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The single-celled parasite known as Toxoplasma gondii infects more than half of the world's human population without creating any noticeable symptoms. Once inside the human body, Toxoplasma rapidly spreads to the heart and other organs. It can even penetrate the tight barrier that normally protects the brain from most pathogens. Yet, the blood of infected persons carries very few freefloating Toxoplasma cells. Scientists have long been puzzled by this ability of Toxoplasma to parasitize the human body without triggering an immune response and without an appreciable presence in the bloodstream. Recent research, however, has shed light on the ways in which Toxoplasma achieves its remarkable infiltration of the human body.

Though there are few individual Toxoplasma cells coursing freely in the blood of an infected person, scientists have discovered that the parasite is quite common in certain cells, known as dendritic cells, involved in the human immune system. Dendritic cells are found in the digestive tract and frequently come into contact with the various pathogens that enter the human body through food and water. When the dendritic cells encounter pathogens, they travel to lymph nodes and relay this information to other immune cells that then take action against the reported pathogen. Scientists have found, however, that Toxoplasma is capable of hijacking dendritic cells, forcing them from their usual activity and using them as a form of transportation to infect the human body quickly. Without this transport mechanism, Toxoplasma could not reach the better-protected areas of the body.

Toxoplasma invades the human body through consumption of the undercooked meat of infected animals, primarily pigs and chickens. Other animals, such as cats, can become infected as well. In fact, cats are a necessary component in the reproductive cycle of Toxoplasma, since the animal's intestines are the parasite's sole breeding ground. Toxoplasma creates egg-like cysts, known as oocysts, in the cats' intestines. These oocysts are shed in the cats' droppings and contaminate ground water and soil, eventually finding their way into the food chain. Because Toxoplasma must somehow find its way into a new host cat in order to reproduce, it cannot kill its current host. Instead, it waits for the host, usually a small rodent, to be eaten by a cat, thus providing Toxoplasma the opportunity to reproduce.

undertheskygymworld.blogspot.in/ The secret of Life ,though,is to fall seven times and to get up eight times. 

1. It can be inferred from the passage that which of the following statements is true of dendritic cells in the human body?   

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2. According to the passage, all of the following are true of Toxoplasma gondii EXCEPT 

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3. The second paragraph performs which of the following functions in the passage?  

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4. Which of the following is the most likely outcome for Toxoplasma cells that invade the human body?    

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5. The author mentions “pigs and chickens” in the final paragraph in order to   

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Concord staked its claim to be the birthplace of Independence during the celebration of "America's jubilee" on April 19, 1825, the fiftieth anniversary of Concord Fight. Concord in 1825 was an expansive town of nineteen hundred inhabitants, thriving with crafts and trade in the village and surrounded by farms prospering on demand from rising urban centers in the long boom that accompanied the opening phase of the Industrial Revolution in the Northeast. It also occupied a prominent place on the political landscape; as a shire town, where the county courts convened, it had risen into a leading center of Middlesex County, and its politicians were major players on that stage. Economic and political ambitions, as well as pride in the past, drove the insistence that Concord was the "first site of forcible resistance to British aggression."

A decade later, by the mid-1830s, with over two thousand inhabitants, Concord was probably at its political and economic pinnacle. The central village hosted some nine stores, forty shops, four hotels and taverns, four doctors and four lawyers, a variety of county associations, a printing office and a post office. Manufacturing was humming, too, with a growing mill village in the west part of town, along the quick-running Assabet River, and rising production of carriages and chaises, boots and shoes, bricks, guns, bellows, and pencils.

But a good many people were left out of the prosperity. In what was still a farming town, 64 percent of adult males were landless, while the top tenth of taxpayers, some fifty men, controlled nearly half the wealth. Those who failed to obtain a stake in society, native and newcomer alike, quickly moved on. The ties that once joined neighbors together were fraying. On the farms, the old work customs - the huskings, roof-raisings, and apple bees - by which people cooperated to complete essential chores gave way to modern capitalist arrangements. When men needed help, they hired it, and paid the going rate, which no longer included the traditional ration of grog. With a new zeal for temperance, employers abandoned the custom of drinking with workers in what had been a ritual display of camaraderie. There was no point in pretending to common bonds.

