Author: ModernMedia

Categories : Surgeries & ProceduresTags :

Surgery to Treat Chronic Rhinosinusitis more Effective than Antibiotics

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Photo by cottonbro studio: https://www.pexels.com/photo/close-up-shot-of-a-person-holding-a-scalpel-5721557/

Chronic rhinosinusitis (CRS), or sinusitis, is a long-term condition affecting one in 10 UK adults. Symptoms include a blocked and runny nose, loss of smell, facial pain, tiredness and worsening of breathing problems, such as asthma. It’s often similar to the symptoms of a bad cold, but it can last for months or even years.

The team carried out a randomised controlled patient trial comparing sinus surgery with long-term use of antibiotics, and a placebo.

More than 500 patients took part from around the UK, and all of them used nasal steroids and saline rinses as part of their usual care – both of which have been shown to help the condition.

The researchers found that surgery was effective at relieving sinusitis symptoms, and trial participants who underwent surgery were still feeling better six months later, according to the findings published in The Lancet. Of those who underwent surgery, 87% said their quality of life had improved six months on.

A three-month course of low dose antibiotics was not found to be helpful as there was no significant difference in outcomes between those on antibiotics and those in the placebo arm of the trial.

The study is part of the MACRO programme, involving a collaborative group of researchers from UCL (the trial’s sponsor), the University of East Anglia (UEA), Guy’s and St Thomas’ NHS Foundation Trust, the University of Southampton, the University of Oxford, UCLH, and Imperial College London. The programme is funded by the National Institute for Health and Care Research.

Lead author Professor Carl Philpott, from UEA’s Norwich Medical School, one of the Chief Investigators of the MACRO trial, said: “What we found is that surgery was effective at reducing symptoms six months on, while taking the course of antibiotics seemed to make little difference. Until now, there was no evidence in the form of a trial that showed sinus surgery works better than medical treatment and access to sinus surgery has been restricted in some parts of the UK in recent years. This could be a real game-changer for sufferers worldwide.

“We hope our findings will help reduce the length of time for patients to get treatment. Streamlining clinical pathways will help reduce unnecessary visits and consultations, and save on healthcare resources.”

For the trial, all participants received nasal steroids and saline rinses as standard care, alongside their randomly allocated treatment option of either sinus surgery, antibiotics or placebo tablets. They were followed up after three and six months, where researchers examined their nose and sinuses, took airflow readings and conducted smell tests, to gauge the success of each treatment in terms of improvement of symptoms, quality of life and possible side effects.

Jim Boardman, MACRO patient representative, said: “I’ve lived under a cloud for years with CRS, as have many others I’ve met with the same condition. There’s a persistent headache and blocked nose along with the loss of sense of smell, which removes a whole dimension of everyday experience and enjoyment. A clear path to successful treatment will be welcomed by all CRS sufferers.”

The researchers are now continuing their research to assess the cost-effectiveness of sinus surgery, while also continuing to follow up trial participants over longer periods of time to see how long the benefits last.

Source: University College London

Categories : Cardiovascular Disease Surgeries & ProceduresTags :

New Studies Explore Early Aspirin Withdrawal and Tailored Antiplatelet Strategies Following PCI

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Percutaneous coronary intervention.
Percutaneous coronary intervention. Credit: Scientific Animations CC4.0

Early withdrawal of aspirin following successful percutaneous coronary intervention (PCI) for acute coronary syndrome and in low-risk patients following an acute myocardial infarction (MI) was the focus of two separate hot line trials presented at ESC Congress 2025. A third trial provided insights into early escalation and late de-escalation of antiplatelet therapy after complex PCI.

In the NEO-MINDSET trial, simultaneously published in NEJM, researchers in Brazil randomised approximately 3400 patients within the first four days of hospitalisation following a successful PCI to either stop treatment with aspirin and receive potent P2Y12 inhibitor monotherapy (ticagrelor or prasugrel) or to receive dual antiplatelet therapy (DAPT) that included aspirin and a potent P2Y12 inhibitor for 12 months.

