際際滷shows by User: Natashamanzoor1 / http://www.slideshare.net/images/logo.gif 際際滷shows by User: Natashamanzoor1 / Sat, 20 Jan 2018 11:30:17 GMT 際際滷Share feed for 際際滷shows by User: Natashamanzoor1 SOS GENE ROLE IN E.COLI /Natashamanzoor1/sos-gene-role-in-ecoli sos-180120113017
In Escherichia coli, different classes of DNA-damaging agents can initiate the SOS response, as described above. Taking advantage of an operon fusion placing the lac operon (responsible for producing beta-galactosidase, a protein which degrades lactose) under the control of an SOS-related protein, a simple colorimetric assay for genotoxicity is possible. A lactose analog is added to the bacteria, which is then degraded by beta-galactosidase, thereby producing a colored compound which can be measured quantitatively through spectrophotometry. The degree of color development is an indirect measure of the beta-galactosidase produced, which itself is directly related to the amount of DNA damage. The E. coli are further modified in order to have a number of mutations including a uvrA mutation which renders the strain deficient in excision repair, increasing the response to certain DNA-damaging agents, as well as an rfa mutation, which renders the bacteria lipopolysaccharide-deficient, allowing better diffusion of certain chemicals into the cell in order to induce the SOS response.[7] Commercial kits which measures the primary response of the E. coli cell to genetic damage are available and may be highly correlated with theA mes Test for certain materials.[8]]]>

In Escherichia coli, different classes of DNA-damaging agents can initiate the SOS response, as described above. Taking advantage of an operon fusion placing the lac operon (responsible for producing beta-galactosidase, a protein which degrades lactose) under the control of an SOS-related protein, a simple colorimetric assay for genotoxicity is possible. A lactose analog is added to the bacteria, which is then degraded by beta-galactosidase, thereby producing a colored compound which can be measured quantitatively through spectrophotometry. The degree of color development is an indirect measure of the beta-galactosidase produced, which itself is directly related to the amount of DNA damage. The E. coli are further modified in order to have a number of mutations including a uvrA mutation which renders the strain deficient in excision repair, increasing the response to certain DNA-damaging agents, as well as an rfa mutation, which renders the bacteria lipopolysaccharide-deficient, allowing better diffusion of certain chemicals into the cell in order to induce the SOS response.[7] Commercial kits which measures the primary response of the E. coli cell to genetic damage are available and may be highly correlated with theA mes Test for certain materials.[8]]]>
Sat, 20 Jan 2018 11:30:17 GMT /Natashamanzoor1/sos-gene-role-in-ecoli Natashamanzoor1@slideshare.net(Natashamanzoor1) SOS GENE ROLE IN E.COLI Natashamanzoor1 In Escherichia coli, different classes of DNA-damaging agents can initiate the SOS response, as described above. Taking advantage of an operon fusion placing the lac operon (responsible for producing beta-galactosidase, a protein which degrades lactose) under the control of an SOS-related protein, a simple colorimetric assay for genotoxicity is possible. A lactose analog is added to the bacteria, which is then degraded by beta-galactosidase, thereby producing a colored compound which can be measured quantitatively through spectrophotometry. The degree of color development is an indirect measure of the beta-galactosidase produced, which itself is directly related to the amount of DNA damage. The E. coli are further modified in order to have a number of mutations including a uvrA mutation which renders the strain deficient in excision repair, increasing the response to certain DNA-damaging agents, as well as an rfa mutation, which renders the bacteria lipopolysaccharide-deficient, allowing better diffusion of certain chemicals into the cell in order to induce the SOS response.[7] Commercial kits which measures the primary response of the E. coli cell to genetic damage are available and may be highly correlated with theA mes Test for certain materials.[8] <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/sos-180120113017-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> In Escherichia coli, different classes of DNA-damaging agents can initiate the SOS response, as described above. Taking advantage of an operon fusion placing the lac operon (responsible for producing beta-galactosidase, a protein which degrades lactose) under the control of an SOS-related protein, a simple colorimetric assay for genotoxicity is possible. A lactose analog is added to the bacteria, which is then degraded by beta-galactosidase, thereby producing a colored compound which can be measured quantitatively through spectrophotometry. The degree of color development is an indirect measure of the beta-galactosidase produced, which itself is directly related to the amount of DNA damage. The E. coli are further modified in order to have a number of mutations including a uvrA mutation which renders the strain deficient in excision repair, increasing the response to certain DNA-damaging agents, as well as an rfa mutation, which renders the bacteria lipopolysaccharide-deficient, allowing better diffusion of certain chemicals into the cell in order to induce the SOS response.[7] Commercial kits which measures the primary response of the E. coli cell to genetic damage are available and may be highly correlated with theA mes Test for certain materials.[8]
