Welcome to the Journal of Articles in Support of the Null Hypothesis
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Why Should I Register and Submit Results? - …
Initially we tested the effect of STAT3 inHER2-positive breast cancer. We wished to determine whether theco-expression of HER2 and ER induced STAT3 phosphorylation, andwhether pSTAT3 promotes stem-like cell phenotype in the breastcancer model. To this end, the basal expression of STAT3 and stemcell markers were examined in various human breast cancer celllines by western blot analysis and real-time PCR. STAT3 wasphosphorylated in MCF7-HER2 cells, but not in MCF7 wild-type(). In addition, STAT3 wasphosphorylated in BT474 as well as at very low level in SKBR3. MCF7wild-type lacks HER2 amplification and SKBR3 lacks ER. This isconsistent with previous data in which MCF7 WT did not typicallyshow phosphorylation of STAT3 (,).Moreover, we found that the stem cell markers, Oct-4 and Sox-2,were expressed in MCF7-HER2 and BT474 cells, but not in MCF7wild-type and SKBR3 ().Real-time PCR analyses confirmed the upregulation of stem cellmarkers in HER2-overexpressing, ER-positive cancer cells (). Our results support thehypothesis that HER2 over-expression and ER positivity promoteSTAT3 phosphorylation and induces the stem cell-like phenotype.
To investigate whether a PQQ-supplemented diet wasable to rescue the premature aging phenotype ofBmi-1/ mice, statistical analysis of thephenotype, body weight and percentage survival was performed forthe different groups of mice. As shown in , when compared with the normaldiet WT mice, the BKO mice who were fed a normal diet exhibited asignificant premature aging phenotype, body weight loss and adecreased percentage survival rate. By contrast, the BKO miceadministered the PQQ-supplemented diet exhibited a partiallyrestored total body size, increased body weight and a prolongedpercentage survival when compared with the BKO mice fed the normaldiet. These results support the hypothesis that thePQQ-supplemented diet partially restored the premature agingphenotype in the Bmi-1/ mice when comparedwith the mice fed a normal diet.
What Is the Purpose of Trial Registration and Results Submission
Usually, the null hypothesis is boring and the alternative hypothesis is interesting. For example, let's say you feed chocolate to a bunch of chickens, then look at the sex ratio in their offspring. If you get more females than males, it would be a tremendously exciting discovery: it would be a fundamental discovery about the mechanism of sex determination, female chickens are more valuable than male chickens in egg-laying breeds, and you'd be able to publish your result in Science or Nature. Lots of people have spent a lot of time and money trying to change the sex ratio in chickens, and if you're successful, you'll be rich and famous. But if the chocolate doesn't change the sex ratio, it would be an extremely boring result, and you'd have a hard time getting it published in the Eastern Delaware Journal of Chickenology. It's therefore tempting to look for patterns in your data that support the exciting alternative hypothesis. For example, you might look at 48 offspring of chocolate-fed chickens and see 31 females and only 17 males. This looks promising, but before you get all happy and start buying formal wear for the Nobel Prize ceremony, you need to ask "What's the probability of getting a deviation from the null expectation that large, just by chance, if the boring null hypothesis is really true?" Only when that probability is low can you reject the null hypothesis. The goal of statistical hypothesis testing is to estimate the probability of getting your observed results under the null hypothesis.
One gene–one enzyme hypothesis - Wikipedia
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