Author: ModernMedia

Brewing Tea Removes Lead from Water

Photo by Joanna Kosinska on Unsplash

Good news for tea lovers: That daily brew might be purifying the water, too. In a new study, Northwestern University researchers demonstrated that brewing tea naturally adsorbs heavy metals like lead and cadmium, effectively filtering dangerous contaminants out of drinks. Heavy metal ions stick to, or adsorb to, the surface of the tea leaves, where they stay trapped.

The study was published in the journal ACS Food Science & Technology.

“We’re not suggesting that everyone starts using tea leaves as a water filter,” said Northwestern’s Vinayak P. Dravid, the study’s senior author. “In fact, we often utilise model experiments and tweak diverse parameters to probe and understand the scientific principles and phenomena involved in capture/release cycles of contaminants. For this study, our goal was to measure tea’s ability to adsorb heavy metals. By quantifying this effect, our work highlights the unrecognised potential for tea consumption to passively contribute to reduced heavy metal exposure in populations worldwide.”

“I’m not sure that there’s anything uniquely remarkable about tea leaves as a material,” said Benjamin Shindel, the study’s first author. “They have a high active surface area, which is a useful property for an adsorbent material and what makes tea leaves good at releasing flavor chemicals rapidly into your water. But what is special is that tea happens to be the most consumed beverage in the world. You could crush up all kinds of materials to get a similar metal-remediating effect, but that wouldn’t necessarily be practical. With tea, people don’t need to do anything extra. Just put the leaves in your water and steep them, and they naturally remove metals.”

Exploring different variables

To conduct the study, the Northwestern team explored how different types of tea, tea bags and brewing methods affect heavy metal adsorption. The various varieties tested included “true” teas such as black, green, oolong and white, as well as chamomile and rooibos teas. They also examined the differences between loose-leaf and commercially bagged tea.

The researchers created water solutions with known amounts of lead and other metals (chromium, copper, zinc and cadmium), and then heated the solutions to just below boiling temperature. Next, they added the tea leaves, which steeped for various time intervals, from mere seconds to 24 hours.

After steeping, the team measured how much of the metal content remained in the water. By comparing metal levels before and after adding the tea leaves, they were able to calculate how much was effectively removed.

Cellulose bags work best — and don’t release microplastics

After multiple experiments, Dravid, Shindel and their team identified several trends. Perhaps somewhat unsurprising: The bag matters. After testing different types of bags without tea inside, the researchers found cotton and nylon bags only absorbed trivial amounts of the contaminants. The cellulose bags, however, worked incredibly well.

The key to a successful sorbent material is high surface area. Similar to how a magnet attaches to a refrigerator door, metal ions cling to the surface of a material. So, the more area for the particles to stick to, the better. Shindel posits that cellulose, which is a biodegradable natural material made from wood pulp, has higher surface area – and therefore more binding sites – than sleeker synthetic materials.

“The cotton and nylon bags remove practically no heavy metals from water,” Shindel said. “Nylon tea bags are already problematic because they release microplastics, but the majority of tea bags used today are made from natural materials, such as cellulose. These may release micro-particles of cellulose, but that’s just fiber which our body can handle.”

Longer steeping time, fewer metals

When comparing different varieties of tea, the researchers discovered tea type and grind played minor roles in adsorbing contaminants. Finely ground tea leaves, particularly black tea leaves, absorbed slightly more metal ions than whole leaves. Again, the researchers attributed this to surface area.

“When tea leaves are processed into black tea, they wrinkle and their pores open,” Shindel explained. “Those wrinkles and pores add more surface area. Grinding up the leaves also increases surface area, providing even more capacity for binding.”

Out of all the experiments, one factor stood out most. Steeping time played the most significant role in tea leaves’ ability to adsorb metal ions. The longer the steeping time, the more contaminants were adsorbed.

“Any tea that steeps for longer or has higher surface area will effectively remediate more heavy metals,” Shindel said. “Some people brew their tea for a matter of seconds, and they are not going to get a lot of remediation. But brewing tea for longer periods or even overnight – like iced tea – will recover most of the metal or maybe even close to all of the metal in the water.”

Future opportunities

Although results depend on several factors – steeping time and water-to-tea ratio, for example – tea preparation removes an amount of lead from water that should be significant from a public health perspective.