SOS GENE ROLE IN E.COLI from Bahaudin zakriya university multan pakistan
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INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflammation,disorders of inflammation,process of invasion of microbes /slideshow/inflammationtypesmorphological-patternsacute-inflammationchronic-inflammationdisorders-of-inflammationprocess-of-invasion-of-microbes-75233451/75233451 natasha-170420140219
Inflame redirects here. For the 2017 Turkish film, see Inflame (film). Toes inflamed by chilblains Inflammation (from Latin inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the bodys inflammatory response the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the bodys immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only urethral inflammation, but clinical health care providers usually]]>

Inflame redirects here. For the 2017 Turkish film, see Inflame (film). Toes inflamed by chilblains Inflammation (from Latin inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the bodys inflammatory response the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the bodys immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only urethral inflammation, but clinical health care providers usually]]>
Thu, 20 Apr 2017 14:02:19 GMT /slideshow/inflammationtypesmorphological-patternsacute-inflammationchronic-inflammationdisorders-of-inflammationprocess-of-invasion-of-microbes-75233451/75233451 Natashamanzoor1@slideshare.net(Natashamanzoor1) INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflammation,disorders of inflammation,process of invasion of microbes Natashamanzoor1 Inflame redirects here. For the 2017 Turkish film, see Inflame (film). Toes inflamed by chilblains Inflammation (from Latin inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the bodys inflammatory response the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the bodys immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only urethral inflammation, but clinical health care providers usually <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/natasha-170420140219-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Inflame redirects here. For the 2017 Turkish film, see Inflame (film). Toes inflamed by chilblains Inflammation (from Latin inflammatio) is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants,[1] and is a protective response involving immune cells, blood vessels, and molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and to initiate tissue repair. The classical signs of inflammation are heat, pain, redness, swelling, and loss of function. Inflammation is a generic response, and therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, which is specific for each pathogen.[2] Too little inflammation could lead to progressive tissue destruction by the harmful stimulus (e.g. bacteria) and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, periodontitis, atherosclerosis, rheumatoid arthritis, and even cancer (e.g., gallbladder carcinoma). Inflammation is therefore normally closely regulated by the body. Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes (especially granulocytes) from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, and is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the bodys inflammatory response the two components are considered together when discussing an infection, and the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the bodys immunovascular response, whatever the cause may be. But because of how often the two are correlated, words ending in the suffix -itis (which refers to inflammation) are sometimes informally described as referring to infection. For example, the word urethritis strictly means only urethral inflammation, but clinical health care providers usually
INFLAMMATION,types,morphological patterns,acute inflammation,chronic inflammation,disorders of inflammation,process of invasion of microbes from Bahaudin zakriya university multan pakistan
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Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,necrosis and apotosis comparison, /Natashamanzoor1/apotosisbiological-changespathways-extrinsic-intrinsic-carcinogenecitynecrosis-and-apotosis-comparison apotosisslides-170419180957