At 12 months, the primary endpoint of death from any cause, MI, stroke or urgent revascularisation had occurred in 119 patients in the monotherapy group and in 93 patients in the DAPT group (p = 0.11 for noninferiority). Researchers also noted that major or clinically relevant nonmajor bleeding occurred in 33 patients assigned to monotherapy vs 82 patients assigned to DAPT. Stent thrombosis occurred in 12 patients in the monotherapy group and in 4 in the dual antiplatelet therapy group.

“We failed to demonstrate the noninferiority of aspirin-free monotherapy initiated immediately after PCI with regard to the ischaemic primary endpoint over 12 months,” said Principal Investigator Pedro Lemos, MD. “Results from the landmark analysis suggest that the excess ischaemic risk with monotherapy occurred in the first 30 days, with comparable outcomes thereafter. Bleeding appeared to be lower at both 30 days and 12 months with monotherapy versus DAPT.”

In TARGET-FIRST, also simultaneously published in NEJM, P2Y12-inhibitor monotherapy was noninferior to continued DAPT with respect to the occurrence of adverse cardiovascular and cerebrovascular events among low-risk patients with acute MI who had undergone early complete revascularisation and had completed one month of DAPT without complications. It also resulted in lower incidence of bleeding events.

Nearly 2000 patients from 40 centres in Europe were randomised to receive P2Y12-inhibitor monotherapy or to continue DAPT for 11 months. A primary-outcome event occurred in 20 patients (2.1%) in the P2Y12-inhibitor monotherapy group and in 21 patients (2.2%) in the dual antiplatelet therapy group (p = 0.02 for noninferiority). Major bleeding occurred in 2.6% of the patients assigned to P2Y12-inhibitor monotherapy group compared with 5.6% of those assigned to DAPT (p = 0.002 for superiority). The incidence of stent thrombosis and serious adverse events appeared to be similar in the two groups, researchers said.

Principal Investigator Giuseppe Tarantini, MD, noted that no previous randomised trials have assessed early aspirin discontinuation in acute MI patients who achieve early, complete revascularisation with modern stents. “These results reflect the benefits of modern stents, high procedural success and optimal medical therapy, making early aspirin discontinuation feasible in this selected population,” he said.

The TAILORED-CHIP trial found early escalation and late de-escalation of antiplatelet therapy is not beneficial in patients with high-risk anatomical or clinical characteristics undergoing complex PCI.

Researchers in South Korea randomised approximately 2000 patients to standard DAPT (clopidogrel plus aspirin for 12 months) or a tailored antiplatelet strategy consisting of early escalation (low-dose ticagrelor at 60mg twice daily plus aspirin for 6 months) followed by late de-escalation (clopidogrel monotherapy for 6 months).

Overall findings showed no significant difference in the incidence of major ischemic events at 12 months with tailored therapy compared with standard DAPT. However, the incidence of clinically relevant bleeding was significantly higher with tailored therapy, according to study investigators.

“Our results suggest that a tailored strategy in patients undergoing complex high-risk PCI does not provide a net clinical benefit,” said Principal Investigator Duk-Woo Park, MD, PhD, FACC. “We observed an increase in bleeding complications without a significant reduction in ischaemic events. This challenges the notion that ‘more is better’ even in carefully selected patients at high ischaemic risk.”

Source: American College of Cardiology

Categories : UrogenitalTags :

Clinical Trial Shows a Constipation Drug Aids Kidney Function

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Human kidney. Credit: Scientific Animations CC0

Chronic kidney disease (CKD) is a major health issue worldwide. Many patients end up requiring regular dialysis to avoid kidney failure and stay alive. Despite the severity of the condition, there are currently no drugs available that improve kidney function. A research group led by Tohoku University Graduate School of Medicine’s Professor Takaaki Abe has found a remarkable solution to treat patients with CKD by co-opting a drug typically used for constipation. This is the first time that this drug (lubiprostone) was shown to prevent the decline of renal function in patients with CKD.

