Chronic obstructive pulmonary disease (COPD) is a complex condition that affects millions worldwide. Researchers have long sought to understand the underlying causes of this debilitating disease. A recent study published in ERJ Open Research has shed new light on the role of carbon build-up in COPD, revealing a significant accumulation of soot-like deposits in the lungs of affected individuals.

The research team, led by Drs James Baker and Simon Lea from the University of Manchester, UK, investigated the impact of carbon exposure on alveolar macrophages – cells that protect the body by engulfing particles and bacteria. In COPD patients, these cells are found to be larger and more prone to inflammation when exposed to carbon.

The study compared samples from 28 people with COPD and 15 smokers without the disease. They discovered a staggering three-fold increase in carbon accumulation within alveolar macrophage cells of COPD patients compared to those who smoked but did not have COPD. Notably, patients with larger deposits of carbon in their alveolar macrophages exhibited worse lung function, as measured by FEV1%.

Dr Lea noted that this build-up of carbon is not a direct result of cigarette smoking, but rather an inherent difference in the form and function of alveolar macrophages between COPD patients and smokers. This raises intriguing questions about the causes of increased carbon levels in COPD patients’ macrophages. Is it because people with COPD are less able to clear the carbon they breathe in? Or is it due to exposure to more particulate matter, which accumulates and contributes to the development of COPD?

The implications of this research are significant, suggesting that reducing pollution in the air we breathe and helping people quit smoking may be crucial steps towards mitigating the risks of COPD. The study also highlights the need for further investigation into how carbon builds up over time and how lung cells respond.

As Professor Fabio Ricciardolo, Chair of the European Respiratory Society’s group on monitoring airway disease, pointed out, “This set of experiments suggests that people with COPD accumulate unusually large amounts of carbon in the cells of their lungs. This build-up seems to be altering those cells, potentially causing inflammation in the lungs and leading to worse lung function.”

The findings of this study offer valuable insights into the complex interplay between environmental and genetic factors in COPD. As researchers continue to unravel the mysteries of this disease, they hope to develop more effective treatments and preventive strategies for patients worldwide.

The risk of blood clots is a serious concern worldwide, with venous thrombosis being one of the most common causes of death globally. A recent study from Lund University in Sweden has shed light on three genetic variants that significantly increase the risk of blood clots in the leg by up to 180%.

While arterial and venous blood clots have different causes and consequences, understanding the risk factors is crucial for prevention and treatment. In Sweden, over 10,000 people suffer from venous thromboembolism each year, with age being a strong risk factor.

“Venous thrombosis is a common disease that has always been somewhat overshadowed by arterial blood clots,” says Bengt Zöller, a specialist in general medicine at Skåne University Hospital and professor of general medicine at Lund University. “However, it’s essential to acknowledge its significance and take steps to prevent it.”
The risk factors for venous thrombosis include age, being overweight or tall, and lack of physical activity. Smoking is considered only a weak to moderate risk factor, while high blood pressure and high levels of blood lipids are associated with arterial clots, not venous ones.

Research suggests that commercial fishermen have a lower risk due to their diet rich in omega-3 fatty acids. Additionally, ultra-processed foods have been linked to an increased risk of blood clots, whereas plant-based diets may reduce this risk.
“Prophylaxis in the form of blood thinners may be particularly important if other risk factors are also present,” advises Zöller.

The three genetic variants identified by Bengt Zöller and his fellow researchers are ABO, F8, and VWF. These variants increase the risk of venous blood clots by 10-30% each, with an individual having five of these gene variants having a 180% higher risk.
“These genetic variants are present in all populations, making it essential to investigate how the number of risk genes affects the duration of treatment with anticoagulants after a blood clot,” concludes Zöller.

To prevent blood clots, one can take steps such as maintaining physical activity, monitoring blood pressure and lipid levels, quitting smoking, and eating a balanced diet rich in omega-3 fatty acids. Tailoring treatment based on risk assessment will become increasingly important in the future.
“Tailoring treatment based on risk assessment will become increasingly important,” concludes Bengt Zöller.

In summary, understanding the three genetic variants that increase the risk of blood clots by up to 180% is crucial for prevention and treatment. By acknowledging these risk factors, individuals can take steps to reduce their likelihood of developing venous thrombosis.
“Blood clot prevention is a vital aspect of healthcare, and awareness about the risks is essential,” emphasizes Zöller.

Chronic renal failure affects millions worldwide, including four million Canadians. Researchers at the Canadian hospital research centre, CRCHUM, have made a world-first breakthrough by identifying microRNA that can protect small blood vessels and support kidney function after severe injury. This advancement has significant implications for early diagnosis and prevention of the disease.

Previously, there was no reliable biomarker to evaluate the health of tiny capillaries in the kidneys or develop targeted approaches to preserve kidney function. A study published in JCI Insight reveals that miR-423-5p microRNA is a promising marker in the blood for predicting the microvascular health of the kidneys.

Researchers Marie-Josée Hébert and Héloïse Cardinal, along with Francis Migneault, have been studying the loss of peritubular capillaries, a conclusive indicator of chronic renal failure. These tiny blood vessels filter waste products out of the blood and transport oxygen and nutrients necessary for the organ’s functions.

Kidney injuries can lead to a decrease in small blood vessels, seriously disrupting kidney function. In people who have received a transplant, if kidney function is severely altered, the kidney’s survival is threatened. Using this biomarker, a test could be developed to evaluate the status of small blood vessels much earlier. Doctors could then better assess microvascular health in higher-risk patients.

This breakthrough has been confirmed in 51 transplant recipients and has shown potential for preventing further damage to kidneys. The researchers are now focused on alternative techniques to transport microRNA or a cocktail to the kidney, which may be useful for other patients with cardiac failure, pulmonary failure, or certain neurodegenerative diseases.

The discovery of miR-423-5p microRNA could have a significant impact on the health of Canadians and potentially lead to new treatments for various medical conditions. Researchers are currently exploring its potential in other areas, such as determining if existing medications impact small blood vessel health in kidney transplant patients.