Category: 8. Health

A research team has evaluated the real-world impact of a community-based pneumococcal vaccination support program for older adults conducted in Sera Town, Hiroshima Prefecture, Japan.

Their work is published in the Journal of Epidemiology on May 5, 2025.

Pneumonia is one of the leading causes of death in Japan. Each year about 74,000 people die from pneumonia with 98 percent of these deaths occurring in people aged 65 and older. The bacteria Streptococcus pneumoniae is the primary cause of pneumonia.

In October 2014, Japan began a nationwide routine vaccination program for the elderly under the National Immunization Program with the 23-valent pneumococcal polysaccharide vaccine (PPSV23). 

Sera Town, a mountainous municipality in eastern Hiroshima Prefecture, jointly planned and implemented a pneumococcal vaccination support program with a research team at Hiroshima University in October 2010-well before the nationwide rollout. The program, which ran until March 2015, aimed to promote community health and provided PPSV23 vaccination to all residents aged 65 and older. The vaccine used in the project was approved in Japan at the time for elderly individuals. As part of this collaborative initiative, a five-year follow-up survey was conducted to assess the vaccine’s preventive effect against pneumonia. 

Specifically, we sought to understand the impact of the PPSV23 vaccine on pneumonia incidence and mortality among the elderly population in a rural setting with a high aging rate.”

Aya Sugiyama, lecturer in the Department of Epidemiology Disease Control and Prevention at the Graduate School of Biomedical and Health Sciences, Hiroshima University

The Sera Town residents who took part in the project ranged in age from 70 to 114 years old, with a median age of 84.

To assess changes in mortality following the introduction of the vaccination program, the researchers used aggregated demographic data from Japan’s vital statistics covering the years 2000 to 2016. They applied an interrupted time series analysis to quantify the level and trend changes in mortality rates over time, specifically looking at the mortality rates before and after the vaccination project was introduced in the town. The study aimed to generate real-world evidence on the effectiveness of vaccination support programs in super-aged societies.

Their analysis of the data showed them that the pneumococcal vaccination support program for older residents in Sera Town was associated with a 25 percent reduction in pneumonia-related mortality. “Notably, it reversed the previously increasing trend in pneumonia mortality in the community,” said Sugiyama.

The study also provided valuable data on the actual incidence of pneumonia among vaccinated older adults, with an incidence rate of 20.3 cases per 1,000 person-years. Scientists use the person-year method in studies where they follow individuals over a period of time. A person-year is one person being followed for one year.

“These findings underscore both the public health significance of local vaccination efforts and the burden of pneumonia in aging populations,” said Sugiyama.

The research team sees the findings as particularly relevant for Japan, which has the most aged population in the world. “With the completion of this evaluation, the next step is to share these findings to inform future discussions on community-based vaccination strategies. While further research is needed, we hope that our results will serve as a reference for regions exploring effective approaches to pneumonia prevention in older adults,” said Sugiyama.

The research team includes Aya Sugiyama, Kanon Abe, Hirohito Imada, Bunlorn Sun, Golda Ataa Akuffo, Tomoyuki Akita, Shingo Fukuma, Junko Tanaka, and Noboru Hattori from Hiroshima University; Masaaki Kataoka from Sera Central Public Hospital; and Kentaro Tokumo from Sera Central Public Hospital, Hiroshima University, and Hiroshima University Hospital.

The research is funded by the Sera Town municipality.

The prevalence of irritable bowel syndrome (IBS) and chronic idiopathic constipation among US adults rose significantly during the COVID-19 pandemic, with a near doubling of the national rate of IBS over 2 years, a study has found.

The uptick is probably due to not only the direct impact of SARS-CoV-2 infection on the gastrointestinal tract but also to the psychological stress associated with pandemic life, the study team said. 

“COVID infection itself can definitely cause gastrointestinal symptoms like diarrhea, nausea, and abdominal pain — and for some people, those symptoms can linger and lead to chronic conditions like IBS,” Christopher V. Almario, MD, MSHPM, lead author and gastroenterologist at Cedars-Sinai Medical Center, Los Angeles, California, told Medscape Medical News. 

“But the stress of living through the pandemic — lockdowns, fear, isolation — also likely played a major role as well in the increased prevalence of digestive disorders. Both the infection itself and the psychological toll of the pandemic can disrupt the gut-brain axis and trigger chronic digestive disorders like IBS,” Almario said. 

The study was published in Neurogastroenterology & Motility.

