Science topics: MedicinePathology
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Pathology - Science topic

The precise study and diagnosis of disease. Clinical, theoretical, experimental pathology, and molecular biology of human disease.
Questions related to Pathology
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I used an IHC staining for Pan-cytokeratin to test for metastasis from breast to brain. I am not sure if the only cells found in brain that are stained brown-ish are the tumor cells from breast cancer that metastasized or could be any other type of cell already present in the brain?
Thanks!
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Sorry for the late response. I would like to correlate with H&E. Can you please share that? Thanks
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A patient with desminopathy survived Covid-19 six months ago without pneumonia, but with a temporary loss of smell and taste. After Covid-19, we note an accelerated progression of desminopathy, penetration accelerates, new muscles are quickly involved in the pathological process, muscle mass decreases, and heart function worsens. Perhaps the infection or its consequences are somehow connected with the mechanism of progression of desminopathy?
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To save life in desminopathy, can the body purposefully reduce muscle mass, for example, due to decreased heart function or for another reason?
It is known that when hypothermia, the body sacrifices limbs for survival. Is it possible with desminopathy a similar phenomenon?
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Dear Mozhgan Norouzi, thank you very much for your reply!
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Currently, the powder form of pilocarpine nitrate is not available in chemical companies in my country..So can i use commercially available pilocarpine nitrate eye drops for intraperitoneal injection in rats (used once to stimulate salivary flow at the time of sacrifice) ?
Thanks in advance.
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I'd like to determine microvessel dimensions in various tumor groups and am looking for an online database to draw pathology slides from.
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نعم ولكن تحتاج الى عملية بحث واسعة وكبيرة للحصول عليه
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Dickson quality index (DQI) = total dry mass / (Shoot:Root ratio + SQ)
Where, Sturdiness quotient (sq) = plant height / root collar diameter
How effective is it to calculate DQI when pathogen inoculation was done while seed-sowing, followed by biological control (Trichoderma/ Pseudomonas/ Botanicals application)?
Thanks!
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The rot starts from the root region being completely dark first then pulpy-like appearance.
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How much literature is there on the use of this scoring system to assess the tumour's response to the neoadjuvant stage of therapy?
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Currently, treatment responses are assessed on the basis of measurement of tumor size before and after treatment with serial conventional radiography, such as chest X-ray, computed tomography (CT) or magnetic resonance imaging (MRI)
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Post mortem sample.
Lungs, 100x, red-oil-O staining.
Regardless of the patient's history, would you consider the finding as a fat embolism?
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Agree with Sarah's comments.
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Hi everyone,
I'm looking for Free speech recognition software for pathology.
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It's not free either, but in my opinion, Dragon is not too bad.
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I work with bat's helminths taxonomy. The ideal is to work on fresh hosts, but some bats species are highly threatened and it's not possible to obtain fresh carcasses or other alternatives. For these cases, I'm thinking about recovering the parasites from bats in biological collections. However the helminths recovering is difficult because of the dehydration and stiffening of the viscera when stored in formaldehyde or alcohol solutions. I've been trying to store some samples in water for some hours or days, but the visceras didn't rehydrate at all. Does anyone have some tips?
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The process of fixation is irreversible - I agree to that.
But I am wondering, why you would like to rehydrate the viscera. Wouldn't it be easier to simply 'wash out' the helminths (I suspect that they are in the lumen of the intestines?), then make a cell block of the fluid and then look an it via microscope?
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Unfortunately, we came across tragedy in our personal apple garden and a few of our trees have majorly infected by Fire Blight pathogenic agent. I have attached a few photos of infected trees, I think there is a relationship between the white stains on the bark of the tree and diseases outbreak. I think the more white spots there are, the more the tree is exposed to the disease. However, this is my experimental understanding and I have no academic expertise in this field. That disease has appeared only on the red apple trees.  
I would be very happy if you put me in the right pass and let me know how I can overcome that disease. 
Sincerely yours 
Bagher
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Below mentioned suggestions might be helpful to you -
Select resistant varieties whenever possible.
  1. Avoid heavy pruning or excess applications of nitrogen fertilizer, both of which encourage new growth.
  2. Avoid planting close to wild plants of hawthorn, apple or pear.
  3. As soon as fire blight is discovered, prune off infected branches 1 foot below the diseased sections and burn them to prevent further infection. Dip pruning shears into a 10% alcohol or bleach solution between each cut to avoid transmitting the disease from one branch to another.
  4. Early applications of liquid copper are effective against this plant problem. Mix 0.5 to 2.0 oz per gallon of water and apply at silver tip and bud break — repeat at 3 to 5 day intervals up to petal fall. Use the lower rate if disease pressure is light and the higher rate when conditions favor heavy disease pressure.
  5. Bacterial spread can be reduced by applications of products that contain Streptomyces lydicus as the active ingredient. To obtain best disease control, applications should be made at the start of the bloom period and every five to seven days thereafter.
  6. SERENADE Garden is a broad spectrum, preventative bio-fungicide recommended for the control or suppression of many important plant diseases. For best results, treat prior to foliar disease development or at the first sign of infection. Repeat at 7-day intervals or as needed.
  7. The systemic action of Organocide® Plant Doctor moves throughout the entire plant to treat most common disease problems. Mix 2-1/2 to 5 tsp per gallon of water and apply to foliage. Spray to run-off, as required for disease control.
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Disclaimer: I am not a microbiologist by profession or training and this is a curious/knowledge question
I have read some old articles that suggest the inoculum concentration to be 10^5 according to EUCAST.
