Chat with us, powered by LiveChat I need help on reviewing and completing a formal report | Collepals Essay Writers

I need help on reviewing and completing a formal report

biology question and need the explanation and answer to help me learn.

Hello friend. I have started and done the intro, methods, results, and some of the discussion but I need you to review those parts I completed and then complete the discussion section and write an abstract for it. All the details are attached for it. Thank you so much looking forwad to a great delivery
Requirements: 6p
what you need to think of when doing this report:
K1. Understanding of the principles of selective toxicity in treating bacterial infections and cancer.
S1. Effective data analysis, drawing appropriate conclusions.
S2. Application of a range of key skills effective written communication, numerical skills, preparation and presentation of scientific reports.
S3. Critical utilization of scientific knowledge and data.
S4. Appropriate use of literature sources.
S5. Ability to work independently.
II. Assessment Criteria
Title: Selective Toxicity Formal Lab Report
Abstract: a brief summary of the method, results and conclusion of the experiment. Easier to do at the end. A single paragraph and written in the present tense. up to 200 words
Introduction:

Back in time Paul Erlich defined chemotherapy as “the use of drugs to injure an invading organism without injury to the host.” (p.207 of the selective toxicity book) The general term of chemotherapy is vastly used to refer to a type of a treatment that is used for cancer; however, there is more to it. Chemotherapy is referred to as a drug when it is meant to be used on humans or animals where it is called agricultural agent when it is used for fungi and insects. (p.3-4 of the selective toxicity book) Today chemotherapies are used for vast number of things that all aim to treat or prevent diseases. Moreover, there are those chemotherapies that work on bacteria only or fungi only and there are those chemotherapies that work on multiple types of organisms. However, most drugs are toxic and threshold poisons.(Chapter 4 of Drug Toxicity and Poisoning by Kavin C. Osterhoudt; Trevor M. Penning) It is important to understand that toxicity in a drug is valuable only when it is selective. (p.4 of the selective toxicity book) An example of drugs selective toxicity is chemotherapy used to treat cancer. The aim of that chemotherapy is only to kill the cancer cells but not other healthy cells of the human body. Selective toxicity of drugs can only be achieved owing to differences in biotransformation processes. (Selective toxicity of antibacterial agents—still a valid concept or do we miss chances and ignore risks? written by )The purpose of this experiment is to investigate the selective toxicity of amphotericin, penicillin and 5-Fluorouracil on the growth of Micrococcus luteus and Pythium spp. Micrococcus luteus is a gram-positive bacterium where Pythium spp. are soil borne pathogens that infect plants and are formally classified as fungi. The experiment investigates how those different drugs affect these two organisms and how selective are they for each of the organisms in the aim of treating bacterial infections and cancer. Based on the mechanisms of action for amphotericin, penicillin and 5-Fluorouracil, Pythium spp should show the largest inhibition to amphotericin where micrococcus luteus should show minimum to no effect to amphotericin and shows the most effect to penicillin.
Methods:
The experement was carried over two weeks:
First week:
4 Petri plates of TSA (Trypticase soy agar) and 4 PDA (Potato Dextrose Agar) Petri plates were provided. First, the 4 TSA plates were labled by the names of the group partners and with the type of chemotharay that was used in later.This experement used Penicillin, 5-flouroaracil, amphotericin and distal water as a negative control. A sterile swab was used to completely swab each of the 4 TSA plates after being put into the culture of M. luteus so to distribute M. luteus over each plate. Then sets of serial dilutions were preformed using sterile distilled water to make 1 x 10-5 M (10 μM) and 1 x 10-6 M (1 μM) concentrations of each chemotharay. Three equally spaced plugs were removed from each plate to form three wells. Those three wells were labeled as -4, -5, -6 to be used later for the different drug concentrations. Finally, 20 µl of each drug concentrations were placed each in their distinguish well. One plate was for Penicillin. Another for 5-flouroaracil and the last two, one had amphotericin concentrations and the other one distilled water. The plates were kept upright all the time and all the 4 plates of TSA were taped up together using sellotape at this point. The plated were then incubated for 2 days at 30oC and then refrigerated. For the PDA plates a “plug” of Pythium spp. was placed in the middle of each plate using a flamed cork borer instead of swabbing the plates with a sterile swab that was put into M. luteus culture. All other steps were taking exactly the same for the BDA as were done for the TSA.