With the loosening of familiar obligations came unprecedented opportunities for personal autonomy and voluntary choice. Massachusetts inaugurated a new era of religious pluralism in 1834, ending two centuries of mandatory support for local churches. Even in Concord, a slim majority approved the change, and as soon as it became law, townspeople deserted the two existing churches - the Unitarian flock of the Reverend Ripley and an orthodox Calvinist congregation started in 1826 - in droves. The Sabbath no longer brought all ranks and orders together in obligatory devotion to the Word of God. Instead, townspeople gathered in an expanding array of voluntary associations - libraries, lyceums, charitable and missionary groups, Masonic lodges, antislavery and temperance societies, among others - to promote diverse projects for the common good. The privileged classes, particularly the village elite, were remarkably active in these campaigns. But even as they pulled back from customary roles and withdrew into private associations, they continued to exercise public power.

1. The passage suggests which of the following about members of the village elite in post-1834 Concord? 
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2. The primary purpose of this passage is to 

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3. According to the passage, which of the following is true of 18th-century Massachusetts residents?

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Lysosomal storage diseases form a category of genetic disorders resulting from defective enzymes that normally function to degrade unneeded molecules in cells. These enzymes do their work in the lysosome, a small compartment in a cell analogous to a garbage disposal. The lysosome contains between thirty and forty different degradative enzymes. When any one of the lysosomal enzymes is defective, the molecules requiring that specific enzyme for their degradation will accumulate and cause that individual's lysosomes to swell enormously. The physiological effects of such swelling on the individual include motor and mental deterioration, often to the point of premature death. But each disease resulting from one specific defective lysosomal enzyme has its own characteristic pathology. The age of onset, rate of progression, and severity of the clinical symptoms observed in patients with the same defective lysosomal enzyme are highly variable. For many years, this variability in patients with the same defective enzyme puzzled scientists. Only recently have researchers begun to answer the riddle, thanks to a genetic analysis of a lysosomal storage disorder known as Tay-Sachs disease. As in most lysosomal storage diseases, patients suffering from Tay-Sachs disease show both mental and motor deterioration and variability in age of onset, progression, and severity. Physicians have categorized the patients into three groups: infantile, juvenile, and adult, based on onset of the disease. The infantile group begins to show neurodegeneration as early as six months of age. The disease advances rapidly and children rarely live beyond 3 years old. The first symptoms of the disease appear in juvenile cases between 2 and 5 years of age, with death usually occurring around age 15. Those with the adult form generally live out a normal lifespan, suffering from milder symptoms than do those with the infantile and juvenile forms. Researchers hoped that the categorization would yield insight into the cause of the variability of symptoms among Tay-Sachs patients, but this turned out not to be the case. In Tay-Sachs disease, undegraded materials accumulate mainly in the lysosomes in the brains of patients, but the kinds of molecules left undegraded and the specific identity of the defective lysosomal enzyme responsible for the malfunction were not discovered until the 1950s and 60s, respectively. The main storage molecule was found to be a lipid-like material known as GM2 ganglioside. The defective enzyme was later identified as hexosaminidase. In 1985, the gene coding for the normal hexosaminidase enzyme was cloned and its DNA sequence determined. Shortly thereafter, the DNA sequences of genes encoding hexosaminidase from many Tay-Sachs patients were studied. It soon became apparent that not one or two but many different types of mutations in the hexosaminidase gene could result in Tay-Sachs disease. Some of the mutations prevented the synthesis of any hexosaminidase, preventing all such enzyme activity in the cell. Patients with this type of mutation all had the infantile form of Tay-Sachs disease. Other mutations were found in certain regions of the gene coding for areas of the enzyme known to be critical for its catalytic activity. Such mutations would allow for only extremely crippled hexosaminidase activity. Most of the patients with these mutations clustered in the juvenile category. Adult Tay-Sachs patients presented mutations in the regions of the hexosaminidase gene that were less important for the enzyme's activity than were those affected in juvenile patients. Scientists quickly hypothesized that the variation in age of onset and severity of Tay-Sachs disease correlated with the amount of residual enzymatic activity allowed by the genetic mutation. Though more research is needed to demonstrate similarity with other lysosomal storage diseases, the work done on Tay-Sachs disease has already offered a promising glimpse into the underlying mechanisms of these disorders.


It can be inferred from the passage that which of the following statements is true of lysosomal storage diseases? 

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