“We noticed that constipation is a symptom that often accompanies CKD, and decided to investigate this link further,” explains Abe. “Essentially, constipation disrupts the intestinal microbiota, which worsens kidney function. Working backwards, we hypothesised that we could improve kidney function by treating constipation.”

To address this issue, the group conducted a multicentre Phase II clinical trial (LUBI-CKD TRIAL) at nine Japanese medical institutions, enrolling 150 patients with moderate CKD. This study evaluated the effects of lubiprostone on kidney function. The results showed that, compared to the placebo group, the decline in kidney function (defined as the estimated glomerular filtration rate: eGFR) was suppressed in a dose-dependent manner in patients treated with 8µg or 16µg of lubiprostone.

The researchers also investigated the mechanism underlying how this effect occurred. They found that lubiprostone increases spermidine production, which improves mitochondrial function by promoting bacterial growth in the gut. The improved mitochondrial function was seen to exert a renoprotective effect – suppressing further kidney damage.

Going forward, the research team has plans to validate the trial results in a larger population (Phase 3 clinical trial) and advance the exploration of biomarkers that predict treatment efficacy. Their goal is to provide each patient with CKD the optimal treatment plan tailored to their needs. This discovery has the potential to significantly transform the conventional approach to CKD treatment, which primarily focuses on reducing uremic toxins.

These findings suggest a new therapeutic strategy in which laxatives suppress renal function decline. This strategy is expected to contribute to the development of treatments for not only CKD, but also mitochondrial dysfunction disorders. The results of this study were published in Science Advances on August 30, 2025.

Source: Tohoku University

Categories : Lab Tests and Imaging NeurologyTags :

Test Detects Brain Cancers in Cerebrospinal Fluid with High Accuracy

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A novel, multi-analyte test developed by researchers at Johns Hopkins Medicine can accurately identify brain cancers using small samples of cerebrospinal fluid (CSF), offering a promising new tool to guide clinical decision-making.

The findings, supported by funding from the National Institutes of Health, were published in Cancer Discovery and demonstrate that combining multiple biological markers, including tumour-derived DNA and immune cell signatures, is more effective for diagnosing central nervous system cancers than using any one marker alone.

“This study highlights how much more information we can gain when we evaluate several analytes together,” says senior study author Chetan Bettegowda, MD, PhD, Professor and Director of the Department of Neurosurgery at the Johns Hopkins University School of Medicine. “The ability to detect cancers with high specificity and also gain insight into the immune environment of the brain could be an important advance in the care of patients with brain tumours.”

To evaluate the potential of a multi-analyte approach, investigators analysed 206 CSF samples, including samples from patients with high-grade gliomas, medulloblastomas, metastases and central nervous system lymphomas. Their test, called CSF-BAM (cerebrospinal fluid–B/T cell receptor, aneuploidy and mutation), measured chromosomal abnormalities, tumour-specific mutations, and T and B cell receptor sequences. In combination, these markers identified brain cancers with more than 80% sensitivity (ability to detect cancer) and 100% specificity (correctly identified those who were cancer-free) in the validation cohort. The 100% specificity means no false positives were recorded among individuals with noncancerous conditions.

The study also showed that the assay could distinguish between the immune cell populations present in cancer and noncancer cases, offering additional biological context that could be helpful in more-challenging clinical scenarios. Investigators say this ability to categorize T and B cell populations in the CSF provides insights into both disease presence and immune response.

“Many patients with brain lesions face invasive diagnostic procedures to confirm a cancer diagnosis,” says Christopher Douville, MD, assistant professor of oncology and a senior study author. “A tool like this could help us make better-informed decisions about who really needs a biopsy and who doesn’t.”

