Category: 8. Health

Cochlear introduced its new smart system in China in June, making the country one of the first global markets to launch the technology – through Hainan, the southern island province, and Hong Kong.

Unlike hearing aids that amplify sound, the implant bypasses damaged hair cells in the inner ear and directly stimulates the auditory nerve with electrical signals from an external processor equipped with a noise-cancelling microphone.

Chief technology officer Jan Janssen said the implant best helped users with severe and profound hearing loss for whom traditional hearing aids were no longer effective.

New research has shown how boys being overweight in early childhood or having chickenpox or another infectious disease in infancy may increase their risk of having chronic disease in later life.

Scientists from the University of Nottingham’s School of Biosciences have analyzed the level of the unique testis hormone biomarker insulin-like peptide 3 (INSL3) in young men at 24 years of age and related this to a range of health and lifestyle factors during their childhood.

The team have previously shown that the biomarker INSL3 in younger men is predictive of chronic disease when they get older. In this new study they found that while most factors had little or no effect, being overweight as a child or young teenager, or having had chickenpox or other infectious disease in early infancy, were significantly associated with a reduction in adult INSL3 by 10 to 15%. This potentially increases the risk of later adult illnesses such as diabetes, cardiovascular disease, bone weakness, or sexual dysfunction.

The study, published today in Andrology is the first to ever examine the impact of childhood diet, health and infections and their long term impact on health across the lifespan.

The research was led by Dr. Ravinder Anand-Ivell, Associate Professor in Endocrinology and Reproductive Physiology, who has previously shown how the unique biomarker INSL3, in aging men is able to predict conditions such as diabetes, cardiovascular disease, or bone weakness, and that low INSL3 in older men has its origins already in younger men.

We know that INSL3 hormone levels in boys and men are a robust biomarker of the testicular capacity to produce the steroid hormone testosterone that is essential not only for reproduction but also for overall healthy well-being. In this new study we have found that there is a clear link between certain health factors in childhood at a time before puberty when the testes are still developing and later men’s health as they age.”

Dr. Ravinder Anand-Ivell, Associate Professor in Endocrinology and Reproductive Physiology, University of Nottingham

In this new study the researchers analysed data from participants in the “Children of the Nineties” cohort of children (the Avon Longitudinal Study of Parents And Children) established by colleagues at the University of Bristol. These boys had been followed clinically from birth and are now in their twenties.

By correlating the levels of INSL3 in the young men from this cohort with a wide range of clinical and lifestyle parameters throughout their childhood and adolescence, the team identified the factors during childhood which could potentially affect mens health as they aged. Importantly, they also identified many other factors which were less important. The key findings showed that being overweight as a child or young teenager, or having had chickenpox or other infectious disease in early infancy both markedly increase the risk to mens health as they age and moreover emphasize the importance of early vaccination.

Dr. Anand-Ivell adds: “By using this new biomarker INSL3 as well as having this childhood health information allows us now to be able to predict those men at risk and thus consider appropriate preventative measures before disease sets in. The next stage of this research is the development of a specialist high-throughput assay which would allow the measurement of INSL3 to be introduced as part of the routine clinical assessment for male healthy aging.”

The genetic mutation causes an enzyme called leucine-rich repeat kinase 2, or LRRK2, to be overactive. Too much LRRK2 enzyme activity changes the structure of brain cells in a way that disrupts crucial communication between neurons that make the neurotransmitter dopamine and cells in the striatum, a region deep in the brain that is part of the dopamine system and is involved in movement, motivation and decision making.

“Findings from this study suggest that inhibiting the LRRK2 enzyme could stabilize the progression of symptoms if patients can be identified early enough,” said Suzanne Pfeffer, PhD, the Emma Pfeiffer Merner Professor in Medical Sciences and a professor of biochemistry. Researchers can mitigate overactive LRRK2 using MLi-2 LRRK2 kinase inhibitor, a molecule that attaches to the enzyme and decreases its activity.

Pfeffer added that because the genetic mutation is not the only way to end up with overactive LRRK2 enzyme, the inhibitor treatment might help with other types of Parkinson’s disease or even other neurodegenerative diseases.

Pfeffer is the senior author of the study published in Science Signaling on July 1. Ebsy Jaimon, PhD, a postdoctoral scholar in biochemistry, is the lead author. The work is part of a longstanding collaboration with Dario Alessi, PhD, at the University of Dundee in Scotland.

Cellular antennae

About 25% of Parkinson’s disease cases are caused by genetic mutations, and the single genetic mutation that makes the LRRK2 enzyme too active is one of the most common. An overactive LRRK2 enzyme causes cells to lose their primary cilia, a cellular appendage that acts like an antenna, sending and receiving chemical messages. A cell that has lost its primary cilia is like your mobile phone when the network is down — no messages come through or are sent.

