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By: G. Ballock, MD
Professor, New York Medical College
The International Panel of Eminent Personalities to Investigate the 1994 Genocide in Rwanda and the Surrounding Events was created by the Organization of African Unity depression symptoms in adolescence buy amitriptyline 25mg lowest price. Throughout our work depression exam order amitriptyline 25mg fast delivery, which began with a meeting in Addis Ababa in October 1998 mood disorder child discount amitriptyline 50mg with amex, we have attempted to function in a manner worthy of this honour and consistent with the gravity of the subject matter anxiety journal articles generic amitriptyline 50 mg otc. The expansive and comprehensive mandate within which we operated appears in full as the first appendix of this report, but we want to reproduce a key portion of it here: the Panel is expected to investigate the 1994 genocide in Rwanda and the surrounding events in the Great Lakes Region. It is therefore expected to establish the facts about how such a grievous crime was conceived, planned and, executed; to look at the failure to enforce the Genocide Convention in Rwanda and in the Great Lakes Region; and to recommend measures aimed at redressing the consequences of the genocide and at preventing any possible recurrence of such a crime. We are conscious of the great expectations that have awaited this report and are grateful at the same time for the realism that has tempered those expectations. Hardly any person to whom we have spoken thinks that the genocide was a simple event or expects that, in some magical way, this Panel will divine simple lessons for the future. On the contrary, in the very course of our investigation, we watched as regional complexities throughout the nations of the Great Lakes Region added complicating new dimensions to our work. The 1994 genocide in one small country ultimately triggered a conflict in the heart of Africa that has directly or indirectly touched at least one-third of all the nations on the continent. This does not mean that we are dealing with an exclusively African phenomenon, however. Of course, there would have been no genocide if certain Rwandans had not organized and carried it out; there is no denying that fundamental truth. Sixty years of colonial domination and the later spread of globalization are integral aspects of the Rwanda story. The truth, as we will see repeatedly in our analysis, is that both the so-called international community and history have had powerful and decisive impacts on Rwanda specifically, and on the Great Lakes Region in general. From the start, we have been acutely conscious of another dimension of our great responsibility in preparing this document: We are an international group asked by the Heads of State of Africa to speak out on an African calamity. A small library of books, reports and studies of the Rwandan genocide has already been published, and it is certain that many more will emerge. But what is notable about the existing material is how much of it has been produced by non-Africans, let alone by non-Rwandans. Nevertheless, we have made a conscious effort to present a report from an African perspective, aimed at both African and international audiences. We have also understood from the outset that the credibility of our findings depends on solid, demonstrable evidence, and we have scrupulously attempted to follow that precept. We met with, listened to , and had extensive dialogues with 270 people in 10 countries, representing every facet of this tragedy: academics; United Nations officials; representatives of Rwandan, neighbouring, and several other governments; survivors; accused perpetrators; refugees; and human rights groups. We have had access to many original documents, and we commissioned studies of our own where there were vacuums to fill. Rwanda has transformed certain of its killing fields into memorial sites, and we visited some of them. We confronted the twisted remains of literally thousands of people still lying in the very classrooms and churches where they had been mercilessly slaughtered only a few years before. It was easy to see, especially in the schools, how many of the murdered were young children. We want to share one such experience here because, for all of us, hearing it ranked among the most traumatic episodes of our lives. It provides basic services for women who were brutalized, physically and sexually, during the genocide. The clinic grew slowly because so many female victims were still terrified after their ordeal, and many were ashamed of what had been inflicted on them. We had already met a number of these women when the clinic supervisor asked us to enter a small room at the back. In this tiny room, we heard from three survivors - three women, sitting side-by-side on a steel cot, who spoke of their tribulations as if in the desperate hope that somehow we could do something. One was a young woman who had been raped repeatedly over several days and then abandoned. The second was a woman who had been beaten and sexually mutilated, and who lived in terror because her attackers, who had been and continued to be her neighbours, still passed freely by her home every day. The third was a woman who was imprisoned, lashed to a bed for several months, and gang-raped continuously. Her final words to us were the stuff of nightmares, vivid, awful, impossible ever to forget. She said, with a chilling matter-of-factness: "For the rest of my life, whether I am eating or sleeping or working, I shall never get the smell of semen out of my nostrils.
