Evaluation of Bali Bombings Legal Responses - 1064 Words

TERRORISM: LEGAL AND NON-LEGAL RESPONSES Evaluate the effectiveness of the legal and non-legal responses to the Bali Bombings The 2002 Bali Bombings were a series of suicide bombing attacks on the popular western tourist district of Kuta, Bali - an island of Indonesia. The attack occurred on October 12, 2002 and took the lives of 202 people; 88 of which were Australian nationals. This response will evaluate the legal and non-legal responses to the Bali Bombings according to the following criteria: resource efficiency, accessibility, enforceability, responsiveness, protection of individual rights, meeting society s needs and the application of the rule of law, and aims to answer the question that, in this case, has justice been†¦show more content†¦In the following days, the AFP conducted thorough forensic investigations into the source of the bombings, as well as the scenes of the crimes. The forensic material was then processed in Australia after an emergency amendment to the Crimes Act, 1901 (Cth) was passed. This speedy response from the nations federal politicians allowed the processing of fore nsic data from offshore (Bali) in the highly sophisticated labs located in Australia. This quick response is what ensured the integrity of the forensics and ultimately what allowed the bombers to be arrested. With the support of forensic examination, the investigation progressed quickly. This led to the arrest by the INP of the first suspect, Amrozi bin Nurhasyim (Amrozi), on November 5, 2002, and the subsequent identification of other suspects. A second joint INP and AFP investigation team was formed to pursue the remaining suspects, which led to the arrest of Imam Samudra and a number of other suspects on 21 November 2002. This was followed by the arrests of Ali Ghufron (Muklas) on December 4, 2002, and Ali Imron on January 12, 2003. The rapid legal responses from the AFP and the Parliament is what allowed the arrest of the bombers, in what was a greatly effective response. Not only was the AFP s response a legal one, but also a non-legal one. A major operation was then undertakenShow MoreRelatedInternational Human Resources3038 Words   |  13 Pagescan be useful, and helps in providing more insight into what is â€Å"normal† as opposed to â€Å"exceptional† in HRM practices and systems (Nankervis, Compton Baird, 2002; Rowley Benson 2002). However, IHRM should not become a description of fragmented responses to distinctive national problems nor about the ‘copying’ of HRM practices, as many of these practices suit national cultures and institutions without necessarily being transferable. Indeed, issues of concern in IHRM are those of consistency or standardizationRead MoreEssay about Restaurant Business Plan10168 Words   |  41 Pagesrestaurants. 2.1.3 Other Issues The economical and the social trends are the once that has the biggest influences. They are evidently affecting everyone living in the macro environment. The other issues will be looking at the political, technological, legal and environmental aspects of the external environment. 2.1.3.1 Political The regulations for import to Australia can be strict. A lot of paper work has to be done to make sure that all assets and groceries that are imported are legally approvedRead MoreExploring Corporate Strategy - Case164366 Words   |  658 Pagesanalysis Corporate governance Stakeholder expectations Social responsibility Culture Competitive strategy Strategic options: directions Corporate-level strategy International strategy Innovation and Entrepreneurship Strategic options: methods Strategy evaluation Strategic management process Organising Resourcing Managing change Strategic leadership Strategy in practice Public sector/not-for-proï ¬ t management Small business strategy ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€"  ââ€" 

Adolf Hitler As A Leader Of The Nazi Germany - 1398 Words

Adolf Hitler was the leader of the Nazi Germany party from 1934 to 1945. During his time of leadership, he initiated fascist policies that ultimately led to World War II. What he is most infamous for the horrendous acts he committed against the Jewish people in Germany as well as other groups of people, such as gypsies, the handicapped, homosexuals, and many others. While Hitler is most known for the genocide he committed, he is also recognized by many historians as a powerful and effective leader. He has many abilities that helped him to lead the German people. Although Adolf Hitler was responsible for the death of millions of human, during the time he led Germany, his effective leadership skills made him one of the most powerful leaders†¦show more content†¦The establishment of the ministry was to ensure the Nazi message through different forms of film, radio, books, educational materials, art, music, and the press. The messages that were conveyed over the media were simp le and agreeable and sought to create subconscious action. The use of this effective propaganda helped to spark a hated for a group of people by a whole population. The use of propaganda brainwashed citizen onto thinking that the source of Germany’s problems were the Jews. The use of propaganda had a powerful appeal to the young people of Germany . Adolf Hitler once said in order to encourage young people to young the Hitler Youth, â€Å"He alone, who owns the youth, gains the future.