From their experiments, the researchers estimate that tea preparation can remediate about 15% of lead from drinking water, even up to lead concentrations as high as 10 parts per million. That estimate applies only to a “typical” cup of tea, which includes one mug of water and one bag of tea, brewed for three to five minutes. Changing the parameters remediates different levels of lead. Steeping for longer than five minutes, for example, adsorbs more lead compared to the average steeping time.

“Ten parts lead per million is obviously incredibly toxic,” Shindel said. “But with lower concentrations of lead, tea leaves should remove a similar fraction of the metal content in the water. The primary limiting factor is how long you brew your tea for.”

In high-resource areas of the world, it’s unlikely that concentrations will reach such high levels. And if there is a water crisis, brewing tea will not solve the problem. But Shindel said the study’s results provide useful new information that could be applied to public health research.

“Across a population, if people drink an extra cup of tea per day, maybe over time we’d see declines in illnesses that are closely correlated with exposure to heavy metals,” he said. “Or it could help explain why populations that drink more tea may have lower incidence rates of heart disease and stroke than populations that have lower tea consumption.”

Source: Northwestern University

Is Red Wine a Healthier Choice than White Wine? Uncorking the Cancer Risks

Photo by Apolo Photographer on Unsplash

Epidemiologists in the School of Public Health conducted a meta-analysis to assess whether red wine protects against cancer, comparing the cancer risks of red wine vs. white wine. It is published in the journal Nutrients.

Alcohol – specifically, the ethanol in alcoholic beverages – metabolises into compounds that damage DNA and proteins, contributing to cancer risk. In 2020, excessive alcohol consumption was linked to more than 740 000 cancer cases worldwide, accounting for 4.1% of all cases.

Despite the classification of alcoholic beverages as Group 1 carcinogens, meaning they are carcinogenic to humans, a common perception is that not all alcoholic beverages are alike. Red wine, in particular, is often considered a healthier choice, and its consumption is on the rise. The popularity of red wine may stem from the widespread belief that its high resveratrol content, an antioxidant with anti-inflammatory properties, offers protective effects against cancer.

Researchers from the Brown University School of Public Health have conducted a study that scours “the vast and often contradictory literature on the carcinogenicity of red and white wine” to assess whether this assumption holds up, and to compare the cancer risks associated with wine type.

“In an effort to better understand the potential impact of wine consumption on cancer risk, we conducted a comprehensive meta-analysis to assess whether red wine is truly a healthier choice than white wine,” said Eunyoung Cho, co-lead author of the study and associate professor of epidemiology and of dermatology at Brown. “Our analysis included as many published epidemiological studies as possible that separately explored the relationship between red and white wine consumption and cancer risk.”

Analyzing 42 observational studies (20 cohort and 22 case-control) involving nearly 96,000 participants, Cho and her team found no overall increased cancer risk from wine consumption, regardless of type. However, they also found no clear evidence that red wine mitigates cancer risk.

Paradoxically, when focusing on cohort studies that follow participants over a long period of time, researchers found that white wine is associated with a 22% increased risk of skin cancer compared to red wine intake.

“The results of our meta-analysis revealed no significant difference in cancer risk between red and white wine overall,” Cho said. “However, we did observe a distinction when it came to skin cancer risk. Specifically, the consumption of white wine, but not red wine, was associated with an increased risk of skin cancer.”

The reasons for this are indeterminate. Researchers suggest that heavy consumption of wine may correlate to high-risk behaviors, such as indoor tanning and inadequate sunscreen use. However, it is unclear why white wine, in particular, is the culprit. 

In an additional twist, the study also found a stronger association between white wine intake and increased overall cancer risk among women. This finding warrants further investigations into potential underlying mechanisms.

The meta-analysis, the first study of its kind, challenges the belief that red wine is healthier than white. It also points to the need for further study into the association between white wine consumption and cancer risk, particularly in women.

Source: Brown University

Prostate Cancer is Not a Death Knell, Study Shows

Credit: Darryl Leja National Human Genome Research Institute National Institutes Of Health

Prostate cancer statistics can look scary: 34 250 U.S. deaths in 2024. 1.4 million new cases worldwide in 2022. Dr Bruce Montgomery, an oncologist at University of Washington, hopes that patients won’t see these numbers and just throw up their hands in fear or resignation.  