We will deal with the role of each of them chronologically depression gad symptoms discount amitriptyline 50 mg overnight delivery,: first before the genocide and then during the genocide anxiety 247 buy amitriptyline 50mg lowest price. Although we have discussed the subject only briefly until now emotional depression definition purchase amitriptyline 25mg with visa, Rwanda in the past decade in fact cannot be understood without France depression test mental health order amitriptyline 25mg with amex. There has always been a vast gulf between the official French account of that role and the interpretation preferred by most disinterested observers; so far as we can determine, few experts in the field accept the official French version. These initiatives have made more conspicuous the decision of the French government not to take a similar step. Indeed, until this moment, there has from official France been no apology, no hint of responsibility, barely even any questioning of its quite public backing of the Rwandan Hutu regime before, during, and after the tragedy. On the contrary, when the Prime Minister at the time of the genocide, Edouard Balladur, backed by three other prominent Cabinet ministers, appeared before a parliamentary inquiry "bristling with indignation,"[4] he asserted that France was "the only country in the international community that tried to act to stop the genocide. But there had always been many critics of the French-Rwandan relationship, both national and international, and their voices continued to grow. Dismissing or ignoring these critics became increasingly awkward, especially after tough, investigative articles in two leading French daily newspapers. Finally, the French establishment agreed in 1998 to set up an unprecedented parliamentary committee to inquire into the Rwandan tragedy. But it concluded that the country bore not the slightest responsibility for any aspect of the genocide. These contradictions were blatant, and politicians and journalists were quick to point them out. Beside the wealth of information contained in the official report, there is an extensive literature analyzing French policy in Africa, some of it focussing specifically on Rwanda. In fact the considerations that drove French policy towards Rwanda are all on the public record, the French establishment never having felt any embarrassment about its African interests and role. No one, not even official French representatives, disagrees that these various considerations were, to one extent or another, the main driving force behind French policy in Rwanda. Its critical involvement during the genocide itself will be dealt with in a subsequent chapter. Relations between representatives of the two governments were unusually close at the personal as well as official levels. In 1975, a military assistance agreement strictly limited the role of French troops in Rwanda to that of instructors. The main goal of the arrangement was to offer technical assistance in the development of a national police force; one clause explicitly prohibited French involvement in military and police affairs. But this was an incorrect interpretation; the agreement still stipulated that training and technical assistance was to be provided to the "gendarmerie Rwandaise," not the army. Among the usual variety of French motives, francophonie unquestionably played a key role. Even warnings of possible genocide were heard, some of them documented in the French parliamentary report itself. Habyarimana must be supported since he was trying to keep the Hutu extremists in check. The French government chose not to use its singular influence at the highest echelons of Rwandan society to demand an end to governmentinitiated violence, a decision that sent its own obvious message. It was impossible to be unaware of the real situation in Rwanda, and it was in the face of this knowledge that France chose to maintain its support for the Habyarimana regime. Indeed, after a ghastly massacre in the south in early 1992, French Ambassador Georges Martres refused to join a delegation of European diplomats in Kigali who met with Habyarimana to express their concern. New massacres of Tutsi had recently taken place, the ethnic climate was growing ever more tense, violence was becoming an everyday occurrence, and the Hutu radicals were already actively organizing their dress rehearsals and compiling their death lists. But in the same month, the International Commission of Inquiry on Human Rights Abuse in Rwanda, a coalition of four international non-governmental organizations committed to human rights, published the results of an investigation it had undertaken. It documented extensive massacres of Tutsi by Hutu, many of them with obvious government connections. The following month, commission members took the report to Paris and Brussels where they held press conferences. The moral legitimation France offered was powerfully reinforced in practical ways.
If exon definition operates mood disorder nos dsm 4 discount 50mg amitriptyline mastercard, then mutating a splice site at the 39-end of an exon should result in loss of recognition of that exon anxiety 1-10 scale buy amitriptyline 25 mg without a prescription, and therefore splicing will skip that exon anxiety 9 year old boy buy amitriptyline 50 mg otc. Furthermore depression years after break up purchase amitriptyline 50mg otc, when cryptic 59-splice sites were used, they were in the intron, rather than the exon, arguing that the intron is the unit being recognized by the yeast spliceosome. Moreover, when the size of an intron was expanded, these cryptic sites could even compete with the normal 59-splice site if they were closer to the 39-splice site, even if they deviated strongly from the consensus sequence. This is consistent with a spliceosome searching for splice sites across an intron, and favoring those that are reasonably close together. This microexon would be skipped in verterbrates because it would be too small to be recognized by exon definition, but it was never skipped in S. Exons are defined by factors bridging across the three exons, as indicated by the arcs above the arrows denoting the borders of the exons. The splice site at the 39-end of the middle exon (yellow) is mutated, as indicated by the X, resulting in loss of recognition of this exon, indicated by the dashed arrow and dashed right end of the arc representing the definition of this exon. Again, the splice site at the 39-end of the middle exon (59-end of the second intron) is mutated. This time, the spliceosome finds a cryptic splice site upstream in the middle exon and splices from there. In exon definition, splicing factors appear to bridge across exons, while in intron definition, the factors bridge across introns. Sometimes, instead of skipping the exon that has a mutation in the splice site at its 39-end, the spliceosome will splice