This document provides an overview of antibiotic classification, mechanisms of action, and development challenges. It discusses how antibiotics are classified into groups based on their mechanisms of inhibiting bacterial cell wall synthesis, protein synthesis, DNA replication, and other targets. Key groups discussed include beta-lactams, glycopeptides, macrolides, aminoglycosides, tetracyclines, quinolones, and others. Each group's mechanism of action and spectrum of activity are described. The document also highlights challenges in antibiotic development and resistance.
This document discusses antimicrobial agents and their mechanisms of action, types, and testing. It covers several topics: disadvantages of taking medication without a doctor's guidance; definitions of antimicrobial agents; mechanisms of action including inhibition of cell wall, membrane, and nucleic acid synthesis; examples of common antimicrobial classes like beta-lactams, aminoglycosides, and quinolones; and methods for testing antimicrobial susceptibility.
Mycobacterium are rod-shaped bacteria that resist decolorization when stained. The genus Mycobacterium contains over 71 species that can infect humans and animals. M. tuberculosis is an intracellular pathogen that causes tuberculosis in humans. It has a complex cell wall containing lipids and prevents the phagosome from fusing with lysosomes, allowing it to survive and replicate inside macrophages. Diagnosis involves microscopy, culture, nucleic acid tests, and the tuberculin skin test. Treatment of tuberculosis in Indonesia follows national guidelines and standards of care.
Cephalosporins are a class of antibiotics derived from the fungus Cephalosporium. They contain a β-lactam ring and are divided into generations based on their antimicrobial spectrum and date of development. They work by inhibiting bacterial cell wall synthesis. Newer generations have increased activity against gram-negative bacteria. Adverse effects include diarrhea, hypersensitivity reactions, and nephrotoxicity in some cases. They are used to treat a variety of bacterial infections. Other β-lactam classes with a similar mechanism of action include monobactams, carbapenems, and carbacephems.
Cephalosporins are a class of antibiotics derived from the fungus Cephalosporium. They contain a β-lactam ring and are divided into generations based on their antimicrobial spectrum and date of development. They work by inhibiting bacterial cell wall synthesis. Newer generations have increased activity against gram-negative bacteria. Adverse effects include diarrhea, hypersensitivity reactions, and nephrotoxicity in some cases. They are used to treat a variety of bacterial infections. Other β-lactam antibiotics with different structures include monobactams, carbapenems, and carbacephems which also have broad-spectrum antibacterial activity.
The document provides information on antibiotics used in pediatric dentistry. It discusses the classification of bacteria and antibiotics, the mechanisms of action of antibiotics including inhibition of cell wall synthesis, cell membrane function, protein synthesis and nucleic acid synthesis. It also covers principles for choosing the appropriate antibiotic, maximum dosage, and commonly used antibiotics like penicillin, erythromycin, clindamycin, amoxicillin, cephalosporins, tetracyclines and metronidazole. Calculations for pediatric antibiotic dosages and classifications of various antibiotics are also summarized.
This document discusses the mechanisms and classifications of various antibiotic classes that act on bacterial cell walls, specifically beta-lactam antibiotics such as penicillins, cephalosporins, monobactams, and carbapenems. It describes how these antibiotics inhibit cell wall synthesis by binding to penicillin-binding proteins and how bacteria have evolved resistance through beta-lactamase enzymes that can hydrolyze the beta-lactam ring and inactivate the antibiotics. The document classifies the different generations of cephalosporins and penicillins based on their antimicrobial spectra and chronological development. It also discusses the characteristics, uses, and resistance mechanisms of representative drugs within each class.
This document provides an overview of different classes of antibiotics, including their mechanisms of action, uses, and side effects. It discusses beta-lactam antibiotics like penicillins and cephalosporins, as well as macrolides, fluoroquinolones, aminoglycosides, tetracyclines, chloramphenicol, glycopeptides and others. Each class is described in terms of its antimicrobial spectrum and applications for treating various bacterial infections. Potential adverse effects are also outlined for safety considerations.
This document discusses antimicrobial agents and their mechanisms of action, types, and testing. It covers several topics: disadvantages of taking medication without a doctor's guidance; definitions of antimicrobial agents; mechanisms of action including inhibition of cell wall, membrane, and nucleic acid synthesis; examples of common antimicrobial classes like beta-lactams, aminoglycosides, and quinolones; and methods for testing antimicrobial susceptibility.
Mycobacterium are rod-shaped bacteria that resist decolorization when stained. The genus Mycobacterium contains over 71 species that can infect humans and animals. M. tuberculosis is an intracellular pathogen that causes tuberculosis in humans. It has a complex cell wall containing lipids and prevents the phagosome from fusing with lysosomes, allowing it to survive and replicate inside macrophages. Diagnosis involves microscopy, culture, nucleic acid tests, and the tuberculin skin test. Treatment of tuberculosis in Indonesia follows national guidelines and standards of care.