“Being diagnosed with prostate cancer is not a death knell,” said Montgomery, senior author of a literature and trial review that appeared in JAMA. Montgomery is the clinical director of genitourinary oncology at Fred Hutch Cancer Center and University of Washington Medical Center, and a professor of medicine and urology at the UW School of Medicine.  

He encourages patients to ask their primary-care doctor specific questions about this cancer too.  Montgomery also encourages his fellow doctors to bring up the question of prostate cancer screening with their patients. 

“Knowing whether there is prostate cancer and how risky it is can be the first step. Not every cancer needs to be treated,” he said. “Sometimes it’s safe to just watch and use active surveillance.”   

A 2024 study coauthored by UW Medicine urologist Dr Daniel Lin showed that active surveillance can be extremely safe: 0.1% of men who opted for surveillance died of prostate cancer after 10 years.  

“We need to realise that prostate cancer is not one disease,” Montgomery said. “As a provider, you need to personalise your approach to the patient you’re seeing and to the disease that they personally are dealing with.” 

For example, if a 50-year-old man develops prostate cancer that is only in the prostate, then more aggressive measures may need to be considered. However, if the disease, which can be slow-moving, develops in an 80-year-old patient, the discussion may be quite different. 

“I’ve seen men that age (80s) develop prostate cancer and they’ve opted for no therapy,” he said. “They know that treatment, such as radiation, might make them feel terrible … so they just say ‘no.’ 

You, as their physician, he noted, must respect that.  

“But if you’re 50 and have 25 to 30 years in which prostate cancer can become a bigger issue, even with the downsides, most patients should get therapy,” he said.  

For more advanced prostate cancer, the number of effective treatments developed has markedly increased, as has the survival rate of men with whose prostate cancer has spread to other parts of their bodies.  

 “Metastatic prostate cancer needs therapy and research over the past 10 to 20 years has improved and continues to improve survival substantially,” he said. “Knowing who needs treatment, which treatment to use and when is both an art and a science.” 

The article covered facts that men and their doctors should know, including: 

  • Approximately 1.5 million new cases of prostate cancer are diagnosed annually worldwide. Approximately 75% of cases are first detected when the cancer is still localised to the prostate. This early detection was associated with a five-year survival rate of nearly 100%.   
  • Management includes active surveillance, prostatectomy surgical removal of the prostate, or radiation therapy, depending on risk of progression. 
  • Approximately 10% of cases are diagnosed after the cancer has spread. This stage of prostate cancer   has a five-year survival rate of 37%.   
  • The most common prostate cancer is adenocarcinoma, a type that starts in gland cells, and the median age at diagnosis is 67 years.  
  • More than 50% of prostate cancer risk is attributable to genetic factors and older age.  

Prostate cancer came to public attention, both nationally and internationally last year, when famed local travel writer, Rick Steves, announced he had developed prostate cancer. He proclaimed last month via his X account, formerly Twitter, that after radiation and surgery at UW Medicine and Fred Hutch, he was cancer free.  

Source: University of Washington School of Medicine/UW Medicine

Research Identifies Beneficial Genetic Changes in Regular Blood Donors

Photo by Charliehelen Robinson on Pexels

Researchers at the Francis Crick Institute have identified genetic changes in blood stem cells from frequent blood donors that support the production of new, non-cancerous cells.

Understanding the differences in the mutations that accumulate in our blood stem cells as we age is important to understand how and why blood cancers develop and hopefully how to intervene before the onset of clinical symptoms.

As we age, stem cells in the bone marrow naturally accumulate mutations and with this, we see the emergence of clones, which are groups of blood cells that have a slightly different genetic makeup. Sometimes, specific clones can lead to blood cancers like leukaemia.

When people donate blood, stem cells in the bone marrow make new blood cells to replace the lost blood and this stress drives the selection of certain clones.

Blood donation impacts makeup of cell populations

In research published in Blood, the team at the Crick, in collaboration with scientists from the DKFZ in Heidelberg and the German Red Cross Blood Donation Centre, analysed blood samples taken from over 200 frequent donors – (three donations a year over 40 years, more than 120 times in total) – and sporadic control donors who had donated blood less than five times in total.

Samples from both groups showed a similar level of clonal diversity, but the makeup of the blood cell populations was different.

For example, both sample groups contained clones with changes to a gene called DNMT3A, which is known to be mutated in people who develop leukaemia. Interestingly, the changes to this gene observed in frequent donors were not in the areas known to be preleukaemic.

