Molecular magnet could improve cancer immunotherapy

According to new research in cell, chemicals that attract specialised immune cells toward tumours could be used to develop better immunotherapies for cancer patients Scientists at the Francis Crick Institute have discovered that immune cells called Natural Killer cells accumulate in tumours and release chemicals that attract specialised dendritic cells (cDC1)-white blood cells known for triggering anti-cancer immune responses to the tumour.

Genes associated with Natural Killer cells and cDC1 correlated with cancer patient survival in a dataset of over 2,500 patients with skin, breast, neck and lung cancers. A similar correlation was seen in an independent group of breast cancer patients, with a particularly positive outcome for women with triple negative breast cancer, which typically has a poor prognosis. The findings have given a renewed appreciation of the importance of Natural Killer cells and cDC1 in the immune response against cancer.

The team showed that prostaglandin E2 (PGE2), a molecule produced by some cancer cells, suppresses Natural Killer cell activity and reduces the responsiveness of cDC1 to the chemical attractants. This suggests that blocking PGE2 with aspirin might help boost the effectiveness of immunotherapies by restoring cDC1 levels in tumours. The research reveals more about the way the body's immune system interacts with cancer, exposing one way in which cancer can avoid attack. It highlight the complexity of this relationship and reveal another way in which the immune system can be harnessed to treat cancer.
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CAR-T- therapy safe and effective for leukemia

Results of the global, multicenter, pivotal phase 2 study that led to the first FDA approval of a gene therapy/cell therapy approach known as CAR T-cell therapy. The therapy, tisagenlecleucel, uses a patient's own white blood cells that have been genetically re-engineered to specifically target and kill cancer cells. It was approved to treat pediatric acute lymphoblastic leukemia (ALL), the most common childhood cancer. Senior authors on the study include Stephan A. Grupp, MD, PhD, of Children's Hospital of Philadelphia and Michael A. Pulsipher, MD, of Children's Hospital Los Angeles (CHLA).

 Researchers evaluate 75 patients between 3 to 21 years of age with relapsed or treatment refractory B-cell ALL. 61% of these patients had relapsed after allogeneic hematopoietic stem cell transplantation, an intensive therapy intended to be curative and whose failure leaves few remaining options. For comparison, the paper cites another FDA-approved therapy for the treatment of children with relapsed or refractory ALL; it produced a response rate of 20% with a median overall survival time of 13 weeks.

Patients who relapsed after transplant or did not respond to treatment - there wasn't much else we had to offer them and often, they went to hospice. Now, instead of sending them to hospice - we treat them with CAR-T-cells, make them better, then send them home. The updated analysis showed an overall remission rate of 81% within 3 months of treatment. All patients who responded to therapy showed no minimal residual disease by flow cytometry - the most sensitive means of analysis.

Overall survival was 90% at 6 months and 76% at 12 months. The median length of remission was not reached, with tisagenlecleucel remaining in the blood for up to 20 months. CAR-T therapy is truly a game changer for pediatric leukemia. Substantial side effects are associated with this therapy; grade 3 or 4 adverse events that may have been related to the therapy occurred in 73% of patients. The most significant side effects included cytokine release syndrome, often requiring admission to an intensive care unit, and neurological events in 40% of
patients.
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Latent HIV reservoirs show resistance to white blood cells

A recent study by researchers at the George Washington University (GW) found that latent HIV reservoirs show resistance to CD8+ T-cells, a type of white blood cell whose primary function is to kill infected cells.

According to Brad Jones, PhD, primary author of the study and assistant professor of microbiology, immunology, and tropical medicine at the GW School of Medicine and Health Sciences, researchers have identified a barrier.

It is difficult to understand the nature of that barrier, they used the most powerful combinations against these cells, and when the dust settled they found that the virus was present at just as high levels as what was started with.

