Compare between the new and the old enforcement arbitration law of Research Paper

Compare between the new and the old enforcement arbitration law of Saudi Arabia and the legal effects on the international agree - Research Paper Example 15). After this law, the previous law was referred to as the old law, which pledged to modernize the nation’s arbitration regime in a number of ways. Most significantly, this new law restrains the nation’s court intervening power with regards to arbitration through acknowledging the parties’ autonomy to deal with the arbitration process (Rawlings et al. 16). The new Saudi Arabian law addresses a vital concern under the old law, which is the power to the nation’s courts to reopen, as well as effectively re-litigate awards on their principles (Jones Day 1). Even though, the new law is an acknowledged enhancement, which promises considerable changes in Saudi Arabia, the event of change in practice remains unclear to date. Much will rely on the text of the executing principles and where the country’s courts stand with regards to the new law (Rawlings et al. 16). Many critics consider that this law slightly killed the independence of the Saudi Arabian co urt system while others argue that the law works to develop the nation, unlike the old law. This paper will take into consideration these arguments and bring out which law is better. It will also discuss the international effects of the legislation of either of the laws in order to note the significance of each. Provision of the Two Laws The New Law Encouraged by the UN Commission of International Trade Law (UNCITRAL) Model Law on International/Foreign Commercial Arbitration, which has been endorsed by a number of regimes, Saudi Arabia’s new law acknowledges parties’ independence to concur on significant aspects of their arbitration process (Rawlings et al. 44). Most importantly, the law respects the right of groups to arbitrate under a governed set of arbitration principles. This is a significant development, which tackles a region of uncertainty, which was present during the old law days. This new law acknowledges parties’ option of governing language, law and arbitrators provided that the sole arbitrator is a qualified lawyer (Rawlings et al. 44). This law also bestows with the entry under the old law for groups to file their agreements with courts for validation prior to commencing arbitration (Jones Day 1). The new law further respects that an agreement between parties can be published in a correspondence among them. The law dictates that arbitrators should have an encouraging obligation to keep groups updated with circumstances, which might lead to a conflict of interest (Rawlings et al. 45). This new law dictates straight procedure for resolving disputes by the arbitral tribunal, such as time restrictions for complaining groups to lodge doubts in the applicable court (Jones Day 1). This eliminates the capacity of groups to oppose to the execution of arbitral awards on such grounds when they did not raise it earlier within the time limit (Rawlings et al. 45). When the groups have not concurred on specific arbitration regulations such as the ICC, the law dictates a detailed arbitration course, which applies by default to all (Jones Day 1). The arbitral award should be granted within a year from the date, which arbitration started depending on the arbitral tribunal's authority to prolong this by an extra 6 months and the groups’ ability to concur with longer extensions. This grants the arbitral board a much more practical timeframe to resolve key commercial disputes, which

Securities Markets 2 (Assignment) Assignment Example | Topics and Well Written Essays - 2500 words

Securities Markets 2 ( ) - Assignment Example The parent company of CAO is China National Aviation Fuel Group Corporation (CNAF), which is the largest state owned enterprise in PRC region (Prima Professional, n.d). The parent company is a well-known aviation transportation and logistics service provider in PRC. CNAF owns 51% of total shares that are issued by CAO. The year, 2005, was not at all good for CAO, since it had to face a loss of $550 million (China Daily Information Company, 2007). The situation led to the collapse of the institution, until it was revived by its parent company. The facts that are learnt from performance of CAO, regarding valuation of derivative, are elaborated in this section (Ernst & Young Global Limited, 2014). The CAO, in the initial period of their business, â€Å"traded in over-the-counter (OTC) swaps and exchange-traded futures† for protecting their business from risks associated with procurement of oils. The company purchased and sold risk free options on behalf of airline companies, who are their clients. So, there is a good source of income for CAO from the bid-ask spread, without exposing the company to vitality of the oil markets. During the third quarter of 2003, the company started to conduct options trades as speculators for earning profit from constructive market movements, which was observed in the oil-related commodities market. The company had started trade on the belief that oil prices will move upward. The trading strategy indicated purchase of call option and sale of put option simultaneously (Amato and Gyntelberg, 2005). Thus, it created a synthetic long position in the oil market, without purchasing the commodity outright. When price of the oil increased, the ca lls, which were purchased earlier, exercised at a profitable rate. The puts were not exercised and the company profited from premiums, which were collected from the options at the time of sale (IBS Case Development Centre, 2010). The put that were sold in the security market were not

The Workplace Challenge Essay Example for Free

The Workplace Challenge Essay Unit 5 serves students ages 14-21. The program matches suitable jobs for every adolescent through evaluation of their interests and developing skills for future jobs. (Shafallah 2007) Aside from these major programs, the school also offers clinical and therapeutic services as well as school health and nutrition oversights. The Students The population of students in Shafallah is 426 who are between ages three to twenty-one years. The students are with mild, moderate, and severe learning challenges. These are children, adolescents, and young adults with Down Syndrome, cerebral palsy accompanied by intellectual or developmental disabilities, and autism spectrum disorders and they make up the majority of our student population. Class size ratio of teachers to students is 1:3 in all school programs except the Autism Unit, where the ratio is 1:2. The Teachers There are currently 125 employed by the school. These are all professionals with varied expertise. Due to the limited professionals who have specific expertise in the fields needed by the school, many, about 25% of the teaching force are foreign nationals from the United States, Canada and other European countries, to serve for at least two (2) years in the school. The remaining 75% are from the different provinces in Qatar. All teachers in the academic unit are degree holders, mostly with masters and doctorate diploma with corresponding licenses in the fields of education, medicine and psychology. The age range is wide, from 25 years to 60. This includes teachers who are at the same time in the management level. The Management Policies and legislations in the school are made by the school board headed by Her Highness Sheikha Moza Bint Nasser Bin Abdullah Al-Missned, the Chairperson of the Supreme Council of Family Affairs. The executive functions are performed by the management team composed of 20 experienced professionals organized in the form of a Management Committee. The head is the Managing Director who is from the United States, followed by an Assistant Managing Director who is from Qatar. 