What do you think of when you hear the word civilization? What are the key features of civilization? In your response, please use at least three examples from the lecture notes and/or textbook.
(You will not see other posts until you post first. Review the rubric in the syllabus for more details about the discussion section.)
Module 1 Notes
Why do we study history? History helps allows us to understand where we have come from and this helps us understand who we are. If I want to understand who you are, I need to know a little about your past. In order to understand our modern civilization, even our world today, we need to understand our past. We are all related to our past, just as we are related to our grandparents and great-great grandparents.
The word history comes from the Greek word historia which means to inquire by investigation. Thatâs why we are going to do in the class — we are going to inquire about the past. Like a psychologist asks about your past in order to understand who you are, we are going to inquire about our own past in order to understand who we are.
Why do we have to study European history in America? Because America descends from European civilization, just as you descent from your parents. European history provides the foundation for modern America. We are related to our European ancestors.
Although humans have existed for over 1 million year, civilization is only about ten thousand years old. Before the advent of civilization, humans were primarily hunter gathers. We lived nomadically, meaning we traveled to where the food was. But civilization dawns about ten thousand years ago and humanity undergoes some radical changes.
Mesopotamia is a region of the world that that produced the Western worldâs first civilization. It lies between the Tigris and Euphrates rivers in modern day Iraq. Sumer was in the Southern part of Mesopotamia where a group of people called Sumerians lived. Sumerian civilization flourished from roughly 5000-1000 BC.
An important development occurred around 5000 BC in Sumeria when people began to organize agriculture into year-round settlements. Before this, humanity was nomadic, meaning they would wander, use resources in a certain area, then leave when the resources became limited. Domesticated animals made advances in farming possible, and humans began to stay in one place, allowing societies to develop.
One of the most important advancements of the Sumerian civilization was irrigation. In order to control water flow, they constructed levees. Before levees and irrigation, humans were at the mercy of weather and flooding rivers, so some years, there would be too much water, while other years, not enough. The Mesopotamians could irrigate and control water flow, allowing them to have a consistent food supply.
Human ingenuity makes life easier!
In fact, wheat grew so well, there were even food surpluses. The people of Sumer used this food surplus to trade with other towns in the region. They received textiles, furniture or raw materials like wood.
There was no currency in ancient Mesopotamia. Everything was done by barter (trade). This economic prosperity caused towns to grow, spread and become large cities. For example, SMC and Santa Monica high school would be small towns, but they grow, eventually come into contact with one another and form a big city. They would gradually evolve into cities with tens of thousands of people. Ur and Uruk are two of the most famous and oldest cities from this period. In some respects, they resemble large cities today.
Sample Solution
higher than, those usually recommended, but within the limits of tolerance of the subjectâ (WHO). Chloroquine CQ resistance is associated with a decrease accumulation of CQ concentration in the food vacuole of parasites, which is the site of action for C (Fidock et al., 2000.). The substitution of lysine to threonine (K76T) at codon 76 of the pfcrt gene is associated with in vivo and in vitro CQ resistance in Africa, South America, and Southeast Asia (Anvikar et al., 2012; Garcia et al., 2004; Ojurongbe. et al., 2007). Sulphadoxine-pyrimethamine(SP) SDX and PYR is inhibiting to the DHPS and DHFR enzymes, respectively, specific point mutations in Pfdhps & Pfdhfr gene encoding these enzymes lead to a lower binding affinity for sulphadoxine-pyrimethamine drugs. High frequency of mutations in codon S108N followed by codon C59R and double mutant (S108N+C59R) genotypes are prevalent in India (Mishra et al. 2012). Apart from this, mutations at codon 51 and 164 are also responsible for increasing the tolerance of parasite towards the drug (Lumb et al. 2009). Pf showed variable levels of resistant to sulphdoxine with sequence variation in dhps gene at codon S436 to A436, A437 to G437, K540 to E540, A581 to G581 and A613 to S/T613. High frequency of mutation in pfdhps gene was observed in Cor-Nicobar Island (Lumb et al. 2009). In Northeastern region of Indian, where witness of treatment failure in AS+ SP regimen, with high prevalence of mutations in dhps gene at codon 436, 437 and 540 (Mishra et al.,2014). Factors influencing emergence and spread resistant parasite Spread of drug resistance rapidly in area of high transmission intensity of malaria incidence because clonal multiplicity increased the level of sexual recombination. If more than one gene is required to encode drug resistance, then recombination slows the evolution of resistance by breaking apart the resistant gene combinations (Hastings & DâAlessandro, 2000). In malaria endemic areas therapeutic responses vary with age as young children have little or no immunity compared with older children and adults. Immunity is play important role to decreases the chance of an infection becoming patients and also better therapeutic responses for any level of resistance [Hastings & Watkins, 2005]. The mutation rate in parasites have influence of the frequency of emerging drug resistance, higher mutation rates facilitate a>
higher than, those usually recommended, but within the limits of tolerance of the subjectâ (WHO). Chloroquine CQ resistance is associated with a decrease accumulation of CQ concentration in the food vacuole of parasites, which is the site of action for C (Fidock et al., 2000.). The substitution of lysine to threonine (K76T) at codon 76 of the pfcrt gene is associated with in vivo and in vitro CQ resistance in Africa, South America, and Southeast Asia (Anvikar et al., 2012; Garcia et al., 2004; Ojurongbe. et al., 2007). Sulphadoxine-pyrimethamine(SP) SDX and PYR is inhibiting to the DHPS and DHFR enzymes, respectively, specific point mutations in Pfdhps & Pfdhfr gene encoding these enzymes lead to a lower binding affinity for sulphadoxine-pyrimethamine drugs. High frequency of mutations in codon S108N followed by codon C59R and double mutant (S108N+C59R) genotypes are prevalent in India (Mishra et al. 2012). Apart from this, mutations at codon 51 and 164 are also responsible for increasing the tolerance of parasite towards the drug (Lumb et al. 2009). Pf showed variable levels of resistant to sulphdoxine with sequence variation in dhps gene at codon S436 to A436, A437 to G437, K540 to E540, A581 to G581 and A613 to S/T613. High frequency of mutation in pfdhps gene was observed in Cor-Nicobar Island (Lumb et al. 2009). In Northeastern region of Indian, where witness of treatment failure in AS+ SP regimen, with high prevalence of mutations in dhps gene at codon 436, 437 and 540 (Mishra et al.,2014). Factors influencing emergence and spread resistant parasite Spread of drug resistance rapidly in area of high transmission intensity of malaria incidence because clonal multiplicity increased the level of sexual recombination. If more than one gene is required to encode drug resistance, then recombination slows the evolution of resistance by breaking apart the resistant gene combinations (Hastings & DâAlessandro, 2000). In malaria endemic areas therapeutic responses vary with age as young children have little or no immunity compared with older children and adults. Immunity is play important role to decreases the chance of an infection becoming patients and also better therapeutic responses for any level of resistance [Hastings & Watkins, 2005]. The mutation rate in parasites have influence of the frequency of emerging drug resistance, higher mutation rates facilitate a>
