I did some research. Here is my conclusion: it is important to control bs spikes. The so-called basal levels primarily inhibit gluconeogenesis, the process whereby glucose is synthesized in the liver. This mechanism provides glucose for glucose-dependent tissues while sugars are not being assimilated from food. Without insulin, blood sugar rises while fasting. But basal levels are not adequate in the face of sugar liberated during digestion of food, especially simple carbohydrates. The digestive process triggers a rapid but transient release of insulin from the pancreas that triggers uptake of glucose by tissues that can sink the excess. In some individuals up to 70 times the basal levels are secreted normally to control exogenous sugar. Excessive sugar causes glycation of protein, whereby crucial proteins are rendered inactive due to permanent binding with sugar that occurs above threshold concentrations. Afrezza closely mimics this normal response to eating, thus preventing glycation. It does so first because it becomes available via the lungs in seconds rather than tens of minutes as is the case with injection. Secondly the molecule does not require preprocessing in the liver before it can be utilized.
What I'm seeing in research papers is that controlling post prandial BS levels decreases the amount of basal insulin needed for control. Taken together this can produce a significant reduction in A1c. A1c is a proxy for tissue damage caused by high blood sugar. Afrezza will eventually get labeled for prediabetics and gestational diabetes IMO
I was a respiratory therapist for over 20 years and did hundreds if not thousands of PFT's. Not one of them was read by a pulmonologist and very few were done in a facility where any physician interpreted the tests. It's a simple procedure to get the FEV1 and there are relatively inexpensive hand held devices to do it. My opinion is that the FDA is captured by BP and the PFT label requirement is the result of competitor pressure on the board. I predict that experience will show that while some reactive bronchospasm occurs no long lasting impairment in pulmonary function will be seen with habitual use.
OK I've watched the arguments and read the decision (again). But I'm not totally clear on what you're saying, save for the speculation bit.
What I see is that SC found that a type 2 agreement is operant, and therefore expectation damages *can* be applied. The problem for VC is that he already found that a lump sum is too speculative, and that specific performance is out because the lats was incomplete; missing essential terms even though economic terms were definite enough to be enforceable. Further clouding the economic terms in the LATS is evidence that there was discussion of differing economic terms after the date of the term sheet.
Now he goes back and reverses himself saying a lump sum is supported by the record by way of expert testimony and a formula he devised to apply it. And yet the economic terms of the LATS provide no means for arriving at a lump sum owing to the temporal and probabilistic characteristics of the proposition.
I think what you're saying is that since there's no clear way to come to a fair and accurate way of determining what the value of the license was in 2006 using either of the two methods available under a type 2 agreement, the court can only award reliance damages.
It may well be the case that the spikes and subsequent damage are what cause derangement in glucose managent. Certainly reduction in the magnitude of sugar levels around mealtime will slow progression of disease. I believe under the right circumstances type 2 diabetes can be reversed. This except from the british journal of anesthesia explains why.
Insulin normally has a tonic inhibitory control (what Schafer termed ‘chalonic’ action) on the supply of energy substrates arising mainly from metabolism in the liver, muscle and adipose tissue. Normally insulin ensures sufficient release of appropriate substrate to allow humans to cope with the eventualities of life in a highly controlled manner. Once insulin deficiency develops this control is lost, and energy substrates are over‐produced and flood the system. The metabolic consequences result from the excess of substrates not (as is often misconceived) by a lack of energy substrate getting to the tissues.
I'm a pre-diabetic, on metformin.
According to the american cancer society you are wrong:
Tobacco smoking is by far the leading cause of small cell lung cancer. Most deaths due to small cell lung cancer are caused by smoking or exposure to secondhand smoke.
FEV1 is all the FDA said. But I understand more comprehensive measurements with a printout are needed for reimbursement of the test these days. If MD didn't care about using the PFT as a revenue generator they could use a very inexpensive device without a printer and just put the FEV1 in the progress notes. We used these flowmeters all the time to monitor asthmatics in the hospital. I see one on ebay with several washable mouthpieces for 50 bucks. The idea is to get a baseline and then monitor to make sure there's no drug-induced sensitivity which would cause wheezing/bronchospasm or inflammatory process that impairs flow. Inhalation of powders in pulmonary disease is well-established. We started using cromyln sodium powder in the early 70's. Since the insulin is synthetic I don't see why there would be any allergic issues. The TS carrier is supposedly inert. I think the concern came from AE of cough in the trials. Some coughing is experienced with other inhaled powders used to treat COPD but the benefit outweighs the side-effect and the cough usually goes away, just like cigarette smoking.
It has been known for months stock would be delisted. If it doesn't hold I will be buying more. All the institutions that can't own pinks are already gone. Today's action is just buzzards looking for bones to pick. Look at all the covering into the close.
scientific journal Basic and Applied Social Psychology has banned articles that use P-values. The problem is that the null hypothesis is ambiguous when applied to propositions that reject it.
" P value calculations tell you only the probability of seeing a result at least as big as what you saw if there is no real effect. (In other words, the P value calculation assumes the null hypothesis is true.) A small P value — low probability of the data you measured — might mean the null hypothesis is wrong, or it might mean that you just saw some unusual data. You don’t know which."
No decision in the appeal. Siga has submitted opening arguments. AFAIK next is PIP rebuttal. Bankruptcy proceedings come up again in June at NY court.
Good find. Explains the clinical picture and the rationale for small N.
The box being the paradox that there can be damages when the amount is arbitrarily chosen. This would seem to be the definition of punative.