Cephalosporins are a class of antibiotics derived from the fungus Cephalosporium. They contain a β-lactam ring and are divided into generations based on their antimicrobial spectrum and date of development. They work by inhibiting bacterial cell wall synthesis. Newer generations have increased activity against gram-negative bacteria. Adverse effects include diarrhea, hypersensitivity reactions, and nephrotoxicity in some cases. They are used to treat a variety of bacterial infections. Other β-lactam classes with a similar mechanism of action include monobactams, carbapenems, and carbacephems.
Cephalosporins are a class of antibiotics derived from the fungus Cephalosporium. They contain a β-lactam ring and are divided into generations based on their antimicrobial spectrum and date of development. They work by inhibiting bacterial cell wall synthesis. Newer generations have increased activity against gram-negative bacteria. Adverse effects include diarrhea, hypersensitivity reactions, and nephrotoxicity in some cases. They are used to treat a variety of bacterial infections. Other β-lactam antibiotics with different structures include monobactams, carbapenems, and carbacephems which also have broad-spectrum antibacterial activity.
The document provides information on antibiotics used in pediatric dentistry. It discusses the classification of bacteria and antibiotics, the mechanisms of action of antibiotics including inhibition of cell wall synthesis, cell membrane function, protein synthesis and nucleic acid synthesis. It also covers principles for choosing the appropriate antibiotic, maximum dosage, and commonly used antibiotics like penicillin, erythromycin, clindamycin, amoxicillin, cephalosporins, tetracyclines and metronidazole. Calculations for pediatric antibiotic dosages and classifications of various antibiotics are also summarized.
This document discusses the mechanisms and classifications of various antibiotic classes that act on bacterial cell walls, specifically beta-lactam antibiotics such as penicillins, cephalosporins, monobactams, and carbapenems. It describes how these antibiotics inhibit cell wall synthesis by binding to penicillin-binding proteins and how bacteria have evolved resistance through beta-lactamase enzymes that can hydrolyze the beta-lactam ring and inactivate the antibiotics. The document classifies the different generations of cephalosporins and penicillins based on their antimicrobial spectra and chronological development. It also discusses the characteristics, uses, and resistance mechanisms of representative drugs within each class.
This document provides an overview of different classes of antibiotics, including their mechanisms of action, uses, and side effects. It discusses beta-lactam antibiotics like penicillins and cephalosporins, as well as macrolides, fluoroquinolones, aminoglycosides, tetracyclines, chloramphenicol, glycopeptides and others. Each class is described in terms of its antimicrobial spectrum and applications for treating various bacterial infections. Potential adverse effects are also outlined for safety considerations.
newer antibacterials are needed because of increasing antimicrobial resistance and no progression in discovery of new drugs as we are kind of stuck with our fight against bugs
This document discusses antibiotic resistance and how it develops. It notes that bacteria can become resistant to antibiotics through spontaneous mutations, acquiring resistance genes from other bacteria, or incomplete treatment that allows resistant strains to survive and multiply. When antibiotics are overused, it creates selective pressure that promotes the spread of resistance. This threatens our ability to treat bacterial infections effectively as more infections become difficult or impossible to treat.
This document provides an overview of antimicrobial resistance. It begins by defining drug resistance as the unresponsiveness of microorganisms to antimicrobial agents. It then discusses the history of resistance, noting that Fleming warned of this danger in 1945. The document outlines the different types of resistance, including natural/primary resistance that microbes innately possess and acquired resistance that develops from use of antimicrobials over time. Microbes can develop resistance through mutation of genetic material or acquisition of new genes. The mechanisms of resistance include drug tolerance, drug destruction, changes to target sites, and altered membrane permeability. Cross-resistance between related drugs is also explained. The document concludes by discussing ways to prevent resistance, including prudent antimicrobial use and
Cephalosporins are a class of semisynthetic, β-lactam antibiotics derived from the fungus Cephalosporium. They are classified into 5 generations based on their year of development and spectrum of activity. Cephalosporins work by inhibiting bacterial cell wall synthesis through binding to penicillin-binding proteins and preventing transpeptidation and cross-linking of peptidoglycan chains. This results in cell lysis and a bactericidal effect. Later generations have increased activity against Gram-negative bacteria and β-lactamase producers. Common uses include respiratory, urinary, skin/soft tissue infections as well as meningitis. Adverse effects are generally mild and include hyper
This document summarizes various classes of antimicrobial agents including their history, mechanisms of action, resistance, and adverse effects. It discusses beta-lactam antibiotics like penicillins and cephalosporins, aminoglycosides, quinolones, and macrolide antibiotics. It provides details on their structures, mechanisms of inhibiting bacterial cell wall synthesis or protein synthesis, and common resistance mechanisms like beta-lactamase production or modification of drug targets.
antimicrobialchemotherapy- Mode of action of antibioticsDevlinaSengupta
The document summarizes the mechanisms of action of antimicrobial agents. It discusses the historical background of antimicrobial use dating back to ancient Peru and China. It then covers the major classes of antimicrobial agents including those that inhibit bacterial cell wall synthesis, cytoplasmic membranes, nucleic acid synthesis, and ribosome function. For each class, it provides details on examples of antimicrobials and their specific mechanisms of inhibiting essential bacterial processes.
