An outbreak of hantavirus on a cruise ship has left three people dead, with another person in intensive care in Johannesburg, the BBC reports. The ship, MV Hondius, departed from Argentina and had completed its cruise in Cape Verde.
Department of Health spokesperson Foster Mohale told the BBC that there were 150 passengers of various nationalities aboard the vessel.
The three victims were all of Dutch nationality. The first, a 70-year old man, suddenly fell ill, developing fever, headache, abdominal pain and diarrhoea, Mohale reported. The man died at the UK island of St Helena. The second, the man’s 69-year old wife, was evacuated to a Johannesburg hospital but also died there. The body of the third victim is awaiting repatriation, along with a guest “closely associated” with them. A 69-year-old man from the UK remains severely ill in a Johannesburg hospital.
Two crewmembers are also understood to be seriously ill but medical authorities in Cape Verde have not given them authority to disembark.
Hantaviruses are a family of viruses spread mainly by rodents, and can cause serious illnesses and death. These viruses cause diseases like hantavirus pulmonary syndrome (HPS) and haemorrhagic fever with renal syndrome (HFRS). About half of patients will develop abdominal symptoms similar to the first passenger who dies.
Speaking to the BBC, microbiologist Siouxsie Wiles speculates on the possibility that additional cases will develop among the ship’s passengers and crew.
“With this incubation period are we going to see more people coming down with the disease in the next days and weeks?”
In a study of adults with advanced prostate cancer taking androgen-receptor pathway inhibitors and different types of anticoagulants, investigators found no evidence of an increase in patients’ bleeding or clotting risks, despite previous lab results that raised alarms. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.
Thromboembolism, caused by a circulating blood clot that gets stuck and causes an obstruction, is the second leading cause of death in people with cancer, surpassed only by progression of the cancer itself. Anticoagulants (blood thinners) are standard therapy to treat or prevent thromboembolism. For individuals with advanced prostate cancer, thromboembolism can be especially worrisome because lab experiments have indicated that androgen-receptor pathway inhibitors, which are recommended for nearly all patients with advanced prostate cancer, can interact with certain anticoagulants – specifically, direct oral anticoagulants (DOACs).
To investigate whether these lab-based findings correlate to real concerns in patients, researchers evaluated outcomes in patients taking both anticoagulants and androgen-receptor pathway inhibitors, including enzalutamide, apalutamide, and abiraterone.
In the retrospective population-based analysis of 2997 Canadian adults with prostate cancer who were prescribed anticoagulants (DOACs or non-DOACs) and enzalutamide or apalutamide between 2012 and 2023, investigators found no increased risks of clotting in the DOAC versus non-DOAC groups. Similarly, investigators compared DOAC and non-DOAC groups combined with abiraterone and did not find an increased risk of bleeding.
“As clinicians, we are faced with the question of choosing the best anticoagulant option for patients on a daily basis, and the complexity further increases in patients with cancer taking many other medications including anticancer therapies that could cause concerning drug–drug interactions,” said lead author Tzu-Fei Wang, MD, of the University of Ottawa at The Ottawa Hospital and the Ottawa Hospital Research Institute. “Our findings suggest that pharmacokinetic drug–drug interaction concerns may not translate into adverse clinical outcomes in the real world. These results can help clinicians and patients feel more confident when managing anticoagulation alongside modern prostate cancer treatments.”
Older people, particularly women, who start treatment with thiazide-type diuretics are at increased risk of developing low sodium levels in the blood. This is shown by a large registry study from the Karolinska Institutet published in JAMA Network Open.
Thiazides are a common group of medicines used to treat high blood pressure. In some cases, however, treatment can lead to hyponatraemia. Low sodium levels can cause symptoms such as fatigue, nausea, confusion and, in severe cases, seizures.
In the study, the researchers compared the risk of hyponatraemia in people who started treatment with thiazides with the risk in people who were instead given calcium channel blockers, another type of blood pressure medication. The study included a total of 159 080 adults in the Stockholm area and is based on data from the so-called Stockholm Sodium Cohort.
The researchers from KI SÖS, Department of Laboratory Medicine and Department of Molecular Medicine and Surgery at KI, followed the participants for the first two years after the start of treatment. The risk was particularly high among older women. Among women aged 80 or over, 2.4% developed severe hyponatraemia. For this group, this meant that one in 53 people treated was affected. In women under 65, however, the risk was low.
“Our findings show that the link between thiazides and low blood sodium levels is very weak in younger people, but clear in older people, particularly in women,” says Cecilia Bergh Fahlén, a PhD student at the Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet.
The researchers believe that the findings may inform clinical decisions regarding the treatment of high blood pressure.
“For vulnerable patients, such as older women, there may be good reasons for considering alternative blood pressure medications. If thiazides are used nonetheless, it is important to monitor sodium levels in the blood”, says Cecilia Bergh Fahlén.
Scientists at Virginia Tech say that the increased risk of cardiovascular disease after menopause may stem not only from declining hormone levels, but also from how those changes influence gene activity.
In a new paper published in the journal Cells, researchers examine growing evidence that declining oestrogen levels can alter epigenetics, the system that controls when genes turn on and off. These changes may help explain why rates of heart disease, diabetes, and other metabolic conditions rise sharply in women after menopause.
In addition, the study identifies a potential link between oestrogen loss, changes in gene regulation, and cardiovascular health. The epigenome, the full set of chemical modifications that regulate gene activity without altering DNA, has been studied extensively in breast cancer, but far less is known about how these mechanisms operate in the heart and cardiovascular system, according to Sumita Mishra, senior author of the study and assistant professor at the Fralin Biomedical Research Institute at VTC.