from a cryptic (previously hidden) splice site, and this cryptic splice site is almost always within that exon (Figure 14. This behavior is most easily explained if the exon is the unit that is being recognized: the spliceosome searches for a splice site in an exon, not in an intron. Moreover, we find that exons in higher eukaryotes tend to be small (usually less than 300 nt), while introns can be enormous-many thousands of nucleotides long. This makes sense if exon definition requires splicing factors to bridge across the exon: the exon cannot be too long for the factors to reach across. Indeed, if exons are artificially expanded beyond about 300 nt, they are usually skipped. In contrast to higher eukaryotes, the fission yeast Schistosaccharomyces pombe appears to use intron definition in splicing. This hypothesis seems plausible in light of the fact that small introns are the rule in both fission and budding yeasts, while there seems to be no limit to exon size. This is just the opposite of the situation in higher eukaryotes, Commitment Several splicing factors play critical roles in commitment, but Xiang-Dong Fu discovered in 1993 that, at least in certain circumstances, a single splicing factor can cause a committed complex to form. We do not know yet exactly how commitment works, although it seems clear that one facet is the attraction of U1 to the commitment complex. The reason is probably that these earlier experiments used crude nuclear extracts that naturally contained splicing factors. This finding suggested that commitment may work differently in yeast than in mammals. However, subsequent work has shown that the commitment complexes of yeast and mammals share many common features. Let us consider some of the proteins involved in bridging between the 59- and 39-ends of the intron in a yeast commitment complex, and compare these with their mammalian counterparts. In 1993, Michael Rosbash and colleagues presented studies designed to find genes that encode proteins involved in the yeast commitment complex. These second mutations could render the yeast strain inviable, even at the low temperature, so such mutations were called "Mutant-u-die," abbreviated Mud. Thus, the second mutations were not lethal in wildtype cells, but they became lethal in cells bearing the first mutation. In this sense, their lethality was "synthetic"-it depended on a conditional lethal mutation already created in the cell. Subsequent work showed that the function of Mud2p depended on a natural sequence at the lariat branchpoint, near the 39-end of the intron.
Oxypurinol inhibits the amidotransferase that initiates degradation of the purine ring system depression symptoms exercise 50mg amitriptyline mastercard. Partial or complete enzymic deficiencies in the salvage of purine bases are characterized by hyperuricemia mood disorder research paper discount amitriptyline 25 mg visa. Carbamoyl phosphate synthetase I is the regulated enzymic activity in pyrimidine ring synthesis mood disorder rapid cycling buy amitriptyline 25 mg line. Methotrexate decreases synthesis of the pyrimidine nucleotide thymidine monophosphate depression symptoms joint pain amitriptyline 25 mg lowest price. Diagnosis: Meconium ileus (obstruction of the ileum by meconium, the first stool produced by newborns) was confirmed by abdominal x-rays. The most common mutation, F508, results in the loss of a codon for phenylalanine and is classified as a frameshift mutation. An amino acid screen revealed that argininosuccinate was increased more than 60-fold over baseline, and citrulline was increased 4-fold. Diagnosis: Urea cycle enzyme defect with neonatal onset Treatment: Hemodialysis was performed to remove ammonia. Sodium phenylacetate and sodium benzoate were administered to aid in excretion of waste nitrogen, as was arginine. Long-term treatment will include lifelong limitation of dietary protein; supplementation with essential amino acids; and administration of arginine, sodium phenylacetate, and sodium phenylbutyrate. The degree of neurologic impairment is related to the degree and extent of the hyperammonemia. Based on the findings, which enzyme of the urea cycle is most likely to be deficient in this patient In individuals with partial (milder) deficiency of urea cycle enzymes, the level of which one of the following would be expected to be decreased during periods of physiologic stress A deep venous thrombosis is a blood clot that occludes the lumen of a deep vein, most commonly in the leg. Thrombin proteolytically activates components of the extrinsic, intrinsic, and common pathways. The other choices decrease the affinity for O2, stabilize the T (tense) or deoxygenated form, and cause a right shift in the curve. Antibiotics in the tetracycline family inhibit protein synthesis by binding to and blocking the A site of the small ribosomal subunit (30S) in prokaryotes. Vitamin C (ascorbic acid) functions as a coenzyme in the hydrolylation of proline and lysine in the synthesis of collagen, a fibrous protein of the extracellular matrix. Vitamin C reduces dietary iron from the ferric (Fe 3+) to the ferrous (Fe 2+) form that is required for absorption. With a deficiency of vitamin C, uptake of dietary iron is impaired and results in a microcytic, hypochromic anemia. Thiamine (vitamin B1) is a coenzyme in the oxidative decarboxylation of pyruvate and -ketoglutarate and, therefore, is important in energy metabolism in most cells. Norepinephrine released from the sympathetic nervous system functions as a neurotransmitter that acts on postsynaptic neurons and causes, for example, increased heart rate. It is also released from the adrenal medulla and, along with epinephrine, functions as a counterregulatory hormone that results in mobilization of stored fuels (for example, glucose and triacylglycerols). Norepinephrine bound to receptors on smooth muscle cells causes vasoconstriction and, thus, raises blood pressure. Their repair involves the excision of an oligonucleotide containing the dimer and replacement of that oligonucleotide, a process known as nucleotide excision repair. Mismatched-base repair involves identification and repair of the newly synthesized (daughter) strand. In prokaryotes, the extent of strand methylation is used to discriminate between the strands. Replication is initiated at specific locations (one in prokaryotes, many in eukaryotes) that are recognized by proteins (for example, DnaA in prokaryotes). Repair can occur independently of replication and, therefore, can be performed outside of the S phase. The enzyme glutathione peroxidase reduces hydrogen peroxide (a reactive oxygen species) to water as glutathionine is oxidized (G-S-S-G). Jaundice (icterus) refers to the yellow color of the skin, nail beds, and sclerae that results from the deposition of bilirubin when the bilirubin level in the blood is elevated (hyperbilirubinemia; see Image C).