† Based off the belief of Hitler, the future of Nazi Germany was in the hands of the children. In 1936, Hitler’s youth grew quickly and had over 4 million members. The youth ranged from the ages of 10 to 18 years old and had separate organizations for boys and girls. The boys were prepped for military service while the girls were prepped for motherhood. The goal of Hitler’s youth was to wean out the weak to make Germany look stronger. By 1936, it was mandatory for all boys a nd girls for the ages of ten to seventeen to join the Nazi youth. While the Hitler Youth was not a militaryShow MoreRelatedAdolf Hitler As A Leader Of Nazi Germany1677 Words   |  7 PagesAdolf Hitler once said â€Å"It is more difficult to fight against faith than against knowledge† (â€Å"30 Eye Catching Hitler Quotes.). In a dictatorship there is one ruler who is in charge of everything in the nation in which he/she rules. Adolf Hitler was born on April 20, 1889 in Braunau am Inn. Hitler also known as Fà ¼hrer; he was chancellor of Germany from 1933 to 1945, and served as dictator from 1934 to 1945. Adolf Hitler was the leader of Nazi Germany, he was one of the initial causes which triggeredRead MoreAdolf Hitler As A Leader Of Nazi Germany1640 Words   |  7 Pages Adolf Hitler is known throughout the world as being the leader of Nazi Germany in the early twentieth century, and ultimately the instigator for World War II. His actions have faced much scrutiny since the conflict was resolved, but the genius behind this war effort is seeded in the politics of his egregious nature. Early Life and Upbringing Hitler was born on April 20, 1889, at Braunau-am-Inn, Austria. Alois,his father, had risen from a poor peasant background to become an Austrian customs officialRead MoreEssay on Adolf Hitler927 Words   |  4 PagesAdolf Hitler Adolf Hitler, to some, was a great ruler, but to others he was a murderer. Hitler was the leader of the Nazi party and was the dictator of Germany. He ordered to have millions of Jews murdered or thrown in prisons. Adolf Hitler was born April 20, 1889, in a small town in Australia called Branuan. His dads name was Alios Hitler and was a customs official. He was 51 years old when Adolf was born. Klara Polz, Adolfs mother, was a farm girl and was 28 when Adolf was bornRead MoreAdolf Hitler As A Post Christ1349 Words   |  6 Pagessometimes refer to Adolf Hitler as a post-Christ Nero because of Hitler s ruthless attitudes and actions towards innocent citizens, similar to Nero when he persecuted Christians during his rule about two thousand years prior(Kershaw). Hitler dealt with a depressing childhood, which included the deaths of his parents and the inability to pursue his dreams as an artist(Knapp). Thereafter, Hitler became interested in politics, as he eventually joined the Small German Workers party(Nazis) and won the faithRead MoreAdolf Hitler And The Barbaric Acts Of Prejudice1134 Words   |  5 PagesAdolf Hitler is most commonly known for the unforgivable acts of prejudice he comm itted throughout the course of his life. His abysmal actions left a scar on the world that could never be healed. However, Hitler possessed extreme intelligence and vocational skills. Although innovative and bright, he became corrupt as he turned against non-Aryans. His dream of pursuing his desire to be an artist slowly drifted from his mind as visions of a pure bred mother Germany came into focus. Hitler’s significantRead MoreThe Rise Of Adolf Hitler1457 Words   |  6 PagesThere are many world leaders in different countries and regions on earth who play a significant role in societies. Their role is significant because they have derived their power from their own birthright or from the people who have elected them. The rise of Dictator Adolf Hitler to supreme power in Nazi Germany would prove to be an event in history that was totally inexplicable in any terms. He was an adventurer who desired to conquer the German people and dominate the entire world, reshaping itRead M oreAdolf Hitler Was A Bad Man827 Words   |  4 