In honor of the Year of the Dragon, we take a look at some potential inspirations for the dragon myth.
Around the world, people are celebrating the Chinese New Year and the start to the Year of the Dragon. This got us wondering: Where did the myth of the dragon come from in the first place? Scholars say that belief in dragons probably evolved independently in both Europe and China, and perhaps in the Americas and Australia as well. How could this happen? Many have speculated about which real-life animals inspired the first legends. Here’s our run-down of the likeliest suspects.
Dinosaurs. Ancient people may have discovered dinosaur fossils and understandably misinterpreted them as the remains of dragons. Chang Qu, a Chinese historian from the 4th century B.C., mislabeled such a fossil in what is now Sichuan Province. Take a look at a fossilized stegosaurus, for example, and you might see why: The giant beasts averaged 30 feet in length, were typically 14 feet tall and were covered in armored plates and spikes for defense.
The Nile Crocodile. Native to sub-Saharan Africa, Nile crocodiles may have had a more extensive range in ancient times, perhaps inspiring European dragon legends by swimming across the Mediterranean to Italy or Greece. They are among the largest of all crocodile species, with mature individuals reaching up to 18 feet in length—and unlike most others, they are capable of a movement called the “high walk,” in which the trunk is elevated off the ground. A giant, lumbering croc? Might be easy to mistake for a dragon.
The Goanna. Australia is home to a number of species of monitor lizards, also referred to as Goannas. The large, predatory animals have razor-sharp teeth and claws, and they are important figures in traditional Aboriginal folklore. Recent studies even indicate that Goannas may produce venom that causes bite victims’ wounds to develop infections after an attack. At least in Australia, these creatures may be responsible for the dragon myth.
Whales. Others argue that the discovery of megafauna such as whales prompted stories of dragons. Ancient humans encountering whale bones would have no way of knowing that the animals were sea-based, and the idea of such gargantuan creatures might well have led people to assume that whales were predatory. Because live whales spend up to 90 percent of their time underwater, they were poorly understood for most of human history.
The Human Brain. The most fascinating explanation involves an unexpected animal: the human. In his book An Instinct for Dragons, anthropologist David E. Jones argues that belief in dragons is so widespread among ancient cultures because evolution embedded an innate fear of predators in the human mind. Just as monkeys have been shown to exhibit a fear of snakes and large cats, Jones hypothesizes that the trait of fearing large predators—such as pythons, birds of prey and elephants—has been selected for in hominids. In more recent times, he argues, these universal fears have been frequently combined in folklore and created the myth of the dragon.
Eli Lilly announced that the experimental drug donanemab showed significant benefits for early Alzheimer’s disease patients.
Beta-Amyloid Plaques and Tau in the Brain
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Alzheimer’s disease affects tens of millions of people every year, slowly stripping away cognitive function. Now, a new drug trial by Eli Lilly might be the best hope yet of slowing the inevitable progression of the disease.
The drug, donanemab, “significantly slowed cognitive and functional decline in people with early symptomatic Alzheimer’s disease,” according to an Eli Lilly statement announcing the trial results. Those patients who received the drug during the 18-month-long Phase 3 trial showed a 35% slower memory decline, cognitive function, and ability to manage common daily tasks, as measured by the integrated Alzheimer’s Disease Rating Scale (iADRS) scale, a key metric in monitoring Alzheimer’s disease progression.
“Based on these results, Lilly will proceed with global regulatory submissions as quickly as possible and anticipates making a submission to the U.S. Food and Drug Administration (FDA)…this quarter,” the company said. “Lilly will work with the FDA and other global regulators to achieve the fastest path to traditional approvals.”
The devastating effects of Alzheimer’s disease on both patients and their families are well-documented, especially given how ineffective previous attempts to slow the progression of the disease have been. With this news, Alzheimer’s sufferers and their families finally have some hope to slow the disease that once seemed as inevitable as it was unstoppable.
