Chest CT Diagnosis and Clinical Management of Drug-related Pneumonitis in Patients Receiving Molecular Targeting ...

Lung Disease News

Dec. 12, 2023 — By monitoring changes in circulating tumor DNA (ctDNA) among 30 patients treated with immunotherapies for metastatic non-small cell lung cancers, researchers were able to determine molecular response ...

Dec. 11, 2023 — Advancements in the care of premature babies are leading to improved survival rates. However, the incidence of neonatal diseases with life-long consequences such as bronchopulmonary dysplasia (BPD) ...

Dec. 6, 2023 — Researchers have identified an allergy pathway that, when blocked, unleashes antitumor immunity in mouse models of non-small cell lung cancer (NSCLC).  And in an early parallel study in humans, ...

Nov. 29, 2023 — The largest review of papers for brain cancer that has spread from the lungs has found abnormalities in the brain cancer and for which licensed drugs could be clinically trialed to find out if they ...

Nov. 17, 2023 — Research shows that some lung cancer cells retain a 'memory' of the healthy cell where they came from -- one that might be exploited to make an emerging type of lung cancer treatment ...

Nov. 14, 2023 — A new study has discovered asbestos exposure led to a higher incidence of asbestos-related lung cancers in British and Australian naval personnel than in other armed ...

Nov. 13, 2023 — Despite the Centers for Disease Control and Prevention warning this year will be potentially dangerous for respiratory illnesses, a third of Americans are not concerned about the threat, according to ...

Sep. 27, 2023 — Experts in cloning and stem cell science are reporting that five lung stem cell variants dominate the lungs of patients with advanced cystic fibrosis, and that these variants drive key aspects of CF ...

Sep. 27, 2023 — Lung fibrosis is a debilitating disease affecting nearly 250,000 people in the U.S. Alone with 50,000 new cases reported each year. There is currently no cure and limited available treatment options, ...

Sep. 21, 2023 — Scientists have shown that their steerable lung robot can autonomously maneuver the intricacies of the lung, while avoiding important lung ...

Sep. 21, 2023 — Small cell lung cancer accounts for about 15 percent of all diagnosed lung cancers and is still associated with a high mortality rate. SCLC tumours often develop resistance to chemotherapy and thus ...

Sep. 13, 2023 — During a bout of influenza, B cells interact with other immune cells and then take different paths to defend the body. One path is the B cells that differentiate into lung-resident memory B cells, or ...

Sep. 12, 2023 — Pneumonia is an infection of the lung alveoli caused by bacteria, viruses or fungi. It is one of the leading causes of morbidity and mortality worldwide, representing a clinical and economic burden ...

Sep. 12, 2023 — An international team of researchers has demonstrated that a combination of inhibitors may suppress tumor growth and prevent relapse in patients with certain cancers, including head and neck squamous ...

Sep. 7, 2023 — Women exposed to air pollution give birth to smaller babies, according to new research. The research also shows that women living in greener areas give birth to bigger babies and this may help ...

Sep. 7, 2023 — Researchers reveal for the first time that high blood sugar levels in type 2 diabetes can play a causal role in lung ...

Sep. 5, 2023 — A new study has shown that a subtype of avian flu virus, endemic in poultry farms in China, is undergoing mutational changes, which could increase the risk of the disease being passed on to ...

Aug. 30, 2023 — Fresh discoveries about a type of immune cells could give lung cancer patients a more accurate prognosis and better identify who will benefit from immunotherapies. Researchers found that the location ...

Aug. 25, 2023 — High levels of some minerals and metals in environmental water supplies may increase the risk of nontuberculous mycobacteria (NTM) pulmonary infections in people with cystic fibrosis, according to a ...

Aug. 24, 2023 — Researchers have discovered a novel approach for engrafting engineered cells into injured lung tissue. These findings may lead to new ways for treating lung diseases, such as emphysema, pulmonary ...