HIV/AIDS treatment currently includes lifelong, antiretroviral therapy while the search for a cure continues. Persistent, latent reservoirs of the virus make efforts to cure infection difficult. In order to eradicate those HIV reservoirs, researchers must find a way to eliminate persistent populations of cells with integrated HIV proviruses.

The paradigm is aimed at combining latency reversing agents (LRA) with immune effectors, such as T-cells, to wake up the virus and kill the reactivated cells.The study found that latent HIV reservoirs exhibit inherent resistance to CD8+ T-cells.

The team conducted their research using the CD8+ T-cells of people living with HIV, in the combination with LRAs to attack and kill the infected cells. The results suggest that cells infected by replication-competent HIV possess inherent resistance to the T-cells, which present an obstacle on the road to curing HIV.
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How immune system's organ regenerates

A molecule called BMP4 that plays a key role in the thymus's extraordinary natural ability to recover from damage. Dr. Jarrod Dudakov of Fred Hutchinson Cancer Research Center, one of the study's leaders, talks about the importance of the thymus, the discoveries he and his colleagues have made about how it regenerates. The researchers hope to translate their work into new therapies to improve the function of the immune system in old age and make immunotherapies more effective.

The thymus is like a boot camp for new recruits to the immune system. From their birthplace in the bone marrow, immature white blood cells go to the thymus to mature into disease-killing machines. A healthy, active thymus gets you a diverse set of different T cells, each equipped to recognize and kill a slightly different foreign target. Thus, the organ is critical for a strong immune system that's ready to prevent any threat.

The thymus is sensitive to damage from everything from infections to life stress, it is also naturally resilient. Its power to bounce back from injury, however, fades with age, and it can take a serious hit from certain aggressive cancer therapies. BMP4, the molecule identified in the team's new study, is only the second known driver of natural thymic regeneration.

 The researchers found that BMP4 is produced by certain cells lining the inside of the organ. That molecule signals other cells of the thymus to turn on genes that promote development and repair.
Now, the team is working to figure out whether there's a master trigger that activates the whole regeneration process and then translate that knowledge into new therapies that help patients.
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Drug for breast cancer gene

The U.S. Food and Drug Administration on Friday approved drug  for treating metastatic breast cancers linked to the BRCA gene mutation. These mutated genes, called BRCA1 and BRCA2, first came to prominence in five years ago. According to FDA, expanding approval of Lynparza (olaparib) to include use against BRCA-linked tumors that have spread beyond the breast. Lynparza is one of a group of powerful new cancer drugs known as PARP inhibitors, and it's the first such drug to be approved for use against breast cancer.

 This approval demonstrates the current paradigm of developing drugs that target the underlying genetic causes of a cancer, often across cancer types. BRCA mutations are involved in up to one in every four breast cancers that are thought to have a hereditary component. These aberrant genes are also implicated in between 5 and 10 percent of non-hereditary breast tumors. When it's functioning properly, BRCA actually helps repair damaged cellular DNA and prevent tumors, but when BRCA1 and BRCA2 go awry they instead encourage breast cancers.

PARP inhibitor medicines such as Lynparza appear to interfere with the function of mutated BRCA with breast cells, causing them to die rather replicate-slowing tumor growth. The safety and effectiveness of Lynparza for women with advanced BRCA-linked breast cancers was established after a trial on patients. The trial measured the length of time the tumors did not have significant growth after treatment. The median progression-free survival for patients taking Lynparza was 7 months compared to 4.2months for patients taking chemotherapy only.

Common side effects of Lynparza include anemia, low white blood cell counts, nausea, fatigue, vomiting, headache, joint pain, increased susceptibility to colds and other respiratory tract infections, and other effects. Because Lynparza can harm a developing fetus, women are advised to use contraception while on the drug. Women should also not breast-feed while using Lynparza.
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HIV virus suppresses virus in humanized mice

A team of Yale researchers tested a new chemical compound that suppresses HIV, protects immune cells, and remains effective for weeks with a single dose. In animal experiments, the compound proved to be a promising new candidate to enhance current HIV treatment regimens-without increasing toxic side effects.