“Over the last 20 years, Lilly scientists have blazed new trails in the fight against Alzheimer’s disease by elucidating basic mechanisms of AD pathology and discovering imaging and blood biomarker tools to track the pathology,” Daniel Skovronsky, M.D., Ph.D., Eli Lilly’s chief scientific and medical officer, and president of Lilly Research Laboratories, said. “We are extremely pleased that donanemab yielded positive clinical results with compelling statistical significance for people with Alzheimer’s disease in this trial. This is the first Phase 3 trial of any investigational medicine for Alzheimer’s disease to deliver 35% slowing of clinical and functional decline.”
Among trial participants, nearly half (47%) of those receiving donanemab experienced no measurable worsening of symptoms after one year (measured as no decline in the sum of boxes of the clinical dementia rating, or CDR-SB), compared to 29% of participants who were on placebo. It is also noted that participants receiving the drug had a 39% lower risk of progressing to the next stage of Alzheimer’s disease compared to those on placebo,
“We are encouraged by the potential clinical benefits that donanemab may provide, although like many effective treatments for debilitating and fatal diseases, there are associated risks that may be serious and life-threatening,” Mark Mintun, M.D., group vice president of Neuroscience Research & Development at Eli Lilly and president of Avid Radiopharmaceuticals, said. “We thank the participants in the clinical trial and their loved ones for their time and commitment to finding solutions for this disease.”
Even advanced Alzheimer’s disease patients may benefit
While the most significant benefits demonstrated in the trial were for those participants in the early stages of the disease, a more limited number of advanced cases were also included in the study of donanemab, and here too there are encouraging results.
In intermediate and advanced Alzheimer’s disease cases, participants show a 29% and 22% slower progression of symptoms, respectively, so even those who have already progressed significantly into the later stages of the disease stand to benefit from the new drug.
Cautious optimism
Given how little good news there has been in the fight against Alzheimer’s disease, it is possible to overhype any progress toward a treatment. It must also be noted that this does not represent a cure for Alzheimer’s disease and that even those who respond well to the new drug are likely to experience declining cognitive functions as the disease progresses, albeit at a slower pace than before.
“It’s modest, but I think it’s real,” Dr. Ronald Petersen, an Alzheimer’s researcher at Mayo Clinic, told Reuters about the new results, “and I think it’s clinically meaningful.”
New treatments hold promise of help for the tens of millions of people suffering from Alzheimer’s disease.
New therapies may offer hope to those with Alzheimer’s disease.
Alzheimer’s is a neurodegenerative disease afflicting more than 55 million people globally.
New treatments are offering some hope for sufferers.
Here, we look at the latest research into causes and treatment options for Alzheimer’s.
Imagine forgetting how to perform simple tasks such as brushing your teeth or losing memories such as graduating college or getting married. As scary as it may sound, this is actually quite common for people with Alzheimer’s disease (AD).
According to the WHO (World Health Organization), around 55 million people worldwide are living with dementia, with the numbers expected to increase to 78 million by 2030. Out of those, around 60-70% of the cases are caused by AD. Alzheimer’s is a neurodegenerative disease, which means that it progressively causes a loss of brain cells and neural connectivity.
The disease is marked by the formation of abnormal protein deposits in the brain, which interfere with the normal functioning of the brain cells, ultimately leading to their death. The exact reason for this protein buildup is not known. However, most experts think it is caused by a combination of genetic, environmental, and lifestyle factors.
In our current understanding of this disease, it has no cure. However, there are many treatment options available that seek to manage the disease and slow its progression , and new research is being conducted every day to find a cure. Early detection and intervention can also help slow the progression of the disease and improve outcomes.
In this article, we take a look at AD in depth, how it affects the brain and its functioning, the risk factors, treatment options, and explore breakthroughs that are moving closer to finding a cure.
Symptoms and diagnosis
One of the biggest challenges with AD is its early detection, as some of the symptoms are similar to normal signs of aging, making early detection difficult. AD is typically seen in people above the age of 65, although in some cases, the symptoms can manifest earlier.
The severity of the disease varies from person to person, with some of the common symptoms including memory loss, difficulty in completing familiar tasks, disorientation, communication problems, changes in mood, decreased judgment, and personality changes.
