Lung cancer causes hypertension

Shortness of breath and respiratory distress often increase the suffering of advanced-stage lung cancer patients. These symptoms can be triggered by pulmonary hypertension, the pulmonary hypertension is due to immune and inflammatory processes triggered by cancer cells. Lung cancer has long since taken on the character of an epidemic: the disease is already responsible for more than a quarter of all cancer deaths, and the trend is rising.

One reason for this is that the prognosis is poor: only one-fifth of patients are still alive five years after diagnosis. This is partly due to the fact that lung cancer is often not recognized until it is in an advanced stage. Another problem is that a variety of different lung cancers exist, each of which requires its own therapeutic concept. Doctors have observed that many patients with progressive lung cancer develop shortness of breath and respiratory distress.

The same symptoms also occur in diseases such as pulmonary arterial hypertension. Scientists measured the diameter of the pulmonary artery of many lung cancer patients using computer tomography. They found thickening of the walls of the pulmonary artery in more than half of the patients. This is a clear indication that these patients also suffer from pulmonary hypertension.

To identify the causes, the lung researchers analyzed three different forms of lung cancer in mice. These were tumour types that grow at different rates and can be experimentally induced in the lungs of mice. All three mouse models showed signs of pulmonary hypertension as tumour growth progressed.

Further experiments showed that the immune cells release various chemical messengers, as is generally observed in inflammatory reactions. Conversely, pulmonary hypertension did not occur when the mice in the experiment lacked functioning immune cells. This is an indication that inflammatory processes triggered by lung cancer may be responsible for pulmonary hypertension.
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The secrets of Ebola

In a comprehensive and complex molecular study of blood samples from Ebola patients in Sierra Leone. Conducting a sweeping analysis of everything from enzymes to lipids to immune-system-associated molecules, the teamfound 11 biomarkers that distinguish fatal infections from nonfatal ones and two that, when screened for early symptom onset, accurately predict which patients are likely to die.

Health workers collected blood samples from patients after they were diagnosed with Ebola and at multiple points thereafter.They obtained 29 blood samples from 11 patients who ultimately survived and nine blood samples from nine patients who died from the virus. For comparison, the research team also obtained blood samples from 10 healthy volunteers with no exposure to Ebola virus.
"Our team studied thousands of molecular clues in each of these samples, sifting through extensive data on the activity of genes, proteins and other molecules to identify those of most interest.

The team found that survivors had higher levels of some immune-related molecules, and lower levels of others compared to those who died. Plasma cytokines, which are involved in immunity and stress response, were higher in the blood of people who perished. Fatal cases had unique metabolic responses compared to survivors, higher levels of virus, changes to plasma lipids involved in
processes like blood coagulation, and more pronounced activation of some types of immune cells.

Pancreatic enzymes also leaked into the blood of patients who died, suggesting that damage from these enzymes contributes to the tissue damage characteristic of fatal Ebola virus disease. The study showed that levels of two biomarkers, known as L-threonine (an amino acid) and vitamin D binding protein, may accurately predict which patients live and which die. Both were present at lower levels at the time of admission in the patients who ultimately perished.

When Ebola virus leads to death, experts believe it is because of overwhelming viral replication. Symptoms of infection include severe hemorrhaging, vomiting and diarrhea, fever and more. In the current Ebola study, the team found that many of the molecular signals present in the
blood of sick, infected patients overlap with sepsis, a condition in which the body in response to infection by bacteria or other pathogens mounts a damaging inflammatory reaction.
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Effects of parents' lifestyle on their children

The importance of parents' characteristics for their children's health is explained by poor living conditions in childhood lead to poverty in adulthood-which affects health and
the transmission of sound or ill health to children. Beyond the obvious common genetic inheritance across generations, parents' health also has an impact on their children's health by imparting habits and lifestyles.

Our research found that if a parent smoked when their child was young, the child was much more likely to smoke as an adult. A person's obesity in later life was more frequent when their parents were smokers and had a problem with alcohol. Obesity was one not only associated with parents having a problem with alcohol it was also associated with parent being smoker. If a person's father smoked when they were 12, they were almost twice as likely to smoke than people whose father did not smoke at all.

If mothers smoked, it increased the risk of their daughters smoking – but not their sons. The risk that a person would smoke was also higher among those whose father was a manual worker, and who had experienced periods of poverty during their childhood. Our findings should give pause for thought to those who devised the new NHS plans to stop smokers or obese patients from having surgery unless they quit smoking or lose weight.

The decision assumes that these patients' poor health is self induced, so they are made to choose between facing the consequences of their lifestyle or demonstrating a commitment to change. These sorts of public health policies don't take into account that lifestyle is strongly associated with circumstances beyond a person's control, especially their childhood circumstances and their parents' health and lifestyles.

Restricting their access to treatment appears especially unfair when people do not have equal opportunities to be in good health and to adopt healthy lifestyles. People would only be responsible for the share that isn't linked to their childhood conditions or their parents' choices. The study shows that, even without making this distinction between responsibility and true responsibility, the control of people on their health choices and their health status is limited.
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Hemlibra for treating hemophilia

 The U.S. Food and Drug Administration today approved Hemlibra (emicizumab-kxwh) to prevent or reduce the frequency of bleeding episodes in adult and pediatric patients with hemophilia A who have developed antibodies called Factor VIII (FVIII) inhibitors. Reducing the frequency or preventing bleeding episodes is an important part of disease management for patients with hemophilia.

Hemophilia A is an inherited blood-clotting disorder that primarily affects males. According to the National Institutes of Health, hemophilia affects one in every 5,000 males born with the condition. Patients with hemophilia A are missing a gene which produces Factor VIII, a protein that enables blood to clot.

