Publisher Health

Blood fat-lowering statins could slow the progression of Alzheimer’s disease, at least for some patients. This is the result of a new study led by Karolinska Institutet published in Alzheimer Research and Therapy. But the researchers are cautious in their interpretations and see the results as a first step in a research journey that may eventually provide the answer.
A new study shows that people with Alzheimer’s dementia deteriorated more slowly in their cognitive functions if they were also treated with a lipid-lowering statin, compared to those who were not treated. However, the study is an observational study where the researchers have compared data on the patients from a registry and therefore cannot answer whether there really is a causal relationship. Thus, the researchers are cautious in their interpretations.
“People with Alzheimer’s dementia treated with statins had better cognitive development over time. However, the results of the study do not mean that we now have evidence that people with dementia should be treated with statins. But on the other hand, we can’t see any support for not doing so. So, if a person needs statins for high blood lipids, a dementia diagnosis should not stop the treatment,” says Sara Garcia-Ptacek, docent of neuroscience and assistant professor at the Department of Neurobiology, Care Sciences and Society, and research leader of the current study.
The reason she emphasizes safety is that statins were initially suspected of causing confusion in patients with dementia. There has therefore been some resistance to prescribing statins to these patients.
The study included data from more than 15 500 patients with dementia who also had an indication for lipid-lowering treatment. Almost 11,000 of them were treated with statins. In general, the patients who were treated with statins had slightly higher values in the cognitive tests carried out, even though they were more likely to have diagnoses such as high blood pressure, cardiovascular disease and diabetes, all of which are risk factors for dementia.
Sara Garcia-Ptacek explains that the research team started with a hypothesis that statins could slow the progression of dementia and cast a fairly wide net to see if they could find evidence of this.
“The basic idea of this study was to pave the way for a more precise cohort study that could eventually lead to a clinical intervention study, which is what is needed to prove a causal link between statins and cognition,” says Sara Garcia-Ptacek.
The idea that statins could affect the risk or progression of dementia is not new. There are even some clinical studies done, but they have all been negative.
“We believe that only certain patients with Alzheimer’s dementia may benefit from statins and that previous clinical trials have been too small to show any significant differences. “Our idea is to try to crystallize which patient groups benefit the most and why, before embarking on clinical trials,” says Sara Garcia-Ptacek.
The research was funded by Region Stockholm, the Swedish Research Council and the Dementia and Margareta af Ugglas Foundation.

