How liver responds to food

Minutes after eating, as nutrients rush into the bloodstream the body makes massive shifts in how it breaks down and stores fats and sugars. Within half an hour, the liver has made a complete switch  from burning fat for energy to storing as much glucose, or sugar, as possible. It's too short a time span for the liver's cells to activate genes and produce the RNA blueprints needed to assemble new proteins to guide metabolism.

Liver cells store up pre-RNA molecules involved in glucose and fat metabolism. ''The switch from fasting to feeding is a very quick switch and human physiology has to adapt to it in the right time frame," says Satchidananda Panda, a professor in the Salk Institute's Regulatory Biology Laboratory. It was known that a RNA-binding protein called NONO was implicated in regulating daily ("circadian") rhythms in the body.

Researchers analyzed levels of NONO in response to feeding and fasting in mice. After the animals ate, speckled clumps of NONO suddenly appeared in their liver cells, newly attached to RNA molecules. Within half an hour, the levels of corresponding proteins-those encoded by the NONO-bound RNA increased.

After mice eat, it looks as if NONO brings all these RNAs together and processes them so they can be used to make proteins. When mice lacked NONO, it took more than three hours for levels of the same proteins involved in processing glucose to increase. During that time lag, blood glucose levels shot up to unhealthy levels.

Since blood glucose levels are also heightened in diabetes, the researchers think that the mice without NONO may act as a model to study some forms of the disease. NONO has been found at high levels in the brain and muscle cells.
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Identical twins share similar genes

An international group of researchers has discovered a new phenomenon that occurs in identical twins: independent of their identical genes, they share an additional level of molecular similarity that influences their biological characteristics. The researchers propose a mechanism to explain the extra level of similarity and show that it is associated with risk of cancer in adulthood.

The characteristics of an individual depend not only on genes inherited from the parents but also on epigenetics, which refers to molecular mechanisms that determine which genes will be turned on or off in different cell types. If we view one's DNA as the computer hardware, epigenetics is the software that determines what the computer can do," said senior author Dr. Robert A. Waterland, associate professor of pediatrics - nutrition at the USDA/ARS Children's Nutrition Research Center and Texas Children's Hospital and of molecular and human genetics at Baylor College of Medicine.

Epigenetics works by adding or removing chemical tags to genes to mark which ones should be used in different cell types. One of the better studied tags, known to play an important role in development. In large group of identical and fraternal twin pairs, Waterland and his colleagues studied a group of genes called metastable epialleles. Previous work indicated that methyl tags are randomly added to metastable epialleles during early embryonic development and maintained throughout life.

The patterns of methyl tags added to metastable epialleles would be equally random in identical twins and fraternal twins, we found that the methylation patterns matched almost perfectly in identical twins, a degree of similarity that could not be explained by the twins sharing the same DNA. Identical twins are formed when the very early embryo - essentially a ball of cells - splits into two parts, and each continues to develop into a separate human being.

Twins inherit an intimate molecular memory of their shared developmental legacy as a single individual. On the other hand, genes at which epigenetic markers are set after the embryo splits can have greater epigenetic differences between the two twins. Epigenetic supersimilarity seems to occur in a relatively small group of genes, but, as the researchers discovered, many of these are associated with cancer. To test whether these epigenetic markers might affect risk of cancer, the scientists in Houston teamed up with cancer epidemiologists running the Cancer Council Victoria's Melbourne Collaborative Cohort Study in Melbourne, Australia.

Analyzing peripheral blood DNA samples from healthy adults show that methylation at epigenetically supersimilar genes is associated with risk of subsequently developing several types of cancer, including lung, prostate and colorectal cancer. This study shows that, at the epigenetic level, identical twins are more similar to each other than previously recognized. Epigenetic supersimilarity affects risk of disease
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Egg cells can remain fresh with epigenetics

Keeping egg cells in stasis during childhood is a key part of female fertility. A team led by Dr Gavin Kelsey in the Babraham Institute and colleagues in Dresden and Munich studied a protein called MLL2 and discovered how it produces a distinctive pattern of epigenetic marks that are needed for egg cell stasis. A fertilised egg cell is the start of every human life. Yet, egg cells are created inside a woman's body before she is birth.

