检索结果-南通市图书馆

Effects of gender-affirming hormone therapy on insulin resistance and body composition in transgender individuals: A systematic review

引用

World Journal of Diabetes 2020年第3期11卷 66-77页

作者： Cassandra Spanos Ingrid Bretherton Jeffrey D Zajac Ada S Cheung Trans Medical research Group Department of Medicine (Austin Health) University of Melbourne

BACKGROUND Transgender individuals receiving masculinising or feminising gender-affirming hormone therapy with testosterone or estradiol respectively,are at increased risk of adverse cardiovascular outcomes,including myocardial infarction and *** may be related to the effects of testosterone or estradiol therapy on body composition,fat distribution,and insulin resistance but the effect of genderaffirming hormone therapy on these cardiovascular risk factors has not been extensively *** To evaluate the impact of gender-affirming hormone therapy on body composition and insulin resistance in transgender individuals,to guide clinicians in minimising cardiovascular *** We performed a review of the literature based on PRISMA ***,Embase and PsycINFO databases were searched for studies examining body composition,insulin resistance or body fat distribution in transgender individuals aged over 18 years on established gender-affirming hormone *** were selected for full-text analysis if they investigated transgender individuals on any type of gender-affirming hormone therapy and reported effects on lean mass,fat mass or insulin *** The search strategy identified 221 *** exclusion of studies that did not meet inclusion criteria,26 were included(2 cross-sectional,21 prospectiveuncontrolled and 3 prospective-controlled).Evidence in transgender men suggests that testosterone therapy increases lean mass,decreases fat mass and has no impact on insulin *** in transgender women suggests that feminising hormone therapy(estradiol,with or without anti-androgen agents)decreases lean mass,increases fat mass,and may worsen insulin *** to body composition were consistent across almost all studies:Transgender men on testosterone gained lean mass and lost fat mass,and transgender women on oestrogen experienced the *** study directly contradicted these trends,though several small st

关键词： Transgender persons Insulin resistance Body composition Gender dysphoria Metabolic syndrome

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

活化的巨噬细胞介导的胰岛异种移植排异反应与细胞因子表达上调的关系

引用

中南大学学报（医学版） 2007年第1期32卷 26-35页

作者： Abhilash P. Chandra Li Ou-yang Jeffrey K. W. Wong Hong Ha Stacey N. Waiters Anita T. Patel Wayne J. Hawthorne Shou-nan YI Centre for Transplantation and Renal research Westmead Millenium Institute University of Sydney at Westmead Hospital Westmead 2145 Australia

目的：笔者以往的实验证明与猪抗原接触过并被CD4^＋T淋巴细胞激活的巨噬细胞能识剐、排斥猪的异种移植物，但不会排斥鼠的同种移植物，这表明在这种特异性移植物免疫识别及破坏过程中移植物及巨噬细胞之间存在着信号联系。方法：在免... 详细信息

目的：笔者以往的实验证明与猪抗原接触过并被CD4^＋T淋巴细胞激活的巨噬细胞能识剐、排斥猪的异种移植物，但不会排斥鼠的同种移植物，这表明在这种特异性移植物免疫识别及破坏过程中移植物及巨噬细胞之间存在着信号联系。方法：在免疫过继转移之前，将胎猪的胰腺碎片移植到非肥胖糖尿病／严重联合免疫缺陷（NOD／SCID）鼠。再从移植了胎猪的胰腺碎片（FPP）并发生排斥反应的受体Balb／c鼠身上分离出巨噬细胞，将这些外源性巨噬细胞植入NOD／SCID鼠。这些外源性的巨噬细胞通过Ly5．1表面抗原或通过CSFE染色标记来追踪。在移植了FPP异种移植物以后的CCR2，CCR5及它们的趋化因子的基因表达可通过实时PCR来评估。结果：形成免疫过继后较早移植的异种移植物出现了免疫排斥，而不是建立免疫过继较长时间后再移植FFP的NOD／SCID鼠。同时，前者可检测出更高水平的趋化因子的基因表达。而且，与未激活的巨噬细胞比较，已经激活的巨噬细胞CCR2，CCR5基因的表达增强更为明显。结论：趋化因子的上调与巨噬细胞的聚集、胰岛移植物的破坏有关。