Published24 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, PA MediaBy Nick TriggleHealth correspondentPatients are being warned to expect major disruption in England as junior doctors begin their 26th day of strike action in their pay dispute.The stoppage, from 07:00, will last three days, with senior doctors drafted in to provide emergency cover.NHS strike action has seen more than 1.1 million appointments and treatments cancelled in the past year.This walkout will be followed by a six-day strike at the start of January, the longest in NHS history.It comes after talks between the British Medical Association (BMA) and government broke down, earlier this month.How double pay rise for senior doctors is backfiringWhy talk of a UK doctor exodus is prematureHow much do junior doctors really get paid? NHS England medical director Prof Sir Stephen Powis said the situation was further complicated by the holiday season – in the coming three weeks, only four weekdays in the NHS are unaffected by holidays or industrial action.”These strikes come at a time that will cause huge disruption to the NHS, with services already feeling the strain of winter pressure,” he said.”Over the holiday period, I would encourage anyone who needs medical help to continue to come forward.”In a life-threatening emergency, call 999 and use A&E in the usual way. For everything else, use 111 online.” But some A&E services are having to close.Cheltenham A&E, for example, will not open during either junior doctor strike, with emergency care provided by Gloucestershire Royal Hospital, run by the same NHS trust.Chief medical officer Dr Ananthakrishnan Raghuram said: “This is a very challenging environment – and decisions have not been taken lightly.”The BMA rejected a last-minute plea by five national organisations, including Age UK and the Patients Association, for the strike action to be downgraded to a partial walkout, with some emergency cover provided by junior doctors. Consultants and specialist doctors would provide life-and-limb cover, the union said.The charities said they were concerned about the risks to elderly patients in particular and warned they could become “stranded” in hospital over the festive period because doctors were too busy covering emergency care to oversee wards.Nearly half of NHS doctors are junior doctors – a group that spans those just out of university through to some who have 10 years or more experience.Two-thirds are members of the BMA – and they will be joined by members of the much-smaller Hospital Consultants and Specialists Association union.Hospitals services are expected to be worst affected but there will also be some disruption to GP care.’I couldn’t wait any longer – I paid for care’Sally Knight started feeling pain in her hip at the start of 2023. It was decided the 69-year-old needed a hip replacement – but after having two appointments cancelled because of strike action and being told the wait could be a year, she decided to pay to have the surgery privately. It cost her more than £13,000.Ms Knight said she had felt she had no choice – the pain had been affecting her daily life.”I feel really frustrated because I’ve worked all my life and paid my dues,” she said.”Yes the help is there – but you have to wait a very long time. I feel very let down.”Sir Julian Hartley, chief executive of NHS Providers, which represents health managers, said this set of strikes meant the “worst fears” of the health service were being realised.”This is the last thing the NHS needs,” he said. “The quality of care will be affected, with efforts to cut waiting lists further dented by these walkouts.” Dr Robert Laurenson and Dr Vivek Trivedi, who co-chair the BMA junior doctors committee, said they were “extremely disappointed” to be taking action again – the last walkout was in early October.”We had hoped that after a much-improved tone and approach from the new health secretary, Victoria Atkins, we were close to a solution to this dispute,” they said.Image source, PA MediaDr Laurenson and Dr Trivedi urged the government to make a new offer – the BMA ended talks after setting a deadline of early December for a resolution.An offer of a pay rise averaging 3%, from January, was being discussed, which would have been on top of the average of nearly 9% junior doctors received in April.But the BMA said that was too little – junior doctors had asked for an extra 35%, to make up for below-inflation pay rises since 2008. “After so many missed opportunities in 2023 to settle the dispute, surely now is the moment to conclude that everyone’s time would be saved by cutting out unnecessary posturing,” Dr Laurenson and Dr Trivedi said.”Patients in need of care deserve nothing less.”Ms Atkins said the strikes would cause “significant disruption”, despite contingency measures. “My door remains open should the BMA cancel these disruptive strikes and come back to the negotiating table, as we were making good progress,” she added.Industrial action in the NHS in England, which began last December with walkouts by ambulance staff and nurses, is estimated to have cost more than £2bn in planning, preparations and paying for cover.A pay offer to NHS staff other than doctors was accepted in May, while strike action by consultants has been put on hold as they vote on a fresh offer from the government. This week, it was announced junior doctors in Wales would strike in January.More on this storyFresh pay offer could end NHS consultant strikesPublished27 NovemberNurses react with fury over doctor pay offerPublished28 NovemberWhat is the NHS pay offer?Published2 MayWhy talk of a UK doctor exodus is prematurePublished9 AugustNHS pay deal signed off for one million staffPublished2 MaySome NHS temporary staff miss out on full pay dealPublished21 JulyHow much do junior doctors really get paid?Published11 AugustRelated Internet LinksStatistics ? Consultant-led Referral to Treatment Waiting Times Data 2023-24.websiteThe BBC is not responsible for the content of external sites.

The Beach Boys’ iconic hit single “Good Vibrations” takes on a whole new layer of meaning thanks to a recent discovery by Rice University scientists and collaborators, who have uncovered a way to destroy cancer cells by using the ability of some molecules to vibrate strongly when stimulated by light.
The researchers found that the atoms of a small dye molecule used for medical imaging can vibrate in unison – forming what is known as a plasmon – when stimulated by near-infrared light, causing the cell membrane of cancerous cells to rupture. According to the study published in Nature Chemistry, the method had a 99 percent efficiency against lab cultures of human melanoma cells, and half of the mice with melanoma tumors became cancer-free after treatment.
“It is a whole new generation of molecular machines that we call molecular jackhammers,” said Rice chemist James Tour, whose lab has previously used nanoscale compounds endowed with a light-activated paddlelike chain of atoms that spins continually in the same direction to drill through the outer membrane of infectious bacteria, cancer cells and treatment-resistant fungi.
Unlike the nanoscale drills based on Nobel laureate Bernard Feringa’s molecular motors, molecular jackhammers employ an entirely different – and unprecedented – mechanism of action.
“They are more than one million times faster in their mechanical motion than the former Feringa-type motors, and they can be activated with near-infrared light rather than visible light,” Tour said.
Near-infrared light can penetrate far deeper into the body than visible light, accessing organs or bones without damaging tissue.
“Near-infrared light can go as deep as 10 centimeters (~ 4 inches) into the human body as opposed to only half a centimeter (~ 0.2 inches), the depth of penetration for visible light, which we used to activate the nanodrills,” said Tour, Rice’s T. T. and W. F. Chao Professor of Chemistry and a professor of materials science and nanoengineering. “It is a huge advance.”
The jackhammers are aminocyanine molecules, a class of fluorescent synthetic dyes used for medical imaging.