I have also read some review articles suggesting 10^8 (0.5McFarland standard)- citing CLSI.
I am not able to download CLSI guidelines, can anyone help me get a copy to read about broth dilution and initial cell density actually prescribed?
Please let me know if these standards have changed? What cell concentration do researchers commonly use to read MIC (in North America or elsewhere)
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In pathological report we often see the sentence: Clinical correlation is recommended.
Can experts let me know whether plant classifications based only on molecular studies is enough to arrive at taxonomic conclusions (like segregation of a new genus, etc) or they should be supported by morphological expressions and their clear cut differences as well?
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This means that it is necessary to take note of all the factors causing this disease through the clinical examination of the patient, and that these examinations should be attached by the physician treating the radiologist so that he can give his medical opinion.
It also applies to plants and others. In general, there must be an integrated medical team that follows up on the situation until it comes out with an accurate diagnostic summary, and similarly for plants and others.
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I am looking for suggestions for credible medical conferences for publication on pathology / infectious diseases.
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Please avoid the Rome conference with everything you have. The journals are bad, very bad (even different journal names on the same PDF) and a google search for "is waset.org legit" has lots of reasons to avoid this completely. One headline on an investigation of them: "How the World Academy of Science, Engineering and Technology became a multimillion dollar organization promoting bullshit science through fake conferences and journals." I am not sure if Lotenna is paid by them to promote the conferences or is just naive, but please do NOT get yourself into that rat hole.
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I have 3 group populations.
Group A has marked nuclear pleomorphism (change in nuclear shape and size), like 1 um, 4um, 2 um, 4um, 6um, 1um, 3um. etc
Group B has also nuclear pleomorphism but not as wide of change as group A
Group C the control group has consistent nuclear size of say 1um for example
I would like to use a stat test to evaluate
1. how significantly different are the groups based on rate of differences
Here are my ideas:
T test probably wont help
I can use clustering analysis
I can do regression analysis
Confidence intervals to show spread of values?
Would ANOVA work?
I just want to visualize and get a P value that these three groups can be different based on variance/change.
Goal is to establish diagnostic criteria based on nuclear size cut offs of either length, width, and circumference of nuclei.
end goal is like 1um - 4um = Grade 1 , 4 - 5um = Grade 2, >6 um = grade 3 and to correlate it to progression free survival.
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One way ANOVA might work but you would need to test its assumptions first, especially homogeneity of variance. Please see my study guide for more information: and the additional material study guide.
If it isn't suitable, apart from Kruskal-Wallis, you can also try Jonckhere-Terpstra which looks for a tend between your groups, which seems to be what you are suggesting.
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COVID-19 is an autoimmune type of disease that is caused (induced) by certain parts of RBD of S protein of SARS-CoV-2.
Atypical pneumonia in SARS-CoV-2 = ILD in myositis/dermatomyositis/antisynthetase/anti-MDA5 syndrome. Exact same CT findings of Ground-glass opacification/opacity (GGO), equal clinical picture, equal laboratory data in patients.
PCR absence of the virus and presence of antibodies with severe symptoms is a concrete sign of autoimmune disease.
More concrete - fast progression of SARS-CoV-2 atypical pneumonia is a result of antinuclear and anticytoplasm autoantibody action on AARS, MDA5.
Vaccines function is to induce immune memory, to tech immune system to produce antibodies fast, memorize immune response, teach and memorize that knowledge.
Current COVID-19 vaccines contain same parts of RBD that cause pathological immune response => it can induce the same immune response as response to SARS-CoV-2 itself + memorize it.
1. This may lead to complications such as autoimmune disease.
2. This may lead to more abnormal immune response if vaccinated individual with memorized immune response will meet a high amount of viral antigens, for example medical personal, front line responders.
In my manuscript I describe the exact pathogenesis of SARS-CoV-2 infections (revealing concrete epitopes) that leads to the COVID, as well as introduce a method of preparation of the vaccine and medicine.
Please, view the brief explanation:
Please, view the complete explanation:
Best Regards,
Mikhail Fedorov
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Abstract: 5 With more than 72 million worldwide recorded cases of COVID-19 so far in 2020, 1.2 million deaths and more than 43 million people recovering from the virus, there a huge risk of further viral spread and mortalities, as well as severe health issues emerging in many survivors. This paper explores the COVID-19 infection mechanism and pathology from a dynorphin and oxytocin neuropeptide framework, and explores the angiotensin system, µ-10 opioid receptor, post viral pathology, and seasonal depression in a literature review and analysis. We details the many factors leading to the well documented elevated pre-infection levels of dynorphin surrounding COVID-19 which may predispose individuals to the virus and detail how oxytocin could be used as prophylactic antiviral, as well as treatment for during and after COVID-19 infection to reduce mortality and residual pathology. Vitamin D 15 and anti-dynorphin agents (hypothetically identified within the actoprotector class) are identified as possible candidates for co-application with oxytocin in a synergistic manner. Furthermore, the paper identifies possible applicability of oxytocin and oxytocin-dynorphin axis adjusting combinations for HIV, which down-regulates the oxytocin receptor and suppresses the immune system. Lastly, the neuropeptides oxytocin and dynorphin are raised 20 as potential biomarkers of disease risk, and assays that can rapidly screen populations for oxytocin and dynorphin levels are proposed, and requires further development.