Second week:
All eight plates were collected and were measured for the size of the zone of inhibition diameter in mm around each well.
Results:
Fig 1. The effect of different Penicillin concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Penicillin.
Fig 2. The effect of different 5-fluorouracil concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of 5-fluorouracil.
Fig 3. The effect of different Amphotericin concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Amphotericin.
Fig 4. The effect of different Penicillin concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Penicillin.
Fig 5. The effect of different 5-fluorouracil concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of 5-fluorouracil.
Fig 6. The effect of different Amphotericin concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Amphotericin.
As shown in figures one to six, TSA plates showed the largest diameter for the zone of inhibitions with Penicillin and the smallest with Amphotericin where it is exactly the opposite for the PDA plates. The two plates of distilled water showed zero inhibition.
Discussion: discuss how your results support or do not support your original hypothesis. based on the lab results. talk about the mechanism of action and why you used dital water as a control.
What do your results show?
How do they compare to expected results?
The mechanism of action of each drug used.
Why did some drugs not work?
up to 1000 word.
The experiment used 3 chemotherapies:
Penicillin
5-flouroaracil
amphotericin
Both Penicillin and 5-flouroaracil uses the same action mechanism which is peptidoglycan. Peptidoglycan is only found in bacteria. Those two drugs affect peptidoglycan and therefore it only affect bacteria and not fungi. Those two drugs cannot pass through the cell wall of fungi. The action mechanism of amphotericin is Classed as an anti-fungal medication. Amphotericin binds to Ergosterol which is found in fungi cell wall. And then it Creates pores that cause leakage of monovalent ions e.g. K+, Na+, H+ and Cl- that triggers cell death.
the chemotherapies such as penicillin would destroy the cell wall of the drugged organisim and therefore this chemotherapies would be able to affect that oragnisim.
Amphotericin affects only fungi but not bacteria. It does not bind to bacteria.
5-flouroaracil would Converted the patient uracil to the “fraudulent” nucleotide fluorodeoxyuridine monophosphate. (fdUMP; an analogue of dUMP) and inhibits thymidylate (dTMP) biosynthesis
The methane group is coming from folic acid
dUMP turn to dtmp
all of this done to stop the replication of DNA.
Distal water was used as a negative control and that is why It had no effect on the organism.
Because there is no ergosterol in bacteria then amphotericin would not affect the bacteria.
Amphotericin: mechanism of action:
Amphotericin is an anti-fungal medication. it binds to ergosterol. Ergosterol is found in fungal cell membranes and has similar functions to cholesterol associated with mammalian cells.It then creates pores that cause leakage of monovalent ions e.g. K+, Na+, H+ and Cl- that ultimately triggers cell death.
Penicillin: mechanism of action
Penicillin is Classed as an anti-bacterial medication. Penicillin inhibits peptidoglycan synthesis on the bacterial cell wall.
5-fluorouracil (5-FU): mechanism of action: got 3 mechanism of actions
1. Classed as an anti-cancer medication
Converted to the “fraudulent” nucleotide fluorodeoxyuridine monophosphate
(fdUMP; an analogue of dUMP) and inhibits thymidylate (dTMP) biosynthesis
2. Inhibits thymidylate synthetase. The C-F bond less susceptible to enzymic
cleavage. Blocks DNA synthesis but not RNA or protein
synthesis
3.Anti-fungal agent flucytosine (5-FC) is converted intrafungally into 5-FU
clear inhibition for Amphotericin on the fungi plate only with no effect on the bacterial plate. the more the concentration the larger the inhibition so -4 has more inhibition than -5 and -5 more than -6.
Penicillin is the opposite of Amphotericin.
References
Title: Selective Toxicity Formal Lab Report
Abstract: a brief summary of the method, results and conclusion of the experiment. Easier to do at the end. A single paragraph and written in the present tense. up to 200 words
Introduction:

Back in time Paul Erlich defined chemotherapy as “the use of drugs to injure an invading organism without injury to the host.” (p.207 of the selective toxicity book) The general term of chemotherapy is vastly used to refer to a type of a treatment that is used for cancer; however, there is more to it. Chemotherapy is referred to as a drug when it is meant to be used on humans or animals where it is called agricultural agent when it is used for fungi and insects. (p.3-4 of the selective toxicity book) Today chemotherapies are used for vast number of things that all aim to treat or prevent diseases. Moreover, there are those chemotherapies that work on bacteria only or fungi only and there are those chemotherapies that work on multiple types of organisms. However, most drugs are toxic and threshold poisons.(Chapter 4 of Drug Toxicity and Poisoning by Kavin C. Osterhoudt; Trevor M. Penning) It is important to understand that toxicity in a drug is valuable only when it is selective. (p.4 of the selective toxicity book) An example of drugs selective toxicity is chemotherapy used to treat cancer. The aim of that chemotherapy is only to kill the cancer cells but not other healthy cells of the human body. Selective toxicity of drugs can only be achieved owing to differences in biotransformation processes. (Selective toxicity of antibacterial agents—still a valid concept or do we miss chances and ignore risks? written by )The purpose of this experiment is to investigate the selective toxicity of amphotericin, penicillin and 5-Fluorouracil on the growth of Micrococcus luteus and Pythium spp. Micrococcus luteus is a gram-positive bacterium where Pythium spp. are soil borne pathogens that infect plants and are formally classified as fungi. The experiment investigates how those different drugs affect these two organisms and how selective are they for each of the organisms in the aim of treating bacterial infections and cancer. Based on the mechanisms of action for amphotericin, penicillin and 5-Fluorouracil, Pythium spp should show the largest inhibition to amphotericin where micrococcus luteus should show minimum to no effect to amphotericin and shows the most effect to penicillin.
Methods:
The experement was carried over two weeks:
First week:
4 Petri plates of TSA (Trypticase soy agar) and 4 PDA (Potato Dextrose Agar) Petri plates were provided. First, the 4 TSA plates were labled by the names of the group partners and with the type of chemotharay that was used in later.This experement used Penicillin, 5-flouroaracil, amphotericin and distal water as a negative control. A sterile swab was used to completely swab each of the 4 TSA plates after being put into the culture of M. luteus so to distribute M. luteus over each plate. Then sets of serial dilutions were preformed using sterile distilled water to make 1 x 10-5 M (10 μM) and 1 x 10-6 M (1 μM) concentrations of each chemotharay. Three equally spaced plugs were removed from each plate to form three wells. Those three wells were labeled as -4, -5, -6 to be used later for the different drug concentrations. Finally, 20 µl of each drug concentrations were placed each in their distinguish well. One plate was for Penicillin. Another for 5-flouroaracil and the last two, one had amphotericin concentrations and the other one distilled water. The plates were kept upright all the time and all the 4 plates of TSA were taped up together using sellotape at this point. The plated were then incubated for 2 days at 30oC and then refrigerated. For the PDA plates a “plug” of Pythium spp. was placed in the middle of each plate using a flamed cork borer instead of swabbing the plates with a sterile swab that was put into M. luteus culture. All other steps were taking exactly the same for the BDA as were done for the TSA.
Second week:
All eight plates were collected and were measured for the size of the zone of inhibition diameter in mm around each well.
Results:
Fig 1. The effect of different Penicillin concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Penicillin.
Fig 2. The effect of different 5-fluorouracil concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of 5-fluorouracil.
Fig 3. The effect of different Amphotericin concentrations on the size of the zone of inhibition for TSA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Amphotericin.
Fig 4. The effect of different Penicillin concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Penicillin.
Fig 5. The effect of different 5-fluorouracil concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of 5-fluorouracil.
Fig 6. The effect of different Amphotericin concentrations on the size of the zone of inhibition for PDA. Bar number 1 represent 100 uM concentration, number 2 represent 10 uM concentration and number 3 represent 1 uM concentration of Amphotericin.
As shown in figures one to six, TSA plates showed the largest diameter for the zone of inhibitions with Penicillin and the smallest with Amphotericin where it is exactly the opposite for the PDA plates. The two plates of distilled water showed zero inhibition.
Discussion: discuss how your results support or do not support your original hypothesis. based on the lab results. talk about the mechanism of action and why you used dital water as a control.
What do your results show?
How do they compare to expected results?
The mechanism of action of each drug used.
Why did some drugs not work?
up to 1000 word.
The experiment used 3 chemotherapies:
Penicillin
5-flouroaracil
amphotericin
Both Penicillin and 5-flouroaracil uses the same action mechanism which is peptidoglycan. Peptidoglycan is only found in bacteria. Those two drugs affect peptidoglycan and therefore it only affect bacteria and not fungi. Those two drugs cannot pass through the cell wall of fungi. The action mechanism of amphotericin is Classed as an anti-fungal medication. Amphotericin binds to Ergosterol which is found in fungi cell wall. And then it Creates pores that cause leakage of monovalent ions e.g. K+, Na+, H+ and Cl- that triggers cell death.
the chemotherapies such as penicillin would destroy the cell wall of the drugged organisim and therefore this chemotherapies would be able to affect that oragnisim.
Amphotericin affects only fungi but not bacteria. It does not bind to bacteria.
5-flouroaracil would Converted the patient uracil to the “fraudulent” nucleotide fluorodeoxyuridine monophosphate. (fdUMP; an analogue of dUMP) and inhibits thymidylate (dTMP) biosynthesis
The methane group is coming from folic acid
dUMP turn to dtmp
all of this done to stop the replication of DNA.
Distal water was used as a negative control and that is why It had no effect on the organism.
Because there is no ergosterol in bacteria then amphotericin would not affect the bacteria.
Amphotericin: mechanism of action:
Amphotericin is an anti-fungal medication. it binds to ergosterol. Ergosterol is found in fungal cell membranes and has similar functions to cholesterol associated with mammalian cells.It then creates pores that cause leakage of monovalent ions e.g. K+, Na+, H+ and Cl- that ultimately triggers cell death.
Penicillin: mechanism of action
Penicillin is Classed as an anti-bacterial medication. Penicillin inhibits peptidoglycan synthesis on the bacterial cell wall.
5-fluorouracil (5-FU): mechanism of action: got 3 mechanism of actions
1. Classed as an anti-cancer medication
Converted to the “fraudulent” nucleotide fluorodeoxyuridine monophosphate
(fdUMP; an analogue of dUMP) and inhibits thymidylate (dTMP) biosynthesis
2. Inhibits thymidylate synthetase. The C-F bond less susceptible to enzymic
cleavage. Blocks DNA synthesis but not RNA or protein
synthesis
3.Anti-fungal agent flucytosine (5-FC) is converted intrafungally into 5-FU
clear inhibition for Amphotericin on the fungi plate only with no effect on the bacterial plate. the more the concentration the larger the inhibition so -4 has more inhibition than -5 and -5 more than -6.
Penicillin is the opposite of Amphotericin.
References