PagesMarch 21, 2017 Adolf Hitler Adolf Hitler was a bad man who did many bad things in his lifetime. He was responsible for the Holocaust and for World War II. Who was Adolf Hitler? What motivated him as dictator of Germany? What did he do in the course of his lifetime? Adolf Hitler was born on April 20th, 1889. He was born in Braunau am Inn, Austria, of German descent (Hitler). Hitler s father s original name was Schicklgruber but he changed it in 1876 to Hitler (Adolf). Hitler had three sistersRead MoreHitler s Impact On The World War II1636 Words   |  7 Pagesa square, saluting and chanting Hitler s name. World War II has begun and many Germans hope for improvements in the economy. Their leader is Adolf Hitler. Adolf Hitler, dictator of Germany in World War II, was a powerful speaker who caused over 5 million deaths in concentration camps. Though Hitler s impact can be felt in modern times, the roots of his atrocious behavior began at childhood—more specifically—high school. Years before Adolf Hitler was born, Hitler s great grandfather, Johann GeorgRead MoreWhy Adolf Hitler Was A Great Leader1200 Words   |  5 Pages31 March 2015 Why Adolf Hitler Was A Great Leader. Can you really call a Murderer a Great Leader? A â€Å"Great Leader† Can be define as a leader who is self aware, self direct, socially aware, visionary, and having the ability to motivate one. Adolf Hitler is self aware, self direct, socially aware, visionary, and having the ability to motivate. From what we know for being a Great Leader we can say Adolf Hitler was a Great Leader. I believe that Hitler was a indeed a â€Å"Great Leader†. Although some believeRead MoreHitler, Stepping Into The Light. . Hitler, Racist And Murderer?1102 Words   |  5 PagesHitler, stepping into the light. Hitler, racist and murderer? Leader and visionary? Or both? Cassi-Dee Muller reports. Adolf Hitler, known for his rise to power, his revolutionary dictatorship and his starting of a world war. But was he simply a bad man with a negative impact on the world? Or was he just being an excellent leader? Born in Austria 1889, Hitler was an average young German until his adult life, where he achieved the position as the leader of the Nazi party. As a Nazi, he believed

Mechanism of Melatonin Stimulation of Growth Hormone Release Via Somatostatin Inhibition free essay sample

Mechanism of melatonin stimulation of growth hormone release via somatostatin inhibition Joseph Angelo Israel Peguit University of the Philippines in the Visayas Cebu College Natural Sciences and Mathematics Division Abstract Secretion of growth hormone is affected by two primary hormones: Growth hormone-releasing hormone and somatostatin. The former is the primary stimulant to promote growth hormone secretion while the latter is the primary inhibitor that prevents growth hormone secretion. Many studies have already shown that melatonin stimulates secretion of growth hormone via somatostatin inhibition but its mechanisms remain unknown. I hypothesized that melatonin inhibits somatostatin at transcription level through inhibition of important somatostatin transcription factors. I collected data from primary and secondary literature to acquire information on the target tissues, receptors and cellular mechanisms of melatonin. I collected information about somatostatin with emphasis on the mechanisms of its expression. Results showed that melatonin inhibits transcription of somatostatin through inhibition of Cyclic-adenosine monophosphate response element binding protein (CREB) which is a constituent of the transcription factors for somatostatin expression. I. Introduction Melatonin is a major secretion of the pineal hormone primarily involved in animal sleeping patterns. For such function, people have been taking melatonin pills over the counter to cure sleeping disorders. Approval from FDA on these melatonin pills is not yet available since the total function of this hormone has not been fully known. However, intensive researches have been going on trying to elucidate the entire function of this hormone. Full understanding on the physiology of this hormone may precede medical innovations as it can help us understand more of our development. One of the ecent discoveries on this hormone is its ability to act as an antioxidant at the same time attenuating the activity of antioxidative enzymes in the body. In connection to its major role of promoting sleep, its medical benefits provide insights to the physiological process happening at the body while at sleep. It has been established that Growth hormone is produced by the anterior lobe of the pituitary gland. It is primarily stimulated by Growth hormone-releasing hormone and primarily inhibited by somatostatin. Secretion