Certain drugs when taken for a prolonged period cause addiction. Discuss the cause, withdrawl symptoms and prevention of addiction due to any one drug.
Certain drugs when taken for a prolonged period cause addiction. Discuss the cause, withdrawl symptoms and prevention of addiction due to any one drug.
Text Solution
AI Generated Solution
|
Topper's Solved these Questions
HUMAN HEALTH AND DISEASE
ICSE|Exercise PREVIOUS YEARS. BOARD PAPER QUESTIONS (Very Short Answer Type Questions)|23 VideosView PlaylistHUMAN HEALTH AND DISEASE
ICSE|Exercise PREVIOUS YEARS. BOARD PAPER QUESTIONS (Short Answer Type-I Questions)|18 VideosView PlaylistHUMAN HEALTH AND DISEASE
ICSE|Exercise PRACTICE QUESTIONS (Short Answer Type-II Questions)|39 VideosView PlaylistEVOLUTION
ICSE|Exercise COMPETITION CORNER (Assertion and Reason Type Questions (For AIIMS aspirants))|26 VideosView PlaylistHUMAN REPRODUCTION
ICSE|Exercise SOURCE BASED QUESTIONS|22 VideosView Playlist
Similar Questions
Explore conceptually related problems
Withdrawal symptoms of certain addictive drugs are?
Watch solution
Define drug addiction. Give the symptoms and control measures of drug addiction.
Watch solution
Knowledge Check
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 22. The general purpose of this passage is to
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 22. The general purpose of this passage is to
A
make an argument
B
raise vital questions
C
introduce a concept
D
call for a course of action
Submit
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 23. As used in line 4, the word" celebrity " most closely means
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 23. As used in line 4, the word" celebrity " most closely means
A
notoriety
B
infamy
C
personage
D
festivity.
Submit
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 24. Based on line 11-22 and the information in the graph, what makes the hemoglobin varieties distinct?
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 24. Based on line 11-22 and the information in the graph, what makes the hemoglobin varieties distinct?
A
Whether there is a carbon nitrogen ring
B
whether there is a red coloration of the blood
C
Variation in the arrangement of metalloprotein chains
D
Variation in the arrangement of polypeptide chains
Submit
Similar Questions
Explore conceptually related problems
Name the bacteria that causes urinary tract infection. What are the symptoms and preventive measures taken for UTI?
Watch solution
Classify various drugs that lead to addiction and discuss their ill effects.
Watch solution
Slow repiration, slow pulse and constriction of pupil occurs due to drug addiction of
Watch solution
A young boy when brought a pet dog home started to complain of watery eyes and running nose. The symptoms disappeared when the boy was kept away from the pet. (a) Name the type of antibody and the chemicals responsible for such a response in the boy. (b) Mention the name of any one drug that could be given to the boy for immediate relief from such a response.
Watch solution
There are few biochemical compounds as familiar to us as hemoglobin, and as the primary transporter of oxygen in our blood, the celebrity of this curious little compound is not without just cause. Vital to almost every known vertebrate, hemoglobin appears within the very first weel of embroyogenesis, and while its role may not change throughout development, its molecular structure undergoes a series of significant transformations. Within the red blood cell, hemoglobin exists as a four-subunit complex, or tetramer, " each subunit of which is made up of one" heme" metalloprotein, and one of several varieties of " globin." Comprised of iron and a carbon-nitrogen ring, heme is responsible for both the oxygen binding capacity of hemoglobin, and for the red coloration of blood. Globin, meanwhile, refers to a folded chain of polypeptides, and it is the combination of these tchains that imparts each type of hemoglobin with its unique characteristics. In humans, six globin chains are expressed sequentially throughout development embroynic hemoglobin, or HbE, is composed of two chains and two chains, both of which are expressedn exclusively during the embryonic period. In the fetal period, another tetramer of two chains and two chains emerges, and persists for the first six months of postnatal life. Due to its high affinity for binding gases, this fetal hemoglobin, or hbF, is able to extract oxygen from low-affinity maternal hemoglobin, and thus plays a crucial role in the oxygenation of fetal tissues. Like HbF, the final two physiologic hemoglobins, hbA and HbA2, also require a pair of a chains, and differ only in being coupled to two chains, and two chains, respectively. typically, both HbA and HbA2 are synthesized at fairly