Wednesday 31 December 2014

Topics of emerging importance:
  • Antimicrobial versus antipathogenic approaches
  • New targets in pathogenic microbes e.g. siderphores, quorum-sensing, efflux pumps

125 comments:

  1. ASSIGNMENT 1: LIST OF ANTIBIOTIC DEGRADING ENZYMES.
    DATE: 28/6/16
    ROLL NO: 15MMB014
    1.Strategy: Hydrolysis
    Enzyme: Amidases
    Antibiotic resistance: Penicillin, cephalosporin
    Organism: Gram negative bacteria

    2.Strategy: Hydrolysis
    Enzyme: Esterases
    Antibiotic resistance: Macrolides
    Organism: E. coli, S. aureus, Pseudomonas aeruginosa

    3.Strategy: Hydrolysis
    Enzyme: Epoxidases
    Antibiotic resistance: Fosfomycin
    Organism: Gram negative bacteria

    4.Strategy: Group transfer
    Enzyme: Thioltransferases
    Antibiotic resistance: Fosfomycin
    Organism: P. aeruginosa, Bacillus subtilis

    5.Strategy: Group transfer
    Enzyme: Nucleotidyltransferases
    Antibiotic resistance: Lincomycin, clindamycin
    Organism: Staphylococcus haemoliticus
    6.Strategy: Group transfer
    Enzyme: ADP-ribosyl transferases
    Antibiotic resistance: Rifampin
    Organism: Mycobacterium tuberculosis

    7.Strategy: Group transfer
    Enzyme: Glycosyl transferases
    Antibiotic resistance: Erythromycin
    Organism: Streptomyces lividans

    8.Strategy: Redox Reactions
    Enzyme: Redox enzymes
    Antibiotic resistance: TypeA streptogramin antibiotic virginiamycin M1
    Organism: Streptomyces virginiae

    9.Strategy: Non-hydrolytic and Non-oxidative cleavage of bond
    Enzyme: Lyases
    Antibiotic resistance: TypeB streptogramin
    Organism: Staphylococci
    REFERENCE: Bacterial resistance to antibiotics: Enzymatic degradation and modification.
    Gerard D. Wright
    (http://www.sciencedirect.com/science/article/pii/S0169409X05000980)

    ASSIGNMENT 2: β-lactamase inhibitors other than Clavulanic acid.
    DATE: 28/6/16
    ROLL NO: 15MMB014
    Sulbactam and Tazobactam
    Reference: Three Decades of β-Lactamase Inhibitors
    Sarah M. Drawz and Robert A. Bonomo

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  2. ASSIGNMENT 1: LIST OF ANTIBIOTIC DEGRADING ENZYMES.
    TYPE OF ENZYME :(1) HYDROLYSIS
    (A) β-Lactamases
    (B) Macrolide esterases
    (C) Epoxidases
    (2) GROUP TRANSFER
    (A) Acyltransferases
    (a) Aminoglycoside acyltransferases
    (b) Chloramphenicol acyltransferases
    (c) Streptogramin acyltransferases
    (B) Phosphotransferases
    (a) Aminoglycoside kinases
    (b) Other antibiotic kinases
    (C) Thioltransferases
    (D) Nucleotidyl transferases
    (E) ADP-ribosyltransferases
    (F) Glycosyltransferases


    ASSIGNMENT 2: β-lactamase inhibitors other than Clavulanic acid.

    (1) Sulbactum
    (2) Tazobactam


    Reference: Bacterial resistance to antibiotics: Enzymatic
    degradation and modification
    (Gerard D. Wright)
    (Advanced Drug Delivery Reviews 57 (2005) 1451–
    1470)

    ROLL NO : 15MMB005

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  3. ASSIGNMENT 3A: List of known Quorum sensing inhibitors
    DATE: 1/7/16
    ROLL NO: 15MMB014

    1.
    QS inhibitor:Halogenated Furanones
    E.g. Brominated furanone C-30 and 5-ethyl-3-hydroxy-4-methyl-2[5H]-furanone
    Source:Red marine alga Delisea pulchra
    Mode of inhibition:binds and increases the turnover rate of LuxR homologue and hence disrupting the AHL-mediated swarming and surface colonization of pathogenic bacterium
    Organism:Serratia liquefaciens
    2.
    QS inhibitor:Methyl anthranilate
    Mode of inhibition:Inhibitor for PQS production resulting in reduced pathogenicity including reduction in the expression of elastase
    Organism:P. aeruginosa
    3.
    QS inhibitor:trans-cinnamaldehyde
    Source:cinnamon oil
    Mode of inhibition:Inhibitor of AI-2 (autoinducer 2)-based QS and virulence
    Organism: Vibrio spp
    4.
    QS inhibitor:Salicylic acid
    Mode of inhibition:repress AHL production
    reduction of bacterial invasion and cytotoxicity to HCE cells
    Organism:P. aeruginosa
    5.
    QS inhibitor:Ellagic acid and fisetin
    Mode of inhibition: drastically attenuate the biofilm formation
    Organism: Streptococcus dysgalactiae
    6.
    QS inhibitor:Andrographolide and curcumin
    Mode of inhibition:significantly repress the QS-regulated virulence, including Pycocyanin and elastase
    Organism:P. aeruginosa

    Reference: Non-antibiotic quorum sensing inhibitors acting against N-acyl homoserine lactone synthase as drug gable target
    target
    Authors:
    Chien-Yi Chang, Thiba Krishnan, Hao Wang, Ye Chen, Wai-Fong Yin,Yee-Meng Chong, Li Ying Tan, Teik Min Chong & Kok-Gan Chan

    http://www.nature.com/articles/srep07245


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  4. IISc researchers find a novel, cheap way to prevent sepsis.
    https://journosdiary.com/2016/09/25/iisc-sepsis-nanovesciles/

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  5. 1. The Intensity of Antibiotic Action
    - Susceptible
    - Intermediate
    - Resistance

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  6. 2. Difference between Pathogenicity and Virulence

    Pathogenicity is the ability to cause a disease in host organisms, whereas virulence is the measurement of the ability to cause a disease in the host organism.

    • Pathogenicity is a qualitative measure, whereas virulence can be represented by a quantitative measure.

    • Pathogenicity is not much suitable to explain the degree of harmfulness of a pathogen, whereas virulence can be used to express the degree of harmfulness of a pathogen.

    • Virulence and pathogenicity have different genetic control.


    -Infectivity
    It is the ability of a pathogen to establish an infection.
    Infectivity has been shown to positively correlate with virulence.


    3.Antibiotics effective at different location
    [1]Cell Wall synthesis - β-lactam antibiotics(penicillin, chloramphenicol0,Fosfomycin,Vancommycin
    [2]Cell membrane synthesis - Polymyxins, Telavancin, Bacitracin
    [3]Protein synthesis - Erythromycin, Streptomycin, Chloramphanicol, Retapamulin
    [4]Nucleic acid synthesis - Doxorubicin, Rifampicin, Actinomycin D
    [5]Metabolic pathway - Sulfadrugs, Trimethoprim

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  7. Qustion: which is the most common antibiotic used in combination with clavulanic acid?
    Answer: Amoxicillin is the most commonly used antobiotic in combination with clavulanic acid under the brand name Bilmox-CV and Blumox-CA

    referance:http://www.drugsupdate.com/brand/showavailablebrands/660/6

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  8. Qustion: WHO priority list of pathogenic organisms for R&D of new antibiotics
    AMR is becoming the most common phenomena among the pathogenic organisms through horizontal gene transfer .So to combat this resistance, new antibiotics needs to be evolved. Due to the limited resources for research, WHO has published the priority list of pathogens so as to guide the researchers to set their research area.
    The pathogens are categorised in three categories:Critical, High,Medium.

