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What happens when a doctor doesn't know the microorganism yet?
<text>What happens when a doctor doesn't know the microorganism yet?</text><reasoning>In empirical therapy, a patient has proven or suspected infection, but the responsible microorganism is not yet unidentified. While the microorgainsim is being identified the doctor will usually administer the best choice of antibiotic that will be most active against the likely cause of infection usually a broad spectrum antibiotic. Empirical therapy is usually initiated before the doctor knows the exact identification of microorgansim causing the infection as the identification process make take several days in the laboratory.</reasoning><output>broad spectrum antibiotic</output>
What happens in empirical therapy?
<text>What happens in empirical therapy?</text><reasoning>In empirical therapy, a patient has proven or suspected infection, but the responsible microorganism is not yet unidentified. While the microorgainsim is being identified the doctor will usually administer the best choice of antibiotic that will be most active against the likely cause of infection usually a broad spectrum antibiotic. Empirical therapy is usually initiated before the doctor knows the exact identification of microorgansim causing the infection as the identification process make take several days in the laboratory.</reasoning><output>a patient has proven or suspected infection, but the responsible microorganism is not yet unidentified</output>
When is empirical started?
<text>When is empirical started?</text><reasoning>In empirical therapy, a patient has proven or suspected infection, but the responsible microorganism is not yet unidentified. While the microorgainsim is being identified the doctor will usually administer the best choice of antibiotic that will be most active against the likely cause of infection usually a broad spectrum antibiotic. Empirical therapy is usually initiated before the doctor knows the exact identification of microorgansim causing the infection as the identification process make take several days in the laboratory.</reasoning><output>before the doctor knows the exact identification of microorgansim</output>
What are antibiotics in chemical terms?
<text>What are antibiotics in chemical terms?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>semisynthetic modifications</output>
What type of antibiotics include penicilin?
<text>What type of antibiotics include penicilin?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>beta-lactam antibiotics</output>
What are the type of antibiotics which are taken from still living things?
<text>What are the type of antibiotics which are taken from still living things?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>aminoglycosides</output>
How are the slufonamides,quinolones, and oxazolidinones created?
<text>How are the slufonamides,quinolones, and oxazolidinones created?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>synthesis</output>
Besides semisytetic modifications, what advances in medicinal chemistry regarding antibacterials?
<text>Besides semisytetic modifications, what advances in medicinal chemistry regarding antibacterials?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>various natural compounds</output>
What is included in the beta-lactam antibiotics?
<text>What is included in the beta-lactam antibiotics?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>penicillins</output>
What is penicillins produced by?
<text>What is penicillins produced by?</text><reasoning>With advances in medicinal chemistry, most modern antibacterials are semisynthetic modifications of various natural compounds. These include, for example, the beta-lactam antibiotics, which include the penicillins (produced by fungi in the genus Penicillium), the cephalosporins, and the carbapenems. Compounds that are still isolated from living organisms are the aminoglycosides, whereas other antibacterials—for example, the sulfonamides, the quinolones, and the oxazolidinones—are produced solely by chemical synthesis. Many antibacterial compounds are relatively small molecules with a molecular weight of less than 2000 atomic mass units.[citation needed]</reasoning><output>fungi</output>
What does the potency of antibacterials depend upon?
<text>What does the potency of antibacterials depend upon?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>concentration</output>
What does this eliminate?
<text>What does this eliminate?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>bacterial infection</output>
What does the bactericidal activitty of antibacterials depend on what?
<text>What does the bactericidal activitty of antibacterials depend on what?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>bacterial growth phase</output>
What besides ongoing metabolic activity is required in bactericidal activity?
<text>What besides ongoing metabolic activity is required in bactericidal activity?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>division of bacterial cells</output>
What does the activity of antibacterials depends on?
<text>What does the activity of antibacterials depends on?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>concentration</output>
What does a successful treatment using antibiotics entail?
<text>What does a successful treatment using antibiotics entail?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial</output>
How do you predict the clinical result?
<text>How do you predict the clinical result?</text><reasoning>The successful outcome of antimicrobial therapy with antibacterial compounds depends on several factors. These include host defense mechanisms, the location of infection, and the pharmacokinetic and pharmacodynamic properties of the antibacterial. A bactericidal activity of antibacterials may depend on the bacterial growth phase, and it often requires ongoing metabolic activity and division of bacterial cells. These findings are based on laboratory studies, and in clinical settings have also been shown to eliminate bacterial infection. Since the activity of antibacterials depends frequently on its concentration, in vitro characterization of antibacterial activity commonly includes the determination of the minimum inhibitory concentration and minimum bactericidal concentration of an antibacterial. To predict clinical outcome, the antimicrobial activity of an antibacterial is usually combined with its pharmacokinetic profile, and several pharmacological parameters are used as markers of drug efficacy.</reasoning><output>several pharmacological parameters are used as markers of drug efficacy</output>
In the build-up to genocide, what have other authors focused on?
<text>In the build-up to genocide, what have other authors focused on?</text><reasoning>Other authors have focused on the structural conditions leading up to genocide and the psychological and social processes that create an evolution toward genocide. Ervin Staub showed that economic deterioration and political confusion and disorganization were starting points of increasing discrimination and violence in many instances of genocides and mass killing. They lead to scapegoating a group and ideologies that identified that group as an enemy. A history of devaluation of the group that becomes the victim, past violence against the group that becomes the perpetrator leading to psychological wounds, authoritarian cultures and political systems, and the passivity of internal and external witnesses (bystanders) all contribute to the probability that the violence develops into genocide. Intense conflict between groups that is unresolved, becomes intractable and violent can also lead to genocide. The conditions that lead to genocide provide guidance to early prevention, such as humanizing a devalued group, creating ideologies that embrace all groups, and activating bystander responses. There is substantial research to indicate how this can be done, but information is only slowly transformed into action.</reasoning><output>structural conditions</output>
What processes are thought to create an evolution toward genocide?
