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December 30, 2013

study showed extensive agricultural use of antibiotics creates public health crisis

Antibiotics discs-howtobioDec. 26, 2013 — “Citing an overabundance in the use of antibiotics by the agriculture and aquaculture industries that poses a threat to public health, economics professor Aidan Hollis has proposed a solution in the form of user fees on the non-human use of antibiotics.”
In a newly released paper published in the New England Journal of Medicine, Hollis and co-author Ziana Ahmed state that in the United States 80 per cent of the antibiotics in the country are consumed in agriculture and aquaculture for the purpose of increasing food production. This flood of antibiotics released into the environment -- sprayed on fruit trees and fed to the likes of livestock, poultry and salmon, among other uses -- has led bacteria to evolve, Hollis writes. Mounting evidence cited in the journal shows resistant pathogens are emerging in the wake of this veritable flood of antibiotics -- resulting in an increase in bacteria that is immune to available treatments.

If the problem is left unchecked, this will create a health crisis on a global scale, Hollis says.

Hollis suggest that the predicament could be greatly alleviated by imposing a user fee on the non-human uses of antibiotics, similar to the way in which logging companies pay stumpage fees and oil companies pay royalties.

antibiotics uses-howtobio
Estimated Annual consumption
 of antibiotics in US.
Data are shown as approximate numbers
of kilograms of antibiotics used per year.
"Modern medicine relies on antibiotics to kill off bacterial infections," explains Hollis. "This is incredibly important. Without effective antibiotics, any surgery -- even minor ones -- will become extremely risky. Cancer therapies, similarly, are dependent on the availability of effective antimicrobials. Ordinary infections will kill otherwise healthy people."

Bacteria that can effectively resist antibiotics will thrive, Hollis adds, reproducing rapidly and spreading in various ways. "It's not just the food we eat," he says. "Bacteria is spread in the environment; it might wind up on a doorknob. You walk away with the bacteria on you and you share it with the next person you come into contact with. If you become infected with resistant bacteria, antibiotics won't provide any relief."

While the vast majority of antibiotic use has gone towards increasing productivity in agriculture, Hollis asserts that most of these applications are of "low value." "It's about increasing the efficiency of food so you can reduce the amount of grain you feed the cattle," says Hollis. "It's about giving antibiotics to baby chicks because it reduces the likelihood that they're going to get sick when you cram them together in unsanitary conditions.

Pig farm-howtobio
A Commercial Pig farming operation- Antibiotics are fed to pigs to speed up growth and increase the
 efficiency of their digestion. Image by Lou Gold (Creative Commons license BY-NC-SA 2.0)
"These methods are obviously profitable to the farmers, but that doesn't mean it's generating a huge benefit. In fact, the profitability is usually quite marginal. "The real value of antibiotics is saving people from dying. Everything else is trivial." While banning the use of antibiotics in food production is challenging, establishing a user fee makes good sense, according to Hollis.

Such a practice would deter the low-value use of antibiotics, with higher costs encouraging farmers to improve their animal management methods and to adopt better substitutes for the drugs, such as vaccinations.Hollis also suggests that an international treaty could ideally be imposed. "Resistant bacteria do not respect national borders," he says. He adds that such a treaty might have a fair chance of attaining international compliance, as governments tend to be motivated by revenue collection.

Hollis notes that in the U.S., a move has been made to control the non-human use of antibiotics, with the FDA recently seeking voluntary limits on the use of antibiotics for animal growth promotion on farms.
He asks: "Is the Canadian government going to take any action to control the use of antibiotics for food production purposes? Health Canada is trying to monitor the use of antibiotics, but has virtually no control over use."

Story Source

The above story is based on materials provided by University of Calgary, via EurekAlert!, a service of AAAS.

Journal reference:
Aidan Hollis, Ziana Ahmed. Preserving Antibiotics, Rationally. New England Journal of Medicine, 2013; 369 (26): 2474 DOI: 10.1056/NEJMp1311479.

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Materials may be edited for content, length and for making it understandable. For original news and know more kindly refer the source and mentioned journal reference.