stable concentrations, though HbA is produced in far greater abundance. Given the tremendous import of these complexes, it should hardly be surprising that errors in their production can yield devastating results. What may be surprising, however, is that these errors_ including sickle-cell desease and thalassemia -are among the most common of all inherited genetic disorders, with an estimated 7% of the world's [population as carrirs, two -thirds of whom reside in Africa. Thalassemia describes a group of dis-orders in which either the a and b chian is quantitativelty reduced. Depending on the mutation, these defects can present with a wide range of anemia-related symptoms, and are particularly prevalent throughout africa, southeast asia, and the Mediterranean. This geographical distribution is anyting but random. Many studies have demonstrated that the production of suboptimal hemoglobin confers a degree of protection against maaria, a potentially deadly infectious disease caused by members of the plasmodium genus. which parazsitize red blood cells. It follows, then that whereas in many regions throughout the world thalassemia may merely constitute disease, in those where malaria is endemic, it represents a favorable evolutionary advantage. Owing to a redundancy in the human genome, thee are four copies of the a globin gene, whi two a -coding regions on weach copy of chromosome 16. For this reason, the spectyrum of severtiy in a thalassemia is particularly broad. For instance, deletion of a single gene will result in a carrier state, and is unlikely to cause clinically acute symptoms. Deletin of all four, meanwhile, leads to a precipitation during the fetal period of nonfunctional y tetramers, also called Hb Barts, and is universally lethal in utero. Similarly. A deletion of three copies typically results in a serious but survivable anemia, and is characterized by the formation of hb barts in the fetal period, and nonfunctional b tetramers, termed HbH, through out adulthood. Predictably, a deletion of two copies produces a still milder anemia, but can be subclassified based on whether the deletions occur on the same chromo some, termed cis deletion. or on opposite chromosomes, termed trans deletion. The trans subtype appears more commonly in the mediterranean, while cis is more often found in Asia. Notably it has been suggested that the cis deletion may contribure to the relatively higher rates of failed prognancies observed in this part of the world. Like its a counterpart, b thalassemia also impairs the production of HbA. However, the symptoms of B thalassemia will not become evident until after the first six months of life, when the concentration of HbF wanes to a critical threshold. Often, a compensatory upregulation in the expression of HbA2 occurs in affected individuals, the effects of which can be pharmaceutically augmented by a drug called hydroxyurea, which induces the expression of HbF in children and adults. 25. Which option gives the best evidence for the answer the previous question?
Watch solution
ICSE-HUMAN HEALTH AND DISEASE -PRACTICE QUESTIONS (Long AnswerType Questions)
- Certain drugs when taken for a prolonged period cause addiction. Discu...
06:41
|
Playing Now - Define drug addiction. Give sources and harmful effects of any four dr...
04:30
|
Play - Name the causative agent of AIDS. What are its symptoms and modes of t...
06:23
|
Play - What is the immune system? What are its main kinds? What is the role o...
04:09
|
Play - Classify various drugs that lead to addiction and discuss their ill ef...
04:54
|
Play - Define immunity. Describe different ways to develop immunity. Write tw...
06:06
|
Play - What is full form of AIDS? How is it transmitted? Draw a labelled diag...
06:24
|
Play - Define immunodeficiency. Give a brief account of AIDS.
06:32
|
Play - Describe different types of immunity found in living organisms
03:23
|
Play - Explain the mode of action of B-lymphocytes and T-lymphocytes.
03:46
|
Play - What are carcinogens? Explain the causes, major types, danger signals ...
09:36
|
Play - Explain the effects of drug addiction on family, society and the addic...
03:51
|
Play - Why do people take to drinking?
01:46
|
Play - What happens when alcohol is taken?
05:25
|
Play - Define drug addiction. Give the symptoms and control measures of drug ...
04:02
|
Play - What are hallucinogens? Give their two examples. Mention their clinica...
04:41
|
Play - What are the properties of acquired immunity? Differentiate between an...
08:09
|
Play - Explain the various types of disorders arising due to improper functio...
04:50
|
Play - What is innate immunity? Differentiate between non-specific and specif...
04:54
|
Play - Differentiate between active immunity and passive immunity. Give any o...
02:38
|
Play