In a healthy brain, many messages are sent back and forth between dopamine neurons in a region of the brain called the substantia nigra and the striatum. These cellular “conversations” are possible because dopamine neuron axons, which are tubular extensions coming off the cell body, reach all the way to the striatum to communicate with neurons and glia, cells that support neuronal function.

An important communication that is disrupted by too much LRRK2 enzyme activity occurs when dopamine neurons are stressed and release a signal in the striatum called sonic hedgehog (named after the cartoon character). In a healthy brain, it causes certain neurons and astrocytes, a type of glial support cell, in the striatum to produce proteins called neuroprotective factors. As their name suggests, these proteins help shield other cells from dying. When there is too much LRRK2 enzyme activity, many of the striatal cells lose their primary cilia — and their ability to receive the signal from dopamine neurons. This disruption in sonic hedgehog signaling means that needed neuroprotective factors are not produced.

“Many kinds of processes necessary for cells to survive are regulated through cilia sending and receiving signals. The cells in the striatum that secrete neuroprotective factors in response to hedgehog signals also need hedgehog to survive. We think that when cells have lost their cilia, they are also on the pathway to death because they need cilia to receive signals that keep them alive,” Pfeffer explained.

Restored cilia were unexpected

The goal of the study was to test if the MLi-2 LRRK2 kinase inhibitor reversed the effects of too much LRRK2 enzyme activity. Because the neurons and glia that were examined in this study were fully mature and no longer reproducing through cell division, the researchers were initially unsure whether cilia could regrow. Working with mice with the genetic mutation that causes overactive LRRK2 and symptoms consistent with early Parkinson’s disease, the scientists first tried feeding the mice the inhibitor for two weeks. There were no changes detected in brain structure, signaling or the viability of the dopamine neurons.

Recent findings on neurons involved in regulating circadian rhythms, or sleep-wake cycles, inspired the researchers to try again. The primary cilia on those cells — which were also no longer dividing — grew and shrank every 12 hours.

“The findings that other non-dividing cells grow cilia made us realize that it was theoretically possible for the inhibitor to work,” Pfeffer said.

The team decided to see what happened after mice with overactive LRRK2 enzyme consumed the inhibitor for a longer period of time; Pfeffer described the results as “astounding.”

After three months of eating the inhibitor, the percentage of striatal neurons and glia typically affected by the overactive LRRK2 enzyme that had primary cilia in mice with the genetic mutation was indistinguishable from that in mice without the genetic mutation. In the same way moving from an area with spotty cell service to one with good service restores our ability to send and receive text messages, the increase in primary cilia restored communication between dopamine neurons and the striatum.

The striatal neurons and glia were again secreting neuroprotective factors in response to hedgehog signaling from dopamine neurons in the same amounts as the brains of mice without the genetic mutation. The hedgehog signaling from dopamine neurons decreased, suggesting they were under less stress. And, indicators of the density of dopamine nerve endings within the striatum doubled, suggesting an initial recovery for neurons that had been in the process of dying.

“These findings suggest that it might be possible to improve, not just stabilize, the condition of patients with Parkinson’s disease,” Pfeffer said.

The earliest symptoms of Parkinson’s disease begin about 15 years before someone notices a tremor. Typically, these symptoms are a loss of smell, constipation and a sleep disorder in which people act out their dreams while still sleeping, according to Pfeffer. She said the hope is that people who have the LRRK2 genetic mutation can start a treatment that inhibits the enzyme as early as possible.

The next step for the research team is to test whether other forms of Parkinson’s disease that are not associated with the LRRK2 genetic mutation could benefit from this type of treatment.

“We are so excited about these findings. They suggest this approach has great promise to help patients in terms of restoring neuronal activity in this brain circuit,” Pfeffer said. “There are multiple LRRK2 inhibitor clinical trials underway, and our hope is that these findings in mice will hold true for patients in the future.”

The study was funded by The Michael J. Fox Foundation for Parkinson’s Research, the Aligning Science Across Parkinson’s initiative and the United Kingdom Medical Research Council.

Incoming information from the retina is channeled into two pathways in the brain’s visual system: one that’s responsible for processing color and fine spatial detail, and another that’s involved in spatial localization and detecting high temporal frequencies. A new study from MIT provides an account for how these two pathways may be shaped by developmental factors.

Newborns typically have poor visual acuity and poor color vision because their retinal cone cells are not well-developed at birth. This means that early in life, they are seeing blurry, color-reduced imagery. The MIT team proposes that such blurry, color-limited vision may result in some brain cells specializing in low spatial frequencies and low color tuning, corresponding to the so-called magnocellular system. Later, with improved vision, cells may tune to finer details and richer color, consistent with the other pathway, known as the parvocellular system.

