For patients struggling to breathe because of acute respiratory failure, clearing mucus from the airways is a routine part of treatment. Mucoactive agents are widely used for this purpose. But after years of clinical use, one question remains: Do mucoactive agents actually help?

To figure this out, researchers designed a large study called the MARCH (Mucoactives in Acute Respiratory Failure: Carbocisteine and Hypertonic Saline) randomized trial, which included nearly 2,000 adults across 71 hospitals in the United Kingdom who were on ventilators and having trouble clearing mucus. The focus of the study was to determine the effectiveness of two widely used mucoactive agents: carbocisteine and hypertonic saline (HTS).

The drugs did not deliver the hoped-for benefits. Those who were on carbocisteine spent about the same amount of time on the ventilator as those who didn’t get any treatment, and the same was true for HTS. Instead, the medications appeared to do more harm than good. Patients treated with these mucoactive agents had side effects like bleeding in the stomach, tightened airways and a drop in blood oxygen levels.

Northwestern Medicine scientists have discovered that one of the body’s most fundamental biological processes—how red blood cells are made—works differently in humans than previously thought, according to a new study published in Nature Genetics. The findings overturn decades of assumptions based largely on animal research, said study senior author Peng Ji, MD, Ph.D., the Marie A. Fleming Research Professor of Pathology.

In the study, Ji and his collaborators used advanced spatial mapping tools to directly observe microscopic environments, known as erythroblastic islands (EBIs), inside intact tissues. EBIs have long been understood to act as “nurseries” where red blood cells mature. But until now, scientists lacked a clear picture of what these structures look like in humans.

“For decades, our understanding of these structures has come almost entirely from mouse studies,” said Ji, who is also vice chair for research in the Department of Pathology. “Most experiments relied on isolating cells and studying them in flat, two-dimensional systems, which disrupt their native organization.”

Lyme disease can be easiest to treat in its earliest stages, but current tests often miss infections during that critical window and cannot tell whether bacteria are still present or were cleared years ago. New research led by Tufts University School of Medicine suggests that a group of immune molecules called anti-lipid antibodies may address these shortcomings.

The findings, published in Infection and Immunity, could lead to improved tests that identify Lyme disease earlier, when antibiotics can best prevent more debilitating disease. They also may help clinicians better identify patients who continue to experience symptoms of infection after treatment—and potentially find new drug targets to help them.

Nearly half a million Americans are diagnosed and treated for Lyme disease each year. Caused by the bacterium Borrelia burgdorferi and spread through the bite of infected blacklegged ticks (also known as deer ticks), the disease can lead to arthritis, neurological problems and heart complications if untreated.