Science topic

Malaria - Science topic

A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.
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Can I perform copy number variant analysis on DNA extracted from asymptomatic malaria patients using qPCR?
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Thank you Fakhr and Hordofa
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With subtle of biological roadblocks and failure of the conventional malaria diagnostic tools to detect low-density parasitaemia, will the current malaria elimination/eradication programs be achievable?
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(PDF) Malaria: an eradicable threat? (researchgate.net)
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It is known that malaria has ruled us for 500,000 years. Since its discovery, microscopy has been a gold standard for diagnosing malaria for more than a century. Since 2010, malaria diagnosis has been expanded through the use of malaria RDTs to reach those in need and limit resources. However, both of these traditional tools produce false-negative results that lead to under-treatment and unwanted costs. Plasmodium parasites seem to learn not to be visible to these tools, except for the NAA methods. The case of P. falciparum is bold and obvious (HRP2/3 gene deletion).
So, can we say that resistance to diagnosis is an emerging problem? Or what other scientific scenarios are there?
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Thanks for your concern, several studies have reported HRP 2/3 gene deletion for P. falciparum. This is a public health threat in malaria diagnosis hence surveillance studies must be done. Kindly read HRP 2/3 gene deletion.
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I want to estimate number of malaria cases averted due to an intervention targeted in reducing malaria incidence. So, how I can estimate it using quarterly incidence survey?
Any suggestion please?
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You can calculate Prevented fraction for the population (PFP) for your outcome (no.of malaria cases averted)
PFP=(incidence rate in the unexposed−incidence rate in the population)/incidence rate in the unexposed
where
The incidence rate in the unexposed refers to no. of malaria cases among people who didn't receive intervention for reducing malaria.
The incidence rate in the population refers to the total no. of malaria cases in the population.
PFP refers to the reduction in the disease burden due to existing exposure levels of intervention, compared with if the whole population was unexposed.
For example, suppose PFP is estimated to be 25%. In that case, it means that, due to existing malaria control activities, malaria incidence is 25% lower than it would have been if the whole population was at risk (no intervention).
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It seems that the issue is not only to develop a vaccine or an effective medical treatment, but is more related to the consequences of an unsanitary environement.
In almost 90 countries and territories, nearly half of the world population lives in areas at risk of malaria transmission.
According to WHO in 2020, 627,000 deaths and 241million clinical cases were caused by malaria. 95% of deaths cases were recorded in Africa.
The Roll Back Malaria partnership launched by WHO, UNICEF, UNDP and the World Bank in October 1998 could not succeed in controlling the spread of the disease.
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Dear colleague,
I fully agree with your statement : «Just eliminate the marshes and stagnant waters (easy said, not done).» It is certainly a hard task to accomplish, but it has to be done.
Many thanks for your useful contribution.
With best regards
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Was wondering if anyone has done any research on cross-border transmission of Malaria between the Shortland Islands (Solomon Islands) and Bougainville (PNG). The two countries are very close to one another at these two points and people travel by sea between these islands. I have not been able to locate any articles.
Kind regards,
Kerre Ann Willsher, PhD,
Rotarians Against Malaria,
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I dont think so.
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Is anyone researching the relationship between malaria and pre eclampsia? Malaria parasites invade the placenta, and are involved with maternal deaths, stillbirth, prematurity and small for gestational age babies. Pre eclampsia emanates from the placenta causing similar problems plus maternal hypertension, oedema and proteinuria, and can move on to eclampsia with fitting and death. Could placental malaria cause pre eclampsia? I was a midwife for many years.
Kerre Ann Willsher, PhD
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This will include checking various literature. Interested though.
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Malaria stain preparation
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Dear Pavan Deshmukh
I propose you a walkthrough of preparation stabilized Wright's stain, dissolve 3.0 g of Wright's stain powder in 1 litre methanol. The composition of the powder was 37% Eosin Y, 33% Methylene Blue and 30% azures and azure eosinate. After 20 minutes of shaking at room temperature and allowing the solution to stand for 2 weeks, undissolved powder was removed by filtration. The filtered stain solution was then diluted to 0.575 absorbence at 650 nm before addition of 0.6% diethylamine hydrochloride stabilizer.
Let me know
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I need an alternative to the use of standard curve for the determination of hemozoin content in the blood of malaria patient.
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@Kang, thank you for this, and the equation; the relationship between absorbance, molar concentration, sample volume and the extinction coefficient please.
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For instance if one wants to assess effects of Malaria on pregnancy outcomes on pregnant mothers with Malaria infection.
Bearing in mind that they have to collect data from patient case notes of these pregnant mothers who had Malaria infection and were previously admitted and delivered their babies at a particular hospital in the past
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I really appreciate the Question.
The d/ce between retrospective cohort(RC) and Cross sectional study(CSS) is
1. RC Assess the outcome whereas CSS asses both outcome and cause of the out come
2. RC is follow up study, CSS is snap shot/see the situation at a point in time
3. RC can help to formulate cause effect relationship but CSS cant.
4. RC have control group CSS dont
Eg1. If there were 2400 workers in a textile factory before 10 year, (at the begnning of 2012) and if u want to asses how the health status of those workers in the last 10 years look like, weather some die before 8/4/3/2/6 year or are healthy. This is dealt by retrospective cohort.
Eg.2 If u want to study the current prevalence of maleria, then the design is cross sectional. No control group you just prepared you, questionnaire go to area/study participants then ask.
Retrospective cohort, you will ask both exposed and non exposed groups
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As known, licorice root is used for the treatment of peptic ulcers, asthma, pharyngitis, malaria, abdominal pain, insomnia and infections.what is the reason of this diversity?
I need a good reference for that.
Best Regards
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Licorice is used to treat dermatitis, liver swelling, mouth sores, and a variety of other ailments, but there is no scientific evidence to back up most of these claims.
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Can anyone help me choose primary antibodies for mouse liver hepatocytes and also in conjunction Cd8 cells. Also Cd3 cells. I want to look at hepatocytes and adjacent immune cells in mice with augmented malaria infections. Thanks. Patrick. I need antibodies that react to mice hepatocytes. And also mouse cd8 and Tcells.