COVID-19 more severely affects people who suffer from a cluster of conditions such as 5 obesity, old age, diabetes, anxiety, addiction and inflammation1, highlighting a potential link between these conditions. This paper explores these links focusing on dynorphins, which is a neuropeptide group heavily involved in pathologies both physical and mental, and oxytocin, a health promoting neuropeptide co-located with dynorphin in magnocellular neurons. In this paper we show how the antagonistic and autoinhibiting effects dynorphin and oxytocin have 10 on each other form an axis, influencing pathology and phenotypic expression between illness and health.
These preprints need urgent peer review - highly relevant to COVID-19 - any help, comment or link appreciated!
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inspiring and brilliant correlation
good luck
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Isolation of anthracnose fungal pathology?
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Anthracnose that affects most of the horticultural crops is usually caused by Colletotrichum sp. The isolation of the pathogen can be carried out in two ways, Viz Tissue bit culture and single spore isolation. In the tissue bit method the affected leaves are surface sterilised with 3% sodium hypochlorite for 2-3 minutes followed by washing in sterilised water 2-3 times, in LAF . The small lesions along with some healthy portion are cultured on PDA or Water agar. After the visible mycelial growth, the culture is purified by subculturing on PDA in culture plates.
In the single spore isolation, affected fruits are collected and stored in moist chamber until sporulation occurs. Then the spores are collected and cultured on sterilised media.
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how we can calculated LOAEL and NOAEL for toxic pathological dose
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You need experiments or observation of toxic effect at different doses.
NOAEL is highest dose at which no toxic effect is not observable
LOAEL is lowest dose at which toxic effect is observable
see attached WHO guidelines
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The physiological interpretation of the nonlinear results are difficult. Some Studies have shown that reduction of IBI (RR) signal complexity (Thuraisingham 2006;Papaioannou et al. 2006) may be a feature of cardiac pathology. On the other hand, for respiration signal Caldirola et al. (2004) found that greater respiratory entropy could be a factor in vulnerability to panic attacks. Whereas other studies have found that 0.1Hz breathing as the most dynamic state which is characterized by a specific complexity pattern and is potentially beneficial for cardiopulmonary rehabilitation and conditioning(Matić et al. 2020 ). So, its confusing how the reduction in complexity via slow rhythmic breathing is actually potentially beneficial where as it is also a a feature of cardiac pathology? Can anyone solve this dilemma?
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Recently, Frontiers gave me the opportunity to express my thoughts on Heart Rate Variability and the future of its use. (Open Access: Interpretation of Heart Rate Variability: The Art of Looking Through a Keyhole, DOI: 10.3389/fnins.2020.609570). In that paper I stress, like Joseph Arpaia in the earlier part of this thread, the multicausality of HRV, which makes it an unreliable source of diagnostic knowledge, if measured for just a short period of time. The case of 0.1 Hz breathing is a case in point: the usual jumpiness of successive intervals, where many systems at the same time influence the start of the next breath, the height of the systolic pressure etc., is now replaced by a steady, self-repeating wave in all of these systems. That destroys the assumptions of the entropy-calculations, resulting in very low numbers, whatever these numbers mean under normal circumstances. (This only works for someone who is not hyper- or hypoventilating). All in all: if one feels comfortable and relaxed breathing for some time at 0.1 Hz, just do it, don’t mind the HRV-numbers.
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I am medical student. I want robbins pathologie fr deutsch pdf . how am I find this book ?
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If you can read and write in English.English version is easily available.
Not aware about Deutsch version at all
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Enantiornithines are now know to have a unique sternal ossification pattern unlike that of any other known archosaur. It is most likely that this unique pattern derives from a mutation in the enantiornithine lineage, but what kind of mechanism could have resulted in such a massive overhaul of the ossification pattern? What is particularly interesting is that despite the change in overall ossification pattern, the adult sternal morphology is not greatly modified (thus not suggesting the ossification pattern changed for functional reasons).
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I am looking for epidemiologyCTE for 2019 or 2020.
also looking for treatment/management studies
studies identifying tau pathology on postmortem studies.
I have a few but struggling to find more recent info, all the help would be appreciated
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The CARE consortium and Boston University CTE Center may be of interest:
The Federal Interagency Traumatic Brain Injury Research (FITBIR) informatics system was developed to share data across the entire TBI research field and to facilitate collaboration between laboratories, as well as interconnectivity with other informatics platforms and may be of interest:
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Excessive exposure to TNF alpha leads to inflammation, oxidative stress, and other pathological responses in cells like endothelial cells. When cells are treated with TNF alpha, will the receptors (R1 or R2) go up (to echo with by TNF alpha) or down (to protect cells from being damaged)? I was not able to find a reference that gives the answer. I would be very appreciated if anyone knows the answer or if there are any references to share?
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Hello, Hongbing!
The two TNF receptor types trigger distinct and common signaling pathways that can work in an interconnected manner.
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I want to know the effect of temperature on the growth of bacteria, as well as on the ability of bacteria to nitrogen fixation.
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I don know
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Hello
Recently, I am curious to know about mechanisms of endometriosis and signaling pathways.
I have a question about the difference between signaling pathways in benign tumors and malignant tumors.
Since I studied, I noticed that the signaling pathway involved in benign and cancerous cells is similar, like MAPK signaling, Wnt Signaling, Apoptosis, Cell adhesion and angiogenesis.
So, what is the difference between endometriosis and ovary cancer in terms of pathway ?
Thank you in advance.
Kimiya
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It would be better to compare benign and malignant conditions in the same organ/tissue: endometriosis vs endometrial cancer, for example, instead of uterus compared with ovary tissue.