of the growth hormone promotes uptake of amino acids, metabolism of fats and bone formation. II. Methodology I collected results from various primary and secondary literatures available online. I selected and analysed a total of thirty-three primary and secondary literatures. In my analysis, I considered the specific tissues that were studied since results do differ even if methodologies are the same. I collated the results obtained through establishing connections to form a cohesive explanation on the mechanism of melatonin to inhibit somatostatin. Nonetheless, all my results are hypothetical as for the moment until physical experimentation must be done. III. Discussion Melatonin Properties It is widely accepted that melatonin (MT) is a neurohormone that is the key regulator of biological rhythms. Intensive study on MT after its discovery demonstrated that it is involved also in, genital development[1], pigment metabolism[8], immune response, neutralization of free radicals[2,3], cell growth and proliferation[4]. The chemical structure of melatonin renders it both lipophilic and partially hydrophilic[7,10]. Such property is very crucial since its transport to different parts of the body does not need specialized mechanisms[7]. MT synthesis primarily occurs in the pineal gland and it has been established that cells from the gastrointestinal tract, retina, ciliary body, lens, Harderian gland, brain, thymus, airway epithelium, bone marrow, gut, ovary, testicle, placenta, lymphocytes and skin altogether produce substantial amounts of melatonin. It exert influences the activity of other tissues via the bloodstream. Biosynthesis The primary production of melatonin occurs in the pineal gland. Synthesis and secretion of melatonin is activated by darkness and suppressed by light. The photic inputs from the retina travel via the retino-hypothalamic tract to the suprachiasmatic nucleus (SCN) of the hypothalamus, then to the superior cervical ganglion and finally to the pineal gland[5,10]. Tryptophan is the main amino acid needed for melatonin production. Melatonin production is a secondary product from serotonin. Serotonin is acted upon by N-acetyltransferase (NAT) and hydroxyindole-O-methyltransferase (HIOMT) to form melatonin. Among the reactions, NAT is considered to be the rate limiting step in the formation of MT. Figure 1 Biosynthetic pathway of Melatonin Synthesis (Tan et. l 2006) or [9] Metabolism Melatonin must be converted to a more hydrophilic form since it is more of lipophilic than is hydrophilic[7,10]. It is then excreted via the kidneys after conversion[10]. The major catabolism of MT happens in the liver. Figure 2 catabolism of melatonin in Liver (Tan et. al 2006) or [9] Melatonin Receptors The receptors for melatonin had already been characteri zed. The subtype Mel1a dominates the receptors found in the SCN[6]. Though the pattern of receptor distribution varies from species to species but in general mammals contain fewer types of receptors than non-vertebrates [7,8]. The types of receptor expressed are Mel 1a (MT1) and Mel 1C [8]. The Pars tuberalis of the pituitary gland also contains a high density of the receptor. However, in humans the receptors are concentrated much on the SCN but are absent in the pars tuberalis (PT)[7,9,10]. This means that any regulation of melatonin on other hormones happen mostly in the SCN in the hypothalamus. The receptors of melatonin belong to the Gi/Go type of the superfamily of G-Protein Coupled Receptors (GPCR)[8]. The G-proteins are coupled to a number of effector systems influencing the intracellular signalling. They are designated as Gi/Go type because of their characteristic being inhibited by the presence of pertussis toxin[8]. Transduction Pathway The effector systems coupled to the melatonin receptors include the Adenylate cyclase, phospholipase C, L-type calcium channels, and ATP-sensitive K+ ion channels[8,6,33]. The inhibition of calcium influx via the L-type calcium channels may be mediated by direct inactivation by the G-protein[6] and/or through induced hyperpolarization by activation of ATP-sensitive K+ channel[6]. Activation of the G-proteins results to activation of ATP-sensitive K+ channels. The active transport of K+ ion intracellularly results to hyperpolarization of the membrane. The hyperpolarization inactivates the voltage-sensitive L-type Ca2+ channels which only opens during membrane depolarization[8,6]. Melatonin receptor activation inhibits activity of Phospholipase C (PLC)[8]. PLC functions to catalyze hydrolysis of phosphatidyl inositol (4,5) bisphosphate to Inositol triphosphate (IP3) and Diacyglycerol (DAG). Inositol triphosphate then functions to activate the IP3-dependent calcium