Researchers say the test could be particularly useful for cases in which conventional imaging or cytology is inconclusive, or in situations when obtaining tissue for diagnosis is risky or not possible. The multi-analyte approach, they say, enables clinicians to better detect cancer and better understand the disease status, supporting a more tailored approach to patient care.

Source: Johns Hopkins Medicine

Categories : Neurodegenerative DiseasesTags :

Experiments Add to Evidence of Links Between Amyloid Deposits in Brain and Bone Marrow

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Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH

A recent study led by a team of researchers at The Johns Hopkins University School of Medicine examining aging mice has provided what is believed to be the first evidence that particles of amyloid beta protein, found in people with Alzheimer’s disease (AD), build up in the bone marrow of the animals, although not in the exact same form as the large, dense plaques found in the brains of people with Alzheimer’s disease.

“Although amyloid buildup has been found in organs outside the brain – such as the heart, kidneys, and nerves – it remains unclear whether similar deposits form in bone or bone marrow with aging or in Alzheimer’s disease,” says contributing study author Mei Wan, PhD, professor of the department of Orthopaedic Surgery. While brain amyloid has been extensively studied for its role in memory loss and neurodegeneration, far less is known about amyloid elsewhere in the body. In fact, almost nothing is known about whether amyloid forms in the skeleton or how it might contribute to age-related bone loss.”

AD is primarily associated with excessive amyloid plaques in the brain. Osteoporosis is a bone disease marked by low bone mineral density with an increased risk of fractures. Recent research suggests these two age-related conditions may be connected, and scientists are beginning to uncover common underlying causes.

Funded by the National Institutes of Health, the study findings, published in Nature Aging, advance scientific understanding of long-suspected similar biological processes that may be at work in osteoporosis – a form of bone loss – and Alzheimer’s dementia, the researchers say. The work may also offer potential new targets for preventing or treating bone loss.  

The buildup of amyloid is triggered by fat cells in the bone marrow, known as bone marrow adipocytes (BMAds), and a protein they release called SAP/PTX2 in aged mice and mice with AD. These amyloid deposits impair bone-building cells (osteoblasts) and activate bone-resorbing cells (osteoclasts), leading to bone loss. In previous mouse models, removing senescent BMAds or blocking SAP/PTX2 have shown to significantly reduce amyloid buildup and restored bone health.

In this study, male and female mice ranging from 4 to 24 months were kept in a temperature-controlled room provided with ongoing access to food and water and exposed to a 12-hour light-dark cycle. Researchers put a concentration of 5mg/ml in the drinking water of the mice aged 18 months and examined the effects CPHPC had on their age-related bone loss. CPHPC (also named Miridesap) is a small molecule compound originally designed to treat amyloidosis which is a rare disease marked by the buildup of amyloid proteins. A control group of mice aged 4, 9, 22 and 24 months were given the same dosage of water without the CPHPC drug  

High-resolution imaging of thigh and shin bones revealed amyloid fibrils forming ring-like structures around BMAds in aged mice and mice genetically engineered to have a form of AD. SAP/PTX2-driven amyloid clumps were found to enhance bone loss.

Study results also showed that CPHPC successfully depleted SAP/PTX2 and reversed bone deterioration in the older mice, suggesting a promising new therapeutic strategy for osteoporosis in the elderly, a strategy that would seek to eliminate aging fat cells or amyloid-promoting proteins.  

Wan adds, “Our study is what we believe to be the first to show that harmful amyloid fibres (Aβ fibrils) build up in the bone marrow of aged mice. We also found that fat cells in the bone marrow release a protein called SAP/PTX2, which plays a major role in triggering this amyloid buildup and damaging bone. These findings uncover a new connection between bone loss and dementia risk and may open the door to new research on how protecting bone health could also help protect brain function.”