The eggs are then kept in stasis throughout childhood until they're needed as an adult. If egg cells don't go into stasis they can't become mature eggs and they will never have the chance to form a new life. Putting an egg cell into stasis involves adding many epigenetic marks throughout its DNA.
Epigenetic marks attached to DNA act as footnotes, indicating which genes are turned 'on' or 'off'.  The team had to create new, highly sensitive ways to detect epigenetic marks in such small numbers of cells.

As eggs develop, a mark called H3K4me3 spreads throughout the genome. Scientists have already seen the same mark close to the start of active genes in many cells, but the team discovered that its role in egg cells is different. They showed that the MLL2 protein is responsible for this unusual placement of H3K4me3 in egg cells.

Without MLL2, most H3K4me3 marks in egg cells are lost and the cells die before getting the chance to form a new life. H3K4me3 is created in two ways. MLL2 can add the H3K4me3 mark without any nearby gene activity while another process, that doesn't use MLL2, places the same mark around active genes .
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How weather increases the risk of cancer

Living in a cold climate could make people more likely to get cancer, people are at greater risk in colder countries because of their genes. The same genes which stop human cells from dying in freezing temperatures are also linked to breast and bowel cancer and leukaemia. A researcher says the genes contributing to cooler climates are the same which increase the risk of malignant tumours forming in the body.

Genetic variants found to be beneficial in extreme environments, can also predispose for cancer. Cell resistance at low temperatures and at high altitude probably increases the probability for malignancy.’Previous research from 2010 found grim weather in northern parts of the world may make men more vulnerable to prostate cancer, perhaps due to a lack of vitamin D from the sun.

However the new study - which compared international rates of cancer with 240 genetic studies of cancer and seven others in cold and high-altitude countries - suggests where people live affects their genes.Extreme cold weather can cause human cells to die, so that people in freezing countries have genetic mutations to prevent cell death and repair DNA.
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Education reduces the risk of Alzheimer's disease

The theory that education protects against Alzheimer's disease has been given further weight by new research. Alzheimer's disease is the leading cause of dementia. Building of 'plaques' and 'tangles' of misshapen proteins lead to the gradual death of brain cells. People affected by Alzheimer's experience memory and communication problems, disorientation, changes in behavior and progressive loss of independence.

The causes of Alzheimer's are largely unknown, and attempts to develop drug treatments to stop or reverse its effects have been disappointing. This has led to increasing interest in whether it is possible to reduce the number of cases of Alzheimer's disease by tackling common risk factors that can be modified.

Many studies have shown that the more years spent in full time education, the lower the risk of Alzheimer's. But it is difficult to unravel whether this is an effect of education improving brain function, or whether it's the case that people who are more educated tend to come from more wealthy backgrounds and therefore have a reduction in other risk factors that cause Alzheimer's disease.

Researchers examined looking DNA and compared genes associated with environmental risk factors – for example, genes linked to educational attainment or to smoking – and seeing which of these genes are also associated with Alzheimer's disease. If a gene is associated with both, then it provides strong evidence that this risk factor really does cause the disease. Researchers studied genetic variants that increase the risk of a variety of different environmental risk factors to see if these were more common in patients with Alzheimer's disease. They found the strongest association with genetic variants that predict higher educational attainment.

This provides further strong evidence that education is associated with a reduced risk of Alzheimer's disease, improving education could have a significant effect on reducing the number of people who suffer from this devastating disease. Exactly how education might reduce the risk of Alzheimer's is uncertain.

Previous studies have shown that the same amount of damage in the brain is associated with less severe and less frequent Alzheimer's in people who have received more education. One possible explanation is the idea of 'cognitive reserve' – the ability to recruit alternative brain networks or to use brain structures or networks not normally used to compensate for brain ageing. Evidence suggests that education helps improve brain wiring and networks and hence could increase this reserve.
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Aspiring improves effectiveness of cancer treatment

Adding aspirin to some existing cancer drugs could increase their effectiveness against a group of tumours resistant to treatment, scientists are hoping clinical trials could soon be underway for people with lung, pancreatic and colorectal cancers that have not responded to other therapies.

Cancers driven by mutations in a group of genes, known as RAS, had a low response to treatments with currently no drug directly targeting them. The group of tumours includes some pancreatic, lung and colorectal cancers with very low survival rates, as well as a small percentage of melanomas.
Addition of aspirin to a cancer inhibitor drug, Sorafenib, strongly enhanced its effectiveness against mouse models of lung cancer and melanoma with RAS mutations.