To test their hypothesis, the researchers trained computational models of vision on a trajectory of input similar to what human babies receive early in life – low-quality images early on, followed by full-color, sharper images later. They found that these models developed processing units with receptive fields exhibiting some similarity to the division of magnocellular and parvocellular pathways in the human visual system. Vision models trained on only high-quality images did not develop such distinct characteristics.

The findings potentially suggest a mechanistic account of the emergence of the parvo/magno distinction, which is one of the key organizing principles of the visual pathway in the mammalian brain.”

Pawan Sinha, MIT professor of brain and cognitive sciences and the senior author of the study

MIT postdocs Marin Vogelsang and Lukas Vogelsang are the lead authors of the study, which appears today in the journal Communications Biology. Sidney Diamond, an MIT research affiliate, and Gordon Pipa, a professor of neuroinformatics at the University of Osnabrueck, are also authors of the paper.

Sensory input

The idea that low-quality visual input might be beneficial for development grew out of studies of children who were born blind but later had their sight restored. An effort from Sinha’s laboratory, Project Prakash, has screened and treated thousands of children in India, where reversible forms of vision loss such as cataracts are relatively common. After their sight is restored, many of these children volunteer to participate in studies in which Sinha and his colleagues track their visual development.

In one of these studies, the researchers found that children who had cataracts removed exhibited a marked drop in object-recognition performance when the children were presented with black and white images, compared to colored ones. Those findings led the researchers to hypothesize that reduced color input characteristic of early typical development, far from being a hindrance, allows the brain to learn to recognize objects even in images that have impoverished or shifted colors.

“Denying access to rich color at the outset seems to be a powerful strategy to build in resilience to color changes and make the system more robust against color loss in images,” Sinha says.

In that study, the researchers also found that when computational models of vision were initially trained on grayscale images, followed by color images, their ability to recognize objects was more robust than that of models trained only on color images. Similarly, another study from the lab found that models performed better when they were trained first on blurry images, followed by sharper images.

To build on those findings, the MIT team wanted to explore what might be the consequences of both of those features – color and visual acuity – being limited at the outset of development. They hypothesized that these limitations might contribute to the development of the magnocellular and parvocellular pathways.

In addition to being highly attuned to color, cells in the parvocellular pathway have small receptive fields, meaning that they receive input from more compact clusters of retinal ganglion cells. This helps them to process fine detail. Cells in the magnocellular pathway pool information across larger areas, allowing them to process more global spatial information.

To test their hypothesis that developmental progressions could contribute to the magno and parvo cell selectivities, the researchers trained models on two different sets of images. One model was presented with a standard dataset of images that are used to train models to categorize objects. The other dataset was designed to roughly mimic the input that the human visual system receives from birth. This “biomimetic” data consists of low-resolution, grayscale images in the first half of the training, followed by high-resolution, colorful images in the second half.

After the models were trained, the researchers analyzed the models’ processing units – nodes within the network that bear some resemblance to the clusters of cells that process visual information in the brain. They found that the models trained on the biomimetic data developed a distinct subset of units that are jointly responsive to low-color and low-spatial-frequency inputs, similar to the magnocellular pathway. Additionally, these biomimetic models exhibited groups of more heterogenous parvocellular-like units tuned predominantly to higher spatial frequencies or richer color signals. Such distinction did not emerge in the models trained on full color, high-resolution images from the start.

“This provides some support for the idea that the ‘correlation’ we see in the biological system could be a consequence of the types of inputs that are available at the same time in normal development,” Lukas Vogelsang says.

Object recognition

The researchers also performed additional tests to reveal what strategies the differently trained models were using for object recognition tasks. In one, they asked the models to categorize images of objects where the shape and texture did not match – for example, an animal with the shape of cat but the texture of an elephant.

This is a technique several researchers in the field have employed to determine which image attributes a model is using to categorize objects: the overall shape or the fine-grained textures. The MIT team found that models trained on biomimetic input were markedly more likely to use an object’s shape to make those decisions, just as humans usually do. Moreover, when the researchers systematically removed the magnocellular-like units from the models, the models quickly lost their tendency to use shape to make categorizations.

In another set of experiments, the researchers trained the models on videos instead of images, which introduces a temporal dimension. In addition to low spatial resolution and color sensitivity, the magnocellular pathway responds to high temporal frequencies, allowing it to quickly detect changes in the position of an object. When models were trained on biomimetic video input, the units most tuned to high temporal frequencies were indeed the ones that also exhibited magnocellular-like properties in the spatial domain.

Overall, the results support the idea that low-quality sensory input early in life may contribute to the organization of sensory processing pathways of the brain, the researchers say. The findings do not rule out innate specification of the magno and parvo pathways, but provide a proof of principle that visual experience over the course of development could also play a role.

“The general theme that seems to be emerging is that the developmental progression that we go through is very carefully structured in order to give us certain kinds of perceptual proficiencies, and it may also have consequences in terms of the very organization of the brain,” Sinha says.