75% or majority of the members of the ManCom are foreign nationals while 25% are from Qatar. The academic and service units are fully manned with leaders but it is noticeable though that in the backhouse, the school has not installed a department that will handle the concerns of human resource or a human resource department. In its absence, the public relations department handles the processing of teachers and other admin staff recruitment. On the surface, observing the transactions in the offices and the other facilities, the movements in the school campus, the school was seemingly operating normally. But as we dig deeper, we would find some areas of major concerns which should be cause for immediate and decisive actions by the school. The school has been experiencing high turnover of teachers for the past two years. Because resignations were frequent, recruitment which is done regularly by the Public Relations Department. The massive tasks in recruitment have eaten up much of the time of the PR staff, so that major functions of the department are de-prioritized. The ManCom with its American Managing Director concentrated on sourcing funds to augment to the schools facilities. The proceeds from the students’ tuition were not sufficient to finance the expansion programs and the upgrading of facilities of the school. The ManCom had to source for international funding agencies for additional support including the schools benefactor and strong advocate, Her Highness Sheikha Moza Bint Nasser Bin Abdullah Al-Missned, the Chairperson of the Supreme Council of Family Affairs, who is also the Chairperson of the school board. In the first quarter of 2007, the ManCom’s attention was called by the school board to solve complaints by the parents and the community about the declining quality of services provided by the school. This resulted to the ManCom’s creation of an adhoc committee to investigate the facts, study the causes of the problems and recommend solutions to the findings. The adhoc committee reported the major findings of their investigation. The complaints of the parents and the community were due to overcrowding of students in classes, where instead of 1:3 ratio, there were 10 students already being handled by each teacher. This was due to the lack of teachers handling specific subjects.

Porters Five Forces model Essay Example for Free

Porters Five Forces model Essay In the banking industry rivalry among its competitors is a pretty common game. A few larger banks always dominate larger markets offering more locations and faster paced technologies for those consumers. Usually in a these larger areas larger banks can thrive because the expectation level of personalization is much lower since consumers don’t feel the need to frequent a location or rely on individuals to help them. While as areas grow smaller in population Small Community banks emerge with a fewer number of larger entities to compete with these banking giants being able to offer a more personalized approach allowing people to rely more on human interacting with technology, not only relying on the technology. Most banks primary function is to lend money of the deposits they gain, so most generally the most competitive is incentives for consumers to keep money on deposit and lower rate loans for consumers to take out. The potential for new competitors is not so common that it happens frequently but in today’s market groups of individuals with large resources who are frustrated with too much structure and to high of fee structures from larger institutions have formed smaller banks or credit unions to supply a need for better priced products, with hopefully a more home town approach with dealing with its customer base. Most markets are set competition mainly coming from outside banks wanting to tap into growing areas to capitalize on possible wealth of clients in that area or high traffic spots that business in that area have attracted. Other areas of new competition doesn’t come directly from a â€Å"NEW† bank but a bank buying out certain branches or absorbing the institution as a whole. This usually changes the dynamic that that competitor usually giving them more resources to utilize and make them more of a competitive force in the banking industry. Sometimes this can also work opposite and help out other banks in the area. If the â€Å"NEW† bank has processes or other items that are not favorable to the community they are in, that company could by an asset to lose it down the road when the client moves business due to not liking the new bank they are at.

Pain Sensation: Nociceptive receptors and transduction

Pain Sensation: Nociceptive receptors and transduction Pain is a subsystem of somatic sensation which includes a wide range of unpleasant sensory and emotional experiences usually associated with actual or potential tissue damage (Das et al., 2005). Over the years, by means of the evolutive process of natural selection, nature has made sure that pain is a bodily signal we cannot ignore. As a matter of fact, sensitivity and reactivity to noxious stimuli are essential to the well-being and survival of an organism. In dangerous circumstances pain tells the subject to get out of that situation immediatly, this is its main function. Without these attributes provided by pain mechanisms, the organism would have no means to prevent or minimize dangerous circumstances (individuals congenitally insensitive to pain are easily injured and most of them die at an early age1). While most of the sensory and somatosensory modalities are primarily informative, pain is a protective modality. Pain perception (also called nociception) doesnt come from excessive stimulation of the same receptors that generate somatic sensations, as someone could even think, it is a properly devoted subsystem. Nociception (from the Latin nocere, to hurt) in fact depends on specifically dedicated receptors and, due to its vital importance, this kind of information travels through redundant pathways. Pain also differs from the classical senses (hearing, smell, taste, touch, and vision) because it is both a discriminative sensation and a graded emotional experience. In the big picture, pain appears as a more complex whole experience than simple somatic sensation; that is why there are still many obscure aspects not completely understood, especially in the field of pain physiology and pharmacology. For this and other reasons, even nowadays, nociception remains an extremely active area of scientific research. 