Personal Essay Example | Topics and Well Written Essays - 2500 words

Personal - Essay Example Each of the section also contains background information of each type of services offered by the bank. The financial banks offer several services for the customers and each of them has different importance for different types of customers. The introduction of technology and the fast growth of internet usage have allowed the financial companies to add more value to the customers without much effort. The beginning of internet banking has made it easier for the customers to conduct their banking activities at ease and at their convenience. Although the mode of banking has evolvedbut the overall concept of individual activities are still the same. This paper is focused on the services offered by HSBC bank in their website. It will cover three basic services in details, which are Banking, Borrowing and Investing. The Qatar branch of HSBC will also be covered in this paper. Savings Bank Account:The banking segment of HSBC offers two types of services, savings account and current account. An individual can choose anyone or both types of account depending on his requirements. The savings account allows an individual to accumulate funds and gain interest on it. It helps the individual to save money for future use. Current Bank Account: The current bank account is particularly for business purposes and offers services, which are exclusive to financial activities of a business. It allows the customers to deal with liquid funds, such as deposit funds, withdraw funds, write check, etc. Moreover, the customers can make unlimited transactions in a day (Money, 2015). HSBC Qatar offers three different types of accounts based on the requirement of the customers. They are Basic Current Account, Advanced Current Account and Premier Current Account. Money Transfer: The money transfer facility of HSBC Qatar allows the customer to transfer funds to different accounts. The customers can transfer money to pay bills, send money to

Gods Existence and Aquinas Objection Essay Example for Free

Gods Existence and Aquinas Objection Essay I was in the debate team in high school. And there were times that our team would take the against side of the statement. In his famous work Prologion, written in 1077-1078, Anselm presents the idea the God exists because God is the greatest thing of all, that the idea of thinking of God exists prove its existence. Hundred of years later, Thomas Aquinas brings up the account that addresses Anselms idea in objection 2 of Question II, First Article of Summa Theologica. Aquinas objects Anselms argument later in his work by attacking the idea that God is something that can be thought greater. To understand Anselms argument for Gods existence, one must first understand the principles that forms the argument. The first principle is the claim that â€Å"nothing greater can be thought. † There is too types of existing, existing in understanding (existing0) and existing in reality (existing1). Then, we try to think of something is existing1. Anselm let â€Å"something† be â€Å"something than which nothing greater can be thought (NGT),† or in another word â€Å"a being than which nothing greater can be conceived† according to the Proslogion. The very first act of thinking that something is existing1 serves as the basis of it existing0. Because in the process of trying to think of something greater, we already establish its existence0. For example, there is a flower A, existing1. This flower A is the most beautiful flower, that this flower is a NGT. In order to prove this flower is NGT, one has to think of all the flower he has seen, flower B, C, or D. In the process of searching through ones mind trying to think of a flower that is more beautiful than flower A, flower A already exists in ones mind, which is existing0. To open his argument, Anselm then said an example of NGT is God. The second principle is the principle of â€Å"thinking of non-existing objects (Principle E). † Anselm uses the example of a painter conceiving the drawing he will paint, then executing his plan in mind to make the painting exists in reality. To breakdown his argument, lets begin with something that exists0. Because one has the ability to imagine that something exists0, one can also imagine that the same thing exists1. This priniciple is the most uncontroversial because it is just a matter of imagination. The fact that one has imagination allows him to imagine whatever he wants. For example, one imagines he won the lottery