The cag Pathogenicity Island of H.pylori: H.pylori is a gram-negative spiral-shaped human pathogen that colonizes the antrum and the corpus of the stomach. The H. pylori PAI was originally named cag (cytotoxin-associated gene) since it was thought to be associated with expression of the vacuolating toxin (VacA). However, it was later shown that both factors, VacA and the PAI, are independent of each other, even though cag-negative strains often do not express VacA. Biopsies from patients with severe gastric diseases showed the presence of cagA gene, establishing a direct correlation of the presence of the cagA gene with disease. Reference: https://www.ncbi.nlm.nih.gov/books/NBK2434/
The story of how Barry Marshall and Robin Warren ingested H pylori to prove it as a causative agent for the peptic ulcer. Please refer to the below link for the story.
Do other mircoorganisms promote the infectivity of v.cholerea as suggested by metchnikoff?? Vibreo cholerea interactions with gastroontestinal tract: lessions from animal studies.
What is the role of normal flora in resistance to cholera??
In a recent Nature paper, to examine microbiota contribution during and after cholera and identify commensals correlated with healing and reconstitution of the microbial community. One particular species may use intercellular communication to stymie Vibrio cholerae pathogenesis, indicating how the microbiota can restrict pathogens. http://www.sciencedirect.com
Why does chemotaxis limit v.cholerea intestinal colonization?? Vibrio cholerae accessory colonisation factor AcfC: a chemotactic protein with a role in hyperinfectivity.
What is the role of normal flora in resistance to cholera? component of the human intestine, bile salt, acts as one of the environmental cues to activate expression of virulence-related gene, leuO. V. cholerae is ingested from contaminated water, it passes into the gastrointestinal tract. “Because we have bile salts present in the small intestines, these bile salts act as a signaling molecule, with ToxR responding and regulating LeuO in response,” explains Ante. ToxR and LeuO are two cholera proteins that play an important role in detecting environmental cues. after sensing environmental molecules, the ToxR sends a signal to the DNA binding domain, which can then regulate the target genes. ToxR signaling has several arms: one is to regulating expression of virulence factors, such as cholera toxin that are important for bile resistance. http://mbioblog.asm.org/mbiosphere/2015/08/bile-resistance-is-futile-how-vibrio-cholera-responds-to-intestinal-environment.html
why does chemotaxis limit V.cholerae intestinal colonization? The inability of the toxR mutant strain to recognize and swim towards mucus is due to their failure to synthesize AcfB, a methyl–accepting chemotaxis protein. AcfB has been shown to be involved in intestinal colonization using the infant mouse model of cholera infection. V. cholerae acfB mutants fail to migrate into the capillary tubes. Vibrio strains carrying a mutation in tcpI, a ToxR regulated gene found within the Vibrio Pathogenicity Island (VPI), which encodes a methyl accepting chemotaxis protein are fully chemotactic towards mucus and galactose-6-sulfate. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872866
Are there any attributes of the O1 O-antigen that particularly promote intestinal colonization? Cholera enterotoxin, which is expressed by Vibrio cholerae O1 and O139. The genes encoding heat-labile and heat-stable toxins are carried on plasmids. Colonization is mediated by one or more proteinaceous fimbrial or fimbrillar adhesins termed colonization factor antigens (CFA). https://academic.oup.com/femsre/article/30/3/382/546603 17mmb023
Are there any attributes of the O1 O-antigen that particularly promote intestinal colonization? another reference-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741415/
Is there physiologically significant cell-to-cell variation in gene expression in vivo? A general dynamic description of protein synthesis was employed to quantify different sources of gene expression noise in cellular systems. To test our approach, we use time-resolved expression data of individual human cells and, from this information, predict the stationary cell-to-cell variation in protein levels in a clonal population. For three of the four human genes investigated, the cellular variations in expression level are not due to fluctuations in promoter activity or transcript copy number, but are almost exclusively a consequence of long-term variations of gene regulatory factors or the global cellular state. reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576406/
Fever, or rise in body temperature, of even just a degree or two can stop a virus's ability to grow.
When the brain increases the body's temperature set point, the body strives to meet that higher temperature. You feel cold because technically you are colder than your body's new set point. In turn, the body works to generate heat to warm itself by contracting and relaxing muscles — hence the shivering, or chills.
Why do we feel cold when we have fever? The link below gives answer to this question https://www.quora.com/Why-do-we-feel-cold-when-we-have-a-fever/answer/Parthiban-Bala?share=6a864aae&srid=lfEq
Why do we feel cold when we have fever? The answer of this question is our body's thermostat's temperature is set at 37°C. When we get infected by any pathogen the temperature of our thermostat increases.Hence to adjust that new thermostat temperature,our body reponses by constricting blood vessels,increasing the rate of metabolism,and shivering,all of which together increases the body temperature,and hence due to this we feel cold during fever.This condition is called chill.In addition to this,when body temperature reaches the temperature setting of thermostat,the chill disappears.The body will maintain this temperature until the job of phagocytes are done.The thermostat is then reset to 37°C.As the infection declines,heat losing mechanism like vasodilation and swaeting happens.The skin become warm and persons become to sweat.This phase of fever is known as crisis which indicates that the body temperature is falling.
How mosquito repellents work? 1.Mosquitoes are attracted to people by the scent of several chemicals we produce: lactic acid and 1-octen-3-ol, two skin compounds produced by our metabolism and sweating, and carbon dioxide, which we exhale. Most mosquito repellents evaporate on the skin and work by blocking a mosquito’s sense of smell, preventing it from finding its target. 2. Vapor-based repellents These ones are liquid based and are electric, implying they are plugged into a socket and used.The liquid (usually in a bottle attached to the main device) is heated enough to vaporize it. This vapor later spreads around the room (diffusion) and cause paralysis to mosquitoes, damaging their nervous system.
Que.function of co-factor in human cell: CCR5 and/or CXCR4 as co-receptors to enter target immunological cells.These receptors are located on the surface of host immune cells whereby they provide a method of entry for the HIV-1 virus to infect the cell.
Que. 1 Da = 1 u = 1.660 538 921(73)×10−27 kg 1 Da = 1 g/mol
Que. fc region is part of antibody or not! Binding specificity for a part of an antibody known as the Fc (Fragment crystallizable) region. Fc receptors bind to antibodies that are attached to infected cells. Fc receptor is a antibody receptor involved in antigen recognition which is located at the membrane of certain immune cells including B lymphocytes, natural killer cells, macrophages, neutrophils, and mast cells.