<text>What processes are thought to create an evolution toward genocide?</text><reasoning>Other authors have focused on the structural conditions leading up to genocide and the psychological and social processes that create an evolution toward genocide. Ervin Staub showed that economic deterioration and political confusion and disorganization were starting points of increasing discrimination and violence in many instances of genocides and mass killing. They lead to scapegoating a group and ideologies that identified that group as an enemy. A history of devaluation of the group that becomes the victim, past violence against the group that becomes the perpetrator leading to psychological wounds, authoritarian cultures and political systems, and the passivity of internal and external witnesses (bystanders) all contribute to the probability that the violence develops into genocide. Intense conflict between groups that is unresolved, becomes intractable and violent can also lead to genocide. The conditions that lead to genocide provide guidance to early prevention, such as humanizing a devalued group, creating ideologies that embrace all groups, and activating bystander responses. There is substantial research to indicate how this can be done, but information is only slowly transformed into action.</reasoning><output>psychological and social</output>
Who revealed the starting points of this evolution to be economic deterioration and political confusion?
<text>Who revealed the starting points of this evolution to be economic deterioration and political confusion?</text><reasoning>Other authors have focused on the structural conditions leading up to genocide and the psychological and social processes that create an evolution toward genocide. Ervin Staub showed that economic deterioration and political confusion and disorganization were starting points of increasing discrimination and violence in many instances of genocides and mass killing. They lead to scapegoating a group and ideologies that identified that group as an enemy. A history of devaluation of the group that becomes the victim, past violence against the group that becomes the perpetrator leading to psychological wounds, authoritarian cultures and political systems, and the passivity of internal and external witnesses (bystanders) all contribute to the probability that the violence develops into genocide. Intense conflict between groups that is unresolved, becomes intractable and violent can also lead to genocide. The conditions that lead to genocide provide guidance to early prevention, such as humanizing a devalued group, creating ideologies that embrace all groups, and activating bystander responses. There is substantial research to indicate how this can be done, but information is only slowly transformed into action.</reasoning><output>Ervin Staub</output>
A history of what is just one factor that contributes to the probability of violence developing into genocide?
<text>A history of what is just one factor that contributes to the probability of violence developing into genocide?</text><reasoning>Other authors have focused on the structural conditions leading up to genocide and the psychological and social processes that create an evolution toward genocide. Ervin Staub showed that economic deterioration and political confusion and disorganization were starting points of increasing discrimination and violence in many instances of genocides and mass killing. They lead to scapegoating a group and ideologies that identified that group as an enemy. A history of devaluation of the group that becomes the victim, past violence against the group that becomes the perpetrator leading to psychological wounds, authoritarian cultures and political systems, and the passivity of internal and external witnesses (bystanders) all contribute to the probability that the violence develops into genocide. Intense conflict between groups that is unresolved, becomes intractable and violent can also lead to genocide. The conditions that lead to genocide provide guidance to early prevention, such as humanizing a devalued group, creating ideologies that embrace all groups, and activating bystander responses. There is substantial research to indicate how this can be done, but information is only slowly transformed into action.</reasoning><output>devaluation of the group</output>
What is one preventive effort in circumventing conditions that lead to genocide?
<text>What is one preventive effort in circumventing conditions that lead to genocide?</text><reasoning>Other authors have focused on the structural conditions leading up to genocide and the psychological and social processes that create an evolution toward genocide. Ervin Staub showed that economic deterioration and political confusion and disorganization were starting points of increasing discrimination and violence in many instances of genocides and mass killing. They lead to scapegoating a group and ideologies that identified that group as an enemy. A history of devaluation of the group that becomes the victim, past violence against the group that becomes the perpetrator leading to psychological wounds, authoritarian cultures and political systems, and the passivity of internal and external witnesses (bystanders) all contribute to the probability that the violence develops into genocide. Intense conflict between groups that is unresolved, becomes intractable and violent can also lead to genocide. The conditions that lead to genocide provide guidance to early prevention, such as humanizing a devalued group, creating ideologies that embrace all groups, and activating bystander responses. There is substantial research to indicate how this can be done, but information is only slowly transformed into action.</reasoning><output>humanizing a devalued group</output>
What two writers examined the lack of an accepted and singular definition for genocide?
<text>What two writers examined the lack of an accepted and singular definition for genocide?</text><reasoning>Jonassohn and Björnson postulate that the major reason why no single generally accepted genocide definition has emerged is because academics have adjusted their focus to emphasise different periods and have found it expedient to use slightly different definitions to help them interpret events. For example, Frank Chalk and Kurt Jonassohn studied the whole of human history, while Leo Kuper and R. J. Rummel in their more recent works concentrated on the 20th century, and Helen Fein, Barbara Harff and Ted Gurr have looked at post World War II events. Jonassohn and Björnson are critical of some of these studies, arguing that they are too expansive, and conclude that the academic discipline of genocide studies is too young to have a canon of work on which to build an academic paradigm.</reasoning><output>Jonassohn and Björnson</output>
The two writers suggested that academics adjusted what in their different definitions to assist them in interpreting events?
<text>The two writers suggested that academics adjusted what in their different definitions to assist them in interpreting events?</text><reasoning>Jonassohn and Björnson postulate that the major reason why no single generally accepted genocide definition has emerged is because academics have adjusted their focus to emphasise different periods and have found it expedient to use slightly different definitions to help them interpret events. For example, Frank Chalk and Kurt Jonassohn studied the whole of human history, while Leo Kuper and R. J. Rummel in their more recent works concentrated on the 20th century, and Helen Fein, Barbara Harff and Ted Gurr have looked at post World War II events. Jonassohn and Björnson are critical of some of these studies, arguing that they are too expansive, and conclude that the academic discipline of genocide studies is too young to have a canon of work on which to build an academic paradigm.</reasoning><output>their focus</output>
What writer joined Jonassohn in the study of the whole of human history?
