Flexibility vs resistance
Common Questions and Answers about Flexibility vs resistance
flexibility
Stretching isn't the best way to improve flexibility—lifting weights through a full range of motion is, according to a recent study at the University of North Dakota. Pausing for 2 to 3 seconds at the "down" position of the lift (where you feel the stretch) without relaxing your muscles is even more effective.
5 mg of entecavir cause resistance in patients who never have been on any nucs and no polymerase resistance detected vs 1mg. My doctor wants me to take 1mg vs 0.5 mg but I have been been on any nucs and show no resistance to any nucs during genotype testing.
Working with a chiropractor, I got a hip flexor malady adjusted; the PT said I needed to work on flexibility. My left leg kind of 'hangs/float' and doesn't extend out normally. I feel it even when I'm walking. The odd part is that I can't really self-correct it with mental striving. I'm thinking it's more than just bad flexibility - wondering if I'm not really neurologically talking to my lower leg?
Strength exercises involve working the muscle against resistance. This can be either with or without weights. Resistance training strengthens the muscle and increases the amount of activity you can do pain-free.
Conditioning exercise, also called aerobic exercise, improves cardiovascular fitness. There are countless benefits to aerobic exercise! Among them, it makes your heart and blood vessels healthier, prevents disability, and improves mood and well-being.
t wear them when playing on the piano/keyboard because I need the flexibility in my wrists (The exact same flexibility that causes me pain).
Does anyone here have a similar situation and/or advice?
tenofovir is the best drug for hbv and the most effective in cancer prevention and it has no resistance.not entecavir which has very low resistance but it has resistance it is not zero, it works less on liver cancer prevention but it is less heavy on kidneys so only if you have kidneys problems it is a better choice.
61) for genotype C vs genotype B, 0.34 (95% CI = 0.21 to 0.57) for precore G1896A vs wild type, and 1.73 (95% CI = 1.13 to 2.67) for BCP A1762T/G1764A vs wild type. Risk was highest among participants infected with genotype C HBV and wild type for the precore 1896 variant and mutant for the BCP 1762/1764 variant (adjusted hazard ratio = 2.99, 95% CI = 1.57 to 5.70, P < .001).
Conclusions HBV genotype C and specific alleles of BCP and precore were associated with risk of HCC.
Would it be doing reps of putting the wrist in flexion with resistance or extension with resistance? Or both perhaps? I also noticed ulnar deviation is weak on that wrist.. could that be linked to pain in push ups or is that unlikely? Thanks for any advice!
we posted so many studies and of course tenofovir is the most potent antiviral for hbv, the only one with 0% resistance on naive patients (no previous use of antivirals) and the only active when resistance to other antivirals is developed.
Usually the result of an increase workload caused by the high resistance the heart pumps against when there is narrow vessels, etc. If the underlying cause can be successfully treated the remodeled heart can return to a normal size.
Six years ago I had an enlarged left venticle and low contractility of the heart's pumping ability. The underlying cause was ischemia (occluded vessels) and vessel stenosis (narrow vessels)causing high blood pressure.
You don't say what you were using before Lantus. If the change has resulted in better control of your blood sugars, that could be why you are gaining weight. (Assuming, of course, you haven't increased food or decreased exercise). Unfortunately, some type 1's do develop insulin resistance after many years especially if during that time you ate carbs pretty freely and bolused for it. Insulin resistance leads to weight gain.
the explanation of why tenofovir is so potent on hbv and makes no resistance was explained by the intracellular levels reached by this drug, it is so bad no study ever showed how all other nucs are extremely poor at this and when i found this comparison i was very very surprised
all ohter drugs are so weak as intracellular levels, just look at lam vs tdf.we dont have etv here but it is probably very poor too.
Viread and Baraclude) is overstated; many patients develop no resistance at all, and the resistance rate, while higher than those for Viread/Baraclude, is not that much higher. Plus, if you do develop resistance, that's when you should start taking Viread (as mono or combo, he didn't say). And Viread is very effective in stopping Hepsera resistance. Recommendation: continue on Hepsera; no Viread until resistance is definitely found.
s benefits are less clear, according to the latest findings from the Pioglitazone vs Vitamin E vs Placebo for the Treatment of Nondiabetic Patients with Nonalcoholic Steatohepatitis (PIVENS) trial, reported online April 28 in the New England Journal of Medicine......."
See: http://www.medscape.com/viewarticle/721221?sssdmh=dm1.615392&src=nldne&uac=39980BG
I hope this helps.
Study Confirms Benefits of Vitamin E in Nonalcoholic Steatohepatitis
Megan Brooks
May 4, 2010 — Supplementation with the natural form of vitamin E (800 IU/day) has beneficial effects in patients with nonalcoholic steatohepatitis (NASH), but pioglitazone's benefits are less clear, according to the latest findings from the Pioglitazone vs Vitamin E vs Placebo for the Treatment of Nondiabetic Patients with Nonalcoholic Steatohepatitis (PIVENS) trial, reported online April 28 in the New England
The mechanism for resistance is differ from antiviral to antiviral. For example, Lamivudine resistance is more on and off. Adefovir is more gradual. Unless you research this area, it's hard to know what exactly is happening. But we do know all antivirals are at risk for resistance over time. And since you are 40 with early cirrohsis, you need the antiviral to stay working for another 30 years or so without resistance, that is a tough goal.
Here is the article I was referring to. I hadn't remembered that it addresses nonalcoholic steatohepatitis and not simple fatty liver so it may not be as applicable as I thought. Nevertheless I will post it.
m still very sceptical in starting the treatment in view of lack of understanding among healthcare group toward drug resistance......Since detection of HBV in 1965, what we are hearing from the so called experts are long-term treatment and then switching the course when resistance developed.....and continue long-term treatment again. I'm starting to understand what my Hepatologist trying to tell me when talking about treatment.
I should also mention that I have Ehlers-Danlos syndrome, flexibility type, although it hasn’t caused me any obvious problems. I don’t have health insurance currently and I’ve already tried a Medrol Dosepak without any relief.
Thanks for ANY insights or suggestions. I’m having a really hard time with this!
for prior null responders - 27% SVR for 1a vs 37% for 1b; for partial prior responders - 47% for 1a vs 68% for 1b; for relapsers no real difference - 84% for 1a vs 88% for 1b.
- cirrhotics did not do as well if they were prior partial responders or null responders but did the same if they were prior relapsers. Partial prior responders: 72% SVR if no or minimal fibrosis; 56% SVR with bridging cirrhosis; 34% if cirrhotic.
hbvdna blips and flactuations lower than 50iu/ml are normal as long as hbvdna gets immediately down to undetactable but if there are no kidneys problems tenofovir is the most safe drug as regards resistance, it is the only hbv drug with no resistance at 4 years and no resistance even if hbvdna is not fully und
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