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scientists reported new genetic risk factor linked to type-II diabetes

Diabetes testing-howtobio
Diabetes mellitus type 2  formerly known as noninsulin
-dependent diabetes mellitus (NIDDM) or adult-onset
diabetes is a metabolic disorder that is characterized by
high blood glucose in the context of insulin resistance
and relative insulin deficiency
Dec. 26, 2013 — “An international team of researchers in Mexico and the United States has uncovered a new genetic clue that contributes to an increased risk of developing type 2 diabetes, particularly the elevated risk among Mexican and other Latin American populations.”

The team, known as the SIGMA (Slim Initiative in Genomic Medicine for the Americas) Type 2 Diabetes Consortium, performed the largest genetic study to date in Mexican and Mexican American populations, discovering a risk gene for type 2 diabetes that had gone undetected in previous efforts. People who carry the higher risk version of the gene are 25 percent more likely to have diabetes than those who do not, and people who inherited copies from both parents are 50 percent more likely to have diabetes. The higher risk form of the gene has been found in up to half of people who have recent Native American ancestry, including Latin Americans. The variant is found in about 20 percent of East Asians and is rare in populations from Europe and Africa.The elevated frequency of this risk gene in Latin Americans could account for as much as 20 percent of the populations' increased prevalence of type 2 diabetes -- the origins of which are not well understood.

"To date, genetic studies have largely used samples from people of European or Asian ancestry, which makes it possible to miss culprit genes that are altered at different frequencies in other populations," said co-corresponding author José Florez, a Broad associate member, an associate professor of medicine at Harvard Medical School and an Assistant Physician in the Diabetes Unit and the Center for Human Genetic Research at the Massachusetts General Hospital. "By expanding our search to include samples from Mexico and Latin America, we've found one of the strongest genetic risk factors discovered to date, which could illuminate new pathways to target with drugs and a deeper understanding of the disease."
A description of the discovery of the newly implicated gene -- named SLC16A11 -- and the consortium's efforts to characterize it, appear online in Nature December 25.

"We conducted the largest and most comprehensive genomic study of type 2 diabetes in Mexican populations to date. In addition to validating the relevance to Mexico of already known genetic risk factors, we discovered a major new risk factor that is much more common in Latin American populations than in other populations around the world. We are already using this information to design new studies that aim to understand how this variant influences metabolism and disease, with the hope of eventually developing improved risk assessment and possibly therapy," said Teresa Tusie-Luna, project leader at the Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán and principal investigator at the Biomedical Research Institute, National University of Mexico.

TD2-SIGMA-press-release-howtobio
The above map shows relative rates of type 2 diabetes in countries in the Americas. By studying Mexican and Latin American populations, the SIGMA Type 2 Diabetes Consortium uncovered a new genetic risk factor for type 2 diabetes that could account for as much as 20 percent of the populations’ increased prevalence of type 2 diabetes — the origins of which are not well understood. (Credit: Image adapted by Lauren Solomon, Broad Communications, from International Diabetes Federation)
This work was conducted as part of the Slim Initiative for Genomic Medicine for the Americas (SIGMA), a joint U.S.-Mexico project funded by the Carlos Slim Foundation through the Carlos Slim Health Institute. SIGMA focuses on several key diseases with particular relevance to public health in Mexico and Latin America, including type 2 diabetes and cancer. The current paper is the team's first report on type 2 diabetes.

"For the Carlos Slim Foundation, the SIGMA project has been a story of total success. Our extraordinary partners, both in Mexico and the U.S., have made it possible to make historic advances in the understanding of the basic causes of type 2 diabetes mellitus. We hope that through our contributions we will be able to improve the ways in which the disease is detected, prevented and treated," said Roberto Tapia-Conyer, CEO of the Carlos Slim Foundation.