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ممكن ذلك من خلال البحث عن احد يساعدك في ذلك
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Currently, I know of BindingDB but there are not enough drug targets when the canonical smile for Chloroquine was inserted. I have checked different database but the feature is missing in all except BindingDB but not enough drug target to conduct network pharmacology. Please help.
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I think the control measure is more important than treatment in prevalent country
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The Anti-Circumsporozoite Antibody Response Of Children To Seasonal Vaccination With The Rts,S/As01e Malaria Vaccine.
Issaka Sagara et al 2021.
Clinical Infectious Diseases, ciab1017,https://doi.org/10.1093/cid/ciab1017
Abstract
A trial in young African children showed that combining seasonal vaccination with the RTS,S/AS01E vaccine with seasonal malaria chemoprevention reduced the incidence of uncomplicated and severe malaria substantially compared to either intervention given alone. This paper reports the anti-circumsporozoite antibody response to seasonal RTS,S/AS01E vaccination in children in this trial.
Abstract
Background
A trial in young African children showed that combining seasonal vaccination with the RTS,S/AS01E vaccine with seasonal malaria chemoprevention reduced the incidence of uncomplicated and severe malaria substantially compared to either intervention given alone. This paper reports the anti-circumsporozoite antibody response to seasonal RTS,S/AS01E vaccination in children in this trial.
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Malaria is not prevalent in our community so there is no idea about
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Can anyone suggest which solvent is used to solubilize beta-hematin or hemozoin (malaria pigment) ?
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Have you tried with HCL? I think it will help.
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Hi everyone, so I have been running some assays in qpcr(presence/absence experiments).
My experiment is on detection of human malaria parasites.
My positive controls show as present and usually above the target threshold.
However my samples are usually below the target threshold although they yield some curves.
The positive controls have Ct's around 20 and the samples Ct's range from 26 to 30. I use 5ul of DNA for this assay.
I ALSO USE THE ABI 7500 FAST REAL TIME MACHINE.
How do I fix this?
PLEASE NOTE: I have attached some pictures of the results
Thanks.
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Irene-Love Amoah Your samples have curves looking like obtained with significant inhibition of PCR. You can try two-three different protocols/kits for DNA extraction.
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Experts say knowing the vectors present is a key factor in putting an end to high malaria prevalence. Nigeria accounts for the highest malaria cases and global malaria death . .. Finding the way forward
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Malaria transmitted by the bite of mosquitoes is a major public health disease in many countries of the world. Anopheles gambiae sensu stricto is the predominant vector responsible for the transmission of malaria in Nigeria .In addition, Anopheles arabiensis is also an important vector that transmit disease.
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I'm working on malaria DNA extraction.
In my lab, we have DNA sampled extracted from patient's whole blood 3 years ago. This sample can be amplified by our primers (designed to be specific to 18s rRNA gene and other gene), so I use it as a positive control.
Recently, I used QIAamp DNA Blood kit (Qiagen) to extract malarial DNA from malaria-infected patients who had high % parasitemia, also including the previously PCR-positive sample. I followed manufacturer's protocol with 200 µl of heparinized whole blood (acute phase within 14 days after admission to clinic). Yield of DNA appears to be good 30-40 ng/ul per each 100 ul elution. My positive control always gave positive PCR results. Unfortunately, extracted DNA from new 13 samples and a previously PCR-positive sample gave negative PCR results.
Possible causes that I am considering are:
- incomplete malarial cell lysis during DNA extraction
- the presence of inhibitor(s)
- low malaria DNA compared to human DNA
What I have tried:
- adding more DNA template for PCR reaction
- using prolonged lysis time and increased temperature
I would like to know what factor I have to adjust?
Thank you for your kind response.
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Iqra, you can try this protocol, it works well when we extract DNA from old samples stored in the freezer:
1. Prepare 1% saponin: 1ml 10% saponin + 9ml UP water
2. Add 1ml of red blood cells (collected with EDTA) to a Corning tube and add 1% saponin to at least 3x the sample volume; vortex;
3. Incubate 5 minutes at 37°C;
4. Centrifuge 3500 rpm for 5 minutes;
5. Remove supernatant, leaving 2ml of pellet.
6. Add 3 to 8ml of UP water; vortex;
7. Centrifuge 3500 rpm for 5 minutes;
8. If necessary, repeat steps 5, 6, and 7 until you get a clear supernatant without hemoglobin.
9. Remove supernatant leaving only a 200μl pellet.
10. Use this 200μl pellet to start extraction with Qiagen.
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Good afternoon ma, my name is Idemudia Nosakhare Lawrence, I am a PhD research student of the University of Benin, Nigeria trying to look at the "Prevalence and Risk Factors of Antibodies to Artemisinin and Artemisinin Resistance Genes amongst Malaria Patients in Benin City, Nigeria. So i want to know how many genes actually codes for artemisinin resistance and how i can do a collaborative study with you ma  
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Thank you for question and answers!
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Hello,
Does anyone have articles about Malaria cases in the Torres Strait? Papua/New Guinean people often seek treatment for a variety of medical conditions at Saibu Island. Relates to border transmission issue.
Kind regards,
Kerre Ann Willsher, PhD
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Please have a look at this document:
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Several studies have proposed that sickle cell trait individuals (HbAS) confer partial protection against Malaria. Even though the mechanism is not clear, various mechanisms have been proposed as a means of malaria resistance by HbAS individuals of which some are sickling of their RBCs and splenic Phagocytosis. Thinking deep into this, I was wondering why then do people with HbSS develop severe malaria because if these mechanisms contribute to people with the Sickle cell trait malaria resistance, then people who are homozygous to the sickle gene should be more resistant to malaria. Any contribution?