This discovery provides an opportunity for new treatments targeting bone aging and Alzheimer’s-associated osteoporosis by focusing on the elimination of senescent fat cells or amyloid-promoting proteins.

Source: Johns Hopkins Medicine

Categories : Lab Tests and ImagingTags :

SAHPRA Approves Mpox Test Using African Medicines Regulatory Harmonisation (AMRH) Continental EUL Procedure

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Mpox (monkeypox) virus. Source: NIH

Pretoria, 27 August 2025 – The South African Health Products Regulatory Authority (SAHPRA) has approved a molecular test kit for Mpox , Cobas MPXV, for use on the Cobas 6800/8800 Systems, within nine working days through a collaborative and harmonised review process under the African Medicines Regulatory Harmonisation (AMRH). Rapid and accurate testing is essential for early detection and to enable timely treatment, and effective containment of the virus.

SAHPRA’s Medical Device Unit, utilising both the World Health Organization (WHO) Emergency Use Listing (EUL) report and the African Medicines Regulatory Harmonisation (AMRH) Continental EUL Procedure, has successfully leveraged reliance mechanisms to facilitate the review and approval of Mpox diagnostic tools. This approach has proven instrumental in accelerating access to critical health technologies, particularly in public health emergencies.

The emergency use approval of the Cobas MPXV for use on the Cobas 6800/8800 Systems, developed by Roche Molecular Systems, Inc. and licensed to Roche Diagnostics South Africa (Pty) Ltd, represents a critical advancement in expanding diagnostic capacity amid Mpox outbreaks. Rapid and accurate testing is essential for early detection, timely treatment, and effective containment of the virus.

 “As part of our efforts to promote regulatory efficiency and responsiveness, SAHPRA has successfully leveraged reliance mechanisms to facilitate the review and approval of Mpox diagnostic tools. This marks a significant milestone in supporting regional and continental harmonisation of the regulatory processes for medical devices, including In-Vitro Diagnostics (IVDs),” says Dr Boitumelo Semete-Makokotlela, SAHPRA’s Chief Executive Officer.

For more information on the AMRH continental EUL listing publication, see here: https://www.nepad.org/news/public-notice-amrh-steering-committee-approves-emergency-use-listing-of-two-mpox

Source: SAHPRA

Categories : Cardiovascular DiseaseTags :

Clinical Trial Challenges 40-year-old Standard of Care for Heart Attack Patients

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Human heart. Credit: Scientific Animations CC4.0

Beta-blocker therapy showed no evidence of an effect on all-cause death, reinfarction or heart failure admission in patients with myocardial infarction (MI) managed invasively who had left ventricular ejection fraction (LVEF) ≥ 40%, according to late-breaking research from the REBOOT trial presented in a Hot Line session today at ESC Congress 20251 and simultaneously published in the New England Journal of Medicine. 

Explaining the rationale for the REBOOT trial, Principal Investigator, Professor Borja Ibáñez from the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC) and Fundación Jiménez Díaz University Hospital, Madrid, Spain, said: “Beta-blockers have long been a foundational treatment after acute MI; however, supporting evidence is derived from trials that predate modern standards of care − before the time of routine reperfusion, invasive management, potent antiplatelet therapies and statins. Re-examining the role of beta-blockers is warranted, particularly among patients with uncomplicated MI and LVEF > 40% in whom the benefits of beta-blockers are not well established, unlike with reduced LVEF (≤ 40%).”  

The investigator-initiated randomised open blinded-endpoint REBOOT trial was conducted at 109 centres across Spain and Italy. Patients with MI (with or without ST-segment elevation) were eligible for enrolment if they underwent invasive management during the index hospitalisation and had a predischarge LVEF > 40%, with no history or signs of heart failure. Patients were randomised 1:1 to beta-blocker or no beta-blocker therapy. The primary endpoint was a composite of all-cause mortality, nonfatal reinfarction or heart failure admission. 