What is Carcinology? Carcinology is a branch of zoology that consists of the study of crustaceans, a group of arthropods that includes lobsters, crayfish, shrimp, krill, barnacles and crabs. Other names for carcinology are malacostracology, crustaceology, and crustalogy. 17mmb023 Jahnavi vyas
que: Five types of cancer ans:carcinoma, sarcoma, melanoma, lymphoma, and leukemia https://www.webmd.com/cancer/understanding-cancer-basics
que: Gait-ataxia Ataxia is defined as the presence of abnormal, uncoordinated movements.This describes signs & symptoms without any specific diseases. An unsteady, staggering gait is described as an ataxic gait because walking is uncoordinated and appears to be 'not ordered'. https://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/movement_disorders/ataxia/conditions/index.html 17mmb023 Jahnavi Vyas
Gait ataxia- Ataxia is typically defined as the presence of abnormal, uncoordinated movements. This usage describes signs & symptoms without reference to specific diseases. An unsteady, staggering gait is described as an ataxic gait because walking is uncoordinated and appears to be 'not ordered'.
Incontinence- Loss of bladder control, varying from a slight loss of urine after sneezing, coughing or laughing, to complete inability to control urination.
How t-cells can hide themselves? Researchers have discovered how Human Immunodeficiency Virus, which causes AIDS, can hide itself in our cells and dodge the attention of our normal defenses. When a normal virus such as the common cold infects people we develop an immune response and produce defense cells which can quickly get rid of the virus. But when HIV infects us it can last for our whole life. HIV does this by successfully hiding from our immune cells, which are seeking to identify and destroy the virus, fooling them into thinking that it is part of the normal trash in a cell rather than being clearly visible on the cell surface.
Broad HIV-1 inhibition in vitro by vaccine-elicited CD8+ T cells in African adults
In first clinical trial in low risk HIV-1-negative adults in Oxford demonstrated the principle that naturally mostly subdominant epitopes, when taken out of the context of full-length proteins/virus and delivered by potent regimens involving combinations of simian adenovirus and poxvirus modified vaccinia virus Ankara, can induce robust CD8+ T cells of broad specificities and functions capable of inhibiting in vitro HIV-1 replication. Here and for the first time, we tested this strategy in low risk HIV-1-negative adults in Africa. We showed that the vaccines were well tolerated and induced high frequencies of broadly HIVconsv-specific plurifunctional T cells, which inhibited in vitro viruses from four major clades A, B, C, and D. Because sub-Saharan Africa is globally the region most affected by HIV-1/AIDS, trial HIV-CORE 004 represents an important stage in the path toward efficacy evaluation of this highly rational and promising vaccine strategy.
Incontinence: Incontinence is describes any accidental or involuntary loss of urine from the bladder (urinary incontinence) or bowel motion, faeces or wind from the bowel (faecal or bowel incontinence).Incontinence is a widespread condition that ranges in severity from 'just a small leak' to complete loss of bladder or bowel control. In fact, over 4.8 million Australians have bladder or bowel control problems for a variety of reasons. https://www.continence.org.au/pages/what-is-incontinence.html 17mmb023 Jahnavi Vyas
DISEASE -a definite pathological process having a characteristic set of signs and symptoms. Disease is caused by extrinsic influences (e.g., virus, bacteria),
Symptom : A physical or mental feature which is regarded as indicating a condition of disease, particularly such a feature that is apparent to the patient.
DISORDER- is a disturbance or derangement that affects the function of mind or body. Disorder is due to intrinsic abnormalities (e.g., birth defects, genetic malfunction)
Polypharmacology approach- The concept of polypharmacology involves the interaction of drug molecules with multiple targets, which may interfere with a single or multiple disease pathways.Computational approaches for polypharmacology modeling will witness rapid growth and wide application in drug discovery.
list of food rich in zinc: Red-Meat,shellfish, legumes,seeds,nuts,eggs,whole grains,milk,dark chocolate,fruits(avocados, blackberries, pomegranates, raspberries, guavas, cantaloupes, apricots, peaches, kiwifruit, and blueberries),vegetables(potatoes and pumpkin) https://www.healthline.com/nutrition/best-foods-high-in-zinc#section9 17mmb023
Therapeutic index- A ratio that compares the blood concentration at which a drug becomes toxic and the concentration at which the drug is effective. The larger the therapeutic index (TI), the safer the drug is. If the TI is small (the difference between the two concentrations is very small), the drug must be dosed carefully and the person receiving the drug should be monitored closely for any signs of drug toxicity.
Combinatorial chesmistry- Combinatorial chemistry is a laboratory technique in which millions of molecular constructions can be synthesized and tested for biological activity. It has generated massive numbers of targeted molecules for testing and the developing techniques of high throughput screening has automated the screening process so larger numbers of biological assays can be done. All this together has reduced the discovery-to-market time from what used to be 10-14 years to 5-8 years.
What is blood-brain barrier? The blood-brain barrier (BBB) is formed by brain endothelial cells lining the cerebral microvasculature, and is an important mechanism for protecting the brain from fluctuations in plasma composition, and from circulating agents such as neurotransmitters and xenobiotics capable of disturbing neural function.
Blood brain barrier 1.It is an endothelial tight junction where endothelial cells are wedged extremely close together. 2. This heavily restricting barrier capacity allows the endothelial cells to tightly regulate CNS homeostasis. 3. CNS endothelial cells have unique properties compared with endothelial cells in other tissues that allow them to tightly regulate the movement of ions, molecules, and cells between the blood and the brain. 4. The tight gap allows only small molecules, fat-soluble molecules, and some gases to pass freely through the capillary wall and into brain tissue. Some larger molecules, such as glucose, can gain entry through transporter proteins.
Blood brain barrier The blood–brain barrier was discovered in the late 19th century, when the German physician Paul Ehrlich injected a dye into the bloodstream of a mouse. To his surprise, the dye infiltrated all tissues except the brain and spinal cord. While this showed that a barrier existed between brain and blood. blood–brain barrier that offers a barrier is the “endothelial tight junction”. Endothelial cells line the interior of all blood vessels. In the capillaries that form the blood–brain barrier, endothelial cells are wedged extremely close to each other, forming so-called tight junctions.
The tight gap allows only small molecules, fat-soluble molecules, and some gases to pass freely through the capillary wall and into brain tissue. Some larger molecules, such as glucose, can gain entry through transporter proteins, which act like special doors that open only for particular molecules.