A balancing act

To understand this better, the Crick researchers edited DNMT3A in human stem cells in the lab. They induced the genetic changes associated with leukaemia and also the non-preleukaemic changes observed in the frequent donor group.

They grew these cells in two environments: one containing erythropoietin (EPO), a hormone that stimulates red blood cell production which is increased after each blood donation, and another containing inflammatory chemicals to replicate an infection.

The cells with the mutations commonly seen in frequent donors responded and grew in the environment containing EPO and failed to grow in the inflammatory environment. The opposite was seen in the cells with mutations known to be preleukaemic.

This suggests that the DNMT3A mutations observed in the frequent donors are mainly responding to the physiological blood loss associated with blood donation.

Finally, the team transplanted the human stem cells carrying the two types of mutations into mice. Some of these mice had blood removed and then were given EPO injections to mimic the stress associated with blood donation.

The cells with the frequent donor mutations grew normally in control conditions and promoted red blood cell production under stress, without cells becoming cancerous. In sharp contrast, the preleukaemic mutations drove a pronounced increase in white blood cells in both control or stress conditions.

The researchers believe that regular blood donation is one type of activity that selects for mutations that allow cells to respond well to blood loss, but does not select the preleukaemic mutations associated with blood cancer.

Interactions of genes and the environment

Dominique Bonnet, Group Leader of the Haematopoietic Stem Cell Laboratory at the Crick, and senior author, said: “Our work is a fascinating example of how our genes interact with the environment and as we age. Activities that put low levels of stress on blood cell production allow our blood stem cells to renew and we think this favours mutations that further promote stem cell growth rather than disease.

“Our sample size is quite modest, so we can’t say that blood donation definitely decreases the incidence of pre-leukaemic mutations and we will need to look at these results in much larger numbers of people. It might be that people who donate blood are more likely to be healthy if they’re eligible, and this is also reflected in their blood cell clones. But the insight it has given us into different populations of mutations and their effects is fascinating.”

Hector Huerga Encabo, postdoctoral fellow in the Haematopoietic Stem Cell Laboratory at the Crick, and first joint author with Darja Karpova from the DKFZ in Heidelberg, said: “We know more about preleukaemic mutations because we can see them when people are diagnosed with blood cancer.

“We had to look at a very specific group of people to spot subtle genetic differences which might actually be beneficial in the long-term. We’re now aiming to work out how these different types of mutations play a role in developing leukaemia or not, and whether they can be targeted therapeutically.”

Source: The Francis Crick Institute

High Temperatures Could Impact the Brain Function of Young Children

Photo by frank mckenna on Unsplash

Exposure to high ambient temperatures is associated with lower connectivity in three brain networks in preadolescents, suggesting that heat may impact brain function. This is the conclusion of a study led by the Barcelona Institute for Global Health (ISGlobal). The results have been published in the Journal of the American Academy of Child & Adolescent Psychiatry

The study involved 2229 children aged 9 to 12 from the “Generation R” cohort in Rotterdam, Netherlands. Functional connectivity data from brain networks, i.e., how different regions of the brain communicate and collaborate, were assessed using resting-state magnetic resonance imaging, when the children were not performing any active tasks. Daily mean temperature estimates were obtained from the UrbClim urban climate model, developed by the Flemish Institute for Technological Research. Temperature values were calculated for the period from 2013 to 2015, assigning daily averages to each participant based on their home address.

Higher ambient temperatures during the week preceding the MRI assessment were associated with lower functional connectivity within the medial parietal, salience, and hippocampal networks, which are essential for proper brain functioning. This implies that brain areas may work less synchronously, affecting processes such as attention, memory, and decision-making. The medial parietal network is related to introspection and self-perception; the salience network detects environmental stimuli and prioritises what deserves our attention; and the hippocampal network is critical for memory and learning.

The research shows that the association between high temperatures and lower functional connectivity was strongest on the day before the brain scan and progressively decreased on subsequent days. In contrast, low average daily temperatures were not associated with functional connectivity.

“We hypothesise that dehydration could explain our findings, as children are particularly vulnerable to fluid loss when exposed to heat, which can affect the functional connectivity of brain networks,” says study lead author Laura Granés, researcher at IDIBELL and ISGlobal.