There is no single diagnostic test for AD. Instead, doctors use a combination of neurological exams, medical history, brain imaging (including CT, PET, and MRI scans), and blood tests to make a diagnosis.
Even though much about the onset of the disease is a mystery, the buildup of proteins in the brain has been linked to neural degeneration. This includes buildup of amyloid beta, which forms senile plaques, and phosphorylated tau protein, which forms neurofibrillary tangles. This buildup generally happens in the hippocampus, which is responsible for memory storage, spatial navigation, and learning.
Risk factors
Despite our limited knowledge of the exact cause of AD, genetics is known to play a role in the development of at least some forms of the disease. The mutation of three genes, amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN 2), is known to cause a type of AD termed familial AD; and presence of one form of the polymorphic protein Apolipoprotein E (APOE) is a strong genetic risk factor for a type of AD termed sporadic AD. The mutations cause the production of abnormal proteins which are associated with AD. In addition, individuals with a genetic predisposition to AD are more likely to develop the disease than those without.
Lifestyle factors such as exercise, sleep, and diet have also been linked to risk. According to the NHS, certain risk factors associated with cardiovascular disease can also increase the risk of AD. These include smoking, obesity, high cholesterol and blood pressure, and diabetes.
However, this hesitancy does not include sleep. Sleep is required for the neural pathways in the brain to function well. Studies have shown that insomnia and sleep deprivation can lead to an accumulation of the amyloid beta protein, as well as the tau protein in the brain.
Therefore, lack of sleep can be a preventable risk factor for neurodegeneration. However, AD is a complex disease with many possible risk factors and it is not caused by lack of sleep alone.
Treatment and management
Even though AD has no known cure, there are several treatment options which can slow the progression of the disease. The treatment itself varies depending on the severity of the disease, as certain medications only work for early-stage AD.
Cholinesterase inhibitors have been shown to help to reduce or control behavioral and cognitive symptoms in early-stage AD. Their purpose is to keep acetylcholine, a neurotransmitter thought to be vital for memory, from breaking down.
Some immunotherapies, such as lecanemab and aducanumab, have also been approved by the FDA for the treatment of early-stage AD. These medications work by reducing beta-amyloid plaques in the brain.
There are also a few treatments available for people with moderate to severe AD. Memantine is a partial N-methyl-D-aspartate (NMDAR) receptor antagonist and helps some people perform day-to-day tasks for longer than they would be able to without the medicine. Scientists think it works by controlling the production of glutamate, which in large amounts can lead to brain cell death.
The FDA has also approved donepezil, which can result in a slight improvement in brain function. However, there is no evidence to suggest that donepezil alters the progression of AD.
Due to the complexity and severity of the disease, the best course of action is early detection, especially for those with a genetic predisposition to the disease. This includes regular checkups and maintaining a healthy lifestyle, with regular exercise and adequate sleep.
A few studies have also suggested cognitive behavioral therapy as a side-effect-free option for neuropsychiatric symptoms. These can help improve the quality of life for individuals with AD and their caregivers but cannot alter the progression of the disease.
Promising advances
Intriguingly, some promising new studies have the potential to point the way to a cure, or at least much more effective treatment.
A new study published in the Annals of Neurology found that suvorexant, a common insomnia medication, decreased the buildup of amyloid beta and tau proteins in the brain.
Suvorexant is a medication commonly prescribed for the treatment of insomnia. The researchers found that suvorexant decreased the concentrations of the proteins in the central nervous system. They suggest that the FDA-approved medication could be repurposed as a treatment for AD.
According to Eli Lilly, their drug donanemab slowed down the progression of AD by a third in clinical trials. Their trials showed that donanemab, given monthly, slowed the progression of Alzheimer’s by about 29% overall and helped patients’ continue more of their daily lives and activities.
However, brain swelling was seen as a common side effect, and two, and possibly three, patients in the study died as a result of its use. Future studies and trials are required to give us more information about the drug and its efficacy and side effects.
Another study, by scientists from John Hopkins University, has identified a sugar molecule the researchers call RPTPζS3L as a potential contributor to AD. RPTPζS3L binds to specific receptors in the brain, thus affecting the brain’s capacity to eliminate harmful proteins that contribute to AD.
