. I am a man who finds comfort and tranquility in routine.

Life seems at its best when there are day-to-day occurrences that I can count on to keep things going smoothly. It is times like those, where routine is available, that I feel the gleeful pleasure in "stepping things up a bit" and deviating from routine. When I *get* to choose to deviate from routine, I often find those moments where life feels its most magical, its most vivid, its most invigorating.

Yet, the lion's share of the times when routine is deviated from, it is not of my doing, it is not of my choice, and it happens in a happenstance, scattered, unpredictable manner. This is typically when life is at its lowest, when my psyche is battered and bruised. It is when I feel surly in my mind, my heart and in my soul.

So, it seems routine is the balance wheel, the fulcrum upon which my mental homeostasis resides. And the deviation from balance is the yin and yang of life... the aspects of the same item that are at polar opposites of each other, yet also the same.

To realize this makes my head spin.

PipeTobacco

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One Year Plus One Day

Yesterday marked my completion of a full 365 days of walking consistently EVERY single day! I shall write about it more soon, but right now I am trying to simply experience the feelings of this accomplishment in a visceral manner. Today was day 366.

PipeTobacco

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Activating Cones!

The following story from Science News is fascinating in that researchers have found a way to treat colorblindness. Color vision is a result of the activity of three different cone cells for different wavelengths of light. These cone cells are embedded in the retina of the eye. Colorblind individuals have at least one cone cell type that is not functional or incompletely functional. This leads to deficits in ability to discern colors. In humans, red/green color blindness is the most frequent, but there are all sorts of variations as well. I hope you find the article interesting.

Monkeys Get Full Color Vision: Males With Red-Green Colorblindness Can Distinguish the Hues After Gene Therapy

By Tina Hesman Saey

Gene therapy gave Dalton a photoreceptor that detects red light and he can now pick out red dots from a gray background and distinguish red and green from other colors. The experiments suggests that color can be added to vision without rewiring the brain to process the new information. Neitz Laboratory, University of Washington

Two male squirrel monkeys now see the world in a whole new way — in full color.

Female squirrel monkeys can see in color, but male squirrel monkeys are normally red-green colorblind because they lack pigments in the retina that detect those wavelengths of light. Now, researchers have performed gene therapy that allowed two male squirrel monkeys named Sam and Dalton to produce proteins that detect red light. As soon as the red-light-harvesting protein was made in the monkeys’ eyes, the animals were able to discriminate between red and green spots in color vision tests, Jay Neitz of the University of Washington in Seattle and his collaborators report online September 17 in Nature.

The experiment wasn’t supposed to work, Neitz says. People born with cataracts don’t develop nerve connections that help the brain make sense of messages sent by the eye. If the defect isn’t corrected early, these people remain essentially blind even if their eyes return to full function later. Because there was no reason to assume color vision was different from other types of vision, the team had assumed it would not be possible to reverse the deficit in an adult animal.

Neitz polled experts in the vision field on whether they thought producing photoreceptors in colorblind adult monkeys could give color vision. “Every single person said, ‘absolutely not.’” But the researchers decided to move forward with the experiment to see if they could get the pigment protein to be made in the eye.

Male monkeys lacking the red photoreceptor protein were given injections of a virus carrying a gene for the protein. Levels of the protein slowly rose in some retinal cells. After 20 weeks, Neitz and his colleagues started to see differences in the way Sam and Dalton performed on daily color vision tests. Around that time, protein production levels peaked and the monkeys have maintained stable color vision for two years since treatment.

Feasting time Digital simulations show what a squirrel monkey named Dalton may have seen before (left) and may now see after (right) gene therapy to correct his color blindness. Researchers say the fact that Dalton can now see in color could mean that full color vision could have evolved in just one genetic step. Neitz Laboratory, University of Washington

In the tests, monkeys were shown three panels with a patch of colored dots on a background of gray dots. If the monkeys press the panel with the dots that match a color cue, the animals get a sip of grape juice as a reward. Even colorblind monkeys guess correctly about a third of the time, Neitz says.