“In the current climate emergency, public health policies aimed at protecting children and adolescents from high temperatures could help mitigate potential effects on brain function,” says Mònica Guxens, ICREA researcher at ISGlobal and senior author of the study.

Implications for mental health

Although brain function alterations have been suggested as a possible mechanism linking temperature and mental health, no study to date has examined the effects of ambient temperature on functional brain networks. In another recent study, the same research team found that exposure to cold and heat can affect psychiatric symptoms such as anxiety, depression and attention problems. In addition, other studies have linked lower connectivity within the brain’s salience network to suicidal ideation and self-harming behaviours in adolescents with depression, as well as to anxiety disorders.

“Given the role of the salience network in suicidal ideation, our findings raise a new hypothesis: high temperatures could decrease the functional connectivity of this network, indirectly contributing to a higher risk of suicide in individuals with pre-existing mental health conditions,” explains Carles Soriano-Mas, researcher at IDIBELL and the University of Barcelona and one of the study’s authors. “While we do not propose that these connectivity changes, triggered by heat exposure, directly induce suicidal behaviours, they could act as a trigger in vulnerable individuals,” adds the researcher. 

Source: Barcelona Institute for Global Health (ISGlobal)

Breakthrough Research Offers Hope for Ischaemic Heart Failure

Right side heart failure. Credit: Scientific Animations CC4.0

Researchers report a groundbreaking discovery in cardiac regeneration that offers new hope for the treatment of ischaemic heart failure. Published in npj Regenerative Medicine, the study reveals a novel approach to promoting cardiomyocyte proliferation.

The paper was authored by researchers at Baylor College of Medicine, the QIMR Berghofer Medical Research Institute in Brisbane, Australia, and collaborating institutions.

“When the heart cannot replace injured cardiomyocytes with healthy ones, it becomes progressively weaker, a condition leading to heart failure. In this study, we investigated a new way to stimulate cardiomyocyte proliferation to help the heart heal,” said co-corresponding author Dr Riham Abouleisa, assistant professor in the Division of Cardiothoracic Surgery at Baylor.

Previous studies showed that calcium plays an important role in cardiomyocyte proliferation. In the current study, Abouleisa and her colleagues explored how modulating calcium influx in cardiomyocytes would affect their proliferation.

“We found that preventing calcium influx in cardiomyocytes enhances the expression of genes involved in cell proliferation,” Abouleisa said. “We prevented calcium influx by inhibiting L-Type Calcium Channel (LTCC), a protein that regulates calcium in these cells. Our findings suggest that LTCC could be a target for developing new therapies to induce cardiomyocyte proliferation and regeneration.”

The study demonstrates that both pharmacological and genetic inhibition of LTCC can induce cardiomyocyte replication and that this occurs by modulating the activity of calcineurin, a known regulator of cardiomyocyte proliferation. This innovative approach showed promising results both in human cardiac slices grown in the lab and in live animals.

Abouleisa and her colleagues’ research highlights the importance of targeting calcium signalling pathways to unlock the regenerative potential of the heart and opens new avenues for developing cardiac regenerative therapies, potentially transforming the treatment landscape for patients suffering from heart failure.

Source: Baylor College of Medicine

Memory is Impaired in Aged Rats After 3 Days of High-fat Diet

Some fast food offerings, such as cheeseburgers, contain more than 60% of calories from fat. Photo by Jonathan Borba

Just a few days of eating a diet high in saturated fat could be enough to cause memory problems and related brain inflammation in older adults, a new study in rats suggests. 

In the study, published in Immunity & Aging, researchers fed separate groups of young and old rats the high-fat diet for three days or for three months to compare how quickly changes happen in the brain versus the rest of the body when eating an unhealthy diet. 

As expected based on previous diabetes and obesity research, eating fatty foods for three months led to metabolic problems, gut inflammation and dramatic shifts in gut bacteria in all rats compared to those that ate normal chow, while just three days of high fat caused no major metabolic or gut changes.

When it came to changes in the brain, however, researchers found that only older rats – whether they were on the high-fat diet for three months or only three days – performed poorly on memory tests and showed negative inflammatory changes in the brain. 

The results dispel the idea that diet-related inflammation in the aging brain is driven by obesity, said senior study author Ruth Barrientos, an investigator in the Institute for Behavioral Medicine Research at The Ohio State University. Most research on the effects of fatty and processed foods on the brain has focused on obesity, yet the impact of unhealthy eating, independent of obesity, remains largely unexplored. 