关键词：巨噬细胞示踪趋化因子异种移植物聚集

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Activation of tyrosine phosphatases in the progression of Alzheimer’s disease

引用

Neural Regeneration research 2020年第12期15卷 2245-2246页

作者： Alexandre F.R.Stewart Hsiao-Huei Chen University of Ottawa Heart Institute OttawaCanada Ottawa Hospital research Institute OttawaCanada

Patients with Alzheimer’s disease(AD)have progressive memory loss,inability to reason,and display anxiety that accelerates disease *** points to two deficits:1)the brain fails to respond to insulin that regulates the formation of neuron connections required to store memories,and 2)deficits arise in the brain’s endogenous cannabinoid signaling that regulates mood and prevents anxiety(Aso and Ferrer,2014).In addition,leptin signaling,important in regulating hypothalamic synaptic plasticity and cognitive function is also affected in AD(McGregor and Harvey,2018).

关键词： Alzheimer endogenous arise

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Low back pain and osteoarthritis pain:a perspective of estrogen

引用

骨研究:英文版 2023年第3期11卷 443-456页

作者： Huiwen Pang Shihui Chen David M.Klyne David Harrich Wenyuan Ding Sidong Yang Felicity Y.Han Australian Institute for Bioengineering and Nanotechnology The University of QueenslandSt.LuciaBrisbaneQLD 4072Australia NHMRC Centre of Clinical research Excellence in Spinal Pain Injury and HealthThe University of QueenslandSt.LuciaBrisbaneQLD 4072Australia Department of Cell and Molecular Biology QIMR Berghofer Medical Research InstituteHerstonQLD 4006Australia Department of Spine Surgery The Third Hospital of Hebei Medical University139 Ziqiang RoadShijiazhuang 050051China Hebei Joint International research Center for Spinal Diseases 139 Ziqiang RoadShijiazhuang 050051China

Low back pain(LBP)is the world's leading cause of disability and is increasing in prevalence more rapidly than any other pain *** disc(IVD)degeneration and facet joint osteoarthritis(FJOA)are two common causes of LBP,and both occur more frequently in elderly women than in other ***,osteoarthritis(OA)and OA pain,regardless of the joint,are experienced by up to twice as many women as men,and this difference is amplified during *** in estrogen may be an important contributor to these pain *** for estrogen have been found within IVD tissue and nearby joints,highlighting the potential roles of estrogen within and surrounding the IVDs and *** addition,estrogen supplementation has been shown to be effective at ameliorating IVD degeneration and OA progression,indicating its potential use as a therapeutic agent for people with LBP and OA *** review comprehensively examines the relationship between estrogen and these pain conditions by summarizing recent preclinical and clinical *** potential molecular mechanisms by which estrogen may relieve LBP associated with IVD degeneration and FJOA and OA pain are discussed.

关键词： agent degeneration pain

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

N-methyl-D-aspartate receptor functions altered by neuronal PTP1B activation in Alzheimer’s disease and schizophrenia models

引用

Neural Regeneration research 2022年第10期17卷 2208-2210页

作者： Alexandre F.R.Stewart Hsiao-Huei Chen Department of Biochemistry Microbiology and ImmunologyUniversity of Ottawaand University of Ottawa Heart InstituteOttawaONCanada Centre for Infection Immunity and InflammationOttawaONCanada Medicine Cellular and Molecular MedicineUniversity of Ottawa Brain and Mind InstituteOttawa Hospital Research InstituteOttawaONCanada

Glutamate is the main exc i tatory neurotransmitter in the brain and binds to two major classes of receptors,theα-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid(AMPA)and the N-methyl-D-aspartate(NMDA)*** AMPA receptors that are immediately activated by glutamate release,NMDA receptors are blocked by magnesium and can only be activated by glutamate after membrane ***,NMDA receptors are only activated after repeated AMPA receptor activation by *** receptors are,for the most part,calcium-permeable *** influx through NMDA receptors modulates synaptic transmission in neurons based on prior history of excitation,and provides a means of scaling the strength of synapses required for Hebbian plasticity.