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I made some research and from the attachEd file which was a research conducted by Natasha Archer and some other scientists, they proposed that low oxygen HbS polymerization leads to stalled growth and replication of the Plasmodium parasite and this is my own understanding. So in this case, the level of parasitemia in HbAS Individuals may not be enough to cause virulent malaria. Now in the case of HbSS individual, even though HbS polymerization might not allow parasites to multiply, that process itself isn’t favorable for micro-circulation of important gases like oxygen which leads to some Vaso-occlusive crises, at least HbAS individuals have the normal gene to compensate for that. I would also like to point the fact that the sickle gene does not protect against being infected by the parasites, but it protects affected individuals from developing severe malaria as a result of the P. falciparum infection. Even though parasites may not be able to multiply in HbSS individuals, those parasites that have already infected also adds up to destruction of their red cells causing their anaemia to be worse, that’s why their affected more by the infection. Impaired spleen activities in people known to have the sickle cell disease doesn’t allow total clearacne of the parasites as well.
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Was wondering if anyone has done any research on cross-border transmission of Malaria between the Shortland Islands (Solomon Islands) and Bougainville (PNG). The two countries are very close to one another at these two points and people travel by sea between these islands. I have not been able to locate any articles.
Kind regards,
Kerre Ann Willsher, PhD,
Rotarians Against Malaria,
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Are there any articles on cross-border transmission of Malaria between West Timor and Timor Leste?
Kind regards,
Kerre Ann Willsher, PhD,
Rotarians Against Malaria,
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Is there any chance by which an individual with sickle cell trait can develop virulent malaria disease as a result of P. falciparum infection?
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Paul Marie Bello Mr. Bello, you are talking about coinfection. Maybe you wish to realize that sickle cell anemia and sickle cell trait are not infectious diseases, but genetic disorders.
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I am a Ph.D student of Public Health Microbiology in a Nigerian University. I will be embarking on a research entitled “Polymorphisms of Plasmodium Merozoite Surface Proteins 1 and 2, kelch13 and pfatpase6Genes in Symptomatic Malaria Patients in Calabar, Nigeria. Please I am seriously in need of a grant to mitigate the expected high cost on this research. Many thanks.
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What is you study protoocol? How many samples have ypu collected? Please provide some details.
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The pandemic has revealed how much the rest of the world has been left behind in terms of pharmaceutical/healthcare research. What models can you offer for kick-starting vibrant local financing of drug development in developing countries?
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Dear Dr. Anyam!
I consider your question to be a highly important one, so I did search for YOU resources you might value:
1) Meganck, R.M., Baric, R.S. Developing therapeutic approaches for twenty-first-century emerging infectious viral diseases. Nat Med 27, 401–410 (2021). https://doi.org/10.1038/s41591-021-01282-0 Free access:
2) Verguet, S., Hailu, A., Eregata, G.T. et al. Toward universal health coverage in the post-COVID-19 era. Nat Med 27, 380–387 (2021). https://doi.org/10.1038/s41591-021-01268-y Free access: https://www.nature.com/articles/s41591-021-01268-y
3) Fontecha, G., Sánchez, A.L. What Will Happen to Biomedical Research in Low-and-Middle Income Countries in the PostCOVID-19 World?. Curr Trop Med Rep 8, 1–5 (2021). https://doi.org/10.1007/s40475-020-00223-0 Free access:
Article Dear Author
4) Anser, M.K., Khan, M.A., Zaman, K. et al. Financial development during COVID-19 pandemic: the role of coronavirus testing and functional labs. Financ Innov 7, 9 (2021). https://doi.org/10.1186/s40854-021-00226-4 Free access:
Yours sincerely, Bulcsu Szekely
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I need to collect dry blood spots on filter papers for future PCR analysis. I'll be collecting the blood samples from patients visiting clinics in a community. What is the procedure? How can I be sure of my sample size? What is the best method of storage?
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This is very helpful. Thanks. Yes dried blood can stay in -21C in a sealed bag.
Sam S
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Malaria is the highest killer disease in Africa, yet no vaccine has been developed against it. Any hope in sight?
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Iam asking about the association between monocyte receptor CD163 and severity of malaria
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Hello everyone,
I am about to do my PhD candidacy exam, and one of the evaluators raised an important point of the genotyping malaria project. Basically, in the malaria field it is very common to genotype different strains by using length markers or just polymorphic markers of the same size. The number of different variations of size or SNPs will determine the number of different clones found in a human host infected with malaria. MOI is define as 'multiplicity of infection' and it basically tells you this number of clones found in an individual. When looking at publications, it is very common to see a MOI of 1, 2, 3, 4, 5, and even 6. However, one of my PhD examiners asked this question:
"How is it possible to have 1 to 6 genotypes of malaria, when its genome is 23'000,000 bases, and it can populate the human host to 1x10^12 cells?"
Since then I am struggling with it and I have narrowed down some evidence to answer this question... In the pathogenesis of malaria, it is common to see a few bottlenecks of transmission. When a mosquito inoculates a human host with the plasmodium parasite, between 10 to 200 circumsporozoites will make it to the liver. After an incubation period of 7 to 10 days, each circumsporozoite will release 30,000 daughter cells into the bloodstream. Each cell will replicate into 8-32 times inside a red blood cell (RBC). So in theory, all of these cells should be clones of the parent cells. However that is not the case given that the average mutation rate of malaria is 4x10e-10 base substitutions per mitosis. How can I answer this question?
In practice is common to see the use of polymorphic genes with a expected heterozygosity close to 1.0, that would yield as many genotype retrievals as possible, and those genes typically vary in size of 300 to 500 base pairs. Some people use a panel of microsatellites to determine these genotypes.
Am I missing a key concept here?
Thanks everyone!
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Though mutation rates are high, not all of them need to be fit. The human body puts forward a very impressive immune defense system, so a majority of mutants that are not very efficient will get weeded out. Added to this, the drug selection pressure will also remove unfit mutants. Therefore, of all the variants only a handful of sucessful genotypes can be isolated.
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For malaria research experts/Scientists
I am experiencing a full explanation of the following concept:
I have been looking at the biological threat of malaria to the control efforts, where the world is in the move to eliminating and eradicating malaria for good.
Looking at different perspectives, I have finally arrived at there could be a real diagnostic resistance in malaria.
Does it give a sense in such a pre-elimination era?