“Unhealthy diets and obesity are linked, but they are not inseparable. We’re really looking for the effects of the diet directly on the brain. And we showed that within three days, long before obesity sets in, tremendous neuroinflammatory shifts are occurring,” said Barrientos, also an associate professor of psychiatry and behavioural health and neuroscience in Ohio State’s College of Medicine.  

“Changes in the body in all animals are happening more slowly and aren’t actually necessary to cause the memory impairments and changes in the brain. We never would have known that brain inflammation is the primary cause of high-fat diet-induced memory impairments without comparing the two timelines.” 

Years of research in Barrientos’ lab has suggested that aging brings on long-term “priming” of the brain’s inflammatory profile coupled with a loss of brain-cell reserve to bounce back, and that an unhealthy diet can make matters worse for the brain in older adults. 

Fat constitutes 60% of calories in the high-fat diet used in the study, which could equate to a range of common fast-food options: For example, nutrition data shows that fat makes up about 60% of calories in a McDonald’s double smoky BLT quarter pounder with cheese or a Burger King double whopper with cheese

After the animals were on high-fat diets for three days or three months, researchers ran tests assessing two types of memory problems common in older people with dementia that are based in separate regions of the brain: contextual memory mediated by the hippocampus (the primary memory center of the brain), and cued-fear memory that originates in the amygdala (the fear and danger center of the brain). 

Compared to control animals eating chow and young rats on the high-fat diet, aged rats showed behaviors indicating both types of memory were impaired after only three days of fatty food – and the behaviors persisted as they continued on the high-fat diet for three months. 

Researchers also saw changes in levels of a range of proteins called cytokines in the brains of aged rats after three days of fatty food, which signaled a dysregulated inflammatory response. Three months after being on the high-fat diet, some of the cytokine levels had shifted but remained dysregulated, and the cognitive problems persisted in behavior tests. 

“A departure from baseline inflammatory markers is a negative response and has been shown to impair learning and memory functions,” Barrientos said. 

Compared to rats eating normal chow, young and old animals gained more weight and showed signs of metabolic dysfunction – poor insulin and blood sugar control, inflammatory proteins in fat (adipose) tissue, and gut microbiome alterations – after three months on the high-fat diet. Young rats’ memory and behavior and brain tissue remained unaffected by the fatty food. 

“These diets lead to obesity-related changes in both young and old animals, yet young animals appear more resilient to the high-fat diet’s effects on memory. We think it is likely due to their ability to activate compensatory anti-inflammatory responses, which the aged animals lack,” Barrientos said. 

“Also, with glucose, insulin and adipose inflammation all increased in both young and old animals, there’s no way to distinguish what is causing memory impairment in only old animals if you look only at what’s happening in the body. It’s what is happening in the brain that’s important for the memory response.” 

Source: Ohio State University

My Five-hour Wait for Treatment at Mamelodi Hospital

Gauteng Health MEC has said Mamelodi Regional Hospital meets National Health Insurance standards, but my experience was not good

The writer waited five hours for treatment for a broken wrist and head injuries at Mamelodi Regional Hospital in Tshwane. Photo: Warren Mabona.

By Warren Mabona

I waited five hours to get medical treatment at Mamelodi Regional Hospital in Tshwane, with a broken wrist and an injured head.

On 19 February 2025 at about 4pm I was walking in Mamelodi West. I was on a journalism assignment, heading to informal settlements that are prone to flooding.

The street was quiet, but I felt safe because I had walked there before. Suddenly, a car stopped in front of me, and two men got out of it and tried to rob me. I ran away and jumped into the stormwater passage, but slipped and fell, hitting my face against the concrete.

When I managed to stand up, I was dizzy and my vision was blurred. I was drenched in dirty water and my belongings — my cell phone, my wallet and my camera bag — were wet.

The men who attacked me were no longer on the street. My right wrist was swollen and painful, an injury above my eye was bleeding profusely, and my head was aching. But I was relieved that I was still alive and I still had all my belongings.

I decided not to call an ambulance, but to walk about 800 metres to Mamelodi Regional Hospital.