Among 8505 patients who underwent randomisation, the mean age was 61 years and 19.3% were women. A total of 10% had a prior MI and 12% were on beta-blocker treatment before the index hospitalisation. 

After a median follow-up of 3.7 years, the primary composite outcome of all-cause death, nonfatal reinfarction or heart failure admission occurred in a similar proportion of patients in each group: 22.5/1000 patient-years in beta-blocker group and 21.7/1000 patient-years in the no beta-blocker group (hazard ratio [HR] 1.04; 95% confidence interval [CI] 0.89 to 1.22; p=0.63). 

All-cause mortality occurred in 11.2 and 10.5/1000 patient-years on beta-blocker therapy and no-beta blocker therapy, respectively (HR 1.06; 95% CI 0.85 to 1.33). Nonfatal reinfarction occurred in 10.2 and 10.1/1000 patient-years, respectively (HR 1.01; 95% CI 0.80 to 1.27), while heart failure admission occurred in 2.7 and 3.0/1,000 patient-years, respectively (HR 0.89; 95% CI 0.58 to 1.38).  

Regarding safety, admission for stroke occurred in 2.6/1000 patient-years in the beta-blocker group and 1.7/1000 patient-years in the no beta-blocker group (HR 1.50; 95% CI 0.90 to 2.49). Admission for symptomatic advanced atrioventricular block occurred in 0.5 of patients in the beta-blocker group and 0.4/1000 patient-years of patients in the no beta-blocker group (HR 1.18; 95% CI 0.40 to 3.50). 

There appeared to be an absence of benefit with beta-blockers across the prespecified subgroups. However, fewer events were noted in patients with mildly reduced LVEF (40−49%) on beta-blockers vs no beta-blockers, although low patient numbers limit interpretability. Women experienced overall more events, especially when on beta-blockers. 

Professor Ibáñez concluded: “Beta-blocker therapy showed no evidence of benefit across the study population of patients with MI managed invasively who had LVEF > 40%. However, as also presented today at ESC Congress, a meta-analysis of data from four trials, including REBOOT, suggest there may be a positive signal in patients with mildly reduced LVEF (40−49%).2” 

Source: European Society of Cardiology

Categories : Cardiovascular DiseaseTags :

Inflammation Marker May ID Unaccounted-for Cardiovascular Risk in Women

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Photo by Teona Swift on Unsplash

Cardiologists have long known that up to half of all heart attacks and strokes occur among apparently healthy individuals who do not smoke and do not have high blood pressure, high cholesterol, or diabetes, the “standard modifiable risk factors” which doctors often call “SMuRFs.” How to identify risk among the “SMuRF-Less” has been an elusive goal in preventive cardiology, particularly in women who are often under-diagnosed and under-treated.

A new study by Mass General Brigham researchers that leverages data from the Women’s Health Study has found hsCRP, a marker of inflammation, can help identify women who are at risk but are missed by current screening algorithms. Results are presented at a late-breaking clinical science session at the European Society of Cardiology Congress (ESC) and simultaneously published in The European Heart Journal.

“Women who suffer from heart attacks and strokes yet have no standard modifiable risk factors are not identified by the risk equations doctors use in daily practice,” said Paul Ridker, MD, MPH, a preventive cardiologist at Mass General Brigham’s Heart and Vascular Institute. “Yet our data clearly show that apparently healthy women who are inflamed are at substantial lifetime risk. We should be identifying these women in their 40s, at a time when they can initiate preventive care, not wait for the disease to establish itself in their 70s when it is often too late to make a real difference.”

As part of the federally funded study, researchers studied 12 530 initially healthy women with no standard modifiable risk factors who had the inflammatory biomarker hsCRP measured at study entry and who were then followed over 30 years. Despite the lack of traditional risks, women who were inflamed as defined by hsCRP levels > 3 mg/L had a 77% increased lifetime risk of coronary heart disease, a 39% increased lifetime risk of stroke, and a 52% increased lifetime risk of any major cardiovascular event.