“These molecules are simple dyes that people have been using for a long time,” said Ciceron Ayala-Orozco, a Rice research scientist who is a lead author on the study. “They’re biocompatible, stable in water and very good at attaching themselves to the fatty outer lining of cells. But even though they were being used for imaging, people did not know how to activate these as plasmons.”
Ayala-Orozco initially studied plasmons as a doctoral student in the research group led by Rice’s Naomi Halas.
“Due to their structure and chemical properties, the nuclei of these molecules can oscillate in sync when exposed to the right stimulus,” Ayala-Orozco said. “I saw a need to use the properties of plasmons as a form of treatment and was interested in Dr. Tour’s mechanical approach to dealing with cancer cells. I basically connected the dots.
“The molecular plasmons we identified have a near-symmetrical structure with an arm on one side. The arm doesn’t contribute to the plasmonic motion, but it helps anchor the molecule to the lipid bilayer of the cell membrane.”
The researchers had to prove that the molecules’ mode of action could not be categorized either as a form of photodynamic or photothermal therapy.
“What needs to be highlighted is that we’ve discovered another explanation for how these molecules can work,” Ayala-Orozco said. “This is the first time a molecular plasmon is utilized in this way to excite the whole molecule and to actually produce mechanical action used to achieve a particular goal ? in this case, tearing apart cancer cells’ membrane.
“This study is about a different way to treat cancer using mechanical forces at the molecular scale.”
Researchers at Texas A&M University led by Jorge Seminario, a quantum chemist and professor of chemical engineering, performed time-dependent density functional theory analysis on the molecular features involved in the jackhammering effect. The cancer studies were performed in mice at the University of Texas MD Anderson Cancer Center in collaboration with Dr. Jeffrey Myers, professor and chair of the Department of Head and Neck Surgery and director of translational research for the Division of Surgery.

A microbial sensor that helps identify and fight bacterial infections also plays a key role in the development of blood stem cells, valuable new insight in the effort to create patient-derived blood stem cells that could eliminate the need for bone marrow transplants.
The discovery by a research team led by Raquel Espin Palazon, an assistant professor of genetics, development and cell biology at Iowa State University, was published last month in Nature Communications. It builds on prior work by Espin Palazon showing that the inflammatory signals that prompt a body’s immune response have an entirely different role in the earliest stages of life, as vascular systems and blood are forming in embryos.
Espin Palazon said knowing that embryos activate the microbial sensor, a protein known as Nod1, to force vascular endothelial cells to become blood stem cells could help develop a method to make blood stem cells in a lab from a patient’s own blood.
“This would eliminate the challenging task of finding compatible bone marrow transplant donors and the complications that occur after receiving a transplant, improving the lives of many leukemia, lymphoma and anemia patients,” she said.
A critical cue
Stem cells are both the factories and the raw materials of a body, repeatedly dividing to self-renew and build new cells for specific tissues. Pluripotent stem cells in embryos can make any kind of cell a body needs, while adult stem cells are limited to producing particular types. Blood stem cells, also known as hematopoietic stem cells, make all of blood’s components. A lifetime supply of blood stem cells is created before birth inside an embryo.
The immune receptor Espin Palazon’s team identified activates in an embryo before endothelial cells start becoming stem cells, priming them for the transition.