and has a million dollars. It is safe to say that one can proceed to think of that million dollars is existing1, regardless of if the million dollars truly exists1. Applying Principle E back to the argument of NGT, if one can imagine NGT in existence0, one can also go ahead and imagine NGT existing1. The third principle is â€Å"thinking something greater than something (Principle G). This principle compares the greatness of existing0 and existing1. Anselm proposes that â€Å"greatness† has two faces: qualitatively and existentially. To further support his argument, Anselm implies that greatness qualitatively means everything positive, such as, more beautiful, more knowledgeable, more influential, etc. Base on this assumption, Anselm argues that, â€Å"Suppose it exists in the understanding alone: then it can be conceived to exist in reality; which is greater. † To apply this principle in daily life, one can relate to a million dollars example above. One can imagine having a million dollars in his mind, but that million dollars doesnt exist1. In another case, one owns a millions dollars, which means that million dollars exists1. The rhetorical question here will be, which case is more appealing to you, which scenario is â€Å"greater? † Back to Anselms claim, the â€Å"it† in his argument is, of course, NGT, which is God. That God exists1 is better than God only exists0 but not exists1. The next principle returns to the basic meaning of NGT. Principle N presents the idea â€Å"if something can be thought to be greater than x, then x is not an NGT. † Assume something is an NGT, nothing greater can be thought. If there is another thing that is greater then it. This â€Å"something† is no longer an NGT. This principle is pretty self-explanatory. To put it in everyday examples, imagine the beautiful flower A is the most beautiful flower in the whole wide world. However, one found another flower more beautiful than A. Now A is no longer an NGT, regardless in existence0 or existence1. Now substitute God in for NGT in the equation. Because Anselm already claimed that God is an NGT, if one can think of something greater than God, God is no longer an NGT. According to the Proslogion, â€Å"God cannot be conceived not to exist. God is that, than which nothing greater can be conceived. That which can be conceived not to exist is not God. † The upcoming principles idea bases that of principle E. Principle T simply proposes the idea that â€Å"an NGT can be thought. † Because one has the ability to think of an object either exists0, exists1, or even both, one can also think of NGT existing0, existing1, or both. The idea that one can think of something is very broad and universal, that â€Å"something† can simply be anything. The final piece of Anselms argument is Principle M. This principle presents the very vague idea that â€Å"if something must be thought as existing1, then it exists1. † If one must think of a flower exists1, then that flower does exist1. Now that all principles Anselm needed to support his argument that God exists are gathered, he begins his argument with a â€Å"fool (thinker)† that â€Å"understands [God] is in his understanding; although he does not understand it to exist. † To fully understand this argument, one has to accept Anselms assumption that God, indeed, is an NGT. The argument that the thinker has the ability to think of NGT existing1 is based on Principle E that if one can think of an object then he can think of it existing1. The idea of thinking NGT exists1 is â€Å"greater† than the idea of thinking NGT exists0 but doesnt exist1 (Principle G); therefore, one can think of something greater than the NGT that exists0 but not in reality. However, this violates the basic meaning of an NGT (Principle N), nothing greater can be thought. So the idea that one can think of something greater than the NGT that exists0 but not in reality is contradictory to the fundamental element of an NGT. Which comes to the agreement that if one think of an NGT it is to be existing1. The conclusion implies the principle that one can thought of NGT exists1 (Principle T). Also, one can and must only think of an NGT exists1. This lead to the final conclusion. If one has no choice but think of something exists1, that something must be existing1 (Principle M). Therefore, an NGT, God, exists. Aquinas gives an condensed version account of Anselms argument in Summa Theologica. In objection 2 of question II, â€Å"Whether the existence of God is self-evident? †, Aquinas addresses the idea much abruptly. He first implies