05.18.02 – Drexel University, PA

May 18th — Last show of the tour. Drexel University. Weather was a bit suspect so they moved the concert indoors to the gymnasium, which is cool — we’ve gotten used to playing gyms on this tour. But at Drexel they also moved the inflatable jousting ring inside. And they moved the mechanical bull inside. And the inflatable laser tag arena. And the puffy-suit sumo wrestling circle.

I met the guys in the opening band “My Morning Jacket” before the show and tried to convey that not all Guster shows are like this one (some have velcro walls too) but it was too late. They were suited up for laser tag before I could finish talking… unfortunately I was one of only like twenty people standing in front of the stage to witness their set, which was excellent. So before we played I decided to make the rounds through the gym with the digital camera to document my surroundings.

And then this robot on wheels came rolling out onto the gym floor. It had some website scrolled across the base of it. His name was the impossibly clever “Gizmo D. Robot.” When I took his picture, he spoke. “Why don’t you take the lens cap off that camera, buddy,” said Gizmo D. Robot. Everyone was looking at me. I checked my camera and said quietly, “But the lens cap is off,” and then the robot came up with the infinitely funny “why don’t you put some film in the camera this time pal.” Ha. Ha. Ha. Ha. Ach. I began to see that this was one of those hilarious insult robots. Please, more funny jokes Mr. Insult Robot! Tell the one about how I forgot to put film in my camera one more time, Mr. Insult Robot!

We bid a fond adieu to the bus after the Drexel show and Pasty was reunited with his car, which looked like this:

Apparently, the same sort of creature that shit on my pants in Nashville had visited Pasty’s car while we were touring. Or maybe it was the same exact creature. Maybe it was following us. An investigation will ensue. For now, if you like reading what I have to say about poop, start clicking on “studio journal” again because we’re going back in the studio in a few weeks to finish our record. Until then, please enjoy this short factual essay I wrote on humans and white feces…

Cholestasis is the clinical condition that results from the impairment of bile secretion. A variety of pathophysiologic mechanisms have been implicated in cholestasis. Functional abnormalities of hepatocytes seen in cholestasis include depressed activites of sinusoidal membrane Na+, K+ -ATPase, reductions in the fluidity of the hepatocyte plasma membrane, decreased basolateral uptake of bile salts and organic anions, altered function of bile salt carrier proteins and microtubules, release of calcium from intracellular stores, and abnormal mitochondrial function with altered cellular redox state and decreased availability of ATP. Canalicular abnormalities include reduction of the microvilli of the canalicular membrane, dilation of the canilicular space, alterations in the canilicular membrane fluidity, and disruption of the pericanilicular actin microfilaments. Perhaps the most important, disruption of tight junctions sealing the canilicular space abolishes both anionic and osmostic gradients necessary for the generation of bile flow and permits back-diffusion of secreted bile components into the plasma. Many of the biochemical abnormalities associated with obstructive cholestasis appear to result from reflux of bile from the canaliculus into the plasma. Biochemically, cholestasis is characterized by the accumulation in plasma of compounds normally secreted into the bile (bilirubin, bile salts). Elevated levels of serum bile salts are the most sensitive indicators of cholestasis. Exclusion of bile from the intestine in severe cholestasis has several consequences. In absence of bile salts, there is moderate malabsorption of fat and severe malabsorption of cholesterol and fat-soluble vitamins. Cholestasis may be associated with specific vitamin deficiency disorders such as night blindness (vit. A), osteomalacia (vit. D), neuropathy (vit. E), or coagulopathy (vit. K). Because bilirubin degradation products are responsible for the normal brown color of stools, pale/white “acholic” stools are occasionally present in advanced cholestatic disorders. Black feces may result from taking drugs, such as bismuth or iron tablets, or from drinking red wine. The presence of blood in the feces may make them either black or bright red in color. This can occur because of infection, ulceration of the intestine or stomach, diverticular disease, malignant or nonmalignant tumors, abrasive foreign bodies, fissures, or hemorrhoids. Pale yellow or white feces suggest a disorder of bile production, usually an obstruction of the bile ducts. In children, greenish feces indicate that food has passed quickly through the digestive tract.

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