Mr. NI:
I was wandering when you will attack me again after my posts on this tread. Obviously didn't pass long. You can't forget my disagreement with you on some companies. I do not think that I am at all important or factor regardless if someone is reading my posts or not.
For other reader, my post on CNSI thread:
techstocks.com
Post upset Mr. NI in that way that he just wait for chance to discredit my opinion on some issue that we discuss. I do not have problem with opponent view but on which way is presented....
In my first response I was generous to him, but this time I will be nasty.
NI wrote: >> I would like to commend you on one very accurate statement; that you are indeed `very short on neurology/CNS disorder.'<<
Even if this is correct, nothing's wrong as it isn't my training, but Mr. NI's mathematical training, basic math science knowledge, is on level of my 6 years old daughter.
NI:>> 2) You make several references to `manipulation' of the data. You clearly do not have any training in clinical research. The fact that 34% of the placebo group had mild strokes compared to 22% of the drug group illustrates the fact that randomization of patient assignment does not assure even distribution of patient attributes.<<
I do not have clinical research experience, do not need to have, but how can you explain that in statistical randomization of the patients, both groups, placebo and drug in double blind study, have almost equal number of the mild stroke patients with facts that one group is twice bigger than other. This is >50% increase in placebo group not a deviation from *even distribution*!!!
>>1) Your make a reference to `other drugs for post-stroke rehabilitation.' Could you please tell me what those drugs are? The only drug approved for stroke is t-PA, which has to be given within 3 hours of the stroke, and is dangerous because of the risk of
increased cerebral hemorrhage.<<
There are several disease conditions in stroke victims and patients which has to be treated seriously. This condition are in medical correlation with stroke not are compensatory for stroke. If Citicoline do not prove reduction in ischemic size/damage ( for which I have doubt), than by you it will be *compesatory drug for stroke*, regardless of the improved neuro-functional recovery. Why is IPIC expanding Citicoline indication in new trials? Yes, you give several good examples and drugs.
NI: >>Secondly, your statement that citicoline `failed' in LOCF analysis (it was significant at .06).......<<
My reading and Interneuron Ph. statement is that by LOCF ( I must say that my view of the LOCF statistic was wrong) analysis of the data (p<0.05 and p<0.08) are not statistically significant. Maybe your math is math without numbers (Did you read today article in LA TIMES on new math?)!
Also, accounting 18 % mortality in both groups and excluding mild stroke distribution, than in placebo group mortality is 27% and in drug is 22%. Was this 20% difference in distribution also deviation from *even* or placebo group is purposely *loaded * with specific stroke patients. IPIC drug's investigators and consultants (Redux) are known for .......
Am I who is manipulating with data? What will be my reasons?
NI:>> The Japanese data is not pivotal, but it is a valuable supplemental source for the NDA, regardless of
mode of administration or dosage.<<
This is mainly incorrect and there are main point. For those who do not know:
1. Citicoline (CTD-choline or Cytidine-diphosphate-choline) in natural compound and precursor for synthesis of the phosphatidylcholine, one of the active components in the synthesis of the phospholipides (biologicaly: membrane formation and repair).
2. Citicoline , in oral administration, degraded by phospholipase in gut, enter in blood as Cytidine (one of the nucleozides) and Choline. Both compound can pass BBB and reach brain tissue/neurons.
3. Citicoline in i.v. infusion circulate in plasma and because it is more polar molecule than its main ingradients (phosphates are polar compounds) its conc. in brain is lower. I was wrong in last post regards the drugs size in Takeda trials (1000mg/daily for two weeks)!
4. In the brain choline can enter biochemical pathway for Citicoline synthesis or form acetylcholine, neurotransmiter wich has several important function in brain bio-chemistry.
The question is there difference in this two administration/drug delivery to brain? Interesting is that in Takeda study there are no side effects as they were associated with higher Citicoline oral dose, as far as I know. Why? Also, it is shown in animal study that large dose of the Citicoline are needed for reduction of the neuronal damage (ischemic size) in stroke model. IPIC trials is at lover dose to eliminate side effects (which can be atributed to elevated acetylcholine conc. in brain) and question is on achieved and distributed level of the Citicoline in brain comparing this two administration. Why Takeda study has better results?
NI:>> 4) Your statement that citicoline is not effective in the first 48 hours `when most neuronal damage is done' is untrue on the first count, partially untrue on the second. Infarct damage continues to expand through the ischemic penumbra for as much as 5-7 days after the infarct.<<
Can you provide data that Citicoline is effective in stroke in the first 48 hr? Where are the study which show Citicoline neuro-effects on infract demage in first 48 hr? Also, will you provide statistical data for infract volume as function of the time. (small math)
NI: >> There were a number of other errors in your postings, but this is enough.<<
There was, are, and will be many errors in my posts. This and other SI thread are to teach and educate any of as. To correct errors. No exceptions. But, your way is disqusting and deserve even worse reply than was this. If you elect to reply than check facts and explain with depth.
Non-neurologist |