The finding builds on the work of senior co-authors Karen S. Anderson and William L. Jorgensen, who used computational and structure-based design methods to develop a class of compounds that target a viral protein essential for HIV to replicate.

The researchers refined this class of compounds to boost potency, lower toxicity, and improve drug-like properties in order to identify a promising preclinical drug candidate. In collaboration with Priti Kumar's lab at Yale, the drug candidate was tested in mice with transplanted human blood cells and infected with HIV.

In the humanized mice, the compound achieved key goals of HIV treatment: It suppressed the virus to undetectable levels in the blood; it protected the immune cells that the virus infects; and it worked synergistically with approved HIV medications, the researchers said.

Additionally, working with Yale drug delivery expert Mark Saltzman and his laboratory, the researchers found that the effects of a single dose of the compound, delivered in a long-acting nanoparticle form lasted for a month. The compound has potential for improving treatment for HIV.
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Are you tired of being tired? Eat these

Are you tired all the time? if yes your level of iron may be low, you can eat the following foods to regain your strength. Egg yolk is a great source of iron. It is needed for production of haemoglobin, the protein in the red blood cells that transports oxygen around the body to produce energy in the muscles, tissues and cells.

A deficiency in iron can lead to a type of anaemia that will leave you feeling drained and weak. This tends to be more common in women, especially if they experience heavy blood loss during menstruation. Eat more of venison than beef, as it contains twice as much iron. Eating Vitamin C-rich foods with plant sources of iron, such as red peppers with tofu or green salad with lentil bake can enhance absorption.

 Brown rice is a good source of fibre-rich complex carbohydrate, eat it regularly with five different fruits and vegetables. Leafy greens such as spinach are packed with magnesium, which makes this a glass of pure energy. If you're low in this mineral, as many people are, you'll feel absolutely drained. Magnesium activates the enzymes that starts energy-production process in the body.

Sardines, salmon, tuna,meat and egg are excellent sources of Vitamin B12. All B vitamins play a crucial part in the supporting our energy levels. B12 works in partnership with folate (Vitamin B9) to form red blood cells and to enhance the absorption of iron in the body. Avoid refined sugar, alcohol, and processed foods. Stay hydrated- water transport nutrients and oxygen around the body in order to support energy production. Dehydration can reduce your energy  and cause fatigue.
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Ogivri for cancer treatment

Food and Drug Administration approved Ogivri (trastuzumab-dkst) as a biosimilar to Herceptin (trastuzumab) for the treatment of patients with breast or metastatic stomach cancer (gastric or gastroesophageal junction adenocarcinoma) whose tumors overexpress the HER2 gene (HER2+).
Ogivri is the first biosimilar approved for the treatment of breast cancer or stomach cancer and the second biosimilar approved treatment of cancer.

Common expected side effects of Ogivri for the treatment of HER2+ breast cancer include headache, diarrhea, nausea, chills, fever, infection, congestive heart failure, difficulty sleeping (insomnia), cough and rash. Common expected side effects of Ogivri for the treatment of HER2+ metastatic stomach cancer include low levels of certain white blood cells (neutropenia), diarrhea, fatigue, low levels of red blood cells (anemia), inflammation of the mouth (stomatitis), weight loss, upper respiratory tract infections, fever, low levels of blood platelets (thrombocytopenia), swelling of the mucous membranes (mucosal inflammation), common cold (nasopharyngitis) and unusual taste sensation (dysgeusia).

Serious expected side effects of Ogivri include worsening of chemotherapy-induced neutropenia. Patients should stop taking Ogivri if cardiomyopathy, life-threatening allergic reactions (anaphylaxis), swelling below the skin (angioedema), inflammation of the lungs (interstitial pneumonitis) or fluid in the lungs (acute respiratory distress syndrome) occur. Patients should be advised of the potential risk to a developing fetus and to use effective contraception.
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Fatty molecules in blood controls malaria parasites

Depletion of a fatty molecule in human blood propels malaria parasites to stop replicating and causing illness in people Plasmodium falciparum is the parasite responsible for malaria. The key molecule the researchers identified has the catchy name of lysophosphatidylcholine LPC. It appears to be a building block the parasites use to construct new cell membranes when they divide. When LPC drops, the parasites can't multiply anymore and commit to a different pathway, but multiply when LPC increases.