In a multicentre phase three trial for non-small cell lung cancer, Sorafenib alone showed a marginal improvement for patients. Latest research suggests its combination with aspirin could benefit patients with RAS mutations who don't otherwise respond to other treatments.
The drug combination could potentially reduce the dose of Sorafenib required, improving quality of life for patients by reducing adverse impacts that can lead some patients to stop treatment.

Combining it with a relatively high dose of aspirin, two molecular processes are activated and together they work to kill RAS mutant cancer cells. This dual activation also might prevent the tumours acquiring resistance to the treatment, which can happen when the inhibitor drug is given alone.
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Managing antibiotics can not reverse the resistance

Researchers have discovered that reducing the use of antibiotics will not be enough to reverse the growing prevalence of antibiotic resistance for some types of bacteria. Besides passing along the genes bestowing antibiotic resistance to their offspring, many bacteria can also swap genes among themselves through a process called conjugation.

The bacteria tested by researchers have fast conjugation rate, even if you don't use antibiotics the resistance can be maintained. Most resistance to antibiotics arises and spreads through natural selection. Some bacteria have genes that help them survive around of antibiotics, they quickly parent the next generation and pass on those genes.

Many of these genes, however, come at a cost. For example, a mutation may allow a bacterium to build a thicker membrane to survive a particular antibiotic, but that mutation might also make it more difficult for the cell to reproduce. Without the selective pressure of antibiotics killing off the competition, bacteria with this mutation should disappear over time.

The results indicate that for bacteria that swap resistance genes simply managing the amount of antibiotics being used will not turn the tide on the growing problem of resistance. To make any headway, drugs will also be needed that stop the sharing of genes and decrease the rate at which they are passed on through reproduction. One of the drugs is a benign natural product and FDA-approved antipsychotic.
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High levels of air pollution increases the risk of heart attack

People with certain blood types are more likely to suffer a heart attack when exposed to high levels of pollution, people who have A, B, or AB blood types have an 'elevated risk', compared to those with the O blood type. Pollution is linked to a raised chance of a heart attack but it is the first time that the risk has also been linked to blood type.

The risk of a heart attack or chest pain doubled for people of type A, B, or AB blood when pollution hits high levels. In comparison, the risk rose by 40 percent for those with type O, according to researchers. The primary mutation we studied differentiates between O blood types and non-O, which includes positive and negative A, B, and AB blood types.

Dozens of genes have been shown in large international studies to predict the onset of coronary artery disease in people who are free of the disease. But the vast majority of people won't have a heart attack unless they already have coronary artery disease. Nor is a heart attack a certainty even with heart disease.

 A level of pollution at which the increased risk occurred for people with non-O blood types is threshold 25 micrograms of pollution per cubic metre. At levels higher than 25 micrograms per cubic metre of pollution, the increase in risk is linear, while below that level there's little if any difference in risk. During a winter inversion, the PM2.5 pollution level can occasionally reach as high as 100 micrograms per cubic metre, but 50 to 60 is more typical.

The researchers found that people with type O blood also have higher risk of heart attack or unstable chest pain in times of high air pollution. Their level of risk is much smaller, at 10 per cent instead of the non-O blood type's 25 per cent per 10 additional micrograms per cubic metre.
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Epigenetic reveals early breast cancer development

Changing the epigenetic code of a single gene is enough to cause a healthy breast cell to begin a chain reaction and become abnormal, Epigenetic changes are a hallmark of cancer, but up until now, it has not been known whether these changes on their own are sufficient to push healthy cells down the cancer path.

 Using a CRISPR-dCas9 epigenetic editing tool, the researchers methylated different genes in healthy breast cells and found that those changes were sufficient to cause the cells to undergo hyperproliferation - abnormally rapid cell division which is an early stage of tumour initiation.

The epigenetic changes are inherited as long as the cell divides, and that the team's manipulations permanently and negatively affected the biology of a normal breast cell from a healthy individual. Epigenetic editing could also be used to design novel therapies by initiating permanent changes to cell biology.

This may be a more viable or alternative way forward for gene editing as any potential mistakes would be less damaging than directly editing the DNA sequence, and epigenetic editing would be more easily reversible if needed. Epigenetic fluctuations happen all the time in human cells. During ageing, human epigenome is progressively distorted.
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How protein breakdown causes leukemias and brain cancer

An enzyme that is responsible for the breakdown of specific amino acids in food plays a key role in the development of leukemias and brain cancer. The researchers have discovered a surprising link between energy metabolism and the epigenetic code. These labels in the DNA of cancer stem cells determine the activity of genes and many cellular functions.