channels in the endoplasmic reticulum to release Ca2+ to the cytosol. On the other hand, DAG activates of Protein Kinase C(PKC)[8,11, 12]. Some studies also showed melatonin can potentiate PLC [12]. In this case, dimerization of G-proteins is to be accounted. Different GPCRs can be expressed in a particular cell type where they can act independently, synergistically or antagonistically [13,14,15]. Recent studies have shown dimerization do not just occur among specific types of GPCRs but also among different types of GPCRs [13,14,15]making the understanding of GPCR signalling pathway even more complicated to understand. What is common among all pertussis-toxin sensitive GPCRs so far studied is their inhibition of adenyl cyclase (AC). Melatonin can inhibit AC by acting upon Gi/Go proteins but its possible though uncertain that dimerization of this type of GPCR with other types can result to AC activation. Activation of adenyl cyclase leads to the increase of cyclic-adenosine monophosphate (cAMP) that is crucial in expression of certain genes. [6,8] Illustration1: Shown is the pituitary transduction pathway of melatonin. Subsequent effects of melatonin on secondary messengers may affect both transcription and secretion of cellular products. The minus sign mean inhibition while a plus sign mean activation. Comparison of Melatonin Pathways in two target organs Pituitary Pathway The primary pathway of melatonin action exhibited in pituitary cells is shown in Figure 1. The differences of the effects of melatonin between pituitary cells and the SCN is due to the differences of GPCR types found between the two tissues. The PLC is inhibited in the pituitary pathway while it is activated in the SCN pathway. Activation is brought about by interactions of Gi/Go and Gq GPCRs on PLC. [16,17] Hypothalamic Pathway via SCN Illustration 2: This is the major pathway of melatonin action in SCN. Major difference from that of the Pituitary pathway is the activation of PLC. Its activation results in the subsequent activation of PKC and release of intracellular Ca2+. These two events may influence the activities of the cell including gene transcription and release of hormones and neurotransmitters. The SCN is the center of melatonin action. Multiple pathways occur at this region at different temporal stages. The PKC activation is known to occur during the dusk and dawn [18] which means that PKC activation in SCN is light-dependent. The activation of PKC proceeds to the activation of circadian rhythmicity, which accounts the importance of its activation in the tissue [18]. SitecAMPINsP3DAG/PKCCalciumCREB SCN-+++- Rat Hypothalamus- Rat Pituitary- Ovine Pituitary Somatostatin Inhibition by Melatonin via the Hypothalamic Pathway Somatostatin Somatostatin (SST) is a small cyclic peptide expressed in the different sites of the body but primarily expressed in the hypothalamus [19]. SST formation starts by proteolytic processing of larger precursor molecules which is the prepro-SS and pro-SS. The cleavage of pro-SS molecules results in the formation of two active forms of SS: SS-14 and SS-28 [19]. Five SSTreceptor (SSTr) subtypes are known to bind to SST. It is important to note that SSTreceptors, like melatonin receptors are coupled specifically to Gi’Go type of G proteins. The cellular mechanisms of SSTreceptor activation include adenylate cyclase inhibition, and prevention of calcium influx in pituitary cells[11]. The action of somatostatin in pituitary cells make it the primary inhibitor of Growth hormone release. Somatostatin inhibition on Growth hormone release Studies have shown that the mechanism of Somatostatin inhibition on GH release is not on transcription level but on the transport of the GH to the extracellular environment[20]. This suggests that the somatostatin influences its effect by changing the intracellular environment to prevent GH release. SST binding to its receptors especially SStr2 lead to the decrease of intracellular calcium concentrations and inhibit transcription of CREB, Protein Kinase and Adenyl Cyclase. In the inhibition of Adenyl Cyclase, intracellular cAMP levels decrease. The subsequent decrease of cAMP lead to the deactivation of Na+ permeable ion channels thus, preventing depolarization. Without depolarization along with inhibition of L-type Ca channels, influx can not happen thus preventing GH secretion via exocytosis. [21] Hypothesis of Melatonin inhibition on Somatostatin Production It has been shown in several studies that melatonin can stimulate GH release via inhibition of somatostatin [20,22,23 ]. It is suggested that the pathway for somatostatin inhibition is via hypothalamic pathway [20] due to the abundance of somatostatin receptors in the