The research was funded by the National Institutes of Health, the Simons Center for the Social Brain, the Japan Society for the Promotion of Science, and the Yamada Science Foundation.

A new study, published recently in Nature Communications, offers the first-ever map of which parts of Chikungunya virus trigger the strongest response from the body’s T cells. 

With this map in hand, researchers are closer to developing Chikungunya vaccines or therapies that harness T cells to strike specific targets, or “epitopes,” to halt infection. The new study also offers important clues for understanding why many people experience chronic, severe joint pain for years after clearing the virus.

Now we can see what T cells are seeing patients with chronic disease.”

Daniela Weiskopf, Ph.D., LJI Assistant Professor, senior author of the new study

This research comes as many mosquito-borne viruses, including Chikungunya, are moving into new areas of the globe.

“Historically, Chikungunya was considered an emerging virus. Now all of Latin America has been exposed,” says Weiskopf. “These mosquitoes are traveling further north, and we need to know what’s going on with this virus before it arrives in the United States.”

T cells jump into action

Chronic Chikungunya virus disease strikes between 30 to 60 percent of those infected-usually women-and causes chronic, severe joint pain. This debilitating joint pain can last for years following the initial viral infection. 

In a study out earlier this year, Weiskopf and her colleagues showed that these patients have a population of inflammatory CD4+ T cells that closely resembles the T cell signature of rheumatoid arthritis, an autoimmune disease.

“So many people, mostly women, have chronic disease following Chikungunya virus infection,” says Weiskopf. “This has an impact on the workforce and impacts the economy. And there’s no treatment.”

Weiskopf and her colleagues are working to understand why these CD4+ T cells linger and cause problems after a person clears the virus. For this study, they investigated whether people who develop chronic disease produce T cells that naturally target a different set of epitopes on Chikungunya virus.

Would a different “flavor” of T cells be more likely to stay in the body after infection?

Weiskopf and her team used a “peptide pool” approach to assemble a map of key T cell epitopes on Chikungunya virus. The researchers broke up the virus into very small amino acid sequences, called peptides. Then they took T cells from people with chronic Chikungunya virus disease and exposed these cells to the pool of peptides.

By stimulating the T cells, the researchers discovered exactly which parts of the virus are most likely to be recognized by T cells. These “immunodominant” regions may prove to be good targets for future Chikungunya treatments.

Rimjhim Agarwal, a UC San Diego graduate student and member of the Weiskopf Lab, spearheaded experiments to learn more about these T cells. Agarwal received funding from The Tullie and Rickey Families SPARK Awards for Innovations in Immunology to take a closer look. 

For her project, funded through the generosity of the Rosemary Kraemer Raitt Foundation Trust, Agarwal compared CD4+ T cells from people with chronic Chikungunya virus disease to people who cleared the virus quickly with no lasting symptoms.

Agarwal found that both patient groups had T cells that targeted the same viral epitopes. People who developed chronic disease did not recognize different proteins of the virus.

Now the question is-why do these T cells stick around to cause inflammation in some but not all people? Weiskopf and Agarwal are now looking at where Chikungunya virus might hide in the body to stimulate a long-term T cell response.

The LJI team also hopes to help other laboratories shed light on how to fight the virus. “Identifying the immunodominant T cell epitopes could seed new research into Chikungunya-specific T cell responses,” says Agarwal.

Individual expectations about one’s health can influence him/her future condition and the speed of the progression of a disease: in fact, a research conducted by researchers of psychology at the Università Cattolica del Sacro Cuore, Milan campus, shows that, after a diagnosis of asthma, people who are optimistic about their health will have a slower progression of the disease.

The study was published in the journal Health Expectations (Wiley) and conducted by full Professor Francesco Pagnini of the Department of Psychology at the Università Cattolica and colleagues.

Professor Pagnini explains: “this study was developed in response to the difficulties reported by patients in managing asthma. Patients helped identify key areas of concern, and their perspectives influenced the choice of outcomes and tools“. Although direct involvement in recruitment and dissemination was limited due to the pandemic, the design and focus of the study were guided by patient priorities, with potential applications in clinical consultations and future co-designed interventions.

Background

After receiving a diagnosis, people often develop expectations about how their condition will evolve, Professor Pagnini explains. This cognitive framework, known as “illness expectations” (IE), comprises future-oriented beliefs about the course of the disease and its symptoms. In chronic conditions such as asthma, IEs can play a crucial role in determining patient-reported outcomes and also variations in clinical markers indicative of disease progression. “In this study, we empirically assessed the impact of IEs on asthma symptoms and respiratory function in patients,” Pagnini affirms.