Treating patients with antimalarial drugs usually kills the replicating parasites, but if you don't also block transmission, the disease will never disappear from the population, they pass into humans through the bite of an infected Anopheles mosquito, congregating first in the liver and later in red blood cells, where they multiply and burst forth in cycles that cause waves of illness.

If the host survive, some of the parasites stop multiplying and follow a different path known as sexual commitment or differentiation. If mosquitoes bite an infected person during this phase, the parasites-now male and female-travel back into the insects and breed. The transmission cycle begins afresh.

When the researchers cultured Plasmodium cells in flasks without their usual bath of human blood serum, the parasites skipped replication and went straight for sexual commitment-hinting that a control switch lurked in the missing blood. The researchers grew Plasmodium with serum. As expected, after a while the parasites lost their zest for replicating and began to undergo sexual commitment. But when the team added fresh serum, the parasites went on replicating. They were indeed grabbing something from the serum.

The researchers decided to separate and study all the serum components to see if they could identify the molecule or molecules at play. We found a single factor that's necessary and sufficient for regulating sexual commitment with each round of parasite replication, the researchers observed that LPC levels dropped. When LPC fell low enough, the parasites switched to sexual commitment.

Plasmodium cells were absorbing LPC from the bloodstream as they prepared to divide. The scientists believe that when the parasites sense that their raw materials are running low, they change strategies. The researchers found similar patterns of LPC depletion in a mouse model of malaria.
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Nanoparticles can limit inflammation

An injection of nanoparticles may boost the immune system when it becomes weak. Inflammation is a double-edged sword. When it works, it helps the body heal and fights off infections. But sometimes, the immune system overreacts. An acute lung injury, sustained by inhaling smoke, for instance, can lead to runaway fluid production that essentially drowns a person.

Experiments in mice suggest that simple plastic nanoparticles, delivered by IV, may be able to keep a type of immune cell called a neutrophil too busy to cause inflammation. Other diseases in which neutrophils cause excessive inflammation include sepsis and the hardening of the arteries, or atherosclerosis.

Researchers designed an experiment injuring part of the blood vessel wall in the microfluidic chips and confirmed that the neutrophils were redirecting their attention from creating inflammation at the injury site to carting the foreign particles away. In mice with acute lung injury, they found that injecting nanoparticles by IV could reduce the number of neutrophils congregating at the injury site by half or more.

The neutrophil concentration was similar to the concentration found in the blood of uninjured mice. Instead, the neutrophils were taking the particles to the liver, where they could be removed from circulation. The chemicals that the team uses to attach the nanoparticles to the blood vessel walls are the same as those used by the neutrophils themselves, a coating that combines nonfouling materials with the targeting chemicals will throw most white blood cells off.
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Reversing damaged heart tissue

It is possible to change fibroblasts -scar tissue cells into cardiomyocytes -heart muscle cells. Researchers used single cell RNA sequencing technology in combination with mathematical modeling and genetic and chemical approaches to delineate the step-by-step molecular changes that occur during cell fate conversion from fibroblast to cardiomyocyte. They reconstructed the routes a single cell could take in this process but also identified underlying molecular pathways and key regulators important for the transformation from one cell type to another.

Embryonic stem cells throughout human body gradually changes into a variety of highly specialized cell types, such as neurons, blood cells, and heart muscle cells. New discovery showed that it is possible to revert terminally differentiated somatic cells to a pluripotent state- cell that can self-produce and potentially turn into any kind of cell in the body. Researchers have also figured out how to convert one kind of differentiated somatic cell type into another without detouring through the pluripotent stage or the original progenitor stage. Such findings shifted the paradigm of cellular hierarchy and revolutionized stem cell research and the field of regenerative medicine.