The frequency pattern for this variant of SLC16A11 is somewhat unusual. Humans as a species first arose in Africa, so nearly all common human genetic variants are present in African populations. However, the SLC16A11 variant -- despite being common in Native American populations -- is largely absent in African populations, and rare in Europeans. In order to understand this unusual pattern, the team conducted additional genomic analyses, in collaboration with Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology, and discovered that the SLC16A11 sequence associated with risk of type 2 diabetes is found in a newly sequenced Neanderthal genome. Analyses indicate that the higher risk version ofSLC16A11 was introduced into modern humans through mixing with Neanderthal.
Inheriting a gene from Neanderthal ancestors is actually not uncommon: approximately 1 to 2 percent of the sequences present in all modern day humans outside of Africa were inherited from Neanderthals. Importantly, neither people with diabetes nor populations of Native American or Latin American ancestry have an excess of Neanderthal DNA relative to other populations.

Since this is the first time SLC16A11 has been highlighted as playing a role in human disease, little information was previously available about its function. The Nature paper reveals some initial clues about its possible connection to type 2 diabetes.SLC16A11 is part of a family of genes that code for proteins that transport metabolites -- molecules involved in the body's various chemical reactions. The SIGMA Type 2 Diabetes Consortium paper reports that SLC16A11 is expressed in the liver, in a cellular structure called the endoplasmic reticulum. The researchers went on to show that altering the levels of the SLC16A11 protein can change the amount of a type of fat that has previously been implicated in the risk of diabetes. These findings have led the team to hypothesize that SLC16A11 may be involved in the transport of an unknown metabolite that affects fat levels in cells and thereby increases risk of type 2 diabetes.

"One of the most exciting aspects of this work is that we've uncovered a new clue about the biology of diabetes," said co-senior author David Altshuler, deputy director and chief academic officer at the Broad Institute and a Harvard Medical School professor at Massachusetts General Hospital (MGH). "We are now hard at work trying to figure out what is being transported, how this influences triglyceride metabolism, and what steps lead to the development of type 2 diabetes."

Story Source

The above story is based on materials provided by Broad Institute of MIT and Harvard.
 
Journal reference:
Amy L. Williams, Teresa Tusié-Luna et al. Sequence variants in SLC16A11 are a common risk factor for type 2 diabetes in Mexico. Nature, 2013; DOI:10.1038/nature12828

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Materials may be edited for content, length and for making it understandable. For original news and know more kindly refer the source and mentioned journal reference.

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Building a Better Malaria Vaccine: Mixing the Right Cocktail

Dec. 27, 2013 — “A safe and effective malaria vaccine is high on the wish list of most people concerned with global health. Results published on December 26 in PLOS Pathogens suggest how a leading vaccine candidate could be vastly improved. The study, led by Sheetij Dutta, from the Walter Reed Army Institute of Research, USA, and colleagues, focused on a protein called AMA1 needed by the Plasmodium falciparum parasite to invade blood cells and cause disease. Study results suggest that a cocktail of AMA1 proteins from only a few different strains can overcome major limitations of an earlier designed version of AMA1-based vaccines."

The challenge with the malaria parasite in general and its AMA1 surface protein in particular is that both exist as multiple strains. Using AMA1 in a vaccine readies the human immune system for subsequent encounters with the parasite, but when such a vaccine was previously tested in humans, it was effective mostly against one particular P. falciparum strain. To explore the potential for a more broadly protective vaccine, the scientists tested different cocktails of AMA1 from different parasite strains for their ability to elicit a diverse range of antibodies that are active in parasite inhibition assays.

They confirmed that a cocktail of AMA1 proteins from three different parasite strains was better than one or two, and one they call Quadvax, which contained AMA1 proteins derived from four different strains, led to an antibody response that was broader than the sum of strain-specific antibodies elicited by the four individual strains. Moreover, Quadvax-elicited antibodies inhibited a range of parasites, including many strains that were different from those in the Quadvax mix. In different laboratory tests, Quadvax-induced antibodies inhibited the growth of 26 different parasite strains, and the scientists suggest that "the combination of four AMA1 variants in Quadvax may be sufficient to overcome global AMA1 diversity."