Additionally, researchers released a new analysis of randomised trial data showing that “SMuRF-Less but Inflamed” patients can reduce their risk of heart attack and stroke by 38% using statin therapy.

“While those with inflammation should aggressively initiate lifestyle and behavioural preventive efforts, statin therapy could also play an important role in helping reduce risk among these individuals,” said Ridker.

Source: Mass General Brigham

Categories : Cardiovascular Disease Mental HealthTags :

A Connection Between Mental Health and Heart Disease, Increased Mortality Risks

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Photo by Alex Green on Pexels

Every 34 seconds, someone in the United States dies from heart disease. As nearly half of the country suffers from some form of cardiovascular disease (CVD), another 1 in 4 adults experience a mental health disorder in their lifetime, signalling an inevitable overlap.

Now, a new report from Emory University shows that certain mental health conditions escalate the risk of developing heart disease by 50–100% – and adverse outcomes from existing heart conditions by 60–170%.

The report, published in The Lancet Regional Health-Europe, summarises cardiovascular health disparities among those diagnosed with depression, anxiety, schizophrenia, bipolar and post-traumatic stress disorders (PTSD). The article is part of a series aiming to raise awareness around disparities in CVD health in four populations: women, the elderly, racial minorities and those with mental health conditions.

Emory University professor Viola Vaccarino, MD, PhD, led this metareview linking mental health conditions to CVD, along with co-authors Amit Shah, MD, and Douglas Bremner, MD, also Emory professors.

The report associated the following conditions and their corresponding risks of developing CVD:

  • Major depression, 72%
  • PTSD, 57%
  • Bipolar disorder, 61%
  • Panic disorder, 50%
  • Phobic anxiety, 70%
  • Schizophrenia, nearly 100%

The research also shows that these conditions are associated with a poorer prognosis, greater risk for readmission and higher mortality from existing heart conditions. For example, major depression more than doubles the mortality rate in those with existing CVD.

Additionally, the report emphasises a bidirectional relationship. “More than 40 percent of those with cardiovascular disease also have a mental health condition,” adds Vaccarino.

The physiology of stress

According to the report, a well-documented relationship exists among depression, schizophrenia, PTSD, and abnormal stress responses in the autonomic nervous system (ANS) and hypothalamic-pituitary adrenal axis (HPA).

The former allows the brain to manage involuntary responses, such as functions of the liver, heart, sweat glands, and eye muscles. ANS also manages both acceleration and deceleration of these functions, regulating inflammatory responses. Since most major organs have ANS nerve endings, this system impacts most bodily functions.

The hypothalamic-pituitary adrenal axis (HPA) also influences immune response and metabolism, which can impact cardiovascular function.

According to the report, dysregulation of these systems creates “adverse downstream effects that can affect cardiovascular risk chronically, including increased inflammation, metabolic abnormalities, high blood pressure, enhanced systemic vascular resistance and autonomic inflexibility.” Inflammation has also been implicated in both the development of heart disease and mental health conditions.

Social determinants and quality of care

The role of social determinants of health in CVD disparities is critical. Those with mental health conditions may face disruptions and barriers in the continuum of care, such as affordability and accessibility. Compromised health literacy or communication can also impede access to health screenings and treatment.

Clinicians could also be challenged to care for patients with certain mental conditions, which can be compounded by stigma and existing models that fragment mental and physical health care. Stigmas are also present in the field of clinical research, where having a mental health condition is often an exclusionary criterion in randomised trials.

Moreover, according to the report, current prediction models don’t account for mental health disorders when forecasting the risk of developing heart disease.

Next steps toward a healthier future

To address the disparities of CVD among people with mental health disorders, the authors recommend an integrated approach with interdisciplinary care encompassing behavioural, mental and cardiovascular health.