that Anselms idea of God is an NGT is equivalent to saying â€Å"things are said to be self-evident which are known as soon as the terms are known,† that the significant of the word â€Å"God† is nothing better can be conceived. He follows the account by stating that the word â€Å"God† â€Å"exists actually and mentally is greater than that which exists only mentally. † Therefore, if the word â€Å"God† is understood mentally it has to be understood to exist actually. Both Anselms argument of Aquinass account of it come to the same conclusion that God exists, that the thought of it existing lead to its real existence. Aquinas objects Anselms idea by stating that not everyone understands the word â€Å"God† will agree that it is an NGT. He follows his objection by stating: Yet, granted that everyone understands that by this name God is signified something than which nothing greater can be thought, nevertheless, it does not therefore follow that he understands that what the name signifies exists actually, but only that it exists mentally. Aquinass main objection is that the idea of NGT can be interpreted that it can only exists mentally. However, for Anselms argument to work, one has to understand that God can exists in reality; therefore, Aquinas further objects Anselms claim by stating those â€Å"who hold God does not exist† will not admit the fact that God is an NGT and it exists in reality. In Anselms defense, he based all his argument on the fact that God is â€Å"a being than which nothing greater can be conceived. † As a true believer of God, Anselm would have simply oppose those who does not believe in God has not fully understand the meaning of â€Å"God†; therefore, they fail to grasp the idea God exists in reality. If one understands God, he will be able to think of Gods existence in mind then agree to think of it in reality. After reading excerpts both from the Proslogion and the Summa Theologica, I am more inclined to support Aquinass claim. Although I do not think Aquinas has successfully destroyed Anselms argument, I think there are more weak links in Anselms argument than that of Aquinass. The most apparent loopholes are Principle M and Principle G. First, Principle M states that if one has to think of something as existing1, then that something has to exists1. However, Anselm neglects the fact that what one believes exists1 does not has to be true. For example, children were told to believe Santa Claus exists in reality and many of them do believe that idea. The contradiction being what those children â€Å"can and must† think exists1, Santa Claus, does not exists1. Second, the positivity of â€Å"greatness† implied in Principle G is too vague. The concept of greatness of reality is â€Å"better† than that of in mind can be subjective. Just because one person thinks the existence in reality is greater than existence in mind does not equal others perception of greatness. With doubts in Principle M and Principle G, I think Aquinas has a stronger position compare to Anselm does.

Clinico-histopathological Spectrum of Cutaneous Vasculitis

Clinico-histopathological Spectrum of Cutaneous Vasculitis Article Type: Original Title: Clinico-histopathological Spectrum of Cutaneous Vasculitis: A Retrospective Study of 62 cases Running Title: A Clinico-pathological study of Cutaneous vasculitis Authors: Nadia Shirazi*, Rashmi Jindal^, Neha Tyagi*, Samarjit Roy^, Meena Harsh,* Sohaib AhmadÇ‚ Affiliation: Department of *Pathology, ^Dermatology and Ç‚Internal Medicine, Himalayan Institute of Medical Sciences. SRH University. Jolly Grant. Dehradun. Uttarakhand. India Corresponding Author: Dr. Nadia Shirazi ABSTRACT Context: Cutaneous Vasculitis is the inflammation of vessel walls which leads to hemorrhagic or ischemic events. The histopathological classification of cutaneous vasculitis depends on the vessel size and the dominant immune cell mediating the inflammation. Object: We studied the etiological factors and clinico-pathological spectrum of patients with cutaneous vasculitis at a tertiary referral centre of north India. Design: Skin biopsies of all patients with clinically suspected cutaneous vasculitis presenting over 5 years , between 2009-2014 were reviewed. Cutaneous vasculitis was classified on the basis of etiology (primary or secondary), on the basis of size of vessel wall as well as on the dominant inflammatory cell infiltrating the vessels. Results: Over 5 years, 62 / 103 patients evaluated for vasculitic syndromes had histologically proven vasculitis. Clinically, vasculitis was primary (77.4%) or secondary (22.5%) to drugs, infections, underlying connective tissue diseases and malignancy. Neutrophilic (n=30), lymphocytic (n=18), eosinophilic (n=10), and granulomatous (n=4) vasculitis were the major histopathological groups. Small vessel involvement was seen in 97% cases. Conclusion: Skin biopsy remains the gold standard for diagnosing cutaneous vasculitis. Small vessel vasculitis is the most common type of cutaneous vasculitis with the dominant cell type being neutrophilic. Eosinophilic infiltrate was exclusively associated with primary vasculitis. Keywords: Cutaneous vasculitis, Small vessel vasculitis, Skin biopsy INTRODUCTION Cutaneous vasculitis (CV) is an inflammatory process of the vessels leading to the destruction of their wall with subsequent hemorrhagic features with or without ischemic necrosis.1 The incidence of cutaneous vasculitis ranges from 15.4 to 29.7 cases per million per year.2,3 The condition usually affects adults with a slight female predominance, however, all ages may be afflicted. CV is classified histo-morphologically on the basis of size of vessel affected (small or medium vessel vasculitis) and on the basis of the dominant cell mediating inflammation- neutrophilic/leukocytoclastic, lymphocytic, eosinophilic and granulomatous. On the basis of etiology, they are classified as primary/idiopathic or secondary to an underlying cause like drug induced, connective tissue disorders, infections, malignancy, etc. Vasculitis in a medium or large vessel is defined as presence of inflammatory cells within their walls, whereas in small vessels diapedesis of various leukocytes often take place and this criteria alone is not significant. It must be associated with signs of vessel damage, such as fibrin within the walls, thrombi or endothelial necrosis. Veins are involved more commonly than arterioles. Clinically, CV can present with a variety of signs and symptoms like urticaria, palpable purpura, ulcers, maculopapular rash, nodules, hemorrhagic vesicles, etc. It can be limited to skin or manifest in other organs like kidney, lungs and heart. Due to this myriad of presentations, CV can mimic a variety of other dermatological and systemic diseases. Skin biopsy remains the gold standard for diagnosis of cutaneous vasculitis complemented by clinical data and relevant haematological and immunological investigations. In this article, we will be presenting the histopathological spectrum of cutaneous vasc ulitis at a single centre of north India. MATERIALS AND METHODS All patients with clinical suspicion of cutaneous vasculitis attending the dermatology OPD between August 2009 and July 2014 at a single tertiary referral centre of north India were included. An informed consent was taken wherever possible in writing. Approval was obtained from the institute’s research committee for compiling the data from the hospital records. A punch biopsy, 4mm in depth was taken from the edge of the lesion. Though efforts were made to collect most of the biopsies within 48 hours of appearance of the suspected vasculitic lesion, a few patients presented as late as 1 -2 weeks. These biopsies were routinely processed and stained with Haematoxylin and Eosin (HE). Serial sections were taken in which no vasculitis was identified on initial section. Elastic tissue staining to assess the damage to the elastic lamina in muscular vessels was also performed. Simultaneously, a hemogram, ESR, kidney and liver functions, rheumatoid factor and immunological tests like AN A and ANCA were also carried out for assessment. Direct immunoflourescence (DIF) could not be undertaken in any case due to poor patient affordability and lack of infrastructure. Patients with thrombocytopenia ( RESULTS Over 5 years a total of 480 skin biopsies were studied out of which 103 cases were performed in those with clinically suspected vasculitis. However, 62 out of these 103 cases were histologically confirmed to have vasculitis; the remaining had unremarkable and non-specific histologic features. Those with positive histological features had a mean age of 44.5 years [range 6-83 years] with the male to female ratio of 1.1:1. The maximum number of patients (n=15) were seen in the age group 31-40 years followed by those in the second decade. Clinically vasculitis was primary (n=48, 77.4%) or secondary (n=14; 22.5%). (Table I) History of drug intake and presence of recent upper respiratory tract infection was seen in 7 and 3 patients respectively. The commonest offending drugs were antibiotics of ÃŽ ²-lactam group and analgesics followed by anti-histaminics. Connective tissue disorders (n=3) and malignancy (n=1) were also found to be the cause of secondary vasculitis. Clinically palpable purpura was the most common finding followed by maculopapular rash.