Lupus increases the risk of dementia

Lupus is a chronic autoimmune disease that causes the body to attack its own healthy cells. It is thought to be caused by genetic and environmental factors. Environmental factors can trigger attacks or 'flare ups. 'Flare ups vary from person to person and are not the same each time. They can be marked by fatigue that can be mild or debilitating. Fatigue is often an early indicator that an attack is about to set in.

Attacks can cause joint and muscle pain and swelling, particularly at the wrists, hands, elbows, knees and ankles. Many people with lupus experience skin problems. The most distinctive marker of lupus is a butterfly-shaped rash on the face. Lupus may also cause light sensitivity, fever, changes in weight and swollen glands. People with lupus sometimes complain of a 'fog,' that can feel like depression or anxiety and sometimes causes them to have difficulty focusing and expressing themselves.

It causes the body’s immune system to break cells in parts of the body including the kidneys, lungs, skin and blood vessels. Lupus may impair memory and cognitive functions. Researchers analyzed data from more than 7,000 people and found that dementia was far more common among people with dementia than those without the disease. Lupus is best known for the damage it does to the kidneys, but its symptoms can be extremely varied, making it very difficult to diagnose.

Experts have identified numerous forms of the disease, including nineteen variations of neuropsychiatric lupus, which affects the central nervous system, including cognitive and memory functions and can even cause psychological and psychiatric symptoms. Some patients refer to a ‘lupus fog,’ a catchall description of the experience of difficulty concentrating, remembering facts, and expressing oneself.

The fog can also come with depression and anxiety, all of which may signal a lupus flare up. Patients who do not have a neuropsychiatric form of lupus are at a greater risk of dementia. Steroids are also associated with memory loss and cognitive impairment in lupus patients.
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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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Cannibal cells prevents cancer growth

Cell cannibalism, also known as entosis, occurs when closer cell kills and digests another cell. Entosis occurs in tumours, it can be triggered when one cell divides to form two.

Cell cannibalism is linked with cancer, dividing cells are cannibalism that kill cancerous cells, this shows that entosis may prevent cancer by causing cancer cells to be destroyed by closer healthy cells.

 Weakened attachments result in multiple cell cannibalism, drugs that weaken cell attachments are  anti-cancer drugs, they are effective for cancer treatment.
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