“We know blood stem cells form from endothelial cells, but the factors that set up the cell to switch identity were enigmatic,” she said. “We didn’t know that this receptor was needed or that it was needed this early, before blood stem cells even form.”
Researchers zeroed in on Nod1 by analyzing public databases of human embryos and studied it using zebrafish, which share about 70% of their genome with humans. Blood stem cell creation tracked closely with Nod1 levels as its effects were inhibited or enhanced.
To confirm Nod1 also plays a role in human blood development, the research team worked with the Children’s Hospital of Philadelphia. Researchers there produce human induced pluripotent stem cells, which are generated from mature samples but genetically reprogrammed to behave like the make-anything stem cells found in embryos. Induced pluripotent stem cells can create most types of blood cells, though not functional blood stem cells. But when researchers took away Nod1, blood production faltered, as it did with blood stem cells in zebrafish.
Seeking self-derived stem cells
Figuring out that Nod1 is a prerequisite for blood stem cells to develop is progress for scientists hoping to design a system for producing blood stem cells from human samples, which could offer a revolutionary new option for patients suffering from blood disorders. Instead of a life-saving infusion of blood stem cells via a transplant of bone marrow, the spongy insides of bones that holds most of a body’s blood stem cells, patients could be treated with stem cells that originated in their own body. Self-derived stem cells could avoid the risks of graft-versus-host disease, a common and potentially deadly reaction that occurs when a patient’s immune system perceives the transplant as a threat to be attacked.
“This would be a huge advancement for regenerative medicine,” Espin Palazon said.

Espin Palazon’s team is continuing to untangle the complex interactions in which blood stem cells arise, including refining the timeline. Understanding when signals are expressed is essential to developing the methods for making blood stem cells.
“The timing is so crucial. It’s like when you’re cooking and you need to add ingredients in a specific order,” she said.
Further research will benefit from the collaboration with Children’s Hospital of Philadelphia, which trained one of the study’s co-authors — Clyde Campbell, adjunct assistant professor of genetics, development and cell biology — on the protocols to create induced pluripotent stem cells.
“My group at Iowa State University will continue working towards a life without blood disorders. I believe our investigations will pave the road to finally create therapeutic-grade blood stem cells to cure blood disorder patients,” Espin Palazon said.
In addition to Espin Palazon and Campbell, other Iowa State co-authors on the study include first author Xiaoyi Cheng, a graduate student; Karin Dorman, professor and Dale D. Grosvenor Chair of genetics, development and cell biology; graduate students Masuma Khatun Usha and Rodolfo Calderon; research associate Elizabeth Snella; and former undergraduate Abigail Gorden. Antonella Fidanza at the University of Edinburgh and Giulia Pavani, Deborah French and Paul Gadue at Children’s Hospital of Philadelphia also contributed to this work.

Physical, sexual, or emotional abuse, or neglect, either alone or combined with other types of childhood trauma, increases the risk of chronic pain and related disability in adulthood, according to new research.
These new findings underscore the urgency of addressing adverse childhood experiences (ACEs) — potentially traumatic events that occur before 18 years of age — and taking steps to mitigate their long-term impact on people’s health.
The study reviews research carried out across 75 years, involving 826,452 adults. Published in the peer-reviewed journal European Journal of Psychotraumatology, it reveals that individuals who have been exposed to various forms of traumatic events in childhood are at an increased risk of experiencing chronic pain and pain-related disability in adulthood, particularly those subjected to physical abuse. The cumulative impact of exposure to multiple ACEs further exacerbates this risk.
“These results are extremely concerning, particularly as over 1 billion children — half of the global child population — are exposed to ACEs each year, putting them at increased risk of chronic pain and disability later in life,” says lead author Dr André Bussières, from the School of Physical & Occupational Therapy at McGill University, in Canada.
“There is an urgent need to develop targeted interventions and support systems to break the cycle of adversity and improve long-term health outcomes for those individuals who have been exposed to childhood trauma.”
ACEs may affect a child or teenager directly through physical, sexual, or emotional abuse, or neglect — or indirectly through exposure to environmental factors like domestic violence, living with substance abuse or parental loss. Chronic pain, affecting between one-third and one-half of the UK population alone, is one of the leading causes of disability worldwide. Long-term painful conditions such as low back pain, arthritis, headache and migraine, can affect a person’s daily functioning to the point they can’t work, eat properly, or participate in physical activities.
Previous research has indicated a positive relationship between exposure to ACEs and chronic pain in adulthood. However, there are still gaps in knowledge — particularly around which type of ACEs are associated with specific pain-related conditions, or whether a dose-response relationship exists.