Why do we need it? The purpose of the blood–brain barrier is to protect against circulating toxins or pathogens that could cause brain infections, while at the same time allowing vital nutrients to reach the brain.
Its other function is to help maintain relatively constant levels of hormones, nutrients and water in the brain – fluctuations in which could disrupt the finely tuned environment.
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.
As the name suggests, this is a barrier between the brain’s blood vessels (capillaries) and the cells and other components that make up brain tissue. Whereas the skull, meninges and cerebrospinal fluid protect against physical damage, the blood–brain barrier provides a defence against disease-causing pathogens and toxins that may be present in our blood. Reference-https://www.google.co.in/amp/s/theconversation.com/amp/explainer-what-is-the-blood-brain-barrier-and-how-can-we-overcome-it-75454
Combinatorial chemistry is a technique by which large numbers of structurally distinct molecules may be synthesised in a time and submitted for pharmacological assay. The key of combinatorial chemistry is that a large range of analogues is synthesised using the same reaction conditions, the same reaction vessels. In this way, the chemist can synthesise many hundreds or thousands of compounds in one time instead of preparing only a few by simple methodology.
About Herpes vitus: Here is a paper that explains how immunological factors may reactivate herpes simplex virus 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045948/
What is blood brain barrier? The (BBB) is formed by brain endothelial cells lining the cerebral microvasculature, and is an important mechanism for protecting the brain from fluctuations in plasma composition. It is also protect from circulating agents such as neurotransmitters and xenobiotics capable of disturbing neural function. https://www.ncbi.nlm.nih.gov/pubmed/12162730 roll no: 17mmb026
define : sarcoma ,carcinoma and lymphoma ? carcinoma:Cancer that begins in the skin or in tissues that line or cover internal organs. reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma. sarcoma:A type of cancer that begins in bone or in the soft tissues of the body, including cartilage, fat, muscle, blood vessels, fibrous tissue, or other connective or supportive tissue. Different types of sarcoma are based on where the cancer forms. For example, osteosarcoma forms in bone, liposarcoma forms in fat, and rhabdomyosarcoma forms in muscle. reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma. lymphoma : Cancer that begins in cells of the immune system. There are two basic categories of lymphomas. One kind is Hodgkin lymphoma, which is marked by the presence of a type of cell called the Reed-Sternberg cell. The other category is non-Hodgkin lymphomas, which includes a large, diverse group of cancers of immune system cells. Non-Hodgkin lymphomas can be further divided into cancers that have an indolent (slow-growing) course and those that have an aggressive (fast-growing) course. reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma.
HIV Causes AIDS: Proof Derived from Koch's Postulates:
Regarding postulate one, PCR testing allows researchers to document cell-associated proviral HIV in persons with AIDS who have been tested (proviral DNA detection is a research test, not one of the common FDA-approved viral load tests). Prior to this technology, HIV was often difficult to find. In addition, combining PCR testing with the common viral load tests has documented the presence of HIV genes as RNA freely floating in the blood plasma, outside of cells, in persons with a positive antibody test not taking anti-HIV medication. (Viral load testing looks for virus; the ELISA and Western blot tests look for antibodies to HIV.) Regarding postulate two, improvements in laboratory culture techniques have allowed the growth of HIV in vitro (in laboratory models) from blood samples obtained from persons with AIDS who have undergone such testing and from almost all persons with a positive antibody test without AIDS who have undergone such testing.
The last two postulates stipulate that inoculating the organism into an animal model (i.e., exposing or infecting the animal) leads to the same disease and that the organism is recoverable from that animal. The evidence satisfying these postulates was established in 1997, when Francis J. Novembre, Ph.D., and colleagues from Emory University in Atlanta, GA, published in the Journal of Virology that a chimpanzee inoculated with HIV ten years earlier had developed an AIDS-defining OI. Prior to the OI, the HIV RNA viral load had increased (partially documenting recovery of the organism from the animal model) and the CD4 cell count had decreased in the chimpanzee. Cultures of blood from the animal also were positive for HIV, establishing recoverability of the organism. Subsequently, blood from that chimp was transfused into a second, healthy chimpanzee. This second chimpanzee later had an increase in the HIV viral load and a decrease in the CD4 cell count.
Prior to this 1997 report, fulfillment of Koch's third and fourth postulates was lacking. Interestingly, the incubation period for clinical AIDS in this chimpanzee, with whom humans share 98% gene homology (structural similarity), was essentially equivalent to the average incubation period in humans -- ten years. This finding and publication were reported in the September 1997 issue of BETA. reference :http://www.thebody.com/content/art2654.html
Define quinolones Quinolones are bactericidal agents that rapidly inhibit DNA synthesis by promoting cleavage of bacterial DNA in the DNA-enzyme complexes of DNA gyrase and type IV topoisomerase, resulting in rapid bacterial death.
explain the genetic basis of acquired resistance to beta lactam antibiotics in s.aureus ? Penicillin-binding protein 2a (PBP2a) of Staphylococcus aureus is refractory to inhibition by available β-lactam antibiotics, resulting in resistance to these antibiotics. The strains of S. aureus that have acquired the mecA gene for PBP2a are designated as methicillin-resistant S. aureus (MRSA). The mecA gene was cloned and expressed in Escherichia coli, and PBP2a was purified to homogeneity. The kinetic parameters for interactions of several β-lactam antibiotics (penicillins, cephalosporins, and a carbapenem) and PBP2a were evaluated. The enzyme manifests resistance to covalent modification by β-lactam antibiotics at the active site serine residue . reference :http://www.jbc.org/content/279/39/40802.full
Define aminoglycosides Aminoglycosides are natural or semisynthetic antibiotics derived from actinomycetes. Aminoglycosides are potent, broad-spectrum antibiotics that act through inhibition of protein synthesis.