    Priority 1: CRITICAL
    1. Acinetobacter baumannii, carbapenem-resistant
    2. Pseudomonas aeruginosa, carbapenem-resistant
    3. Enterobacteriaceae, carbapenem-resistant, ESBL-producing
    Priority 2: HIGH
    1. Enterococcus faecium, vancomycin-resistant
    2. Staphylococcus aureus, methicillin-resistant, vancomycin-intermediate and resistant
    3. Helicobacter pylori, clarithromycin-resistant
    4. Campylobacter spp., fluoroquinolone-resistant
    5. Salmonellae, fluoroquinolone-resistant
    6. Neisseria gonorrhoeae, cephalosporin-resistant, fluoroquinolone-resistant
    Priority 3: MEDIUM
    1. Streptococcus pneumoniae, penicillin-non-susceptible
    2. Haemophilus influenzae, ampicillin-resistant
    3. Shigella spp., fluoroquinolone-resistant

    referance:http://www.who.int/mediacentre/news/releases/2017/bacteria-antibiotics-needed/en/

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  9. Question: Is there any other category of organism between resistant and sensitive?
    Yes, there is another category of organisms which lie between sensitive and resistant i.e. Intermediate susceptible.
    Sensitive organism: A bacterial strain is said to be susceptible to a given antibiotic when it is inhibited in vitro by a concentration of this drug that is associated with a high chances of therapeutic success.
    Resistant organism: A bacterial strain is said to be resistant to a given antibiotic when it is inhibited in vitro by a concentration of this drug that is associated with a high chances of therapeutic failure.
    Intermediate organism: The sensitivity of a bacterial strain to a given antibiotic is said to be intermediate when it is inhibited in vitro by a concentration of this drug that is associated with an uncertain therapeutic effect.
    Referance: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701059/

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  10. which is the latest antibiotic?

    Baxdela (delafloxacin) is an recently approved antibiotic by FDA on 19 th june 2017. It is used for treatment of acute bacterial skin and structure infections (ABSSSI) caused by gram positive including MRSA and MSSA and gram negative bacteria.

    Mode of action (fluoroquinolone antibacterial)

    inhibit bacterial topoisomerase 4 and topoisomerase 2 (DNA gyrase)

    dosage
    injection - 300 mg by intravenous infusion over 60 min every 12 hours
    orally (tablets) - 450 mg orally every 12 hours for 5-14 days total duration

    side effects
    nausea, diarrhea, headache, transaminase elevation, vomiting

    Reference - http://www.centerwatch.com/drug-information/fda-approved-drugs/drug/100207/baxdela-delafloxacin-tablets-and-injection

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  11. which is the most widely used clavulanic acid preparation ?

    Augmentin - amoxicillin/clavulanic acid this is the most widely used clavulanic acid preparation

    Refernce - www.sciencedirect.com

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  12. what is the difference between pathogenicity, virulence and infectivity?

    Pathogenicity - the ability of an organism to cause disease. It is composed of two factors
    - infectivity
    - virulence

    Infectivity - the ability to infect and colonize a host

    Virulence - the ability to cause host cell damage

    Reference - http://academic.pgcc.edu/~kroberts/Lecture/Chapter%2014/virulence.html

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  13. List Of enzymes (other than β-lactamases) that degrades antibiotics :-
    1) Macrolide esterases
    2) Expoxidases
    3)Lyases (cleave C-C, C-O, C-N, C-S Bond)

    Certain enzymes are responsible to cause antibiotic resistance by modifying anibiotics rather than actually degrading them.
    Some of the enzymes are :-
    - Acyltransferases
    - Aminogylcoside Acetyltransferases
    - Chloramphenicol Acetyltransferases
    - Streptogranin Acetyltransferases
    - Phosphotransferases
    - ADPribosyltransferases

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  14. Question: How organisms develope antimicrobial resistance?
    There are two ways of doing the same.
    A)Via Genetic changes:

    1.Mutational resistance: results into decreased affinity towards drug, decrease drug uptake, over expression of efflux pumps, changes in metabolic pathways so as altering the targets of the antibiotic

    2.Horizontal gene transfer: Aquisition of gene coding for amtimicrobial resistance via three major routes; conjugation, transduction, transformation.

    B)Via mechanistic changes:

    1.Modification of antibiotic molecule:
    a>chemical alteration of antibiotic:acetylation(aminoglycosides, chloramphenicol), phosphorylation (aminoglycosides, chloramphenicol),adenylation (aminoglycosides, lincosamides)

    b>Destruction of the antibiotic molecule:
    beta lactemase and other enzymes

    2.Efflux pumps:
    five families discovered:i) the major facilitator superfamily (MFS), ii) the small multidrug resistance family (SMR), iii) the resistance-nodulation-cell-division family (RND), iv) the ATP-binding cassette family (ABC), and v) the multidrug and toxic compound extrusion family (MATE).

    These families differ in terms of structural conformation, energy source, range of substrates they are able to extrude and in the type of bacterial organisms in which they are distributed.

    3.Changes in Target Sites
    a>Target protection
    b>modification of target site by mutation or enzymatic reaction.


    Referance:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/

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  15. Que-Which are the drug degrading enzyme other than β-lactamases?
    Ans-Based on 2 strategy:
    1.Hydrolysis: include β-Lactamases, Macrolide esterases, Epoxidases.
    2.Group transfer: include Acyltransferases, Aminoglycoside acetyltransferases, Chloramphenicol acetyltransferases, Streptogramin acetyltransferases, Phosphotransferases, Aminoglycoside kinases, Thioltransferases Nucleotidyltransferases, ADP-ribosyltransferases and Glycosyltransferases.

    Other: include Redox enzyme and Lyases.

    Reference: http://www.sciencedirect.com/science/article/pii/S0169409X05000980

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  16. Riboswitches: this video explains nicely about riboswitches
    https://www.youtube.com/watch?v=Fi9OKd9hpNw

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  17. list of antibiotic target

    cell wall - ampicillin, penicillin, amoxicillin, cefradina
    cell membrane - polymyxin B
    protein synthesis - gentamycin, tetracycline, kanamycin
    nucleic acid - nalidixic acid, rifampicin, delafloxacin
    metabolic pathways - sulfonamids, trimethoprim, dapsone

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  18. Is there any intermediate between susceptible and resistant?

    yes

    sensitive - get killed at normal dose

    intermediate - require higher dose and response towards antibiotic is lower than that of sensitive

    resistant - not get killed at any dose

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  19. drug inhibitor other than beta lactamase

    Penicillinase producing Neisseria gonorrhoeae (PPNG) have penicillinase plasmid which inhibit penicillin

    chloramphenicol acetyltransferase inactive chloramphenicol

    aminoglycoside transferase (AAC) modify amino group of aminoglycoside and inactivate it

    aminoglycoside nucleotide transferase (ANT) and aminoglycoside phosphotransferase (APH) modify hydroxyl group of aminoglycoside and not allow them to bind with ribosome

    hydrolytic enzymes hydrolyses streptogramin B

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  20. Basic information about quorum sensing

    Quorum sensing is the regulation of gene expression in response to cell population density

    standard quorum sensing pathway include bacterial population, signaling molecule (autoinducers) and expression of behavioral gene. As bacterial population increases they will produce and release chemical signal known as autoinducer which is detected by bacterial population and so they will express the gene for virulence, HGT, biofilm formation, and Competence

    gram negative bacteria uses acetylated homoserine lactones as autoinducers

    gram positive bacteria use processed oligopeptides as autoinducer

    reference - pubmed

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  21. Basic information about Riboswitches

    Riboswitches is a common means of genetic regulation at the mRNA level in the bacterial kingdom found in 5'UTR region of mRNA having two domain

    aptamer domain- have ligand binding pocket
    expression platform- regulate transcription and translation machinery

    when ligand bind to aptamer domain it undergoes conformational change coupled with expression platform that instruct transcription and translational machinery

    Alao support RNA world hypothesis - modern riboswitch allows formation of stem loop structure that act as antiterminator when ligand bind to optamer which shows that in ancient time RNA world organism have optamer for regulation without protein

    Riboswitch relation with antibiotic resistant and novel target - riboswitch in leader RNA of the resistance gene that encodes the AAC and AAD enzyme confer resistant to aminoglycoside antibiotic . so if a metabolite is designed that bind to receptor gene regulated by riboswitch than resistant can be overcome

    reference - pubmed

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  22. Question: what is quorum sensing?