2. Pain Sensation Nociceptive receptors and transduction Pain sensation begins with relatively unspecialized free nerve cell endings called nociceptors. Like other somatic sensory receptors, they transduce a variety of noxious stimuli into receptor potentials, which in turn trigger action potentials in the pain nerve fibers (afferents). These action potentials are transmitted to the spinal cord and then, through the brainstem, to the thalamus and the somatic sensory cortex according to specific pathways2. Nociceptors are widespread distributed, they also show different degrees of sensitiveness and specialization. There are nociceptors in the skin, in the joints and also in visceral organs, but none of them is found inside the central nervous system (CNS)1. In contrast with somatic sensory receptors (responsible for the perception of innocuous mechanical stimuli), the axons associated with nociceptors conduct relatively slowly, being only lightly myelinated or, more commonly, unmyelinated2. Thus, according to the different kind of axon, there are faster or slower pain pathways. In particular, pain receptors can fall into four major categories depending on their response to the different types of stimulation caused by the damage: mechanosensitive nociceptors: respond to mechanical stimulation and have A-delta fibers, bigger axons with faster conduction velocity; mechanothermal nociceptors: respond to thermal stimuli, A-delta fibers; chemical nociceptors: respond to chemical substances, A-delta fibers; polymodal nociceptors: respond to high intensity stimuli of the previous three types and have C fibers, smaller and unmyelinated axons with slower conduction velocity. The cell bodies of these primary pain-neurons are located in the dorsal root ganglia (for body afferents) and in the trigeminal ganglia (for face afferents)1,2. The transduction of nociceptive signals, which starts with the nociceptive receptors, is a complex task. Tissue damage results in the release of a variety of chemical substances which triggers the response of nociceptors. Some of these substances activate the transmembrane transient receptor potential (TRP) channels, which in turn initiate action potentials2. Another characteristic feature of nociceptors is their tendency to be sensitized by prolonged stimulation, making them respond to other sensations as well in certain circumstances. This prolonged stimulation increases the release of chemical substances, making nociceptors sensitized and reducing their response threshold. Actually, within a few seconds after the injury, an area of some centimeters around the injured site shows reddening caused by vasodilation. This inflammation becomes maximal after about ten minutes and this region shows a lowered pain threshold (hyperalgesia) in response to additional noxious stimuli. This effect is also referred to as peripheral sensitization, in contrast to central sensitization that can occur at higher levels in the dorsal horn1. Although it is still unknown whether nociceptors respond directly to the noxious stimulus or indirectly by means of one or more endogenous chemical intermediaries released from the traumatized tissue, the activation of nociceptors initiates the process by which pain is experienced: these receptors relay information to the CNS about the intensity and location of the painful stimulus. Pain classification The result of sudden painful stimulation can be divided into two categories of sequential sensations separated by a short time interval. A sharp first pain, immediately after the damage, its followed some seconds later by additional, diffuse and longer-lasting second pain sensation. The temporal interval between these two separate sensations is due to the difference between fast transmitting A-delta fibers and slow transmitting C fibers. This phenomenon is also known as double pain sensation. Pain has also been classified into three major types1: Pricking pain: is also called fast pain or sensory pain (first pain) and arises mainly from the skin, carried by A-delta fibers which permit discrimination and localization of the pain. Burning pain: is caused by inflammation, burned skin and is carried by C fibers. This type of pain is a more diffuse, slower to onset, and longer in duration (second pain). Like pricking pain, burning pain arises mainly from the skin, but it is not distinctly localized. Aching pain: is a sore pain which arises mainly from the viscera and somatic deep structures. This pain is carried by the C fibers from the deep structures to the spinal cord and is not distinctly localized. Pain pathways The neural pathway that conveys pain (and temperature) information from the periphery of the body to the higher centers of the CNS is often referred as the anterolateral system (or ventrolateral column). This pathway is physically separated from the system that conveys mechanosensory information like touch and pressure (dorsal column-medial lemniscus pathway). However, even though the dorsal route has been always considered a touch pathway functionally separate from the anterolateral pathway, recent reports indicate that the dorsal column can carry noxious information from the viscera and widespread skin regions as well1. Anyway, the main difference between these two systems remains the site of decussation: while the dorsal column is an ipsilateral tract until the medulla (where synapses and decussates), the anterolateral system makes early synaptic connections and decussates right away in the spinal cord, becoming a contralateral tract. Composing the anterolateral system, there are three major ascending tracts: the neospinothalamic tract (the main, central pain pathway, phylogenetically younger, with few synapses), the paleospinothalamic tract and the archispinothalamic tract (which constitute minor parallel pain pathways, phylogenetically older and multisynaptic tracts)1. Every pain tract is made of three kinds of pseudounipolar neurons: first-order, from free nerve endings (nociceptors) to the dorsal horns of the spinal cord; second-order, from the dorsal horns to the thalamus; and third-order, from the thalamus to the primary somatic sensory cortex. The cell bodies of first-order neurons are located in the dorsal root ganglia (DRG) for all three pathways. a) The neospinothalamic tract (central pathway) constitutes the classical anterolateral system. This pathway is responsible