Direct cardiac reprogramming, a promising approach for cardiac regeneration and disease modeling that direct conversion of cardiac non-myocytes into induced cardiomyocytes (iCMs) that closely resemble endogenous CMs. Like any reprogramming process, the many cells that are being reprogrammed don't do so at the same time.

Cellular reprogramming is heterogeneous, which makes it difficult to study using traditional approaches.
Using microfluidic single-cell RNA sequencing techniques, addressed the two main issues of 'asynchronous' programming and heterogeneous cell populations. They analyzed global transcriptome changes during fate conversion from fibroblasts to iCMs.
Using mathematical algorithms, they identified molecularly distinct subpopulations of cells along the reprogramming pipeline.

After a heart attack, cardiac fibroblasts around the injured area are immediately activated and become highly proliferative but this proliferative capacity decreases over time. How to take advantage of the varied cell cycle status of fibroblasts over the progression of a heart attack and its aftermath would certainly broaden the application of cellular reprogramming for patients and optimize outcomes. The molecular features of subpopulations of fibroblasts were differentially suppressed during reprogramming, suggesting that the susceptibility of cells to be reprogrammed varies.

This susceptibility coincides with the timing of cardiomyocyte differentiation during heart development. The signatures in the intermediate populations that seem to appear earlier in heart development were more resistant to the alterations. This suggests that the recent epigenetic memories of cells might be more easily erased, and so the fibroblast subpopulations with such epigenetic features are more easily converted into cardiomyocytes. Adjusting epigenetic memories not just changing their current epigenetic status could be crucial for changing a cell fate for therapeutic value.
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Links between microbiomes and autoimmune disorders

Bacteria in human body have all kinds of positive effects on our health, the bacteria in the gut have many beneficial functions. They help in digestion, prevent infection by pathogens and strengthen immune system to fight diseases.

A new function of a protein in the gut microbiome reveals potential impacts for those who suffer from inflammatory bowel disease IBD. A protein expressed by gut bacteria called Bacteroides works to prevent IBD by rapidly recruiting white blood cells to kill a cell of the immune system that is responsible for orchestrating IBD.

However, there is a flipside to the protein's call for help. In some people, the white blood cells overreact to the presence of the IBD bacteria. This is what causes problems like IBD, it's not the bacteria itself, but the immune system's severe reaction triggered by the protein.

These same overstimulated white blood cells are also the cells that cause other autoimmune disorders like diabetes, this discovery demonstrates the effect the gut microbiome has on the immune system and unearths a novel mechanism through which changes in the gut microbiome can increase the risk of autoimmune disorders.
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Yescarta for cancer treatment

Yescarta is a chimeric antigen receptor T cell CAR T therapy for the treatment of adult patients with relapsed or refractory large B-cell lymphoma after two or more lines of systemic therapy.
Active ingredient in Yescarta is axicabtagene ciloleucel, inactive ingredient is albumin (human); DMSO.

Yescarta is a treatment for your non-Hodgkin lymphoma. It is used when you have failed at least two other kinds of treatment. Yescarta is different from other cancer medicines because it is made from the user's white blood cells, which have been modified to recognize and attack the lymphoma cells.

Before you receive Yescarta, you will get three days of chemotherapy to prepare your body. When your Yescarta is ready, your healthcare provider will give it to you through a catheter placed into your vein-intravenous infusion.

Yescarta may cause side effects that are life-threatening and can lead to death. Call or see your healthcare provider or get emergency help right away if you have fever, difficulty breathing, shaking chills, confusion, dizziness, severe nausea, vomiting, diarrhea, fast or irregular heartbeat, severe fatigue and weakness.
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Fat cells for treating leukemia

Killing cancer cells indirectly by powering up fat cells in the bone marrow could help acute myeloid leukemia patients. Researchers discovered that boosting adipocytes, or fat cells, located in the bone morrow suppressed cancerous leukemia cells.