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When it comes to Ambivalence, it can be a symptom of mental illness but it is also something we experience in our everyday life ( I certainly do, and my wife hates it) . Where would you draw the line between normal ambivalence and pathological ambivalence? Also what is the role of attitudes (if any) towards the object? I wrote an article about attitudes a while ago. The article can be found here:
The word is free..
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Dear Sir, Henrik G.S. Arvidsson Before anyone reaches a point where He/She has absurd thoughts of killing their spouses is the time when He/She should draw a line between normal or pathological ambivalence.
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I am testing J20 mice (AD model) in the Y-maze and I would like to see the progression of the cognitive decline by testing at early and late stages of the amyloidosis pathology. However I have not been able to find any paper describing the repetitive use of the Y-maze test. I was wondering whether someone knows if mice can be re-tested after a few months or if the re-exposure to the same test could be a confounding factor for the analysis.
Thanks in advance!
Yasmina
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Yes, after 2 weeks
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When a corona (+)ve patient wins the war against the virus and become healthy. What is the probability that the coronavirus will not be transferred to the next generation of that healthy patient in the future? How does it affect the genes of a corona (+)ve patient?
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COVID-19 is not a genetic disease.
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A study by Peeters et al. (2017) suggests that sugar traps cancer in a 'vicious cycle' which make it more aggressive and harder to treat (1). On the question-and-answer site Quora, Ray Schilling, MD, concludes: "there is a connection between the consumption of sugar and starchy foods and various cancers in man. Animal experiments are useful in suggesting these connections, but many clinical trials including the Women’s Health Initiative have shown that these findings are also true in humans. It is insulin resistance due to sugar and starch overconsumption that is causing cancer" (2).
References
1. Peeters K, Van Leemputte F, Fischer B, Bonini BM, Quezada H, Tsytlonok M, Haesen D, Vanthienen W, Bernardes N, Gonzalez-Blas CB, Janssens V, Tompa P, Versées W, Thevelein JM. Fructose-1,6-bisphosphate couples glycolytic flux to activation of Ras. Nat Commun 2017; 8: 922. doi: 10.1038/s41467-017-01019-z. https://www.nature.com/articles/s41467-017-01019-z.pdf
2. Schilling R. Why isn't sugar portrayed as bad like cigarettes? https://www.quora.com/Why-isnt-sugar-portrayed-as-bad-like-cigarettes
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The fact that cancer cells use more sugar than non-cancer cells, known as the Warburg effect, appears to form the basis of the current question. Nevertheless, it is not yet known if this effect is merely a symptom of cancer or whether it is the cause of cells becoming cancerous. Evidence indicating the way cancer cells metabolize sugar is not conclusive, either. Considering refined or added sugar, the bulk of the available evidence indicates that sugar is not a carcinogen. There is no evidence that eating sugar causes cancer or speeds up its growth. There is also no evidence that eliminating dietary sugar causes cancer to shrink or disappear. However, it is known that eating excess sugar, especially added sugars, can contribute to many chronic diseases such as obesity and diabetes, which are potential risk factors for several types of cancer.
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As we know, not long ago the WHO named Wuhann Pneumonia (SARS-COV 2): Covid-19 (from Coronavirus Disease 2019), which has become a serious pandemic and health emergency with multiple pathological manifestations; Within this framework, we will focus on Covid-19 and prostate cancer: In fact, links between the two have recently been found (Montopoli et al.-Universitá della Svizzera) showing that patients with this type of cancer who receive treatment for androgen inhibition or deprivation have a four times lower risk of being infected by Covid versus those who were not treated like this; It has also been observed -as the eminent Spanish urologist J. Castiñeiras indicates- that men with Coviid-19 but with higher levels of androgens than women die more from this coronavirus
...... Thus, the antiandrogens used in prostate cancer and the TMPRSS2 protease inhibitors may be the therapeutic options of choice in those suffering from prostate cancer and Covid-19 ... but, if this is the case -as the en- Would it be advisable to give antiandrogenic drugs and / or TMPRSS2 protease inhibitors in all adult patients, even without prostate cancer, and also in women?
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Thank you, dear Dra Manal; You are very gentle and kind; may God bless and protect you
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Hello,
I am looking for an image dataset of large stained histology section (WSI). We aim at image registration and in particular, registration of large consecutive histological sections where for each slice different stain is used (such as Cc10, CD31, He, Ki67, proSPC, CNEU, ER, PR).
We have released our dataset for this task, but we feel it can be further enlarged. So we are looking for a reference to other similar data or someone interested in collaboration.
Thanks
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Stanford Tissue Microarray Database
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I am interested in regions of the human brain with both relatively high and low oxygen tension. However, it is difficult to find any data on this, especially for the "steady state" and not in pathology. Does anybody have an idea where to find this?
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If the inter-capillary distances are similar, and the rate of oxygen consumption by murine and human brain tissue is similar the steady state O2 levels will be too.
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I want to know how to look/methods of(analyze and scoring) in different parts pathological section like stroma, Ductal epithelial, epithelial lining, luminal epithelial etc. in a different pathological tissue slide.
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Hi all,
Does eosin stains collagen in IHCs in typical H&E staining? Please share your thoughts below as comments. Please add a reference if possible (much appreciated).
Best,
J.
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Thank you..!!
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A biosafety level is the level of the biocontainment precautions required to isolate dangerous biological agents in an enclosed facility. The levels of containment range from the lowest biosafety level 1 to the highest at level 4. In the United States, the Centers for Disease Control and Prevention (CDC) have specified these levels. In the European Union, the same biosafety levels are defined in a directive. Sabanci University is following the same directive in accordance with Turkish biological safety regulation.