<text>What writer joined Jonassohn in the study of the whole of human history?</text><reasoning>Jonassohn and Björnson postulate that the major reason why no single generally accepted genocide definition has emerged is because academics have adjusted their focus to emphasise different periods and have found it expedient to use slightly different definitions to help them interpret events. For example, Frank Chalk and Kurt Jonassohn studied the whole of human history, while Leo Kuper and R. J. Rummel in their more recent works concentrated on the 20th century, and Helen Fein, Barbara Harff and Ted Gurr have looked at post World War II events. Jonassohn and Björnson are critical of some of these studies, arguing that they are too expansive, and conclude that the academic discipline of genocide studies is too young to have a canon of work on which to build an academic paradigm.</reasoning><output>Frank Chalk</output>
With whom was Leo Kuper paired in research that focused on 20th century works?
<text>With whom was Leo Kuper paired in research that focused on 20th century works?</text><reasoning>Jonassohn and Björnson postulate that the major reason why no single generally accepted genocide definition has emerged is because academics have adjusted their focus to emphasise different periods and have found it expedient to use slightly different definitions to help them interpret events. For example, Frank Chalk and Kurt Jonassohn studied the whole of human history, while Leo Kuper and R. J. Rummel in their more recent works concentrated on the 20th century, and Helen Fein, Barbara Harff and Ted Gurr have looked at post World War II events. Jonassohn and Björnson are critical of some of these studies, arguing that they are too expansive, and conclude that the academic discipline of genocide studies is too young to have a canon of work on which to build an academic paradigm.</reasoning><output>R. J. Rummel</output>
Two women and what man concentrated on post World War II events?
<text>Two women and what man concentrated on post World War II events?</text><reasoning>Jonassohn and Björnson postulate that the major reason why no single generally accepted genocide definition has emerged is because academics have adjusted their focus to emphasise different periods and have found it expedient to use slightly different definitions to help them interpret events. For example, Frank Chalk and Kurt Jonassohn studied the whole of human history, while Leo Kuper and R. J. Rummel in their more recent works concentrated on the 20th century, and Helen Fein, Barbara Harff and Ted Gurr have looked at post World War II events. Jonassohn and Björnson are critical of some of these studies, arguing that they are too expansive, and conclude that the academic discipline of genocide studies is too young to have a canon of work on which to build an academic paradigm.</reasoning><output>Ted Gurr</output>
What is part of hje the make up of bacterial strains?
<text>What is part of hje the make up of bacterial strains?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>Intrinsic antibacterial resistance</output>
What is exchanged between between bacterial strains or species via plasmids that have this resistance?
<text>What is exchanged between between bacterial strains or species via plasmids that have this resistance?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>antibacterial resistance genes</output>
What can be absent from the bacterial genome?
<text>What can be absent from the bacterial genome?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>antibiotic target</output>
When does the spread of antibacterial resistance frequently occurs/
<text>When does the spread of antibacterial resistance frequently occurs/</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>vertical transmission</output>
What does some resistance come from?
<text>What does some resistance come from?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>mutation</output>
What method of spread can occur in antibacterial resistance?
<text>What method of spread can occur in antibacterial resistance?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>vertical transmission of mutations</output>
What do plasmids do in resistance?
<text>What do plasmids do in resistance?</text><reasoning>Several molecular mechanisms of antibacterial resistance exist. Intrinsic antibacterial resistance may be part of the genetic makeup of bacterial strains. For example, an antibiotic target may be absent from the bacterial genome. Acquired resistance results from a mutation in the bacterial chromosome or the acquisition of extra-chromosomal DNA. Antibacterial-producing bacteria have evolved resistance mechanisms that have been shown to be similar to, and may have been transferred to, antibacterial-resistant strains. The spread of antibacterial resistance often occurs through vertical transmission of mutations during growth and by genetic recombination of DNA by horizontal genetic exchange. For instance, antibacterial resistance genes can be exchanged between different bacterial strains or species via plasmids that carry these resistance genes. Plasmids that carry several different resistance genes can confer resistance to multiple antibacterials. Cross-resistance to several antibacterials may also occur when a resistance mechanism encoded by a single gene conveys resistance to more than one antibacterial compound.</reasoning><output>carry several different resistance genes</output>
What is a modern common occurence with antibiotics?
<text>What is a modern common occurence with antibiotics?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>resistance of bacteria</output>
When was the Luria-Delbruck experiment?
<text>When was the Luria-Delbruck experiment?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>1943</output>
Which two antibiotics that have high efficacy are much less useful now?
<text>Which two antibiotics that have high efficacy are much less useful now?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>penicillin and erythromycin</output>
What does emergence of resistance reflect?
<text>What does emergence of resistance reflect?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>evolutionary processes</output>
What is the purpose of antibiotic treatment?
<text>What is the purpose of antibiotic treatment?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>survive high doses of antibiotics</output>
When was antibacterial-resistance demonstrated?
<text>When was antibacterial-resistance demonstrated?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>1943</output>
Who made the demonstration in 1943?