The findings suggest that oestrogen-related gene regulation pathways, long studied in cancer biology, may also play an important role in cardiometabolic health. Heart disease is the leading cause of death for women, and risk increases during and after the menopause transition, according to the National Heart, Lung, and Blood Institute.
“For years, we’ve focused on oestrogen loss as the primary driver of increased heart disease risk after menopause,” Mishra said. “What’s becoming clear is that the story is more complex. By reframing menopause-related health risks around gene regulation, this work points to new directions for future treatments that may extend beyond hormone therapy to more directly target these regulatory pathways.”
In addition, genetic predisposition and environmental factors, such as diet, exercise, and metabolic disease, likely interact with these pathways to shape cardiovascular risk after menopause, beyond what hormone replacement alone can address.
Rather than identifying a single new mechanism, the results of the study offer a new way of understanding the problem by connecting hormone loss to longer-term changes in how the body regulates interconnected systems involved in cardiovascular and metabolic health.
The study also highlights that many existing interventions used to manage cardiometabolic disease in postmenopausal women, including lipid-lowering therapies, glucose-lowering agents such as GLP-1 receptor agonists and SGLT2 inhibitors, and lifestyle interventions such as diet and exercise, may intersect with gene regulatory pathways influenced by oestrogen.
Emerging evidence suggests that these strategies can modulate metabolic and inflammatory signalling networks and, in some cases, the way DNA is packaged and regulated, helping to link current therapies to menopause-associated biological changes.
The researchers also highlight a gap in current knowledge, noting that much of the mechanistic evidence comes from laboratory and preclinical studies, and that more research in humans is needed to understand how these processes unfold over time.
Looking ahead, ongoing studies in the Mishra laboratory will focus on understanding how metabolic and gene-regulatory pathways are integrated in cardiometabolic disease, including in postmenopausal health.
The new study also aligns with ongoing research in the Mishra laboratory focused on heart failure with preserved ejection fraction (HFpEF), a form of heart disease that disproportionately affects women and becomes more prevalent after menopause. HFpEF is closely linked to obesity and metabolic dysfunction and remains a major unmet clinical challenge.
In related work published in Hypertension, the Mishra team investigated how oestrogen-dependent signaling pathways in the heart and vasculature are altered after menopause, contributing to changes in vascular function and metabolic regulation.
Together, these findings emphasise a broader research focus on how hormonal signalling interacts with molecular pathways that govern cardiometabolic health in postmenopausal women. This growing body of work may help guide the development of more targeted strategies to prevent and treat cardiovascular disease in this population.
Mishra is a member of the Center for Exercise Medicine Research and the Center for Vascular and Heart Research at the Fralin Biomedical Research Institute. She is also an assistant professor in the Department of Human Nutrition, Foods, and Exercise in the College of Agriculture and Life Sciences.
Phase II trial reveals that both – alone or in combination – can improve cognitive function in patients receiving chemotherapy.
Photo by Tima Miroshnichenko on Pexels
Up to 80% of people who receive chemotherapy experience cancer-related cognitive impairment, which most commonly involves mild-to-moderate changes such as difficulty paying attention, memory lapses, and struggles with multitasking. A new Phase II trial found that exercise and low-dose ibuprofen can each help to lessen cognitive problems and help protect patients’ cognitive function. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.
Both exercise and anti-inflammatory medications can improve cognitive outcomes in a variety of disease settings, but little is known in the setting of cancer. Because exercise and ibuprofen both reduce inflammation through different pathways, their combined use could potentially have additive or synergistic effects on lessening cancer-related cognitive impairment.
To investigate, researchers randomized 86 patients with cancer receiving chemotherapy who reported cognitive problems to four study arms for six weeks: Exercise for Cancer Patients (EXCAP) + low-dose ibuprofen, EXCAP + Placebo, low-dose ibuprofen only, and Placebo only. (EXCAP is a home-based, low-to-moderate intensity, progressive walking and resistance exercise prescription.)
After six weeks, participants in the EXCAP + Placebo group demonstrated significantly better attention performance compared with the Placebo group. The ibuprofen-only group also showed greater improvements than the Placebo group. Compared with Placebo participants, both EXCAP + ibuprofen and EXCAP + Placebo participants exhibited improvements on a measure that assessed how often friends, family, or coworkers have commented on or noticed the patient’s cognitive difficulties. However, the ibuprofen group showed less improvement on a measure of short-term verbal memory compared with those not on ibuprofen, which needs to be further investigated.
The findings suggest that exercise can positively impact cognitive function in individuals receiving chemotherapy. Ibuprofen may also help improve some cognitive functions, but perhaps to a lesser (and less consistent) extent. Phase III trials are needed to explore these findings further.
“We are encouraged by the findings of this trial that suggest possible benefits of both interventions for some cognitive domains. Clearly, we saw a more pronounced effect with exercise, which is notable considering the multiple health benefits of exercise for cancer survivors,” said lead author Michelle C. Janelsins, PhD, MPH, of the University of Rochester and the Wilmot Cancer Institute. “This is one of the first studies specifically designed to assess these interventions for cancer-related cognitive impairment during chemotherapy in patients with multiple diseases using both performance-based cognitive assessments and patient-reported outcomes.”
Dr Janelsins noted that future studies should consider modifying the duration and dose of both the exercise and low-dose ibuprofen interventions. She also stressed that any intervention for cognitive problems should be discussed with a health care provider to ensure there are no contraindications.