I need an experts' view here and stretched my neck to read your prompt responses
Is anyone interested?
please don't hesitate to contact me @:
Abdissa BH
Thanks
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Sorry, I did not understand your phrase "diagnostic resistance". Do you mean to say there is a problem in the investigation, confirmation and reporting of malaria cases ? Can you point out some literature that explains the concept ?
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Malaria caused by Malaria parasites (Plasmodium species) is transmitted by Mosquitoes. Malaria especially in the sub-Saharan African region remains a major public health due to associate high mortality and morbidity particularly in the under-five.
Mosquitoes repellents are a major tool for the control of spread of the disease.
What is your take on the above question?
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Dear Prof. Alegbeleye, in Venezuela since there is a hyperinflation, and we don't have money to buy repellers, I personally have started to use several herbs.
One of them is called locally "ruda", another one are eucalipto leaves. Both have a strong smell that repels mosquitoes.
We have now a zika epidemic again, I guess, and our legs and arms are bitten all time by Dengue, Zika and Malaria mosquitoes (white legs) in most cities and fields. SARS-CoV-20 quarantine makes it worse.
But there aren't statistics provided by health authorities, hereby is hard to prove it, otherwise, my legs and arms are bitten, and I know what I have.
Sometimes these herbs work as repellents, it depends on the local weather. If it becomes warmer is hard to stop the mosquitoes, if it is colder, the herbs help. That is what I observe now.
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The theme of World Malaria Day 2020 is "Zero malaria starts with me." It is a grass-root campaign with an objective to keep malaria high on political agenda, mobilize additional resources and empower communities to take ownership of malaria prevention and care.
The Corona virus has shut down large-scale treatment and prevention programs around the globe, which could send malaria deaths skyrocketing this year. Malaria may back again in its devastating form in Corona crisis and will be the major killer in 2020.
(Source: June 12, FP News & WHO)
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Malaria is a constant disease
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Some researchers have claimed that Hydroxychloroquine (HCQ) can enter cells and make the environment more "alkaline" by soaking up protons. Many publications discuss only 2 nitrogen atoms that can accept a proton, however the molecule possesses 3, and therefore I would be interested to learn about the transport of HCQ, which is in the diacid form in the commercial Sulfate compound, is potentially in a triacid form in the stomach and is known to be predominantly in the diacid form in Blood at pH 7.4.
There is research demonstrating that the acid form is hydrophobic, compared to the neutral compound, which accounts for its much lower activity against Plasmodium, in which the neutral compound is lipophylic.
How many molecules of HCQ per cell have been found in clinical settings, and would this have any real impact on internal pH compared to natural buffers?
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The environment that's supposed to be made more alkaline is only the endosomal compartment, not the entire cell or body. Naturally, endosomes slowly become more acidic, on their way to becoming lysosomes. Many viruses sense this acidification, and use it as a trigger to fire their endosome escape functions and enter the cytoplasm. If this fails, the virus will likely be destroyed once the lysosomes become mature and loaded with protease & RNAse.
To prevent endosome acidification, a traditional chemical buffering system is likely not the correct mechanism. This would more likely be achieved by a specific phamacological mechanism, like interrupting membrane integrity or inhibiting a proton transporter. I have seen remarkably little work on this, and all of it only in cell culture.
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The world war started in silence against the unseen enemy since the beginning of 2020. Just created black smokes disturbing global temperature and so many showdowns were completed all over the world to set the accuracy of nuclear weapons for many decades. Nature has showed its revenge by the smallest weapon so far and we are calling it the deadliest one in this 21st century.
We know about the global influenza pandemic of 1918-1919, which killed more than 20 million people worldwide, and the HIV/AIDS pandemic, which began to accelerate in the early 1980s and continues unabated in some parts of the world. In addition, at least 30 other new and reemerging diseases and syndromes have been recognized since the 1970s
New diseases are superimposed on endemic diseases such as diarrheal diseases, malaria, tuberculosis (TB), and measles, which continue to exact a huge toll. Indeed, malaria and TB, among others, are reemerging in a drug-resistant form. Today, infectious diseases remain the leading cause of death worldwide. Many pathogens are becoming increasingly resistant to standard antimicrobial drugs, making treatment difficult and in some cases impossible. Moreover, chronic conditions generally considered noninfectious actually have been found to have a microbial etiology.
New and Reemerging Diseases: The Importance of Biomedical Research
Anthony S. Fauci
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Despite the fact that emerging and re-emerging diseases pose a serious threat to public health in developing as well as developed nations, we are destroying our ecosystem by damaging the forest. We have published many papers on emerging and re-emerging zoonoses. All our papers are easily available at the Research Gate and Academic.
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If there is any ongoing projects on identifying cures for COVID-19 or an alternative one for Malaria, I'll love to know and most likely be involved if there is a chance, thanks
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Current situation of COVID19 is playing a huge impact on community and the health professionals in Bangladesh like any other affected country. But as a developing country with dense population it is almost impossible to identify and point out the COVID19 cases in mass population living in a non understanding situation. Curretly the testing facility for COVID19 is not available except only one centere in the capital of of Bangladesh. Also this is the time of viral flue presenting with similar symptoms like COVID19 infection. A broad spectrum antibiotic is given to treat and prevent secondary infection during this time in most of the patients. Besides as tropical country malaria is a common disease; often the treatment of malaria is offered based on symptoms only. Chloroquine has been described as a potential anti 2019-nCoV drug along with other antiviral agents. Currently Faviparavir is not available in Bangladesh. So my question is can we prescribe a early treatment in combination with Chloroquine and Azithromycin with or without Glucocorticoids (Depending on cases only) in all the suspected COVID19 cases as a routine (unless there is any existing contraindication to these drugs)? What could be the outcome? What difficulties we might face? What might be the potential risk and befinit situation regarding this regiment?
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NIH begins clinical trial of hydroxychloroquine and azithromycin to treat COVID-19. The Phase 2b trial will enroll approximately 2,000 adults. Though a small trial data from China (DOI: 10.1016/j.ijantimicag.2020.105949) showed promise. While other studies from New York (DOI:10.1001/jama.2020.8630) show no benefit. The data from the NIH trial can clarify the doubt better.
