The Half Decent Pharmaceutical Chemistry Blog

I'm proud of the way this blog is going on. Honestly, when I began, it was more because Mitch had asked me rather than a personal need.
Approximately two months later, I have definitely changed my mind: I'm so fond of this blog.

Yes, so far, I've almost lectured the readers, but things are going to change.
Today this half decent blog made a giant, significant leap towards FAME. There is a very prestigious site linking to this plucky new kid on the block: The Half Decent Pharmaceutical Chemistry Blog is now listed on Sciencebase.

For what concerns the weeks ahead, pharmaceutical chemistry is going to make his debut on these pages. And it'll have a massive impact with organic chemistry (syntheses and properties of drugs, biological pathways explained from a chemical point of view) ruling the place.

Moreover, many other themes will be discussed here, as well as those you can already find it.

As you can see, many important people already read The Half Decent Pharmaceutical Chemistry Blog.
Don't you want to join us?

Language distinguishes humans from the other hominids (chimpanzees, gorillas, and orangutans). We can point out three major aspects of language: writing, reading and speaking, which is the easiest to explain, from a nonscientific point of view.

Interestingly, languages have some points in common in every culture: every person learns it at an early stage of life and every language presents its own syntax (subject, verb and complement: what varies is the order) and grammar (every language has rules).

Towards the end of the 19th century, Paul Broca and Carl Wernicke found the two, most important areas of human brain linked to the ability to speak.
Both studied a pathology generally called aphasia (inability to speak). It has to be pointed out that aphasia can mean either the inability to understand heard words or to speak. And that made a huge difference.
The two aphasias, in fact, depends on which of the two areas has been damaged: Wernicke's or Broca's area.

Both areas are in the left brain in right handed people. In 70% percent of left handed humans, they are on the same side, while the remaining 30% is divided into a 15% who has them on the right and a 15% in both hemispheres.

Wernicke's area is in the posterior temporal lobe and surrounds the primary auditory area. That is quite obvious, because of the links between listening and speaking.
Words reach A1 and, then, Wernicke's area, which contains sound images of heard words. Hence, thanks to this area, we can comprehend the words we hear.

The information is sent to the Broca's area by the arcuate fasciculus. Broca's area is situated in the left inferior frontal region and creates those programmes for moving the organs we use to articulate words (mouth, tongue, etc.).

It has to be said that there are other parts of our brain, which are involved in speaking: the supplementary language area and some zones of motor and somatosensory cortex.

For what concerns aphasias, according to the different functions of the damaged regions, we can explain the three different types: a damage of the Wernicke's area will result in a receptive aphasia (the patient can't understand any language) and one of the Broca's area in an expressive aphasia (the patient understand what heard but won't be able to repeat it or to reply).
A problem with the auxiliary areas causes a problem of speech arrest: the patient is likely to develop a variable inability to conclude phrases.

Generally speaking, drugs are divided in agonist and antagonist molecules. Basically, the agonist triggers a biological response, while the antagonist doesn't.

Pharmacologists have always tried to explain how the biological effect is correlated with the binding of the molecule to its target. During their studies, scientists have pointed out differences among the agonists and, therefore, two subtypes of agonists were defined: partial and inverse agonists. Antagonists were subclassified too.
Partial agonists are unable to trigger the maximum response; inverse agonists, on the other hand, reduce the baseline activity of the target.

Clark was one of the first to formulate a theory that explained the aforementioned relationship: he said there is a linear dependence between responce and number of receptors occupied by the molecule (or, in other words, its concentration).
Clark's theory has been corrected, as time passed:new discoveries showed, in particular, that proteins are actually in a dynamic equilibrium between an active and an inactive form.
Consistently, an agonist(A) will bind to the active form of the receptor R (R*), while an antagonist will form an adduct with the inactive form.

Basal activity will be due to the number of receptors normally in the active form.

Let's go back to the definition of inverse agonist, now. We said these molecules bind to the receptor and REDUCE its basal activity.
Since the chances of a response are tightly linked to the active form, inverse agonists have an extremely higher affinity for the inactive form R, rather than R*.
Inverse agonists will bind to R, reducing the number of active receptor.
To sum up, agonists move the equilibrium to R*, inverse agonists to R.

According to its definition, an antagonist will not reduce the basal activity: it'll solely NOT trigger any additional biological effect, but it will leave unaltered the basal activity of the protein.
We should therefore consider our antagonist as the fulcrum of a balance, on whose  plates agonism (hence, R*, in order to trigger the biological respose) and inverse agonism (hence, R, in order to decrease the baseline response) were placed.