Besides varying a lot from strain to strain, AMA1 also contains less variable (conserved) exposed parts (so-called epitopes) on its surface. The researchers found that vaccination with Quadvax yielded not only antibodies against the variable epitopes, but also against more conserved epitopes of the AMA1 protein. Such antibodies were not seen when using individual strains for immunization, but Quadvax appeared to enhance the immunogenicity -- the ability to provoke an antibody response -- of these conserved parts of the protein. Since the epitopes are identical across strains, the resulting antibodies are broadly active rather than strain-specific.

howtobio
Human red blood cells are
surrounded and invaded by
malaria parasites (purple). 
Credit: Sheetij Dutta, CC-BY
The scientists conclude "we had set out to study broadening of antibody responses achieved by mixing AMA1 proteins and were surprised and delighted to find not only greater variety of strain-specific antibodies but also increased antibodies against conserved epitopes were induced by the Quadvax. Perhaps even more exciting, when mixed, combinations of these antibodies were synergistic in their broad inhibition of many parasite strains. Novel conserved epitopes described here can be targets for further improvement of the vaccine. Most importantly, our data strongly supports continued efforts to develop a blood stage vaccine against malaria."
                                                          
In spite of the extreme variability, a vaccine containing only a few diverse AMA1 strains, the scientists hope, could provide universal coverage by redirecting the immune response towards conserved epitopes. The next steps will be to test human-use formulations of Quadvax in primate models and in a human blood-stage challenge model.

Story Source

The above story is retrieved from materials provided by Public Library of Science.

Journal reference:
Sheetij Dutta, Lisa S. Dlugosz, Damien R. Drew, Xiopeng Ge, Diouf Ababacar, Yazmin I. Rovira, J. Kathleen Moch, Meng Shi, Carole A. Long, Michael Foley, James G. Beeson, Robin F. Anders, Kazutoyo Miura, J. David Haynes, Adrian H. Batchelor. Overcoming Antigenic Diversity by Enhancing the Immunogenicity of Conserved Epitopes on the Malaria Vaccine Candidate Apical Membrane Antigen-1.PLoS Pathogens, 2013; 9 (12): e1003840 DOI:10.1371/journal.ppat.1003840

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Materials may be edited for content, length and for making it understandable. For original news and know more kindly refer the source and mentioned journal reference.

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December 27, 2013

Antioxidant drug knocks down multiple sclerosis-like disease in mice

<a href="http://www.random42.com/multiple-sclerosis#images">random42 medical animation</a>

December 27, 2013- “Researchers at Oregon Health & Science University have discovered that an antioxidant designed by scientists more than a dozen years ago to fight damage within human cells significantly helps symptoms in mice that have a multiple sclerosis-like disease.”

The antioxidant — called MitoQ — has shown some promise in fighting neurodegenerative diseases. But this is the first time it has been shown to significantly reverse an MS-like disease in an animal.
The discovery could lead to an entirely new way to treat multiple sclerosis, which affects more than 2.3 million people worldwide.Multiple sclerosis occurs when the body’s immune system attacks the myelin, or the protective sheath, surrounding nerve fibers of the central nervous system. Some underlying nerve fibers are destroyed. Resulting symptoms can include blurred vision and blindness, loss of balance, slurred speech, tremors, numbness and problems with memory and concentration.

The antioxidant research was published in the December edition of Biochimica et Biophysica Acta Molecular Basis of Disease. The research team was led by P. Hemachandra Reddy, Ph.D., an associate scientist in the Division of Neuroscience at OHSU’s Oregon National Primate Research Center.
P-Hemachandra-Reddy
P. Hemachandra Reddy, Ph.D. who
led the research is associate scientist
in the division of Neuroscience at
Oregon  National Primate Research
Center


To conduct their study, the researchers induced mice to contract a disease called experimental autoimmune encephalomyelitis, or EAE, which is very similar to MS in humans. They separated mice into four groups: a group with EAE only; a group that was given the EAE, then treated with the MitoQ; a third group that was given the MitoQ first, then given the EAE; and a fourth “control” group of mice without EAE and without any other treatment.

After 14 days, the EAE mice that had been treated with the MitoQ exhibited reduced inflammatory markers and increased neuronal activity in the spinal cord — an affected brain region in MS — that showed their EAE symptoms were being improved by the treatment. The mice also showed reduced loss of axons, or nerve fibers and reduced neurological disabilities associated with the EAE. The mice that had been pre-treated with the MitoQ showed the least problems. The mice that had been treated with MitoQ after EAE also showed many fewer problems than mice who were just induced to get the EAE and then given no treatment.