To help address these gaps, the authors carried out a systematic review that included 85 studies. Of those, results from 57 studies could be pooled in meta-analyses. They found that: Individuals exposed to a direct ACE, whether physical, sexual, or emotional abuse, or neglect, were 45% more likely to report chronic pain in adulthood compared to those not exposed. “These results underscore the urgency of addressing ACES, particularly in light of their prevalence and health repercussions,” says the senior author Professor Jan Hartvigsen, from the University of Southern Denmark.
“A more nuanced understanding of the precise relationship between ACEs and chronic pain will empower healthcare professionals and policymakers to devise targeted strategies to help diminish the long-term impact of early-life adversity on adult health.”
The authors propose that future research should delve into the biological mechanisms through which ACEs affect health across the lifespan, aiming to deepen understanding and develop ways to mitigate their impact.

A collaborative effort between the University of Córdoba and IMIBIC uses, for the first time, changes in sweat metabolism to diagnose the severity of sleep apnea
In Greek, apnea (ἄπνοια) denotes the “absence of breathing.” Hence, obstructive sleep apnea is a disease defined by interruptions in breathing, which recurs while the person suffering from it is asleep. A feeling of breathlessness, fatigue and drowsiness are symptoms that patients suffer. This disease is also related to the incidence of cardiovascular disorders, so to deal with these related problems, adequate diagnosis of the severity of the disease is necessary.
Alterations in the metabolism of people with sleep apnea are key to determining the severity of the disease. These changes are usually analyzed in blood or urine. However, in search of a less invasive and more accessible alternative, a team from the Department of Analytical Chemistry at the University of Córdoba and the Maimonides Institute for Biomedical Research in Córdoba (IMIBIC), formed by researchers Laura Castillo, Mónica Calderón, Feliciano Priego and Bernabé Jurado, has verified, for the first time, the potential of sweat samples to ascertain the severity of sleep apnea.
“By analyzing sweat metabolome and its alterations, mainly at night, we were able to see what stage of the disease the patients were in,” explains Laura Castillo, the study’s lead author. For her, the advantages of using sweat over other samples are clear: “it is a non-invasive and clean sample since, unlike the case with blood, we don’t have to remove proteins, and it’s much easier to analyze and detect metabolites.”
In this study, sweat samples from before and after sleep were analyzed from a series of individuals with sleep apnea at different stages, as well as from a control group without the disease.
In these samples, using the gas chromatography technique, coupled with high-resolution mass spectrometry, 78 metabolites were identified and their changes were studied, mostly related to energy production and oxidative stress. “We could see how the sweat metabolism itself indicates those alterations during sleep as a result of which the person’s energy production worsens and their oxidative stress increases,” says Castillo. Thus, with a personalized follow-up using the sweat excreted during the sleep of a person with the disease, its development can be tracked, and its possible effects, such as cardiovascular problems, can be monitored. This metabolomic profile also made it possible, in the trial, to distinguish between those who suffered from the disease and those who did not have it and belonged to the control group.
An index to learn more about the disease
In addition to establishing sweat as a good sentinel when it comes to determining the stage of the disease, this work also reveals the importance of taking into account the oxygen desaturation index when diagnosing it.
The diagnosis of sleep apnea is currently based on the Apnea-Hypopnea Index (AHI), which measures sleep apnea based on the episodes of shortness of breath one suffers per hour (for example, the disease is severe when one has 30 or more episodes per hour). According to the team, this index “does not provide all the information about the disease or the patient’s situation at a given time” since it counts how many events there are, but not their severity.
Therefore, in their study they also verify the importance of using the oxygen desaturation index, which shows how serious the episodes are by measuring the number of events in which oxygen saturation has decreased by more than 3%. After verifying the linear relationship between this index and the AHI, its validity has been confirmed, since, in addition to the data provided by the AHI, it also measures severity, taking into account oxygen saturation loss.