The brain has multiple defense mechanisms designed to protect it from the adverse effects of cellular dehydration mood disorder nos icd 10 buy amitriptyline 25mg low price. As the serum [Na+] rises anxiety or asthma amitriptyline 25 mg discount, water moves from the intracellular to the extracellular space to return the serum osmolality to the normal range mood disorder light therapy order amitriptyline 25mg visa. Almost immediately depression yeast infection purchase amitriptyline 50mg fast delivery, there is an increase in the net leak of serum electrolytes (primarily Na+ and K+) into the intracellular space, which increases intracellular osmolality. Additionally, there is an increased production of cerebrospinal fluid, with movement into the interstitial areas of the brain. Within the subsequent approximately 24 hours, the brain cells produce organic solutes. The increase in intracellular osmolality restores intracellular volume, thereby decreasing the adverse clinical impact of hypernatremia. The increase in transcellular transport of electrolytes is somewhat transient, because over time, it interferes with normal cellular function. Cellular adaptation by the production of idiogenic osmoles requires days to reach full effect. Idiogenic osmoles clearly serve a protective role, but their removal is also slow (days) when isotonicity has been reestablished. The clinical implication of the slow removal of these idiogenic osmoles is that correction of hypernatremia (hypertonicity) must be gradual to avoid cellular swelling or cerebral edema. Any clinical condition associated with increased water loss or decreased water intake predisposes to hypernatremia. Generally speaking, for hypernatremia to occur, the rate of water excretion must exceed that of water intake. An exception to this basic principle, occurring less commonly, is hypernatremia secondary to sodium loading. Examples of conditions that lead to increases in insensible losses include fever, burns, open wounds, and hyperventilation. Although hypernatremia is due to an imbalance of water homeostasis, there may also be a concomitant salt disturbance. Hypernatremia can be seen in patients who are hypovolemic, euvolemic, or hypervolemic. These individuals have sustained losses of both sodium and water but with a relatively greater loss of water. They usually manifest typical signs of volume depletion, such as tachycardia and orthostatic hypotension. These patients have a normal total body sodium (and are therefore euvolemic), but they are depleted in total body water. As in the evaluation of hypovolemic hypernatremia, euvolemic hypernatremia can be further categorized into renal and extrarenal causes. Additionally, dysregulation of the aquaporin-2 channel can be seen with hypercalcemia. Decreased protein intake leads to decreased urea production and, therefore, a decreased medullary gradient with inability to maximally concentrate the urine. Insensible losses are the primary source of electrolyte-free water loss in this subgroup of patients. Increased insensible losses occur via the skin (burns, sweat), respiratory tract (tachypnea), or both. Most often, they have normally functioning kidneys but lack adequate water intake. Idiopathic hypodipsia occurs, but identification of an impaired thirst mechanism as the primary disorder causing hypernatremia should lead to a more thorough neurologic investigation to rule out the presence of hypothalamic tumors or disorders. This relative hypervolemic hypernatremic state reflects an imbalance of both water and salt. Commonly, the physician might be concerned that administration of the free water necessary to correct the serum [Na+]. However, because of the normal distribution of water, <10% of the administered water, either intravenously or enterally. Additionally, it is imperative to understand that further diuresis to obtain a net negative sodium balance will exacerbate the hypernatremia by increasing free water urinary losses, and therefore it must be considered in calculating the free water deficit. The amount, route, and rate of replacement depend on the severity of symptoms, rate of onset, concurrent clinical conditions, and volume status.
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