Acute myeloid leukemia AML is an aggressive type of blood cancer that often relapses in the wake of successful initial treatment. Stem cells that are resistant to therapy are believed to be responsible. Reseachers examined patient samples by comparing the composition of proteins of AML stem cells and leukemia cells without stem cells properties.

The investigators found suspiciously high levels of an enzyme called BCAT1 in the stem cells. These levels rose even higher during a cancer recurrence. The researchers considered this to be a clue that BCAT1 might be linked to therapy resistance. Cancer researchers have suspected for some time that the BCAT1 enzyme, which is responsible for the breakdown of specific proteins in food, plays a role in the development of malignant tumors.

 They discovered that an overproduction of BCAT1 increases the aggressiveness of malignant brain tumors and breast cancer. BCAT1 reduces the levels of this key molecule and this leads to increased levels of chemical labels in the DNA. The tiny methyl groups that are attached to DNA determine whether particular genes are active or silent and, thus, have an immense impact on all cellular functions.

They increase cancer-promoting methylation of DNA. AML is known for an extremely heterogeneous pattern of genetic alterations. However, misregulated methylation with its drastic consequences for the whole cell appears to be a common characteristic of this malignant disease.

The finding that BCAT1 drives cancer-promoting methylation in AML stem cells and other cancer stem cells opens up new options for therapy. A blockade of the enzyme using a targeted agent might normalize DNA methylation and thereby reduce cancer spread and therapy resistance.
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Traffic jam causes tumor growth

When cells lose track of their orientation, they can start to grow out of control, and develop into cancer. Researchers has identified a new regulator for cell orientation, offering a future target for precision medicine in cancer treatment.

Tissues in the breast, pancreas, colon and lungs are all organised as single cell layers called epithelia. Cells sit side by side, and use internal signals to orient themselves. The signals for telling which way is up are connected to the waste handling system, a series of miniature vesicle sorting stations.

Traffic jam in the sorting inside cells can cause tumor development Liver Kinase B1 LKB1 activity promotes tumor growth. Human cells contain tumor suppressor genes that act as gate-keepers to prevent tumor growth. One such classical tumor suppressor, Liver Kinase B1 LKB1 was identified as being responsible for the hereditary cancer predisposition syndrome, Peutz-Jeghers syndrome.

It has later been shown to be mutated in a range of cancers, including lung and colon cancer. The new results suggest that the enzyme LKB1 exists on vesicle sorting stations and is shut off in normal cells, but the traffic jam allows LKB1 to remain active for a longer time.

High activity of LKB1 contributes to tumor growth by sending confusing signals to the cell about which way is up. The researchers investigated epithelial tissues in the fruit fly Drosophila melanogaster, a powerful animal model system for medical research, in addition to human cells grown in 3-D cultures in the laboratory.

In both systems, high activity of LKB1 increased stress signals in the cells and disrupted cellular orientation. Targeting LKB1 as potential therapy, researchers tested the effect of genetically removing LKB1 from cells that otherwise would form tumors due to loss of orientation.

Reducing LKB1 activity restored normal epithelial organization and prevented
tumor growth. These results suggest that pharmacological inhibition of LKB1 may be beneficial as treatment in some cancer types. It will be important to determine if pharmacological agents can specifically target LKB1 in animals or in human cells in culture, and how such potential treatment may be transferred to the clinic.
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Chemotherapy may have effects on intergenerational fertility

Chemotherapy treatment can damage the fertility of women and their children. The treatment can reduce the levels of fertility and chance of having children. Women and men are encouraged to freeze their eggs or sperm before treatment.

But when chemotherapy patients have children naturally, it was usually assumed that their ability to reproduce was unaffected. Children born to women who have had chemotherapy have 72 per cent fewer children of their own than members of the general population.

The effect seems to mainly affect women. Children of men who had chemotherapy treatment may have a similar number of children compared to members of the general population of the same age. Daughters of women who had chemotherapy had 71 per cent fewer children than the general population. Sons of female chemotherapy patients had 87 per cent fewer children.