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Genome sequencing helps find vital information, for example the strain type, virulence, location of origin and differences between strains transmitted within the country and in other countries
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You can find a centralized database of genomes on https://www.gisaid.org/ . To access them, you have to register and it can take some time to actually obtain the info. Nevertheless, you can see the authors of the publications and contact them directly.
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) with disease progression, a significant decrease in olfaction is noted. How can this fact be explained?
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I agree with Japneet Kaur. The problem in the cilia of olfactory sensory neurons. The myofibrilar myopathy is a genetic disease that associated with the primary ciliary dyskinesia. The primary ciliary dyskinesia resulted in defective cilia and olfactory receptors.
Attached, please find the article describing both myofibrilar myopathy and primary ciliary dyskinesia.
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Deaer Researchers,
I have isolated 20 to 30 fungal isolates from fruit and now have pure colonies . so i want to identify them on morphologically which fungi are those,
some isolates have spore and i have taken there pictures by microscope and morphologically compared with the available fungi. but
how can compare and identify the the remaining isolates who have no spores but have hyphae, ?
other then ITS or RNA methods.
thanks
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Based on gross and microscopic morphology, one can identify several fungal isolated up to Genus level.
We have developed PHOL stain (1990) and Narayan stain (1997) for the morphological studies of fungi. Also, we have developed Pal sunflower seed medium (1980) for rapid isolation and presumptive identification of Cryptococcus neoformans from clinical and environmental sources including fruits and vegetables.
You are interested, you may please download all our papers from Research Gate.
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COVID- 19
Respiratory infections can be transmitted through droplets of different sizes: when the droplet particles are >5-10 μm in diameter they are referred to as respiratory droplets, and when then are <5μm in diameter, they are referred to as droplet nuclei. According to current evidence, COVID-19 virus is primarily transmitted between people through respiratory droplets and contact routes.2-7 In an analysis of 75,465 COVID-19 cases in China, airborne transmission was not reported.
Droplet transmission occurs when a person is in in close contact (within 1 m) with someone who has respiratory symptoms (e.g., coughing or sneezing) and is therefore at risk of having his/her mucosae (mouth and nose) or conjunctiva (eyes) exposed to potentially infective respiratory droplets. Transmission may also occur through fomites in the immediate environment around the infected person. Therefore, transmission of the COVID-19 virus can occur by direct contact with infected people and indirect contact with surfaces in the immediate environment or with objects used on the infected person (e.g., stethoscope or thermometer). 
Airborne transmission is different from droplet transmission as it refers to the presence of microbes within droplet nuclei, which are generally considered to be particles <5μm in diameter, can remain in the air for long periods of time and be transmitted to others over distances greater than 1 m. 
In the context of COVID-19, airborne transmission may be possible in specific circumstances and settings in which procedures or support treatments that generate aerosols are performed; i.e., endotracheal intubation, bronchoscopy, open suctioning, administration of nebulized treatment, manual ventilation before intubation, turning the patient to the prone position, disconnecting the patient from the ventilator, non-invasive positive-pressure ventilation, tracheostomy, and cardiopulmonary resuscitation. 
There is some evidence that COVID-19 infection may lead to intestinal infection and be present in faeces. However, to date only one study has cultured the COVID-19 virus from a single stool specimen.  There have been no reports of faecal−oral transmission of the COVID-19 virus to date.
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The virus is primarily spread between people during close contact, often via small droplets produced by coughing, sneezing, or talking. While these droplets are produced when breathing out, they usually fall to the ground or onto surfaces rather than remain in the air over long distances.People may also become infected by touching a contaminated surface and then touching their eyes, nose, or mouth. The virus can survive on surfaces for up to 72 hours. It is most contagious during the first three days after the onset of symptoms, although spread may be possible before symptoms appear and in later stages of the disease.
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Khem Raj Meena I agree with you. But everyone is scared again of the vaccination because of the numerous rumours around it
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A hospital-acquired infection (HAI), also known as a nosocomial infection, is an infection that is acquired in a hospital or other health care facility. To emphasize both hospital and nonhospital settings, it is sometimes instead called a health care–associated infection (HAI or HCAI).
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Please see the following RG link.
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Biological techniques are methods or procedures that are used to study living things. They include experimental and computational methods, approaches, protocols and tools for biological research.
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We know that frontline healthcare workers including doctors and nurses get COVID-19 from patients via direct contact. Do laboratory workers who collect nasal swab/ blood specimen or perform PCR test also get COVID-19?
Is there any laboratory acquired corona case reported?
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While laboratory-acquired infections with the Severe Acute Respiratory Syndrome coronavirus (the original SARS-CoV from 2003) have been reported previously in laboratories performing virus propagation, to date, laboratory-acquired infection has not been reported for SARS-CoV-2 (https://www.gov.uk/government/publications/wuhan-novel-coronavirus-guidance-for-clinical-diagnostic-laboratories/wuhan-novel-coronavirus-handling-and-processing-of-laboratory-specimens).
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any idea a bout how bacterial infection due to tissues pathology this could be a link between them or not.
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hello,
yes , effect any type of bacterial infection on histological structure will be a link between them .
there are many articles about this.
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Tissue slide images are used to detect cancer using deep learning most of the work is done what are the new challenges
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Preston Guynn thank you sir for your suggestion
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Any therapeutic drug used for a disease whose pathology does not relate to DNA would bind with DNA anyway. In this case, is it desirable that the drug should be groove binder or intercalator so as to cause minimum alteration in DNA?