(Figure I). Three-quarters of granulomatous vasculitis presented clinically with symptoms of allergic granulomatosis; 25% (n=4/17) of leukocytoclastic vasculitis presented clinically with features of microscopic polyangiitis. Among the haematological parameters, a raised ESR was the most consistent finding. (Tables II III). Most of these were small vessel (venules and arterioles) vasculitis (n=60, 97%). Only 2 cases showed medium vessel vasculitis particularly associated with panniculitis. Depending upon the dominant cell mediating inflammation, the dominant cell type was neutrophilic (n=30), lymphocytic (n=18), eosinophilic (n=10), and granulomatous (n=4). Histopathological evaluation in neutrophilic vasculitis showed transmural infiltration of vessel wall with neutrophils (Figure II). Fibrinoid necrosis, neutrophilic debris with or without extravasated red cells were features of leucocytoclastic vasculitis. Lymphocytic vasculitis is shown in Figure III. Epithelioid granulomas were seen surrounding and destroying the vessel wall in granulomatous vasculitis with transmural vessel wall infiltration by lymphocytes and polymorphs (Figure IV). Medium vessel vasculitis showed infiltration by neutrophils in vessel wall which was associated with septal panniculitis. (Figure V). Six of the 10 cases with urticarial vasculitis had an eosinophilic infiltrate; the remaining showed lymphocytes predominantly. Clinically most cases (n=8; 47%) of idiopathic vasculitis were of neutrophilic type. Drug reaction was the commonest cause of secondary vasculitis (n=7) and most of these (n=4, 57%) showed lymphocytic infiltrate (Table IV). DISCUSSION Cutaneous vasculitis presents as a mosaic of clinical and histological findings due to varied pathogenic mechanisms.3 Even in the presence of suggestive dermatological lesions, biopsy showed histological features in nearly 60% cases. We observed primary vasculitic syndromes leading to cutaneous histologic changes in 77% of all cases. Joint pain and swelling was the main presenting feature, palpable purpura and maculopapular rash were the predominant clinical cutaneous markers and raised ESR was a consistent feature. Mostly small vessels were affected and neutrophils predominated in infiltrates. However, there was a substantial overlap in the calibre of the vessel, the cellular infiltrate and the clinical diagnosis. Our observations corroborate with the case series of Carlson et al in terms of the dominance of primary vasculitis and lack of organ involvement.3 Raised ESR was also observed by Ekenstam et al and Gupta et al.4, 5 Arthralgia was the commonest systemic manifestation also observed by Gupta et al. 5 Neural and renal involvement was seen in 15 (24.1%) and 18 (29%) patients respectively in our series. Earlier studies showed visceral involvement is seen in 6, 7, 8 Fatal disease occurs in a minority (3, 8 Different therapeutic approaches are the main reason for sub-classifying vasculitis. Avoidance or treatment of the causative factor may cure or limit the activity of secondary vasculitis; whereas immunosuppressive therapy is the treatment of choice for primary vasculitis. Given this broad range of presentations of cutaneous vasculitis and the numerous disorders that can mimic vasculitis, it is not surprising that it is difficult to correctly and confidently classify these patients. 9 Currently the most widely adopted vasculitis classification system is that of Chapel Hill Consensus Conference (CHCC) which is based on pathologic criteria . 10 The other widely used system is that of the American College of Rheumatology (ACR) which is based on clinical findings. 11-18 As yet, no ideal system of classification exists for vasculitis. 3, 19, 20 The most accepted classification is one which distinguishes between primary and secondary vasculitis, recognizes the dominant blood vessel size involved as well as incorporates patho-physiological markers such as direct immune-fluorescence (DIF) and ANCA.21,22 Therefore the classification of cutaneous vasculitis into specific syndromes is best first approached morphologically by determining vessel size and principal inflammatory response. 