 This may be caused by epigenetics or changes which can be compared to switches that turn on or off certain genes in the DNA passed on to a person’s offspring. Recent studies have found that, smoking causes epigenetic changes in DNA. Chemotherapy given to women may have intergenerational effects on fertility.
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How to turn scar tissue into healthy tissue

Limited therapeutic options and the heart's inability to regenerate healthy cells after heart attacks are parts of factors that cause sudden death in heart attack patients. Scientists are exploring ways to reprogram scar tissue cells into healthy heart muscle cells to reduce death.

Creation of cardiomyocytes with genetic signatures that closely mimic those found in healthy adult heart muscle cells can solve the problem. The other reprogramming approach leads to the creation of cardiomyocytes with more embryonic cell signatures.

The differences in the cardiomyocytes generated using these two methods are
Cardiomyocytes, the cells responsible for the beating of the heart, are essential to repairing the heart after injury. But after injury, such as a heart attack, many of these cells are irreversibly lost; they've been turned into scar tissue cells.

The replacement of these lost cells with patient-specific cardiomyocytes has gained attention as a potential therapy because existing healthy heart tissue better accepts these cells and because of increased recovery rates. Patient-specific cardiomyocytes also offer unique advantages for drug screens to help doctors identify each patient's drug type and dosage.

There are presently two widely practiced approaches to generate patient-specific cardiomyocytes.
In the first approach, an adult connective cell called a fibroblast is reprogrammed back into a naïve embryonic stem cell-like state. Once in this naïve state, the cell has the potential to develop into any cell type in the body, but scientists direct it to develop into a cardiomyocyte. These newly created cardiomyocytes are called induced pluripotent stem cell cardiomyocytes iPSC-CM.

In the second approach called direct cardiac reprogramming, a fibroblast is directly converted into a cardiomyocyte, without having to first be reprogrammed into a naïve embryonic stem cell. These new cardiomyocytes are called induced cardiomyocytes iCM. The researchers found that both methods resulted in cells with classic cardiomyocyte molecular features. However, by comparing the unique set of genes activated or not activated in each group of cells, the researchers found that iPSC-CMs more closely resembled embryonic cardiomyocytes, while iCMs more closely resembled adult cardiomyocytes.

Researchers also found that iPSC-CMs feature more active genes and a higher number of genes poised to be either activated or repressed a trait more commonly found in potent cells.
Metabolically, iPSC-CMs had a higher expression of glycolytic genes while iCMs had a higher expression of genes involved in fatty acid oxidation, the primary means of energy production in adult hearts.

In iPSC-CMs, heart muscle cells called sarcomeres, which give the heart a striated look, were less organized than in iCMs. The contractibility of cardiomyocytes as measured by the intake and removal of calcium was also greater in iCMs, suggesting that iCM cells are more mature than iPSC-CM cells.
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Folic acid may reduce autism risk from pesticide

Taking folic acid during the window around conception reduced the risk associated with pesticides, researchers examined many children who had been diagnosed with ASD, the researchers interviewed their mothers about their household pesticide exposure during pregnancy, folic acid and B vitamin intake.

Children whose mothers took 800 or more micrograms of folic acid and other prenatal vitamins had a lower risk of developing autism spectrum disorder ASD even when their mothers were exposed to household or agricultural pesticides.

Mothers who took less than 800 micrograms and encountered household pesticides had higher risk of having a child who developed an ASD than their counterparts who took 800 micrograms of folic acid or more and were not exposed to pesticides.

The risk increased for women exposed several times, women with low folic acid intake who were exposed to agricultural pesticides during a window from three months before conception to three months afterward were at higher risk. Folic acid can reduce the risk of developing autism but it can not prevent it completely. Avoiding chronic pesticide before and during pregnancy can prevents ASD.

Folate plays a critical role in DNA methylation- a process by which genes are turned off or on, as well as in DNA repair and synthesis. These are important during periods of rapid growth when there are lots of cells dividing in developing fetus. Taking folic acid can improve genomic functions.
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Fetal gene can cause preeclampsia

Preeclampsia is a pregnancy complication characterized by high blood pressure and signs of damage to kidneys and liver. Preeclampsia usually starts after 20 weeks of pregnancy in women whose blood pressure had been normal. Slight rise in blood pressure may be a sign of preeclampsia.

Pregnant women risk of preeclampsia can be linked in some cases to genes from fetus. Preeclampsia usually starts with a problem in the placenta, which is mainly composed of fetal cells.
Researchers analysed a large number of women, and discovered several genetic variables that identified  the same gene associated with the risk.

The genetic variants identified by the researchers are associated with the FLT-1 gene, which encodes a protein that, in soluble form, is known as a biomarker for preeclampsia.