关键词： PTP1B aspartate NMDA

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Biological function of Presenilin and its role in AD pathogenesis

引用

Translational Neurodegeneration 2013年第1期2卷 95-107页

作者： Shuting Zhang Mingming Zhang Fang Cai Weihong Song Townsend Family Laboratories Department of PsychiatryBrain Research CenterGraduate Program in NeuroscienceThe University of British Columbia2255 Wesbrook MallVancouverBC V6T 1Z3Canada

Presenilins(PSs)are the catalytic core of γ-secretase ***,the mechanism of FAD-associated PS mutations in AD pathogenesis still remains *** we review the general biology and mechanism of γ-secretase and focus on the catalytic components–presenilins and their biological functions and contributions to the AD *** functions of presenilins are divided into γ-secretase dependent and γ-secretase independent *** γ-secretase dependent functions of presenilins are exemplified by the sequential cleavages in the processing of APP and Notch;the γ-secretase independent functions of presenilins include stabilizing β-catenin in Wnt signaling pathway,regulating calcium homeostasis and their interaction with synaptic transmission.

关键词： complex. function cleavage

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Metabolic alterations and vulnerabilities in hepatocellular carcinoma

引用

Gastroenterology Report 2021年第1期9卷 1-13,I0001页

作者： Daniel GTenen Li Chai Justin L.Tan Cancer Science Institute of Singapore National University of SingaporeSingapore Harvard Stem Cell Institute Harvard Medical SchoolBostonMAUSA Department of Pathology Brigham&Women’s HospitalHarvard Medical SchoolBostonMAUSA Experimental Drug Development Centre Agency for ScienceTechnology and Research(A*STAR)Singapore Genome Institute of Singapore Agency for ScienceTechnology and Research(A*STAR)Singapore

Liver cancer is a serious *** is ranked as the cancer with the second highest number of cancer-related deaths *** carcinoma(HCC),which arises from transformed hepatocytes,is the major subtype of liver *** accounts for 85%of total liver-cancer *** important aspect of HCC that has been actively studied is its *** the liver as the primary site of numerous metabolic processes in the body,it has been shown that the metabolism of HCC cells is highly dysregulated compared to that of normal *** is therefore crucial to understand the metabolic alterations caused by HCC and the underlying mechanisms for these *** deeper understanding will allow diagnostic and therapeutic advancements in the treatment of *** this review,we will summarize the current literature in HCC metabolic alterations,induced vulnerabilities,and potential therapeutic interventions.

关键词： hepatocellular carcinoma(HCC) metabolism metabolic vulnerability targeted therapy

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

P450-mediated dehydrotyrosine formation during WS9326 biosynthesis proceeds via dehydrogenation of a specific acylated dipeptide substrate