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I am working on liver stage malaria infection.
Please I need:
1. A simplified method of inoculation.
2. A less expensive method of determining the parasite count in the liver.
Thank you.
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Though I never had an opportunity to work on Malaria, I have inoculated the yeast cells of Cryptococcus neoformans in Swiss Albino mice through intro-cerebral route to produce meningo-encephalitis.
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Regarding a research on the effects of humidity to the transmission of Bancroftian filariasis.
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Think as a result of taking precautions and preventing disease
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Covid infections as of today can be dependent variable. Prevalence of TB or Malaria (per 10000 population) in all countries can be independent variable. The problem is a majority of countries have Covid but zero TB or Malaria. Correlation turns out to be positive at p 0.05 . What could be wrong in my design of study?
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Secondly, whether you include the countries with zero TB, you should both consider the statistical principle and practical meaning of your results. I'm not sure what kind of correlation you used, so suggest you to refer to the statistical book and see if your data met the use condition. If met, then you could consider whether the results of including and excluding zero TB countries are the same. If not, think about the differences and which one is more feasible.
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how H CQ+Azi acts against covid 19?
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Kindly discuss your ideas and viewpoints on the probable correlation between the SARS CoV-2 and the malarial parasites.
It is generally observed that the cases of people affected with the COVID-19 is more prevalent in countries where there is very few cases of people suffering from Malaria and vice versa.
As an example we can cite many African countries and tribal areas of India, which have not been seriously hit by COVID-19. At the same place the European countries which had negligible cases of malaria, have turned into the global epicentre for this ongoing pandemic.
It draws a generic attention towards the epidemiological analysis when we considerably observe that even Hydroxychloroquinone and Chloroquinone is commonly prescribed nowadays as an alternative treatment for COVID-19 in many countries. Where these drugs are commonly prescribed for the treatment of malaria.
Even it is quite surprising to speculate - places in central Asia(Mangolia) where liver cancer cases are the maximum, we can observe a very less no. of COVID-19 cases.
So there must/might be any specific underlying mechanism that could be similar in both these pathogens - one a deadly virus and another a detrimental plasmodium!
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What about testing facilities / stigma / cost / hospital attendence?
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Development of the vaccine against the malaria has long been worked upon what is its clinical outcome any experience regarding its current status ?
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Please go through the following link:
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In my country, Jordan, the borders have been closed, tracking cases infected with the virus inside Jordan, quarantine, and the use of malaria treatment for some cases infected with the virus, the curfew for long periods of time with the end of the week the curfew extends to 48 hours, the suspension of work in most sectors, and distance education Online, is this correct?
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Quarantine is a good measure; the anti-malaria treatment with chloroquine/hydroxychloroquine is not established but discussed as an option (clinical trials are currently performed), it is an off-label use but may be justified; curfew of 48 hours appears very short (in other countries it is for several weeks), physical distance is the most important measure. Stay healthy and please follow the recommendations!!
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What is the pathogenesis of anemia caused by malaria?
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Please take a look at the following RG link.
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The COVID-19 pandemic is one of the worst challenges the modern medicine has ever encountered. There is no standard treatment for this infection, and there are many ongoing clinical trials to find a possible treatment regimen. Among different tested medications, chloroquine was promising likely by having immunomodulating properties.
Strangely, the highest mortality rates of the COVID-19 have been reported in the developed countries with robust healthcare systems. The tropical countries have witnessed less fatal cases (1). The less fatality of this virus in these regions (with a high prevalence of malaria) may be related to Hemoglobin structure. Given the natural selection, the structure of Hemoglobin in these regions is slightly different than the rest of the world (e.g., high prevalence of the Hemoglobin S). It is possible that altered Hemoglobin not only helps these people to survive malaria but the COVID-19 virus as well. We suggest adding medications capable of changing the hemoglobin structure to COVID-19 clinical trials. Increasing hemoglobin F level may have a therapeutic effect in these patients (higher levels of hemoglobin F can be a reason for lower mortality in children as well). In this context, “Pomalidomide” appears to be a suitable candidate. Its role in increasing Hemoglobin F level as well as immunomodulatory effects have been well documented (2-4). The same as chloroquine, Pomalidomide can regulate the cytokines. By increasing the Hemoglobin F and immunomodulation, pomalidomide can have dual effects on this infection.
Ehsan Sotoudeh MD
Red Crescent Iranian Hospital in Dubai, Dubai, UAE
Houman Sotoudeh MD
University of Alabama at Birmingham, Alabama, USA
1. Coronavirus COVID-19 Global Cases by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU).
2. Chanan-Khan AA, Swaika A, Paulus A, et al. Pomalidomide: the new immunomodulatory agent for the treatment of multiple myeloma. Blood Cancer J 2013; 3: e143.
3. Meiler SE, Wade M, Kutlar F, et al. Pomalidomide augments fetal hemoglobin production without the myelosuppressive effects of hydroxyurea in transgenic sickle cell mice. Blood 2011; 118(4): 1109-12.
4. Richardson PG, Mark TM, Lacy MQ. Pomalidomide: new immunomodulatory agent with potent antiproliferative effects. Crit Rev Oncol Hematol 2013; 88 Suppl 1: S36-44.
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Never use it in COVID-19, due to a plethora of side effects and teraatogenicity.
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The COVID-19 pandemic is one of the worst challenges the modern medicine has ever encountered. There is no standard treatment for this infection, and there are many ongoing clinical trials to find a possible treatment regimen. Among different tested medications, chloroquine was promising likely by having immunomodulating properties.
Strangely, the highest mortality rates of the COVID-19 have been reported in the developed countries with robust healthcare systems. The tropical countries have witnessed less fatal cases (1). The less fatality of this virus in these regions (with a high prevalence of malaria) may be related to Hemoglobin structure. Given the natural selection, the structure of Hemoglobin in these regions is slightly different than the rest of the world (e.g., high prevalence of the Hemoglobin S). It is possible that altered Hemoglobin not only helps these people to survive malaria but the COVID-19 virus as well. We suggest adding medications capable of changing the hemoglobin structure to COVID-19 clinical trials. Increasing hemoglobin F level may have a therapeutic effect in these patients (higher levels of hemoglobin F can be a reason for lower mortality in children as well). In this context, “Pomalidomide” appears to be a suitable candidate. Its role in increasing Hemoglobin F level as well as immunomodulatory effects have been well documented (2-4). The same as chloroquine, Pomalidomide can regulate the cytokines. By increasing the Hemoglobin F and immunomodulation, pomalidomide can have dual effects on this infection.