I went to the casualty unit, expecting that I would receive treatment quickly. At the front desk, a clerk took more than 20 minutes to fill in my file. He said the hospital’s computer system was offline and he had to fill in the file with a pen. I then went to sit at the reception area. My head was aching and I repeatedly requested headache tablets from the nurses, who gave me two tablets after 30 minutes. But my pain lingered.

The wound on my face was still bleeding and my wrist was swollen and bent. About 40 minutes after my arrival, a nurse cleaned my wound and wrapped it with a bandage, stopping the bleeding.

At about 8pm, a man sitting next to me said he had arrived at the hospital at 2pm after falling from scaffolding at a construction site. He was still waiting for his X-ray results.

I went for X-rays and long afterwards, at about 10pm, I had a cast put on my wrist. I was given injections which helped with the pain. I was discharged at 11pm and went home.

In September last year, the Gauteng MEC for Health Nomantu Nkomo-Ralehoko said that Mamelodi Regional Hospital was the first hospital in Gauteng ready to meet National Health Insurance (NHI) standards.

In response to GroundUp’s questions, Gauteng Department of Health spokesperson Motalatale Modiba said a triage priority system is followed at the hospital, meaning that four patients with critical wounds that required life-saving emergencies were attended to first. He said this affected my waiting time for wound care and the application of a cast.

“You were classified as Orange P2, that is a person who is in a stable condition and is not in any immediate danger, but requires observation,” said Modiba.

“At the time of your arrival, the casualty unit had 31 other patients to be seen. These include four critical cases in the resuscitation unit, ten trauma cases, 16 medical cases and four pediatric cases,” he said.

Modiba confirmed that the hospital’s computer system was offline when I arrived.

I asked Modiba whether the Gauteng Department of Health can still confidently regard this hospital as NHI-ready despite the slow delivery of medical services I experienced. Modiba said: “Mamelodi Regional Hospital remains committed to provide best healthcare services.”

Republished from GroundUp under a Creative Commons Attribution-NoDerivatives 4.0 International License.

Read the original article.

Oxytocin Can ‘Pause’ Pregnancy After Conception

Photo by Pavel Danilyuk on Pexels

Oxytocin, a hormone already known for its role in childbirth, milk release, and mother–infant bonding, may have a newfound purpose in mammalian reproduction. In times of maternal stress, the hormone can delay an embryo’s development for days to weeks after conception, a new study in rodents shows. According to the authors, the findings about so-called “diapause” may offer new insights into pregnancy and fertility issues faced by humans.

Led by researchers at NYU Langone Health, the study explored diapause, in which an embryo temporarily stops growing early in its development before it attaches to the lining of its mother’s uterus, a key step leading to the formation of the placenta. Known to occur in species as varied as armadillos, giant pandas, and seals, diapause is thought to have evolved to help expectant mothers preserve scarce resources (e.g., breast milk) by delaying birth until they have enough to successfully take care of their offspring.

Although recent studies have uncovered evidence that a form of diapause may occur in humans, the underlying mechanisms behind it have until now remained unclear.

The findings in mice showed that one type of stress that may cause diapause is milk production and release (lactation), as it requires a mother to expend bodily resources nursing already-born pups, and supplying nutrients to pups growing in the womb, at the same time. The study revealed that the time between conception and birth, typically 20 days for these animals, was delayed by about a week in pregnant rodents that were already nursing a litter.

Further, the research team showed that this delay was brought about by a rise in the production of oxytocin, levels of which are known to go up as a mother lactates. To confirm this role for the hormone, the researchers exposed mouse embryos in the lab to a single dose (either 1 microgram or 10 micrograms) of oxytocin, and found that even these small amounts delayed their implantation in the uterus by as much as three days. The team found that the chemical did more than just pause pregnancy: oxytocin surges that were large enough to mimic the amounts and timing measured during nursing caused loss of pregnancy in the mice in nearly all cases.

“Our findings shed light on the role of oxytocin in diapause,” said study co-author Moses V. Chao, PhD, a professor at NYU Grossman School of Medicine. “Because of this newfound connection, it is possible that abnormalities in the production of this hormone could play roles in infertility, premature or delayed birth, and miscarriage.”

A report on the findings appears in Science Advances in a special issue focused on women’s health.

In another part of the study, the team searched for a mechanism that would allow embryos to react to an oxytocin surge. They found that the hormone can bind to special proteins called receptors on the surface of a layer of cells known as the trophectoderm, which surrounds the early embryo and eventually forms the placenta.