“Sometimes they get on a streak, so those first couple of days when they were on a streak, we tried not to get too excited,” he says. “But by the end of the week it became clear that this was not random chance.”

Sam and Dalton could consistently pick out red, green, blue and yellow dots from the gray background and discriminate between the colors. Before the gene therapy, they could only discriminate yellow and blue. The speed at which the monkeys learned the new colors indicates that no brain rewiring was required for the feat, unlike that needed to restore other types of vision such as distinguishing objects.

The achievement is causing a stir among vision scientists and may have implications for understanding the evolution of color vision, says Bevil Conway, a neuroscientist at Wellesley College in Massachusetts.

“Somehow the brains of these monkeys are already wired to decode these color signals,” Conway says. That fact raises the possibility that “the evolution of color vision may have required just one genetic switch.”

But, Conway says, there is an important disclaimer. “We have no idea if this would work in humans or that it would be a delightful experience for the people post-surgery.” People who have surgery to repair sight lost in childhood often report that their new vision is confusing and disorienting, he says. Adding color could prove to be similar.

Other scientists who originally thought color vision couldn’t be generated in adult animals are impressed by Neitz’s achievement.

“They certainly have added some color vision,” says Gerald Jacobs, a neuroscientist at the University of California, Santa Barbara. “I find the measurements compelling.”

Still, the monkeys’ actual sensation of color — what it looks like to them — remains a mystery.

“The achievement is technically amazing and conceptually very cool,” says Melissa Saenz, a neuroscientist at Caltech in Pasadena, Calif. But even though the monkeys can discriminate some new wavelengths of light, “there's no evidence that the monkeys perceive a new dimension of color,” she says. For example, the monkeys may now perceive red and green as different shades of yellow and blue, colors the animals already knew.

“If it doesn't involve experiencing new sensations of color, it would not dramatically change the experience of colorblind people if the treatment were applicable to humans,” Saenz says.

* * * * *

Very fascinating and enjoyable to read about.

PipeTobacco

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My Exhaustion Continues

I feel myself slipping into the feelings of despair and exhaustion again. I must struggle against it. I wonder if it is the decreasing light levels and decreasing day lengths.

I have a Human Use Committee Meeting later this morning. They are always such a joy as well, so that may be a contributing factor. Yet, as I am a Don Quixote sort of person, I feel it is my duty to "fight the good fight" and tilt at these sorts of annoying windmills to try to promote what is right, just and proper for people.

PipeTobacco

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National Health Care Now!

I am trying to not get too worked up about this because it is the same old b*llsh*t like always in terms of politics.... but....

I am annoyed as hell about the current yammerings from politicians and pundits about the "national health care debate". We finally have a president again that is trying to do something that will help the PEOPLE of our nation and improve the quality of life for our society. All people should be able to have access to health care regardless of their economic background, their job, or their age and stage in life.

The politicians and pundits who keep working to minimize and negate the idea that PEOPLE should have guarantees about having health care are rude, obnoxious, evil little people who only wish to greedily hoard their own riches. Even more obnoxious is that these politicians and pundits use unscrupulous tactics to sway many to their side. They prey on the idiots and the unaware in our nation and make up foolish and hyperbole filled arguments designed to make the masses who haven't got a "clue" so to speak duck-step into the old Reagen-era notion of "Oh my God, Govermnment is the root of all evil." and "You'll give me a "national plan" only over my dead body!"

It is foolish, stupid and frustrating as hell. How can any REASONABLE person who believes in social justice, fair governance, and a society about PEOPLE not corporate profit not see that HEALTH INSURANCE CORPORATIONS are about THEIR OWN PROFIT, and do not give a damn (really) about the health and well being of any of their "clients".