Ehsan Sotoudeh MD
Red Crescent Iranian Hospital in Dubai, Dubai, UAE
Houman Sotoudeh MD
University of Alabama at Birmingham, Alabama, USA
1. Coronavirus COVID-19 Global Cases by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins University (JHU).
2. Chanan-Khan AA, Swaika A, Paulus A, et al. Pomalidomide: the new immunomodulatory agent for the treatment of multiple myeloma. Blood Cancer J 2013; 3: e143.
3. Meiler SE, Wade M, Kutlar F, et al. Pomalidomide augments fetal hemoglobin production without the myelosuppressive effects of hydroxyurea in transgenic sickle cell mice. Blood 2011; 118(4): 1109-12.
4. Richardson PG, Mark TM, Lacy MQ. Pomalidomide: new immunomodulatory agent with potent antiproliferative effects. Crit Rev Oncol Hematol 2013; 88 Suppl 1: S36-44.
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Pomalidomide has severe side effects and is certainly not a candidate for treating COVID-19. The most common side effects include diseases of the blood and lymphatic system, including anemia (45.7%), neutropenia (45.3%) and thrombocytopenia (27%), as well as general complaints at the site of administration, including fatigue (28.3 %), pyrexia (21%) and peripheral edema (13%). Infections and infestations, including pneumonia, are also common (10.7%). Peripheral neuropathies were noted in 12.3% of the patients and venous embolic or thrombotic events (VTE) occurred in 3.3% of the patients. The most commonly reported grade 3 or 4 adverse reactions include neutropenia (41.7%), anemia (27%), thrombocytopenia (20.7%), and infections or infestations, including pneumonia (9%). (WP)
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It is said that chloroquine (Anti protozoal drug and has anti inflammatory property usually used to treat malaria and a few chronic inflammatory diseases) assumes to be effective in limiting the replication of SARS-CoV-2 (virus that causes COVID-19) in vitro. [Cortegiani, Andrea; Ingoglia, Giulia; Ippolito, Mariachiara; Giarratano, Antonino; Einav, Sharon (10 March 2020). "A systematic review on the efficacy and safety of chloroquine for the treatment of COVID-19". Journal of Critical Care. doi:10.1016/j.jcrc.2020.03.005. ISSN 0883-9441. PMID 32173110.]
Hydroxychloroquine have similar actions but more available in some countries.
Azithromycin an antibacterial drug used to treat many bacterial infections. It is also used to treat malaria in addition to other drugs.
Do you believe in that Hydroxychloroquine (HCQ) and Azithromycin are effective against SARS-CoV2 (Causes of COVID-19)? If your answer is yes, would please explain, how?
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No Evidence of Rapid Antiviral Clearance or Clinical Benefit with the Combination of Hydroxychloroquine and Azithromycin in Patients with Severe COVID-19 Infection
Jean Michel Molina et al.
PII: S0399-077X(20)30085-8
Reference: MEDMAL 4279
To appear in: Médecine et Maladies Infectieuses
Received Date: 28 March 2020
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Good day house.
I am conducting a research on hemoparasites like plasmodium, hemoproteus, leucocytozoon (Phylum Apicomplexans). Before running my PCR, I intend to check my PCR primers using in silico PCR in the UCSC Genome browser. But I can't find any genome for protozoans/parasites, rather only genomes for the hosts of these parasites are there - homo sapiens, megabats, microbats etc.
Please how do I go about this? I mean which genome can I use on the UCSC genome browser to conduct in silico PCR for protozoans/parasites given that their genomes are not listed?
Secondly, what tools can I use to assess my PCR primers? I mean tools that will easily tell me whether there are hairpins in my primers and possibility of self dimer?
Thanks.
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I just saw your message. Please check with if the assembly is same as you used previously
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How to use malaria parasite prevalence data to determine endemicity
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According to biomedical.net. Crude and age specific all-cause/malaria-specific mortality rates were calculated by dividing the deaths in each group with the total person-years observed (pyo) in that group.
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Indonesia committed to go for malaria elimination, step by step islands wise, beginning in 2010 until 2030, in east part of Indonesia ( Maluku and Papua ).
Indonesia malaria prevalence is on all stages, high endemic need to have control program , meso endedic, low endemic to non endemic areas. This comiitment supported by top leaders as well as inside the MoH organization from central level down to Health centre, It needs all stake holders to work together, supported by community itself.
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The public awareness of malaria needs to improve continuously. Health education campaigns should focus on basic malaria knowledge, Careful planning is required to ensure that even the sparse area of a country are incorporated into the malaria health promotion system to sustain elimination of malaria itself.
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The early stage of malaria parasite life cycle is mainly in the liver, I want to believe continuous life cycle of this parasite in its host could lead to liver damage or may be something as serious as cancer.
How can the long term impact of this parasite on the liver be assessed?
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Please have al look at our paper:#
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Doing a Comparative study on the Cytokine profile of Symptomatic and Asymptomatic Malaria individuals.
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Hi Arrey,
I suggest you should use gene expression method, ELISA has a lot of limitation.
In gene expression you will used real time PCR.
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HMSS- hyper reactive malarial splenomegaly syndrome, is one of the chronic form of malaria. it commonly occurs in peoples from malaria endemic areas who have recurrent malarial attacks.