Growing Burden of Gut Disorders 

Disorders of gut-brain interaction (DGBIs) are a heterogeneous group of conditions in which gastrointestinal symptoms occur without any detectable structural or biochemical abnormalities in the digestive tract. They include IBS, functional dyspepsia, and chronic idiopathic constipation, among others. 

DGBIs are highly prevalent. Research has shown that nearly 40% of people in the US meet Rome IV criteria for at least one DGBI. 

Almario and colleagues assessed trends in prevalence of these conditions during the COVID-19 pandemic. Starting in May 2020 through May 2022, they conducted a series of online surveys with more than 160,000 adults aged 18 or older using validated Rome IV diagnostic questionnaires. 

Results showed that during the pandemic, IBS prevalence rose from 6.1% in May 2020 to 11.0% by May 2022, an increase of 0.188% per month (adjusted P < .001). 

Chronic idiopathic constipation showed a smaller but statistically significant increase, from 6.0% to 6.4% (0.056% per month; adjusted P < .001). 

Within the IBS subtypes, mixed-type IBS showed the largest relative increase (0.085% per month), followed by IBS with constipation (0.041% per month) and IBS with diarrhea (0.037% per month). 

There were no significant changes in the prevalence of other DGBIs, such as functional bloating, functional diarrhea, or functional dyspepsia, during the study period. 

Almario told Medscape only about 9% of those surveyed reported a positive COVID test at the time of the surveys, but that figure probably underrepresents actual infections, especially in the early months of the pandemic. “Most of the survey responses came in during the earlier phases of the pandemic, and the percentage reporting a positive test increased over time,” he explained. 

Almario also noted that this study did not directly compare digestive disorder rates between infected and uninfected individuals. However, a separate study by the Cedars-Sinai team currently undergoing peer review addresses that question more directly. “That study, along with several other studies, show that having COVID increases the risk of developing conditions like IBS and functional dyspepsia,” Almario said. 

Taken together, the findings “underscore the increasing healthcare and economic burden of DGBI in the post-pandemic era, emphasizing the need for targeted efforts to effectively diagnose and manage these complex conditions,” they wrote. 

“This will be especially challenging for healthcare systems to address, given the existing shortage of primary care physicians and gastroenterologists — clinicians who primarily manage individuals with DGBI,” they noted. 

Support for this study was received from Ironwood Pharmaceuticals and Salix Pharmaceuticals in the form of institutional research grants to Cedars-Sinai. Almario has consulted for Exact Sciences, Greenspace Labs, Owlstone Medical, Salix Pharmaceuticals, and Universal DX.

Disrupted care during the covid-19 pandemic led to sharp increases in other non-covid causes of illness and death, particularly mental health disorders, malaria in young children, and stroke and heart disease in older adults, finds a study published by The BMJ today.

For example, new cases of depressive disorders rose by 23% in 5-14 year-olds and malaria deaths rose by 14% in children under five years old from 2020-2021.

The researchers say future responses to potential pandemics or other public health emergencies of international concern “must extend beyond infection control to address long term, syndemic health impacts.”

Most healthcare services were severely affected during the pandemic, hindering efforts to prevent and control many conditions. Yet an in-depth analysis of the pandemic’s impact on other causes of illness and death is still needed.

To address this, researchers in China used data from the Global Burden of Disease Study 2021 to simulate the burden of 174 health conditions in 2020 and 2021 across various regions, age groups, and sexes.

A total of 204 countries and territories were included in the analysis. The main measures of interest were incidence (number of new cases), prevalence (number of people living with a condition), deaths, and disability adjusted life years (DALYs) – a combined measure of quantity and quality of life.

Depressive and anxiety disorders, along with malaria, were the most notably affected, with a significant rise in disease burden compared with other causes.

For example, age standardised DALY rates for malaria rose by 12% (to 98 per 100,000). DALY rates for depressive and anxiety disorders also rose by 12% (to 83 per 100,000) and 14% (to 74 per 100,000), respectively, especially among females.

Age standardised incidence and prevalence rates for depressive disorders rose by 14% (to 618 per 100,000) and 10% (to 414 per 100,000), respectively, while anxiety disorders saw a 15% rise (to 102 and 628 per 100,000).

Prevalence rates for heart disease also saw notable increases, particularly among individuals aged 70 and above (169 per 100,000 for ischaemic heart disease and 27 per 100,000 for stroke). 

There was also a significant (12%) increase in the age standardised death rate due to malaria, particularly among children under five years old in the African region.

The researchers acknowledge that their methods may not fully capture the complexity and variation of pandemic-related disruptions, and say factors such as uneven quality of data across regions, potential underreporting, and delayed diagnoses during the pandemic, may have affected the accuracy of their results.