The study

‘We involved a group of 310 people diagnosed with asthma who were followed for a period of 6 months, with three assessment points, measuring the level of asthma control with the Asthma Control Test (ACT), while respiratory function was assessed through forced expiratory volume in 1 second (FEV1) using spirometry,’ he explains. At the beginning of the study, we assessed each person’s IE using the validated Illness Expectation Test (IET), which captures both explicit (conscious) and implicit (unconscious) expectations.

It emerged that people with more negative explicit IE about their asthma reported worse symptoms over time. Explicit IE about symptom progression was also associated with changes in lung function, with more negative expectations predicting greater decline in respiratory performance, the professor adds.

These findings suggest that IE may be significantly associated with asthma outcomes, highlighting their potential relevance in understanding patient experiences and symptom perception. “In experiments with patients affected by other diseases, such as multiple sclerosis, we obtained similar results”, the expert continues.

The hypothesis suggested to explain these results is that, as with the placebo effect, what happens is that if I have an idea about the world and the future that awaits me, that idea will prevail, largely influencing behaviour and thus, for example, modifying adherence to therapies and clinical recommendations, he concludes.

Study design

This randomized controlled trial was conducted in two different Family Health Centers (FHCs) in a province in eastern Turkey. A schematic of the experimental design is given in Fig. 1. This randomized controlled experimental design was conducted in accordance with the CONSORT checklist steps.

Setting and sample

The sample size for this study was determined by G power analysis. The population of the study consisted of 1442 women aged between 45 and 54 years and registered to Family Health Centers No. 1 and 3 in a city center, according to the updated data from Tunceli Provincial Health Directorate in 2018. The sample of the study was determined based on a similar study [11], using the Menopause-Specific Quality of Life (MENQOL) and the Health Promoting Lifestyle Profile II (HPLPL II). A power analysis was conducted, using G*Power 3.1.9.2 and considering the total MENQOL score after education, with an effect size of 0.48, standard deviation of 7.22, power of 0.80, β of 0.05, and α of 0.05. Accordingly, the sample was determined to consist of 136 menopausal women, including 68 in the experimental group and 68 in the control group. A computer-generated random number table was used, which can be used when the sample size is n < 100. For selecting women in the sample, those in the age group of 45–54 years were numbered according to their registration number in the FHCs, using simple random sampling method and a random number table. To prevent cross-contamination between the groups, data for the experimental group were collected from the Health Center No. 1, and data for the control group were collected from the Health Center No. 3. Similarly, in FHC No. 1 and 3, there are 4 physicians, 4 family health personnel, 2 auxiliary health personnel, 4 polyclinics, 1 nurse room, 1 vaccination room, 1 pregnant-baby monitoring room, 1 intervention room and 1 training room. During the practice, no intervention regarding MG was performed on menopausal women in FHCs.

Ethical approval

For conducting the study, an ethical approval was obtained from the Munzur University Scientific Research and Publication Ethics Committee (Date: 03/09/2018/4579) and written permissions from the Tunceli Provincial Health Directorate and the responsible physicians of Health Centers No. 1 and 3. The participants were informed about the purpose of this study, and their written informed consent was obtained using an informed consent form. Compliance with ethical principles was ensured at every stage of the study. Additionally, permission was obtained for using both HPLPL II and MENQOL. No interventions were conducted on women in the control group until the experimental research was completed. After the post-test was administered to women in the experimental and control groups, those in the control group also participated in a motivational interviewing session upon their wishes.

Participants

Between August 15, 2018, and December 30, 2019, the eligibility of women registered with two different FHCs in the city center of Tunceli was evaluated for inclusion in this study. A total of 8 women from the experimental group, 6 women due to transportation difficulties, moving to another city, caring for family members, treatment of secondary disease, and 2 women due to inaccessibility, were excluded from the study. In addition, a total of 9 women from the control group were excluded from the study 5 of them could not be reached and 4 did not participate in the post-test without submitting any reason.

Inclusion criteria

The inclusion criteria were as follows: (1) being literate; (2) being able to make a conscious decision to participate in the study, being able to communicate verbally, and being able to sign a consent form; (3) having had menopause naturally and within the last 3 years; (4) being sexually active; (5) having no hormone replacement therapy.

Exclusion criteria

The exclusion criteria were as follows: (1) unwilling to continue the study; (2) having a psychiatric diagnosis according to the FHC records.

Termination criteria of the study

The termination criteria were as follows: (1) intending to leave the study and (2) move to another city.

Study protocol

The search was randomized by a computer programming module (http://www.randomizer.org/form.htm) designed for controlled trials; a randomization list was prepared, and the participants were randomly assigned either to the experimental group (n = 68) or to the control group (n = 68).

Instruments for evaluation

The following measurement tools were used in this study.