“The tight connection between cardiovascular and psychological health warrants changes in the health care system that are more amenable to patients with comorbidities,” says Vaccarino. “A clinical team would be ideal for the care of these patients – a team of specialists, social workers, and nursing staff who work in collaboration to provide multidisciplinary care and resources.” 

The report concludes that closing the health disparity gap upholds the rights of those living with a mental health condition to achieve the highest level of health and fully participate in society. 

Source: Emory University

Categories : Regenerative Medicine Skeletal SystemTags :

Repurposed Multiple Sclerosis Drug Could Help Bones Heal Faster

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Photo by Tima Miroshnichenko on Pexels

Researchers at the University of Arizona College of Medicine – Tucson found evidence that a drug that improves the ability to walk in people with multiple sclerosis can also make bone fractures heal faster.

The findings help further the understanding of specific factors involved in the bone healing process, and potentially open avenues for new therapeutic approaches.

“Broken bones are typically slow to heal in many people, and they can impact lives for months and in different ways. People lose time at work and daily activities at home with family and friends are impacted,” said senior author John Elfar, MD, professor, surgeon and chair of the Department of Orthopaedic Surgery at the U of A College of Medicine – Tucson. “This drug has the potential to change that.” 

Elfar partnered with Prem Kumar Govindappa, PhD, DVM, an assistant professor in the department, on the preclinical study that showed treatment with the drug 4-aminopyridine, or 4-AP, resulted in leg fractures healing faster and stronger than without the drug. The paper was published in The Journal of Bone and Joint Surgery.

“Mice with bone fractures healed quicker and were stronger after they healed after treatment with 4-AP,” said Elfar said, who is a member of the university’s BIO5 Institute. “We saw more bone mass and less intermediate cartilage, meaning there was accelerated bone healing.” 

The drug is approved for use in chronic neurological conditions, where it helps with walking by improving how signals from the brain and spinal cord reach limbs.

The team also saw improvements in bone mass and the ability to bear weight after treatment with 4-AP. Collagen deposition and bone mineralization, both of which are necessary for bone healing, also received a boost. Collagen forms the structural foundation of bones. In bone mineralization, minerals like calcium and phosphate join the newly forming bone matrix, strengthening and hardening the bone.

“We found that every fine-tuned measure of the strength of bone was better after administering 4-AP to mice,” Elfar said. “We also found more BMP2 protein in bone-forming cells at the fracture site, which again told us we found something that could accelerate the process.”

Examining human bone cells exposed to 4-AP in a dish, the scientists saw increased production of bone morphogenetic protein, or BMP2, a bone-building substance used clinically to help with some kinds of bone repair. BMP2 prompted the production of stem cells that become cells called osteoblasts, which are essential to form new bone.

The research team also measured 4-AP’s effects on human bone narrow mesenchymal stem cells and human osteoblast cells in the lab. 4-AP increased the conversion of the stem cells into osteoblasts and the latter’s ability to migrate and grow, which are essential to the healing process.

Elfar said that 4-AP’s role in driving BMP2 gene and protein activity is key to its bone healing effects, and using 4-AP to prompt BMP2 production in the body could be especially important.

“BMP2 is a hormone the body makes to accelerate bone healing,” Elfar said. 

BMP2 is known to modulate bone healing and is approved for use in certain medical procedures, including spinal fusion and sinus reconstruction surgery. An artificial version that has orthopedic medicine uses can have side effects, though, including bone resorption and cervical spine swelling. Finding a way to channel naturally produced BMP2 could improve bone healing while avoiding such problems.

The scientists previously showed that 4-AP could prevent bone and muscle loss in a mouse model of nerve damage. Similarly, they saw indications of 4-AP’s healing effects for wound, nerve and limb injuries. 

The researchers plan to eventually test 4-AP’s potential use in healing bones in a clinical trial. They also want to better understand the drug’s effects on BMP2 production, and more broadly, on the biology of healing bone.

Source: University of Arizona