Notably, mouse embryos that were genetically altered to disable oxytocin receptors lived long enough to implant into their mother’s placenta at much lower rates than normal embryos. This suggests that the ability to respond to oxytocin spikes and therefore go into diapause is somehow important for the developing pups’ survival, says Dr. Chao, who plans to examine this protective function in more detail.

“Despite being extremely common, infertility and developmental issues that can arise during pregnancy remain poorly understood and can have a lasting, devastating impact on parents and their children,” said study senior author Robert Froemke, PhD, professor of genetics. “Having a deeper understanding of the factors that contribute to these problems may allow experts to better address them in the future.”

The researchers next plan to examine how cell growth gets turned back on after diapause, Dr Froemke says. In addition, the team plans to explore how diapause may affect offsprings’ health and development after birth, and determine whether and how their discoveries can inform reproductive medicine.

Dr Froemke cautions that while the study results are promising, mice and humans have significant differences in their reproductive processes, despite both being mammals. He adds that the current investigation did not assess the role that other pregnancy-related hormones, such as oestrogen and progesterone, may play in diapause.

Source: NYU Langone Health / NYU Grossman School of Medicine

Leakiness of First Blood–brain Barrier Layer Results in Cognitive Deficits

a, Diagram of the BBB and brain endothelial glycocalyx layer. b, TEM of cortical capillaries with lanthanum nitrate staining from young (3-month-old) and aged (21-month-old) mice. Scale bars, 1 µm. Source: Shi et al., Nature, 2025.

A study published in Nature reveals how a key component of the blood–brain barrier (BBB), the endothelial glycocalyx layer, becomes dysregulated in ageing, causing the BBB to become compromised. The researchers also investigated the possibility of to restore this layer’s integrity, reducing neuroinflammation and restoring cognitive function.

The BBB is a highly specialised safeguard keeping the brain separate from harmful factors, such as toxins and also albumin, IgG and fibrinogen (and, unfortunately, many medications which could otherwise treat brain disease). The leakage of such blood-derived molecules into the brain has been shown to trigger neuroinflammatory changes and create a neurotoxic brain environment. The part of the BBB directly in contact with the blood is the endothelial glycocalyx layer, a carbohydrate-rich meshwork mostly composed of proteoglycans, glycoproteins and glycolipids that coats the BBB lumen. Yet the endothelial glycocalyx’s composition and role is poorly understood despite it being the first layer of interface between the blood and brain.

The researchers found that the brain endothelial glycocalyx is highly dysregulated during ageing and neurodegenerative disease. Two mucin-type O-glycan biosynthetic enzymes, C1GALT1 and B3GNT3 were also found to be downregulated mouse models of ageing and in the brains of Alzheimer’s and Huntington’s disease patients. To test these, the researchers used adeno-associated viruses (AAV) in young mice to turn down the expression of C1GALT1 and B3GNT3. These mice showed signs of BBB leakage and in severe cases, brain haemorrhaging occurred in mice.

In samples from the brains of Alzheimer’s patients, the researchers also observed reduced C1GALT1 in microvessels.

To test if it was possible to restore the BBB’s ability to protect the brain against harmful blood-borne molecules, they administered AAVs in aged mice to restore levels of B3GNT3 and C1GALT1.

Assessing cognitive function, they found that aged mice treated with B3GNT3 via an AAV displayed improvements in spatial working memory in a maze test and hippocampal-dependent learning and memory in a fear conditioning test. Aged mice treated with C1GALT1 did not improve in the maze test, and no significant difference was observed in cued freezing in the fear conditioning among the three aged groups.

Although the study shows that increasing C1GALT1 and B3GNT3 reduces BBB permeability and improves brain health, the precise mechanisms that underlie these beneficial effects remain unclear. The researchers believe that by limiting the nonspecific uptake of blood-derived molecules, the brain can be protected. But C1GALT1 and B3GNT3 are also likely to influence a wide range of proteins and glycan structures and in order to further understand brain ageing and rejuvenation it is therefore crucial to understand the molecular pathways affected by them.

The authors concluded: “Cumulatively, our findings provide a detailed compositional and structural mapping of the ageing brain endothelial glycocalyx layer and reveal important consequences of ageing- and disease-associated glycocalyx dysregulation on BBB integrity and brain health.”