    Quorum sensing is the regulation of gene expression in response to fluctuations in cell-population density. Quorum sensing bacteria produce and release chemical signal molecules called autoinducers that increase in concentration as a function of cell density. The detection of a minimal threshold stimulatory concentration of an autoinducer leads to an alteration in gene expression.

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  24. Question: Which processes are controlled by quorum sensing?

    Processes like symbiosis, virulence, competence, conjugation, antibiotic production, motility, sporulation, and biofilm formation are controlled by quorum sensing.

    Referance:http://www.annualreviews.org/doi/abs/10.1146/annurev.micro.55.1.165?journalCode=micro

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  25. Class of autoinducers
    Autoinducers belong to three classes:
    1) Acylated Homoserine Lactones,AHLs : used by Gram negative bacteria ,also referred as AI-1
    2) Oligopeptide signals: used by Gram positive bacteria
    3) AI-2, Autoinducer-2:4,5-dihydroxy-2,3-pentanedione , DPD ; used by both Gram positive and Gram negative bacteria
    Other quorum sensing signals beyond these classes include:-
    PQS -Pseudomonas Quinolone Signal
    DSF -Diffusible Signal Factor (present in Xanthomonas campestris)
    AI-3 - Autoinducer-3 (present in EHEC , Enterohemorrhagic Escherichia coli)


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  26. What are characteristics of an ideal antimicrobial agent?

    Solubility in body fluids to be transported in the body and reach the infectious organisms

    Selective toxicity: they must be more toxic to microorganisms than to host cells

    Toxicity is not easily altered: should have a standard toxicity and not be made more or less toxic by interactions with foods or other drugs

    Non allergenic: should not cause an allergic reaction

    Stability: maintenance of a constant, therapeutic concentration in blood and tissue fluids – should have the same therapeutic activity over many hours

    Resistance by microorganisms not easily acquired

    Long shelf-life

    Reasonable cost

    Narrowest sprectrum with fewest side effects

    Referance:https://www.coursehero.com/file/p6pmhvd/The-characteristics-of-an-ideal-antimicrobial-agent-is-o-Solubility-in-body/

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  27. Question: What are the examples and mode of action of anti-biofilm agents?

    prevention of attachment to surface: Minocyclin, rifampin, silver nanoparticles.

    Distruption of biofilm architecture: Decenoic acid and mixture of D amino acids when attach with biofilm releases the amyloid fibers which are the main component of extracellular matrix.

    Matrix targeting enzymes:1)depolymarization of polysachharide: triclosan, dispersin B
    2)cleavage of eDNA: DNase I enzyme
    3)disteuption of extra cellular matrix: Lysostaphin

    Immunotherapy:antibody against cell anchored adhernce proteins and various exotoxins

    Bacterio phage: Phage possess specific enzymes that degrades polysachharides

    signal transduction interferance:stopping the quorum sensing at any point like production & sensing of autoinducers, activation of genes with the help if autoinducing peptides.

    Referance:https://academic.oup.com/femspd/article/70/3/231/567328/Anti-biofilm-agents-recent-breakthrough-against

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  28. Question:Why our immune system is silent against normal flora?
    Answer: Our human body contains 100 triliian bactrial calls majorly colonizing GI track,but they do not provoke any immune response being foriegn element.The answer is 'Intestinal selection'

    T-cells under go 'thymic selection' where they are tought not to attack self tissues and organs via exposing them to self-antigens.So that they remember the self tissues when they leave the thymus after developement.

    After leaving thymus second education is given in GI track where ILCs(Innate T cells)teach not to attack benificial bacteria vi MHCII presentation.(Intestinal selection)

    Thus, our immunesystem do not generate immune response against normal bacteria.


    Reference:https://medicalxpress.com/news/2015-04-immune-cells-beneficial-bacteria.html

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  29. which is the most widely used antifungal which is toxic to humans?

    Amphotericin B - used to treat system mycoses but cause nephrotoxicity in humans and so is replaced by Azoles

    Reference - https://www.ncbi.nlm.nih.gov/pubmed/11154026

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  30. Is brain suppose to be sterile ?

    Generally, yes brain is suppose to be sterile and it only contains microorganism in some disease condition

    Reference - Todar's online text book of bacteriology

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  31. How immune system tolerate indigenous microbiota?

    Immune system tolerate indigenous microbiota by the following ways
    1) depending upon nature of pathways combination of TLRS activate signaling pathways which can detect pathogen only
    2) indigenous microbiota induce release of factors which have anti-inflammatory response
    3) macrophage suppress the pro-inflammatory molecules released by indigenous microbiota but are unable to suppress pro-inflammatory molecules when released by pathogens
    4) basolateral or intracellular surface have recognition sequence and so when pathogen came in contact with this surface are get recognized and killed whereas indigenous microbiota are colonized on upper surface only
    Reference - Microbial inhabitants of humans - Micheal wilson

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  32. How Does Cranberry Juice Prevent Urinary Tract Infections?

    The bacteria responsible for more than 95 percent of urinary tract infections are a pathogenic strain of the same E. coli bacteria found in the lower intestine. The problematic strain of E. coli carries on its surface tiny arm-like appendages called fimbriae that anchor the bacteria to the surfaces of urinary tract cells.

    Camesano's work shows that cranberry juice blocks the E. coli fimbriae from grabbing onto urinary tract cells. Cranberries contain large amounts of a chemical called proanthocyanidin, or PAC. PAC functions almost like a shield it forces the fimbriae to crumple so they can't attach to surface of the cells in the urinary tract.

    https://amp.livescience.com/32722-how-does-cranberry-juice-prevent-urinary-tract-infections.html

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  33. Question:What is DGGE analysis?

    DGGE is a particular type of gel electrophoresis in which a constant heat (about 60ºC) and an increasing concentration of denaturing chemicals are used to force DNA molecules to unwind.

    In DGGE, DNA, which is negatively charged, is attracted by the positive electrode and forced to migrate through the pores of a polyacrylamide gel. Once it reaches the concentration of denaturing reagents at which it unwinds, it is said to have melted.

    This determines the melting domains which are defined as stretches of base pairs with an identical melting temperature.

    Any variation of DNA sequences within these domains will result in different melting temperatures, thus causing different sequences to migrate at different positions in the gel

    This provides DGGE with the power to distinguish between mutated and wild type sequences without prior knowledge of what these sequences are.

    Reference:https://www.scq.ubc.ca/denaturing-gradient-gel-electrophoresis-dgge-an-overview/

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  34. If acid and other digestive juices in our stomach are so strong, How bacteria can survive in that environment?

    They can survive by sheer luck if you eat a lot of them, or if some physical barrier protects them from the acid. For example, this can happen if they are hidden in the middle of a large morsel of food, and the interior was not sufficiently exposed to stomach acid. (So there's another reason to eat slowly and chew your food well!)