Description of the major classes of antimicrobial drug, resistant mechanisms developed by bacteria to combat the action of antimicrobials, and the control measures needed to limit this horizontal gene transfer.
To understand the mechanisms of antimicrobial action and the classification of antimicrobial drugs.
To explain the process of microbial resistance.
To understand the spread of resistant microbes.
Outlines the prevention of microbial resistance.
This document discusses antibiotics, including their classification, mechanisms of action, uses, and side effects. It covers several classes of antibiotics such as penicillins, cephalosporins, and their generations. Antibiotics work by inhibiting bacterial cell wall synthesis, disrupting cellular membranes, or interfering with protein, nucleic acid, or folic acid synthesis. Their use requires consideration of the infecting organism, patient factors, and development of resistance. Combination antibiotic therapy can have additive, synergistic, or antagonistic effects.
Multi drug resistance molecular pathogenesisAlagar Suresh
The document discusses multi-drug resistance and antibiotic resistance. It provides background on the history of antibiotics and resistance. It then covers the major topics of how antibacterial resistance develops through various mechanisms like mutations, plasmids, efflux pumps, and inactivating enzymes. The document also discusses the Indian scenario of rising drug resistance and the growing problem of NDM-1 enzyme production. It concludes by outlining some strategies to address resistance like developing new antibiotics, prudent antibiotic use, and alternative approaches like phage therapy and quorum sensing inhibition.
This document provides an overview of chemotherapy and antimicrobial agents. It discusses the types of bacteria, classification of antimicrobials, mechanisms of action and resistance. Specific drug classes are covered in detail including penicillins, cephalosporins, tetracyclines, macrolides, aminoglycosides, and fluoroquinolones. Adverse effects and clinical uses are described for each class. The document aims to educate students on the general concepts of antimicrobial therapy and properties of commonly used antibiotic drugs.
1) Antibiotics are compounds that kill or inhibit the growth of bacteria and are produced by microorganisms. They work by being more toxic to invading bacteria than the human host.
2) The document discusses several classes of antibiotics including penicillin, cephalosporins, aminoglycosides, macrolides, tetracyclines, chloramphenicol, glycopeptides, and fluoroquinolones. It describes their mechanisms of action and antimicrobial spectrums.
3) Antibiotic resistance has become a major problem as bacteria evolve and develop resistance through both natural and acquired mechanisms such as long-term antibiotic use.
1 Antibiotics resistance mechanism and Antibiotics Stewardship program.pptxchristomlin11
This document discusses antibiotic resistance and stewardship. It begins by outlining the mechanisms of action of different classes of antibiotics and how bacteria develop resistance. It then covers the classification of resistance as intrinsic or acquired, and describes various mechanisms of acquired resistance mediated by chromosomal mutations or mobile genetic elements. The document also addresses current issues regarding resistance in important pathogens like MRSA, ESBL-producing Enterobacteriaceae, Acinetobacter, and gonorrhea. It concludes by discussing strategies for prudent antibiotic use and the importance of antibiotic stewardship programs.
Lecture 6 protein synthesis inhibiting antibioticsana munir
This document discusses several classes of antibiotics that inhibit protein synthesis in bacteria. It focuses on chloramphenicol, aminoglycosides, and tetracyclines. Chloramphenicol inhibits peptide bond formation on bacterial ribosomes. Aminoglycosides interfere with protein initiation by causing incorrect mRNA reading. Tetracyclines prevent amino acid attachment to bacterial ribosomes. All three classes bind to different sites on the bacterial ribosome to inhibit protein synthesis and treat various bacterial infections, but have potential toxic side effects when used.
Drug resistance occurs when microorganisms become unaffected or resistant to drugs like antimicrobials that were previously able to treat them. Resistance can be natural or acquired through mutations over time when exposed to drugs. It poses a major clinical problem. Many bacteria have become multidrug-resistant, including Staphylococcus aureus and Streptococcus pneumoniae. Resistance occurs through various mechanisms like drug inactivation, alteration of drug targets, or reducing drug accumulation in microbes. The spread of resistance is promoted through incomplete treatment courses and overuse of antibiotics. New drug development aims to overcome resistance mechanisms.
Antimicrobial resistance develops through natural mutation and transfer of resistance genes between bacteria. When antibiotics lose effectiveness against bacterial infections, treatment becomes difficult and transmission of disease increases. Strategies to address antimicrobial resistance include monitoring antibiotic use, restricting non-therapeutic use in animals, improving antibiotic stewardship in healthcare, reducing inappropriate outpatient use through education, and developing rapid diagnostics and new drugs.
This document provides an overview of various classes of antibacterial agents, including their mechanisms of action, spectra of activity, and important considerations. It discusses β-lactam antimicrobials like penicillins and cephalosporins which inhibit cell wall synthesis, as well as glycopeptides, aminoglycosides, tetracyclines, macrolides, and others which inhibit bacterial protein synthesis. It also covers quinolones and folate inhibitors which interfere with nucleic acid synthesis. For each class, key representatives and their distinguishing properties are outlined.
This document provides information on various types of antibiotics:
- It discusses the discovery and timeline of important antibiotics such as penicillin, streptomycin, and sulfonamides.
