Withdrawal effects are generally associated with drugs that induce feelings of euphoria by stimulating the reward center of the brain, either directly (cocaine, morphine) or indirectly (alcohol, nicotine). The classic hallucinogens have little effect on the dopaminergic pathways and hence do not cause serious withdrawal effects as observed with ...
What are the most popular theories in a nutshell?
To date, the mechanism of action of paracetamol is not fully understood. There are some experimental evidences, but it is difficult to put things togheter. It is now clear that paracetamol acts contemporaneously via at least three pathways:
The inhibition of cyclo-oxigenase (COX)
The main mechanism ...
Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse.
Given that you ask
...how to make GABA pass the blood brain barrier?
I assume that
You wish to elevate GABA by exogenously administering a compound;
That compound has to cross the blood-brain barrier (...
This is a tough topic, have a look at the following references and see, if they can help you:
Structural modelling and dynamics of proteins for insights into drug
Ligand entry pathways in the ligand binding domain of PPARγ receptor
Pathway and mechanism of drug binding to G-protein-coupled receptors
Molecular Dynamic Simulation and Inhibitor ...
No, orally taken painkillers act systemically.
Taking a painkiller orally results in the drug being taken up into the bloodstream by the digestive system. From there it can potentially reach all tissues.
In other words, a pain response does not act as a chaperone. A hypothetical drug that would home in on tissues with a pain ...
Short answer: different people have different amount of active receptors.
In treatment, combination scores of Pharmacodynamics and Pharmacokinetics determine the final effect of the drug.
Receptors determine many effects of the drug in many pathways.
Different people also sense pains differently (Psychology).
The purpose of treatment is ...
From the dedicated cisplatin website and Drugbank it appears its use is quite diverse and not confined to testicular cancers. Further, your linked (Siddick, 2003) paper mentions on the first line of its abstract that cisplatin has clinical activity against a wide variety of solid tumors.
Cisplatin.org mentions that cisplatin finds use as chemotherapy ...
As Christiaan already pointed out, this depends on the pharmacokinetic and pharmacodynamic parameters. The effective drug concentration depends on the drug-receptor association constant and the drug degradation constant (for a highly simplified model). The degradation/removal depends on the abundance of the enzyme catalyzing this reaction.
Ethanol is ...
Absolutely, the two I've had the most success are working with a radiolabeled and a fluorescently labeled version of the drug. Many drugs autofluoresce as well and this can be easily tracked.
When it's labeled as mentioned above microscopy or a luminometer, spectrophomoter or a scintillation counter can evaluate fractions or whole cells, or purified ...
Regarding the tissue partition coefficient, Li et al. said: "By using such a parameter, it is assumed that there is the same transfer kinetics of nanoparticles from blood into tissues as from tissues back into blood circulation, and an equilibrium of concentrations between blood and tissue exists. These assumptions may not be appropriate for nanoparticles."
To go the PBPK route:
I would recommend using the organism parameters and structure from the whole body platform model by Shah and Betts.
Shah, D.K. & Betts, A.M. J Pharmacokinet Pharmacodyn (2012) 39: 67. doi:10.1007/s10928-011-9232-2
They have assigned a plasma space volume, plasma flow, blood cell space volume and blood cell flow for each organ and ...
Any apparently "magical" powers of cisplatin in testicular cancer have more to do with the disease than the drug.
Unlike the similarly male-specific prostate cancer, testicular cancer is generally seen in young men in their 20s or 30s (click on "number of new cases and deaths"). This paper suggests, as is generally thought to be the case for earlier-onset ...
Most NSAIDs derive their analgesic effects from inhibit the cyclooxygenase (COX) enzymes that produce the prostaglandin-H2 precursor to the prostaglandins that sensitize neurons to pain.
Edit: With respect to where this takes place, the COX enzymes are expressed in inflamed tissues as well as constitutively in the stomach and kidney. The prostaglandins ...
I don't know of any interesting mechanism that is specific to pain killers, so I will instead answer for drugs in general.
Drug action is a complex process consisting of many steps. Let's take a simple example: A systemic direct inhibitor of a kinase. This drug would need to*:
Be absorbed into your bloodstream
Remain in your bloodstream for sufficient time
I wasn't sure when I first read this, but this is actually a very interesting question.
Right now there seem to be two completely divorced lines of inquiry that researchers are pursuing with respect to the antimalarial drugs.
One group of researchers is working on working out the mechanism by which say, chloroquine and its ilk bind to and interfere with ...
Your source (DrugBank via PubChem) is describing the typical pharmacokinetic information (ADME, absorption, distribution, metabolism, excretion) on Providine-Iodine, under the assumption it is not absorbed. It's true, a thing that is not absorbed has no volume of distribution, is not metabolized, and is not eliminated.
Though Providine-Iodine is not ...
All things being equal, does that mean an administration of a drug will be twice as potent if the bioavailability is doubled?
Bioavailability is initially taught, and sometimes reported as a proportion, $F$, the concentration in drug in plasma under a test condition (typically oral administration) over the concentration of of the same dose of the drug under ...
The Wikipedia page for vascular endothelial growth factor (VEGF) looks pretty useful - it explains that VEGF stimulates the growth of blood vessels. If this gets out of balance, for example in diabetic retinopathy and wet form age-related macular degeneration, one treatment is to attempt to reduce levels of VEGF in the circulation, using monoclonal ...
From your article:
Sig-1Rs localize at the interface between the endoplasmic reticulum (ER) and mitochondrion, which is known as the mitochondria-associated ER membrane (MAM).
Consequently, they are found in a variety of areas within the central nervous system as well as in other types of cells throughout the body (notably cardiac cells).
An important ...