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End aside, sniggering excepted. The only parts I am interested in are the clamps and the appetite scores no food intakes in this one. So we have a low insulin clamp and a high insulin clamp looking a lot like this: Friday, August 03, Holiday reading. I'm off on vacation for a while so the next posts are likely to be delayed. If anyone would like a light summary of the ideas I'm thinking about, this is a nice review: Yin and Yang of hypothalamic insulin and leptin signaling in regulating white adipose tissue metabolism For a level deeper of understanding you just need to add in that saturated fats have an FADH2: NADH ratio around 0.

NADH ratio of well below 0. Because a core function of insulin is the inhibition of lipolysis. Posted by Peter at Friday, August 03, 2 comments: Wednesday, August 01, Insulin makes you hungry 4 unless you keep it out of your brain. Especially via the brain. Where insulin detemir doesn't go. People will be aware that insulin detemir is really strange stuff.

There are perfectly respectable papers showing that it cannot enter the brain and blocks the entry of normal insulin in to the brain too or that it is fantastic at entering the brain, much better than more normal insulins. There are probably more studies in the latter camp but my biases push me towards the former camp. The nature of the researchers also tends to push me towards the former camp. I posted on insulin detemir here and here to explain my point of view.

Now there is this paper: Just eyeballing the insulin doses used we can assume that the plasma insulin levels were a reasonable approximation for humans in the normal post prandial period, ie physiological fed-state rather than pharmacological.

The research group is completely wedded to the idea that central insulin is an appetite suppressant and that weight gain from any insulin therapy is only a reaction to recurrent hypoglycamia. As there is no hypoglycaemia during the clamps their presumption is that this neutral insulin infusion results in a reduced food intake.

As insulin detemir gives less food intake after a normoglycaemic clamp than neutral insulin does, then their conclusion is that insulin detemir is having a more potent central appetite suppressing effect than the neutral insulin. They are so confident about this that the inclusion of a control situation, where saline was infused without any insulin and appetite was checked after this, was considered un-necessary.

This really is the level of research in the "satiety" insulin camp. Posted by Peter at Wednesday, August 01, 10 comments: Insulin makes you hungry 4 unless you keep it out of your brain. Monday, July 30, Insulin makes you hungry 3 a matter of semantics and free fatty acids. There is absolutely nothing technically incorrect with the description of the results contained within the title of this paper: Effects of insulin-induced hypoglycaemia on energy intake and food choice at a subsequent test meal They gave a small dose of insulin low enough to not need rescue glucose within the study period as a single bolus, waited for 20 minutes then offered the subjects an eat-as-much-as you-like buffet.

This is what the glucose levels did. Posted by Peter at Monday, July 30, 5 comments: Insulin makes you hungry 3 a matter of semantics and free fatty acids. Tuesday, July 24, Insulin makes you hungry 2 even in the presence of hyperglycaemia.

This is the paper cited by Woo: Posted by Peter at Tuesday, July 24, No comments: Insulin makes you hungry 1. If you want to think about the central effects of insulin you could do a great deal worse than working through this paper: Brain insulin controls adipose tissue lipolysis and lipogenesis It is jammed full of exquisite quotes: Thus, at the doses administered, brain insulin infusion inhibited lipolysis to a similar extent as that achieved with peripheral hyperinsulinemia" Here it is in pictures.

What does a CNS infusion of insulin do to lipolysis, at what are purported to be physiological dose rates? Obviously, it does exactly what peripheral insulin does, but using minuscule amounts; it suppresses lipolysis: Posted by Peter at Tuesday, July 24, 3 comments: Sunday, July 22, Butter gives you fatty liver! This paper is an absolute gem: It contains no trace of understanding in its entirety, but the numbers in the results are fascinating.

How do we sum it up? If you pay people to over eat kcal per day for three weeks they gain weight and they gain liver fat. Posted by Peter at Sunday, July 22, 14 comments: Butter gives you fatty liver! Tuesday, July 17, Oops. OMG, just seen how many comments are awaiting moderation now I'm back to occasional posting. I'll see what I can do, if desperate I'll just delete the spam and hit post for them all.

Apologies for the inattention over the past few weeks Posted by Peter at Tuesday, July 17, No comments: Woo had a bit of a rant about acipimox. Here's my simplified idea. I've been interested in acipimox, in a round about sort of a way, for a very long time.

To me, the core fascination is that it is not only an effective suppressor of lipolysis, but it is pretty well weight-neutral and it most certainly does not result in weight gain.

Which, you have to admit, is interesting. How can this be? I feel something of a clue can be found in the studies using a similar drug, nicotinic acid. Both drugs effectively suppress plasma free fatty acids via the same receptor but the neatest study happens use nicotinic acid. People may recall that I posted about the role of FFAs in the secretion of insulin as demonstrated by an isolated rodent pancreatic preparation, some time ago.

