Effects of stress on sperm

Children of stressed fathers are at greater risk of developing PTSD and depression, according to a new study. Researchers found life's pressures can change the DNA of a man's sperm - leading to brain development changes in his yet unborn baby. It's widely known that a mother's environment during pregnancy, including factors such as poor diet, stress and infection, can negatively impact the offspring.

Learning how a father's behavior and environment can impact his child's development could lead to the detection and prevention of many mental health disorders. Researchers have known for years that stress can increase the risk of mental disorders,' Dr Tracy Bale, professor of neuroscience at the University of Maryland School of Medicine, told Daily Mail Online. 'What’s interesting here is that we are finding intergenerational effects.'

Researchers, led by Dr Bale, conducted a mice experiment to examine how a father's lifestyle impacts his children. Previously, the team has found male mice experiencing chronic periods of mild stress passed down genetic coding for a less effective hormonal response to stress in children. Three major hormones are released by the nervous system when the body is under stress. These are adrenaline, cortisol and norepinephrine. Collectively, these hormones send human bodies into ''fight''mode, which is important to the body's ability to cope with the effects of stress.

Stress resulted in changes in sperms genetic material known as microRNA, which plays a key role in which genes become functional proteins. These changes in stress reactivity have been linked to some mental disorders, including depression and PTSD.

In the new study, presented at the 2018 AAAS annual meeting in Austin, Texas, Dr Bale and her colleagues unraveled new details about the microRNA changes in the sperm. The caput epididymis, the structure where sperm matures, release vesicles which contain microRNA that can fuse with sperm to change its cargo delivered to the egg. When males mice were stressed, the caput epididymis responded by altering the content of these vesicles.

This suggests even mild environmental stress, such as workplace stress, can have a significant impact on the development and potentially the health of future offspring. This is through a process known as epigenetics where DNA is changed through lifestyle factors such as diet, exercise - or even stress. Scientists have known a mother's environment during pregnancy can damage a fetus by diet, stress or infection affecting the expression of certain genes in the same way.

Father's stress can affect offspring development by altering important aspects of his sperm. Her previous studies on the placenta have revealed novel sex differences during pregnancy that may predict increased pre-natal risk for neurodevelopmental disorders in males. Historically, most research on how a parent's lifestyle, behavior and environment can affect their children has focused on the mother. But scientists have recently been paying increasing attention to how a father's health impacts his children.
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Mechanism behind autoimmune disorder

Northwestern Medicine scientists discovered a previously-unknown mechanism of disease behind a specific autoimmune disorder. The scientists observed antibodies that targeted phosphatidylethanolamine, an important phosopholipid, from within the endosomes of cells. This discovery was the first observation of a pathogenic mechanism behind anti-phosphatidylethanolamine (aPE) autoimmunity, an immune system disorder that's been correlated with thrombosis, transplant failure and pregnancy loss.

It was first reported decades ago, but exactly how aPE autoimmunity worked had remained a mystery despite a large body of literature documenting its prevalence, according to Ming Zhao, PhD, associate professor of Medicine in the Division of Cardiology and senior author on the paper. Autoimmune diseases usually develop when antibodies-proteins which neutralize pathogens erroneously attack cells while circulating through the bloodstream. To target those cells, the antibodies bind to accessible antigen targets on the exterior surface of cells.

The internalization happens through the endosome, a part of the cell that samples the external environment and gathers in signaling molecules. In this case, the endosome also draws in the antibodies, making the cells vulnerable.This creates an opportunity for anti-PE antibodies that are brought into the cells to bind to the PE in these tiny vesicles and attack the cells from within a miniature 'Trojan Horse' process, this causes chaos within the cell, sending it into an inflammatory state, leading to a greater risk of blood clot formation and pregnancy complications.

It's important to note the inflammatory response may be the principal effect of aPE because it means anti-inflammatory treatment is likely to be more effective than anti-coagulants. These novel discoveries shed light on how cellular vulnerability to aPE is mediated and explain some of its clinical symptoms, according to the study. Because endosomes are an integral part of nearly every type of cell, linking the activity of aPE antibodies to clinical symptoms will be a priority for scientists in future investigations.
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How hepatitis C hides in the body

The Hepatitis C (HCV) virus is invisible to the immune system by breaking down communication between the immune cells, it builds virus factories that multiply easily. It takes one to three months from infection to disease, it can lead to liver failure and death. Hepatitis C virus is transmitted through blood and infects the cells in the liver, it is difficult to detect because it does not have symptoms when you get infected.

The virus causes chronic infection that lasts a lifetime. It may take decades before the infection leads to liver failure or cancer, so a lot of people are unaware that they have the virus in their body. They only notice it when they get seriously ill, which may be too late for the treatments that are available. Hepatitis C virus destroys important proteins in the immune system to promote its own growth. The ability to directly manipulate their host cells is the reason some viruses are very harmful to human.

Human cells have a complex inner structure that is divided into different areas, with different sacs that are formed from fatty membranes. Viruses that have the same genetic material as HCV (positively polarized single-stranded RNA) cause major changes in these membrane sacs.

Liver cells infected with HCV had altered membrane sacs. To study whether the IRGM protein caused the changes, researchers employed the CRISPR-Cas system, a technique that is used for regulating cells, in this case to turn off the IRGM protein in the liver cells. When the IRGM is removed from the liver cells, the virus is unable to grow.

The reason for this is that the hepatitis C virus utilizes some of the cells, called the Golgi apparatus, where the protein IRGM has an important function. The Golgi apparatus is a kind of transport centre in the cells. It packs proteins into small sacs called vesicles and sends them where they need to go within the cell, or out to other cells.

The hepatitis C virus utilizes this to build its virus factories by taking over and redirecting these vesicles with the necessary building blocks to the site where the factories are being built. These vesicles are rich in lipids that the virus is entirely dependent on to anchor its factory construction.

When this protein is removed, the virus is no longer able to infiltrate the Golgi apparatus and thus it can't build up its secret network of virus factories. Hepatitis C is transmitted via the blood. Infection is spread primarily through unclean syringes, non-sterilized medical devices, or unsafe blood transfusions.
HVC can also be passed on from mother to child, and through bodily fluids.
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