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1 2024-07-25

CRI Associate Professor Prashant Mishra,M.D.,Ph.D.,Xun Wang,Ph.D.,and colleagues have found that hepatocytes,the cells responsible for most liver function,normally use their mitochondria to process fatty acids,a key energy source during regeneration.When their mitochondria are damaged,hepatocytes turn on PDK4–a metabolic enzyme that restricts cells from shifting to an alternative energy source–and cells die.“There are good and bad sides of metabolic flexibility.Although metabolic flexibility has been largely described as beneficial because it gives cells the ability to tolerate shifting environments or alternative nutritional sources,our findings suggest flexibility can also be detrimental by allowing damaged cells to survive,”Dr.Mishra said.“With mitochondrial damage,liver cells actively suppress flexibility–a good thing if it prevents the damage from spreading.”CRI scientists initially studied the mitochondria of healthy liver cells,both under normal and regenerative conditions.Their analyses showed fatty acids from other parts of the body were transported through the blood to the liver to fuel regeneration.When researchers blocked fatty acid transit,heathy livers were flexible and shifted to other energy sources,including sugars like glucose.Researchers then examined livers from mice with mutations in their mitochondrial genes.Damaged liver cells were unable to use fatty acids during regeneration and did not shift to other energy sources,preventing livers from regenerating.To understand why the flexibility was suppressed by mitochondrial mutations,Mishra Lab members examined genes that control acell’s ability to use alternate energy sources.Results showed increased levels of the PDK4 gene–a negative regulator of apathway needed to generate energy from glucose.When researchers blocked PDK4,damaged cells in the liver became metabolically flexible and were able to use other energy sources to spread and duplicate. 查看详细>>

来源:达拉斯德克萨斯大学西南医学中心 点击量: 0

2 2024-07-22

n their latest study,Iwasaki’s team analyzed blood samples from patients in the Mount Sinai-Yale Long COVID study.This cohort of over 215 Long COVID patients is part of acollaboration between Iwasaki and David Putrino,PhD,professor in the Department of Rehabilitation and Human Performance at Icahn School of Medicine at Mount Sinai in New York City.As part of this joint effort,Putrino’s clinic obtained blood samples from patients enrolled in the study.Iwasaki’s laboratory then purified antibodies from the blood and transferred them into healthy mice.Next,the researchers led by Keyla Sá,a postdoctoral fellow in Iwasaki’s lab,conducted multiple behavioral experiments to look for Long COVID symptoms.While many of these experiments found no significant difference between the experimental and control mice,a few revealed striking changes in those that received antibodies.In one such experiment,researchers placed the mice on aheated plate and measured how long it took for them to react.Some mice that received antibodies reacted significantly more quickly to the heat,indicating aheightened sensitivity to pain.The researchers went back and identified the patients whose antibodies had been injected into the mice.Interestingly,these patients reported pain as one of their Long COVID symptoms.Another experiment was the rotarod test,in which researchers placed mice on arotating cylinder to measure coordination and balance.Mice that received antibodies were more likely to struggle to stay on the apparatus.Once again,when the researchers looked at the source of these antibodies,they learned that they were mostly from patients who reported suffering from dizziness.The mice also underwent agrip strength test,in which researchers measured the force applied by the animals to agrid apparatus.A group of mice were found to have reduced muscle strength if they received antibodies from patients reporting tinnitus and headache.Thus,antibodies capable of impairing muscle function are found in patients with these symptoms.How exactly these antibodies cause pathology needs more study. 查看详细>>