3 This is the first case series classifying cutaneous vasculitis based on the vessel calibre and histo-morphologic features from the north Indian state of Uttarakhand. Though, the referral centre caters to a million people, this data cannot be extrapolated to the general population as the people are treated in the periphery by practitioners, the data of which is non-existent. A major limitation of our study was the non-availability of direct immunofluorescence which is considered very important for delineating the immunoglubulin type. Nevertheless, since this facility is not available in most of the Indian subcontinent and there is a lack of expertise in the field of dermatopathology, our data merits attention. CONCLUSION Vasculitis occurs as a primary disorder or secondary to various medical conditions, the treatment differing accordingly. The severity may range from a self-limited condition to a life threatening disorder with multiple organ failure. Skin biopsy is an important tool in arriving at a definitive diagnosis duly complemented by clinical features, pertinent laboratory data, serological evaluation, ANCA with or without direct immunofluorescence. REFERENCES 1. Carlson JA, Cavaliere LE, Grant-Kels JM. Cutaneous Vasculitis: diagnosis and management. Clin Dermatol 2006; 24: 414-29. 2. Chen KR, Carlson JA. Clinical approach to cutaneous vasculitis. Am. J Clin Dermatol 2008; 9: 71-92. 3. Carlson JA, Ng BT, Chen KR. Cutaneous vasculitis update: diagnostic criteria, classification, epidemiology, etiology, pathogenesis, evaluation and prognosis. Am J Dermatopathol 2005; 27 (6): 504-28. 4. Ekenstam E, Callen JP. Cutaneous leukocytoclastic vasculitis-clinical and laboratory features of 82 patients seen in private practice. Arch Dermatol 1984;120: 484-9 5. Gupta S, Handa S, Kanwar AJ, Radotra BD, Minz RW. Cutaneous Vasculitides: Clinico-pathological correlation. Indian J Dermatol Venereol Leprol 2009;75:356-62 6. Fiorentino DF. Cutaneous Vasculitis. J Am Acad Dermatol 2003; 48(3): 311-40 7. Carlson JA, Chen KR. Cutaneous vasculitis update: small vessel neutrophilic vasculitis syndromes. Am J Dermatopathol 2006; 28(6): 486-506 8. Tai YJ, Chang AH, Williams RA et al. Retrospective analysis of adult patients with cutaneous leukocytoclastic vasculitis. Australas J Dermatol 2006; 47(2): 92-6 9. Carlson JA, Chen KR. Cutaneous pseudovasculitis. Am J Dermatopathol 2007; 29(1): 44-55. 10. Jennette JC, Falk RJ, Andrassy K et al. Nomenclature of systemic vasculitides: proposal of an international consensus conference. Arthritis Rheum 1990; 33 (8): 1135-6. 11. Fries JF, Hunder GG, Bloch DA et al. The American college of Rheumatology 1990 criteria for the classification of vasculitis: Summary. Arthritis Rheum 1990, 33(8):1135-6. 12. Leavitt Ry, Fauci AS, Bloch DA et al. The American college of Rheumatology 1990 criteria for the classification of wegener’s granulomatosis.1990;33(8):1101-7 13. Masi AT, Hunder GG, Lie JT, et al. The American College of Rheumatology 1990 criteria for the classification of Churg-Strauss Syndrome (allergic granulomatosis and angitis). Arthritis Rheum 1990; 33(8): 1094-100 14. Hunder GG, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of giant cell arteritis. Arthritis Rheum 1990; 33(8): 1122-8 15. Mills JA, Michel BA, Bloch DA et al. The American College of Rheumatology 1990 criteria for the classification of Henoch-Schonlein purpura. Arthritis Rheum 1990; 33(8): 1114-21. 16. Calabrese LH, Michel BA, Bloch DA et al. The American College of Rheumatology 1990 criteria for the classification of hypersensitivity vasculitis. Arthritis Rheum 1990; 33(8): 1108-13. 17. Lightfoot Jr RW, Michel BA, Bloch DA et al. The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. Arthritis Rheum 1990; 33(8): 1088-93. 18. Arend WP, Michel BA, Bloch DA et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990; 33(8): 1129-34. 19. Callen JP. Cutaneous vasculitis: what have we learned in the past 20 years? Arch Dermatol 1998;134(3):355-7 20. Jennette JC, Falk RJ. Do vasculitis categorization systems really matter? Curr Rheumatol Rep 2000; 2(5): 430-8 21. Sunderkotter C, Sindritaru A. Clinical classification of vasculitis. Eur J Dermatol 2006; 16(2):114-24. 