Introductory information form

The introductory information form was prepared by the researcher in line with the literature [24,25,26,27,28,29,30]. It consists of a total of 10 questions about the menopausal women’s socio-demographic characteristics (age, education level, income level, place of residence for the longest time) and history of menopause (duration of being in menopause, training on menopause, thoughts about menopause and coping methods for menopausal complaints).

Health promoting lifestyle profile II (HPLPL II)

The HPLPL II was prepared by Walker et al. in 1987 [31]. This scale is suitable for use in research to evaluate health promotion behaviors within the framework of the health promotion model [11]. The scale includes six dimensions, namely, nutrition, physical activity, stress management, interpersonal relationships, responsibility for health, and spiritual growth (52 items in total). The items are scored based on a 4point Likert scale (never, sometimes, often, and usually). The total score of the scale ranges from 52 to 208. The score of each dimension is calculated separately and a higher scores mean better health. The Cronbach’s alpha coefficient was found as 0.92 for the total scale and ranged between 0.64 and 0.80 for its dimensions, suggesting that the Turkish version of the scale has sufficient validity and reliability [32]. In the present study, the Cronbach’s alpha value of the scale was 0.88.

Menopause-Specific quality of life (MENQOL)

The MENQOL was developed by John R. Hilditch et al. in 1996 to create a health-specific quality of life scale for menopausal women [33], and its Turkish validity and reliability study was conducted by Kharbouch and Şahin in 2007 [34]. This is a 7-point Likert-type scale containing 29 items and consists of four domains: vasomotor, psychosocial, physical and sexual. Each item is scored from “0” to “6”, where “0” refers to “not bothersome” and “6” to “extremely bothersome”. A higher scale score indicates greater severity of the complaint. The Cronbach’s alpha coefficient of the scale domains was found to range between 0.81 and 0.89 [34]. In the present study, the Cronbach’s alpha value of the scale domains ranged between 0.71 and 0.83.

Nursing interventions

Since the method is a technique that generally requires expertise, it is recommended that practitioners undergo a certain training and certification process in order to apply the technique effectively. The researcher participated in the motivational interviewing program and received a certificate prior to the application in this study. Additionally, expert opinions were received from 5 experts during the preparation of motivational interviewing steps. The nursing intervention was applied to 68 menopausal women included in the experimental group. A total of 9 sessions were conducted, including 1 preparation session, 6 motivational interviews, 1 initial follow-up interview one week after the intervention, and 2 follow-up interviews 4 weeks after the initial follow-up. Considering the interactive training method, the motivational interviewing sessions were conducted in the training room of the Health Center in groups of 10 at three different days (Monday, Thursday, Friday) once a week, through face-to-face sessions each lasting 50–60 min. During the interviews, the women were provided with counseling to activate their own sources of motivation, develop healthy lifestyle behaviors and improve their quality of life specific to menopause. The specific contents of the interventions were as follows:

During the research period, no interventions were applied to women in the control group by the researcher, and they filled in the data collection forms simultaneously with those in the experimental group. During the application, no interventions of motivational interviewing were conducted for menopausal women at the FHCs.

Statistical analysis

The data were coded and statistically analyzed using the Statistical Package for Social Science (SPSS 24) software package. Fisher’s exact test and chi-square test were employed by the researcher to determine the homogeneity of women in the experimental and control groups. The effects of healthy lifestyle behaviors and menopausal-specific quality of life between the groups were analyzed using independent samples t-test and repeated measures ANOVA. Cohen’s d value was calculated to determine the effect size for women in the experimental and control groups. The results were evaluated at a 95% confidence interval and a significance level of 0.05.

According to the Ministry of Health (MoH), in the first five months of 2025, the country recorded 22,974 dengue cases and five deaths. This indicates that risks remain, especially in the context of overlapping outbreaks such as dengue, hand-foot-and-mouth disease, and COVID-19 increasing in some localities.

At the end of May, the MoH issued an urgent directive calling for strengthened leadership, surveillance, and communication to reduce dengue-related fatalities.

Dengue was previously known for having an outbreak cycle of about once every five years, with a clear “quiet period”. But now, epidemiological patterns have changed alarmingly. It is no longer seasonal and has spread geographically.

Information about the unpredictable developments, burdens, and risks posed by dengue was shared by experts at a recent online talk show organised by Suc khoe & Doi song, the official media voice of the MoH, in collaboration with Takeda Vietnam Pharmaceuticals Limited. Takeda has made significant efforts to support the health sector by raising community awareness about dengue. The talk show was held under the theme: “Towards zero dengue deaths: Collective disease prevention with integrated solutions”.

Dr. Vo Hai Son, deputy director of the Vietnam Administration of Disease Prevention, said, “Previously, high case numbers followed a cycle of about five years, but now it has changed, and high case numbers appear roughly every two years.” He further explained that urbanisation, migration, and easier travel between regions have facilitated the wider and harder-to-control spread of dengue fever.

