You WILL Enjoy the Recession

Hey, Let's Invest In Greece!

Heh.

From Two Tonys (Letter 15)

Two Tonys - A whacker of men and Mafia associate serving multiple life sentences for murders and violent crimes. Left bodies from Tucson to Alaska, but claims all his victims "had it coming." Diagnosed with liver cancer, and is fighting to prolong his life.

I’m still in the medical complex, but this is all up in the air. What makes me suspicious is they’re treating me too nice. (We’ll see.) They might send me back to a yard or keep me here. I can’t get to the decision maker.

Hey, I’m real proud of you. Not only as a true friend, but also for your achievements. I know you’ll keep it up and the sky’s the limit. Maybe you’ll even make it to the Larry King Show. Pond to pond of course. All I ask is as you struggle on, stop and give me a good thought. Now get your bald ass in there and get on with it.

L&R from over the Atlantic!

Two Tonys

Click here to read Letter 14

Two Tonys is dying, and really appreciates your comments.

Post comments below or email them to writeinside@hotmail.com. To post a comment if you do not have a Google/Blogger account, just select anonymous for your identity.

If you would like to write to Two Tonys or send him a book or a magazine subscription, then please email me for instructions on mailing things to the prison.

Shaun Attwood

Iron Man’s Freedom (Part 2)

Iron Man - A martial-arts expert and personal trainer whose crimes include smashing someone’s door down: "I didn’t hurt anyone. I just wanted my fuckin’ money." His workouts are brutal. "I’ll have you in the best shape of your life by the time you get out," he told me.

I am working 12 hour days, and making serious money. Air conditioning is a very lucrative trade. I handle sales and service for my company, and I am the top seller in the company. They issued a company vehicle to me my second day on the job.

My reputation in Tucson is already spreading. Just today I got a call from the General Manager of a rival A/C company asking me to come work for him. I declined his offer because I am happy where I am at, and even more importantly, the guy I work for now really went out of his way to help me get set up when I first got out. You know how I am, I am loyal to those who have shown loyalty to me.

Got my own pad now, and I work-out at the YMCA's here in Tucson. There are several of them, so I just hit whichever one I am closest to when I finish my last service call for the day.

Anyway, it is getting late and I have a big day tomorrow.

Take care and know in your heart that it is with love and respect that I remain,

Your Friend and Brother,

Iron Man

Click here to read Iron Man’s previous blog.

Click her for the fight story, Iron Man v Snake Eyes

Our prison friends appreciate your comments.

Email comments for Iron Man to writeinside@hotmail.com or post them below. To post a comment if you do not have a Google/Blogger account, just select anonymous for your identity.

Shaun Attwood

Commercial Bank Profits

Thought this chart would make those of you in the Capposphere a little smiley today.

Now imagine if banks were to have just paid the ole Captain a mere $10 billion to tell them not to make bad loans as a consulting fee.

Fructose -- Protective?

Fructose and Tagatose Protect Against Oxidative Cell Injury by Iron Chelation

Abstract

To further investigate the mechanism by which fructose affords protection against oxidative cell injury, cultured rat hepatocytes were exposed to cocaine (300 ) or nitrofurantoin (400 ). Both drugs elicited massively increased lactate dehydrogenase release. The addition of the ketohexoses -fructose (metabolized via glycolysis) or -tagatose (poor glycolytic substrate) significantly attenuated cocaine- and nitrofurantoin-induced cell injury, although both fructose and tagatose caused a rapid depletion of ATP and compromised the cellular energy charge. Furthermore, fructose, tagatose, and sorbose all inhibited in a concentration-dependent manner (0–16 mM) luminol-enhanced chemiluminescence (CL) in cell homogenates, indicating that these compounds inhibit the iron-dependent reactive oxygen species (ROS)-mediated peroxidation of luminol. Indeed, both Fe²⁺ and Fe³⁺ further increased cocaine-stimulated CL, which was markedly quenched following addition of the ketohexoses. The iron-independent formation of superoxide anion radicals (acetylated cytochrome c reduction) induced by the prooxidant drugs remained unaffected by fructose or tagatose. The iron-chelator deferoxamine similarly protected against prooxidant-induced cell injury. In contrast, the nonchelating aldohexoses -glucose and -galactose did not inhibit luminol CL nor did they protect against oxidative cell injury. These data indicate that ketohexoses can effectively protect against prooxidant-induced cell injury, independent of their glycolytic metabolism, by suppressing the iron-catalyzed formation of ROS. 

Cell protection by fructose is independent of adenosine triphosphate (ATP) levels in paracetamol injury to rat liver slices

Abstract

Fructose protects cells against several types of injury but the mechanism of protection is uncertain. We have used paracetamol injury in rat liver slices as a model system to investigate the role of ATP levels in protection by fructose. Fructose depletes ATP levels in a concentration-dependent fashion in liver slices obtained from non-induced rats. Liver slices recover their ATP levels in the presence of fructose concentrations up to 10 mM. However, in the presence of 20 mM fructose, ATP levels are depleted for the duration of 240 min incubation. Adenine at 100 μM reverses the ATP depletion induced by 20 mM fructose in slices over 240 min incubation. Liver slices obtained from phenobarbitoneinduced rats were exposed to 10 mM paracetamol for 120 min and, then, incubated without paracetamol, with or without fructose for another 240 min. Introduction of 10 mM or 20 mM fructose in the second stage of incubation prevents paracetamol-induced injury. Fructose at 20 mM induces a rapid and marked depletion in slice ATP levels and these remain low throughout the second 240 min incubation period. Fructose at 10 mM maintains high ATP levels, even in paracetamol-treated slices. There is a profound protective effect against paracetamol-induced injury by either concentration. This suggests that protection is not dependent on high or on low ATP levels. Incubation of paracetamoltreated slices in the presence of 20 mM fructose plus 100 μM adenine in the second 240 min incubation period still results in the same level of protection as with 20 or 10 mM fructose alone while reversing the ATP depletion observed with 20 mM fructose.

Protection of cellular and mitochondrial functions against anoxic damage by fructose in perfused liver

Abstract

In anoxic perfused liver, conversion of fructose to lactate was greatly increased to about 3 μmol/min per g liver. This increase in lactate implied that the same amount of ATP was also produced. The rate of metabolism of glucose was less than 10% of that of fructose, as judged by rate of production of lactate. In anoxic liver perfused with fructose, the ATP levels of both the tissue and mitochondria remained high, despite lack of oxygen, thus preventing enzyme leakage and preserving processes requiring ATP, such as bile excretion and urea formation. The mitochondrial oxidative phosphorylation capacity of anoxic liver perfused with fructose was also unimpaired. Spectral analysis of light transmitted through the liver revealed that the mitochondrial electron transfer system was in the completely reduced state during anoxia, indicating that the mitochondria were incapable of synthesizing ATP. These results suggest that fructose metabolism during anoxia resulted in sufficient production of ATP for maintaining the physiological functions of the cells and the oxidative phosphorylation capacity of their mitochondria.

Sheriff Joe Arpaio Gags on Prison Punishment Loaf