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Well, firstly, it is quite wrong and a misconception that any therapeutic drug will eventually bind to DNA, it only occurs in the event of the drug target being nucleic acids. There exists other drugs which will only, and specifically target only specific metabolic, signaling enzymes and microtubules . Now to answer your question regarding Intercalator vs groove binder,
1. DNA intercalators are a group of compounds with diverse structure and the ability to bind firmly but reversibly to DNA by intercalation of a flat, aromatic chromophore between the base pairs. The only recognised forces that maintain the stability of the complex, even more than DNA alone, are van der Waals, hydrogen bonding, hydrophobic effects, and/or charge transfer forces. Classical intercalators have a straight, heteroaromatic ring which comes in between two neighbouring base pairs. Interaction leads to structural changes of the DNA molecule resulting in the partial unwinding of the DNA molecule and extension of DNA chain by one base pair.
2. Minor groove DNA binding compounds are a new family of antineoplastic drugs with representatives already in the process of clinical testing. The structure of these molecules is characterised by several connected aromatic rings that allow freedom of movement and torsion. Binders usually have a characteristic curved shape compatible with the DNA minor groove. This formed complex is stabilised with hydrophobic interactions. Also, DNA binders do not cause significant structural changes in the DNA molecule and no change to the DNA free energy structure. Only in cell level, DNA minor groove binders stop the cell cycle in its G2-M phase.
SO, THE END NOTE - keeping in mind the above points about the Intercalators and the groove binder, definitely Intercalating agents (and drugs) like amonafide, Pyrazolacridine etc pose a greater threat to the DNA as compared to Groove Binders.
I am attaching the links to certain research materials and articles which might help you for further reference and study,
Mišković K, et al. ANTINEOPLASTIC DNA BINDING COMPOUNDS
Kubota Y, et al. INTERCALATION AND GROOVE BINDING MODES
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It is well known that most of the pathological protein deposits contain several different components/proteins, along with the main protein constituent. What are the proteins or components that commonly found in ATTR deposits?
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Dear Behnam,
Thanks for these references, I should have a close look at these.
Best regards,
Mahafuzur
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Can biofilms be seen by pathologists when they do lab studies? For example, if a human has a biofilm in their colon and does a colonoscopy with biopsies sent to the pathologist, could the doctor doing the scope and/or the pathologist reviewing the biopsy actually be able to identify the biofilm? Or is the biofilm too microscopic for even today's advanced imaging.
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not all bacterial may be see in slides , but in general we can see the bacterial colonies in infected tissue section, especially in severe bacterial infection
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is there anyone who study PDL1expression in PB lymphocytes by flow cytometry in healthy controls and in pathological cases ( cancer)
Oddly, we found that healthy controls express more PDL1 than patients with cancer. Any explanation?
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Hi Daniela,
PD-L1 can be constitutively expressed in peripheral lymphocytes from healthy and cancer patients, some issues to consider are:
The panel you are using for analyzing PD-L1 expression and whether you included the corresponding flow cytometry controls.
The parameter you are using to evaluate PD-L1 expression (% or MFI)
If you are running paired samples from cancer and healthy subjects at the same time in the flow cytometer.
Is the distribution of lymphocytic populations similar between cancer and healthy donors? If there is a reduction in one particular population, this might account for a reduced expression of this molecule
Are you stimulating the cells to evaluate the expression of PD-L1? Some stimuli might be too aggressive for lymphocytes from cancer patients and cause cell death.
I hope this helps.
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The global average surface temperature rose 0.6 to 0.9 degrees Celsius (1.1 to 1.6° F) between 1906 and 2005, and the rate of temperature increase has nearly been doubled in the last 50 years. Temperatures are certain to go up further and may lead to fast genetic mutations in some pathogenic microbes to become accustomed to the new climate and proliferate resistant gene distribution over geographies. In addition, the overuses of antibiotics is also triggering the issues at a great step. Near about 10 most deadly bacterial pathogens have already been registered as antibiotic-resistant. Mycobacterium tuberculosis is one of them, that has already been created a huge challenge to overcome in their own right and will only become harder to control as their resistance to antibiotics grows. The development of new antibiotics is slow and difficult work but bacterial resistance is decreasing our arsenal of existing drugs posing a catastrophic threat as ordinary infections become untreatable.
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Addressing the global shortage of, and access to, medicines and vaccines
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My research budget is limited and I want to publish my article in the cheapest way possible. I wanted to find out between behavioral and pathological and other methods. What methods could I choose to publish my article?
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Hi
you can measure telomer length
telomers are critical sequence in chromosomes and they're length directly connect with aging
and for your article you can try free charges journals just like Andrew mentioned
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A patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) was recommended to refuse toothpaste. He continued to brush his teeth twice a day with a toothbrush with only water. As a result, within one month we noted a significant increase in strength and muscle mass in this patient. The patient did not take any medications during this period. After 30 days, the muscle condition returned to its original level. How can this positive effect be explained?
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The toothpaste may affect gut microbiota balance of the digestive tract thus affecting natural PH levels. The triclosan is proving s extremely aggressive. https://stm.sciencemag.org/content/10/443/eaan4116
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I am a Commercial Cannabis Production student looking to identify these fungal colonies based on their morphology on PDA plates. These samples were taken from various locations on campus, and we are to use our resources to identify what they are.
Any personal expertise or links to other helpful resources would be much appreciated!
Thanks in advance.