for the immediate awareness of a painful sensation and for the understanding of the exact location of the painful stimulus. The first-order nociceptive afferents enter the spinal cord via the dorsal roots of the DRG and, when these projecting axons reach the dorsal horns of the spinal cord, they branch into ascending and descending collaterals, forming the tract of Lissauer2. Once within the dorsal horn, these afferents make synaptic connections with second-order neurons located in Rexeds laminae (layer I to V). Axons of these second-order neurons then cross the midline of the spinal cord, decussating in the anterior white commissure, and ascend to the brainstem in the contralateral (anterolateral) quadrant. Most of the pain fibers from lower extremities of the body and below the neck terminate, through the brainstem, in the ventral posterior lateral nucleus (VPL) of the thalamus. The VPL, which serves as a relay station, is thought to be mainly concerned with discriminatory functions1. Finally, here axons of second-order neurons synapse with third-order neurons that send the signal to the primary and secondary somatosensory cortex (SCI and SCII, respectively). Unlike the rest of bodily afferents, first-order nociceptive neurons from the head, face and intraoral structures have somata in the trigeminal ganglion. Trigeminal fibers enter the pons, descend to the medulla (forming the spinal trigeminal tract) and make synaptic connections in the spinal trigeminal nucleus, then cross the midline and ascend as trigeminothalamic tract (or trigeminal lemniscus). Axons from the second-order neurons terminate in a variety of targets in the brainstem and thalamus, but the discriminative aspects of facial pain are thought to be mediated by projections to the ventral posterior medial nucleus (VPM) of the thalamus and by projections (from here) to primary and secondary somatosensory cortex2. All of the fibers terminating in VPL and VPM are somatotopically oriented and still here the information supplied by different somatosensory receptors remains segregated. Axons from the thalamus synapse with third-order neurons of the SCI, which includes Brodmanns Areas 3a, 3b, 1 and 2. Each of these cortical areas contains a separate and complete representation of the body: they are somatotopically organized maps representing the human body (from the foot up to the face) in a medial to lateral arrangement2. b) The paleospinothalamic tract is a parallel pathway where the emotional response to pain is mediated1. This tract also activates brainstem nuclei which are the origin of descending pain-suppression pathways which regulate the sesation of noxious inputs at the spinal cord level. In the paleospinothalamic tract the majority of the first-order nociceptive neurons make synaptic connections with second-order neurons in Rexeds layer II (substantia gelatinosa). These second-order neurons also receive input from mechanoreceptors and thermoreceptors, and thats why the anterolateral system is also responsible for temperature perception1. The nerve cells that compose the paleospinothalamic tract are multireceptive or wide dynamic range nociceptors. Most of their axons cross and ascend in the spinal cord primarily in the anterior region and thus form the anterior spinal thalamic tract (AST). These second-order fibers contain several tracts and each of them makes a synaptic connection in different locations: in the mesencephalic reticular formation (MFR) and in the periaqueductal gray (PAG), forming the spinoreticular tract; in the tectum, also known as the spinotectal or spinomedullary tract; in the midline thalamic nuclei, forming the spinothalamic tract. Altogether these three fiber tracts are thus known as the paleospinothalamic tract, which is in part bilateral, because some of the ascending fibers do not cross to the opposite side of the cord1. Finally, from the thalamic nuclei, these fibers synapse bilaterally in the somatosensory cortex. Pain is a complex experience processed by a diverse and distributed network of neurons and brain regions. In addition to the sensory-discriminative aspects (carried by the neospinothalamic tract) there are also affective-motivational components of pain2. In the paleospinothalamic pathway there are extensive connections between the thalamic nuclei and the limbic areas such as the cingulate gyrus and the insular cortex. The insular cortex integrates the sensory input with the cognitive components. The limbic structures (amygdala, superior colliculus) project to the hypothalamus and initiate visceral responses to the pain. The thalamic nuclei also projects to the frontal cortex, which in turn is linked to the limbic structures involved in processing the emotional components of pain1. c) The archispinothalamic tract is another parallel pathway, phylogenetically the oldest that carries noxious information1. The characteristics of this tract are very similar to the ones found in the previous pathway. First-order nociceptive neurons make synaptic connections in Rexeds layer II (substantia gelatinosa). From here, second-order fibers ascend and descend in the spinal cord surrounding the grey matter to end synapsing with cells in the reticular formation and in the periaqueductal gray. Further diffuse multisynaptic pathways ascend to the diverse nuclei of thalamus and send collaterals to the hypothalamus as well as the limbic system nuclei. These fibers, like for the paleospinothalamic tract, mediate visceral, emotional and autonomic reactions to painful stimuli. In short, because of the importance of warning signals of dangerous circumstances, several nociception pathways are involved to transmitting these signals and some of them are redundant. The neospinothalamic tract conducts fast pain (via A-delta fibers) and provides information of the exact location of the noxious stimulus. The multisynaptic paleospinothalamic and archispinothalamic tracts conduct slow pain (via C fibers), a pain which is chronic and harder to localize. Through these patways, pain activates many different brain areas which link together sensation, perception, emotion, memory and motor reaction1. 