I hope that Obama does not waffle on the notion of a "government option" in terms of his health care reform. If he does, then I suspect all will be lost. Additionally, I hope that Obama does not get beaten down by all this yammering and b*llsh*t from the extreme right and give up. WE NEED HEALTH CARE REFORM AND WE NEED A "GOVERNMENT OPTION" so that we are able to treat our nation's citizens fairly.... not in the biased, discriminatory manner we do now by giving people different coverage based upon what their employer is willing to cough up money for. It is stupid that we are even having this debate. We should have had national health care for all when Theodore Roosevelt first suggested it long ago. We should have had it when Clinton tried in the 90s. It is utterly assinine that we do not have national health care.

PipeTobacco

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Day 360

It is amazing to think of the milestone in just a few days. Today is 360 days of consistency in walking EVERY day between 4-5 miles. I am glad I have done this, and hope that I will continue to do so every day.

PipeTobacco

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Tired Tuesday

I am not sure what is afoot, but I am doggedly tired. I wanted to stop in briefly to make sure I posted, but I am mentally exhausted and no thoughts appear possible in my brain.

PipeTobacco

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Feeling Hot Blooded

The most interesting news flash I have read in the last week concerned the findings of some researchers at the University of Michigan who have found a knockout mouse that will "burn" (aka metabolize) excess fat instead of store it in the body. This of course could have tremendous impact for our nation of obese people. Here is a synopsis from Science News:


Mice With Mutation Feel the Burn: Without Immune Gene, Rodents in a New Study Make Heat Not Fat

By Tina Hesman Saey

September 3rd, 2009

Resisting weight gain Two mice were fed high-fat diets for several months. But the mouse on the left, genetically engineered to lack an immune system gene, put on less weight than the mouse on the right.

Mice with a mutation in an immune gene don’t get fat, they burn it.

A gene that helps regulate inflammation also stops fat cells from wasting energy. When the gene, called I kappa B kinase epsilon or IKKε, is missing, mice turn a high-fat diet into heat instead of body fat, a new study in the Sept. 4 Cell shows.

If the gene works the same way in humans as in mice, it could be a new target for antiobesity drugs.

Scientists previously learned that low-level inflammation produced by obesity could trigger type 2 diabetes. But the details of the connection are still unclear, says Alan Saltiel, a cell biologist and endocrinologist at the University of Michigan in Ann Arbor. In the new study, Saltiel and his colleagues fed mice a high-fat diet and discovered that levels of IKKε were elevated in the liver and fat tissue of the mice, compared with mice on a regular chow diet. IKKε is known to be involved in regulating inflammation, and the researchers thought the molecule might be the link between diet and diabetes that they were looking for.

“What I expected was that if we knocked out this gene we’d get rid of the link between obesity and diabetes,” by eliminating inflammation, Saltiel says. He didn’t suspect that the connection would be severed further up the chain — preventing mice from getting obese in the first place.

IKKε is a largely overlooked member of a family of four kinases known to be involved in inflammation, says Gökhan Hotamisligil, a professor of genetics and metabolism at Harvard University Medical School in Boston. Researchers have paid more attention to IKKε's siblings IKKα and IKKβ, but those two forms don't become more active in fat cells, or adipocytes, in response to obesity. Yet drugs that inhibit all the IKK kinases improve inflammation and symptoms of diabetes, leaving researchers with a mystery about which form of kinase forges a link between obesity and disease.

“For quite a while we had gaps in the understanding of how adipocytes promote inflammation,” Hotamisligil says. “This study sheds some light that IKKε could be tipping the balance in adipocytes,” causing the fat cells to release inflammatory chemicals.

Mice lacking the gene increase production of an energy-burning protein called uncoupling protein or UCP1, the researchers discovered. The protein is found in mitochondria, the power plants of the cell. Excess UCP1 causes fat cells to burn more energy and release it as heat, akin to an incandescent light bulb that sheds heat along with light.

Normally, IKKε “keeps the brakes on the expression of UCP1 in white fat,” Saltiel says. “When we knocked out IKKε, we released the brakes.”