- It describes different classes of antibiotics based on their mechanism of action including cell wall inhibitors, protein synthesis inhibitors, and DNA/RNA synthesis inhibitors.
- It summarizes production methods for commonly used antibiotics like penicillin, cephalosporins, and aminoglycosides which are produced through fermentation using specific microorganisms and nutrient conditions.
newer antibacterials are needed because of increasing antimicrobial resistance and no progression in discovery of new drugs as we are kind of stuck with our fight against bugs
This document discusses antibiotic resistance and how it develops. It notes that bacteria can become resistant to antibiotics through spontaneous mutations, acquiring resistance genes from other bacteria, or incomplete treatment that allows resistant strains to survive and multiply. When antibiotics are overused, it creates selective pressure that promotes the spread of resistance. This threatens our ability to treat bacterial infections effectively as more infections become difficult or impossible to treat.
This document provides an overview of antimicrobial resistance. It begins by defining drug resistance as the unresponsiveness of microorganisms to antimicrobial agents. It then discusses the history of resistance, noting that Fleming warned of this danger in 1945. The document outlines the different types of resistance, including natural/primary resistance that microbes innately possess and acquired resistance that develops from use of antimicrobials over time. Microbes can develop resistance through mutation of genetic material or acquisition of new genes. The mechanisms of resistance include drug tolerance, drug destruction, changes to target sites, and altered membrane permeability. Cross-resistance between related drugs is also explained. The document concludes by discussing ways to prevent resistance, including prudent antimicrobial use and
Cephalosporins are a class of semisynthetic, β-lactam antibiotics derived from the fungus Cephalosporium. They are classified into 5 generations based on their year of development and spectrum of activity. Cephalosporins work by inhibiting bacterial cell wall synthesis through binding to penicillin-binding proteins and preventing transpeptidation and cross-linking of peptidoglycan chains. This results in cell lysis and a bactericidal effect. Later generations have increased activity against Gram-negative bacteria and β-lactamase producers. Common uses include respiratory, urinary, skin/soft tissue infections as well as meningitis. Adverse effects are generally mild and include hyper
This document summarizes various classes of antimicrobial agents including their history, mechanisms of action, resistance, and adverse effects. It discusses beta-lactam antibiotics like penicillins and cephalosporins, aminoglycosides, quinolones, and macrolide antibiotics. It provides details on their structures, mechanisms of inhibiting bacterial cell wall synthesis or protein synthesis, and common resistance mechanisms like beta-lactamase production or modification of drug targets.
antimicrobialchemotherapy- Mode of action of antibioticsDevlinaSengupta
The document summarizes the mechanisms of action of antimicrobial agents. It discusses the historical background of antimicrobial use dating back to ancient Peru and China. It then covers the major classes of antimicrobial agents including those that inhibit bacterial cell wall synthesis, cytoplasmic membranes, nucleic acid synthesis, and ribosome function. For each class, it provides details on examples of antimicrobials and their specific mechanisms of inhibiting essential bacterial processes.
Description of the major classes of antimicrobial drug, resistant mechanisms developed by bacteria to combat the action of antimicrobials, and the control measures needed to limit this horizontal gene transfer.
To understand the mechanisms of antimicrobial action and the classification of antimicrobial drugs.
To explain the process of microbial resistance.
To understand the spread of resistant microbes.
Outlines the prevention of microbial resistance.
This document discusses antibiotics, including their classification, mechanisms of action, uses, and side effects. It covers several classes of antibiotics such as penicillins, cephalosporins, and their generations. Antibiotics work by inhibiting bacterial cell wall synthesis, disrupting cellular membranes, or interfering with protein, nucleic acid, or folic acid synthesis. Their use requires consideration of the infecting organism, patient factors, and development of resistance. Combination antibiotic therapy can have additive, synergistic, or antagonistic effects.
Multi drug resistance molecular pathogenesisAlagar Suresh
The document discusses multi-drug resistance and antibiotic resistance. It provides background on the history of antibiotics and resistance. It then covers the major topics of how antibacterial resistance develops through various mechanisms like mutations, plasmids, efflux pumps, and inactivating enzymes. The document also discusses the Indian scenario of rising drug resistance and the growing problem of NDM-1 enzyme production. It concludes by outlining some strategies to address resistance like developing new antibiotics, prudent antibiotic use, and alternative approaches like phage therapy and quorum sensing inhibition.
This document provides an overview of chemotherapy and antimicrobial agents. It discusses the types of bacteria, classification of antimicrobials, mechanisms of action and resistance. Specific drug classes are covered in detail including penicillins, cephalosporins, tetracyclines, macrolides, aminoglycosides, and fluoroquinolones. Adverse effects and clinical uses are described for each class. The document aims to educate students on the general concepts of antimicrobial therapy and properties of commonly used antibiotic drugs.
1) Antibiotics are compounds that kill or inhibit the growth of bacteria and are produced by microorganisms. They work by being more toxic to invading bacteria than the human host.