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  35. http://probiotics.org/the-best-probiotic-brands-a-comparison/
    Its a link to the top 10 available brands producing probiotic combination using various strains.

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  36. https://m.nootriment.com/lactobacillus-bulgaricus-streptococcus-thermophilus/
    Why Lactobacillus bulgaris and Streptococcus thermophilus is used as probiotics???? This link will somewhat help you out to solve this question.

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  37. This comment has been removed by the author.

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  38. Question: Why S.thermophilus is used as the prebiotic strain?
    Answer: S.thermophilus can maintain healthy colon health and also boosts immune system.
    It breaksdown lactose into acid so it is given to the persons who are lactose intolerant as probiotics .
    It is also used to treat AAD( antibiotic assiciated diarrohea) during chemotherapy.
    Reference:https://m.nootriment.com/lactobacillus-bulgaricus-streptococcus-thermophilus/

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  39. Que-Benefits of Streptococcus thermophilus probiotic.
    Ans-Increase immunity.
    -Prevent ulcers caused by H.pylori.
    -Decrease AIDS symptoms.
    -Decrease chance of kidney stone.
    -Improve lactose digestion.
    -Reduce antibiotic associated diarrhoea.
    -Decrease ulcerative colitis symp

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  40. Q-Mechanism of cholera toxin?

    When cholera toxin is released from the bacteria in the infected intestine, it binds to the intestinal cells known as enterocytes (epithelial cell ) through the interaction of the pentameric B subunit of the toxin with the GM1 ganglioside receptor on the intestinal cell, triggering endocytosis of the toxin. Next, the A/B cholera toxin must undergo cleavage of the A1 domain from the A2 domain in order for A1 to become an active enzyme. Once inside the enterocyte, the enzymatic A1 fragment of the toxin A subunit enters the cytosol, where it activates the G protein Gsa through an ADP-ribosylation reaction that acts to lock the G protein in its GTP-bound form, thereby continually stimulating adenylate cyclase to produce cAMP. The high cAMP levels activate the cystic fibrosis transmembrane conductance regulator (CFTR), causing a dramatic efflux of ions and water from infected enterocytes, leading to watery diarrhoea

    Ref-https://www.ebi.ac.uk/interpro/potm/2005_9/Page2.htm

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    Replies
    1. For the figure of this mechanism go to the reference site

      Delete
  41. Who was Metchnikoff and what was his discovery?

    His chief contribution was in the field of immunology.He discovered the phagocytes and the phenomena of phagocytosis. He established the concept of cell mediated immunity.
    Elie Metchnikoff also theorized that health could be enhanced and senility(old age) delayed by manipulating the intestinal microbiome with host-friendly bacteria found in yogurt.
    ref:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859987/
    https://en.wikipedia.org/wiki/%C3%89lie_Metchnikoff

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  42. Question: One dalton represents how much amount of weight?

    One dalton or the atomic mass unit(amu) represents the mass of one proton or one neutron.

    one dalton is equal to 1.66*10−27 kg

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  43. http://www.hpppi.iicb.res.in/btox/

    The above link of database will provide information about the microbial toxins.

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  44. The above database was developed and published by

    DBETH: A Database of Bacterial Exotoxins for Human

    Abhijit Chakraborty,1 Sudeshna Ghosh,1 Garisha Chowdhary,2 Ujjwal Maulik,2 and Saikat Chakrabarti1,*

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3244994/

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  45. why hydrogen peroxide produced by probiotic strain will cause harm to other pathogenic microbes and not to human cells?

    This is because human cells have strategies such as catabolism of ROS using enzymes (catalase SOD etc) and maintain homeostasis by repairing ROS mediated damage to overcome the harmful effect of ROS.

    Even some microorganism produce enzyme to metabolize ROS and hence they can cause infection

    Reference : Beyond oxidative stress: an immunologist’s guide to reactive oxygen species
    Carl Nathan1,2 and Amy Cunningham-Bussel1,2

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4250048/

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  46. Biological answer behind consumption of curd and sugar while going out for good work

    Curd i considered as the cooling food (it reduces acidity and burning sensation in stomach)(reduces pitta according to ayurveda)
    Sugar provides instant glucose to body and hence take care of supply of energy to brain and body

    so, this combination is beneficial and keeps mind and body healthy and fresh. Therefore there is a indian tradition of eating mixture of curd and sugar while going for some good work.

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  47. origin of crohn's disease

    It is an inflammatory bowel disease that may affect any part of GI tract from mouth to anus

    sign and symptoms include - abdominal
    pain,diarrhea,fever,weight loss

    The exact cause is unknown and thought to be occurred because of environmental and genetic factor.
    About 70 genes are thought to be involved in crohn's disease and thus may be is of genetic origin

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  48. list of zinc rich food

    cereals (whole grain)
    meat (chicken)
    pomegranates
    soyabeab
    peas
    dark choclate
    spinach
    almonds
    peanuts (groundnuts)
    walnuts

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  49. Amount of blood and plasma in body

    Human's contains blood about 7% of their body weight
    Man - 5.5 liters and Women - 3.4 liter but this amount vary from person to person.
    Plasma makes up to about 55% of total volume of body's blood

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  50. what is the meal of male anopheles mosquito? Did they bite humans or not?

    Male anopheles mosquito feed on nectar and other source of sugars and not bite the humans.

    Female anopheles mosquito also feed on nectar like male but they require protein and iron present in human blood to nurture their egg and hence they bite humans.

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  51. Why Camel's milk is consumed?

    Camel milk comes loaded with antimicrobial proteins, which can help keep our immune systems functioning at their best. Specifically, camel’s milk is rich in micro-sized immunoglobulin, which can help target and neutralize foreign antigens. The small size of the antimicrobial agents is key – because these proteins are so tiny they can cross the blood-brain barrier and get nutrients into and toxins out of normally hard-to-reach cells.

    It’s an excellent source of probiotics, which promote the growth of healthy bacteria in the digestive system.

    Camel’s milk is a natural source of an insulin-like protein, which means drinking it can help regulate glucose levels.

    Camel’s milk is loaded with complex fatty acids, which can boost levels of HDL (“good”) cholesterol while reducing levels of LDL (“bad”) cholesterol. As a result, camel’s milk appears to counteract arteriosclerosis while reducing the risk of stroke, hypertension and heart disease.

    ReplyDelete
  52. Which food are rich in gOS?(Galacto-oligosachharides)
    Lentils, Chickpeas, Green peas, Lima beans, Kidney beans

    ReplyDelete
  53. Are prebiotics the answer for the lactose intolerance?
    Yes.
    As we age, our bodies express less and less of the enzyme lactase that helps our bodies break down the lactose in milk and other dairy products, and develope lactose intolerance.

    prebiotics-'gOS' was given to the patients of lactose intolerance and their gut microbiome was checked for any difference. The microbiome shifted to the more lactose fermenting bacteria and was capable of utilizing lactose without any help from human enzymes.

    Hence, reshaping the gutmicrobiome with the help of prebiotic can solve the problem of lactose intolerance.

    ReplyDelete
  54. Can our microbiome help to solve the crimes?

    Scientists have shown that human dead body evolves in a predictable way, hinting at a new way to determine time of death.

    ReplyDelete
  55. What are PAINS?
    Pan-assay interference compounds are chemical compounds that give false positives in high-throughput screens.PAINS tend to nonspecifically react with numerous biological targets rather than specifically affecting one desired target.

    ReplyDelete
  56. What are psycobiotics?

    They are prebiotic strain that can produce and react on neuroactive substances and confer mental health.