Ref.: Krause KM, Serio AW, Kane TR, Connolly LE. Aminoglycosides: An Overview. Cold Spring Harb Perspect Med. 2016;6(6):a027029. Published. doi:10.1101/cshperspect.a027029
mechanisms responsible for antimicrobial resistance? From an evolutionary perspective, bacteria use two major genetic strategies to adapt to the antibiotic “attack”, i) mutations in gene(s) often associated with the mechanism of action of the compound, and ii) acquisition of foreign DNA coding for resistance determinants through horizontal gene transfer (HGT). In general, mutations resulting in antimicrobial resistance alter the antibiotic action via one of the following mechanisms, i) modifications of the antimicrobial target (decreasing the affinity for the drug, see below), i) a decrease in the drug uptake, ii) activation of efflux mechanisms to extrude the harmful molecule, or iv) global changes in important metabolic pathways via modulation of regulatory networks. Thus, resistance arising due to acquired mutational changes is diverse and varies in complexity. reference :https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/
Define toxic shock syndrome (TSS) Toxic shock syndrome (TSS) is a cluster of symptoms that involve many systems of the body. Certain bacterial infections release toxins into the blood stream, which then spreads the toxins to body organs. This can cause severe damage and illness. The following bacteria commonly cause TSS: Staphylococcus aureus Streptococcus pyogenes Clostridium sordellii
Quinolone-- Quinolones act by the rapid inhibition of bacterial DNA synthesis, leading to cell death. The primary targets are DNA gyrase and topoisomerase IV which are involved in the maintenance of the superhelical structure of DNA.
Polypharmacology for complex diseases is likely to involve multiple drugs acting on distinct targets that are part of a network regulating physiological responses. Drug-target networks can be used to identify multiple targets and to determine suitable combinations of drug targets or drugs. Thus, the discovery of new drug therapies for complex diseases may be greatly aided by systems biology.
Reverse pharmacology-- Drug discovery, at the bedside, is followed in reverse pharmacology (RP) by the relevant science of drug development for safety, efficacy, and mechanistic understanding. Such a transdisciplinary structured path can explore the large potential for novel drugs. The phytoactives can be novel scaffolds for new drugs.The delay in drug discovery can be eliminated by reverse pharmacology (RP).
Distinguish between resident and transient microbes. Resident microbes are those which stays in the place permanently, without causing any disease eg. Streptococci on skin. transient flora, episodic microorganisms found on or in a person. Some of these cause no trouble, like tourists passing through a city, while others are most definitely trouble, like terrorists coming into a city to wreak havoc.
Transient microorganisms, like the yeast Candida, can cause vaginitis, while Norovirus is a contagious virus that can give you the stomach flu. It's not found in your gut on a normal basis, but if you eat or drink it in your food, you might feel pretty bad for a few days.
An enterotoxin is a protein exotoxin released by a microorganism that targets the intestines. Enterotoxins are chromosomally encoded or plasmid encoded exotoxins that are produced and secreted from several bacterial organisms. They are often heat-stable, and are of low molecular weight and water-soluble Exotoxins are the ones which are secreated by the living cell and disrupts the cellular metabolism of others.
When cholera toxin is released from the bacteria in the infected intestine, it binds to the intestinal cells known as enterocytes (epithelial cell in above diagram) 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.
Mechanism of antibiotic resistance, 1) Drug inactivation 2) Alteration of target and or binding site 3) Alteration of metabolic pathway 4) Reduced drug Accumulation 5) Active efflux 6) mutation
Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS), also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension, multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also include severe myalgia, vomiting, diarrhea, headache, and nonfocal neurologic abnormalities.
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
A quinolone antibiotic is any member of a large group of broad-spectrum bactericides that share a bicyclic core structure related to the compound 4-quinolone. They are used in human and veterinary medicine to treat bacterial infections, as well as in animal husbandry.
Mode of action - Quinolones act by the rapid inhibition of bacterial DNA synthesis, leading to cell death. The primary targets are DNA gyrase and topoisomerase IV which are involved in the maintenance of the superhelical structure of DNA.
Que: Make a list of disease caused by staphylococcus Ans:Boils,Impetigo, cellulitis, Staphylococcal scalded skin syndrome,food poisoning, septicaemia,Toxic shock syndrome, Septic arthritis. Ref: https://www.myoclinic.org 17mmb016
Que: which are the bacteria involved in gas production in canned food? Ans: Thermophilic anaerobic spoilage is caused by anaerobic Thermoanaerobacter and Thermoanaerobacterium with the production of large quantities of H2 and CO2 gases, and causing sour fermentation at high temperatures in medium‐acid canned foods. Some species of spore forming psychrophilic bacteria have the ability to spoil refrigerated canned foods with production of gas, off‐flavors, and odors. Ref:https://onlinelibrary.wiley.com/doi/10.1002/9781119237860.ch22 17mmb016
The cag Pathogenicity Island of H.pylori:
ReplyDeleteH.pylori is a gram-negative spiral-shaped human pathogen that colonizes the antrum and the corpus of the stomach.
The H. pylori PAI was originally named cag (cytotoxin-associated gene) since it was thought to be associated with expression of the vacuolating toxin (VacA). However, it was later shown that both factors, VacA and the PAI, are independent of each other, even though cag-negative strains often do not express VacA.
Biopsies from patients with severe gastric diseases showed the presence of cagA gene, establishing a direct correlation of the presence of the cagA gene with disease.
Reference: https://www.ncbi.nlm.nih.gov/books/NBK2434/
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DeleteHimani zaveri
Helicobacter pylori: A Nobel pursuit?
ReplyDeleteThe story of how Barry Marshall and Robin Warren ingested H pylori to prove it as a causative agent for the peptic ulcer. Please refer to the below link for the story.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2661189/
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Himani Zaveri
Do other mircoorganisms promote the infectivity of v.cholerea as suggested by metchnikoff??
ReplyDeleteVibreo cholerea interactions with gastroontestinal tract: lessions from animal studies.
https://www.researchgate.net/publication/26879738_Vibrio_cholerae_Interactions_with_the_Gastrointestinal_Tract_Lessons_from_Animal_Studies.
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ReplyDeleteWhat is the role of normal flora in resistance to cholera??
ReplyDeleteIn a recent Nature paper, to examine microbiota contribution during and after cholera and identify commensals correlated with healing and reconstitution of the microbial community. One particular species may use intercellular communication to stymie Vibrio cholerae pathogenesis, indicating how the microbiota can restrict pathogens.
http://www.sciencedirect.com
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DeleteWhy does chemotaxis limit v.cholerea intestinal colonization??
ReplyDeleteVibrio cholerae accessory colonisation factor AcfC: a chemotactic protein with a role in hyperinfectivity.
https://www.nature.com/articles/s41598-018-26570-7
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DeleteWhat is the role of normal flora in resistance to cholera?
ReplyDeletecomponent of the human intestine, bile salt, acts as one of the environmental cues to activate expression of virulence-related gene, leuO.