来源:耶鲁大学 点击量: 0

3 2024-07-21

Two-dimensional(2D)materials have atomic-level thickness and excellent mechanical and physical properties,with broad application prospects in fields such as semiconductors,flexible devices,and composite materials.Due to their extremely low bending stiffness,single-layer 2D materials will undergo out-of-plane deformation when subjected to geometric constraints,forming ripples,buckling,wrinkling,or even creases,which can significantly affect their mechanical,electrical,and thermal properties.Their mechanical stability also directly affects the lifespan and service performance of devices based on suspended 2D materials,such as micro/nanoelectromechanical systems(M/NEMS),resonators/oscillators,nano kirigami/origami,proton transport membranes,and nanochannels.Clarifying the mechanical stability mechanisms of 2D materials and achieving overall control of their instability behaviours is crucial for the mechanical applications of 2D materials and other atomically thin films.A research team led by Professor Yang Lu from the Department of Mechanical Engineering at the University of Hong Kong(HKU)has made asignificant breakthrough in this area by providing anew method for assessing instability in atomically thin films.In collaboration with researchers from the University of Science and Technology of China,Professor Lu’s team proposed a“push-to-shear”strategy to achieve in situ observation of the in-plane shear deformation of single-layer 2D materials for the first time,achieving controllable tuning of the instability characteristics of 2D materials.Combining theoretical analysis and molecular dynamics simulations,the mechanical principles and control mechanisms of multi-order instability in atomically thin films were revealed.The results have been published in the academic journal Nature Communications with the paper titled“Tuning Instability in Suspended Monolayer 2D Materials”.The team is planning to collaborate with industrial partners to develop anew type of mechanical measurement platform for atomically thin films,which utilizes in-situ micro/nanomechanical techniques to achieve high-throughput mechanical property measurements while also enabling deep strain engineering of the materials’device physical properties.“This research breakthrough overcomes the difficulty of controlling the instability behaviour of suspended single-atom-layer 2D materials,achieving the measurement of the bending stiffness of single-layer graphene and molybdenum disulfide(MoS2).The study also provides new opportunities for modulating the nano-scale instability morphology and physical properties of atomically thin films,”said Professor Lu.“We developed aMEMS-based in-situ shearing device to control the instability behaviour of suspended single-layer 2D materials,which is also applicable to other atomically thin films.We further investigated the evolution of the wrinkle morphology of 2D materials induced by instability,uncovering different instability and recovery paths dominated by changes in the wavelength and amplitude of wrinkles,and providing anew experimental mechanics method for assessing the instability behaviour and bending performance of atomically thin films.In addition,the local stress/strain and curvature changes related to the instability process of 2D materials have important applications in physical and chemical fields,such as changing the electronic structure by adjusting the wrinkled morphology and establishing fast proton transport channels(see Figure 1).”Professor Lu added.“This research has achieved controllable instability modulation of atomically thin materials represented by 2D materials.Compared to traditional tensile strain engineering,shear strain can deeply regulate the band structure of 2D materials.In the future,we will continue to advance this research and ultimately hope to achieve an integrated design of mechanics and functionality in low-dimensional materials under deep strain,”said Dr Hou Yuan,the first author of the paper and apostdoctoral fellow in Professor Lu’s group. 查看详细>>

来源:香港大学 点击量: 7

4 2024-07-18

The concept of short-range order(SRO)—the arrangement of atoms over small distances—in metallic alloys has been underexplored in materials science and engineering.But the past decade has seen renewed interest in quantifying it,since decoding SRO is acrucial step toward developing tailored high-performing alloys,such as stronger or heat-resistant materials.Understanding how atoms arrange themselves is no easy task and must be verified using intensive lab experiments or computer simulations based on imperfect models.These hurdles have made it difficult to fully explore SRO in metallic alloys.But Killian Sheriff and Yifan Cao,graduate students in MIT’s Department of Materials Science and Engineering(DMSE),are using machine learning to quantify,atom-by-atom,the complex chemical arrangements that make up SRO.Under the supervision of Assistant Professor Rodrigo Freitas,and with the help of Assistant Professor Tess Smidt in the Department of Electrical Engineering and Computer Science,their work was recently published in The Proceedings of the National Academy of Sciences.Interest in understanding SRO is linked to the excitement around advanced materials called high-entropy alloys,whose complex compositions give them superior properties.Typically,materials scientists develop alloys by using one element as abase and adding small quantities of other elements to enhance specific properties.The addition of chromium to nickel,for example,makes the resulting metal more resistant to corrosion.Unlike most traditional alloys,high-entropy alloys have several elements,from three up to 20,in nearly equal proportions.This offers avast design space.“It’s like you’re making arecipe with alot more ingredients,”says Cao.The goal is to use SRO as a“knob”to tailor material properties by mixing chemical elements in high-entropy alloys in unique ways.This approach has potential applications in industries such as aerospace,biomedicine,and electronics,driving the need to explore permutations and combinations of elements,Cao says. 查看详细>>