    They cando it via various ways:
    1)Lactobacillus bravis and Bifidobacterium dentium have shown to produce large amount of GABA -a neurotransmitter involved in suppression of anxiety and depression.
    2)probiotic Lactobacillus rhamnosus (JB-1) appeared to reduce the levels of stress-induced corticosterone and relieve in stress.
    3)Oral administration of Lactobacillus acidophilus has shown to reduce pain by inducing opioid and cannabinoid receptors in the intestinal epithelial cells

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  57. Why chills and fever fills at the same time in malaria?

    The rupture of red blood cells by merozoites releases hemozoin and toxins (such as red cell membrane lipid, glycosyl phosphatidyl inositol anchor of a parasite membrane protein), which could directly stimulate macrophages and other cells to release of cytokines such as TNF and interleukin-1 from macrophages, resulting in chills and high grade fever.Chills are caused by rapid muscle contraction and relaxation. Muscle contraction and relaxation are the body's way of producing heat when it feels cold, though we feel chills and fever at the same time in malaria.

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  58. Why we feel cold even if our body temperature is high when we have fever?


    Whenever White blood cells encounter any harmful micro- organism in body they release protein called pyrogen. These chemicals are then carried by the blood to a part of brain known as hypothalamus, which regulates body temperature.

    Pyrogens inhibit heat-sensing neurons & excite cold -sensing ones. This make the hypothalamus think the body is cooler than it actually is. In response to this illusion hypothalamus sets a temperature which is higher than normal.

    The blood vessels of skin constriction to increase blood supply to the vital organs . This reduces heat loss through skin & cause the person to feel cold.

    Additionally our skin sensors measure relative temp. instead of absolute temp. so person fells cold during fever as the core body temp. is high.

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  59. what is artemether?

    It is a methyl ether derivative of artemisinin

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  60. This comment has been removed by the author.

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  61. ‌Artemisinin is available as its derivatives, artemether, artesunate and arteether.
    ‌Artemether is a medication used for the treatment of malaria. The injectable form is specifically used for severe malaria rather than quinine.  It may not be as effective artesunate. It is given by injection in a muscle. It is also available by mouth in combination with lumefantrine, known as artemether/lumefantrine.

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  62. Who discovered Plasmodium falciparum?

    Charles Louis Alphonse Laveran, a French army surgeon stationed in Constantine, Algeria, was the first to notice parasites in the blood of a patient suffering from malaria. This occurred on the 6th of November 1880. For his discovery, Laveran was awarded the Nobel Prize in 1907.

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  63. Though suffering from fever we suffer from cold and shivering

    Because in order to clear pathogen our immune system release pyrogens which signals thermostatic center of brain (hypothalamus) to rise the temperature of body as pathogen will die at slight increase in temperature of the body. At that time only thermostat temperature had been increase and our body is at normal temperature and so to balance this response to raising the temperature occur like cold along with shivering which encourages behavioural response bo get blanket for raising the body temperature.

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  64. we also sweat with fever

    Reason behind this is when the pathogen is cleared immune system stop releasing pyrogens and so thermostat came to normal but now the body's temperature is higher and hence to decrease the temperature sweating occurs .

    very much similar like in case of exercise

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  65. Full form of TCP - type 4 pillus in V.cholera infection .

    - Toxin-coregulated pillus

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  66. E.coli in stomach is beneficial whereas in vagainal tract is harmful ?

    Because UTI (urinary tract infection) is caused by uropathogenic E.coli (UPEC) which is different from strain present in stomach and they have variety of virulence factors (VFs) such as adhesins, alpha hemolysin toxin,protectins, outer membrane protease T (OmpT),uropathogenic specific protein(Usp). They also produce biofilm. All this is responsible for UTI .
    This VFs are not present in strains which are in stomach hence E.coli in vagainal tract is harmfull and stomach is beneficial .

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  67. Why our immune system is not responding against our human microbiota?

    T cells, that are made in the thymus and are trained there to kill-off foreign microbes and other intruders that make their way into the human body. But why don’t these T cells attack helpful bacteria in the GI tract?
    T cells are again educated in the gut to not attack beneficial bacteria but when this education is disrupted, it can lead to disease. For example, inflammatory bowel diseases like Crohn’s disease and ulcerative colitis occur when the immune system attacks the GI tract and bacteria in the GI tract.

    In the thymus, T cells that could attack the body are destroyed before they are released into circulation. In the gut, a type of cell called innate lymphoid cells (ILCs) educate the T cells to not attack beneficial bacteria. These ILCs had previously been found to make a physical barrier between the bacteria in the gut and the immune system.

    https://drive.google.com/file/d/1MZHTFY-JE-LxcDfV5QVKWIDwYWJz2jML/view?usp=drivesdk

    17mmb012

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  68. The immune system is capable of recognizing pathogenic ("bad") bacteria, either by components of the innate (non-specific) or adaptive (specific) immune system. Pathogenic bacteria will have antigen on their surface that mark them as 'foreign', leading to an immune response targeted to the bacteria.Initiation of immune response relies on detection of PAMPs.These are present on microorganisms and not the host cells. For eg. Some bacteria have lps on their surface and not on the mammalian cells which makes them prone to immune attack and so they are targetted and killed.

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  69. Different type of pathogenic E.coli

    Enterotoxigenic E. coli (ETEC)
    Enteroinvasive E. coli (EIEC)
    Enteropathogenic E. coli (EPEC)
    Enterohemorrhagic E. coli (EHEC)
    Ueopathogenic E. coli (UPEC)

    textbookofbacteriology.net/e.coli_4.html
    Enteroaggregative E. coli (EAEC)

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  70. On the type of virulence factor present and host clinical symptoms, E. coli strains are categorized into different pathotypes:
    (1) enteropathogenic E. coli (EPEC), causes diarrhea in children and animals
    (2) enterohemorrhagic E. coli (EHEC), is responsible for hemorrhagic colitis and hemolytic-uremic syndrome
    (3) enterotoxigenic E. coli (ETEC), causes traveler's diarrhea
    (4) enteroaggregative E. coli (EAEC), causes persistent diarrhea in humans, and diffusely adherent E. coli (DAEC), a subclass of enteroaggregative E. coli causes diarrhea in children
    (5) enteroinvasive E. coli (EIEC), causes watery diarrhea and dysentery
    (6) uropathogenic E. coli (UPEC), causes urinary tract infections in humans and animals
    (7) neonatal meningitis E. coli (NMEC), is responsible for meningitis and sepsis

    reference:Differentiation of Escherichia coli Pathotypes by Oligonucleotide Spotted Array

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  71. Enterotoxigenic ecoli (ETEC)
    Enteropathogenic ecoli (EPEC)
    Enteroinvasive ecoli (EIEC)
    Enterohemorrhagic ecoli (EHEC)
    Uropathogenic ecoli (UPEC)

    PAMPs - pathogen associated molecular patterns are moleculez associated with group of pathogens, that are recognized by cells of innate immune system. They are recognized by pattern recognition
    receptors such as toll like receptors.

    How humans immune system is silent even in presence of microbes?
    Our bodies coevolved with bacteria over a million of years.microbes gradually came to help regulate bodily processes from digestion to energy processing to immune defenses.the body had to develop mechanisms by which it "tolerates" the presence of potentially helpful bacteria, not attacking them as foreign invaders. Complicating matters, many species -- including those in the Helicobacter family -- are helpful, or at least harmless, normally, but cause disease when genetic or environmental factors alter the normal balance.
    http://www.sciencedaily.com

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  72. Pathogenic E.coli strains are-
    1.Enterotoxigenic E.coli (ETEC)
    2.Enteropathogenic (EPEC)
    3.Enteroinvasive(EIEC)
    4.Verotoxin producing E.coli
    5.E.coliO157:H7 strain is enterohemogrrhagic
    6.E.coli O121 strain
    7. E.coli K1 strain

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  73. This comment has been removed by the author.