<text>Who made the demonstration in 1943?</text><reasoning>The emergence of resistance of bacteria to antibiotics is a common phenomenon. Emergence of resistance often reflects evolutionary processes that take place during antibiotic therapy. The antibiotic treatment may select for bacterial strains with physiologically or genetically enhanced capacity to survive high doses of antibiotics. Under certain conditions, it may result in preferential growth of resistant bacteria, while growth of susceptible bacteria is inhibited by the drug. For example, antibacterial selection for strains having previously acquired antibacterial-resistance genes was demonstrated in 1943 by the Luria–Delbrück experiment. Antibiotics such as penicillin and erythromycin, which used to have a high efficacy against many bacterial species and strains, have become less effective, due to the increased resistance of many bacterial strains.</reasoning><output>Luria–Delbrück</output>
What type of organism has been reported to have worked on infections?
<text>What type of organism has been reported to have worked on infections?</text><reasoning>The effects of some types of mold on infection had been noticed many times over the course of history (see: History of penicillin). In 1928, Alexander Fleming noticed the same effect in a Petri dish, where a number of disease-causing bacteria were killed by a fungus of the genus Penicillium. Fleming postulated that the effect is mediated by an antibacterial compound he named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized some of its biological properties, and attempted to use a crude preparation to treat some infections, but he was unable to pursue its further development without the aid of trained chemists.</reasoning><output>mold</output>
Who noticed in a lab the antibacterial characteristics of mold?
<text>Who noticed in a lab the antibacterial characteristics of mold?</text><reasoning>The effects of some types of mold on infection had been noticed many times over the course of history (see: History of penicillin). In 1928, Alexander Fleming noticed the same effect in a Petri dish, where a number of disease-causing bacteria were killed by a fungus of the genus Penicillium. Fleming postulated that the effect is mediated by an antibacterial compound he named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized some of its biological properties, and attempted to use a crude preparation to treat some infections, but he was unable to pursue its further development without the aid of trained chemists.</reasoning><output>Alexander Fleming</output>
What mold did Fleming notice had antibacterial properties?
<text>What mold did Fleming notice had antibacterial properties?</text><reasoning>The effects of some types of mold on infection had been noticed many times over the course of history (see: History of penicillin). In 1928, Alexander Fleming noticed the same effect in a Petri dish, where a number of disease-causing bacteria were killed by a fungus of the genus Penicillium. Fleming postulated that the effect is mediated by an antibacterial compound he named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized some of its biological properties, and attempted to use a crude preparation to treat some infections, but he was unable to pursue its further development without the aid of trained chemists.</reasoning><output>penicillin</output>
What did Fleming initially think a good use would be for it?
<text>What did Fleming initially think a good use would be for it?</text><reasoning>The effects of some types of mold on infection had been noticed many times over the course of history (see: History of penicillin). In 1928, Alexander Fleming noticed the same effect in a Petri dish, where a number of disease-causing bacteria were killed by a fungus of the genus Penicillium. Fleming postulated that the effect is mediated by an antibacterial compound he named penicillin, and that its antibacterial properties could be exploited for chemotherapy. He initially characterized some of its biological properties, and attempted to use a crude preparation to treat some infections, but he was unable to pursue its further development without the aid of trained chemists.</reasoning><output>chemotherapy</output>
What are strains that are resistant to antibiotics called sometimes?
<text>What are strains that are resistant to antibiotics called sometimes?</text><reasoning>Antibacterial-resistant strains and species, sometimes referred to as "superbugs", now contribute to the emergence of diseases that were for a while well controlled. For example, emergent bacterial strains causing tuberculosis (TB) that are resistant to previously effective antibacterial treatments pose many therapeutic challenges. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. For example, NDM-1 is a newly identified enzyme conveying bacterial resistance to a broad range of beta-lactam antibacterials. The United Kingdom's Health Protection Agency has stated that "most isolates with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections."</reasoning><output>superbugs</output>
What was a once almost controlled disease that is coming back do to resistance?
<text>What was a once almost controlled disease that is coming back do to resistance?</text><reasoning>Antibacterial-resistant strains and species, sometimes referred to as "superbugs", now contribute to the emergence of diseases that were for a while well controlled. For example, emergent bacterial strains causing tuberculosis (TB) that are resistant to previously effective antibacterial treatments pose many therapeutic challenges. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. For example, NDM-1 is a newly identified enzyme conveying bacterial resistance to a broad range of beta-lactam antibacterials. The United Kingdom's Health Protection Agency has stated that "most isolates with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections."</reasoning><output>tuberculosis</output>
How many new infections of resistant TB are reported per year?
<text>How many new infections of resistant TB are reported per year?</text><reasoning>Antibacterial-resistant strains and species, sometimes referred to as "superbugs", now contribute to the emergence of diseases that were for a while well controlled. For example, emergent bacterial strains causing tuberculosis (TB) that are resistant to previously effective antibacterial treatments pose many therapeutic challenges. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. For example, NDM-1 is a newly identified enzyme conveying bacterial resistance to a broad range of beta-lactam antibacterials. The United Kingdom's Health Protection Agency has stated that "most isolates with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections."</reasoning><output>half a million</output>
What is the acronym used to describe resistant TB?
<text>What is the acronym used to describe resistant TB?</text><reasoning>Antibacterial-resistant strains and species, sometimes referred to as "superbugs", now contribute to the emergence of diseases that were for a while well controlled. For example, emergent bacterial strains causing tuberculosis (TB) that are resistant to previously effective antibacterial treatments pose many therapeutic challenges. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide. For example, NDM-1 is a newly identified enzyme conveying bacterial resistance to a broad range of beta-lactam antibacterials. The United Kingdom's Health Protection Agency has stated that "most isolates with NDM-1 enzyme are resistant to all standard intravenous antibiotics for treatment of severe infections."</reasoning><output>MDR-TB</output>
What is one potential issue with drinking alcohol while taking antibiotics?
<text>What is one potential issue with drinking alcohol while taking antibiotics?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>decreased effectiveness</output>
Do all antibiotics interact dangerously with alcohol?