3. Pain Modulation When talking about pain, we always have to consider and keep in mind the discrepancy between the objective reality of a painful stimulus and the subjective rsponse to it. Modern studies have provided considerable insight into how circumsatnces affect pain perception-interpretation and, ultimately, into the pharmacology of the pain system2. For many years it has been suggested that somewhere in the CNS there should be some neuronal circuits modulating incoming painful informations. Evidence for an intrinsic analgesia system was demonstrated by intracranial electrical stimulation of certain brain sites1,3. The circuit consisting of the periaqueductal gray matter (PAG), the raphe nuclei (RN), the locus coeruleus (LC) and the caudate nucleus (CN) contributes to the descending pain suppression mechanism, which inhibits incoming pain information at the spinal cord level6. Stimulation of such areas produce analgesia without behavioral suppression; indeed, touch, pressure and temperature sensation remain intact1. At the interneuronal level, opiate receptors activation causes hyperpolarization of the neurons, which in turn results in the inhibition of firing and in the release of substance P (a neurotransmitter involved in pain transmission) that blocks pain transmission1. In addition to descending projections, also local interactions between mechanoreceptive afferents and neural circuits within the dorsal horn can modulate the transmission of nociceptive informations to higher centers2. Observations by Melzack and Wall led to the idea that concomitant activation of the large myelinated fibers associated with low-threshold mechanoreceptors can mediate the flow of pain. This mechanism, also known as Gate Control Theory13, predicts that (at the spinal cord level) non-noxious stimulation will produce presynaptic inhibition on dorsal root nociceptor fibers and thus blocking incoming noxious information from reaching the CNS1 (i.e. non-painful input closes the gates to other painful inputs, which results in prevention and suppression of pain sensation). This explains also why if you, for example, stub a toe, a natural and effective reaction is to vigorously rub the site of injury for a couple of minutes2. However, there are many different factors that can influence the way we understand pain. Doubtless, three of these are: drugs, prior injuries and, more broadly speaking, circumstances. a) Drugs The brain has a neuronal circuit and endogenous substances to modulate pain. There are two primary types of drugs that work on the brain: analgesics and anesthetics1. The term analgesic refers to a drug that relieves pain without loss of consciousness, whereas the term anesthetic refers to a drug that depresses the CNS. Anesthetics are characterized by the absence of perception for all sensory modalities, including loss of consciousness, but without loss of vital functions. The areas that produce analgesia when stimulated are also responsive to exogenously administered opiate drugs2. As a matter of fact, the most effective clinically used drugs for producing temporary relief from pain are the opioid family, which includes morphine and heroin1. Unluckily, several side effects resulting from opiate use include tolerance and drug dependence (addiction). In general, these drugs modulate the incoming pain information as well as relieve pain temporarily, and are also known as opiate producing analgesia (OA). Opioidergic neurotransmission is found throughout the brain and spinal cord and appears to influence many CNS functions: opioids exert marked effects on mood, cognition and motivation1 (e.g. producing euphoria). The analgesic action of opiates implied the existence of specific brain and spinal cord receptors for these drugs long before the receptors were actually found. Since such receptors are unlikely to have evolved in response to the exogenous administration of opium and its derivates, the convinction grew that endogenous opiate-like compounds must exist in order to explain the evolution of these receptors in the body2. Nowadays, three classes of opioid receptors have been identified: ÃŽÂ ¼ (mu), ÃŽÂ ´ (delta) and ÃŽÂ º (kappa). All three classes are widely distributed in the brain, and particularly in the PAG, which is the site for higher cortical control of pain modulation in humans8. Moreover, three major classes of endogenous opioid peptides that interact with them have been recognized in the CNS: ÃŽÂ ²-endorphins, enkephalins and the dynorphins. Enkephalins are considered the putative ligands for the ÃŽÂ ´ receptors, ÃŽÂ ² endorphins for the ÃŽÂ ¼-receptors, and dynorphins for the ÃŽÂ º receptors1. The opioid peptides modulate nociceptive input mainly in two ways: blocking neurotransmitter release by inhibiting Ca2+ influx into the presynaptic terminal; or opening potassium channels, which hyperpolarizes neurons and inhibits spike activity. The various types of opioid receptors are distributed differently within the central and peripheral nervous system and this can explain many unwanted side effects following opiate treatments1. (For example, ÃŽÂ ¼-receptors are widespread in the brain stem parabrachial nuclei, which is a respiratory center. Inhibition of these neurons elicits also respiratory depression). In addition to opiates, the other big family of analgesia producing drugs is represented by the cannabinoids. Like opiates, cannabinoids produce analgesia when microinjected in the PAG and pain itself serves as a trigger for endocannabinoid release3. Results from the study by Walker et al. (1999) indicate that anandamide (an endogenous cannabinoid) fulfills the requirements for a nonopiate mediator of endogenous pain suppression and these data support the existence of endogenous cannabinergic circuitry in the dorsal and lateral PAG. Even if the opiate and cannabinoid mechanisms partially overlap anatomically, the endogenous opiate system is activaetd by intense and prolonged stimuli (such as high threshold electrical stimulation), while endogenous cannabinoids occur mostly in tonic pain suppression, during tests that do not produce significant stress or fear3. Cannabinoids have been used to treat pain for centuries and cannabis is still used despite its illegal status in most parts of the world. The spontaneous and stimulated release of anandamide in a pain-suppression circuit suggests that such drugs may form the basis of a modern pharmacotherapy for pain, particularly in instances where opiates are ineffective3. b) Previous injury A curious effect, well known and documented in clinical literature, is referred to as phantom limb sensation. Following the amputation of an extremity, nearly all patients have an illusion that the missing limb is still present. Although this illusion usually diminishes over time, it persists in some degree throughout the amputees life, and can often be reactivated2. A reasonable explanation for this phenomenon is that the central sensory processing apparatus continues to operate indipendently of the periphery, giving rise to these bizarre sensations. Indeed, considerable functional reorganization of the somatotopic maps in the primary somatosensory cortex occurs immediately after the amputation and tends to evolve for several years2. Neurons that have lost their original inputs respond to tactile stimulation of other (near) body parts, and so it is not unusual for the patient to perceive a phantom limb as a whole and intact, but displaced from the real location. These and further ev idences suggested then that a full representation of the body exists indipendently of the peripheral elements that are mapped2. Anyways, the major problem following phantom limbs phenomena