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  74. bacterial pathogenicity depends on structure:
    S-layers are proteins in the outermost cell envelope of a broad range of bacteria. S-layers are composed of a single protein or glycoprotein.
    S
    layers have been associated with a number of possible functions that relate to pathogenicity. S-layers can function as adhesins, enabling the bacterium to adhere to host cell membranes and tissue surfaces in order to colonize. Many of the cell-associated protein adhesins used by pathogens are components of the S-layer. The S-layer may protect bacteria from harmful enzymes or changes in pH. Like many other surface components, S-layers contribute to virulence by protecting the bacterium against complement and attack by phagocytes.

    Ref: online textbook of bacteriology
    17mmb013

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  75. 4 types of pathogenic E. coli

    Enteropathogenic E. coli
    Enterotoxigenic E. coli
    Uropathogenic E. coli
    Shigella-like or Invasive E. coli

    Ref. Classification of Pathogenic Escherichia coli According to Serotype and the
    Production of Virulence Factors, with Special Reference
    to Colonization-Factor Antigens (research paper)

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  76. The mucosa also needs to respond rapidly to the arrival of potentially harmful
    organisms and so must be able to recognise such organisms and distinguish them from
    members of its indigenous microbiota. The mechanisms responsible for such tolerance
    and discrimination are only now beginning to be elucidated and what little is known
    has generally come from studies involving the intestinal mucosa. The ability of human
    cells to recognise conserved microbial structural components known as “pathogen-
    associated molecular patterns” (PAMPs). PAMPs include molecules such as LPS, LTA,
    peptidoglycan, lipoproteins, and proteins (i.e., modulins). And these are recognized
    by a system involving proteins known as Toll-like receptors (TLRs). The term PAMP, it
    must be said, is something of a misnomer because the molecules included in this term
    are also present in the vast majority of non-pathogenic species – a more appropriate
    terminology would be MAMPs (i.e., microbe-associated molecular patterns). At present,
    ten different TLRs have been identified and each recognises one or more MAMPs. For ex-
    ample, TLR4, TLR2, and TLR5 recognise LPS, peptidoglycan, and flagellin, respectively.
    In the case of LPS, a co-receptor (CD14) is necessary to activate signalling via TLR4.
    Interaction of the TLR with its ligand activates a signalling pathway in the host cell,
    which induces some response such as the production of cytokines and macrophage
    activation. Combinations of TLRs are thought to be used by host cells to recognise a
    specific microbe, or type of microbe, and so may be able to distinguish between indige-
    nous microbes and exogenous pathogens. Depending on the nature of the microbe, a
    specific set of TLR signalling pathways would be activated and the net signal generated
    may be recognised by the host as being characteristic of a “friendly” or “aggressive”
    microbe and an appropriate response generated. In intestinal epithelial cells, however,
    TLR and/or CD14 expression is strongly down-regulated; therefore, these cells do not
    respond to PAMPs such as LPS so that no inflammatory response is elicited. Although
    this may account for the non-inflammatory relationship that exists between members
    of the indigenous microbiota and intestinal epithelial cells, it does not explain how the
    mucosa can mount an inflammatory response when it is needed (i.e., when challenged
    by pathogenic microbes). One possibility is that the recognition/response system may
    be located intracellularly or on the basolateral surface of the epithelial cells. It would,
    therefore, be activated only when a pathogen invaded the cell or when it gained access
    to its basolateral surface.
    For entire text reference is Microbial Inhabitants Book (2005)chapter 1:An introduction to human microbe symbiosis

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  77. The initiation of an immune response against an invading species relies on the detection of pathogen associated molecular patterns (PAMPs). PAMPs are molecular structures that are present in microorganisms, but not in host cells. In addition to being distinctly non-mammalian, another critical feature of PAMPs is that they are conserved amongst microbes. This means that PAMPs tend to be molecules that serve critical functions for microbial survival, and thus they are seen in an array of microbial species, including pathogens (microbes that make us sick) and commensals (microbes that have neutral or beneficial effects on our health).
    Antimicrobial peptides, which are chemicals made by immune cells that can directly kill bacteria. They’re like antibiotics made by your own body, and they are an important innate defense mechanism against bacterial infection.So the commensal bacteria might be resistant to antimicrobial peptides, which would allow them to survive in the host. Thus one can say that commensal bacteria adapted to live in our bodies have evolved mechanisms to tolerate antimicrobial peptides, while pathogens have not.
    ref: http://www.because-science.org/blog/2015/1/27/why-dont-we-kill-our-microbiota

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  78. The intestinal mucosa contains many IgA-secreting plasma cells, and secreted IgA plays a critical role in host defense against pathogenic bacteria. Importantly, IgA regulates the ecological balance of commensal bacteria; in other words, IgA regulates the composition and character of intestinal microflora. For example, the lack of activation-induced cytidine deaminase (AID), which results in a defect in class-switch recombination and, thereby, a lack of IgA-producing cells in the intestine, leads to excessive anaerobic expansion in the small intestine, particularly of segmented filamentous bacteria (SFB) The addition of IgA rescues the aberrant SFB expansion in the small intestine of AID-/- mice.63 Bacteroides thetaiotaomicron is otherwise commensal to the host, but in the absence of IgA, it elicits a robust innate immune response including the induction of inducible nitric oxide synthase (iNOS).64 Thus mucosal IgA can determine the nature of bacteria and is required for keeping commensal bacteria “commensal” to the host.


    The immunosuppressive activity of Treg cells is due, at least in part, to their capacity to hydrolyze extracellular ATP through the enzymatic activity of CD39 and CD73 expressed on their membranes.60,61 CD39 is an ectoenzyme that hydrolyzes ATP/UTP and ADP/UDP to the respective nucleosides, such as AMP. CD73 is an ecto-5′-nucleotidases that degrades extracellular nucleoside monophosphates to nucleosides (e.g., adenosine). Adenosine activates adenylyl cyclases by triggering the cognate Gs-protein coupled receptor A2a, which has a non-redundant role in the attenuation of inflammation and tissue damage in vivo.62 Thus extracellular ATP and its metabolites ADP, AMP and adenosine are critical factors, produced by intestinal commensal bacteria, that profoundly affect the intestinal immune system.

    Ref. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023604/#!po=26.6393

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  79. Brain is one organ that is assumed to be sterile but it probably may not be true. For example AIDS is a disease that damages the blood-brain barrier which might lead to presence of bacteria in the brain. Autopsy-derived cerebral white matter was obtained from AIDS patients; controls included material from individuals who died of other causes (including cerebral infarction, meningitis, and encephalitis), and also brain tissue collected during surgical resection for epilepsy. Total RNA was prepared, copied into DNA, and subjected to massively parallel sequencing. The results showed that all patient samples contain sequence tags for alpha-proteobacteria.


    Reference -http://www.virology.ws/2013/06/28/bacteria-in-our-brains/

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  80. Do human brains carries microbes?
    The authors performed deep sequencing of white matter-derived RNA from 4 HIV patients, 4 other disease controls and 2 cerebral surgical resections from epilepsy patients, and found alpha-proteobacteria in all of them as well as some herpes viruses and bacteriophages.