V. cholerae is ingested from contaminated water, it passes into the gastrointestinal tract. “Because we have bile salts present in the small intestines, these bile salts act as a signaling molecule, with ToxR responding and regulating LeuO in response,” explains Ante. ToxR and LeuO are two cholera proteins that play an important role in detecting environmental cues.
after sensing environmental molecules, the ToxR sends a signal to the DNA binding domain, which can then regulate the target genes. ToxR signaling has several arms: one is to regulating expression of virulence factors, such as cholera toxin that are important for bile resistance.
http://mbioblog.asm.org/mbiosphere/2015/08/bile-resistance-is-futile-how-vibrio-cholera-responds-to-intestinal-environment.html
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why does chemotaxis limit V.cholerae intestinal colonization?
ReplyDeleteThe inability of the toxR mutant strain to recognize and swim towards mucus is due to their failure to synthesize AcfB, a methyl–accepting chemotaxis protein. AcfB has been shown to be involved in intestinal colonization using the infant mouse model of cholera infection. V. cholerae acfB mutants fail to migrate into the capillary tubes. Vibrio strains carrying a mutation in tcpI, a ToxR regulated gene found within the Vibrio Pathogenicity Island (VPI), which encodes a methyl accepting chemotaxis protein are fully chemotactic towards mucus and galactose-6-sulfate.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872866
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Are there any attributes of the O1 O-antigen that particularly promote intestinal colonization?
ReplyDeleteCholera enterotoxin, which is expressed by Vibrio cholerae O1 and O139. The genes encoding heat-labile and heat-stable toxins are carried on plasmids. Colonization is mediated by one or more proteinaceous fimbrial or fimbrillar adhesins termed colonization factor antigens (CFA).
https://academic.oup.com/femsre/article/30/3/382/546603
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Are there any attributes of the O1 O-antigen that particularly promote intestinal colonization?
ReplyDeleteanother reference-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741415/
Is there physiologically significant cell-to-cell variation in gene expression in vivo?
ReplyDeleteA general dynamic description of protein synthesis was employed to quantify different sources of gene expression noise in cellular systems. To test our approach, we use time-resolved expression data of individual human cells and, from this information, predict the stationary cell-to-cell variation in protein levels in a clonal population. For three of the four human genes investigated, the cellular variations in expression level are not due to fluctuations in promoter activity or transcript copy number, but are almost exclusively a consequence of long-term variations of gene regulatory factors or the global cellular state.
reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576406/
Why we get chills during fever?
ReplyDeleteFever, or rise in body temperature, of even just a degree or two can stop a virus's ability to grow.
When the brain increases the body's temperature set point, the body strives to meet that higher temperature. You feel cold because technically you are colder than your body's new set point. In turn, the body works to generate heat to warm itself by contracting and relaxing muscles — hence the shivering, or chills.
Reference-https://www.everydayhealth.com/cold-and-flu/why-do-we-get-chills-with-a-fever/
Why do we feel cold when we have fever?
ReplyDeleteThe link below gives answer to this question
https://www.quora.com/Why-do-we-feel-cold-when-we-have-a-fever/answer/Parthiban-Bala?share=6a864aae&srid=lfEq
17mmb025 Himani Zaveri
Why do we feel cold when we have fever?
ReplyDeleteThe answer of this question is our body's thermostat's temperature is set at 37°C. When we get infected by any pathogen the temperature of our thermostat increases.Hence to adjust that new thermostat temperature,our body reponses by constricting blood vessels,increasing the rate of metabolism,and shivering,all of which together increases the body temperature,and hence due to this we feel cold during fever.This condition is called chill.In addition to this,when body temperature reaches the temperature setting of thermostat,the chill disappears.The body will maintain this temperature until the job of phagocytes are done.The thermostat is then reset to 37°C.As the infection declines,heat losing mechanism like vasodilation and swaeting happens.The skin become warm and persons become to sweat.This phase of fever is known as crisis which indicates that the body temperature is falling.
17mmb008 Neha Jha
Q-1mm³ is how much L?
ReplyDeleteSo 1L = 10,00,000mm³,hence 1mm³=1×10-6.
17mmb008 Neha Jha
How mosquito repellents work?
ReplyDelete1.Mosquitoes are attracted to people by the scent of several chemicals we produce: lactic acid and 1-octen-3-ol, two skin compounds produced by our metabolism and sweating, and carbon dioxide, which we exhale. Most mosquito repellents evaporate on the skin and work by blocking a mosquito’s sense of smell, preventing it from finding its target.
2. Vapor-based repellents
These ones are liquid based and are electric, implying they are plugged into a socket and used.The liquid (usually in a bottle attached to the main device) is heated enough to vaporize it. This vapor later spreads around the room (diffusion) and cause paralysis to mosquitoes, damaging their nervous system.
Que.function of co-factor in human cell:
ReplyDeleteCCR5 and/or CXCR4 as co-receptors to enter target immunological cells.These receptors are located on the surface of host immune cells whereby they provide a method of entry for the HIV-1 virus to infect the cell.
Que. 1 Da = 1 u = 1.660 538 921(73)×10−27 kg
1 Da = 1 g/mol
Que. fc region is part of antibody or not!
Binding specificity for a part of an antibody known as the Fc (Fragment crystallizable) region. Fc receptors bind to antibodies that are attached to infected cells.
Fc receptor is a antibody receptor involved in antigen recognition which is located at the membrane of certain immune cells including B lymphocytes, natural killer cells, macrophages, neutrophils, and mast cells.
17mmb023 Jahnavi Vyas
What is Carcinology?
ReplyDeleteCarcinology is a branch of zoology that consists of the study of crustaceans, a group of arthropods that includes lobsters, crayfish, shrimp, krill, barnacles and crabs. Other names for carcinology are malacostracology, crustaceology, and crustalogy.
17mmb023 Jahnavi vyas
que: Five types of cancer
ReplyDeleteans:carcinoma, sarcoma, melanoma, lymphoma, and leukemia
https://www.webmd.com/cancer/understanding-cancer-basics
que: Gait-ataxia
Ataxia is defined as the presence of abnormal, uncoordinated movements.This describes signs & symptoms without any specific diseases. An unsteady, staggering gait is described as an ataxic gait because walking is uncoordinated and appears to be 'not ordered'.
https://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/movement_disorders/ataxia/conditions/index.html
17mmb023 Jahnavi Vyas
Gait ataxia-
ReplyDeleteAtaxia is typically defined as the presence of abnormal, uncoordinated movements. This usage describes signs & symptoms without reference to specific diseases. An unsteady, staggering gait is described as an ataxic gait because walking is uncoordinated and appears to be 'not ordered'.