is constituted by the fact that up to 85% of the amputated patients develop also phantom pain4. The description of this common unease can vary from a tingling or burning sensation to some more serious and debilitating issues. Phantom pain, in fact, is one of the more frequent causes of chronic pain syndromes and is extraordinarily difficult to treat2. Neverthless there is no really effective treatment, a study by Jahangiri et al. (1994) demonstrated that preoperative epidural infusion of morphine, bupivacaine and clonidine significantly reduces the incidence of phantom limb pain and phantom limb sensation. Moreover, this kind of treatment has been shown as safe for use on general surgical wards with a low incidence of minor side-effetcs4. Other than amputations, pain perception may also be modulated in certain stressful situations. Exposure to a variety of painful or stressful events produces an analgesic reaction, and this phenomenon is called stress induced analgesia (SIA). It has been considered that SIA can provide insights into both the psychological and physiological factors that activate endogenous pain control and opiate systems1. (For example, soldiers wounded in battle or athletes injured in sports events sometimes report that they do not feel pain during the battle or game; however, they will experience the pain later after the battle or as game has ended). Some studies demonstrated in animals that electrical shocks cause stress-induced analgesia3 and it has been suggested that endogenous drugs, (opiates or cannabinoids) released in response to stress, inhibit pain by activating the midbrain descending system1. Based on these and other experiments, it is assumed that the stress experienced by the soldiers and the athletes suppressed the pain which they would later perceive. c) Circumstances The experience of pain is highly variable between individuals: this highly subjective perception has a complex and often non linear relationship between nociceptive input and pain sensation5. From human experimentation we know that a variety of pain modulatory mechanisms exist in the nervous system, and these systems can be accessed either pharmacologically or through contextual and cognitive manipulation7,6. Various mental processes such as attention, emotional state, past experiences, memories, beliefs and feelings have been shown to influence pain perception and bias nociceptive processing in the humain brain9. All these top-down factors can be grouped together in the category of circumstances that either enhance or diminish pain sensation in regard to dedicated modulatory circuits. Among the cognitive variables influencing pain, the brain mechanisms underlying attentional control have been probably the most extensively studied5. A number of reports show the important role of attentional state in modulating the activity of primary somatosensory areas7. Thus, pain is perceived as less intense when individuals are distracted from it, as proved in an interesting study by Das et colleagues (2005). This research provides strong evidence supporting virtual reality (VR) based games in providing analgesia and positive influence on children with acute burn injuries, with minimal side effects10. VR can be considered an intermediary between reality and computer technology, and its ability to immerse the user interacting with the artificial environment is central in this kind of approach. However, attentional processes interact with mechanisms supporting the formation of expectations about pain and reappraisal of the experience5. The ability to predict the likelihood of an aversive event is an important adaptive capacity11. Our subjective sensory experiences are thought to be heavily shaped by interactions between expectations and incoming sensory information12 and this cognitive factor is important also for pain perception: positive expectations (i.e., expectations for decreased pain) produce a reduction in perceived pain that rivals the effects of a clearly analgesic dose of morphine12. These evidences provide also a neural mechanism that can, in part, explain the positive impact of optimism in chronic disease states. In fact, perceived control, attentional control and the descending pain modulatory system are involved in the placebo-induced analgesia, which is a clinical example of cognitive pain modulation that decreases pain intensity and cerebral responses to pa in5. Such top-down modulatory mechanism is a robust and clinically important phenomenon, which can be demonstrated in approximately one-third of the population9. Moreover, placebo analgesia requires the activation of endogenous opioid-mediated inhibition and neuroimaging techniques showed that there is also overlapping among brain sites activated by opioids and those that are activated during placebo analgesia9. Also the emotional state driven by the (experimental) context alters the attitude of patients and can produce powerful effects on pain perception7. In general, negative emotions increase pain, whereas positive ones decrease it14,7. Neverthless the brain mechanisms underlying these effects remain largely unknown, the prefrontal cortex, as well as parahippocampal and brainstem structures, are thought to be involved in the emotional regulation of pain14. According to Roy et al. (2009) cognitive and emotional processes induced by pleasant or unpleasant pictures interact with pain perception and modulate the responses to painful electrical stimulations in the right insula, paracentral lobule, parahippocampal gyrus, thalamus, and amygdala14. Not only, recent studies suggested that emotionally laden images representing human pain had a unique capacity to enhance pain reports15, in the suggestive perspective that search for the neural bases of human empathy with huge social implications. Thus, even though is well-established that mood selectively alters the affective-reactive response to pain (also called pain tolerance), the interpretation for some of these studies is sometimes difficult, since they do not always clearly dissociate changes in mood from changes in attention7. In fact, other studies showed that emotions can have a direct effect on attention to pain, leading to what is called attentional bias toward pain-related informations, which does not ensure the absence of covariate processes7. In the end, the available data indicate that emotion and selective attention may both interact modulating pain perception and cortical responses. But the observations that emotional manipulations alter pain unpleasantness more than pain sensation, while attention alters both pain sensation and unpleasantness, suggest that different modulatory circuits are involved7 and that they act through at least partially distinct mechanisms, which can be separated by appropriate experimental settings15. All this multiplicity of mechanisms underlying the emotional modulation of pain is reflective of the strong and reciprocal interrelations between pain and emotions, and emphasizes even more the powerful effects that emotions can have on pain perception14. 