Cell death, particularly apoptosis, is probably one of the most widely-studied subjects among cell biologists. Understanding apoptosis in disease conditions is very important as it not only gives insights into the pathogenesis of a disease but may also leaves clues on how the disease can be treated. In cancer, there is a loss of balance between cell division and cell death and cells that should have died did not receive the signals to do so. The problem can arise in any one step along the way of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely in human subjects.. It is used, in contrast to necrosis, to describe the situation in which a cell actively pursues a course toward death upon receiving certain stimule]]>

Cell death, particularly apoptosis, is probably one of the most widely-studied subjects among cell biologists. Understanding apoptosis in disease conditions is very important as it not only gives insights into the pathogenesis of a disease but may also leaves clues on how the disease can be treated. In cancer, there is a loss of balance between cell division and cell death and cells that should have died did not receive the signals to do so. The problem can arise in any one step along the way of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely in human subjects.. It is used, in contrast to necrosis, to describe the situation in which a cell actively pursues a course toward death upon receiving certain stimule]]>
Wed, 19 Apr 2017 18:09:57 GMT /Natashamanzoor1/apotosisbiological-changespathways-extrinsic-intrinsic-carcinogenecitynecrosis-and-apotosis-comparison Natashamanzoor1@slideshare.net(Natashamanzoor1) Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,necrosis and apotosis comparison, Natashamanzoor1 Cell death, particularly apoptosis, is probably one of the most widely-studied subjects among cell biologists. Understanding apoptosis in disease conditions is very important as it not only gives insights into the pathogenesis of a disease but may also leaves clues on how the disease can be treated. In cancer, there is a loss of balance between cell division and cell death and cells that should have died did not receive the signals to do so. The problem can arise in any one step along the way of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely in human subjects.. It is used, in contrast to necrosis, to describe the situation in which a cell actively pursues a course toward death upon receiving certain stimule <img style="border:1px solid #C3E6D8;float:right;" alt="" src="https://cdn.slidesharecdn.com/ss_thumbnails/apotosisslides-170419180957-thumbnail.jpg?width=120&amp;height=120&amp;fit=bounds" /><br> Cell death, particularly apoptosis, is probably one of the most widely-studied subjects among cell biologists. Understanding apoptosis in disease conditions is very important as it not only gives insights into the pathogenesis of a disease but may also leaves clues on how the disease can be treated. In cancer, there is a loss of balance between cell division and cell death and cells that should have died did not receive the signals to do so. The problem can arise in any one step along the way of apoptosis.Apoptosis is an ordered and orchestrated cellular process that occurs in physiological and pathological conditions. It is also one of the most studied topics among cell biologists. An understanding of the underlying mechanism of apoptosis is important as it plays a pivotal role in the pathogenesis of many diseases. In some, the problem is due to too much apoptosis, such as in the case of degenerative diseases while in others, too little apoptosis is the culprit. Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die. The mechanism of apoptosis is complex and involves many pathways. Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. Despite being the cause of problem, apoptosis plays an important role in the treatment of cancer as it is a popular target of many treatment strategies. The abundance of literature suggests that targeting apoptosis in cancer is feasible. However, many troubling questions arise with the use of new drugs or treatment strategies that are designed to enhance apoptosis and critical tests must be passed before they can be used safely in human subjects.. It is used, in contrast to necrosis, to describe the situation in which a cell actively pursues a course toward death upon receiving certain stimule
Apoptosis,biological changes,pathways extrinsic, intrinsic, carcinogenecity,necrosis and apotosis comparison, from Bahaudin zakriya university multan pakistan
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https://cdn.slidesharecdn.com/profile-photo-Natashamanzoor1-48x48.jpg?cb=1622184387 https://cdn.slidesharecdn.com/ss_thumbnails/sos-180120113017-thumbnail.jpg?width=320&height=320&fit=bounds Natashamanzoor1/sos-gene-role-in-ecoli SOS GENE ROLE IN E.COLI https://cdn.slidesharecdn.com/ss_thumbnails/natasha-170420140219-thumbnail.jpg?width=320&height=320&fit=bounds slideshow/inflammationtypesmorphological-patternsacute-inflammationchronic-inflammationdisorders-of-inflammationprocess-of-invasion-of-microbes-75233451/75233451 INFLAMMATION,types,mor... https://cdn.slidesharecdn.com/ss_thumbnails/apotosisslides-170419180957-thumbnail.jpg?width=320&height=320&fit=bounds Natashamanzoor1/apotosisbiological-changespathways-extrinsic-intrinsic-carcinogenecitynecrosis-and-apotosis-comparison Apoptosis,biological c...