来源:麻省理工学院 点击量: 17

5 2024-07-18

DALLAS–July 18,2024–Cancer cells salvage purine nucleotides to fuel tumor growth,including purines in foods we eat,an important discovery with implications for cancer therapies from research by Children’s Medical Center Research Institute at UT Southwestern published in Cell.CRI Assistant Professor Gerta Hoxhaj,Ph.D.,and her team have challenged the long-standing belief that tumors primarily acquire purine nucleotides–building blocks for DNA,which is required for cellular growth and function–by constructing them from scratch via de novo synthesis.The Hoxhaj Lab’s newest research shows tumors also significantly use the more efficient salvage,or recycling,pathway to acquire purines.“For more than 70 years,drugs targeting purine nucleotides have been acornerstone of cancer treatment,but these treatments have limitations,and drug resistance often develops,”Dr.Hoxhaj said.“Our research illuminates the contributions of both pathways–de novo and salvage–and highlights the crucial,yet previously overlooked,role the salvage pathway plays in tumor growth.”Dr.Hoxhaj,with co-authors Diem Tran,Ph.D.,Rushendhiran Kesavan,Ph.D.,and Dohun Kim,B.S.,used isotope tracing to follow the de novo and salvage purine pathways across normal mouse tissues and avariety of cancer types,including breast,kidney,colon,and liver cancers.Normal tissue analyses showed the kidney salvaged the most purines,which could explain why people with kidney disease are at higher risk for gout.Gout,a type of arthritis linked to uric acid buildup,may be caused by the kidney’s inability to process uric acid,a purine byproduct.When conducting the same analyses on tumors,CRI researchers discovered cancer cells use both de novo and salvage pathways to fulfill their constant need for purines.Additionally,tumors grew faster in mice given ahigh dose of oral nucleotides,indicating purines from the diet contribute to cancer growth. 查看详细>>

来源:达拉斯德克萨斯大学西南医学中心 点击量: 105

6 2024-07-17

“There is great interest in reducing senescence to slow or reverse aging or aging-associated diseases.We discovered anoncoding RNA that when inhibited strongly impairs senescence,suggesting that it could be atherapeutic target for conditions associated with aging,”said Joshua Mendell,M.D.,Ph.D.,Professor of Molecular Biology and amember of the Harold C.Simmons Comprehensive Cancer Center at UT Southwestern.He is also aHoward Hughes Medical Institute Investigator.Dr.Mendell led the study with co-first authors Yujing Cheng,Ph.D.,recent graduate of the Genetics,Development,and Disease graduate program,and Siwen Wang,M.D.,a former postdoctoral researcher,both in the Mendell Lab.Cellular senescence is a“double-edged sword,”Dr.Mendell explained.Cells sometimes undergo senescence when acancer-causing mutation arises,halting uncontrolled cell division and preventing tumors from developing.On the other hand,too much senescence contributes to aging and degenerative diseases.The Mendell Lab has long studied noncoding RNAs,finding new roles for these molecules in both health and disease.In this newest study,he and his colleagues used atechnique for regulating gene activity called CRISPR interference to individually inactivate thousands of noncoding RNAs in human cells that carried acancer-causing mutation.Usually,this mutation prompts cells to become senescent;however,inactivating anoncoding RNA involved in senescence caused the cells to continue dividing.These experiments quickly revealed apreviously unrecognized regulator of senescence called SNORA13,a member of afamily of noncoding RNAs known as small nucleolar RNAs that are thought largely to function as guides for chemical modification of other RNA molecules.A series of additional experiments showed that SNORA13 plays another important and unexpected role:slowing down the construction of ribosomes,cellular machines that synthesize proteins.Dr.Mendell explained that cellular stress–prompted by acancer-causing mutation,for example–can perturb ribosome assembly and push cells into senescence.However,removing SNORA13 caused cells to ramp up ribosome assembly,blocking the quality control that would normally trigger senescence and allowing cells to continue dividing. 查看详细>>