22. Watts RA, Scott DG. Classification and epidemiology of the vasculitides. Baillieres Clin Rheumatol 1997; 11 (2): 191-217 Table I. Causes of vasculitis in our study (n=62) Causes Number (%) Histomorphology Primary 48 (77.4) Neutrophilic (n=22) Lymphocytic (n=13) Eosinophilic (n=10) Granulomatous (n=3) Secondary 14 (22.5) Drugs 7 (50) Neutrophilic (n=3) Lymphocytic (n=3) Eosinophilic (n=1) Infections 3 (21.4) Neutrophilic (n=2) Granulomatous (n=1) Connective tissue disorders 3 (21.4) Lymphocytic (n=3) Malignancy 1 (7.1) Neutrophilic (n=1) Table II: Clinical features of cases with histologically proven vasculitis Clinical feature Number (%) Arthralgia/ arthritis 45 (72.5) Palpable purpura 34 (54.8) Maculopapular rash 18 (29.0) Fever 15 (24.1) Urticaria 12 (19.3) Nodule 4 (6.4) Papule 4 (6.4) Ulcer 2 (3.2) Haematuria 1 (1.6) Table III: Laboratory parameters of patients of patients with histologically proven vasculitis Parameter Positive Negative Not done Anemia 12 30 20 Raised ESR 50 12 Leukocytosis with neutrophilia 11 31 20 Eosinophilia 4 38 20 Thrombocytopenia 8 42 12 Kidney function tests 4 58 ANA 12 22 28 Anti-ds DNA 6 28 28 ANCA 16 46 CRP 12 26 24 Anti HCV 5 57 ASO titre 8 15 39 Table IV: Association of histomorphological diagnosis with clinical impression HISTOPATHOLOGICAL DIAGNOSIS CLINICAL DIAGNOSIS Primary Small Vessel Vasculitis (n=48) Neutrophilic / Leukocytoclastic (n=22) Vasculitis(n=8) Pustular dermatosis (n=5) Microscopic polyangiitis (n=4) Rheumatoid vasculitis (n=2) Hypersensitivity vasculitis (n=1) Erythema Elevatun Diutinum (n=1) Henoch-Schonlein Purpura (n=1) Lymphocytic (n=13) Chronic Urticaria (n=4) Perniosis (n=3) Pityriasis Lichenoides (n=2) Atrophie Blanche (n=2) Erythema Annulare Centrifugum (n=1) Polymorphous Light Eruptions (n=1) Eosinophilic (n=10) Urticarial vasculitis (n=6) Prurigo nodularis (n=2) Hypersensitivity vasculitis (n=1) Granuloma faciale (n=1) Granulomatous (n=3) Allergic granulomatosis (n=2) Churg-Strauss Syndrome (n=1) Secondary Small Vessel Vasculitis (n= 12) Neutrophilic (n=6) Drug reaction (n=3) Behcet’s disease (n=1) Sweets syndrome (n=1) Acute neutrophilic dermatosis (n=1) Lymphocytic (n=5) Drug reaction (n=4) Discoid lupus erythematosis (n=1) Granulomatous (n=1) Wegener’s granulomatosis (n=1) Medium vessel vasculitis (n=2) Neutrophilic (n=2) Polyarteritis Nodosa (n=2) LEGENDS Figure I: Palpable purpura Figure II: H E (20x10X): Neutrophilic vasculitis Figure III: HE (10x10X): Lymphocytic vasculitis Figure IV: HE (20x 10X): Granulomatous vasculitis Figure V: HE (20x10X): Medium vessel vasculitis with panniculitis

Panama :: Essays Papers

Panama The official name of Panama is the Republic of Panama or (Repà ºblica de Panamà ¡). Panama is located on the narrowest and lowest part of the Isthmus of Panama that links North America and South America. This part of the isthmus is situated between 7 ° and 10 ° north latitude and 77 ° and 83 ° west longitude. Panama is slightly smaller than South Carolina, approximately 77,082 square kilometers. The country’s two coastlines are referred to as the Caribbean and Pacific, rather than the north and south coasts. To the east is Colombia and to the west Costa Rica. Pacific. Dominant features of their landform is highlands forming the continental divide. The higher elevations near borders with Costa Rica and Colombia. The highest point in the country is the Volcà ¡n Barà º which rises to almost 3,500 meters. The lowest elevation is in the middle of the country where it is crossed by the Panama Canal. Most of the population is on the Pacific side of the divide. The population of the country is around 2.8 million with a growth rate of 1.5%. The racial and ethnic groups are 65% mestizo, 14% African descent, 10% Spanish descent, 10% Indian. The religion is 85% Roman Catholic, 5% Protestant, and 5% Islamic. Spanish is the official language, though United States influence and the canal zone reinforce the use of English as a second language. Panama's arts show its ethnic mix. Indian tribes, West Indian groups, mestizos, Chinese, Middle Eastern, Swiss, Yugoslav and North American immigrants have all offer contributed ingredients to the culture. Traditional arts are woodcarving, weaving, ceramics and mask-making. The capital city is Panama City with major cities of Colon, Bocas del Toro, Potobelo, El porvenir, Santiago, Tocumen, La Palma, David, Balboa, and el Dorado. Political culture traditionally characterized by personalism, the tendency to give one's political loyalties to an individual rather than to a party. Politics from 1968 until his death in 1981 dominated by General Omar Torrijos Herrera, Their form of government is Executive under provisions of their 1972 Constitution, as amended in 1978 and 1983. The chief executive is president of the republic, he is assisted by two vice presidents, all elected by popular vote for five-year terms. The unit of currency is the Balboa which is equal to the United States dollar. Balboas are available only in coins.