After three months on a high-fat diet, the mice with the mutation gained an average of 12 grams, while normal mice gained about 20 grams. Both types of mice on a normal diet weighed about 32 grams on average. Although the mutant mice still gained some weight, the researchers say that it wasn’t enough to trigger the inflammation and diabetes associated with obesity.

It is clear that removing IKKε changes the mice’s energy balance, says C. Ronald Kahn of Harvard University Medical School’s Joslin Diabetes Center in Boston, but the mechanism for the change still isn’t understood. Kahn suspects that the mutant mice have more energy-burning brown fat cells, which are rich in UCP1, mixed in with white fat.

The researchers think that IKKε works mainly in fat and the liver, but since this study removed the gene from every cell in the body, the team cannot be sure where the gene exerts its influence most strongly, says Philipp Scherer, director of the Touchstone Diabetes Center at the University of Texas Southwestern Medical Center at Dallas. “These improvements could be secondary to improvements in other tissues,” he says. It will be important to know which tissues are affected if drugs that suppress IKKε are developed for use in people.

Previous studies have shown that mice lacking the immune gene are more susceptible to deadly viral infections. But Saltiel says that potential drugs inhibiting IKKε to fight obesity probably wouldn’t turn the gene off completely, leaving enough activity to combat infections. White blood cells from the mutant mice in the new study responded normally to a substance designed to mimic a bacterial infection.

I know two of the endocrinologists who were part of the research team involved with this work. It is a remarkable finding and could someday be enormously beneficial.

PipeTobacco

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Weekend Frivolities

Last weekend (the extended Labor Day Weekend which lasted from Friday through Monday) was spent up at my wife's one lineage's annual family reunion. The reunion meant four days of camping, four days of no showers, huge amounts of sunscreen, a firepit, a campfire, a cake walk, a booze walk, and food in quantities and types beyond imagine. The person hosting the event's four acres of land (roughly 16,000 square meters of land) had over 75 massive RVs scattered across the property. These big behemoth homes on wheels looked much like the following samples:

Big & New RV
Used RV
Very Used RV
Pop-Up Camper Tents
Other Vehicles Present Converted into RVs #1
Other Vehicles Present Converted into RVs #2
and even an occasional
Tent

A good time was had by most everyone, and we all suffered the headaches, tummy aches, and other maladies associated with excesses of such kinds of our choosing during the event.

I believe I am going to go head to my elderly father-in-laws to check how he is recovering from the festivities and to perhaps share a few libations and bowls of pipe tobacco with him this afternoon.

PipeTobacco

P.S. Please also take a brief, but sad and heartfelt moment of remembrance for those who lost their lives as a part of the September 11, 2001 tragedy that happened 8 years ago today.

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Does Exercise Make A Person Less Contemplative?

One thing that I have noticed of late is that I am LESS contemplative than I had been during most of my life. Please do not get me wrong... I still contemplate and ponder pretty much anything under the sun for a good part of the day. But, and I am not sure if this is a good or a bad thing... I *think* there may be a correlation between my consistency in exercise and my amount of contemplation.

It is as if my walking (which is accomplished solo at least 98% of the time) has somehow altered the amount of time in which I spend "in my head" so to speak. This has probably been very good at decreasing the percentage of the time in which I feel moody/depressed, but perhaps it may have decreased my creativity as well?

An interesting idea, I will have to contemplate further... or maybe I will just go for a walk.

PipeTobacco

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09/09/09

In my fondness for numbers and patterns and symmetry, today is a true humdinger! September 9th, 2009 can be listed as 09/09/09 !

Perhaps I should drink 9 shots of Wild Turkey to celebrate?

PipeTobacco

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352nd Day!

Today marks the 352nd day of my consistency in exercise. I am very happy with my having stuck with it so far. A very big anniversary mark is very quickly approaching! I hope that I continue to be consistent.

PipeTobacco

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Rats Are People Too!