-Carling
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I suggest you please go for microscopic Lacto-Phenol Cotton Blue staining both for hyphal structure and spore morphology (at 450X and 1000X magnifications), on the basis of which the identification of fungal strains are made.
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For pathological investigation of sensory and motor nerves in lumber region of rat how to isolate and preserve
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In order to harvest the dorsal root ganglion, first perform intracardiac perfusion with PBS containing heparin followed by 4% PFA or 10% neutral buffered formalin. Once this is complete, you will decapitate, use a scalpel to cut rostral-caudal though the skin and fascia. Remove the overlying musculature. Then starting rostral, use a bone nipper or rongeur to cut the spinal column at 10 and 2 o'clock and remove each lamina one by one in this fashion. Once you have performed laminectomy through the lumbar region, you will slowly cut the dorsal and ventral spinal roots, beginning at the cervical region and moving down one level at a time till you free the spinal cord. Be careful to cut these roots as close to the spinal cord as possible or you may remove the DRG by mistake. Once the cord is removed, you should be able to visualize the dorsal root ganglion. USe the images in the linked publication to determine the exact lumbar DRG you want to isolate. At this point, you want to slowly break away the bone that encircles the DRG so that is can be freed. There is a lot of connective tissue so be sure that you have cut throughthis as well. Then you can carefully grab the DRG by one of the protruding nerve roots, careful not to grab the actual ganglion or you can crush the tissue of interest. You can either count down to the level from the floating rib or up via the sciatic nerve. The images should be very helpful.
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The data available in most publications are from 2005 or earlier, was wondering if any one knew of a more recent dependable source?
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Please see the following RG link.
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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 have specimens stored in Formalin 10% for more than 6months.( Due to no resident pathologist in Country). Could they still be processed for His to pathology?
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The quick answer is that it depends on the prep. The length of fixation can vary depending on histology, antibody work, or in situ hybridization work. We can leave samples in fixative for months and still get good results, however if you are doing an in situ hybridization protocol such as RNAscope, than the most you want to fix is for 24-36 hours due to the amount of cross-linking which has to be broken by pretreatments. We routinely fix overnight and rinse the tissue. Sometimes we even stored in buffer for up to a few days. We fix with 4% paraformaledehyde in 1 x PBS, as previous experience using 3% Gluteraldehyde reduced antigens resulting in a less bright signal.
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Dear colleagues;
I look for young scientists for authoring a book deals with subjects belongs to medical biochemistry. Are you interested?
A priority is to the English native speakers
Regards;
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Am very much interested. please how do i contact you . And again what are the subjects of interest
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I have stained some sections of mouse intestinal epithelium for phosphorylated ERK. I would like to count the number of DAB positive cells, and express that as a % of the total number of cells present. I have a few questions - also please see the attached image as an example of the staining.
- What software would you recommend?
- Does anyone know of any fairly specific guides I can find to help me with this?
- Any other guidance?
Thank you for your responses.
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Hi Sarah,
Provided the staining was performed optimally, try QuPath, an user-friendly, open-source program developed by the University of Edinburgh:
Official web site with program to download:
Full instructions here:
Another open source option - Orbit (instructions included):
I hope this helps :)
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Dear,
I am trying to use a 1% agarose gel to replace the current in use HistoGel from Richard-Allan scientific. The HistoGel has tend to dissolve when it goes thru the tissue processor (excelsior).
Now my 1% agarose has dissolved as well. Only some some fragments of the lager pieces where found back.
Please help?
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It was a heating problem. A new tissue processor has fixed the problem and the HistoGel is stable. Thank you
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In a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state), a significant loss of muscle mass is observed after a night's sleep, with its replacement by adipose tissue. How to reduce muscle loss during sleep?
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Dear Ali Javadmanesh, Adrian Fierl, Abdulnabi Abdullamer Matruod, thank you very much for your answers!
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A few (unilateral) adult cochlear implant recipients experience an ipsilateral vestibular deficit after (uneventful) surgery.
Any clues/opinions about the possible underlying pathologic mechanisms?
many thanks
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Valeria Tananska Has given a very comprehensive list of all relevent articles.
Children often show deficits only on assessment ...and most of the time the post surgery vestibular symptoms are temporary ..
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Is there any relation between colchicine ( for FMF  long term) and lung cancer,
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Please refer following article:
Tumor Biology 37 (8), 10653-10664, 2016
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Dr. Gillson did so much research in HPV field and I would like to contact her for more information.
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Kindly go through the following PDF attachment.
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John Huntley and myself are currently guest-editing two volumes for Topics in Geobiology on the evolution and fossil record of parasitism and are having trouble finding a researcher to contribute a chapter on The Evolution and fossil record of gastropods as vectors and hosts for parasites. Gastropods are common intermediate hosts for various parasites which in some cases can even cause characteristic diseases and pathologies. Would there be any (paleo)ecologists, paleontologist, parasitologists or evolutionary paleobiologist who might be able contribute such a chapter this year. We will sent it out for review in addition to reviewing it ourselves. Please sent me an private message or e-mail with a potential outline or potential contributors.
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Follow
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Biological agents (viruses, insects, bacteria, etc) can become resistant to countermeasures (engineered host resistance, drugs, pesticides, etc), but the resistance often comes with a cost. In the absence of the countermeasure, resistant mutants are often less fit and less competitive than wild-type counterparts.
Consequently, I'm wondering if there are any real-world examples of a previously resistant organism becoming susceptible over time in the absence of the countermeasure.
For instance, an insect pest that develops resistance to a pesticide but then loses resistance when that pesticide isn't used for several years.