<text>Do all antibiotics interact dangerously with alcohol?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>moderate alcohol consumption is unlikely to interfere with many common antibiotics</output>
Is it OK to drink alcohol while taking any antibiotic?
<text>Is it OK to drink alcohol while taking any antibiotic?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>there are specific types of antibiotics with which alcohol consumption may cause serious side-effects</output>
How common is the belief that alcohol and antibiotics should never be mixed?
<text>How common is the belief that alcohol and antibiotics should never be mixed?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>widespread</output>
What can alcohol and certain antibiotics cause?
<text>What can alcohol and certain antibiotics cause?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>decreased effectiveness of antibiotic therapy</output>
What is unlikely to interfere with with many common antibiotics?
<text>What is unlikely to interfere with with many common antibiotics?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>alcohol consumption</output>
What belief should bever be mixed widespread?
<text>What belief should bever be mixed widespread?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>alcohol and antibiotics</output>
What common drug can reduce antibiotic effectiveness?
<text>What common drug can reduce antibiotic effectiveness?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>alcohol</output>
What type of antibiotic is most likely to be a problem with alcohol?
<text>What type of antibiotic is most likely to be a problem with alcohol?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>specific types of antibiotics with which alcohol consumption may cause serious side-effects</output>
Should alcohol be used while on antibiotics?
<text>Should alcohol be used while on antibiotics?</text><reasoning>Interactions between alcohol and certain antibiotics may occur and may cause side-effects and decreased effectiveness of antibiotic therapy. While moderate alcohol consumption is unlikely to interfere with many common antibiotics, there are specific types of antibiotics with which alcohol consumption may cause serious side-effects. Therefore, potential risks of side-effects and effectiveness depend on the type of antibiotic administered. Despite the lack of a categorical counterindication, the belief that alcohol and antibiotics should never be mixed is widespread.</reasoning><output>alcohol and antibiotics should never be mixed</output>
What was the first available antibiotic?
<text>What was the first available antibiotic?</text><reasoning>The first sulfonamide and first commercially available antibacterial, Prontosil, was developed by a research team led by Gerhard Domagk in 1932 at the Bayer Laboratories of the IG Farben conglomerate in Germany. Domagk received the 1939 Nobel Prize for Medicine for his efforts. Prontosil had a relatively broad effect against Gram-positive cocci, but not against enterobacteria. Research was stimulated apace by its success. The discovery and development of this sulfonamide drug opened the era of antibacterials.</reasoning><output>Prontosil</output>
What company developed Prontosil?
<text>What company developed Prontosil?</text><reasoning>The first sulfonamide and first commercially available antibacterial, Prontosil, was developed by a research team led by Gerhard Domagk in 1932 at the Bayer Laboratories of the IG Farben conglomerate in Germany. Domagk received the 1939 Nobel Prize for Medicine for his efforts. Prontosil had a relatively broad effect against Gram-positive cocci, but not against enterobacteria. Research was stimulated apace by its success. The discovery and development of this sulfonamide drug opened the era of antibacterials.</reasoning><output>IG Farben</output>
Who led the team that came up with Prontosil?
<text>Who led the team that came up with Prontosil?</text><reasoning>The first sulfonamide and first commercially available antibacterial, Prontosil, was developed by a research team led by Gerhard Domagk in 1932 at the Bayer Laboratories of the IG Farben conglomerate in Germany. Domagk received the 1939 Nobel Prize for Medicine for his efforts. Prontosil had a relatively broad effect against Gram-positive cocci, but not against enterobacteria. Research was stimulated apace by its success. The discovery and development of this sulfonamide drug opened the era of antibacterials.</reasoning><output>Gerhard Domagk</output>
What prize did Domagk get for his work?
<text>What prize did Domagk get for his work?</text><reasoning>The first sulfonamide and first commercially available antibacterial, Prontosil, was developed by a research team led by Gerhard Domagk in 1932 at the Bayer Laboratories of the IG Farben conglomerate in Germany. Domagk received the 1939 Nobel Prize for Medicine for his efforts. Prontosil had a relatively broad effect against Gram-positive cocci, but not against enterobacteria. Research was stimulated apace by its success. The discovery and development of this sulfonamide drug opened the era of antibacterials.</reasoning><output>1939 Nobel Prize for Medicine</output>
What is a way of improperly using antibiotics for those traveling?
<text>What is a way of improperly using antibiotics for those traveling?</text><reasoning>Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections such as the common cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect them". Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics.</reasoning><output>prophylactic antibiotics</output>
What can happen if a doctor doesn't prescribe to a person's weight and prior use?
<text>What can happen if a doctor doesn't prescribe to a person's weight and prior use?</text><reasoning>Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections such as the common cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect them". Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics.</reasoning><output>failure of medical professionals to prescribe the correct dosage</output>
What are 3 other common forms of bad antibiotic practices?
<text>What are 3 other common forms of bad antibiotic practices?</text><reasoning>Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections such as the common cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect them". Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics.</reasoning><output>failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery</output>
What happens when a cold is treated with antibiotics?
<text>What happens when a cold is treated with antibiotics?</text><reasoning>Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections such as the common cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect them". Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics.</reasoning><output>Inappropriate antibiotic treatment</output>
What do doctors usually do when a patient seems to want antibiotics even though they may not be right?
<text>What do doctors usually do when a patient seems to want antibiotics even though they may not be right?</text><reasoning>Common forms of antibiotic misuse include excessive use of prophylactic antibiotics in travelers and failure of medical professionals to prescribe the correct dosage of antibiotics on the basis of the patient's weight and history of prior use. Other forms of misuse include failure to take the entire prescribed course of the antibiotic, incorrect dosage and administration, or failure to rest for sufficient recovery. Inappropriate antibiotic treatment, for example, is their prescription to treat viral infections such as the common cold. One study on respiratory tract infections found "physicians were more likely to prescribe antibiotics to patients who appeared to expect them". Multifactorial interventions aimed at both physicians and patients can reduce inappropriate prescription of antibiotics.</reasoning><output>prescribe antibiotics</output>
In the 1990s, how many people were indicted for war crimes that were officially defined as genocide?