The production of healthy red blood cells is critical for those with acute myeloid leukemia but is sometimes overlooked as conventional treatments focus on killing the leukemia cells alone. Patients with this disease suffer from anemia and infection due to the failure of healthy blood production.

A drug used to moderate diabetes that induces fat cell production in the bone marrow was used for leukemia patients and was found to help foster red blood cell production as well as suppress leukemic disease.

The drug suppressed the cancer cells and bolstered the healthy cells, allowing them to regenerate in the new drug-induced environment. The drug activates blood regeneration and may provide benefits for those waiting for bone marrow transplants by activating their healthy cells.
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Post trauma stress disorder may increase the risk of lupus

Lupus is an incurable autoimmune disease that causes kidney inflammation and can affect many organs in the body like joints, skin, blood cells, brain, heart, lungs and kidney.

Lupus can be difficult to diagnose because lupus flares can be as minor as a rash, but can also come with muscle pain, joint pain and fatigue. Severe flare ups can cause fluid to build up around the heart and cause kidney failure.

Women who have post traumatic stress disorder PTSD or have experienced trauma may develop lupus. There is a correlation between PTSD and lupus in women than any other risk factor.

PTSD has been associated with other autoimmune diseases like cardiovascular problems. PTSD creates constant state of anxiety and defense. In these states, the heart rate goes up, and cortisol release is less controlled, which leads to an inflammation. This stress response causes lupus.

Lupus is an enigmatic disease; it affects different organs, the disease can be genetic, it may be triggered by infections, drugs and sunlight. Presently, there is no cure for lupus, the available treatments can control the symptoms.
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Kymriah for treating acute lymphoblastic leukemia

Kymriah (tisagenlecleucel) suspension for intravenous infusion, it is a prescription cancer treatment used in patients up to 25 years old who have acute lymphoblastic leukemia (ALL) that is either relapsing or refractory.

 Kymriah is made from your white blood cells, your healthcare provider has to take some of your blood called leukapheresis. Your blood cells are frozen and sent to the manufacturing site to make Kymriah.

 Your healthcare provider may give you chemotherapy for a few days to prepare your body. When your body is ready, your healthcare provider will give you Kymriah. The drug can increase the risk of life-threatening infections that may lead to death.

Having Kymriah in your blood may cause a false-positive HIV test result by some commercial tests. Kymriah may cause side effects that are life-threatening like: difficulty breathing, fever, shaking chills, confusion, severe nausea, vomiting, diarrhea, severe muscle or joint pain, very low blood pressure and dizziness.
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Benznidazole drug for treating American trypanosomiasis

Benznidazole belongs to a group of medicines called antiprotozoals. It is used to treat an infection called American trypanosomiasis.
Benznidazole works by killing the protozoa.

Take the medicine with meals, after breakfast and after supper, to decrease the chance of stomach upset. If you get an upset stomach (diarrhea, nausea, stomach pain, or vomiting) and it continues, check with your doctor.

Although rare, Benznidazole can lower the number of white blood cells in the blood, increasing the chance of getting an infection. It can also lower the number of platelets, which are necessary for proper blood clotting.

Common side effects of this drug are-
Convulsions (seizures); numbness, tingling pain, or weakness in hands or feet; reddish discoloration of skin,
fever or chills; pinpoint red spots on skin; skin rash; sore throat; unusual bleeding or bruising.

Other side effects are- abdominal or stomach pain; diarrhea; nausea; vomiting, confusion; dizziness; headache; restlessness; temporary loss of memory; trouble in sleeping; difficulty concentrating; unusual tiredness and fatigue.
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Zika virus weakened immune system and deformed fetus

The Zika virus increases in pregnant women by suppressing their dampened immune systems and attacks their natural defenses, which allows the virus to directly attack the fetus. A woman's immune system naturally suppresses itself during pregnancy to keep the body from recognizing the fetus as a foreign body and attacking it, Zika uses this process, turning pregnant woman's immune defense so the virus can spread without any hindrance.