Patients may experience repeated episodes of serious bleeding, primarily into their joints, which can be severely damaged as a result. Some patients develop an immune response known as a FVIII inhibitor or antibody. The antibody interferes with the effectiveness of currently available treatments for hemophilia.

Hemlibra is a first-in-class therapy that works by bridging other Factors in the blood to restore blood clotting for these patients. Hemlibra is a preventative (prophylactic) treatment given weekly via injection under the skin (subcutaneous).

Patients treated with Hemlibra reported an improvement in hemophilia-related symptoms (painful swellings and joint pain) and physical functioning (pain with movement and difficulty walking) compared to patients who did not receive prophylactic treatment. Common side effects of Hemlibra include injection site reactions, headache, and joint pain (arthralgia).

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Vaping can cause birth defects

Vaping while pregnant could cause babies to be born with disfiguring birth defects to their faces and heads. Exposure to e-cigarette vapor damaged cells that would eventually become facial features in ways that could cause facial clefts and uneven growth of facial structures. The Centers for Disease  Control and Prevention CDC and doctors already recommend that no form of smoking – including vaping – is safe for pregnant women.

As many as 19.4 percent of young adults thought that e-cigarettes caused ‘no harm,’ according to CDC data collected between 2013 and 2014. More than half of the same age group believed that they were only ‘moderately harmful.’ Studies have shown that e-cigarette vapor does have fewer toxins, but the products are so new that their effects aren’t fully understood.

They discovered that the mixture of liquids to create the novel flavors of e-cigarette vapor were responsible for the worst damage to the developing fetus. Most flavors led to only minor effects, like slightly smaller than normal faces. But one unnamed flavor in particular consistently caused the most damage. All of the frogs exposed to that flavor had significant facial clefts.

E-cigarettes use a heating mechanism to heat e-liquids and convert them into flavored vapor. The liquids contain nicotine, as well as propylene, glycol, vegetable glycerine and flavoring compounds. The ingredients used to make the various flavors are a bit of a mystery. Researchers  analyzed 159 varieties of flavored vape liquids, and found that more than two thirds used a compound called diacetyl, which is linked to a popcorn lung.

Previous research linked flavoring in e-liquids to heart defects in developing zebrafish, brain development delays in mice, and the release of at least two carcinogens. The researchers tested six different e-liquids, with nicotine strengths varying from six mg/ml to 24 and one or more flavoring additives. Two varieties had only one flavor each: red tobacco and menthol. They also tested a liquid flavored with both milk and dark chocolate, and one with melon and candy.

The most dramatic defects were tied to the two liquids with the greatest number of different flavors. One used strawberry, almond, caramel, vanilla, biscuit and Vienna cream flavorings, and the other had cereal, berries, cream and citrus. Both of the many-flavored varieties led to dramatically cleft faces or other facial birth defects in the frogs they were tested on.

Facial and mouth clefts are gaps in the middle of the face that can affect both soft muscle and skin tissue and bones. They are rare in humans, effecting only about 1 in every 150,000 babies born worldwide. Depending on how severe the cleft is, they may be reparable with surgery, but if left untreated can also make it difficult for people with cleft faces and palates to eat, make them prone to ear infections and hearing loss, speech and language impairments and dental problems.
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Anti-malarial drug for Zika virus treatment

Medication used to prevent and treat malaria may also be effective for Zika virus. The drug, called chloroquine, has a long history of safe use during pregnancy. Zika causes mild flu-like symptoms. But in pregnant women, the virus can cause serious birth defects in babies-including microcephaly-a neurological condition in which newborns have unusually small heads and fail to develop properly.

Presently, there is no treatment or way to reverse the condition. The latest research suggests the anti-malaria drug chloroquine may be an effective drug to treat and prevent Zika infections. Reseachers examined the effect of chloroquine in human brain organoids and pregnant mice infected with the virus, and found the drug markedly reduced the amount of Zika virus in maternal blood and neural progenitor cells in the fetal brain.

Pregnant mice received chloroquine through drinking water in dosages equivalent to acceptable levels used in humans. Although chloroquine did not completely clear Zika from infected mice it did reduce the viral load, suggesting it could limit the neurological damage found in newborns infected by the virus.
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Naturally acquired immunity against Zika virus

During their study of Zika infection in pregnant mice, the researchers built-up immunity in previously infected mothers that continued into pregnancy and protected fetal tissues. Because the mothers had already cleared their non-symptomatic Zika infections, they developed high levels of protective immunoglobulin antibodies against the virus that researchers found in the animals. Detection of these protective antibodies points to the possibility of developing diagnostic tests to identify naturally immune women and distinguish them from women at high risk of infection.

The ability to identify high-risk women would help develop focused therapeutic strategies for prevention, combining protective antibodies with an eventual vaccine, which could synergistically provide more a robust level of protection against Zika. Built-up immunoglobulin antibodies protect against Zika infection in mothers and their developing fetal offspring.

Researchers said expectant mothers are susceptible to Zika infection compared to non-pregnant women. If the virus is active during pregnancy, it usually spreads to vital tissues of a developing fetus. Because Zika virus infection in healthy non-pregnant women is mostly asymptomatic, many women of reproductive age in high-risk regions have a cleared infection before pregnancy.

Susceptibility to Zika virus infection was markedly reduced in mice that had previously cleared a prior infection compared to those undergoing a first infection during pregnancy. Mice that didn't have prior Zika infections developed clinical symptoms and sharply increased levels of Zika virus in their blood, which spread to fetal tissues.

Zika virus could not be found in most of the baby mice from mothers with resolved infection prior to pregnancy. Protection found in Zika-resistant mice could be transferred to susceptible mice with Zika virus neutralizing antibodies found in the blood of mice with prior asymptomatic infection.
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