Tuesday, December 12, 2023

Monday, December 11, 2023

Wednesday, December 6, 2023

Wednesday, November 29, 2023

Friday, November 17, 2023

Tuesday, November 14, 2023

Monday, November 13, 2023

Wednesday, September 27, 2023

Thursday, September 21, 2023

Wednesday, September 13, 2023

Tuesday, September 12, 2023

Thursday, September 7, 2023

Tuesday, September 5, 2023

Wednesday, August 30, 2023

Friday, August 25, 2023

Thursday, August 24, 2023

Wednesday, August 16, 2023

Friday, August 11, 2023

Wednesday, August 9, 2023

Tuesday, August 8, 2023

Tuesday, July 25, 2023

Thursday, July 20, 2023

Friday, July 7, 2023

Thursday, June 22, 2023

Thursday, June 8, 2023

Thursday, June 1, 2023

Wednesday, May 24, 2023

Friday, April 21, 2023

Friday, March 31, 2023

Tuesday, March 28, 2023

Friday, March 17, 2023

Wednesday, March 15, 2023

Monday, March 13, 2023

Friday, March 10, 2023

Thursday, March 9, 2023

Wednesday, March 8, 2023

Monday, February 27, 2023

Thursday, February 23, 2023

Wednesday, February 22, 2023

Wednesday, February 8, 2023

Wednesday, February 1, 2023

Thursday, January 19, 2023

Thursday, January 12, 2023

Monday, January 9, 2023

Thursday, January 5, 2023

Wednesday, January 4, 2023

Wednesday, December 28, 2022

Monday, December 26, 2022

Thursday, December 22, 2022

Wednesday, December 21, 2022

Tuesday, December 6, 2022

Monday, December 5, 2022

Friday, December 2, 2022

Thursday, December 1, 2022

Wednesday, November 30, 2022

Tuesday, November 29, 2022

Tuesday, November 22, 2022

Monday, November 21, 2022

Thursday, November 17, 2022

Wednesday, November 16, 2022

Tuesday, November 15, 2022

Tuesday, November 8, 2022

Thursday, November 3, 2022

Wednesday, November 2, 2022

Wednesday, October 26, 2022

Tuesday, October 25, 2022

Monday, October 17, 2022

Monday, October 10, 2022

Tuesday, October 4, 2022

Tuesday, September 27, 2022

Friday, September 23, 2022

Thursday, September 22, 2022

Monday, September 19, 2022

Friday, September 16, 2022

Thursday, September 15, 2022

Wednesday, September 14, 2022

Tuesday, September 13, 2022

Thursday, September 8, 2022

Tuesday, September 6, 2022

Monday, September 5, 2022

Friday, September 2, 2022

Thursday, September 1, 2022

Wednesday, August 31, 2022

Thursday, August 25, 2022

Thursday, August 18, 2022

Tuesday, August 9, 2022

Monday, August 8, 2022

Tuesday, August 2, 2022

Monday, August 1, 2022

Thursday, July 28, 2022

Nintedanib Reveals Remarkable Efficacy In Alleviating Progressive Pulmonary Fibrosis Symptoms

In the groundbreaking INBUILD trial, researchers discovered that nintedanib can significantly improve the lives of patients suffering from progressive pulmonary fibrosis (PPF). Nintedanib holds promise not only in reducing the progression of dyspnea, fatigue, and cough but also in mitigating the overall impact of ILD over 52 weeks in patients grappling with PPF.

The trial results were published in the journal European Respiratory Journal.

Pulmonary fibrosis, a condition characterized by scarring of the lungs, often leads to symptoms such as dyspnea (shortness of breath) and cough, profoundly impacting patients' daily lives. Hence, researchers conducted a trial, that focused on the effects of nintedanib on PPF symptoms using the Living with Pulmonary Fibrosis (L-PF) questionnaire to assess changes in patients' conditions.

The trial included 663 patients with fibrosing interstitial lung disease (ILD), excluding idiopathic pulmonary fibrosis, but with more than 10% lung involvement on high-resolution computed tomography (HRCT) scans and evidence of ILD progression within the past 24 months. Patients were randomly assigned to receive either nintedanib or a placebo, with researchers analyzing L-PF questionnaire scores from baseline to week 52 using mixed models for repeated measures.

Findings:

The results revealed a significant positive impact of nintedanib on patients' lives compared to the placebo group.

Those receiving nintedanib experienced smaller increases (worsenings) in adjusted mean L-PF questionnaire total scores (0.5 versus 5.1) at week 52.

This trend was also observed in symptom scores (1.3 versus 5.3), dyspnea (4.3 versus 7.8), and fatigue (0.7 versus 4.0).

One notable finding was the decrease in L-PF questionnaire cough score in the nintedanib group, in stark contrast to the placebo group where cough scores increased (-1.8 versus 4.3).

Additionally, the impacts of ILD, as assessed by the L-PF questionnaire impact score, decreased slightly in the nintedanib group while increasing in the placebo group (-0.2 versus 4.6).

These positive outcomes were consistent across different patient subgroups, including those with a usual interstitial pneumonia-like fibrotic pattern on HRCT and those with other fibrotic patterns on HRCT.

The findings suggest that nintedanib has the potential to not only reduce the worsening of dyspnea, fatigue, and cough but also mitigate the overall impact of ILD over 52 weeks in patients with progressive pulmonary fibrosis. This breakthrough offers hope to individuals grappling with the debilitating effects of pulmonary fibrosis, as it paves the way for improved treatment strategies and enhanced quality of life for those affected by this challenging respiratory condition. As researchers continue to unravel the complexities of pulmonary fibrosis, advancements like these represent a significant step forward in the pursuit of better therapeutic options and increased well-being for patients.