<text>In the 1990s, how many people were indicted for war crimes that were officially defined as genocide?</text><reasoning>About 30 people have been indicted for participating in genocide or complicity in genocide during the early 1990s in Bosnia. To date, after several plea bargains and some convictions that were successfully challenged on appeal two men, Vujadin Popović and Ljubiša Beara, have been found guilty of committing genocide, Zdravko Tolimir has been found guilty of committing genocide and conspiracy to commit genocide, and two others, Radislav Krstić and Drago Nikolić, have been found guilty of aiding and abetting genocide. Three others have been found guilty of participating in genocides in Bosnia by German courts, one of whom Nikola Jorgić lost an appeal against his conviction in the European Court of Human Rights. A further eight men, former members of the Bosnian Serb security forces were found guilty of genocide by the State Court of Bosnia and Herzegovina (See List of Bosnian genocide prosecutions).</reasoning><output>About 30</output>
Convicted perpetrators Popovic and Beara were found guilty of genocide despite what evasive action?
<text>Convicted perpetrators Popovic and Beara were found guilty of genocide despite what evasive action?</text><reasoning>About 30 people have been indicted for participating in genocide or complicity in genocide during the early 1990s in Bosnia. To date, after several plea bargains and some convictions that were successfully challenged on appeal two men, Vujadin Popović and Ljubiša Beara, have been found guilty of committing genocide, Zdravko Tolimir has been found guilty of committing genocide and conspiracy to commit genocide, and two others, Radislav Krstić and Drago Nikolić, have been found guilty of aiding and abetting genocide. Three others have been found guilty of participating in genocides in Bosnia by German courts, one of whom Nikola Jorgić lost an appeal against his conviction in the European Court of Human Rights. A further eight men, former members of the Bosnian Serb security forces were found guilty of genocide by the State Court of Bosnia and Herzegovina (See List of Bosnian genocide prosecutions).</reasoning><output>several plea bargains</output>
Tolimir was found guilty of both genocide and what other charge?
<text>Tolimir was found guilty of both genocide and what other charge?</text><reasoning>About 30 people have been indicted for participating in genocide or complicity in genocide during the early 1990s in Bosnia. To date, after several plea bargains and some convictions that were successfully challenged on appeal two men, Vujadin Popović and Ljubiša Beara, have been found guilty of committing genocide, Zdravko Tolimir has been found guilty of committing genocide and conspiracy to commit genocide, and two others, Radislav Krstić and Drago Nikolić, have been found guilty of aiding and abetting genocide. Three others have been found guilty of participating in genocides in Bosnia by German courts, one of whom Nikola Jorgić lost an appeal against his conviction in the European Court of Human Rights. A further eight men, former members of the Bosnian Serb security forces were found guilty of genocide by the State Court of Bosnia and Herzegovina (See List of Bosnian genocide prosecutions).</reasoning><output>conspiracy to commit genocide</output>
Another charge beyond the act of genocide and for which Krstic and Nikolic were found guilty was what?
<text>Another charge beyond the act of genocide and for which Krstic and Nikolic were found guilty was what?</text><reasoning>About 30 people have been indicted for participating in genocide or complicity in genocide during the early 1990s in Bosnia. To date, after several plea bargains and some convictions that were successfully challenged on appeal two men, Vujadin Popović and Ljubiša Beara, have been found guilty of committing genocide, Zdravko Tolimir has been found guilty of committing genocide and conspiracy to commit genocide, and two others, Radislav Krstić and Drago Nikolić, have been found guilty of aiding and abetting genocide. Three others have been found guilty of participating in genocides in Bosnia by German courts, one of whom Nikola Jorgić lost an appeal against his conviction in the European Court of Human Rights. A further eight men, former members of the Bosnian Serb security forces were found guilty of genocide by the State Court of Bosnia and Herzegovina (See List of Bosnian genocide prosecutions).</reasoning><output>aiding and abetting genocide</output>
Three others were charged with participating in genocides in Bosnia by which country's courts?
<text>Three others were charged with participating in genocides in Bosnia by which country's courts?</text><reasoning>About 30 people have been indicted for participating in genocide or complicity in genocide during the early 1990s in Bosnia. To date, after several plea bargains and some convictions that were successfully challenged on appeal two men, Vujadin Popović and Ljubiša Beara, have been found guilty of committing genocide, Zdravko Tolimir has been found guilty of committing genocide and conspiracy to commit genocide, and two others, Radislav Krstić and Drago Nikolić, have been found guilty of aiding and abetting genocide. Three others have been found guilty of participating in genocides in Bosnia by German courts, one of whom Nikola Jorgić lost an appeal against his conviction in the European Court of Human Rights. A further eight men, former members of the Bosnian Serb security forces were found guilty of genocide by the State Court of Bosnia and Herzegovina (See List of Bosnian genocide prosecutions).</reasoning><output>German courts</output>
What is the name of a US government agency tasked with trying to stop improper use of antibiotics?
<text>What is the name of a US government agency tasked with trying to stop improper use of antibiotics?</text><reasoning>Several organizations concerned with antimicrobial resistance are lobbying to eliminate the unnecessary use of antibiotics. The issues of misuse and overuse of antibiotics have been addressed by the formation of the US Interagency Task Force on Antimicrobial Resistance. This task force aims to actively address antimicrobial resistance, and is coordinated by the US Centers for Disease Control and Prevention, the Food and Drug Administration (FDA), and the National Institutes of Health (NIH), as well as other US agencies. An NGO campaign group is Keep Antibiotics Working. In France, an "Antibiotics are not automatic" government campaign started in 2002 and led to a marked reduction of unnecessary antibiotic prescriptions, especially in children.</reasoning><output>US Interagency Task Force on Antimicrobial Resistance</output>
Which agencies control this task force?