Incontinence-
Loss of bladder control, varying from a slight loss of urine after sneezing, coughing or laughing, to complete inability to control urination.
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DeleteHow t-cells can hide themselves?
ReplyDeleteResearchers have discovered how Human Immunodeficiency Virus, which causes AIDS, can hide itself in our cells and dodge the attention of our normal defenses. When a normal virus such as the common cold infects people we develop an immune response and produce defense cells which can quickly get rid of the virus. But when HIV infects us it can last for our whole life. HIV does this by successfully hiding from our immune cells, which are seeking to identify and destroy the virus, fooling them into thinking that it is part of the normal trash in a cell rather than being clearly visible on the cell surface.
https://www.sciencedaily.com/releases/2008/03/080331223838.htm
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DeleteBroad HIV-1 inhibition in vitro by vaccine-elicited CD8+ T cells in African adults
ReplyDeleteIn first clinical trial in low risk HIV-1-negative adults in Oxford demonstrated the principle that naturally mostly subdominant epitopes, when taken out of the context of full-length proteins/virus and delivered by potent regimens involving combinations of simian adenovirus and poxvirus modified vaccinia virus Ankara, can induce robust CD8+ T cells of broad specificities and functions capable of inhibiting in vitro HIV-1 replication. Here and for the first time, we tested this strategy in low risk HIV-1-negative adults in Africa. We showed that the vaccines were well tolerated and induced high frequencies of broadly HIVconsv-specific plurifunctional T cells, which inhibited in vitro viruses from four major clades A, B, C, and D. Because sub-Saharan Africa is globally the region most affected by HIV-1/AIDS, trial HIV-CORE 004 represents an important stage in the path toward efficacy evaluation of this highly rational and promising vaccine strategy.
https://doi.org/10.1038/mtm.2016.61
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DeleteIncontinence:
ReplyDeleteIncontinence is describes any accidental or involuntary loss of urine from the bladder (urinary incontinence) or bowel motion, faeces or wind from the bowel (faecal or bowel incontinence).Incontinence is a widespread condition that ranges in severity from 'just a small leak' to complete loss of bladder or bowel control. In fact, over 4.8 million Australians have bladder or bowel control problems for a variety of reasons.
https://www.continence.org.au/pages/what-is-incontinence.html
17mmb023 Jahnavi Vyas
Disease vs Symptom vs Disorder
ReplyDeleteDISEASE -a definite pathological process having a characteristic set of signs and symptoms. Disease is caused by extrinsic influences (e.g., virus, bacteria),
Symptom : A physical or mental feature which is regarded as indicating a condition of disease, particularly such a feature that is apparent to the patient.
DISORDER- is a disturbance or derangement that affects the function of mind or body. Disorder is due to intrinsic abnormalities (e.g., birth defects, genetic malfunction)
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List of food rich in zinc-
ReplyDeleteMeat,shellfish, legumes,seeds,nuts,eggs,whole grains,milk,dark chocolate.
Polypharmacology approach- The concept of polypharmacology involves the interaction of drug molecules with multiple targets, which may interfere with a single or multiple disease pathways.Computational approaches for polypharmacology modeling will witness rapid growth and wide application in drug discovery.
ReplyDelete17mmb007
Deletelist of food rich in zinc:
ReplyDeleteRed-Meat,shellfish, legumes,seeds,nuts,eggs,whole grains,milk,dark chocolate,fruits(avocados, blackberries, pomegranates, raspberries, guavas, cantaloupes, apricots, peaches, kiwifruit, and blueberries),vegetables(potatoes and pumpkin)
https://www.healthline.com/nutrition/best-foods-high-in-zinc#section9
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Therapeutic index- A ratio that compares the blood concentration at which a drug becomes toxic and the concentration at which the drug is effective. The larger the therapeutic index (TI), the safer the drug is. If the TI is small (the difference between the two concentrations is very small), the drug must be dosed carefully and the person receiving the drug should be monitored closely for any signs of drug toxicity.
ReplyDeletehttps://aidsinfo.nih.gov/understanding-hiv-aids/glossary/865/therapeutic-index#
Hinal mehta- 17mmb007
DeleteCombinatorial chesmistry- Combinatorial chemistry is a laboratory technique in which millions of molecular constructions can be synthesized and tested for biological activity. It has generated massive numbers of targeted molecules for testing and the developing techniques of high throughput screening has automated the screening process so larger numbers of biological assays can be done. All this together has reduced the discovery-to-market time from what used to be 10-14 years to 5-8 years.
ReplyDeletehttp://www1.udel.edu/chem/C465/senior/fall00/DrugDiscovery/WhatisCombinatorialChemistry.htm
Hinal mehta- 17mmb007
DeleteWhat is blood-brain barrier?
ReplyDeleteThe blood-brain barrier (BBB) is formed by brain endothelial cells lining the cerebral microvasculature, and is an important mechanism for protecting the brain from fluctuations in plasma composition, and from circulating agents such as neurotransmitters and xenobiotics capable of disturbing neural function.
https://www.ncbi.nlm.nih.gov/pubmed/12162730
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Jahnavi vyas
Blood brain barrier
ReplyDelete1.It is an endothelial tight junction where endothelial cells are wedged extremely close together.
2. This heavily restricting barrier capacity allows the endothelial cells to tightly regulate CNS homeostasis.
3. CNS endothelial cells have unique properties compared with endothelial cells in other tissues that allow them to tightly regulate the movement of ions, molecules, and cells between the blood and the brain.
4. The tight gap allows only small molecules, fat-soluble molecules, and some gases to pass freely through the capillary wall and into brain tissue. Some larger molecules, such as glucose, can gain entry through transporter proteins.
Blood brain barrier
ReplyDeleteThe blood–brain barrier was discovered in the late 19th century, when the German physician Paul Ehrlich injected a dye into the bloodstream of a mouse. To his surprise, the dye infiltrated all tissues except the brain and spinal cord. While this showed that a barrier existed between brain and blood.
blood–brain barrier that offers a barrier is the “endothelial tight junction”. Endothelial cells line the interior of all blood vessels. In the capillaries that form the blood–brain barrier, endothelial cells are wedged extremely close to each other, forming so-called tight junctions.
The tight gap allows only small molecules, fat-soluble molecules, and some gases to pass freely through the capillary wall and into brain tissue. Some larger molecules, such as glucose, can gain entry through transporter proteins, which act like special doors that open only for particular molecules.