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Major criteria include the following:
1. Gross splenomegaly 10 cm or more below the costal margin in adults for which no other cause can be found
2. Elevated serum IgM level 2 standard deviations or more above the local mean 3. Clinical and immunologic responses to antimalarial therapy
4. Regression of splenomegaly by 40% by 6 months after start of therapy
5. High antibody levels of Plasmodium species (≥ 1:800)
Minor criteria include the following:
1. Hepatic sinusoidal lymphocytosis
2. Normal cellular and humoral responses to antigenic challenge, including a normal phytohemagglutination response
3. Hypersplenism
4. Lymphocytic proliferation
5. Familial occurrence
It is possible that some of the cases with negative blood films and QBC would have been found positive by the more sensitive PCR. It has recently been suggested by McGregor et al. [1] that subjects with a positive PCR would be more likely to respond to ther-apy than negative subjects, indicating a role of molecular diagnosis in the case definition of the syndrome.
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The indication of tetracyclines in treatment or prophylaxis of malaria is documented well, but the mechanism seems hidden. 
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In Plasmodium falciparum, doxycycline has been observed to block the expression of apicoplast genes, leading to nonfunctional apicoplasts in subsequent progeny, and impeding the development of viable parasites.
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Glucose 6 phospho-dehydrogenase deficiency predisposes malaria patients receiving drugs like primaquine to develop hemolytic anemia.
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The results of some support the limited historical evidence of low G6PD deficiency prevalence in Ethiopia. The A376G (A)mutation observed is a mild deficiency causing around 85% of thenormal enzymatic activity with little clinical significance. The more severe G6PD deficiencyallelic types, G202A (A-) and C563T (Mediterranean), common in Africa were not observed, supporting the safe use of primaquine especially the single low dose for falciparum in Ethiopia.
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Studies have shown poor healthcare professionals' prescription/counselling practices and patients' in-ability to correctly follow their medication regimens as some of the common causes of malaria treatment failure among patients, kindly share your perceptions on the topic, for the purpose of creating awareness.
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MDR malaria, poor nutrition & associated complications, preexisting diseases, reinfestation, carrier, etc are factors of relapses.
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How long does it last? Can it prevent attacks altogether?
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Yes! Please go through the following RG links.
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This is very important if we must prevent deaths especially in children.
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Clinical Aspects and Treatment of Severe Malaria
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In the last few months I observed some acute leukemias associated with positive malaria or with history of recurrent malaria manifestations.
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How the malaria parasite increases the risk of blood cancer
in this link;
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I am working on the association of CLEC4C rs12310416 polymorphism with clinical malaria in children in South Western Nigeria, however, I need a publication that has worked on this before so I can see the primers they used and the restriction enzymes I can use for my research
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Thank you very much Fred,
I'll sure go through the attachments.
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The signs and symptoms of malaria are quite nonspecific - one of the few real distinguishing features is its periodic febrile paroxysms. Hence, what should be the basis for administration of pre-referral artesunate? Is just a history of periodic fever enough? Should you just use a Rapid Diagnostic Test (RDT) to confirm the diagnosis?
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Please, always try to confirm the diagnosis by microscopy, RDT or PCR. Never give Artesunate alone, always in a combination therapy, due to the emergence of possible resistance to artemisinins.
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Any suggestions? I'm trying to get some help by OPS or UNICEF
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¡Por favor infórmeme exactamente sobre sus intereses!
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We have developed a SYBR Green method to reveal our antiplasmodial assays but we have experienced some troubles when testing some pure polyphenols. The fluorescence level of the corresponding wells in the plate was much lower than negative control and thus, inhibition level was higher than 200% for known inactive compounds such as gallic acid. Has anyone observed same interferences ?
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https://apps.who.int › iris › bitstream › handle ›
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I am currently looking for academic professional that can accept my studentship for PhD program in any of the following research area:
1. Antimalarial or anticancer novel compound synthesis and biochemical evaluation.
2. Structural biology of uncharacterized enzyme target for malarial or cancer therapy.
3. And other related research topics.
These studies will involve the use of bioinformatics/computational and biochemical/biophysical techniques.
Country of interest: Brazil, USA, Germany and other available countries.
Kindly let me know your willingness
Kind regards.
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Do you have your own funds?
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Sofola (Delgoa bay), Mozambique, was renown among Portuguese as the Biblical Orphis, with streets paved with gold. Antonio Manutius, in 1538 , recalls this alluvional gold was almost extinguished when Portuguese "conquered it" (before being wipe out by malaria, the proof Romans already knew and used the place). But I consider the last deadly cyclones, in that poor country so dramatically affected, may have unveil new gold deposits. What is your opinion at the respect?
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Most of rich deposited mine/ oil/ Gold ..... countries always suffer from poverty which shows that political approaches of abusing .. ..
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I am currently carrying ou a study on Plasmodium faclciparum malaria and concomitant bacteria infection. I will need an expart to collaborate with especially in molecular epidemiology, and immunology with the possibility to carryout a sandwich PhD study.
Sequel to this I will like to have your kind suggestions that may be of help
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You have to write those persons who are working in your area for research for collaboration.
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I am working on a research to determine the endemicity classes of different regions in a country which means that each region has to have one endemicity class. I am looking for ways of using different classes for each region to come up with my results
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Thanks for all the tips! This was extremely helpful
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I am working on the effect of malaria parasitaemia on cardiac metabolism in adults, the parameters of interest include Lipid profile, Troponin1,Ck Mb, uric acid, Tibc and myoglobin
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Thanks for all the tips! This was extremely helpful
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Dear All,
Kindly, share with me any resources and/or knowledge and experiences regarding studies measuring the efficacy of SP and insecticide treated net, either as independent or combined as interventions against malaria.
There are enough studies, even by WHO, indicating that SP drug (for pregnant women) and ITN are very effective interventions when used as directed and so are highly recommended. But i have not found information in quantitative terms (if any), up to what percentage (say 90%, 55%, etc.) of protection/prophylactic effect the SP drug and/or the ITN provide for the user against malaria infection.
Thank you in advance for your time and for sharing.
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Please, just look the early papers on inttermittent preventive treatment (IPTi and IPTp).
Good luck!
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how does alkaline phosphotatse mediate the pathophysiology of congenital malaria
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@Ishag Adam, yes that's correct. But it's role in placental Malaria as a biomaker for the organ is the question under study
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I trained my deep learning model on several blood smear datasets, each include a certain blood disease: leukemia,malaria,iron-deficiency.