“The MitoQ also significantly reduced inflammation of the neurons and reduced demyelination,” Reddy said. “These results are really exciting. This could be a new front in the fight against MS.”

White mouse
Mice were  induced to contract a disease called experimental
autoimmune encephalomyelitis,which is similar to MS in 
humans to build model for MS studies.
Even if the treatment continues to show promise, testing in humans would be years away. The next steps for Reddy’s team will be to understand the mechanisms of MitoQ neuroprotection in different regions of the brain, and how MitoQ protects mitochondria within the brain cells of the EAE mice. Mitochondria, components within all human cells, convert energy into forms that are usable by the cell.
There is a built-in advantage with MitoQ. Unlike many new drugs, MitoQ has been tested for safety in numerous clinical trails with humans. Since its development in the late 1990s, researchers have tested MitoQ’s ability to decrease oxidative damage in mitochondria.

“It appears that MitoQ enters neuronal mitochondria quickly, scavenges free radicals, reduces oxidative insults produced by elevated inflammation, and maintains or even boosts neuronal energy in affected cells,” said Reddy. The hope has been that MitoQ might help treat neurodegenerative diseases like Alzheimer’s and Parkinson’s. Studies evaluating its helpfulness in treating those diseases are on going.

Story Source

The above story is retrieved from materials provided  at the News Events Page of Oregon Health and Science University Portland, Ore.

Journal reference:
Peizhong Mao, Maria Manczak, Ulziibat P. Shirendeb, P. Hemachandra Reddy, MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1832, Issue 12, December 2013, Pages 2322-2331, ISSN 0925-4439, http://dx.doi.org/10.1016/j.bbadis.2013.09.005.

Note:
Materials may be edited for content, length and for making it understandable. For original news and know more kindly refer the source and mentioned journal reference.

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Harmless Members of Microbiome Spark Immune Reaction in Chronic rhinosinusitis

Dec. 24, 2013- “Saint Louis University researchers have analyzed the microbiomes of people with chronic rhinosinusitis and healthy volunteers and found evidence that some chronic sinus issues may be the result of inflammation triggered by an immune response to otherwise harmless microorganisms in the sinus membranes.”

Chronic stuffy nose? Could be your microbiome
Chronic rhinosinusitis, the inflammation of the sinus
 and nasal passages lasting more than three months
The findings, recently published in JAMA Otolaryngology – Head & Neck Surgery, support mounting evidence that inflammation may be the cause of most chronic rhinosinusitis (CRS) instead of bacterial infection. Study author Rajeev Aurora, Ph.D., professor of molecular microbiology and immunology at Saint Louis University, says that the paper sheds new light on the spectra of microorganisms that live in our bodies and our own immune response to those organisms.

Chronic rhinosinusitis, the inflammation of the sinus and nasal passages lasting more than three months, is one of the most common chronic conditions in the U.S. The condition can be challenging for doctors to treat because the underlying mechanisms causing the condition are not well understood. While antibiotics can help some patients, others are not helped by drugs or more invasive treatments, such as surgery to open up sinuses. Doctors have proposed any number of causes, included allergy, immune deficiency, cystic fibrosis, gastroesophageal reflux, and structural abnormalities, but questions remain about the origin of the condition.

Aurora_300
Study author Rajeev Aurora, Ph.D., professor
 of molecular microbiology and immunology at
 Saint Louis University, says that the paper
 sheds new light on the spectra of microorganisms
 that live in our bodies and our own immune response
 to those organisms.
As scientists are learning more about the body’s microbiome, the specific colonies of microorganisms like bacteria that live in various places in the body, including the mouth, the intestinal tract, and skin, they are becoming aware that the clusters of microbiota can be remarkably different from each other from place to place in the same person, as well as from the microbiota of other people.