Why do we need it?
The purpose of the blood–brain barrier is to protect against circulating toxins or pathogens that could cause brain infections, while at the same time allowing vital nutrients to reach the brain.
Its other function is to help maintain relatively constant levels of hormones, nutrients and water in the brain – fluctuations in which could disrupt the finely tuned environment.
Reference: http://theconversation.com/explainer-what-is-the-blood-brain-barrier-and-how-can-we-overcome-it-75454
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.
ReplyDeletehttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4292164/
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DeleteThis comment has been removed by the author.
ReplyDeleteAs the name suggests, this is a barrier between the brain’s blood vessels (capillaries) and the cells and other components that make up brain tissue. Whereas the skull, meninges and cerebrospinal fluid protect against physical damage, the blood–brain barrier provides a defence against disease-causing pathogens and toxins that may be present in our blood.
ReplyDeleteReference-https://www.google.co.in/amp/s/theconversation.com/amp/explainer-what-is-the-blood-brain-barrier-and-how-can-we-overcome-it-75454
Combinatorial chemistry is a technique by which large numbers of structurally distinct molecules may be synthesised in a time and submitted for pharmacological assay. The key of combinatorial chemistry is that a large range of analogues is synthesised using the same reaction conditions, the same reaction vessels. In this way, the chemist can synthesise many hundreds or thousands of compounds in one time instead of preparing only a few by simple methodology.
ReplyDeleteReference-http://www.combichemistry.com/principle.html
About Herpes vitus:
ReplyDeleteHere is a paper that explains how immunological factors may reactivate herpes simplex virus 1.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045948/
This comment has been removed by the author.
ReplyDeleteWhat is blood brain barrier?
ReplyDeleteThe (BBB) is formed by brain endothelial cells lining the cerebral microvasculature, and is an important mechanism for protecting the brain from fluctuations in plasma composition. It is also protect from circulating agents such as neurotransmitters and xenobiotics capable of disturbing neural function.
https://www.ncbi.nlm.nih.gov/pubmed/12162730
roll no: 17mmb026
define : sarcoma ,carcinoma and lymphoma ?
ReplyDeletecarcinoma:Cancer that begins in the skin or in tissues that line or cover internal organs.
reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma.
sarcoma:A type of cancer that begins in bone or in the soft tissues of the body, including cartilage, fat, muscle, blood vessels, fibrous tissue, or other connective or supportive tissue. Different types of sarcoma are based on where the cancer forms. For example, osteosarcoma forms in bone, liposarcoma forms in fat, and rhabdomyosarcoma forms in muscle.
reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma.
lymphoma : Cancer that begins in cells of the immune system. There are two basic categories of lymphomas. One kind is Hodgkin lymphoma, which is marked by the presence of a type of cell called the Reed-Sternberg cell. The other category is non-Hodgkin lymphomas, which includes a large, diverse group of cancers of immune system cells. Non-Hodgkin lymphomas can be further divided into cancers that have an indolent (slow-growing) course and those that have an aggressive (fast-growing) course.
reference:https://www.cancer.gov/publications/dictionaries/cancer-terms/def/carcinoma.
Foods containing Zinc: Oysters, beef, crab, lobster, pork, beans, chicken, yogurt, cashews, chickpeas, cheese, oats, milk, almond, kidney beans, green peas
ReplyDeleteRef.: https://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/
17MMB006- Avinash Dutta
HIV Causes AIDS: Proof Derived from Koch's Postulates:
ReplyDeleteRegarding postulate one, PCR testing allows researchers to document cell-associated proviral HIV in persons with AIDS who have been tested (proviral DNA detection is a research test, not one of the common FDA-approved viral load tests). Prior to this technology, HIV was often difficult to find. In addition, combining PCR testing with the common viral load tests has documented the presence of HIV genes as RNA freely floating in the blood plasma, outside of cells, in persons with a positive antibody test not taking anti-HIV medication. (Viral load testing looks for virus; the ELISA and Western blot tests look for antibodies to HIV.)
Regarding postulate two, improvements in laboratory culture techniques have allowed the growth of HIV in vitro (in laboratory models) from blood samples obtained from persons with AIDS who have undergone such testing and from almost all persons with a positive antibody test without AIDS who have undergone such testing.
The last two postulates stipulate that inoculating the organism into an animal model (i.e., exposing or infecting the animal) leads to the same disease and that the organism is recoverable from that animal. The evidence satisfying these postulates was established in 1997, when Francis J. Novembre, Ph.D., and colleagues from Emory University in Atlanta, GA, published in the Journal of Virology that a chimpanzee inoculated with HIV ten years earlier had developed an AIDS-defining OI. Prior to the OI, the HIV RNA viral load had increased (partially documenting recovery of the organism from the animal model) and the CD4 cell count had decreased in the chimpanzee. Cultures of blood from the animal also were positive for HIV, establishing recoverability of the organism. Subsequently, blood from that chimp was transfused into a second, healthy chimpanzee. This second chimpanzee later had an increase in the HIV viral load and a decrease in the CD4 cell count.
Prior to this 1997 report, fulfillment of Koch's third and fourth postulates was lacking. Interestingly, the incubation period for clinical AIDS in this chimpanzee, with whom humans share 98% gene homology (structural similarity), was essentially equivalent to the average incubation period in humans -- ten years. This finding and publication were reported in the September 1997 issue of BETA.
reference :http://www.thebody.com/content/art2654.html
Define quinolones
ReplyDeleteQuinolones are bactericidal agents that rapidly inhibit DNA synthesis by promoting cleavage of bacterial DNA in the DNA-enzyme complexes of DNA gyrase and type IV topoisomerase, resulting in rapid bacterial death.
Ref.: Quinolones: a comprehensive review.
DeleteCatherine M. Oliphant, Gary M. Green
Am Fam Physician. 2002 Feb 1; 65(3): 455–464
explain the genetic basis of acquired resistance to beta lactam antibiotics in s.aureus ?
ReplyDeletePenicillin-binding protein 2a (PBP2a) of Staphylococcus aureus is refractory to inhibition by available β-lactam antibiotics, resulting in resistance to these antibiotics. The strains of S. aureus that have acquired the mecA gene for PBP2a are designated as methicillin-resistant S. aureus (MRSA). The mecA gene was cloned and expressed in Escherichia coli, and PBP2a was purified to homogeneity. The kinetic parameters for interactions of several β-lactam antibiotics (penicillins, cephalosporins, and a carbapenem) and PBP2a were evaluated. The enzyme manifests resistance to covalent modification by β-lactam antibiotics at the active site serine residue .
reference :http://www.jbc.org/content/279/39/40802.full
Define aminoglycosides
ReplyDeleteAminoglycosides are natural or semisynthetic antibiotics derived from actinomycetes. Aminoglycosides are potent, broad-spectrum antibiotics that act through inhibition of protein synthesis.