4. Conclusions In conclusion, in the CNS, much of the information from the nociceptive afferent fibers results from excitatory discharges of multireceptive neurons. The pain information in the CNS is controlled by ascending and descending inhibitory systems that can exert both facilitatory and inhibitory effects on the activity of neurons using endogenous opioids or other substances as mediators. In addition, a powerful inhibition of pain-related information occurs in the spinal cord. These inhibitory systems can be activated by brain stimulation, intracerebral microinjection of morphine, and peripheral nerve stimulation1. However, pain is an extremely complex perceptual and cognitive experience that is influenced also by many top down factors such as past sensations, expectations, the context within which the noxious stimulus occurs, the attentional and emotional state. Therefore, for all these reasons, the response to pain can often vary considerably from subject to subject. Case Report: Use of Valproate in Kleine Levin Syndrome Case Report: Use of Valproate in Kleine Levin Syndrome Successful use of Valproate in Kleine Levin Syndrome: a case report and review of cases reported from India Abstract Kleine-Levin Syndrome (KLS) is characterized by recurrent episodes of hypersomnia and other symptoms and it is a really challenging for the physician, since its causes are not yet clear, and available treatment options are not having adequate support. Here we are reporting a case with successful use of Valproate in KLS and also reviewing the cases reported from India. Introduction Kleine-Levin Syndrome (KLS) is a rare disorder which mainly affects adolescent boys and characterized by recurrent episodes of hypersomnia, and sometime along with hyperphagia, behavioral and cognitive disturbances, and hypersexuality (Yao et al., 2013). Several medications (stimulants, lithium, valproate, antipsychotics, antidepressants) have been reported to provide variable benefit in different symptoms, with lithium being the most widely used drug (Arnulf et al., 2005 2012). We are presenting a case of KLS, who had complete remission with valproate and also reviewing the cases reported from India. Case details: A 17 year old single male student of 12th standard, presented to our psychiatric outpatient clinic in September 2004 with hypersomnolence, low mood, decreased appetite and interest in studies, social and sexual disinhibition (such as singing obscene songs loudly at home, and touching unconsenting females’ including mother’s body parts- limbs, face and genitalia). Onset was acute, without any elicitable precipitating factor and course was episodic with average 7-10 days episode in every month for last four months and he maintained completely well in interepisodic period. Provisional diagnosis of recurrent depressive disorder (brief episodes) was kept and he was started on Sertraline (50 mg), on which he responded well. He remained asymptomatic for nearly nine months, but started having similar episodes again from mid 2005, due to which Sertraline was gradually hiked up to 150 mg/day, but of no use. Hence he was admitted in our inpatient setting in March, 2006 for diagnostic evaluation and further management. After detailed evaluation, it was found that his sadness was not pervasive and depressive cognitions and associated disturbances were not present and hypersomnia remained predominant complaint as initially he was sleeping 16-20 hours per day. He was also not responding with these medications, hence differential diagnosis of KLS vs. depression was kept and later finalized to KLS. His heamogram, renal functions, liver functions, blood sugar, routine urine, thyroid functions were within normal limits and chest X ray, ECG, EEG, and MRI brain were nor mal. In view of good literature support Lithium was started from 600 mg/day and hiked to 900 mg/day (serum level 0.8 mEq/liter). On which he has shown significant improvement initially for six month but later again started experiencing similar symptoms. He also had three episodes of fall, unresponsiveness and epileptiform discharge in EEG twice. Hence in view of seizure disorder and lack of response, Neurologist’s consultation was sought, who opined to start antiepileptic medication. Hence lithium was switched to Valproate (750 mg/day) in December 2006, on which he maintained completely well for 4 years, except brief reemergence of symptoms on discontinuing Valproate, which improved completely on resuming the medication. Valproate was gradually tapered and stopped in January 2011 on insistence of patient and family with discussing its pros and cons. Now index case has been maintaining well off Valproate for last three years without any episode of hypersomnolence, sexual disin hibition, sadness, or epileptic seizure. Discussion Based on historical reports by Kliene and Levin, KLS was essentially described and termed by Critchley (1962). Thereafter many researchers have reported their cases and reviewed cases with KLS (Arnulf et al., 2005 2012). Here we are reporting a case with KLS, who responded well with Valproate, after diagnostic dilemma and different psychotropic medications and also reviewing the other cases reported from India. In our electronic search for Indian studies on Kliene-levin syndrome, by using PUBMED and Google Scholar, we could find 15 cases reported from India (Aggarwal et al., 2011; Mendhekar et al., 2001; Prabhakaran et al., 1970; Shukla et al., 1982; Sagar et al., 1990; Narayanan et al., 1972; Agrawal Agrawal, 1979; Malhotra et al., 1997; Gupta et al., 2011). Of them 13 were males and 2 females, similar to male preponderance reported in the literature (Arnulf et al., 2005 2012). While presenting to psychiatric services their age was between 9 to 26 years and they had onset between 7 to 24 years of age. In two-third of patients (10 out of 15 patients) it was preceded with fever and their episodes of somnolence were lasted from 3 days to 10 weeks. Hypersomnia and hyperphagia were present in all, while two-third of patients also had social and sexual disinhibition (11 out of 15 patients). Other symptoms were cognitive disturbances (low intelligence quotient, impaired memory, confusion, and a cademic decline), irrelevant talk, and perceptual disturbances. Nearly one-third of patients improved spontaneously without any medication, while rest was given lithium, carbamazepine, methyl amphetamine, dextro amphetamine, and modafinil. Longest asymptomatic follow-up period is reported for 2 years (Aggarwal et al., 2011) (as depicted in table-1). Though literature supported lithium for higher response rate (Arnulf et al., 2005 2012), but index patient had remarkable response with Valproate, not with lithium, like earlier two reports (Crumley, 1997; Adlakha Chokroverty, 2009). Like earlier report (Adlakha Chokroverty, 2009), index patient also improved on lower dose of Valproate (divalproate 750 mg vs. 500 mg Valproate). Compared to other cases reported from India (Aggarwal et al., 2011; Gupta et al., 2011), index patient had longest follow-up (7 years) and remained asymptomatic in this period, except small exacerbation on discontinuation of Valproate treatment, which improved completely on resuming the drug. Similar to our patient, anticonvulsants (like Valproate) are the preferred treatment for KLS patient, and may also offer benefits in case of comorbid epilepsy (Yao et al., 2013). Valproate may be a good alternative to lithium in terms of efficacy as well as side effect profile. References Yao, C.C., Lin, Y., Liu, H.C., Lee, C.S., 2013. Effects of various drug therapies on Kleine–Levin syndrome: a case report. Gen Hosp Psychiatry. 