Groundbreaking University of Limerick, Ireland research has shed new light on the link between childhood adversity and future risk of death.
A major international study led by researchers at UL and published in the journal of Psychosomatic Medicine: Journal of Biobehavioral Medicine has examined the association between adverse childhood experiences and the increased risk of premature mortality.
Adverse childhood experiences such as emotional and physical abuse, household instability, socioeconomic climate and ill health can lead to people having a shorter life, but it was not clear how.
The researchers believed that, as individuals with these adverse experiences in their childhood can suffer from lower self-acceptance and purpose in life, that these could be a pathway or a ‘mechanism’ linking these experiences to future mortality risk.
The new study, which followed 6,128 people across 24 years in the United States, found that self-acceptance — positive attitudes towards oneself and acknowledging and accepting multiple aspects of yourself — and purpose in life — a sense of a goal-directed direction in life — do explain part of the reason why childhood adversity is related to future longevity.
The project was led by Associate Professor of Psychology at University of Limerick Dr Páraic Ó Súilleabháin, Director of the Personality, Individual Differences and Biobehavioural Health Laboratory and member of the Health Research Institute.
The work was conducted in collaboration with others from University of Limerick, West Virginia University, Open University of the Netherlands, University of Minnesota, and Florida State University.

Commenting on the study, Dr Ó Súilleabháin said: “It is very important to find the ways in which experiences such as these early in life can have an impact across our lives. We have previously found that these experiences are related to a shortening of life expectancy. It is important to understand the mechanisms linking them, so that ways to increase life expectancy can be identified.
“We found that self-acceptance and purpose in life are very important in the link between these childhood experiences and risk of death in adulthood. In other words, of all the possible factors in the link between childhood adversity and risk of future death, it appears that self-acceptance and purpose in life are two important drivers.”
The research team used the ‘Midlife in the United States Survey’ to test whether these factors were indirect pathways that increased the association between adverse childhood experiences and mortality hazards over 24 years of follow-up.
They included 20 possible childhood adversities, and the results show that adverse childhood experiences do significantly increase mortality risk and that self-acceptance and purpose does account for a percentage of those — effects which withstood a range of adjustments and sensitivity analyses, according to the researchers.
Given that self-acceptance and purpose can change through intervention, these factors may be useful targets for individuals with adverse childhood experiences that could reduce the health risks in later life, Dr Ó Súilleabháin explained.
“Research suggests that self-acceptance and purpose can change through intervention. These interventions are not just needed at the individual level, but also at the societal level,” Dr Ó Súilleabháin explained.
“For instance, while it is relatively straightforward to think of avenues with various therapies and so on, it is incredibly challenging for someone to foster self-acceptance and purpose without basic needs being met in healthcare, housing, education, and so on.
“Impacting self-acceptance and purpose in life in adulthood for those who have had childhood adversity, may ultimately impact their longevity,” Dr Ó Súilleabháin added.

Down syndrome, a congenital disorder stemming from abnormal cell division and differentiation, is most common in newborns fated to neurodevelopmental delays and other health complications.
The genetic defect causes the dysfunction of the protein kinase DYRK1A, which is encoded on chromosome 21 and is deeply associated with both Down syndrome and autism spectrum disorder. DYRK1A has attracted attention as a target molecule for treating various diseases, but specific cellular mechanisms regulating the enzyme DYRK1A have yet to be made clear.
Now, researchers at Kyoto University have identified the FAM53C protein and its DYRK1A-inhibiting effect that keeps the protein kinase inactive inside the cytoplasm.
“Our findings demonstrate the important role of the intracellular regulatory mechanism of DYRK1A in the normal development and function of the neuropsychiatric system,” says first author Yoshihiko Miyata at KyotoU’s Graduate School of Biostudies.
“The molecular regulation of the highly complex development and activity of the human brain fascinates me,” adds Miyata. In addition to neuropsychiatric symptoms, Down syndrome may also cause early onset of Alzheimer’s disease, type 2 diabetes, and facial maldevelopment.
“Given DYRK1A’s significance, we have explored potential molecules serving as its interacting counterpart,” says Miyata.
DYRK1A controls many biological functions, including the development and function of the nervous system. At the cellular level, this critical protein phosphorylates various other proteins in the cytoplasm and nucleus to regulate the cell cycle, cell differentiation, cytoskeletal formation, and DNA damage response.
After identifying DCAF7/WDR68 as a major binding protein for DYRK1A in a previous study, Miyata’s team used mass spectrometry to uncover other interacting proteins that modulate DYRK1A’s function and cellular location. Notably, the structurally flexible FAM53C protein binds directly to a region of DYRK1A responsible for protein phosphorylation. This interaction reduces DYRK1A’s kinase activity, securely anchoring DYRK1A within the cytoplasm but outside the cell nucleus, as in normal brain tissue.
“The FAM53C-mediated regulation of the protein kinase activity may significantly impact gene expression regulation caused by normal and aberrant levels of DYRK1A, giving us many potential clinical insights,” suggests Miyata.