As an endocrinologist who works with rats (human and non-human), the following article drew my attention. It was posted by Science News on August 31st:

Oh, Rats — There Go the Snails

Introduced rodents crash a once-thriving population in Hawaii
By Susan Milius

Paradise in trouble In a meadow on the Hawaiian island of Molokai (left), populations of Partulina redfieldi tree snails (right) shrank some 80 percent within two years after rats discovered them.courtesy of Michael G. Hadfield

Rats keep getting into paradise. And when they discover a taste for escargot, it’s an infernal problem for native populations.

At a study site high in the mountains on the Hawaiian island of Molokai, tree snails of the species Partulina redfieldi thrived for 12 years and then declined catastrophically, says zoologist Michael G. Hadfield of the University of Hawaii at Manoa. The culprits were introduced rats that started scouring trees for snails, Hadfield and Jennifer Saufler, now at University College London, report in the August Biological Invasions.

Rats have hitchhiked along as people settled the globe and have changed their new homes by feasting on native species such as snails and ground-nesting birds. The Molokai study provides an unusual look at rat damage because the team collected data before and after a burst of attacks, Hadfield says.

The Hawaiian islands once had extraordinary snails, about 750 species found nowhere else, Hadfield notes. All together the islands once hosted more snail species than did the other 49 states and Canada combined. Darwin contemplated Hawaiian snail variation, and the showy species in the Achatinellinae subfamily, which live in trees, have become a classic example of the wide diversity of species that can develop on islands.

Shells bitten by rats tipped off researchers that the introduced rodents were feasting on the Partulina redfieldi, a species found only on the island of Molokai.

But more than 70 percent or so of those 750 species have gone extinct, including some of the storied tree snails, Hadfield says. As part of a broad research program on snail biology and conservation, he and his colleagues started in 1983 to monitor P. redfieldi snails in ohia trees dotting a mountain meadow.

These snails spend their entire lives, which can last 18 years or more, in one tree, the researchers found. And biology doesn’t make for fast comebacks. P. redfieldi has to reach 3 to 5 years of age before reproducing, and even then the snails have, through live birth, only about five babies a year.

Despite this leisurely reproductive biology, snail numbers in four meadow trees at least doubled during the first dozen years of the study. From 1995 through 1996, though, the snail numbers plunged more than 80 percent, the researchers report. At the same time, the number of rat-chewed shells found under the trees jumped. Hadfield says he thinks the number of rats boomed, and then some of them “discovered that the trees were full of dinner.”

“Rats are copycats,” he says. Other research has shown that a few rats discovering a banquet can inspire others to visit and feed repeatedly.

After Hadfield first saw the devastation, The Nature Conservancy started setting out poisoned bait to reduce the rat numbers. But Hadfield’s team reports that the snail population stayed small through 2006.

“There has been a fairly long-standing interest in the role of rats in Pacific island ecosystems,” says archaeologist Stephen Athens of the International Archaeological Research Institute, an independent research organization in Honolulu. “What seems to have changed is a new appreciation of how truly devastating rats can be.”

Athens says the study doesn’t have hundreds of years of data to address the big question of what rats have done to Hawaiian ecosystems untouched by humans, but it should help resource managers try to save what’s left of the snail species.

Predators loom large in the uncertain future of Hawaii’s once-glorious snails, Hadfield says. Native snails are falling prey to three rat species that now prowl the islands and to an introduced flatworm and a predatory snail. These menaces haven’t completely killed any hope Hadfield has for preserving the remnants of Hawaii’s snails. Yet, he says his new analysis suggests snail preservationists are going to have to get tough.

While introduced species can and are a nemesis for many native populations, it still seems rough to be so anti-rat.

PipeTobacco

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Off to the Wild

I am heading to the North Country for my wife's family's Annual Reunion. Four big nights of camping, eating, drinking and merriment (I hope). Wish me luck!