This research could have significant consequences for the diagnosis and treatment of AD. If RPTPζS3L can be used as a diagnostic marker for AD, it would allow doctors to make a much faster diagnosis and therefore provide earlier treatment options.
Further, the discovery of this protein provides a possible target for the development of novel therapies for AD.
Conclusion
Early detection and treatment is the best way to deal with AD, especially in people who have a genetic predisposition.
The new studies and research offer a ray of hope to those going through this experience, as breakthroughs might be just around the corner.
A new link is found between Alzheimer’s transmission and discontinued treatments, shedding light on the disease’s enigma.
Alzheimer’s disease is known to be caused by an abnormal build-up of proteins in the brain cells and around it. One of the proteins involved in creating this disease is the amyloid-beta protein, as its deposits form plaques around the brain cells.
Age is a significant risk factor for Alzheimer’s as the likelihood of developing this disease doubles every five years after one hits the 65-year mark. This condition can also be inherited on rare occasions as it is sometimes genetic.
A new study by a team of UCL and UCHL researchers has provided further evidence that this condition could have also been medically acquired due to amyloid-beta protein transmission
The people described in this paper had all received treatments with a type of human growth hormone extracted from the pituitary glands of deceased individuals(cadaver-derived human growth hormone or c-hGH) at an early age. This same treatment was administered to over 1,800 people in the United Kingdom alone between 1959 and 1985.
This treatment was only withdrawn in 1985 after it was recognized that some batches of the c-hGH were contaminated with infectious proteins called prions. Surprisingly, these infectious proteins caused Creutzfeldt-Jakob disease in some people.
Some of the people who got CJD through the c-hGH treatment had prematurely developed deposits of the amyloid-beta protein in their brains as the samples of c-hGH were all contaminated with amyloid-beta.
Study finds rare cases of Alzheimer’s in middle-aged people
This new Nature Medicine paper, reported by a UCL publication, focused on eight people. These people, all of whom had been treated with c-hGH in childhood, were referred to UCLH’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London. Five of them had symptoms of dementia, with all five of them meeting the diagnostic criteria for Alzheimer’s.
This happened despite being between 38 and 55 years old when these neurological symptoms first surfaced, proving that their symptoms are not associated with age. The team also ruled out genetic conditions as the reason behind this condition in all five people after testing their samples.
This leaves only the c-hGH treatment they had received as children as the only plausible reason for the Alzheimer’s diagnosis.
Fortunately, there are no new risks of transmitting this disease medically as the c-hGH treatment has been discontinued, and there have been no other medical procedures reported to be linked to Alzheimer’s transmission.
However, these findings have highlighted the importance of properly reviewing measures to eliminate the transmission of infectious proteins implicated in accidental transmission of CJD.
“There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care. The patients we have described were given a specific and long-discontinued medical treatment, which involved injecting patients with the material now known to have been contaminated with disease-related proteins,” said the lead author of the research, Professor John Collinge, Director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, in a press release.
Co-author Professor Jonathan Schott (UCL Queen Square Institute of Neurology, honorary consultant neurologist at UCLH, and Chief Medical Officer at Alzheimer’s Research UK) added:
“It is important to stress that the circumstances through which we believe these individuals tragically developed Alzheimer’s are highly unusual, and to reinforce that there is no risk that the disease can be spread between individuals or in routine medical care.
He noted: “These findings do, however, provide potentially valuable insights into disease mechanisms, and pave the way for further research which we hope will further our understanding of the causes of more typical, late-onset Alzheimer’s disease.”
‘The last time Earth was as warm as today was a full 125 thousand years ago, and temperatures are still rising rapidly.’
January 2024 sees record-breaking temperature, warmest month ever-recorded
Meanwhile, 2023 crossed the temperature threshold of 1.5 degrees Celsius in July, with countries worldwide facing severe heatwaves—for instance, wildfires in the US, Canada, and Southern Europe in just that month.