引用

Acta Pharmaceutica Sinica B 2023年第8期13卷 3561-3574页

作者： Songya Zhang Lin Zhang Anja Greule Julien Tailhades Edward Marschall Panward Prasongpholchai Daniel J.Leng Jingfan Zhang Jing Zhu Joe A.Kaczmarski Ralf B.Schittenhelm Oliver Einsle Colin J.Jackson Fabrizio Alberti Andreas Bechthold Youming Zhang Manuela Tosin Tong Si Max J.Cryle CAS Key Laboratory of Quantitative Engineering Biology Shenzhen Institute of Synthetic BiologyShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Institut für Biochemie Albert-Ludwigs-Universitat FreiburgFreiburg 79104Germany Department of Biochemistry and Molecular Biology the Monash Biomedicine Discovery InstituteMonash UniversityClayton 3800VICAustralia EMBL Australia Monash UniversityClayton 3800VICAustralia ARC Centre of Excellence for Innovations in Peptide and Protein Science Clayton 3800VICAustralia Department of Chemistry University of WarwickGibbet Hill RoadCoventry CV47ALUK School of Life Sciences University of WarwickGibbet Hill CampusCoventry CV47ALUK research School of Chemistry the Australian National UniversityActon 2601ACTAustralia Monash Proteomics and Metabolomics Facility Monash UniversityClayton 3800VICAustralia Institute of Pharmaceutical Sciences Albert-Ludwigs-Universitat Freiburg79104Germany

WS9326A is a peptide antibiotic containing a highly unusual N-methyl-E-2-3-dehydrotyrosine(NMet-Dht)residue that is incorporated during peptide assembly on a non-ribosomal peptide synthetase(NRPS).The cytochrome P450 encoded by sas16(P450Sas)has been shown to be essential for the formation of the alkene moiety in NMet-Dht,but the timing and mechanism of the P450Sas-mediatedα,β-dehydrogenation of Dht remained ***,we show that the substrate of P450Sas is the NRPS-associated peptidyl carrier protein(PCP)-bound dipeptide intermediate(Z)-2-pent-1′-*** demonstrate that P450Sas-mediated incorporation of the double bond follows N-methylation of the Tyr by the N-methyl transferase domain found within the NRPS,and further that P450Sas appears to be specific for substrates containing the(Z)-2-pent-1’-enyl-cinnamoyl group.A crystal structure of P450Sas reveals differences between P450Sas and other P450s involved in the modification of NRPS-associated substrates,including the substitution of the canonical active site alcohol residue with a phenylalanine(F250),which in turn is critical to P450Sas activity and WS9326A ***,our results suggest that P450Sas catalyses the direct dehydrogenation of the NRPS-bound dipeptide substrate,thus expanding the repertoire of P450 enzymes that can be used to produce biologically active peptides.

关键词： Cytochrome P450 Non-ribosomal peptide synthetase Protein crystal structure Enzyme mechanism Natural products Peptideantibiotic

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models

引用

Neural Regeneration research 2021年第1期16卷 129-136页

作者： Shelly A.Cruz Zhaohong Qin Konrad M.Ricke Alexandre F.R.Stewart Hsiao-Huei Chen Ottawa Hospital research Institute Neuroscience ProgramUniversity of OttawaOttawaONCanada Brain and Mind Institute University of OttawaOttawaONCanada Department of Biochemistry Microbiology and ImmunologyUniversity of OttawaOttawaONCanada Cellular and Molecular Medicine University of OttawaOttawaONCanada Department of Medicine University of OttawaOttawaONCanada Centre for Infection Immunity and InflammationUniversity of OttawaOttawaONCanada University of Ottawa Heart Institute OttawaONCanada

Ischemic brain injury causes neuronal death and *** activates protein-tyrosine phosphatase 1B(PTP1B).Here,we tested the significance of PTP1B activation in glutamatergic projection neurons on functional recovery in two models of stroke:by photothrombosis,focal ischemic lesions were induced in the sensorimotor cortex(SM stroke)or in the peri-prefrontal cortex(peri-PFC stroke).Elevated PTP1B expression was detected at 4 days and up to 6 weeks after *** ablation of PTP1B in neurons of neuronal knockout(NKO)mice had no effect on the volume or resorption of ischemic lesions,markedly different effects on functional recovery were *** stroke caused severe sensory and motor deficits(adhesive removal test)in wild type and NKO mice at 4 days,but NKO mice showed drastically improved sensory and motor functional recovery at 8 *** addition,peri-PFC stroke caused anxiety-like behaviors(elevated plus maze and open field tests),and depression-like behaviors(forced swimming and tail suspension tests)in wild type mice 9 and 28 days after stroke,respectively,with minimal effect on sensory and motor ***-PFC stroke-induced affective disorders were associated with fewer active(FosB+)neurons in the PFC and nucleus accumbens but more FosB+neurons in the basolateral amygdala,compared to sham-operated *** contrast,mice with neuronal ablation of PTP1B were protected from anxiety-like and depression-like behaviors and showed no change in FosB+neurons after peri-PFC *** together,our study identifies neuronal PTP1B as a key component that hinders sensory and motor functional recovery and also contributes to the development of anxiety-like and depression-like behaviors after ***,PTP1B may represent a novel therapeutic target to improve stroke *** procedures for animal use were approved by the Animal Care and Use Committee of the University of Ottawa Animal Care and Veterinary Service(protocol 1806)on July 27,2018.