The protein contributes to damaging the mother's vascular system causing high blood pressure and an increased amount of protein in the urine. This happens as a result of problems with the placenta, essentially because fetal cells in the placenta produce the protein.

The risk of the disease may be because changes in the gene affect how the protein works and how it affects the mother. This is a fetal gene that gives the mother an increased risk of developing preeclampsia.
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Statins reduce the risk of breast cancer

Lowering cholesterol activity reduces the risk of breast cancer, oestrogen hormone helps cancer to spread, that is why women are given anti-hormone treatments after chemotherapy and surgery.

Women whose genes encourage the production of  cholesterol are prone to breast cancer, statins can reduce the levels of cholesterol, taking statins to lower cholesterol could prevent breast cancer.

Statins interrupt the enzymatic reduction of HMG-CoA to mevalonate. This prevents synthesis of cholesterol.
Taking statins can reduce the risk of breast cancer. Statin is a form of medicine that is used to decrease the amount of low-density lipoprotein LDL cholesterol in the blood.

Researchers followed up women both with and without a high cholesterol aged and compared it to mortality rates and breast cancer developments, they discovered that women taking statins have lower risk of developing cancer.
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Effects of long, mysterious strip of RNA on sperm count

Scientists have discovered part of genetic material known as lncRNAs that help sperm develop. Male mice lacking a particular lncRNA have low sperm count, this shows that lncRNAs could represent novel infertility drug targets.

The strands, called long non-coding RNAsor lncRNAs don't seem to encode proteins, but have been implicated in everything from cancer to brain function. Many are located in the testes, suggesting they could contribute to infertility.

Researchers collected and measured lncRNA levels during the process of cellular differentiation that leads to sperm production. They found that specific lncRNAs are associated with each stage of sperm development.

The researchers also identified lncRNAs and mRNAs that are testes-specific -- that is, not found in other human or mouse tissues. Genetically-modified male mice lack one particular lncRNA. They used these mice to assess how the loss of this one lncRNA affects overall mouse fertility.

 Mice provide a model to study human sperm development as the process is highly conserved between the two species. Researchers discovered massive changes in lncRNAs produced in cells that eventually increase mouse sperm. Each stage of sperm development was associated with different lncRNAs. This shows that lncRNAs are important for creating complex biological process.

Many of the lncRNAs were strictly found in mouse testes, a subset of lncRNAs are able to escape gene silencing processes that help turn off unnecessary genes on the X and Y sex chromosomes during sperm development. The X and Y sex chromosomes determine whether a sperm will produce a male or female embryo. lncRNA could serve as a potential therapeutic target for male infertility drugs.
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Lockdown gene to increase IVF success rate

In Vitro Fertilization IVF is an assisted reproductive technology, it is the process of fertilization by extracting eggs, retrieving sperm and manually combining an egg and sperm in a laboratory dish. The embryo is then transferred to the uterus.

Human egg and sperm cells have their genes trained to fertilize. After fertilization, the developing embryo begins the genetic program that turns a single cell into a healthy fetus.

Epigenetic changes to the DNA, like the removal of methyl group locks by enzymes, which allows many more genes to be read. Some genes need to be locked down during development, as their genetic messages cause problems for the embryo.

Everything that goes wrong in embryos has the potential to cause infertility or early pregnancy abortions. The scientists sequenced the RNA of more than 30 embryos lacking Trim28 and discovered that Rbmy1a1 gene was unusually active.

The enzyme encoded by Rbmy1a1 produces mRNA transcripts which are harmful to the developing embryo. Detecting the activity of detrimental genes like Rbmy1a1 before an embryo is implanted could improve rates of IVF success.
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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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Genetic blood tests can expose cancer

Genetic blood test might expose different types of cancer at early stage,
the blood test discovered blood from DNA fragments released by cancerous tumours.

Examining DNA fragments for mutations found in cancer- causing genes leads to the discovery of blood of many early stage cancers. It exposed colon, breast, lung and ovarian cancers.

Early detection of cancers can leads to effective treatment from onset and save many lives, the test can screen out people without cancer. Genetic blood test for cancer must expose DNA mutations linked to cancer and ignore harmless mutations that is always present in healthy humans.

Exposing cancer and early treatment is the most important aspect of the discovery, differentiating deadly cancers that will hurt people from cancers that may not is very important for the success of the blood test.
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