Further reading: Effects of nintedanib on symptoms in patients with progressive pulmonary fibrosis. DOI: 10.1183/13993003.00752-2023

Genetic Malfunction Causes Rare Lung Disease? Study Finds Defective Cell Function That Was Previously Unknown

One of the most significant cells in the body is the macrophage. This immune cell, dubbed "big eater" in Greek, eats and breaks down dangerous substances like dust, debris, bacteria, and cancer cells. Macrophages play a particularly important role in the lungs, where they combat bacterial infections and remove excess surfactant, a lipid- and protein-rich covering that is essential for lung health but can accumulate sticky matter if left unchecked.

The study found that the children are missing half of their alveolar macrophages, which are located in the air sacs of the lungs.(Shutterstock)

Researchers from Rockefeller University and other institutions have discovered a hereditary illness that causes defective cell function that was previously unknown.

Hindustan Times - your fastest source for breaking news! Read now.

By noticing an unexpected link between a particular subset of sick kids, the researchers were able to make their breakthrough. These nine youngsters had fought lifelong battles with life-threatening conditions such as progressive polycystic lung disease, pulmonary alveolar proteinosis (PAP), and recurring viral and bacterial infections that frequently left their lungs riddled with cysts and left them gasping for air.

But as genomic data revealed, the children shared another characteristic: the absence of a chemical receptor that is supposed to call alveolar macrophages into action. It's the first time that this missing receptor, called CCR2, has been linked to disease. The researchers, including Rockefeller's Jean-Laurent Casanova and Institut Imagine's Anna-Lena Neehus, recently published their results in Cell.

The study also found that the children are missing half of their alveolar macrophages, which are located in the air sacs of the lungs.

"It was surprising to find that CCR2 is so essential for alveolar macrophages to properly function," said Casanova. "When it comes to lung defense and clean-up, people without it are operating at a double loss."

More formally known as C-C motif chemokine receptor 2, CCR2 sits on the surface of alveolar macrophages, a kind of monocyte (or white blood cell). It responds to the presence of a chemical ligand, or binding molecule, known as CCL-2, which is also expressed by monocytes.

The receptor and ligand work together to summon macrophages to the site of an infection, and to maintain the appropriate level of surfactant; too little can lead to collapsed lung tissue, and too much can result in narrowed airways.

It was among these immune cells that first author Neehus, of Casanova's lab at the Institut Imagine in Paris, was seeking evidence of genetic deficiencies that might alter their behaviour. While combing through the genomic data on 15,000 patients in a database, she found two Algerian sisters, then aged 13 and 10, who'd been diagnosed with severe PAP, a syndrome in which surfactant builds up and the gas exchange that takes place in alveoli is hindered.

About 90 per cent of PAP cases are caused by antibodies that cripple a protein that stimulates the growth of infection-fighting white blood cells. The girls, however, didn't have the PAP autoantibodies. Instead, they had no CCR2--a newly identified genetic mutation. Perhaps its lack was connected to their pulmonary conditions, Neehus thought. "It looked interesting and promising," she recalled.

She soon found seven other children in the cohort who had the same CCR2 mutation and serious lung conditions: two more pairs of siblings, and one trio of siblings. They were from the United States and Iran.

To explore the impact the variant might have on the children, the researchers analysed the children's clinical histories, lung tissue samples, and genetic data.

Several key findings emerged. "First we discovered that these patients have only half the normal counts of pulmonary alveolar macrophages, which explains the different types of lesions they have across the pulmonary tissues," says Casanova. With only half a crew, the reduced clean-up unit couldn't keep up with its workload, leading to tissue injury.

The macrophages were otherwise normal, as were the children's other immune cells.Without CCR2 signalling, monocytes have no idea where they're needed. In the study, a live-imaging analysis of the monocytes from the lungs of a 10-year-old girl with CCR2 deficiency showed the cells milling about aimlessly, unsure where to go. (See gif at top.) In contrast, live imaging of monocytes from a healthy control patient shows them migrating in the same direction, summoned by the teamwork of CCR2 and CCL-2.

This directionlessness also makes those with a CCR2 deficiency more susceptible to mycobacterial infections, because the macrophages can't find their way to the tissue clusters where mycobacteria take up residence, and thus digest the invaders.

This had dire effects for three of the children in the study, who developed bacterial infections after being vaccinated with a live-attenuated substrain of Mycobacterium bovis, an agent of tuberculosis. Their immune systems failed to assemble a legion of macrophages at the vaccination site in the shoulder, causing tissue destruction or hard nodes that had to be surgically removed, or lymph node infections. (All of the children were effectively treated with antibiotics.)

The children inherited the deficiency from their parents--and yet their parents were healthy. "Each of the parents carries one disease copy of the gene, and both parents gave the affected copy to their children," said Neehus. "The parents aren't affected because they each only have one copy, whereas the kids have two."

Several children were the result of consanguineous marriages, in which the parents are related. The offspring of such pairings have a higher risk of inheriting the mutation that causes CCR2 to disappear.

---