PipeTobacco

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Linear Squiggles

I have been making a concerted effort to get back into the regular posting "groove" so to speak. I must say it has been helpful for me as it helps me to re-establish routine and patterns in my life. I am hopeful my readership will continue to return, as I so very much appreciate all of you and especially your comments. I apologize for my sporadic postings until this week.

While the Summer is now gone (at least metaphorically, as I am in academia, and we are now in the Fall Semester), I must say I am glad to be back in routine. Normally I really enjoy the break during Summer, and while I did like this Summer, it was so different than usual, that it was a time that kept me on my toes and out of patterns and routine. I have painted and/or redecorated 9 rooms in my home (only one small bathroom left to go), and I must admit I and my wife and kids are all pleased with the transformation. Yet, I am more pleased to be very nearly done with the chaos.

PipeTobacco

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What About the Jeep Patriot?

In terms of the vehicles I drive, I am a bit non-conformist, but also greatly desiring of driving something I like and enjoy. I typically wish to have a vehicle that has the features I like in it (generally versatile (hence no MG or Fiat convertibles, or Jeep Wranglers, all of which I really like), manual transmission, air conditioning, small engine, good (at least bearable) gas mileage, and something "esoteric" or "quirky" about it). Vehicles in the past that I have had that fit this bill include (I have had other vehicles that did not fit the above criteria that I will save for a future discussion on vehicles I do not like):

1965 Volkswagen Beetle
1974 Chevrolet Vega
1976 Chevrolet Chevette
1979 Volkswagen Rabbit Diesel
1980 Renault LeCar
1984 Volkswagen Rabbit Pickup
1996 Pontiac Grand Am
1998 Chevrolet S-10 Pickup

The 1998 Chevrolet S-10 Pickup is what I typically dive day-to-day. My family has several other pricier, bigger, "better" vehicles, but I have always been drawn more to the "small and quirky". Hence, although I am the patriarch of the family, I primarily drive the smallest, oldest, most "beat-up" vehicle in the family. But my Chevrolet S-10 Pickup is now getting a bit wheezy (110,000 miles (roughly 177,000 kilometers)) and I have started to look around at possible replacements. Strangely enough, what has captured my attention is the Jeep Patriot! It is a bit larger than my truck, but gets better gas mileage, can be purchased with a manual transmission, and gives me that "quirky" sort of vibe.

Here are few more images of the Jeep Patriot:

Jeep Patriot #1
Jeep Patriot #2
Jeep Patriot #3
Jeep Patriot #4

If any of you may have had this vehicle, please tell me of your opinion. Also, everyone, please give me your opinion on the aesthetics or other aspects of this vehicle I am feeling passion about.

PipeTobacco

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Happy 345 Day!

As a person who is very comforted, intrigued, and drawn to patterns, symmetry, and shapes, I was quite happy to realize that today is a definite "pattern" day in my effort to maintain my exercise regime. Today is the 345th day of my walking/jogging each day for 4-5 miles.

The pattern 3-4-5 is comforting and mentally attractive to me. I am not sure how many of you feel similarly about numbers, colors, shapes, etc. But, as odd as it may sound in my writing it here, I have definite opinions/preferences about numbers, colors, and letters. Here is a sample:

Esthetically pleasing numbers (seen in Arial, Times Roman, or Schoolbook Font):

0 - the oval shape is artistic in appearance
3 - the shape and the image of three is attractive
4 - the shape is beautiful
6 - the rounded shapes such as this are "elegant" to my mind
9 - similar to the "6" above

Neutral numbers to me include:

1 - bland
5 - not particularly inspiring
7 - too common as a "preferred" number

Numbers I typically "dislike" (sounds a bit harsh, but I mean esthetically, I find them unattractive:

2 - not sure why, but to me it is a disappointing appearing shape
8 - while at first glance, you may think I would like the double rounded shape, but in my mind the number feels "over the top" or too "aggressive"

If you find this sort of topic interesting, perhaps I will continue with it for my opinions of colors, shapes, letters and other items.

PipeTobacco