However, they say their analysis offers broader scope than previous studies and provides actionable, policy relevant recommendations to improve health system preparedness.

As such, they conclude: “These findings underscore the urgent need to strengthen health system resilience, enhance integrated surveillance, and adopt syndemic-informed strategies to support equitable preparedness for future public health emergencies.”

This study highlights how data can guide smarter recovery to ensure that future health crises disrupt lives less and afflict populations more evenly, say researchers in a linked editorial.

By integrating these insights into post-pandemic plans, countries can improve resilience, they write. Concrete steps include allocating budgets for essential services in emergencies, reinforcing primary health care, expanding disease surveillance networks, and prioritising universal health coverage with a focus on disadvantaged or marginalised communities.

“Ultimately, recognising and planning for the pandemic’s indirect toll will save lives and leave health systems stronger and fairer for future public health emergencies,” they conclude.

Researchers at McMaster University, Cleveland Clinic and Case Comprehensive Cancer Center have uncovered how a protein long associated with Alzheimer’s disease helps lung cancer spread to the brain – a discovery that offers hope that existing Alzheimer’s drugs could be repurposed in preventing cancer’s spread.

The study, published in Science Translational Medicine on July 2, 2025, details how the protein (BACE1) is instrumental in the development of brain metastases – tumours that spread to the brain from cancers originating elsewhere in the body – in people with lung cancer. These tumours occur in up to 40 per cent of patients with non-small cell lung cancer.

We’ve always associated BACE1 with Alzheimer’s disease, so to find it playing a major role in lung cancer brain metastases is an important discovery. It’s a reminder that cancer can hijack biological pathways in ways we don’t yet fully understand.”

Sheila Singh, senior author, director of McMaster’s Centre for Discovery in Cancer Research and professor with the Department of Surgery

To make the discovery, researchers used a cutting-edge gene activation technique known as a genome-wide in vivo CRISPR activation screen. The technique allowed researchers to systematically activate thousands of genes one by one in lung cancer cells and put the modified cells into mice. When BACE1 was switched on, the cancer cells were far more likely to invade the brain.

BACE1 has long been linked to Alzheimer’s disease, the most common form of dementia. In people with Alzheimer’s, BACE1 cuts a protein called APP, triggering the formation of sticky plaques in the brain.

Currently, there are limited therapies available once cancer has spread to the brain. However, researchers say the discovery of BACE1 does offer hope as a drug developed for Alzheimer’s could be repurposed.

The therapy uses a drug called Verubecestat that blocks BACE1 activity. Researchers found that mice given Verubecestat had fewer and smaller tumours, and also lived longer. The drug had shown promise in Alzheimer’s patients but a Phase 3 clinical trial was discontinued in 2018 after a committee determined it was unlikely that positive benefit/risk could be established.

“The discovery of BACE1 opens the door to repurposing existing treatments like Verubecestat to potentially prevent or slow the spread of lung cancer to the brain, where treatment options are currently very limited,” Singh says.

The team say more research is needed to better understand the effectiveness of the therapy in preventing the spread of lung cancer to the brain.

“This study highlights how interdisciplinary partnerships can lead to breakthroughs in understanding and treating devastating diseases like brain metastases,” said Shideng Bao, a researcher in Cleveland Clinic’s Department of Cancer Biology, a corresponding author on the paper. “By identifying BACE1 as a key player in the spread of lung cancer to the brain, we’ve uncovered a promising new avenue for therapeutic intervention that could ultimately improve outcomes for patients.”

The Sheila Singh Lab collaborated with Cleveland Clinic and Case Comprehensive Cancer Center on the research. Singh and her colleagues are world leaders in brain cancer research, previously discovering a pathway used by cancer cells to infiltrate the brain, as well as new therapeutic approaches.

The study was supported by funding from the Boris Family Fund for Brain Metastasis Research, the Canadian Cancer Society, the Canadian Institute of Health Research, the Cancer Research UK Lung Cancer Centre of Excellence the Cleveland Clinic Foundation and Lerner Research Institute, and a Sir Henry Wellcome Fellowship.

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A team of researchers from Japan has developed a method for generating alveolar epithelial type 2 (AT2)-like cells from mouse embryonic fibroblasts without using stem cell technology. Remarkably, this process, which typically takes a month with conventional stem cell differentiation, has been reduced to just 7 to 10 days.