tissue. The mechanism of inhibition is not known in any literature found. Thus, it is a point in this section to trace the main effects of melatonin on the secondary messengers in SCN of hypothalamus. Melatonin’s mode of inhibition is on transcription level or on transportation level. Nonetheless, I contend that melatonin’s inhibition may be possibly at transcription level. Melatonin can possibly affect inhibition of somatostatin in two ways. It can affect by increasing the SST receptor-effector system [20] and /or affecting transcription of somatostatin by inhibition of important transcription factors needed for transcription of somatostatin. Via SST receptor-effector system The sst receptors and the G-proteins coupled to them constitute the receptor system of SST. While the effector system is composed of the various effects of the activation of the G-proteins caused by the binding of the ligand on the sst receptors. Both melatonin and somatostatin receptors are of Gi/Go type of GPCR as characterized by their sensitivity to Pertussis toxin. A possible mechanism that melatonin can attenuate the SST receptor-effector system is through dimerization. Melatonin coupling to its receptors may induce somatostatin-like intracellular effects since the same type of G-proteins are acted upon. Somatostatin has been proven to inhibit its own transcription through a negative feedback loop though no literature on its mechanism has been found yet. The mechanism of the negative feedback may be the same mechanism of melatonin on inhibition. One study showed that somatostatin can also inhibit CREB along with cAMP and Protein Kinase A [25]. The inhibiton of CREB, which is one of the transcription factor for SST transcription may mediate the negative feedback[26]. Via Inhibition of transcription factors needed for somatostatin expression Not much literature of the mechanism of somatostatin secretion is present. It is possible that the effect of melatonin on the secondary messengers influence SST expression. Camp-response element binding protein (CREB) is an important component for SST transcription to proceed. [25,26,27] CREB is constitutively bound to cAMP-response element (CRE), an enhancer of SST gene. Calcium concentrations, cAMP and Nitric Oxide influence CREB phosphorylation[26,28,29]. The CREB phosphorylation recruits CBP, a Histone Acetyl transferase (HAT) which will initiate assembly of basal transcription factors[27, 30]. Phosphorylation of CREB can be induced by Mitogen-activated protein kinase (MAPK) [28] and by Protein Kinase A (PKA) [30]. MAPK-induced phosphorylation may occur at the serine 142 residue. Phosphorylation at this region results in the separation of CREB from SST-CRE and transcription is unable to proceed [31,32]. However, phosphorylation of CREB at the serine 133 residue via protein kinase A result to transcription[31]. The MAPK pathway is activated by the influx of calcium [30] while PKA is activated by increase in cAMP levels[30]. Conclusion The action of melatonin is best manifested in pars tuberalis of the pituitary and the suprachiasmatic nucleus of the hypothalamus owing to the high density of melatonin receptors expressed. Differences in the action of melatonin between the pituitary and hypothalamus is attributed to differential activation of melatonin receptors on G-proteins. Melatonin receptors in SCN of hypothalamus activate both Gq and Gi/Go types of G-Proteins to activate PLC. While mel receptors in pituitary cells act via Gi/Go type only that results in inactivation of PLC. The somatostatin receptor, just like the melatonin receptors also belong the superfamily of G protein-Coupled Receptors (GPCR). Somatostatin receptors are also coupled to Gi/Go G-proteins just like mel receptors. I hypothesize that the similarity of the coupled G-proteins could explain the contention that melatonin attenuates the somatostatin receptor-effector system. I also hypothesize that the mechanism melatonin inhibition on somatostatin resembles that of the feedback regulation of somatostatin to itself. The possible regulation of melatonin on somatostatin synthesis may be at transcriptional level. This regulation may not be direct inhibition but induced through changes of the secondary messengers. Inhibition of melatonin on adenyl cyclase prevents phosphorylation of one of the transcription factors of Somatostatin gene. It is only through phosphorylation that CREB can assemble the basal transcription factors. Phosphorylation of CREB may be through Calcium-induced MAPK pathway of cAMP-dependent Protein Kinase A activation. However, the phosphorylation of CREB via MAPK pathway does not promote Somatostatin transcription due to different phosphorylation of residue.