Aurora and his research team decided to study the microorganisms that live in the sinus membrane to learn more about their role in CRS. Their initial hypothesis was a simple one: using newly available sequencing techniques, they would compare the bacteria and other microbiota in the sinuses of healthy people and those with CRS, and, if they could pinpoint specific bacteria in those with CRS, they would have their culprit.
In order to access the sinus membrane, Aurora collaborated with assistant professor of otolaryngology at SLU Thomas Sanford, M.D. to collect samples from patients who were undergoing surgery. Thirty patients had chronic rhinosinusitus and 12 were healthy controls, undergoing surgery for other reasons.
Once the samples were gathered, researchers examined two particular microbe genes – bacterial 16S and fungal 18S ribosomal RNA genes– and analyzed them with deep sequencing techniques.
Sanford_300
Thomas Sanford, M.D., assistant professor of
 otolaryngology at SLU,   collected samples
 from patients who were undergoing surgery.
“It turned out that the CRS and control groups were very similar, and the differences were not of the type that that would cause disease,” Aurora said. “It did not appear that a particular microorganism was acting as a pathogen.

“So, we turned to look at the immune system.”
And, indeed, Aurora and his team found that the immune system of those with CRS was activated by the microbiota of healthy individuals.

Further study findings suggested that bacteria and fungi are not causing an infection in the sinuses, but rather, that the immune system was responding to commensals, microorganisms that, themselves, do not harm the human body. When the immune system reacts in a hyper-responsive way, unnecessarily fighting off a harmless microorganism, it can initiate an immune response like inflammation. The body can then get locked into a cycle where inflammation generates more inflammation, causing a chronic condition.

“Patients with CRS are hyper-responsive to normal microbiota,” said Aurora. “Our take-home message is that the problem doesn’t lie in the microbiota. The inflammatory response and the resulting damage from the prolonged inflammation are caused by the body’s own immune response to harmless microbiota.”

For future studies, Aurora is left with another important question to answer. If the immune system is activated in response to commensals, why are only nasal and sinus microbiota and not those in the gut or skin involved?

There is no evidence, for example, that people with CRS also have colitis, another inflammatory condition. It appears that there is some specificity to the reaction to the microbiota in the nasal passages, and future research will explore why the inflammatory reaction appears to be so localized.

There is no evidence, for example, that people with CRS also have colitis, another inflammatory condition. It appears that there is some specificity to the reaction to the microbiota in the nasal passages, and future research will explore why the inflammatory reaction appears to be so localized.

Listen to an explanation of how scientists think the microbiome, disease, and the immune system are related. SLU researcher Rajeev Aurora, Ph.D., builds on the work of scientists Lora Hooper, Ph.D. and Jeffery Gordon, M.D., who described mutualism, the continuum of microbes that range from helpful to harmful.


Story Source

The above story is based on materials provided by  Saint Louis University, Spain.

Journal reference:
Aurora R, Chatterjee D, Hentzleman J, Prasad G, Sindwani R, Sanford T. Contrasting the Microbiomes From Healthy Volunteers and Patients With Chronic Rhinosinusitis. JAMA Otolaryngol Head Neck Surg. 2013;139(12):1328-1338. doi:10.1001/jamaoto.2013.5465.

Note:
Materials may be edited for content, length and for making it understandable. For original news and know more kindly refer the source and mentioned journal reference.

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December 26, 2013

Microbial Staining 101: A Beginners Guide Of Microbial Staining

Most cells and tissues either eukaryotic or prokaryotic are colourless, transparent and lack contrast when viewed either by naked eyes or through microscopic arrangements. This is almost impossible to visualize and  examine these cells in normal conditions. In order to visualize them, providing essential  appropriate contrast into the specimen is important.Two basic methods of contrast development; viz-Optical (using a specific configuration of microscope components) and  staining samples with particular dye are frequently either in alone mode or in combination. In microbial examinations study of size, shape, different cellular structures for characterization of microbial groups largely depends on these staining procedures. We at Howtobio decided to write a complete series dedicated to microbial staining procedures. This series will provide you all the information, required to perfectly stain microorganisms. We will publish articles in several consecutive parts during upcoming weeks. This part is the first part of the series and in this part we  will talk about  the basics of stains and staining in this article.

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