Assoc. Prof. Dr. Pham Quang Thai, vice head of the Infectious Diseases Control Department at the National institute of Hygiene and Epidemiology, stated from an epidemiological perspective that dengue has now spread across provinces, including mountainous areas that previously recorded very few cases. This development means that everyone needs to be more proactive in responding to the disease.

Negligence and improper handling

Although general awareness about dengue has improved, according to experts, a significant portion of the population remains negligent and mismanages the illness, leading to cases of late hospitalisation, severe disease progression, and even death.

Assoc. Prof. Dr. Do Duy Cuong, director of Bach Mai Institute of Tropical Medicine, said, People with a fever may assume it is due to other illnesses like the flu, but in reality some cases show no clear symptoms, and patients arrive at the hospital late, already in shock or with multiple organ failure.

Misinterpretation of symptoms causes many people to self-treat at home, missing the “golden period” for intervention and facing unpredictable risks

A typical case shared by Cuong involved a male student from the countryside living in rented accommodation in Hanoi. Due to poor living conditions, when he had a fever, he just stayed in his room and ate sparsely. He was only admitted to hospital on the fifth day, when his condition had worsened, and he was showing signs of shock and haemoconcentration.

Additionally, dengue is caused by a virus and has no specific cure. The unauthorised use of antibiotics, corticosteroids, or IV fluids without a doctor’s prescription is a serious mistake that can worsen the illness.

Comprehensive collaboration towards zero dengue deaths

To cope with the increasingly complex dengue epidemiology, reduce fatalities, and effectively control outbreaks, experts emphasise the need for a comprehensive strategy including vector control, epidemiological surveillance, early warning systems, behavioural communication, and strengthening of the health system. Among these, vaccination, a new solution endorsed by the World Health Organisation (WHO), is a part of the overall strategy, enabling proactive prevention and reducing the risk of severe disease progression.

Sharing at the talk show, MSc. Dr. Vo Hai Son emphasised the importance of controlling disease vectors, along with proactive actions from everyone: “Social measures, together with the proactiveness in each locality, neighbourhood, and household, will make people aware of the risks of infection and death due to dengue. From there, we will coordinate with the health sector to eliminate mosquito larvae and mosquitoes. This will help enhance disease and vector control.”

Adding to the vector control solution, Assoc. Prof. Dr. Pham Quang Thai also pointed out the unpredictable challenges in urban environments. “Some people say their apartment is on the 30th floor and they don’t see mosquitoes, so they believe they’re safe. But don’t assume that. Mosquitoes are very smart. They don’t fly directly from the first to the 30th floor, but instead ascend step by step, breeding on each floor. As a result, even the highest floors of apartment buildings will have mosquitoes.”

High-rise apartment buildings are not safe zones for dengue. Mosquitoes will still breed and transmit dengue if not properly controlled

From the perspective of an enterprise accompanying Vietnam’s health system, Benjamin Ping, general manager of Takeda, said, “We believe that multi-sectoral collaboration plays a key role because no single unit or organisation can effectively control dengue alone.”

Ping also emphasised the necessity for cooperation between the government, the health sector, businesses, and the community. He stated that Takeda is committed to contributing to collective efforts by strengthening healthcare system capacity, supporting community communication, and ensuring sustainable access to vaccinations as an integral part of the disease control strategy.

Additionally, the role of health education is indispensable. It is necessary to implement diverse, official, and continuous campaigns to raise community awareness, help people understand the disease correctly, recognise early symptoms, avoid negligence, and seek medical care in time. In addition, vaccination is also considered one of the proactive preventive solutions, helping to reduce severe cases and fatalities caused by dengue.

The WHO is currently recommending the use of Takeda’s dengue vaccine for certain populations in countries with high transmission rates and significant dengue burden. This vaccine has been approved in 40 countries, with over 15 million doses distributed globally.

Disclosure

This content was jointly developed by the Sức khỏe & Đời sống Newspaper, and has been professionally reviewed and approved by the Vietnam Association of Preventive Medicine with the aim of raising public awareness. It is intended solely for public informational purposes and should not be used for the diagnosis or treatment of any health condition. This material is not a substitute for professional medical advice. Please consult your physician for further guidance. C-ANPROM/VN/NON/0034

Experts discuss dengue fever prevention in Vietnam Takeda, a global biopharmaceutical company, hosted a series of meetings in Ho Chi Minh City and Hanoi on September 26-27 to discuss the essential role of vaccines in an integrated dengue prevention strategy in Vietnam and globally.

Integrated solutions for dengue fever prevention in Vietnam Dengue vaccines being available in Vietnam contributes to strengthening the prevention and control strategy for this infectious disease, but synchronised implementation of multiple solutions is needed to ensure vaccine sustainability.