The core concept here is that insulin secretion is dependent on the chain length and saturation of the FFAs used for perfusing the pancreas along with the glucose. This phenomenon appears to be well appreciated by the authors of this next paper same research group: Circulating fatty acids are essential for efficient glucose-stimulated insulin secretion after prolonged fasting in humans So what happens to in-tact humans when you fast them for 24 hours to raise FFAs and then bolus them with intravenous glucose?

Or fast them, artificially drop their FFAs with nicotinic acid, and then bolus them with glucose? This is what happens: Posted by Peter at Tuesday, July 17, 8 comments: Monday, May 28, Speculation on the effect of subcutaneous adipocytes implanted in to the mesentery of mice. Taking a piece of subcutaneous fat from a sacrificed mouse and implanting in to the mesentery of a recipient mouse causes weight loss in the recipient , starting once the surgery has healed. We know that healing takes something just over six weeks: Posted by Peter at Monday, May 28, 6 comments: Speculation on the effect of subcutaneous adipocytes implanted in to the mesentery of mice.

Sunday, May 20, Guddling in the dark for a respiratory quotient 2. Multiple papers have values that don't make sense, which is an issue making me doubt my sanity and is damaging to my personal extensive set of confirmation biases. They also produce basic contradictions of the physiology of the oxidation of glucose vs the oxidation of fatty acids. But now I think I can go back and explain much of the peculiarity in this image from Kahn's group, the one which triggered this previous post.

Two sets of mice, on the same chow, having sustained differences in RQ, in a way I couldn't understand: Posted by Peter at Sunday, May 20, 12 comments: Guddling in the dark for a respiratory quotient 2.

I picked up this paper via Face-ache so cannot recall to whom I should credit for the find. The post is also highly speculative. Higher h Respiratory Quotient and Higher Spontaneous Physical Activity in Nighttime Eaters It's worth noting that the difference is small but probably biologically significant. Statistically p is less than 0. Before we think about it we need some background.

That comes from the same group in an earlier paper: Posted by Peter at Saturday, May 12, 21 comments: Nighttime Eaters have an elevated RQ on a given macro ratio diet. Friday, April 13, AHA approved egg!

One of the full size chickens miss-fired yesterday and produced this minute egg: Posted by Peter at Friday, April 13, 19 comments: Monday, April 09, Pasta for weight loss. This paper hit T'internet recently and has been cited all over the place: Effect of pasta in the context of low-glycaemic index dietary patterns on body weight and markers of adiposity: I've greyed it out so no-one is tempted to read it in full, the flavour is all you need: Show me how After you enable Flash, refresh this webpage and the presentation should play.

View by Category Toggle navigation. Products Sold on our sister site CrystalGraphics. Antigen differences between the donor and the recipient Thoracotomy is reserved for nondiagnostic BAL with high risk of infection.

Viral CMV pneumonia fatal in gt 85, treated with ganciclovir 2. Surgical resection of localized lesion. Other infections PCP, legionella, nocardia, treatment same as in usual patients 35 Idiopathic pneumonia Early idiopathic pneumonia no proven treatment biopsy diffuse alveolar damage Late idiopathic interstitial pneumonia pathology mononuclear cells interstitial infiltrates, may be immunologically mediated process management same as managing idiopathic pulmonary fibrosis, immunosuppression to control the GVHD 36 Infection Control oral bactrim for the 2 weeks prior to BMT, twice weekly after PMN engraftment laminar airflow LAF environment for neutropenia reduce infection, but reduce mortality only in aplastic anemia oral nonabsorbable antibiotics for GI decontamination eliminate G , not G - LAF decreases incidence of acute GVHD prophylactic acyclovir after BMT suppress HSV infection 37 Sepsis Syndrome bacteremia in 50 marrow recipients G - , G coagulase - staphylococci, yeast candida viral infection CMV seen in previous infected patients who develop acute GVHD.

CMV viremia high cardiac output, low SVR, sepsis syndrome coexist with acute GVHD empiric antibiotic coverage, modified with culture results and endemic infection and resistance pattern careful iv volume expansion. Whether your application is business, how-to, education, medicine, school, church, sales, marketing, online training or just for fun, PowerShow.

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It serves many important functions involving red blood cells and immunity. The organ may need to be removed from the body due to an accident or various disorders or conditions. After surgery, you will need to follow certain nutrition guidelines to promote health and recovery.

Talk with your doctor and registered dietitian for the best lifestyle and nutrition advice after your splenectomy. A splenectomy is a medical technique used to remove the spleen by several incisions. The two main types of spleen surgery performed by doctors are open splenectomy and laparoscopic splenectomy, according to MayoClinic.

Both types of spleen surgery are performed using general anesthesia and involve several incisions in the body. After surgery, your doctor may require you to follow a special diet and refrain from any physical activity. A clear liquid diet includes any colorless or clear food and beverage. A clear liquid diet is typically recommended by a doctor immediately following spleen surgery, says the University of Texas Southwestern Medical Center at Dallas. A clear liquid diet is typically prescribed by doctors after surgery to support nutrition and energy for patients when they are unable to tolerate regular foods.

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