2) The document discusses several classes of antibiotics including penicillin, cephalosporins, aminoglycosides, macrolides, tetracyclines, chloramphenicol, glycopeptides, and fluoroquinolones. It describes their mechanisms of action and antimicrobial spectrums.
3) Antibiotic resistance has become a major problem as bacteria evolve and develop resistance through both natural and acquired mechanisms such as long-term antibiotic use.
1 Antibiotics resistance mechanism and Antibiotics Stewardship program.pptxchristomlin11
This document discusses antibiotic resistance and stewardship. It begins by outlining the mechanisms of action of different classes of antibiotics and how bacteria develop resistance. It then covers the classification of resistance as intrinsic or acquired, and describes various mechanisms of acquired resistance mediated by chromosomal mutations or mobile genetic elements. The document also addresses current issues regarding resistance in important pathogens like MRSA, ESBL-producing Enterobacteriaceae, Acinetobacter, and gonorrhea. It concludes by discussing strategies for prudent antibiotic use and the importance of antibiotic stewardship programs.
Lecture 6 protein synthesis inhibiting antibioticsana munir
This document discusses several classes of antibiotics that inhibit protein synthesis in bacteria. It focuses on chloramphenicol, aminoglycosides, and tetracyclines. Chloramphenicol inhibits peptide bond formation on bacterial ribosomes. Aminoglycosides interfere with protein initiation by causing incorrect mRNA reading. Tetracyclines prevent amino acid attachment to bacterial ribosomes. All three classes bind to different sites on the bacterial ribosome to inhibit protein synthesis and treat various bacterial infections, but have potential toxic side effects when used.
Drug resistance occurs when microorganisms become unaffected or resistant to drugs like antimicrobials that were previously able to treat them. Resistance can be natural or acquired through mutations over time when exposed to drugs. It poses a major clinical problem. Many bacteria have become multidrug-resistant, including Staphylococcus aureus and Streptococcus pneumoniae. Resistance occurs through various mechanisms like drug inactivation, alteration of drug targets, or reducing drug accumulation in microbes. The spread of resistance is promoted through incomplete treatment courses and overuse of antibiotics. New drug development aims to overcome resistance mechanisms.
Antimicrobial resistance develops through natural mutation and transfer of resistance genes between bacteria. When antibiotics lose effectiveness against bacterial infections, treatment becomes difficult and transmission of disease increases. Strategies to address antimicrobial resistance include monitoring antibiotic use, restricting non-therapeutic use in animals, improving antibiotic stewardship in healthcare, reducing inappropriate outpatient use through education, and developing rapid diagnostics and new drugs.
This document provides an overview of various classes of antibacterial agents, including their mechanisms of action, spectra of activity, and important considerations. It discusses β-lactam antimicrobials like penicillins and cephalosporins which inhibit cell wall synthesis, as well as glycopeptides, aminoglycosides, tetracyclines, macrolides, and others which inhibit bacterial protein synthesis. It also covers quinolones and folate inhibitors which interfere with nucleic acid synthesis. For each class, key representatives and their distinguishing properties are outlined.
This document provides information on various types of antibiotics:
- It discusses the discovery and timeline of important antibiotics such as penicillin, streptomycin, and sulfonamides.
- It describes different classes of antibiotics based on their mechanism of action including cell wall inhibitors, protein synthesis inhibitors, and DNA/RNA synthesis inhibitors.
- It summarizes production methods for commonly used antibiotics like penicillin, cephalosporins, and aminoglycosides which are produced through fermentation using specific microorganisms and nutrient conditions.
Similar to antibiotic_classification_and_mechanisms_mhs.pdf (20)
This document discusses plant physiology and the relationship between plants and water. It specifically mentions transport of water and transpiration as key topics. The document was prepared by a group of 4 students: Alvenaya Hindayageni, Fadhila Humaira, Fira Wahyuni Putri, and Bilu Priscilia.
This document discusses plant taxonomy and classification. It describes the three subkingdoms that make up the plant kingdom: Protophyta, Thallophyta, and Embryophyta. Key characteristics and examples are provided for each subkingdom and their constituent phyla. The document also examines the class Angiospermae in depth, describing the distinguishing features of monocotyledons and dicotyledons. Common medicinal plant families from each group are listed. The structure of flowers and systems used to diagram and describe their parts are also summarized.
Sexuality - Issues, Attitude and Behaviour - Applied Social Psychology - Psyc...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
When I was asked to give a companion lecture in support of ‘The Philosophy of Science’ (https://shorturl.at/4pUXz) I decided not to walk through the detail of the many methodologies in order of use. Instead, I chose to employ a long standing, and ongoing, scientific development as an exemplar. And so, I chose the ever evolving story of Thermodynamics as a scientific investigation at its best.
Conducted over a period of >200 years, Thermodynamics R&D, and application, benefitted from the highest levels of professionalism, collaboration, and technical thoroughness. New layers of application, methodology, and practice were made possible by the progressive advance of technology. In turn, this has seen measurement and modelling accuracy continually improved at a micro and macro level.
Perhaps most importantly, Thermodynamics rapidly became a primary tool in the advance of applied science/engineering/technology, spanning micro-tech, to aerospace and cosmology. I can think of no better a story to illustrate the breadth of scientific methodologies and applications at their best.