35, 102.e7-102.e9. Arnulf, I., Zeitzer, J.M., File, J., Farber, N., Mignot, E., 2005. Kleine-Levin syndrome: a systematic review of 186 cases in the literature. Brain. 128, 2763-76. Arnulf, I., Rico, T.J., Mignot, E., 2012. Diagnosis, disease course, and management of patients with Kleine-Levin syndrome. Lancet Neurol. 11, 918-28. Critchley, M., 1962. Periodic hypersomnia and megaphagia in adolescent males. Brain. 85, 627–56. Aggarwal, A., Garg, A., Jiloha, R.C., 2011. Kleine-Levine syndrome in an adolescent female and response to modafinil. Ann Indian Acad Neurol. 14, 50-2. Mendhekar, D.N., Jiloha, R.C., Gupta, D., 2001. Kleine-levin syndrome : a report of two cases. Ind J Psychiatry. 43, 276-8. Prabhakaran, N., Murthy, G.K., Mallya, U.L., 1970. A Case of Kleine-Levin Syndrome in India. Br J Psychiatry. 117, 517-519. Shukla, G.D., Bajpai, H.S., Mishra, D.N., 1982. Kleine-levin syndrome: a case report from India. Br J Psychiatry. 141, 97-98. Sagar, R.S., Khandelwal, S.K., Gupta, S., 1990. Interepisodic morbidity in Kleine-Levin syndrome. Br J Psychiatry. 157, 139-141. Narayanan, H.S., Narayanan Reddy, G.N., Rama Rao, B.S., 1972. A case of Kleine-levine syndrome. Ind J Psychiatry. 14, 356-358. Agrawal, A.K., Agrawal, A.K., 1979. Kleine-levin syndrome: a case report. Ind J Psychiatry. 21, 286-287. Malhotra, S.M., Das, M.K., Gupta, N., Muralidharan, R, 1997. A Clinical Study of Kleine-levin syndrome evidence for hypothalamic-pituitary axis dysfunction. Biol Psychaitry. 42, 299-301. Gupta, R., Lahan, V., Srivastava, M., 2011. Kleine-Levin syndrome and idiopathic hypersomnia: Spectrum disorders. Ind J Psychol Med. 33, 194-8. Crumley, F.E., 1997. Valproic acid for Kleine-Levin syndrome. J Am Acad Child Adolesc Psychiatry. 36, 868-9. Adlakha, A., Chokroverty, S., 2009. An adult onset patient with Kleine-Levin syndrome responding to valproate. Sleep Med. 10, 391-3. Table-1: Reported cases with Kleine Levin syndrome from India

whistleblowers :: essays research papers

Because of certain events and media scandals that have surrounded the business community a former forgotten kind of employees has regained importance they are called the whistleblowers. Their importance has reached such tremendous heights that they were named in Time magazine’s 2002 Persons of the year because of their crucial involvement in the Enron case and many others that followed after that. The dictionary definition states that whistleblower as â€Å"One who reveals something covert or informs against another person†. Whistleblowers can get their title no matter what position of the company they occupy as long as they have reliable information any employee can inform of unethical procedures or illegal that the company they are working for might be engaging. There are many cases where whistleblowers have been the key part in the prosecution of CEOs directors, financial consultants, etc. that had been engaging in illegal procedures and that if there have not be because of the whistleblowers aide the authorities would have never even notice those felonies. There are many examples one that is cited on the article is the case of James Alderson a chief financial officer in a small hospital that sued the company that acquired the hospital a large medical company called Quorum Health Group Inc. part of Columbia/HCA Company because he found out that the kept two sets of books for preparing healthcare costs for Medicare patients one that was sent to the Federal government with highly inflated costs and the other one that detailed actual cost of operations. The case started in 1990 and ended until 2003 we also have to consider that in 1990 the business environment did not have the huge concerns that we have today over the management of financial information and there were not many laws to aide whistleblowers in their cause. But since that time new policies and laws have emerged to support whistleblowers and there is a greater focus of executives over ethical issues. By blowing the whistle Alderson knew that he was jeopardizing his career and he did he had to finance the whole case with his checkbook, he lost his job and had

of mice and men :: essays research papers

Why do we have dreams? We have dreams because that is what we want in life. With out a dream we would have no reason to live. In the book Of Mice And Men there is lennie an george who share a dream of copanionship. Lennie is a large, mentlly handicapped man. Lennie need George because of his handicap. He would be all alone and probably grow up to be ignorant and may hurt other people. For example in the beginning of the book he drinks some water out of a rivver that isn't running. George tell him he shouldn't drink water that isnt running because it may have bacteria in it. Lenny had no response to George. This prove lennies ignorance. He is because he had killed Curly's Wife, a mouse, and a puppy. Lennie killed Curly's Wife because she asked him if he want edth feel her soft hair. Lennie felt her hair and got carried away. She had gotten frightend and started screaming. lennie got frieghtend and started to shack here and then ended up breaking her neck. George is a small man. He to ok care of Lennie since Lennie was a little boy. George needs Lennie because George gets Lennies paycheck. He get Lennies paycheck to help them get closer to their dream. George also needs Lennies freindship. In the book George says "Guys like us, that work on ranches are the lonliest guys in the world. They got no family. They dont belong no place." and Lennie says "But not us! an' why? Because I got you to look after me an' you got me to look after you and thats why." This quotation tells us why they have their dream and why it is so importantto them. George and Lenny's dreamis to own a ranch. George in the book, says, "We'll have a big vegtable patch an' rabbit hutch an' chickens. And when it rains in the winter we'll just say "The hell with goin to work" and we'll biuld up a fire in the stoveand set around it an' listen to the rain come down on the roof.