Describe and discuss, orally and/or in writing, the emergence of Western culture and civilization from paleo- and neolithic societies through Mesopotamia, Ancient Egypt, the Levant, and Persia; Ancient and Hellenistic Greece; the Roman Republic and Empire; and the origins and development of Judaism, Christianity, and Islam; Europeâs Middle Ages; Crusades; demographic and urban change; the Renaissance; and the Reformation.
Critically examine and interpret both primary and secondary sources, attentive to such concepts as historical agency, context (both domestic and global), perspective (including race, class, gender, and ethnicity), and multi-causation (conjuncture), relating such material fully to the course content.
Categorize and analyze in a historical manner major political, economic, social, cultural, and international events, trends, and themes related to the course content and discuss their historical significance.
Draw connections between comparable and/or contrasting time periods and regions related to the course content and discuss the value of historical knowledge and analysis for understanding change and continuity.
Demonstrate, in written work, understanding of history as a discipline characterized by the critical analysis and synthesis of factual evidence.
Describe and discuss, orally and/or in writing, the emergence of Western culture and civilization from paleo- and neolithic societies through Mesopotamia, Ancient Egypt, the Levant, and Persia; Ancient and Hellenistic Greece; the Roman Republic and Empire; and the origins and development of Judaism, Christianity, and Islam; Europeâs Middle Ages; Crusades; demographic and urban change; the Renaissance; and the Reformation.
Demonstrate the ability to interpret historical information by applying analytical skills used by historiansâsuch as synthesizing evidence from both primary and secondary sources, comparing and contrasting multiple perspectives, contextualizing information, and/or identifying causes and effects of change and continuityâto the course content.
Sample Solution
Malaria is a life-threatening disease and is widespread in the tropical and subtropical regions mainly around the equator. Malaria is a protozoan disease and transmitted through infected female anopheles mosquitoes. There are five Plasmodium species which can infect human beings namely Plasmodium falciparum (Pf), Plasmodium vivax (Pv), Plasmodium malariae (Pm), Plasmodium ovale (Po) and Plasmodium knowlesi (Pk). In India, Pf and Pv are equally contributing to the malaria burden in the country, but a gradual increase in Pf cases is observed since last five years. According to NVBDCP, around 0.88 million malaria cases were reported in India and amongst them 0.46 million are Pf cases as it is more virulent (NVBDCP 2013). The highest number of malaria cases reported in India were from Odisha (25.6%) followed by Chhattisgarh (13.3%), Jharkhand (11.6%), Madhya Pradesh (8.7%), Gujarat (6.7%), Maharashtra (5.2%), other states (14.3%) and North Eastern states, which contributes 8.3% malaria cases in the country (NVBDCP-2013). In the past, chloroquine (CQ) was effective for treating nearly all malaria cases. However, CQ resistance of Pf was first reported in Assam, India in 1973 (Sehgal et al.1973) and number of studies until 1977 indicated widespread presence of CQ resistance Pf in Assam, Arunachal Pradesh, Mizoram and Nagaland. Since then drug resistance has been reported from several other parts of the country (Dua et al; 2003, Baruah et al; 2005, Valecha et al; 2009). Epidemiological studies have also confirmed the association of CQ resistance with a mutation in the transporter gene pfcrt. The amino acid substitution at pfcrt codon 76 (K to T) have shown a determinant association with the resistant phenotype (Lopes et al.1993, Babiker et al. 2001). The transporter for CQ resistance is located in the membrane of the food vacuoles where CQ is suggested to act by binding to hematin, a toxic by-product from the digestion of hemoglobin, thereby preventing synthesis of non-toxic hemozoin (Fitch et al. 1998, Bray et al. 1998). To overcome the problem of CQ drug resistance, sulphadoxine-pyrimethamine (SP) combination was recommended by the National Programme in the country (National antimalarial programme, 1982). SP acts by interfering with two enzymes in the biosynthesis of folate. Sulphadoxine(SDX) is analogous to p-amino benzoic acid and competitively inhibits dihydropteroate synthase (DHPS) while pyrimethamine (PYR) is a competitive inhibitor of dihydrofolate reductase (DHFR). The inhibiti>
Malaria is a life-threatening disease and is widespread in the tropical and subtropical regions mainly around the equator. Malaria is a protozoan disease and transmitted through infected female anopheles mosquitoes. There are five Plasmodium species which can infect human beings namely Plasmodium falciparum (Pf), Plasmodium vivax (Pv), Plasmodium malariae (Pm), Plasmodium ovale (Po) and Plasmodium knowlesi (Pk). In India, Pf and Pv are equally contributing to the malaria burden in the country, but a gradual increase in Pf cases is observed since last five years. According to NVBDCP, around 0.88 million malaria cases were reported in India and amongst them 0.46 million are Pf cases as it is more virulent (NVBDCP 2013). The highest number of malaria cases reported in India were from Odisha (25.6%) followed by Chhattisgarh (13.3%), Jharkhand (11.6%), Madhya Pradesh (8.7%), Gujarat (6.7%), Maharashtra (5.2%), other states (14.3%) and North Eastern states, which contributes 8.3% malaria cases in the country (NVBDCP-2013). In the past, chloroquine (CQ) was effective for treating nearly all malaria cases. However, CQ resistance of Pf was first reported in Assam, India in 1973 (Sehgal et al.1973) and number of studies until 1977 indicated widespread presence of CQ resistance Pf in Assam, Arunachal Pradesh, Mizoram and Nagaland. Since then drug resistance has been reported from several other parts of the country (Dua et al; 2003, Baruah et al; 2005, Valecha et al; 2009). Epidemiological studies have also confirmed the association of CQ resistance with a mutation in the transporter gene pfcrt. The amino acid substitution at pfcrt codon 76 (K to T) have shown a determinant association with the resistant phenotype (Lopes et al.1993, Babiker et al. 2001). The transporter for CQ resistance is located in the membrane of the food vacuoles where CQ is suggested to act by binding to hematin, a toxic by-product from the digestion of hemoglobin, thereby preventing synthesis of non-toxic hemozoin (Fitch et al. 1998, Bray et al. 1998). To overcome the problem of CQ drug resistance, sulphadoxine-pyrimethamine (SP) combination was recommended by the National Programme in the country (National antimalarial programme, 1982). SP acts by interfering with two enzymes in the biosynthesis of folate. Sulphadoxine(SDX) is analogous to p-amino benzoic acid and competitively inhibits dihydropteroate synthase (DHPS) while pyrimethamine (PYR) is a competitive inhibitor of dihydrofolate reductase (DHFR). The inhibiti>