This can lead to the conclusion that antagonism doesn't REALLY exist, but is a mere pharmacologic, theoretical artifact, with no correspondence in a real biological system.

Yesterday, after posting my last message here, I suddenly found myself under the attack of evil forces, that thought, although this is likely to be the oldest computer in the Western world, this was a comfortable place for making some noise.

I like this computer and using it makes me feel proud. It's like an old sport car (like a Jaguar from the Sixties): any one can drive a brand new Mercedes S-class, just a few can live an old convertable, every day, sun, rain or snow.
In order to do it, the machine has to be treated gently and you must know it quite well.

As I said, despite having 64MB of RAM and Pentium III 450MHz, XP works very well: with my DSL connection, I can check the forums on chemicalforums.com, use messenger and listen to one of my MP3s with media player (10th edition, baby!).
There are certainly a few drawbacks: for example, I can't install a recent, decent, anti virus. What I will use, from now on, to protect this old fellow is a free firewall (XP has one, but I wouldn't rely on it too much).
I have to say that, once graduated (2 years), my family (yes, all of them, not only my parents: we are Italian, we are not very rich) will buy me a laptop, since I want to go abroad for a PhD. But this is a different story.

So, yesterday, I was hit by, above all, an enormous number of ad-wares.
I managed (fighting my way through windows constantly popping up) to download a free trial version of Panda Antivirus 2007, install it and run it. A high number of viruses and ad-wares was found. But, as I discovered, the most vicious of them survived.
I tried the Active Scan (over  night, I went to bed at 2am), which, finally, wiped out the viruses (that had increased in number, meanwhile) but can't remove ad/spy-wares: it only tells you where and how many they are.

This morning (woke up at 7) I was really disappointed: before going to the University I tried to manually delete all the files, but couldn't find all of them (c'mon, I didn't have enough time).
However, once at the university, I explained to my friends my problem: they had two different opinions (namely, Ad-Aware and Avast!).
I said that I would have entitled computing guru one of them, according to the outcome.

Well, thing is I opted for a third solution: I reinstalled the free trial but, this time, I updated its files first.
And, this time, it was all nice and smooth! 15 ad-wares detected and destroyed!

Oh, yes, I'm so proud of my old-fashioned sport coupé!

By the way, after a promising start, Chemblogs, now, looks like an abandoned building, with three or four people living in. It reminds me the final, well-known, scene of Blade Runner.
I hope Mitch will NOT think about shutting everything down: I really like writing a blog.

This is probably the first The-Half-Decent-Pharmaceutical-Chemistry-Blog-ish post. In fact, I put a nice artwork in order to smart up the whole thing.
You can say it's a double inspiration: Andy Warhol's Mao's portrait has been a frequent memory while studying how human brain analyzes colours.
So, this is my tribute to Andy Warhol: it's called Four Colours.

Atoms and molecules absorb light with a certain wavelength and the colour we perceive is its complementary. The object reflects or emits light with the remaining wavelengths.

Everybody knows we have two kinds of photoreceptors, namely cone and rod cells: cones are less common among the animals and fewer than rods in human retina.
Cones are concentrated in the part of the retina called fovea, which is the one we see with in daylight: we use to move it to focus our attention.
There are three different types of cones (Trichromatic Theory), generally referred as Blue, Green and Red. However, considering the sensitivity of their pigments, it is definitely more correct to name them S-, M- and L-cells (small, medium and long wavelength). Or, if you like colours, Blue, Bluish-Green and Yellowish-Green.

According to the wavelength of the light emitted by the object, the three cones are differently stimulated and their responses, in terms of frequency of action potential, vary.
Cone cells are connected to parvocellular ganglion cells only. The information, then, goes through magnocellular layers of the lateral geniculate nucleus and, reaches the primary visual cortex (V1).

Blobs are a group of cells of V1, located in the third layer. Blobs process colour information as cone cells, with the cells activated by specific wavelengths.
The information is sent to V2 rough stripes and, finally,the analysis of colour finishes in V4, where there are neurons which are sensitive to a small range of wavelength: this guarantees a very accurate analysis.
V4 cells are responsible for colour constancy too: looking at a complex scene (i.e. with varying lightning conditions), the colours of objects do not change.
In the end, the processed data are transmitted to the association temporal cortex.