Sensing clinical

On the whole, there is enough evidence that HTs, overall ETs, exert positive effects in the human body and may play a major role in the prevention and management of several diseases. However, more research is needed to fully understand whether ETs and/or likely their in vivo metabolites are the responsible compounds linked to the health-promoting features of foodstuffs that are rich in ETs. In this sense, clinical studies with purified extracts may shed light on this question. In addition, human trials should include enough subjects to avoid the... 

Clinically Efficacy. It is evident from the mechanism of action of antihistamines and the etiology of allergic diseases that antihistamines in no sense achieve a cure of the patient s allergy. After the adrninistration of a therapeutic dose, a temporal blockade of the effects of histamine is obtained. Whereas classical antihistamines needed at least twice daily adrninistration, for most of the more recently introduced agents adrninistration once daily is sufficient. 

E. J. Ariens, Stereochemistry, a basis for sophisticated non-sense in pharmacokinetics and clinical pharmacology, Eur. J. Clin. Pharmacol. 1984, 26, 663-668. 

MDA had unique psychoactive properties that were different from hallucinogens such as LSD or mescaline. While MDA in high doses appears to be hallucinogenic or psychotomimetic, it seems not to have been used for this effect, but rather for its effects on mood production of a sense of decreased anxiety and enhanced self-awareness. Even early reports described the desire of MDA users to be with and talk to other people (Jackson and Reed 1970). MDA is also the only substituted amphetamine that received serious clinical study as an adjunct to psychotherapy (Yensen et al. 1976). 

Rules and filters do exceptions exist Off course they do. Common sense is required. There is a natural priority order in drug discovery decision making. Clinical information trumps all. Next in importance is high quality experimental evidence, e.g., in vivo animal experiments. Rules and filters come into play when clinical and experimental data is lacking. 

The clinical scenario and the severity of the volume abnormality dictate monitoring parameters during fluid replacement therapy. These may include a subjective sense of thirst, mental status, skin turgor, orthostatic vital signs, pulse rate, weight changes, blood chemistries, fluid input and output, central venous pressure, pulmonary capillary wedge pressure, and cardiac output. Fluid replacement requires particular caution in patient populations at risk of fluid overload, such as those with renal failure, cardiac failure, hepatic failure, or the elderly. Other complications of IV fluid therapy include infiltration, infection, phlebitis, thrombophlebitis, and extravasation. 

Although one cannot readily identify any comprehensive, official pronouncement on the topic of development bioequivalency, it is apparent that in many cases FDA officials have adopted a pragmatic and common-sense approach to problems of this type. Obviously, in development bioequivalency our fundamental objective should be, for example, to build an appropriate bridge between F3 and F3 and F2 and F3 such that it is legitimate to use data obtained in clinical trials with F3 and F2 to support a conclusion of safety and efficacy for F3. Depending on how substantial the differences are between Fi and F3 and F2 and F3, the required bridge can be very simple or possibly more elaborate. 

Dozens of clinical trials plus decades of clinical practice plus millions of content patients can t be that wrong. Whatever the bias in whatever the study, common sense clearly says the sum of the parts attesting antidepressants efficacy blatantly outnumbers the evidence showing the opposite. The use of these antidepressants is now deeply rooted and well-established in medical society worldwide, it s safe, it works, and there s no shadow of doubt about it.2... 

Although the therapeutic effectiveness of antidepressants seemed astonishing 40 years ago and still seems indisputable to many people today, it is, in fact, an illusion. As I have shown earlier in this book, the difference between the effects of antidepressants and placebos is clinically insignificant, despite clinical-trial methods that ought to enhance it. But strangely enough, it is not the ineffectiveness of antidepressants that seals the fate of the chemical-imbalance theory. Rather, it is their effectiveness. The problem is that too many different types of antidepressants work too well for the theory to make physiological sense. 

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