Ref.: Krause KM, Serio AW, Kane TR, Connolly LE. Aminoglycosides: An Overview.
Cold Spring Harb Perspect Med. 2016;6(6):a027029.
Published. doi:10.1101/cshperspect.a027029
mechanisms responsible for antimicrobial resistance?
ReplyDeleteFrom an evolutionary perspective, bacteria use two major genetic strategies to adapt to the antibiotic “attack”, i) mutations in gene(s) often associated with the mechanism of action of the compound, and ii) acquisition of foreign DNA coding for resistance determinants through horizontal gene transfer (HGT).
In general, mutations resulting in antimicrobial resistance alter the antibiotic action via one of the following mechanisms, i) modifications of the antimicrobial target (decreasing the affinity for the drug, see below), i) a decrease in the drug uptake, ii) activation of efflux mechanisms to extrude the harmful molecule, or iv) global changes in important metabolic pathways via modulation of regulatory networks. Thus, resistance arising due to acquired mutational changes is diverse and varies in complexity.
reference :https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/
Define toxic shock syndrome (TSS)
ReplyDeleteToxic shock syndrome (TSS) is a cluster of symptoms that involve many systems of the body. Certain bacterial infections release toxins into the blood stream, which then spreads the toxins to body organs. This can cause severe damage and illness.
The following bacteria commonly cause TSS:
Staphylococcus aureus
Streptococcus pyogenes
Clostridium sordellii
Ref.: https://www.hopkinsmedicine.org/healthlibrary/test_procedures/urology/toxic_shock_syndrome_tss_85,P00653
Quinolone--
ReplyDeleteQuinolones act by the rapid inhibition of bacterial DNA synthesis, leading to cell death. The primary targets are DNA gyrase and topoisomerase IV which are involved in the maintenance of the superhelical structure of DNA.
https://www.sciencedirect.com/topics/medicine-and-dentistry/quinolone
Hinal mehta- 17mmb007
DeleteProperty of polypharmacology approach--
ReplyDeletePolypharmacology for complex diseases is likely to involve multiple drugs acting on distinct targets that are part of a network regulating physiological responses. Drug-target networks can be used to identify multiple targets and to determine suitable combinations of drug targets or drugs. Thus, the discovery of new drug therapies for complex diseases may be greatly aided by systems biology.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068535/
Hinal mehta- 17mmb007
DeleteReverse pharmacology--
ReplyDeleteDrug discovery, at the bedside, is followed in reverse pharmacology (RP) by the relevant science of drug development for safety, efficacy, and mechanistic understanding. Such a transdisciplinary structured path can explore the large potential for novel drugs. The phytoactives can be novel scaffolds for new drugs.The delay in drug discovery can be eliminated by reverse pharmacology (RP).
https://www.sciencedirect.com/topics/medicine-and-dentistry/reverse-pharmacology
Hinal mehta- 17mmb007
DeleteDistinguish between resident and transient microbes.
ReplyDeleteResident microbes are those which stays in the place permanently, without causing any disease eg. Streptococci on skin.
transient flora, episodic microorganisms found on or in a person. Some of these cause no trouble, like tourists passing through a city, while others are most definitely trouble, like terrorists coming into a city to wreak havoc.
Transient microorganisms, like the yeast Candida, can cause vaginitis, while Norovirus is a contagious virus that can give you the stomach flu. It's not found in your gut on a normal basis, but if you eat or drink it in your food, you might feel pretty bad for a few days.
An enterotoxin is a protein exotoxin released by a microorganism that targets the intestines. Enterotoxins are chromosomally encoded or plasmid encoded exotoxins that are produced and secreted from several bacterial organisms. They are often heat-stable, and are of low molecular weight and water-soluble
ReplyDeleteExotoxins are the ones which are secreated by the living cell and disrupts the cellular metabolism of others.
Mode of action of cholera enterotoxin,
ReplyDeleteWhen cholera toxin is released from the bacteria in the infected intestine, it binds to the intestinal cells known as enterocytes (epithelial cell in above diagram) 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.
Mechanism of antibiotic resistance,
ReplyDelete1) Drug inactivation
2) Alteration of target and or binding site
3) Alteration of metabolic pathway
4) Reduced drug Accumulation
5) Active efflux
6) mutation
Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection with either Staphylococcus aureus or group A Streptococcus (GAS), also called Streptococcus pyogenes. It is characterized by high fever, rash, hypotension, multiorgan failure (involving at least 3 or more organ systems), and desquamation, typically of the palms and soles, 1-2 weeks after the onset of acute illness. The clinical syndrome can also include severe myalgia, vomiting, diarrhea, headache, and nonfocal neurologic abnormalities.
ReplyDeleteFunction of CxCr4 and CCr5
ReplyDeleteThe 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
A quinolone antibiotic is any member of a large group of broad-spectrum bactericides that share a bicyclic core structure related to the compound 4-quinolone. They are used in human and veterinary medicine to treat bacterial infections, as well as in animal husbandry.
ReplyDeleteMode of action -
Quinolones act by the rapid inhibition of bacterial DNA synthesis, leading to cell death. The primary targets are DNA gyrase and topoisomerase IV which are involved in the maintenance of the superhelical structure of DNA.
Que: Make a list of disease caused by staphylococcus
ReplyDeleteAns:Boils,Impetigo, cellulitis, Staphylococcal scalded skin syndrome,food poisoning, septicaemia,Toxic shock syndrome, Septic arthritis.
Ref: https://www.myoclinic.org
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Que: which are the bacteria involved in gas production in canned food?
ReplyDeleteAns: Thermophilic anaerobic spoilage is caused by anaerobic Thermoanaerobacter and Thermoanaerobacterium with the production of large quantities of H2 and CO2 gases, and causing sour fermentation at high temperatures in medium‐acid canned foods. Some species of spore forming psychrophilic bacteria have the ability to spoil refrigerated canned foods with production of gas, off‐flavors, and odors.
Ref:https://onlinelibrary.wiley.com/doi/10.1002/9781119237860.ch22
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