来源:达拉斯德克萨斯大学西南医学中心 点击量: 81

7 2024-07-11

A research team from The Chinese University of Hong Kong(CUHK)’s Faculty of Medicine(CU Medicine)has conducted alarge cohort study among 1,627 children with and without autism spectrum disorder(ASD)and found alterations in four kingdoms of the gut microbial species including archaea,bacteria,fungi and viruses in children with ASD.Using machine learning,they developed apanel of 31 multikingdom and functional markers that showed high diagnostic performance for ASD and has great potential as aclinical diagnostic tool.The findings were published in Nature Microbiology.In apilot study,the researchers also showed that modulation of the gut microbiome alleviated symptoms of anxiety in children with ASD,introducing the possibility of anew therapeutic paradigm for the condition.Multikingdom gut microbial markers facilitate ASD diagnosis ASD is aneurodevelopmental condition characterised by impairment in social communication,and restrictive and repetitive behaviour.Genetic and environmental factors contribute to the pathogenesis of ASD but emerging evidence suggests that impaired cross-talk between the gut microbiome and central nervous system,dubbed the gut-brain axis,may contribute to the development of ASD.According to the latest estimation from CU Medicine,approximately 2.54%of children in Hong Kong has ASD,and the incidence has been rising in recent years.The CU Medicine research team performed metagenomic sequencing on faecal samples from 1,627 children with or without ASD,aged one to 13 years old from five independent cohorts.Subjects were recruited from the Child and Adolescent Psychiatric Services of the Department of Psychiatry at Alice Ho Miu Ling Nethersole Hospital of the Hospital Authority’s New Territory East Cluster from 2021 to 2023.The team analysed faecal samples and clinical data including diet,medication and co-morbidities.The researchers identified apanel of novel gut microbiome markers including 14 archaea,51 bacteria,seven fungi,18 viruses,27 microbial genes and 12 metabolic pathways that were altered in children with ASD.Using machine learning approaches,they then developed anovel,non-invasive diagnostic model based on apanel of 31 multikingdom and functional markers that showed ahigh diagnostic accuracy for ASD.Dr Su Qi,Research Assistant Professor in the Department of Medicine and Therapeutics at CU Medicine,said,“Bacterial composition has been shown to be altered in ASD but the contribution of other components of the microbiome including the archaea,fungi,viruses,microbial genes or functional pathways remains unexplored.We found that the 31-microbiome panel has asensitivity of 94%and specificity of 93%for the diagnosis of ASD,and maintained asensitivity of 91%in children from an independent hospital cohort and ayounger community cohort from one to six years old.”Professor Siew Ng,Croucher Professor in Medical Sciences at CU Medicine,Director of the Microbiota I-Center(MagIC),and New Cornerstone Investigator added,“The diagnosis of ASD is challenging and requires regular developmental assessment in children who show signs of atypical social and language development.Diagnosis is often delayed especially in younger children who may only have mild symptoms and this could lead to delayed intervention.This,to our knowledge,is the first study to demonstrate the robustness and utility of anon-invasive biomarker to diagnose and predict ASD across different ages,gender and settings.” 查看详细>>