    Reference-
    https://www-forbes-com.cdn.ampproject.org/v/s/www.forbes.com/sites/quora/2017/08/09/do-human-brains-carry-microbiota-scientists-cant-agree/amp/?amp_js_v=a2&amp_gsa=1&usqp=mq331AQCCAE%3D#referrer=https://www.google.com&amp_tf=From%20%251%24s&ampshare=https%3A%2F%2Fwww.forbes.com%2Fsites%2Fquora%2F2017%2F08%2F09%2Fdo-human-brains-carry-microbiota-scientists-cant-agree%2F

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    Replies
    1. But this showed the presence of microbes in only the infected patients but not in healthy individual.

      Delete
  81. Human brain is not sterile.
    1)At the time of some disease like AIDS
    blood brain barrier may lead to some damage at that micro organisms can cross that membrane.
    2) Blood brain barrier may becomes more permeable at the time of inflammation so bacteria like borrelia,streptococci etc may be present in brain.
    3)Even in the absence of inflammation also microbes are present in brain .because of LYMPHATIC SYSTEAM OF HUMAN BODY.

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  82. Human brain is not sterile.
    1)At the time of some disease like AIDS
    blood brain barrier may lead to some damage at that micro organisms can cross that membrane.
    2) Blood brain barrier may becomes more permeable at the time of inflammation so bacteria like borrelia,streptococci etc may be present in brain.
    3)Even in the absence of inflammation also microbes are present in brain .because of LYMPHATIC SYSTEAM OF HUMAN BODY

    ReplyDelete
  83. Is human brain is sterile??

    To determine the microbes are present in brain or not they do studay of AIDS known to damage the blood-brain barrier, might lead to the presence of bacteria in the brain.white matter was obtained from AIDS patients;The results showed that all patient samples contain sequence tags for alpha-proteobacteria

    To demonstrate that live alpha-proteobacteria are present in the brain specimens, Sequence analysis of mouse brain RNA done seven weeks later revealed mainly alpha-proteobacteria. Transfer of the bacteria was not observed after heat-treatment of the brain homogenate.

    Ref.-http://www.virology.ws/2013/06/28/bacteria-in-our-brains/

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  84. Liebig's law: This law states that in environments where multiple nutrients are in relatively low concentrations, only one nutrient will affect the growth of the organism. This implies that the evolutionary response of the population would be dictated by the most growth‐limiting nutrient. Alternatively, it is possible that an initial adaptation to the most limiting nutrient results in other nutrients present in low concentration affecting the evolutionary dynamics of the population.

    Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528229/

    Shelford's law of tolerance: A law stating that the abundance or distribution of an organism can be controlled by certain factors (e.g. the climatic, topographic, and biological requirements of plants and animals) where levels of these exceed the maximum or minimum limits of tolerance of that organism.

    Ref: https://www.encyclopedia.com/plants-and-animals/zoology.../shelfords-law-tolerance

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  85. pH of different parts of GI tract-
    Saliva-(6.5-7.5 for a minute)
    Upper stomach(fundus)-4-6.5
    Lower stomach-1.5-4
    Duodenum-7-8.5
    Small intestine-4-7
    Large intestine-4-7
    Allegany Nutrition
    The Human Digestive Tract pH Range Diagram


    The pH is a way of measuring how acidic or alkaline the body is. The pH in the human digestive tract varies greatly (see Human Digestive Tract pH Range Chart on the left side). The pH of saliva is usually between 6.5 – 7.5. After we chew and swallow food it then enters the fundic or upper portion of the stomach which has a pH between 4.0 – 6.5. This is where “predigestion” occurs while the lower portion of the stomach is secreting hydrochloric acid (HCI) and pepsin until it reaches a pH between 1.5 – 4.0. After the food mixes with these juices it then enters the duodenum (small intestine) where the pH changes to 7.0 – 8.5. This is where 90% of the absorption of nutrients is taken in by the body while the waste products are passed out through the colon (pH 4.0 – 7.0).

    Reference-https://www.alleganynutrition.com/supporting-pages/the-human-digestive-tract-ph-range-diagram/

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  86. Primary colonization- The group of organisms that first establish the attachment to a particular site.

    Secondary colonization- After primary colonization, substances excreted and secreted by microbes serve as nutrients ,thus creating opportunities for colonization of other organisims.

    Autogenic succesion- a change in composition of community arising from microbial community.

    Allogenic community- a change in composition of community due to external non-microbial factors.

    Climax community- combination of positive and negative nutritional interactions together affecting the physicochemical features of site gives rise to climax community.

    Resilience- Body recovering to its original state from infection.

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  87. ph of different parts of GI track

    saliva- 6.5 – 7.5
    fundic or upper stomach-4.0 – 6.5
    lower stomach-1.5 – 4.0 because this part contain HCL and Pepsin
    Lower stomach-1.5-4
    Duodenum-7-8.5
    Small intestine-4-7
    Large intestine-4-7

    For checkeing the ph range they use Measurements with pH-sensitive, radiotransmitting capsules are highlighted

    Ref.https://www.alleganynutrition.com/supporting-pages/the-human-digestive-tract-ph-

    ReplyDelete
  88. The human gut microbiome as source of innovation for health: Which physiological and therapeutic outcomes could we expect?
    https://www.ncbi.nlm.nih.gov/pubmed/28131442

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  89. Review
    The Human Gut Microbiome: From Association to Modulation
    Author links open overlay panelThomas S.B.Schmidt1JeroenRaes23PeerBork1456
    Show more
    https://doi.org/10.1016/j.cell.2018.02.044

    17mmb021

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  90. Organisms used for production of vitaminB-12
    Pseudomonas denitrificans,Propionibacterium shermanii,Sinorhizobium meliloti,Salmonella typhimurium,Bacillus megaterium,Halobacterium sp.Rhodobacter capsulatus,R.sphaeroides,E.coli.

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  91. Industrial production of vitamin B12:
    Commonly used microorganisms for induatrial production of vitamin B12 are
    1. Pseudomonas denitrificans
    2. Propionibacterium shermanii
    3. Bacillus megaterium
    4. Streptomyces olivaceus
    A hybrid strain obtained by protoplast fusion between Protaminobacter rubber and Rhodopseudomonas spheroides resulting in Rhodopseudomonas protamicus helps to increase the production of vitamin B12.

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  92. Bacteria used in synthesizing Vitamin B12 are:

    Large scale industrial production of vitamin B12 occurs via microbial fermentation, predominantly utilizing Pseudomonas denitrificans, Propionibacterium shermanii, or Sinorhizobium meliloti, Bacillus megaterium etc.

    Ref: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282855/

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  93. List of bacteria used for vitamin B12 production are:
    1.Pseudomonas denitrificans
    2.Propionibacterium shermanii
    3.Sinorhizobium meliloti
    4.Escherichia coli
    5.Salmonella typhimurium

    Ref:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282855/

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  94. Orgenisms used for production of Vitamine-B12

    Pseudomonas dentrificans
    Rhodobacter capusulatus
    Salmonella typhimurium
    Bacillus megaterium
    Propionibacterium shermanii etc.

    For large scale production of Vitamine B12 by organisms like,Pseudomonas denitrificans, Propionibacterium shermanii, or Sinorhizobium meliloti
    Many genes involved in vitamin B12 biosynthesis in S. typhimurium have been shown to be functional in E. coli . Transfer of 20 genes from the S. typhimurium cob locus allowed the production of vitamin B12 in E. coli

    Ref. Microbial production of vitamin B12: a review and future perspectives
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5282855/

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  95. Industrial production of B12 is achieved through fermentation of selected microorganisms.Streptomyces griseus, a bacterium once thought to be a yeast, was the commercial source of vitamin B12 for many years. The species Pseudomonas denitrificans and Propionibacterium freudenreichii subsp. shermanii are more commonly used today.These are frequently grown under special conditions to enhance yield, and at least one company uses genetically engineered versions of one or both of these species. Since a number of species of Propionibacterium produce no exotoxins or endotoxins and are generally recognized as safe (have been granted GRAS status) by the Food and Drug Administration of the United States, they are presently the FDA-preferred bacterial fermentation organisms for vitamin B12 production.