Researchers tested African and Asian strains of Zika in the blood samples of healthy men, women and pregnant women. Researchers discovered that the Asian strain of Zika targets monocytes, which are white blood cells that mount the body's immune defense by destroying viruses and bacteria, people can survive the attack, but pregnant women cannot because Zika exploits the existing process by which the body protects a fetus from immune attack. Zika virus suppresses immune system like HIV.

The virus goes in, multiplies, grows and then crosses the placenta attack the fetus and cause disease. The blood of pregnant women infected with Zika also showed abnormally high expression of two genes that have been previously associated with pregnancy complications. Microcephaly have been associated with mothers who were infected with the Zika virus before giving birth, a pregnant women naturally have higher levels of immune-suppressing M2 macrophages to prevent the womb from rejecting the fetus.

However, the Asian Zika virus boosts M2 macrophage reproduction, decreasing the infection fighting process and encouraging immune suppression. Researchers discovered that the Asian Zika virus is more dangerous during first and second trimester, when the virus can increase immune suppression. During the third trimester, the blood of infected pregnant women and non-pregnant women were about the same.

During pregnancy, the host body is prone to opportunistic infection
Previous clinical studies showed that Zika virus infection during the first and second trimesters of pregnancy are strongly associated with fetal abnormalities. These anomalies cause brain damage and developmental delays in babies even if they are born with normal-sized heads.
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Breakfast is important for proper development

Breakfast is the most important meal of the day, starting the morning with a meal is important for teenagers and children. Skipping breakfast could leads to low brain function. Children who did not eat breakfast each day lacked proper nutrients that are essential for healthy growth.

Skipping breakfast can leads to iron, folate, calcium and iodine deficiencies which can leads to development of different diseases. Iron circulates oxygen throughout the body, iron deficiency leads to less oxygen circulation which can affect red blood cells.

Inadequate oxygen leads to fatigues, children become tired easily with poor oxygen circulation. Not having enough oxygen can affect how well their brain functions as well as their immune system's ability to keep the body healthy.

Iron is essential in maintaining healthy cells, hair and skin. The amount of iron that children need depends on their age. Calcium is necessary for strong bones and teeth. Calcium deficiency can cause problems with a child's hormone release and their muscle contractions.

Iodine is important for good thyroid health. Children who do not get proper amounts of iodine can experience slow mental development. Skipping breakfast daily leads to low levels of folate. Folate is essential for proper nutrients absorption.
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Genetic variants determined strength of immune system

Genetic differences in human affects cellular response to infections. Defense against microbial pathogens is carried out by white blood cells. White blood cells activate cellular defense programs and repressing the expression of hundreds of genes when they come across microbes.

Human immune system plays a central role in autoimmune inflammatory diseases, cancer, metabolism and aging. The researchers discovered hundreds of genes where the response to immune stimulus depended on the genetic variants possessed by the individual.

These genes demonstrate that genetic variation has an important role in how the human immune system works.
The study discovered genetic variants whose effects on gene regulation was different depending on the different infectious state of the cells.

Genetic disease risk is sometimes driven not by genetic variants causing constant cellular dysregulation, but by causing a failure to respond properly to environmental conditions such as infection.

Researchers analyzed how cells from different individuals respond to infection by measuring gene expression both during the early and late immune response.

 Integrating the gene expression profiles with genome-wide genetic data of each individual, they were able to discovered how genetic variants affect gene expression and how this genetic effect changes with immune stimulus.

Diseases have both genetic and environmental risk factors.
The analyses of gene expression patterns provide comprehensive information about the immune responses and show wide variation among individuals exposed to different pathogens at different time.

The research identified population differences in immune response and demonstrated that immune response modifies genetic associations to disease.
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