来源:香港中文大学 点击量: 335

8 2024-07-10

A model co-designed by aprofessor at Anglia Ruskin University is expected to reduce the need for chemotherapy in up to 38%of breast cancer patients who would previously have been advised to consider the treatment.The latest version of the PREDICT Breast model,published in the npj Nature journal and launched this week,uses the latest breast cancer survival data as well as taking into account the benefits and harms of chemotherapy and radiotherapy.PREDICT Breast was initially launched in 2010 by Gordon Wishart,Professor of Cancer Surgery at ARU and then Director of the Cambridge Breast Unit at Cambridge University Hospitals NHS Foundation Trust,and Paul Pharoah who at the time was Professor of Cancer Epidemiology at University of Cambridge.They brought together ateam of leading clinicians and scientists to develop and validate the PREDICT Breast model,which was based on Cancer Registry data from the UK.PREDICT Breast has been continuously updated since its launch and allows estimation of 10 and 15-year survival,as well as the absolute benefits of chemotherapy,trastuzumab,hormone therapy and bisphosphonates,to allow appropriate use of these therapies.The model is currently used worldwide by over 40,000 clinicians and their patients each month.The new version has been largely unfunded,but the recently published data is now being followed up by afurther study in the United States,using data from the SEER(Surveillance,Epidemiology,and End Results programme)database.Professor Wishart,now Chief Medical Officer at Check4Cancer alongside his visiting role at ARU,said:“Chemotherapy can cause significant physical effects such as nausea,weight loss,fatigue,bleeding,bruising and increased risk of infection.The data from the new model shows that for asignificant number of women with breast cancer,chemotherapy can be safely avoided. 查看详细>>

来源:Cambridge Network 点击量: 21

9 2024-07-10

A newly discovered hormone that keeps the bones of breastfeeding women strong could also help bone fractures heal and treat osteoporosis in the broader population.Researchers at UC San Francisco and UC Davis showed that in mice,the hormone known as Maternal Brain Hormone(CCN3)increases bone density and strength.Their results,published July 10 in Nature,solve along-standing puzzle about how women’s bones remain relatively robust during breastfeeding,even as calcium is stripped from bones to support milk production.“One of the remarkable things about these findings is that if we hadn’t been studying female mice,which unfortunately is the norm in biomedical research,then we could have completely missed out on this finding,”said Holly Ingraham,PhD,the senior author of the new paper and aprofessor cellular molecular pharmacology at UCSF.“It underscores just how important it is to look at both male and female animals across the lifespan to get afull understanding of biology.”More than 200 million people worldwide suffer from osteoporosis,a severe weakening of the bones that can cause frequent fractures.Women are at particularly high risk of osteoporosis after menopause because of declining levels of the sex hormone estrogen,which normally promotes bone formation.Estrogen levels are also low during breastfeeding,yet osteoporosis and bone fractures are much rarer during this time,suggesting that something other than estrogen promotes bone growth. 查看详细>>

来源:加州大学旧金山分校 点击量: 56

10 2024-07-09

近日,中国科学院近代物理研究所的科研人员与来自法国、芬兰、南非和英国等国家的合作者首次成功测量了β缓发质子核镧-120的激发态结构,在质子滴线原子核的质子中子相互作用和形状演化的研究中取得重要进展,相关成果于近期发表在Physics Letters B上。理论预言,当位于中重质量区的原子核靠近N="Z线时,质子-中子相互作用会增强,并对激发态的结构产生重要影响。同时,原子核可能伴随形状的演化,呈现出“橄榄球”(长椭球),甚至是稀有的“南瓜形”(扁椭球)、“梨形”(八极形变)和“猕猴桃形”(三轴形变)。因此,通过实验测量奇特核的激发态性质对于检验相关理论模型至关重要。为了探索极端丰质子镧原子核的结构演化及其背后的物理机制,近代物理所和法国巴黎萨克雷大学的研究人员主导开展了寻找镧-120激发态的实验。镧-120是一种稀有的β缓发质子核,于1984年首次发现。由于熔合蒸发反应生成镧-120的截面极小,反应产物十分复杂,因此分离及鉴别镧-120极其困难。在过去的40年中,实验物理学家一直未能成功测量到镧-120的激发态。研究团队利用芬兰于韦斯屈莱大学重离子加速器上的质量分析谱仪和伽马探测器阵列,结合多种时间空间关联测量技术,首次在实验上建立了镧-120的激发态能级结构,发现镧-120的奇偶能级劈裂符合系统性,但是它的电磁跃迁比显著不同。结合理论模型,研究团队发现镧-120展现出一种稀有的三轴形变,并且质子-中子相互作用在描述质子滴线奇奇核的结构中扮演着重要角色。该研究得到了国家自然科学基金、中法科研伙伴交流计划项目和中国科学院未来伙伴网络专项的支持。 查看详细>>

来源:中国科学院大学 点击量: 559

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