Scientists have been warning about the climate crisis we face today for decades. Earlier in August last year, NASA’s Goddard Institute for Space Studies (GISS) declared July 2023 as the hottest month on record since 1880, reported Interesting Engineering.
13.14 degrees Celsius–average Jan temperature
This finding was based on an analysis of surface air temperature data from the ERA5 reanalysis dataset, which showed that the average surface air temperature for January 2024 was 13.14 degrees Celsius (55 degrees Fahrenheit).
According to Copernicus, this temperature was 0.70 degrees Celsius (33 degrees Fahrenheit) above the 1991-2020 average for January and 0.12 degrees Celsius (32 degrees Fahrenheit) higher than the previous warmest January, which occurred in 2020.
Moreover, January 2024 marked the eighth consecutive month that set a record for being the warmest for that respective month of the year.
The global temperature anomaly for January 2024 was also emphasized in the report, as it was observed to be lower than those of the last six months of 2023 but higher than any before July 2023.
This warming trend is denoting and highlighting the ongoing impact of climate change, with January 2024 being significantly warmer than estimates for the January average during the pre-industrial period (1850-1900).
Global average temp surpassed the 1991-2020 average & the pre-industrial average
The report further highlighted that the global mean temperature for the preceding twelve months (February 2023 to January 2024) was the highest on record, exceeding both the 1991-2020 average and the pre-industrial average by significant margins.
According to NASA, in August 2023, the temperature was 0.43 degrees Fahrenheit (0.24 degrees Celsius) warmer than any other July in NASA’s record, and it was 2.1 Fahrenheit (1.18 Celsius) warmer than the average July between 1951 and 1980.
Surface air temperature anomaly for January 2024
Now, January is seeing a slide with scientists claiming uprisings of El Niño already underway.
Professor Chris Merchant, a Professor in Ocean and Earth Observation from the University of Reading, stated:
“After the string of record-breaking months in 2023, it is no great surprise that January 2024 is another record-breaker for global temperature. A relatively strong El Nino is still in progress, which increases global temperatures a notch, and underlying this is the relentless rise of temperature as human activity adds more carbon dioxide and methane to the atmosphere.”
Merchant noted that 2023 stood out as even warmer than expected, and 2024 may well do likewise. This has alerted people worldwide, with governments looking to develop policies concerning global warming and climate change, emphasizing moving away from fossil fuels.
“There is great progress in the transition to clean energy. But we need progress that is five times faster, and most political leaders still don’t seem to get what is at stake. We need them to wake up,” added Merchant.
“The last time Earth was as warm as today was a full 125 thousand years ago, and temperatures are still rising rapidly. A full 12 months has just been recorded as being 1.5 degrees Celsius above pre-industrial conditions,” stated Professor Richard Allan, Professor in Climate Science from the University of Reading.
“The Paris climate agreement sought to ensure the climate over a longer 20 or 30-year period is limited to 1.5 degrees Celsius above pre-industrial levels, and all of the evidence shows we are close to smashing through this barrier,” he added.
“But the fact remains that only with rapid, massive, and sustained cuts in greenhouse gas emissions across all sectors of society can we avoid the progressive worsening of extreme weather and sea level rise beyond progressively more dangerous warming levels.”
Hummus on the moon? Student grows world’s first chickpeas in moondust
Jessica Atkin, a graduate student at Texas A&M University developed a special soil amendment to overcome the obstacles of lunar dust’s quality and fertility.
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Jessica Atkin, a graduate student at Texas A&M University, has achieved a remarkable feat: she has grown chickpeas on simulated moondust, paving the way for future lunar agriculture.
The challenge of lunar farming
Atkin, pursuing her degree in the Department of Soil and Crop Sciences, has always been fascinated by space exploration. She decided to take on the challenge of growing crops on the moon, where the conditions are very different from Earth.
“The moon has no soil, only dust,” she explained. “The dust is very fine and has no organic matter, nutrients, or microbes that plants need. It also has harmful elements like iron and aluminum that can damage plant cells. And, of course, there is less gravity, more radiation, and extreme temperatures.