Concerns mount over potential dengue fever outbreaks At a recent scientific symposium on dengue vaccines in Ho Chi Minh City, experts warn that dengue fever is shifting from a seasonal outbreak to a year-round public health threat, with treatment costs in some cases approaching $40,000.

Perfluoroalkyl and polyfluoroalkyl substances (PFAS) have the nickname ‘forever chemicals’ thanks to their persistence in the environment. While a handful of bacteria are known to mop up these insidious compounds, it’s unclear whether any of our own microflora hide such a talent.

A new study by an international team of researchers has shown how several species of human gut bacteria can absorb and store PFAS. Potentially, boosting these types of bacteria in our bodies could stop the chemicals from negatively impacting our health.

“We found that certain species of human gut bacteria have a remarkably high capacity to soak up PFAS from their environment at a range of concentrations, and store these in clumps inside their cells,” says Kiran Patil, a molecular biologist from the University of Cambridge in the UK.

“Due to aggregation of PFAS in these clumps, the bacteria themselves seem protected from the toxic effects.”

Related: ‘Game Changer’: Hot New Tech Turns Forever Chemicals Into Valuable Resource

Through detailed lab tests, the researchers found a total of 38 different gut bacterial strains able to absorb forever chemicals at a variety of concentrations, with the fiber-degrading bacterium Bacteroides uniformis one of the best at the job.

In experiments with Escherichia coli, the team also discovered certain mechanisms that could make bacteria more or less effective at taking on board PFAS – something that will be useful if this absorption can be bioengineered in the future.

The researchers found that PFAS were effectively locked away in the bacteria that could handle the chemicals, the bacteria clustering together in a way that reduces their surface area and possibly protects the microorganisms from being harmed themselves.

Further tests on mice with nine of these bacteria species implanted in their guts showed that the microbes were able to quickly absorb PFAS, which was excreted from the mice through their feces. As levels of forever chemicals increased, the microbes worked harder at soaking them up.

“The reality is that PFAS are already in the environment and in our bodies, and we need to try and mitigate their impact on our health now,” says molecular biologist Indra Roux from the University of Cambridge.

“We haven’t found a way to destroy PFAS, but our findings open the possibility of developing ways to get them out of our bodies where they do the most harm.”

PFAS are found in everything from cosmetics to drinking water to food packaging, and have become embedded in so many manufacturing processes that it would now be almost impossible to avoid them completely. What’s less clear is the harm they might be doing to our bodies, though they’ve already been linked to a number of health issues – including kidney damage.

The bacteria’s ability to remove PFAS from human bodies remains to be seen. It is possible, the researchers say, that probiotic dietary supplements may be developed to boost the right mix of gut microbes and help safely clear out PFAS from our systems.

“Given the scale of the problem of PFAS ‘forever chemicals’, particularly their effects on human health, it’s concerning that so little is being done about removing these from our bodies,” says Patil.

The research has been published in Nature Microbiology.

Food labeling is out of step with healthy diet recommendations and could be improved by including nutrient release rates, according to University of Queensland Emeritus Professor Mike Gidley.

The researcher at UQ’s Queensland Alliance for Agriculture and Food Innovation said nutrition was currently communicated in two ways, by a food’s nutrient composition and by the diversity of wholefoods in the diet.

“At the moment people pick and choose which of these food languages works best for them, but something is missing,” Emeritus Professor Gidley said.

“Composition defines nutritional value by the nutrients and calorific energy the food contains, measured against daily consumption targets.

“Whole food tends to be what health agencies emphasize because that is where the strongest evidence for human health benefits has been found.

“The problem is if you measure food in terms of how much protein, carbs or fat it contains, it’s not enough to judge nutritional value.

“Some unhealthy foods have similar compositions to healthy options.

“And whole foods generally have a slow and steady nutrient release, while nutrients in fabricated ingredient foods are generally more rapidly released, a difference which is not addressed if nutrition value is only based on composition.

“A better labeling system would include the rate at which an individual component – protein, starch, fat, sugar – is delivered, or predicted to be delivered to the body.

“If we can incorporate nutrient release rates, we can bridge the gap between the two types of nutrition communication.”

Emeritus Professor Gidley said further research was needed before his proposal could become a reality.

“We need more data on real people and how they digest their food, which is a major science challenge because it happens dynamically in the body and needs to be measured non-invasively,” he said.

“We need to know not only how quickly nutrients go into us but also how much nourishes our gut microbiota, which is increasingly recognized as playing an important part of human health.

“Secondly, we need global collaboration to define a standardized analytical method to predict nutrient release from foods using a laboratory method.

“My guess is the first stage would be moving towards a fast, medium or slow kind of classification system.

“It won’t happen immediately, but without talking about it, nothing will happen, so this proposal is a conversation starter.”

Emeritus Professor Gidley’s opinion piece was published in Nature Food.