Maria Theresa of Prussian law

Starting in and around the year 1740 with the crowning of Maria Theresa as empress, began the buildup of the Prussian army. In the eighteenth century commenced the rein of the â€Å"Prince of Prussia†. By mid century, despite only having 3 million inhabitants it had the third strongest army in Europe. It was planning to take over Austria. According to the author, Ozment, the key to Prussia’s dominance and success was due to its ability to conquer and build because of long lived kings. Frederick I crowned himself the King of Prussia in 1701 and openly challenged Austria.His son, Frederick William I brought back Prussian virtues of discipline, obedience and piety. Between him and his son, the army quadrupled in size. An integration of religion and social reform transformed the country. This served to enlighten and educate the populace. Prussia attacked Austria three times, won the Silesian war, increased its landmass by half and revenues by a third. Prussia later suffered a few defeats when attacked by other European countries in the battle of Kolin and others.But the embattled Prussia returned at Rossbach, thought to be their greatest victory. By war’s end, a large amount of the country was destitute and 1/10th of its prewar population had perished. But Frederick aimed to build and rebuild. His reign was deemed enlightened absolutist because it was â€Å"hierarchical and strong-armed, yet optimistic and progressive for the times†. The ruler enabled free press, economic development and the codification of Prussian law.. Frederick believed that the power of Prussia was in its army and he developed it. He also created a strong centralized government and even ruled over the Prussian nobles who wanted their estates, serf and etc. He was also philosophically aligned with John Locke, another enlightened thinker and â€Å"father of liberalism†. Frederick also followed the model that a ruler was authoritative over individuals because he represented and enforced order in order to make individual freedoms possible.

naive american bloodline essays

naive american bloodline essays In my family, keeping the Native American blood line strong has always been somewhat important, especially to my grandfather. He is a hundred percent Cherokee Indian and he looks just like the guy on the back of the buffalo nickel. He hoped for me to carry on the Native American blood line. I had dated several girls in my life and none of them were Native American and it was not for a lack of trying, there just are not many Native American girls in the state of Florida or in any other state for that matter. My brother and sister gave up on the idea years ago and married outside of the blood line. They claimed it was too difficult to do, so it was up to me to find a true Indian girl, to fall in love with and hopefully make my grandfather proud of me. To begin with, I had to do a lot of preliminary dating to find just the right woman. First of all, I searched all over the place. I went to a Pow Wow with my grandfather at the fair grounds in Orlando and that only depressed me even more. All it turned out to be was a glorified tourist trap and a shell of how the Native American people have been forced to be remembered. I tried searching for peoples last names on the web and phone book that sounded Native American. I also went to the library and looked for genealogy records on microfilm for Native Americans in my local area and still no luck. I began to think that maybe my brother and sister were not wrong for giving up. I, too was about too give-up the search. In addition to being Indian, I had decided that love was a very important deciding factor in selecting my soul mate. If I stopped pressuring myself, then maybe I would be able to find love. One sunny day in June of 1995, I was working on the monorail and I spotted this stunningly gorgeous girl. She had the most beautiful long and curly black hair. I felt that I must meet her. So, when my monorail entered the station, I got off of the train and approached her. I told he ...