Ptinue Continued Research

Hofmann worked for Bayer, which then named acetylsalicylic acid compound aspirin. Aspirin became commercially available in 1899 and today it is estimated that over a trillion aspirin tablets have been consumed by those in need of its curative effects.

In the movie, Whale Rider, there are great examples of Joseph Campbell’s article, Four Functions of Myth, which are: mystical myth, cosmological myth, social myth, and psychological myth. In the film, Whale Rider, Pai discovers her sense of self as she reinvents the Maori tribe’s creation myth to save the dying culture.

Escitalopram was discovered in 1997 and submitted to the Food and Drug Administration for approval in the United States of America in 2001. It was approved for the treatment of major depressive disorder in 2002 and for the treatment of generalized anxiety disorder in

The new drug blocks the sodium channel 1.7 according to the channel's level of activity - the more active the channel is the stronger will be the drugs hampering effect. Current drugs, in comparison, block the sodium channels without accounting for the activity level, which results in unecessary side effects. Sodium channels are located in nerve cell membranes. Their activation triggers the sensation of pain, the severity of which is proportional to the channels' activity level. According to the Zurich researchers, trigeminal neuralgia is believed to stem from a nerve deficiency or damage at the base of the skull. Given that local injections cannot reach this region, drugs are the first line of defense against the

Chronic migraine is a debilitating condition with over $1 billion in medical cost and $16 billion in lost productivity per year in the United States. (25) Here we examine the efficacy of onabotulinumtoxinA [botox] injections versus topiramate as prophylactic therapy for chronic migraine (CM) in adults. Chronic migraine (CM) is a specific and relatively newly defined sub-type of Chronic Daily Headache (CDH) defined as “more than fifteen headache days per month over a three month period of which more than eight are migrainous, in the absence of medication over use. Episodic migraine is the other migraine sub-type, which is defined as less than 15 headache days per month.” (14)

This was the simplest way to obtain all the drug information needed from the package insert. The approved indication for this drug is PAH for patients in WHO functional classes II-III. Treprostinil is classified as a prostanoid drug meaning that its mechanism of action causes vasodilation of arterioles, which halts proliferation of smooth muscle cells and platelet aggregation. For patients without hepatic impairment, treprostanil is started at a dose of 0.25 mg BID or 0.125 mg TID. Every 3-4 days the dose is increased by 0.25-0.5 mg BID or 0.125 mg TID. The goal is to titrate up to the maximal tolerated dose. The use of treprostinil is contraindicated in patients with moderate to severe hepatic impairment (Child Pugh Class B and C), but can be used for those with mild impairment (Child Pugh Class A). In this case, the initial dose would be 0.125 mg BID and is increased by 0.125 mg BID every 3-4 days as the patient can tolerate. Oral treprostinil has a 17% bioavailability, with maximum concentration occurring approximately 4 to 6 hours after administration. The absorption of this drug is increased with the administration of food. The AUC increased by 49% and the Cmax by 13% following a meal in healthy participants. Also, treprostinil is highly protein bound. The drug is mainly hepatically metabolized by enzyme CYP2C8 and is excreted mostly as metabolites and very little as the parent drug. Treprostinil has drug interactions with anti-hypertensive medications due to risk of hypotension and CYP2C8 inhibitors. Common adverse effects include: headache, diarrhea, nausea and flushing. Rare adverse drug reactions include: hypokalemia, pain in jaw and abdominal discomfort. Precautions and warnings are an increased risk of bleeding, rebound PAH symptoms after sudden discontinuation, increased drug release when taken with alcohol, and aggravation of

The first theory is cortical spreading depression (6). A wave of decreased electrical activity of the nerves in a patient’s brain leads to a change in neural and vascular function (6). In response, an aura is present prior to a migraine. Furthermore, hyper excitability of trigeminal nerves activates the discharge of substance P, neurokinin, and Calcitonin Gene-Related Peptide, all of which are neuropeptides associated with inflammatory processes (8). These substances cause the release of pro-inflammatory mediators in the brain and for vasoconstriction then vasodilation to occur, leading to a migraine (4).