Current Ms word generated power point presentation covers major details about the micronuclei test. It's significance and assays to conduct it. It is used to detect the micronuclei formation inside the cells of nearly every multicellular organism. It's formation takes place during chromosomal sepration at metaphase.
The debris of the ‘last major merger’ is dynamically youngSérgio Sacani
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Authoring a personal GPT for your research and practice: How we created the Q...Leonel Morgado
Thematic analysis in qualitative research is a time-consuming and systematic task, typically done using teams. Team members must ground their activities on common understandings of the major concepts underlying the thematic analysis, and define criteria for its development. However, conceptual misunderstandings, equivocations, and lack of adherence to criteria are challenges to the quality and speed of this process. Given the distributed and uncertain nature of this process, we wondered if the tasks in thematic analysis could be supported by readily available artificial intelligence chatbots. Our early efforts point to potential benefits: not just saving time in the coding process but better adherence to criteria and grounding, by increasing triangulation between humans and artificial intelligence. This tutorial will provide a description and demonstration of the process we followed, as two academic researchers, to develop a custom ChatGPT to assist with qualitative coding in the thematic data analysis process of immersive learning accounts in a survey of the academic literature: QUAL-E Immersive Learning Thematic Analysis Helper. In the hands-on time, participants will try out QUAL-E and develop their ideas for their own qualitative coding ChatGPT. Participants that have the paid ChatGPT Plus subscription can create a draft of their assistants. The organizers will provide course materials and slide deck that participants will be able to utilize to continue development of their custom GPT. The paid subscription to ChatGPT Plus is not required to participate in this workshop, just for trying out personal GPTs during it.
ESR spectroscopy in liquid food and beverages.pptxPRIYANKA PATEL
With increasing population, people need to rely on packaged food stuffs. Packaging of food materials requires the preservation of food. There are various methods for the treatment of food to preserve them and irradiation treatment of food is one of them. It is the most common and the most harmless method for the food preservation as it does not alter the necessary micronutrients of food materials. Although irradiated food doesn’t cause any harm to the human health but still the quality assessment of food is required to provide consumers with necessary information about the food. ESR spectroscopy is the most sophisticated way to investigate the quality of the food and the free radicals induced during the processing of the food. ESR spin trapping technique is useful for the detection of highly unstable radicals in the food. The antioxidant capability of liquid food and beverages in mainly performed by spin trapping technique.
6. Challenges of antibiotic development
• the global antibiotic resistance pandemic heralds a post
antibiotic era as bad as the pre antibiotic era.
• there is also a decline in the development of new antibiotic
classes as pharmaceutical companies direct their effort and
funding to chronic illnesses with a potential for long term
revenue
• between 1998 and 2003 only 9 new antibiotics compared to 16
new ones betweeen 1983 and 1987.
• following 911, drug companies are directing their efforts to
drugs and vaccines for fighting bioterrorism,
7. History of antibiotic development
1928 :Alexander Fleming noted
mould of the genus penicillium
contaminating one of his cultures
preventing the growth of bacteria.
1935: Domagk , sulphonamide –
synthetic dye
1941: clinical trials of penicillin-
Florey and Chain
8.
9. Bacteriostatic vs bactericidal activity
• Bactericidal- kill susceptible bacteria; bacteriostatic-inhibit growth of
bacteria, hosts immune responses necessary to eradicate baceria
• Not absolute terms: action depends on in vitro growth conditons, bacterial
density, test duration
• Bactericidal action necessary in endocarditis, meningitis, osteomyelitis,
neutropenia – host immune system not adequate in these sites and
consequences of incomplete killing grave
• Disadvantage of bactericidal: rapid bacterial lysis in meningitis with
overwhelming inflammatory response with increased mortality
• Advantage of bacteriostatic: clindamycin in staph TSS effective in inhibiting
TSST-1 production without excessive inflammatory response
10.
11. Mechanisms of action
•antibiotics act by disrupting various molecular targets
within bacteria and cell surface, preventing growth or
initiating killing.
•3 broad mechanisms:
•Disrupt bacterial cell envelope
•Block production of new proteins
•Inhibit DNA replication
12.