<text>Which agencies control this task force?</text><reasoning>Several organizations concerned with antimicrobial resistance are lobbying to eliminate the unnecessary use of antibiotics. The issues of misuse and overuse of antibiotics have been addressed by the formation of the US Interagency Task Force on Antimicrobial Resistance. This task force aims to actively address antimicrobial resistance, and is coordinated by the US Centers for Disease Control and Prevention, the Food and Drug Administration (FDA), and the National Institutes of Health (NIH), as well as other US agencies. An NGO campaign group is Keep Antibiotics Working. In France, an "Antibiotics are not automatic" government campaign started in 2002 and led to a marked reduction of unnecessary antibiotic prescriptions, especially in children.</reasoning><output>US Centers for Disease Control and Prevention, the Food and Drug Administration (FDA), and the National Institutes of Health (NIH)</output>
When did the French start going after overuse of antibiotics?
<text>When did the French start going after overuse of antibiotics?</text><reasoning>Several organizations concerned with antimicrobial resistance are lobbying to eliminate the unnecessary use of antibiotics. The issues of misuse and overuse of antibiotics have been addressed by the formation of the US Interagency Task Force on Antimicrobial Resistance. This task force aims to actively address antimicrobial resistance, and is coordinated by the US Centers for Disease Control and Prevention, the Food and Drug Administration (FDA), and the National Institutes of Health (NIH), as well as other US agencies. An NGO campaign group is Keep Antibiotics Working. In France, an "Antibiotics are not automatic" government campaign started in 2002 and led to a marked reduction of unnecessary antibiotic prescriptions, especially in children.</reasoning><output>2002</output>
What do anitibiotics mostly target?
<text>What do anitibiotics mostly target?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>bacterial functions or growth processes</output>
Which two types of antibiotics target the cell wall?
<text>Which two types of antibiotics target the cell wall?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>penicillins and cephalosporins</output>
Which type of antibiotic goes after the cell membrane?
<text>Which type of antibiotic goes after the cell membrane?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>polymyxins</output>
What 3 types go after protein synthesis?
<text>What 3 types go after protein synthesis?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>(macrolides, lincosamides and tetracyclines</output>
Besides sprectrum of activity and chemical structure, how can antibacterial antibiotics classified?
<text>Besides sprectrum of activity and chemical structure, how can antibacterial antibiotics classified?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>mechanism of action</output>
What is another name used for bacterial cell wall?
<text>What is another name used for bacterial cell wall?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>penicillins and cephalosporins</output>
whats another word for cell membrane?
<text>whats another word for cell membrane?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>polymyxins</output>
How many new classes of antibacterial antibiotics was introduced in the late 2000's/
<text>How many new classes of antibacterial antibiotics was introduced in the late 2000's/</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>four</output>
What three ways are antibiotics classified?
<text>What three ways are antibiotics classified?</text><reasoning>Antibacterial antibiotics are commonly classified based on their mechanism of action, chemical structure, or spectrum of activity. Most target bacterial functions or growth processes. Those that target the bacterial cell wall (penicillins and cephalosporins) or the cell membrane (polymyxins), or interfere with essential bacterial enzymes (rifamycins, lipiarmycins, quinolones, and sulfonamides) have bactericidal activities. Those that target protein synthesis (macrolides, lincosamides and tetracyclines) are usually bacteriostatic (with the exception of bactericidal aminoglycosides). Further categorization is based on their target specificity. "Narrow-spectrum" antibacterial antibiotics target specific types of bacteria, such as Gram-negative or Gram-positive bacteria, whereas broad-spectrum antibiotics affect a wide range of bacteria. Following a 40-year hiatus in discovering new classes of antibacterial compounds, four new classes of antibacterial antibiotics have been brought into clinical use in the late 2000s and early 2010s: cyclic lipopeptides (such as daptomycin), glycylcyclines (such as tigecycline), oxazolidinones (such as linezolid), and lipiarmycins (such as fidaxomicin).</reasoning><output>mechanism of action, chemical structure, or spectrum of activity</output>
When did the EU ban antibiotics for speeding up growth?
<text>When did the EU ban antibiotics for speeding up growth?</text><reasoning>The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as growth-promotional agents since 2003. Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.[citation needed] However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills (S.742 and H.R. 2562) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed. These bills were endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA).</reasoning><output>2003</output>
What report caused the UK to worry about resistance?
<text>What report caused the UK to worry about resistance?</text><reasoning>The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as growth-promotional agents since 2003. Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.[citation needed] However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills (S.742 and H.R. 2562) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed. These bills were endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA).</reasoning><output>Swann report 1969</output>
What 3 US organizations have called for the banning of antibiotics in the production of food animals?
<text>What 3 US organizations have called for the banning of antibiotics in the production of food animals?</text><reasoning>The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as growth-promotional agents since 2003. Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.[citation needed] However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills (S.742 and H.R. 2562) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed. These bills were endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA).</reasoning><output>American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)</output>
Name two US bills that want to ban antibiotics in food production?
<text>Name two US bills that want to ban antibiotics in food production?</text><reasoning>The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as growth-promotional agents since 2003. Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.[citation needed] However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills (S.742 and H.R. 2562) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed. These bills were endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA).</reasoning><output>S.742 and H.R. 2562</output>
What 3 medical associations supported the bills?