Atkin developed a special soil amendment to overcome these obstacles and improve the lunar dust’s quality and fertility. She worked with Sara Oliveira Santos, a doctoral student at Brown University, who helped her solve the water retention and drainage issues of the dust.
The secret ingredients: Fungi and worms
Atkin’s soil amendment consists of two main components: beneficial fungi and vermicompost. The fungi, which form a symbiotic relationship with the plant roots, help protect the plants from the toxic elements in the dust. They also enhance the plant’s ability to absorb water and nutrients.
The vermicompost, the product of worm digestion, provides organic matter and nutrients to the dust. Atkin said that worms could be brought to the moon and fed with the astronauts’ biowaste, such as food scraps, clothing, and hygiene items.
Atkin chose chickpeas as her crop because they are legumes that can benefit from the fungi. They are also protein-rich and use less water and nitrogen than other crops.
Varying degrees of chlorophyll can be seen in the chickpea moondust study at five weeks.
A breakthrough
Atkin and her team managed to grow chickpeas to seed in up to 75% lunar dust simulant, a mixture that mimics the composition of the real moon dust. This is the first time anyone has done this, and it has huge implications for the future of space exploration.
Atkin said her research could enable astronauts to grow their food on the moon, reducing their dependence on prepackaged supplies. This would save costs and resources and improve the astronauts’ health and morale.
However, she also acknowledged some limitations and challenges. For instance, the chickpeas took longer to mature on the moon dust than on Earth, showing signs of stress. She said that she will continue to study the effects of multiple generations of plants and the possibility of growing other crops.
“The novelty about using vermiculture is that it can all be done in space, whether in a space station or on the moon, reducing the need for resupply missions,” she said.
This study was published in a preprint paper posted on biorxiv.
Study abstract:
Food sustainability is one of the most significant barriers to long-term space travel. Providingresources from Earth is not cost-efficient, and resupply missions are not viable to meet the needsof long-term life in deep space conditions. Plants in space can provide a source of nutrition andoxygen, reducing the reliance on packaged foods, reducing resupply needs, and extending theduration of missions. Using lunar regolith simulant, we employ a novel methodology to createa sustainable and productive growth medium to support the cultivation of horticultural cropson the Moon. Implementing microbial soil regeneration mechanisms derived from Earth, weleverage the interaction between Arbuscular Mycorrhizal Fungi (AMF) and Vermicompost (VC) tocreate a fertile LRS matrix. These amendments can sequester toxic contaminants, improve soilstructure, and increase plant stress tolerance. We demonstrate the ability to produce chickpea(Cicer arietinum) in lunar regolith simulant augmented with AMF and VC under climate-controlledconditions. We cultivated chickpea to seed in a mixture containing 75% Lunar Regolith Simulant.Preliminary results suggest that higher LRS contents induce heightened stress responses. However,plants grown in 100% LRS inoculated with arbuscular mycorrhizal fungi demonstrated an averagetwo-week survival extension compared to non-inoculated plants. This study provides, for the firsttime, a baseline for chickpea germination in varying mixtures of LRS and VC and will inform futurestudies as humanity goes back to the Moon
Men who regularly lift heavy objects at work have almost 50 percent higher sperm concentration and count,
As infertility is becoming a common problem of late, and medical professionals are scrambling to find solutions to nullify this rising trend. Researchers have found a link between male fertility and occupational factors, such as physical demands and work schedules.
The Harvard Medical School (HMS) and Brigham and Women’s Hospital collaborative effort found that men who “regularly lift heavy objects at work have higher sperm counts than men whose work is less physically demanding,” a press release said. The study, published in the journal Human Reproduction, is “part of the Environment and Reproductive Health (EARTH) cohort, aimed to examine how environmental chemicals and lifestyle choices affect reproductive.
benefits asso
ciated with exercise in humans is well known, including those observed on reproductive health, “but few studies have looked at how occupational factors can contribute to these benefits,” said first author Lidia Mínguez-Alarcón, HMS assistant professor of medicine at Brigham and Women’s and a co-investigator of the EARTH study.
40% of infertility cases are caused by factors affecting men
Data has shown that men are responsible for nearly half of the issues related to infertility. Factors such as sperm count, semen quality, and sexual function are found to be the main restricting factors for such a predicament.