13. GROUP EXAMPLES MOA PROPERTIES
Beta-lactams Penicillins
Cephalosporins
Carbapenems
monobactams
Inhibit cell wall
synthesis
Bactericidal
Time dependent
Long PAE on g+ve
(carbapenems
also g -ve)
Glycopeptides Vancomycin
Teichoplanin
Telavancin
Inhibit cell wall
synthesis
Time dependent
PAE
Macrolides and
ketolides
Azithromycin
Telithromycin
Erythromycin
clarithromycin
Inhibit protein
synthesis
Bacteriostatic
Time and
concentration
dependent
Long PAE
Aminoglycosides Gentamicin
Amikacin
Tobramycin
Netilmicin
streptomycin
Inhibit protein
synthesis
Bactericidal
Concentration
dependent
PAE
14. GROUP EXAMPLES MoA PROPERTIES
Tetracyclines and
Glycylcyclines
Tetracycline
Tigecycline
Doxycycline
Minocycline
Inhibit protein
synthesis
Bacteriostatic
Time dependent
Long PAE
Quinolones Ciprofloxacin
Norfloxacin
Levofloxacin
moxifloxacin
Inhibit DNA gyrase Bactericidal
Conc. dependent
Long PAE
Quinolones Ciprofloxacin
Norfloxacin
Levofloxacin
moxifloxacin
Inhibit DNA gyrase Bactericidal
Conc. dependent
Long PAE
lincosamides clindamycin Inhibits protein
synthesis
Bactericidal/ static
Time depedent
PAE
Streptogramins Quinupristin/
dalfopristin
Inhibits protein
synthesis
Bactericidal
PAE
Conc.dependent
15. GROUP EXAMPLES MOA PROPERTIES
oxalidinones linezolid Inhibits protein
synthesis
Bacteriostatic
Time dependent
PAE
lipopeptides daptomycin Destroys cell
membrane
structure
Bactericidal
Conc.dependent
Long PAE
polymixins Colistin
Polymixin B
Destroys cell
membrane
structure
Bactericidal
Conc.dependent
PAE
ansamycins rifampicin Inhibits protein
synthesis
Bactericidal
Long PAE
chloramphenicol Inhibits protein
synthesis
Bacteriostatic
Sulfa drugs Sulfamethoxazole-
trimehoprim
dapsone
Inhibits DNA
synthesis
Bactericidal
Conc.dependent
16. Structure of the bacterial cell wall
• Rigid peptidoglycan layer –
alternating amino sugars(NAG and
NAM) crosslinked by peptide
chains
• Transpeptidation is the final stage
in cross linking of the linear glycan
chains.
17. Cell wall synthesis inhibitors: β lactam antibiotics
• the β lactam ring mimics the D-alanyl-
D alanine portion of the peptide chain
that is normally bound by pbps that
assemble the peptidoglycan layer
• This prevents cross linking of the
glycan strands leading to bacterial lysis
β lactam ring
18. Beta lactams
penicillins cephalosporins carbapenems monobactams
1st gen 2nd gen 3rd gen 4th gen 5th gen
Natural penicillins
Penicillin G
Penicillin V
Benzathine P
Procaine P
Penicillinase R
Methicillin
Nafcillin
Cloxacillin
aminopenicillins
Amoxycillin
ampicillin
Extended spectrum
Ticarcilin
Piperacilin
carbenicillin
Imipenem
Meropenem
Ertapenem
aztreonam
Cefadroxil
Cephalexin
Cephradine
cefazolin
Cefaclor
Cefamandole
Cefuroxime
cefoxitin
Cefotaxime
Ceftazidime
ceftriaxone
cefepime Ceftaroline
ceftobiprole
19. Spectrum of activity: Penicillins
Natural penicillins
G+ve bacteria: streptococci,L.
monocytogenes some anaerobes,
some spirochaetes, G-ve:
N.meningitidis,some H. Infl
Penicilinase R
S. aureus, S. Epidermidis
Aminopenicillins
Similar to natural penicillins with
additional G-ve:E.coli, P. Mirabilis,
S.enterica, Shigella spp.
Aminopenicillin/ B lactamase
Inhibitors
Sulbactam and clavulanate
inactivate the B lactamases and
broaden aminopenicillin activity:
Some S. Aureus, many
enterobacteriaceae, clostridia except
difficile, Bacteroides spp
Extended spectrum
p. aeruginosa
20. Spectrum of activity: Cephalosporins
• Each successive generation has
broader activity against aerobic G-
ves.
• Limited activity against anaerobes
• Lack activity against L.
Monocytogenes and enterococci
• 1st gen: good cover for aerobic
G+ve cocci(staph/strep), some G-
ves.
• 2nd gen: increased activity against
aerobicG-ve and
facultative(E.coli,P.mirabilis,H.infl,B
.fragilis
• 3rd gen: in addition, activity against
B burgdorferi, greater activity
against aerobic G-ve than 2nd gen,
shortlived activity against
enterobacteriaceae, no activity
against p.aeroginosa except
ceftazidime
• 4th and 5th gen: good
antipseudomonal and antistaph
cover, also enterobacteriaceae
21. Carbapenems
•Very broad spectrum (G+ve and –ves, anaerobes)due to:
•Small molecules with charge characteristics that allow
them to use porins in the OM of G-ve bacteria to access
the PBPs
•Resistant to B lactamases
•Affinity to broad range of PBPs
22. Monobactams
• Aztreonam
• Single Beta lactam ring
• Very good G-ve cover(Neisseria, Haemophilus spp. Intermediate on
P.aeruginosa), poor activity on G+ves, anaerobes
• No cross reaction in Beta lactam allergy
23. Cell wall synthesis inhibitors: Vancomycin
• like beta lactams,binds to the D-
alanyl-D-alanine portion of the
peptidoglycan layer preventing the
pbps from adding them to the
pepidoglycan layer
• Effective against nearly all aerobic
and anaerobic G+ves including C.