Or, a chronic infection that is initially treated with a drug, develops resistance, but then becomes susceptible to that drug after a prolonged period of no treatment.
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The best example is the acquired resistance of insects to insecticides. When there is selection of pressure on a population of a pest insect through the continued application of the same insecticidal molecule with the same mode of action, more than 80% of the population acquires resistance in a few generations, but if the insecticide is no longer applied, the populations will become susceptible again in a few generations.
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Hello and good day - I am most interested in your work. As an infrared thermographer, inflammation is the most common finding. I agree with your assessment that MD is the axis of rotation for health/pathology. Much success to you.
Sincerely,
Dr. Jeff Prystupa
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think you
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The difference Warburg effect in cancer metabolism from Pasteur effect in able-bodied metabolism is explained by pathologic shift normal flow energy into pathologic flow energy with disordered normal fluctuation positive gain entropy into negative gain entropy according famous Glansdorff and Prigogine theory.
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Thank you for the article. I have familiarized myself with Abstract of this article which was studied role environmental matrix of cancer cells and metastatic niche via hydroxyliated collagen, i.e. modificated collagen but not production collagen. This interesting work does not reject above presented cancer metabolism mechanism as "aerobic glycolysis" of Warburg effect.
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Hi,
I have a question for unbiased quantification method for tumor section staining.
I am currently doing TUNEL assay on primary breast tumor (Triple negative breast cancers) sections from mice. I have notice that the quantification data is very sensitive to where I take an image of.
In my case, the size of primary tumors were more than 400mm3 when they were collected. And all the tumors, regardless of sham or treatment groups, had varying degrees of necrotic or apoptotic core, which may be attributed to restricted oxygen and nutrition transport?
1.I assume that you should exclude those apoptotic or necrotic core tissues? Then, can I assume that event of necrotic or apoptotic core in primary cancer is completely independent of treatment (chemotherapy)?
2. For TUNEL assay, I observe the TUNEL staining of necrotic tissues that does not colocalize with DAPI staining. And these necrotic tissues, outside of core necrotic tissue, are more frequently observed in drug -treatment group. Would you still consider including those regions without DAPI colocalization?
If anybody give me general guideline for quantification of TUNEL staining or IHC staining, it would be great. I would like to get an experts opinion and be consistent and unbiased in quantification of primary tumor tissue staining.
Thanks!!
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Hello
We stopped using TUNEL as a demonstration of apoptotic cells a long time ago, mainly as a result of the issues you are finding. The TUNEL assay gives far too many false positives, which can result from anoxia, necrosis or even physical shear damage to the tissue. The assay is difficult to perform reproducibly, even on automated platforms.
We now use cleaved caspase 3 IHC, which is fantastically reproducible, easily automated, easy to quantitate and far less likely to give false positives. The antibody is from Abcam (ab13847).
Cheers
Kevin
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I wish to know more about the role of transaminase, alkaline phosphate and creatinekinase in fish clinical diagnosis or pathology
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High levels of transaminase can indicate hepatic damage, skeletal and cardiac muscle damage (ischemia), septicemia, and toxemia.
High levels of alkaline phosphate indicate: biliary obstruction, extensive or generalized bone disease, neoplasms, or septicemia.
high levels of creatinekinasa can indicate: acute and chronic renal failure, obstruction of the primary urinary flow and rupture of the bladder.
Is important to note that these analytes are an orientation tool for diagnosis, do not specify directly damage to tissues or organs.
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I have stored the rat's organ at -80°C. How can I do the histopathology of the hippocampus of rats brain? Because at room temperature organ became melted & flexible.
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1. Defrost the hippocampus.
2. Immediately make an incision by the midline in the tissue with a scalpel.
3. Then put the sample in 10% formalin pH 7.2 to fix it for at least 2 hrs.
4. Perform the inclusion in paraffin and continue with the histopathology routine technique ...
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I have frozen rat kidney and I want to do a histological or pathological study. Can I use frozen tissue or I have to defrost them? If I defrost them, will the integrity of the tissue be destroyed after defrosting or not? Thanks for your attention
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Since the project concerns EM, Ratan, it would be memorable to take similar tissue properly treated and embedded and compare it to the tissue that had been stored frozen, then treated and embedded. You will be shocked to see what happens to the organelles and membranes by unfixed freezing then thawing. Structures such as glycogen, ER, microbodies, mitochondrial cristae, may be almost unrecognizable. This is why, for pathology, such tissue may only be useful at a gross pharmochemical level, and not structural. Once membrane barriers are compromised, you can't be sure where the target compound had been located in the cell, or whether it was intracellular or extracellular.
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Fluorescent intensity of cytosolic GFP of bacterial cell is assumed to be equal to their cell volume? what does it mean?. could anybody explain it why cytosolic GFP? and their intensity considering cell volume.
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Not equal to, but in direct proportion to the cell volume. The fluorescence intensity of GFP expressed as a cytosolic protein is directly proportional to the amount of GFP present, which in turn is directly proportional to the number of cells expressing it. The volume of cytosol is also, of course, directly proportional to the number of cells. Hence, the GFP fluorescence is directly proportional to the volume of cytoplasm of the cells expressing it.
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In our lab, we freeze tissue samples from mice (embedded in OCT); we used to have a few problems with this method, using the standard plastic 15 mm cryomolds (frozen with dry ice & alocohol; or sometimes liquid nitrogen instead) -
1) It was very time-consuming. We would hold each individual cryomold over a beaker f