Many genetic factors are also clearly an indicative of the susceptibility to migraine headaches. While the exact mechanism remains uncertain, it is thought that migraines are caused by genetic abnormalities that cause hyper-excitability of the nervous system. The nerve terminals release neurotransmitters such as substance P, neurokinin A (NKA), and calcitonin gene-related peptide (CGRP), which then binds to the receptors on intracranial blood vessels, causing vasodilation, mast cell degranulation, increased vascular permeability and blood vessel edema, plasma protein extravasation, and sterile inflammation. The cranial nerves are then reactivated causing the pain experienced during a migraine.

Migraine is a form of neurovascular pain syndrome with alters central neuronal processing by activating the brain stem nuclei, cortical hyper excitability, and spreading cortical depression ("Migraine: Headache: Merck Manual Professional", n.d.). Migraine also affects the trigeminovascular system, which triggers neuropeptide release and causes painful inflammation in cranial vessels and the dura mater ("Migraine: Headache: Merck Manual Professional", n.d.). Migraine attacks are not caused by a primary vasvular event, but episodic and varies among different patients (Goadsby, Lipton, & Ferrari, 2002).

After the successful synthesis, studies on Piracetam were done from all around the world to focus on specific aspects such as to improve memories and the neuroprotection on patients with the Alzheimer’s disease. These studies expanded to other racetams such as Aniracetam and Oxiracetam. Aniracetam was developed by Hoffman-La Roche in 1970’s which contributes to the neurotransmission by activating the Acetylcholine receptors. Oxiracetam was developed in 1993. Its main goal is to improve the capacity to process information. Racetams were revolutionary because there are no side effects and they combine both physiological and medical

Classification can be difficult, however, due to overlapping effects. Sicilian Gambit, can more accurately show receptor blocking properties, but is very complex and hard to memorize. Due to those factors the Vaughan-Williams classification is used (Homound, 2008). The Vaughan-Williams classification has five levels. Class I slow electrical conductions in the heart by sodium channel blockers. Class II are beta-blockers, which reduce the transmission of impulses within conduction by blocking sympathetic nervous system stimulation. Class III agents prolong the repolarization of the cell membrane by blocking the potassium channels. Class IV is calcium-channel blockers. They reduce the movement of ions during the calls action potentials. And lastly class V are variable mechanisms, an example of this would magnesium sulfate. (Levine) (www.drugs.com). They can also be classified clinically by agents that work on ventricular arrhythmias and supraventricular arrhythmias. Ventricular arrhythmias tend to be more serious and are treated with medications like lidocaine and moricizine. Supraventricular arrhythmias are less serious and may not even require treatment

Using rat models of neuropathic pain, Nav 1.7 selective blockers have been seen to be successful in inhibiting Nav 1.7 activity (4).

Jae Y. Choe, PhD., Drug action and interactions: antihistaminic drugs. Unites States: McGriw Hill Medical; 1937, p. 93-94.

Eicosapentaenoyl serotonin is a hybrid molecule patterned after arachidonoyl serotonin. Arachidonoyl serotonin is an inhibitor of fatty acid amide hydrolase (FAAH) and also acts as an antagonist of transient receptor potential vanilloid-type 1 (TRPV1) channels. Arachidonoyl serotonin is analgesic, reducing both acute and chronic peripheral pain in rodents [1, 2]. The effects of replacement the arachidonoyl portion with eicosapentaenoic acid have not been investigated. Replacement of arachidonate with saturated 11- or 12-carbon fatty acids generated compounds that potently inhibited capsaicin-induced TRPV1 channel activation with an IC50 of 0.76 μM. This compound showed no effects on wblocking FAAH-mediated hydrolysis of arachidonoyl ethanolamide

Throazine, other major tranquilizers developed 1952 - The French psychiatrists Jean Delay and Pierre Deniker report that Thorazine ® calms hospitalized chronic schizophrenic patients without causing clinically significant depression. The drug is called 'hibernotherapie' because patients became quiet, like