To substantiate it, a previous study done by the EARTH team found that among men seeking fertility treatment, sperm count and quality declined by as much as 42 percent between 2000 and 2017.
“Further, there is increasing evidence that male infertility is associated with common chronic diseases such as cardiovascular disease and autoimmune disease, highlighting the broader importance of male reproductive health,” said Mínguez-Alarcón.
Physically active men at work have higher sperm concentration and count
The study was done using the data collected by the EARTH study, which was done by the Harvard T. Chan School of Public Health and Mass General Brigham, to gauge the impact of environmental and lifestyle factors on fertility. The study sourced medical information from over 1,500 men and women seeking medical assistance for infertility. The current study took a subset of 377 male partners in couples seeking treatment at a fertility center from the collected data.
A thorough analysis revealed that men who reported more physically strenuous activities at work had 46 percent higher sperm concentration percent and 44 percent higher total sperm count compared to those with less physical jobs. Also, the according to the team, men who reported more physical activity at work had higher levels of the male sex hormone testosterone and, counterintuitively, the female hormone estrogen.
“Contrary to what some people remember from biology class, ‘male’ and ‘female’ hormones are found in both sexes, but in different amounts. In this case, we hypothesize that excess testosterone is being converted into estrogen, a known way for the body to keep normal levels of both hormones,” said Mínguez-Alarcón. The results proved that physically demanding jobs and rotating or evening shift occupations may be associated with higher testicular function in men measured as higher sperm concentrations and counts and higher serum testosterone and estradiol levels.
The team plans to confirm if these findings will hold for men from the general population. The researchers also hope future studies will reveal the underlying biological mechanisms. “Uncovering actionable steps people can take to improve their fertility stands to benefit all of us, not just couples trying to conceive,” according to Mínguez-Alarcón
Four weeks of shift work could disrupt women’s biological clocks, says study.
Previous studies have shown that younger women who work late night shifts and are exposed to that environment for long durations might possibly need fertility treatment, as this may impair fertility and gestational success. But does that also hold true for women who are doing shift work?
Possibly, but the underlying mechanisms of these changes have not yet been fully understood.
A new study presented at the 25th European Congress of Endocrinology has attempted to decode how a shift in the sleep-wake cycle affects fertility in female mice.
The team carried out their experiments in an animal-based model by constantly shifting the Circadian rhythm, the 24-hour internal clock in our brain that tells us to sleep when it’s dark, wake when it’s light, and regulates the cycle of alertness
These clocks regulate various biological functions and processes, including the sleep-wake cycle, hormone secretion, digestion, and reproduction, but can easily be disrupted by inappropriate light exposure, such as light at night, said the press release.
“The circadian rhythm not only requires proper functioning of the master biological clock, but also a synchronised activity of numerous secondary clocks found in other brain areas and peripheral organs, including reproductive organs,” said lead researcher Marine Simonneaux.
The team changed the patterns of light exposure that the female mice were receiving by 10 hours across four weeks. They found that the hormone which triggers ovulation, luteinizing hormone, was abolished in the mice over the weeks, thus reducing their fertility.
Simonneaux added, “The decreased fertility is due to an alteration of the master circadian clock signalling towards the hypothalamic reproductive circuit. Specifically, our research shows that four weeks of chronic shift exposure impairs the transmission of light information from the master biological clock to the kisspeptin neurons, known to drive the timing of the pre-ovulatory luteinising hormone surge.”
Researchers from the Institute of Cellular and Integrative Neurosciences (INCI) and the University of Strasbourg presented their findings at the 25th European Congress of Endocrinology in Istanbul, Turkey.
Hinting at more research to come, which will focus on whether other additional internal clocks are altered after shift work-like patterns, Simonneaux added, “Understanding the precise mechanisms by which circadian disruption alters the reproductive function is important, as it may pave the way for potential preventive and therapeutic interventions to reduce some of the negative effects of shift work on women’s fertility.”