difficile, no activity on G-ves
• Emerging R against enterococci
24. Antibiotics that inhibit protein synthesis
Antibiotics that inhibit protein synthesis
tetracycline aminoglycosides macrolides others
Tetracycline
Oxytetracycline
Demeclocycline
Minocycline
doxycycline
Streptomycin
Neomycin
Gentamicin
Amikacin
tobramycin
Erythromycin
Clarithromycin
Azithromycin
Roxithromycin
spiramycin
Chloramphenicol
Oxalidinones
Ketolides
Lincosamides
streptogramins
25. Protein synthesis in ribosomes
• Ribosomes in bacteria – 70s(50s
&30s);eukaryotes 80s
26. mechanisms of protein synthesis inhibitors
• Interact with various
components of the bacterial
ribosome and inhibit its function
27. Aminoglycosides
★positive charge allows them to bind
to the negatively charged outer
membrane with formation of
transient holes through which
antibiotic molecules move.
★ penetrate the inner cytoplasmic
membrane and bind the 30S
subunit of the bacterial ribosome
inhibiting synthesis of new proteins
from mRNA
★ Good activity against aerobic G-
ves, no activity on anaerobes
28. Macrolides
• bind tightly to the 50s
subunit preventing exit of
the newly synthesized
peptide and hence blocking
protein production.
• Active against a broad variety
of bacteria: some G+ves, G-
ves, atypicals, some
mycobacteria and
spirochaetes
29. Tetracyclines and Glycylcyclines
• interact with the 30s subunit
of the bacterial ribosome
and prevent binding by tRNA
molecules blocking protein
synthesis
• Active against some aerobic
G+ves, some aerobic G-ves,
atypicals and spirochaetes
30. Chloramphenicol
• binds the 50s subunit of the
ribosome blocking the binding of
tRNA loaded with an amino acid
• Less limited use in resource rich
due to toxicity concerns-reversible
dose dependent BM suppression
• Broad spectrum: aerobic G+ves,
aerobic G-ves, anaerobes and
atypicals
31. Clindamycin
• Lincosamide antibiotic
• bind to the 50s subunit of the
bacterial ribosome and inhibit
protein synthesis
• Active against aerobic G+ves and
anaerobes
• No activity on aerobic G-ves
• Associated with C. Difficile colitis
32. Streptogramins
• quinipristin/dalfopristin are
two macrocyclic compounds
each of which binds to the
50s subunit of thebacterial
ribosome to inhibit proten
synthesis
• Work synergistically against
G+ves including MRSA,
penicillin R strep pneumo,
some VRE
33. Linezolid
• oxazolidinones
• bind to the 50s subunit of the
ribosome preventing association
with the 30s subunit
• also inhibits protein syntheis by
preventing formation of the first
peptide bond
• Activity against aerobic G+ves
including MRSA,VRE but not
approved for penicillin R sterp
pneumo
34. Antimetabolites:Sulfa drugs
• trimethoprim-sulfamethoxazole
and dapsone
• Inhibitors of folic acid
synthesis(bacteria cannot use
preformed folic acid)
• tmp inhibits bacterial growth by
preventing the synthesis of
tetrahydrofolate
• Sulfonamides and sulphones- PABA
analogues, competitive inhibition
of dihydropteric acid
• Broad variety of aerobic G+ve and
G-ve susceptible. No activity on
atypicals and anaerobes
35. Inhibitos of DNA synthesis:Quinolones
• All except nalidixic acid have
fluorine added to enhance potency
• Bind to the A sub-unit of DNA
gyrase, prevent supercoiling of
DNA
• Broad variety: G+ve, G-ve, atypicals
and mycobacteria
36. Inhibitors of RNA synthesis:Rifamycins
• Inhibit bacterial RNA
polymerase
• Activity against staph, N.
Meningitidis and H. Influenza
• Used in combination
treatment for mycobacterial
infections
37. Metronidazole
• Small molecule that can passively
diffuse into bacteria.
• Has a nitro group that must be
reduced(accept electrons) for it to be
active.
• Anaerobic bacteria can donate
electrons to this nitro group enabling it
to form free radicals that lead to
breaks in DNA molecules and
subsequent cell death
• Active against G+ve and –ve anaerobes
including C. Difficile and
microaerophilic H. pylori
38. Tigecycline
• Structurally related to minocycline
• Binds 30s preventing entry of tRNA similar to TTCs
• Has an additional N,N,-dimethylglycylamido group that increases affinity
for the ribosomal target – broader spectrum , less R
39. Lipopeptides
• Daptomycin
• lipid portion inserts into the bacterial cytoplasmc menbrane forming an
ion conducting channel that allows ions to escape from the bacterium
leading to cell death
• Active against aerobic G+ves, also MRSA, penicillin R S.pneumo, some
VRE
• No activity against G-ves,poor activity in lungs
40. Lipoglycopeptide: telavancin
• New antibiotic for vancomycin R organisms
• Dual mechanism of action: cell wall synthesis inhibiton –binds to the
terminalacyl-d-alanyl-d-alanine chains preventing cross-linking; disrupts
cell membrane as well