However, i would appreciate to know if there is any dataset that contains other blood diseases or any datasets that contain multi-label samples of these diseases ( for example blood smear image of a patient who is diagnosed with both leukemia and anemia) for multi-label classification.
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I do the same things, but using CBC tests performed by hematological analyzer. I study and create ML models for classifications blood diseases
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I administered alcohol to animals and inoculate them with malaria parasite. The second group was given alcohol without infection. I carried out BAC analysis and discovered that group with infection had higher BAC compared to group without infection.
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sorry I cant get your exact question
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MEFLOQUINE – QUESTIONS ON THE CLINICAL STUDIES
De Souza 1983 A phase I clinical trial of mefloquine in Brazilian male subjects.
Mefloquine, given as a single oral dose of 1000 mg, was compared with a standard antimalarial, sulfadoxine-pyrimethamine, for tolerance and safety in adult male Brazilians from an endemic area.
Usually, phase I studies with new drugs are conducted in normal healthy individuals.
This study, however, differed from the standard practice in that the study group was from a target population, with previous experience of malaria, multiple helminth infections, anaemia, defective nutrition, and enlarged livers and spleens.
The mean Hb was 7.3 mmol/ litre (range, 5.7-8.52) on day 0, and 8.58 mmol/litre (range, 6.16-9.95) on day 63.
The method of selection explains the low body weights, low values for RBC, Hb, erythrocyte volume fraction, and plasma proteins, and high eosinophil count seen in some of the subjects on day - 2. Some also had enlarged livers and spleens and slightly raised SGOT and SGPT values
Thus, it can be considered that the volunteers in the trial were representative of a population in the endemic areas where the use of mefloquine is envisaged.
Question 1
How many illnesses other than malaria were exhibited by the patients in the study
Question 2
Were these the best people for clinical trials to be conducted on for the prevention of malaria
Question 3
Were these the best people for clinical trials of how the drug would perform in a more genetically distinct population?
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Indigenous populations should definitely take part in clinical trials especially if they end up being the target population for the drug. The oddity in this study is the involvement of the target group in phase I of the trial. It is not the current standard since phase I should be performed on healthy individuals with a clean baseline to assess drug tolerance, dosing and safety, in an ideal setting. The indigenous population with comorbidities could have been included in phase III or phase IIIb; when the suitability of the drug in patients with comorbidities and genetic variation is assessed. This would provide the real world risk-benefit analysis of the drugs. The population in this study represent the findings in most patients in the malaria-endemic areas. A drug that may not have significant side effects in phase I may produce marked ADR when combined with the comorbidities and other drugs used to treat the comorbidities. Even hemolysis in case of G6PD would be catastrophic in people with such low Hbs. Not to mention the effect on the under nutrition with low plasma proteins on drug distribution and metabolism. These factors may be missed if such at-risk populations only had drug exposure during Phase IV since pharmacovigilance and ADR reporting systems are relatively poor.
Question 1
How many illnesses other than malaria were exhibited by the patients in the study?
The patients at least 4 illnesses other than malaria, assuming the enlarged spleen was not caused by malaria. Hyperreactive Malarial Splenomegaly Syndrome (HMSS) could have been responsible for all the findings in the volunteers.
Question 2
Were these the best people for clinical trials to be conducted on for the prevention of malaria?
These volunteers would end up being beneficiaries of such a drug trial. However, the population was not ideal to test the efficacy of malaria prophylaxis as the patients may already have had malaria exposure, especially with signs of Hyperactive malarial spleen seen in chronic malaria infestations. They may also have had some partial malaria resistance from repeated exposure. Malaria prevention clinical trials should ideally be performed in malaria naïve patient with new exposure to the risk of malaria, like travelers from non-malaria endemic sites.
Question 3
Were these the best people for clinical trials of how the drug would perform in a more genetically distinct population?
These people may have represented the sickest people with chronic or recurrent malaria. Hence the safety assessment of the drug in phase III or IIIb would be important. However, there were too many confounders present in this group to give a real picture of the drug’s efficacy or safety. It was more likely to attribute any ADR to the comorbidities, drug interactions or chronic malarial infection than a genetic distinction of the population. Especially without controls from the same environment without those diseases/complications to compared to healthy participants of other races in Phase I or II of the clinical trial. Generally, large numbers of people are required to detect rare events in the sub-population with distinct genetic make-up. Hence phase IV clinical trials provide more data on unexpected outcomes due to genetic variations.
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Hi,
Please I need your response to the above question.
I want to test the effectiveness of a malaria RDT kit in the field using blood samples that will be collected from consenting human participants.
In my protocol, the gold standard for comparison is questioned?
What do you think should be the gold standard for comparison? Is it microscopy or PCR or …..?
Thank you
Soniran O.T.(PhD)
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Microscopy is considered standard for clinical diagnostic purposes. For a research, I would suggest PCR since microscopy is subject to the possibility of bias (false negative/positive) due to its dependent operator experience. Also, submicroscopic malaria can be detected my PCR. Best,
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Malaria systems immunology: Plasmodium vivax induces tolerance during primary infection through dysregulation of neutrophils and dendritic cells. Vallejo AF, Read RC, Arevalo-Herrera M, Herrera S, Elliott T, Polak ME. J Infect. 2018 Nov;77(5):440-447.
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Good day house.
Please I want to screen about 100 DNA samples extracted from bats' blood for Plasmodium and its relatives. For the PCR I need positive control. Is it right for me to extract DNA from a Malaria Parasite positive human blood sample as the positive control?
Thanks
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No, the species will be different, although some may be very close. A review of the literature may provide what you need, contact the authors and local zoology people. Good Luck with your research.
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Why don't children with  sickle cell disease have a similar protection?
Why is the protection specific for falciparum malaria and not other types of malaria?
Why is the protection partial?
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Sickle cell anaemia is a hereditary disease caused by a recessive gene. This gene causes the production of abnormal haemoglobin as a result, the shape of the red blood cells (RBCs) containing it becomes distorted and sickle shape.