<text>What 3 medical associations supported the bills?</text><reasoning>The emergence of antibiotic resistance has prompted restrictions on their use in the UK in 1970 (Swann report 1969), and the EU has banned the use of antibiotics as growth-promotional agents since 2003. Moreover, several organizations (e.g., The American Society for Microbiology (ASM), American Public Health Association (APHA) and the American Medical Association (AMA)) have called for restrictions on antibiotic use in food animal production and an end to all nontherapeutic uses.[citation needed] However, commonly there are delays in regulatory and legislative actions to limit the use of antibiotics, attributable partly to resistance against such regulation by industries using or selling antibiotics, and to the time required for research to test causal links between their use and resistance to them. Two federal bills (S.742 and H.R. 2562) aimed at phasing out nontherapeutic use of antibiotics in US food animals were proposed, but have not passed. These bills were endorsed by public health and medical organizations, including the American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA).</reasoning><output>American Holistic Nurses' Association, the American Medical Association, and the American Public Health Association (APHA)</output>
What was the first antibiotic developed from nature?
<text>What was the first antibiotic developed from nature?</text><reasoning>In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and 80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World War II. Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that period were not shared between the Axis and the Allied powers during the war.</reasoning><output>tyrothricin</output>
When was tyrothricin created?
<text>When was tyrothricin created?</text><reasoning>In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and 80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World War II. Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that period were not shared between the Axis and the Allied powers during the war.</reasoning><output>1939</output>
What also happened in 1939 besides tyrothricin?
<text>What also happened in 1939 besides tyrothricin?</text><reasoning>In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and 80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World War II. Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that period were not shared between the Axis and the Allied powers during the war.</reasoning><output>start of World War II,</output>
Who discovered tyrothricin?
<text>Who discovered tyrothricin?</text><reasoning>In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and 80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World War II. Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that period were not shared between the Axis and the Allied powers during the war.</reasoning><output>Rene Dubos</output>
What was tyrothricin used for during the war?
<text>What was tyrothricin used for during the war?</text><reasoning>In 1939, coinciding with the start of World War II, Rene Dubos reported the discovery of the first naturally derived antibiotic, tyrothricin, a compound of 20% gramicidin and 80% tyrocidine, from B. brevis. It was one of the first commercially manufactured antibiotics universally and was very effective in treating wounds and ulcers during World War II. Gramicidin, however, could not be used systemically because of toxicity. Tyrocidine also proved too toxic for systemic usage. Research results obtained during that period were not shared between the Axis and the Allied powers during the war.</reasoning><output>wounds and ulcers</output>
What do vaccines need to work?
<text>What do vaccines need to work?</text><reasoning>Vaccines rely on immune modulation or augmentation. Vaccination either excites or reinforces the immune competence of a host to ward off infection, leading to the activation of macrophages, the production of antibodies, inflammation, and other classic immune reactions. Antibacterial vaccines have been responsible for a drastic reduction in global bacterial diseases. Vaccines made from attenuated whole cells or lysates have been replaced largely by less reactogenic, cell-free vaccines consisting of purified components, including capsular polysaccharides and their conjugates, to protein carriers, as well as inactivated toxins (toxoids) and proteins.</reasoning><output>immune modulation or augmentation</output>
What type of vaccines have saved millions of lives?
<text>What type of vaccines have saved millions of lives?</text><reasoning>Vaccines rely on immune modulation or augmentation. Vaccination either excites or reinforces the immune competence of a host to ward off infection, leading to the activation of macrophages, the production of antibodies, inflammation, and other classic immune reactions. Antibacterial vaccines have been responsible for a drastic reduction in global bacterial diseases. Vaccines made from attenuated whole cells or lysates have been replaced largely by less reactogenic, cell-free vaccines consisting of purified components, including capsular polysaccharides and their conjugates, to protein carriers, as well as inactivated toxins (toxoids) and proteins.</reasoning><output>Antibacterial vaccines</output>
What types of vaccines have been phased out?
<text>What types of vaccines have been phased out?</text><reasoning>Vaccines rely on immune modulation or augmentation. Vaccination either excites or reinforces the immune competence of a host to ward off infection, leading to the activation of macrophages, the production of antibodies, inflammation, and other classic immune reactions. Antibacterial vaccines have been responsible for a drastic reduction in global bacterial diseases. Vaccines made from attenuated whole cells or lysates have been replaced largely by less reactogenic, cell-free vaccines consisting of purified components, including capsular polysaccharides and their conjugates, to protein carriers, as well as inactivated toxins (toxoids) and proteins.</reasoning><output>Vaccines made from attenuated whole cells or lysates</output>
In what city did Frédéric achieve celebrity status?
<text>In what city did Frédéric achieve celebrity status?</text><reasoning>In Paris, Chopin encountered artists and other distinguished figures, and found many opportunities to exercise his talents and achieve celebrity. During his years in Paris he was to become acquainted with, among many others, Hector Berlioz, Franz Liszt, Ferdinand Hiller, Heinrich Heine, Eugène Delacroix, and Alfred de Vigny. Chopin was also acquainted with the poet Adam Mickiewicz, principal of the Polish Literary Society, some of whose verses he set as songs.</reasoning><output>Paris</output>
Who was the principal of the Polish Literary Society that Frédéric became acquainted with?
<text>Who was the principal of the Polish Literary Society that Frédéric became acquainted with?</text><reasoning>In Paris, Chopin encountered artists and other distinguished figures, and found many opportunities to exercise his talents and achieve celebrity. During his years in Paris he was to become acquainted with, among many others, Hector Berlioz, Franz Liszt, Ferdinand Hiller, Heinrich Heine, Eugène Delacroix, and Alfred de Vigny. Chopin was also acquainted with the poet Adam Mickiewicz, principal of the Polish Literary Society, some of whose verses he set as songs.</reasoning><output>Adam Mickiewicz</output>