关键词： adhesive removal test anxiety depression elevated plus maze forced swimming test Iba1 interleukin-1β microglia open field test tail suspension test tumor necrosis factor-α

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Spinal cord injury reprograms muscle fibroadipogenic progenitors to form heterotopic bones within muscles

引用

Bone research 2022年第2期10卷 310-325页

作者： Hsu-Wen Tseng Dorothée Girard Kylie A.Alexander Susan M.Millard Frédéric Torossian Adrienne Anginot Whitney Fleming Jules Gueguen Marie-Emmanuelle Goriot Denis Clay Beulah Jose Bianca Nowlan Allison R.Pettit Marjorie Salga François Genêt Marie-Caroline Le Bousse-Kerdilès Sébastien Banzet Jean-Pierre Lévesque Mater research Institute-The University of Queensland WoolloongabbaQLDAustralia Institut de Recherche Biomédicale des Armées(IRBA) INSERM UMRS-MD1197 ClamartFrance INSERM UMRS-MD 1197 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance INSERM UMS-44 Universitéde Paris-SaclayHôpital Paul BrousseVillejuifFrance UPOH(UnitéPéri Opératoire du Handicap Perioperative Disability Unit)Physical and Rehabilitation Medicine departmentRaymond-PoincaréHospitalAssistance Publique-Hôpitaux de Paris(AP-HP)GarchesFrance Universitéde Versailles Saint Quentin en Yvelines UFR Simone Veil-SantéEND:ICAP INSERM U1179Montigny le BretonneuxFrance

The cells of origin of neurogenic heterotopic ossifications(NHOs), which develop frequently in the periarticular muscles following spinal cord injuries(SCIs) and traumatic brain injuries, remain unclear because skeletal muscle harbors two progenitor cell populations: satellite cells(SCs), which are myogenic, and fibroadipogenic progenitors(FAPs), which are mesenchymal. Lineage-tracing experiments using the Cre recombinase/Lox P system were performed in two mouse strains with the fluorescent protein Zs Green specifically expressed in either SCs or FAPs in skeletal muscles under the control of the Pax7 or Prrx1 gene promoter, respectively. These experiments demonstrate that following muscle injury, SCI causes the upregulation of PDGFRα expression on FAPs but not SCs and the failure of SCs to regenerate myofibers in the injured muscle, with reduced apoptosis and continued proliferation of muscle resident FAPs enabling their osteogenic differentiation into NHOs. No cells expressing Zs Green under the Prrx1 promoter were detected in the blood after injury, suggesting that the cells of origin of NHOs are locally derived from the injured muscle. We validated these findings using human NHO biopsies. PDGFRα+mesenchymal cells isolated from the muscle surrounding NHO biopsies could develop ectopic human bones when transplanted into immunocompromised mice, whereas CD56+myogenic cells had a much lower potential. Therefore, NHO is a pathology of the injured muscle in which SCI reprograms FAPs to undergo uncontrolled proliferation and differentiation into osteoblasts.

关键词： progenitor injuries muscles

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：