    The total world production of vitamin B12, by four companies (the French Sanofi-Aventis and three Chinese companies) in 2008 was 35 tonnes.

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  96. Lactobacillus rhamnosus GG:
    L.rhamnosus that was isolated in 1983 from the intestinal tract of a healthy human being by Sherwood Gorbach and Barry Goldin.the 'GG' derives from the first letters of their surnames.

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  97. genetically engineered probiotic strain in market:
    genetic engineering using recombinant-DNA technology has been employed, to improve the flavor and stability of buttermilk through metabolic engineering of L. lactis subsp. diacetyllactis
    In L. lactis, a-acetolactate can be decarboxylated by a-acetolactate decarboxylase to form acetoin, a compound without the desired flavor. Inactivating the gene encoding a-acetolactate decarboxylase, aldB, increases the availability of a-acetolactate for chemical oxidation.

    https://www.cell.com/trends/biotechnology/pdf/S0167-7799(03)00251-8.pdf

    17mmb023

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  98. 1 Lactobacillus rhamnosus GG (LGG), ATCC 53103 was originally isolated from fecal samples of a healthy human adult bySHETWOOD GORBACH and BARRY GOLDWIN, explaining its typical surname letters GG
    2

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  99. Lactobacillus rhamnosus GG, isolated from the intestinal tract of a healthy human by Dr. Sherwood Gorbach and Dr. Barry Goldin from Boston, they filed for a patent in April of 1985, and called it “GG” as of their last names.

    17mmb021
    https://www.powerofprobiotics.com/Lactobacillus-rhamnosus-GG.html

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  100. Lactobacillus rhamnosus GG is isolated by healthy human's fical sample by two scientest Sherwood Gorbach and Barry Goldwin, So from theirs Surname's 1st letter its write as GG

    ReplyDelete
    Replies
    1. Ref: Towards a better understanding of Lactobacillus rhamnosus GG ...https://www.ncbi.nlm.nih.gov › articles

      Delete
  101. Question :-genetic eng. Probitics in use
    Grangette et al. has used a mutant of Lactobacillus plantarum with impaired capacity to incorporate D-alanine in teichoic acids. This mutant , was found to be more protective in a mouse model of colitis than wild type strain. Moreover, the lipoteichoic acid deficient L. acidophilus enhances . IL-10 production by dendritic and macrophage and down-regulates IL-12 and TNF-á under in vitro conditions
    17mmb019

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  102. Pathogenic strains are the ones that have the ability to cause a disease or infection. These strains can cause extinction of the biological species by killing them through various different mechanisms. The pathogenic strain can never be extinct as they acquire resistance to antibiotics if treated repeatedly with antibiotics but there is an exception which is shown in this research article below.

    https://www.google.co.in/amp/s/amp.livescience.com/15826-black-death-bacteria-extinct.html

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  103. Evolutionary rescue occurs when a population in a given environment is expected to go extinct, but nonetheless persists because evolution by natural selection increases fitness rapidly enough to prevent extinction (see [1]). This is a process that is likely to be a recurrent and widespread feature of the coevolutionary dynamics of hosts and pathogens, defining both realized host ranges for pathogens and the responses by each to environmental change.
    http://www.ncbi.nlm.nih.gov>articles

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  104. Why does susceptibility to infection of suckling mice increases with age?
    The experiment performed is described below in the research paper.
    http://iai.asm.org/content/73/2/1232.full

    Is QS important for colon?
    It helps in bacterial cell to cell communication.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1111840/

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  105. Function of CxCr4 and CCr5

    The chemokine receptor CXCR4 is broadly expressed in cells of both the immune and the central nervous systems and can mediate migration of resting leukocytes and haematopoietic progenitors in response to its ligand

    CCr5 - This protein is expressed by T cells and macrophages, and is known to be an important co-receptor for macrophage-tropic virus, including HIV, to enter host cells. Defective alleles of this gene have been associated with the HIV infection resistance.

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  106. 4 phases of cell division are- G1-S-G2-M

    The cell cycle is a four-stage process in which the cell increases in size (gap 1, or G1, stage), copies its DNA (synthesis, or S, stage), prepares to divide (gap 2, or G2, stage), and divides (mitosis, or M, stage).

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  107. full form of DOTS - Directly observed treatment short-course.
    In DOTS, healthcare workers observe patients as they take their medicine.

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  108. foods rich in zinc :-
    Legumes ( chick peas, beans)
    seeds ( sesame seeds, pumpkin, Flax )
    nuts ( cashew, almonds)
    Milk and Cheese (100 grams of cheddar cheese contains about 28% of a man’s daily recommended amount of zinc)
    whole Grains ( Wheat, quinoa , rice, oats)
    Dark chocolates (a 100-gram (3.5-ounce) bar of 70–85% dark chocolate contains 3.3 mg of zinc, or 30% of a man's recommended amount) etc

    more such items rich in Zinc - https://www.healthline.com/nutrition/best-foods-high-in-zinc

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  109. BLOOD BRAIN BARRIER -
    Blood vessels are critical to deliver oxygen and nutrients to all of the tissues and organs throughout the body. The blood vessels that vascularize the central nervous system (CNS) possess unique properties, termed the blood–brain barrier, which allow these vessels to tightly regulate the movement of ions, molecules, and cells between the blood and the brain. This precise control of CNS homeostasis allows for proper neuronal function and also protects the neural tissue from toxins and pathogens, and alterations of these barrier properties are an important component of pathology and progression of different neurological diseases.

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  110. I'm 15 years old. I was born with HIV my mother passed away because of the HIV infection And I regret why i never met Dr Itua he could have cured my mum for me because as a single mother it was very hard for my mother I came across Dr itua healing words online about how he cure different disease in different races diseases like HIV/Aids Herpes,Parkison,Asthma,Autism,Copd,Epilepsy,Shingles,Cold Sore,Infertility, Chronic Fatigues Syndrome, Lupus Cure,Fibromyalgia,Love Spell,Prostate Cancer,Lung Cancer,Glaucoma.,psoriasis,Cirrhosis of Liver, Cataracts,Macular degeneration, Chrons disease,Infectious mononucleosis.,Cardiovascular disease,Lung disease.Enlarged prostate,Osteoporosis.Alzheimer's disease,psoriasis,Bipolar Disorder,Dementia.,Tach Disease,Breast Cancer,Blood Cancer,Colo-Rectal Cancer,Love Spell,Chronic Diarrhea,Ataxia,Arthritis,Amyotrophic Lateral Scoliosis,Stroke,Fibromyalgia,Fluoroquinolone ToxicitySyndrome Fibrodysplasia Ossificans ProgresSclerosis,Weak Erection,Breast Enlargment,Penis Enlargment,Hpv,measles, tetanus, whooping cough, tuberculosis, polio and diphtheria)Diabetes Hepatitis even Cancer I was so excited but frighten at same time because I haven't come across such thing article online then I contacted Dr Itua on Mail drituaherbalcenter@gmail.com/ . I also chat with him on what's app +2348149277967 he tells me how it works then I tell him I want to proceed I paid him so swiftly Colorado post office I receive my herbal medicine within 4/5 working days he gave me guild lines to follow and here am I living healthy again can imagine how god use men to manifest his works am I writing in all articles online to spread the god work of Dr Itua Herbal Medicine,He's a Great Man.

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