Study abstract:
In female mammals, the timing of the preovulatory LH surge depends on the combination of the positive estrogen feedback and a circadian signal which synchronizes the LH surge with the transition between the resting and active period at the end of the follicular phase, when arousal is maximal. Previous results have demonstrated that a functional biological clock, located in the suprachiasmatic nucleus (SCN), is required for optimal female fertility. In this context, we have investigated the consequences a chronodisruptive environment could have on the female mammals’ gonadotropic axis using a female mouse model of shiftwork. This is a relevant issue since an increasing number of women are working in non-standard work schedules in our modern 24 h/7 d society, and shift work is associated with reproductive deficits. Adult female mice were either kept in regular light/dark schedules or exposed to a model of shift work conditions (3 weeks rotation a 10-hour phase advance for three days and a 10-hour phase delay for four days). Daily rhythms in SCN vasopressin-containing neurons, kisspeptin neurons, LH secretion on the day of proestrus, as well as fertility parameters, were compared between both groups of mice. The chronodisruptive protocol reduces the number of the vasopressin neurons known to transmit the daily information to the kisspeptin neurons, abolished activation of kisspeptin neurons typically observed at the light/dark transition, and reduced the amplitude and altered the timing of the preovulatory LH surge. Furthermore, when female mice exposed to chronic shift are mated with a male, the number of gestation is reduced as compared to those observed in control female mice. Our results indicate that chronic shift desynchronizes the hypothalamic-pituitary-ovarian axis. Notably, chronic exposure to disrupted light/dark cycles impairs the vasopressin-induced daily activation of kisspeptin neurons which can explain the altered LH secretion and the reduced fertility in female mice. In future experiments, we will investigate whether peripheral clocks within the gonadotropic axis are also altered by chronic shift. Altogether, these experiments will provide a better understanding of circadian disruption’s potential on the daily reproductive rhythms of female mammals.
Placental organoid (circle in the centre). Trophoblast cells are invading out of the organoid, mimicking placental cells invading the uterus in the early weeks of pregnancy.
Researchers have created “mini-placentas,” which serve as biological models of the initial phases of placental development.
This laboratory-created artificial placental organoid has the potential to reveal key details about the early stages of pregnancy, which is often referred to as the “black box of human development.”
Researchers at the University of Cambridge created these mini-placentas, also known as trophoblast organoids. Trophoblast cells provide nourishment to the embryo and contribute significantly to the creation of the placenta.
Early phases of placental development
The team hopes that their model could potentially enhance experts’ understanding of pregnancy disorders, including pre-eclampsia, and could lay the groundwork for future therapeutic advancements
Pre-eclampsia, which affects around six out of every hundred first pregnancies, is a disorder characterized by elevated blood pressure when pregnant. It can pose serious health concerns to both the mother and the baby.
“The study shows that it is possible to experiment on a developing human placenta, rather than merely observe specimens, in order to study major disorders of pregnancy,” mentioned the release.
Furthermore, this small organoid might help researchers better understand how the placenta interacts with the womb’s inner lining (endometrium).
The interactions between the cells of the endometrium and the placenta play a crucial role in determining the success of a pregnancy. These interactions play a vital role in amplifying the maternal blood supply to the placenta, which is required for the proper growth and development of the fetus.
Insights into pregnancy disorders
Professor Ashley Moffett, from the Department of Pathology at the University of Cambridge, highlighted the importance of studying the first few weeks of placental development.
“Most of the major disorders of pregnancy – pre-eclampsia, stillbirth, growth restriction, for example – depend on failings in the way the placenta develops in the first few weeks. This is a process that is incredibly difficult to study – the period after implantation, when the placenta embeds itself into the endometrium,” Moffett explained.
Moffett further added in the release: “Over the past few years, many scientists – including several at Cambridge – have developed embryo-like models to help us understand early pre-implantation development. But further development is impeded because we understand so little about the interactions between the placenta and the uterus.”
These lab-grown placenta models have the potential to advance reproductive disease research and help discover future therapies for problems affecting early pregnancy.
The development and study of mini-placentas represent a significant step forward in the effort to enhance mother and fetal health throughout pregnancy.
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