The new approach, published in npj Regenerative Medicine, may have significant implications for the treatment of respiratory diseases such as interstitial pneumonia and chronic obstructive pulmonary disease (COPD), which currently have limited treatment options. AT2 cells are critical for lung health, as they produce surfactant and help in alveolar repair. In severe lung diseases, these cells can be depleted or impaired, underscoring the potential therapeutic value of regenerating AT2 cells.

New approach to generating AT2-like cells

Induced pluripotent stem cell (iPSC)-based methods have enabled the creation of AT2 cells, but this process is expensive and time-consuming, inspiring researchers to search for faster alternatives.

“The advent of the induced pluripotent stem cell (iPSC) technology in 2006 has enabled the generation of AT2 cells in approximately one month, but this method is costly and carries risks of tumor formation and immune rejection,” explained Professor Makoto Ishii of Nagoya University Graduate School of Medicine.

“To overcome these disadvantages, we focused on direct reprogramming instead. The direct reprogramming approach produces AT2-like cells in just 7 to 10 days, with lower tumor risk and potential for autologous use,” Ishii said.

The researchers focused on reprogramming mouse fibroblasts to produce AT2-like cells, known as induced pulmonary epithelial-like cells (iPULs), in a significantly shorter period.

First, the researchers identified 14 candidate genes associated with lung development. By studying expression levels of the AT2 cell marker, surfactant protein-C (Sftpc), they were able to determine a combination of four genes with the highest reprogramming efficiency – Nkx2-1, Foxa1, Foxa2 and Gata6 – that were most effective in inducing AT2-like cells.

These genes were introduced into a 3D culture of mouse fibroblasts expressing green fluorescent protein (GFP) in response to Sftpc. Approximately 4% of the cells exhibited GFP positivity in 7 to 10 days, indicating the successful induction of iPULs.

Transplantation into mouse lungs

Following this, the researchers isolated the GFP-positive cells using flow cytometry and analyzed them. The purified iPULs displayed lamellar body-like structures, which are characteristic of normal AT2 cells. A transcriptomic analysis revealed that the gene expression profiles of the iPULs closely resembled those of native AT2 cells.

To test the functionality of these iPULs, the researchers transplanted them into mice with interstitial pneumonia. After 42 days, the transplanted cells successfully engrafted into the alveolar region. Notably, some of the cells differentiated into alveolar epithelial type 1 (AT1)-like cells, which are vital for lung tissue regeneration.

With the successful demonstration of the reprogramming of fibroblasts into AT2-like cells in mice, the researchers say that their next step will be to explore the potential for using this technology in human cells. The ultimate goal is to develop a safe regenerative therapy using a patient’s own fibroblasts, Ishii added.

Reference: Morita A, Ishii M, Asakura T, et al. Direct reprogramming of mouse fibroblasts into self-renewable alveolar epithelial-like cells. npj Regen Med. 2025;10(1):30. doi: 10.1038/s41536-025-00411-4

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X-rays of the ankle showed swelling in the soft tissue but without some signs of infection. The doctors wondered if the man had osteomyelitis, an infection in the bone, which can be a complication in people with diabetic ulcers. The large size and duration of the ulcer matched with a bone infection, as well as some elevated inflammatory markers he had on his blood tests.

To investigate the bone infection further, they admitted the man to the hospital and ordered magnetic resonance imaging (MRI). But the MRI showed only a soft-tissue defect and a normal bone, ruling out a bone infection. Another MRI was done with a contrast agent. That showed that the man’s large arteries were normal and there were no large blood clots deep in his veins—which is sometimes linked to prolonged standing, as the man did at his laundromat job.

As the doctors were still working to root out the cause, they had started him on a heavy-duty regimen of antibiotics. This was done with the assumption that on top of whatever caused the ulcer, there was now also a potentially aggressive secondary infection—one not knocked out by the previous round of antibiotics the man had been given.

With a bunch of diagnostic dead ends piling up, the doctors broadened their view of possibilities, newly considering cancers, rare inflammatory conditions, and less common conditions affecting small blood vessels (as the MRI has shown the larger vessels were normal). This led them to the possibility of a Martorell’s ulcer.

These ulcers, first described in 1945 by a Spanish doctor named Fernando Martorell, form when prolonged, uncontrolled high blood pressure causes the teeny arteries below the skin to stiffen and narrow, which blocks the blood supply, leading to tissue death and then ulcers. The ulcers in these cases tend to start as red blisters and evolve to frank ulcers. They are excruciatingly painful. And they tend to form on the lower legs, often over the Achilles’ tendon, though it’s unclear why this location is common.