Scientists from the University of Rochester say deep learning can supercharge a technique that is already the gold standard for characterizing new materials. In an npj Computational Materials paper, the interdisciplinary team describes models they developed to better leverage the massive amounts of data that X-ray diffraction experiments produce.
During X-ray diffraction experiments, bright lasers shine on a sample, producing diffracted images that contain important information about the material’s structure and properties. Project lead Niaz Abdolrahim, an associate professor in the Department of Mechanical Engineering and a scientist at the Laboratory for Laser Energetics (LLE), says conventional methods of analyzing these images can be contentious, time-consuming, and often ineffective.
“There is a lot of materials science and physics hidden in each one of these images and terabytes of data are being produced every day at facilities and labs worldwide,” says Abdolrahim. “Developing a good model to analyze this data can really help expedite materials innovation, understand materials at extreme conditions, and develop materials for different technological applications.”
The study, led by Jerardo Salgado ’23 MS (materials science), holds particular promise for high-energy-density experiments like those conducted at LLE by researchers from the Center for Matter at Atomic Pressures. By examining the precise moment when materials under extreme conditions change phases, scientists can discover ways to create new materials and learn about the formation of stars and planets.
Abdolrahim says the project, funded by the US Department of Energy’s National Nuclear Security Administration and the National Science Foundation, improves upon previous attempts to develop machine learning models for X-ray diffraction analysis that were trained and evaluated primarily with synthetic data. Abdolrahim, Associate Professor Chenliang Xu from the Department of Computer Science, and their students incorporated real-world data from experiments with inorganic materials to train their deep-learning models.
More X-ray diffraction analysis experimental data needs to be publicly available to help refine the models, according to Abdolrahim. She says the team is working on creating platforms for others to share data that can help train and evaluate the system, making it even more effective.

In a phase-one human clinical trial, a University of Houston pharmacist researcher has demonstrated that a newer generation tetracycline antibiotic, called Omadacycline, may be a promising tool in combating the resilient bacteria Clostridioides difficile (C diff), which causes an infection often picked up in hospitals. C diff brings on diarrhea and colitis, an inflammation of the colon, and is responsible for nearly 500,000 infections annually in the United States.
The fight against C diff takes its toll internally, including a significant disruption of gut microbiota, usually by broad-spectrum antibiotics, leading to loss of colonization resistance to C difficile. Omadacycline demonstrated a low likelihood of causing C diff in clinical trials, but no one understood why.
Kevin Garey, Robert L. Boblitt Endowed Professor of Drug Discovery at the UH College of Pharmacy, assessed the pharmacokinetics and gut microbiome effects of oral Omadacycline in comparison to Vancomycin, another possible C diff drug. Vancomycin is used to treat C diff but is not good at eliminating it over the long-term. Garey’s team investigated whether Omadacycline, given orally, achieves high concentration in the gut and the effect on the gut microbiome, the healthy bacteria that lives in the colon.
“Our research shows off the coolness of the microbiome. Omadacycline caused a distinctly different effect on the microbiome than Vancomycin. This could explain why Omadacycline is a safe drug to give to patients at high risk for C diff infection. This could become a new method in drug development to see if antibiotics are not only killing the bacteria causing infections (the bad bugs) but not causing harm to the beneficial microbes that live in our body (the good bugs),” said Garey, whose results were published in The Journal of Infectious Diseases. “I would hope that this becomes a normal part of the antibiotic drug development process.”
In the study, 16 healthy volunteers tolerated Omadacycline with no safety differences compared to the other antibiotic. A rapid initial increase in fecal concentration of Omadacycline was observed compared to Vancomycin, with maximum concentrations achieved within 48 hours. Rapid increase is a good thing — it means the active drug is getting to the site of the infection faster.
“Both the Omadacycline and Vancomycin groups showed significant changes in their microbiomes when we looked at how diverse they were internally (alpha diversity). However, when we compared the changes between the two groups (beta diversity), they were noticeably different from each other,” reported Garey.
Garey’s team includes Jinhee Jo, assistant professor, University of Houston College of Pharmacy; and Blake M. Hanson and Hossaena Ayele, The University of Texas Health Science Center at Houston School of Public Health.