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Diagnostic and therapeutic challenges of gastrointestinal angiodysplasias: A critical review and view points

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World journal of Gastroenterology 2019年第21期25卷 2549-2564页

作者： Diego García-Compeán ángel N Del Cueto-Aguilera Alan R jiménez-Rodríguez josé A González-González héctor j maldonado-garza Gastroenterology Service and Department of Internal Medicine Faculty of Medicine University Hospital "Dr. José E. González"Universidad Autónoma de Nuevo León

Gastrointestinal angiodysplasias (GIADs), also called angioectasias, are the most frequent vascular lesions. Its precise prevalence is unknown since most of them are asymptomatic. however, the incidence may be increasing since GIADs affect individuals aged more than 60 years and population life expectancy is globally increasing worldwide. They are responsible of about 5% to 10% of all gastrointestinal bleeding (GIB) cases. Most GIADs are placed in small bowel, where are the cause of 50 to 60% of obscure GIB diagnosed with video capsule endoscopy. They may be the cause of fatal severe bleeding episodes;nevertheless, recurrent overt or occult bleeding episodes requiring repeated expensive treatments and disturbing patient’s quality-of-life are more frequently observed. Diagnosis and treatment of GIADs (particularly those placed in small bowel) are a great challenge due to insidious disease behavior, inaccessibility to affected sites and limitations of available diagnostic procedures. hemorrhagic causality out of the actively bleeding lesions detected by diagnostic procedures may be difficult to establish. No treatment guidelines are currently available, so there is a high variability in the management of these patients. In this review, the epidemiology and pathophysiology of GIADs and the status in the diagnosis and treatment, with special emphasis on small bowel angiodysplasias based on multiple publications, are critically discussed. In addition, a classification of GIADs based on their endoscopic characteristics is proposed. Finally, some aspects that need to be clarified in future research studies are highlighted.

关键词： Angiodysplasias Angioectasias Vascular malformations Epidemiology Pathogenesis Endoscopic treatment Somatostatin analogues

Meckel's diverticulum diagnosis by video capsule endoscopy: A case report and review of literature

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World journal of Clinical Cases 2018年第14期6卷 791-799页

作者： Diego García-Compeán Alan R jiménez-Rodríguez Angel N Del Cueto-Aguilera Gilberto herrera-Quinones josé A González-González héctor j maldonado-garza Gastroenterology Service and Department of Internal Medicine Faculty of Medicine University Hospital "Dr. José E. González" Universidad Autónoma de Nuevo León Monterrey 64700 Nuevo León México

BACKGROUND Meckel's diverticulum(MD) occurs predominantly in children and adolescents. It is rarely diagnosed in adults. Preoperative diagnosis is difficult due to low sensitivity of the radiological imaging studies. The role of video capsule endoscopy(VCE) in the diagnosis of MD is unknown, and the endoscopic patterns are not defined. We will describe four of our cases of MD evaluated with VCE and make a review of the literature focusing on the endoscopic characteristics.CASE SUMMARY We present four cases of MD confirmed by surgery. They were all adult males with ages going from 18 to 50 years, referred to our service from 2004 to 2018, due to obscure gastrointestinal bleeding(OGIB). Theyhad a history of 1 mo to 10 years of overt and occult bleeding episodes. Laboratory blood test showed an iron-deficiency anemia from 4 to 9 g/dL of hemoglobin that required multiple hospitalizations and blood transfusions in all cases. Repeated upper digestive endoscopies and colonoscopies were negative. Small bowel was examined with VCE, which revealed double lumen images in all cases, one with polyps and three with circumferential ulcers in the diverticulum. however, based on VCE findings, preoperative diagnosis of MD was suggested only in two patients. Capsule was retained in one patient, which was recovered with surgery. The anatomopathological report revealed ulcerated ectopic gastric mucosa in all cases.CONCLUSION VCE is useful for the diagnosis of MD. however, endoscopic characteristics must be recognized in order to establish preoperative diagnosis.

关键词：梅克尔憩室治疗方法临床分析内镜

Mitochondrial dysfunction as a target in spinal cord injury:intimate correlation between pathological processes and therapeutic approaches

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Neural Regeneration Research 2023年第10期18卷 2161-2166页

作者： julieta Schmidt héctor Ramiro Quintá Universidad de Buenos Aires CABAArgentina Laboratorio de Medicina Experimental“Dr.j.Toblli” Hospital AlemánCABAArgentina Consejo Nacional de Investigaciones Científicas y Técnicas-CONICET CABAArgentina Rehabilitation Medicine Department University of MinnesotaTwin CitiesMINUSA

Traumatic spinal cord injuries interrupt the connection of all axonal projections with their neuronal targets below and above the lesion site. This interruption results in either temporary or permanent alterations in the locomotor, sensory, and autonomic functions. Damage in the spinal tissue prevents the re-growth of severed axons across the lesion and their reconnection with neuronal targets. Therefore, the absence of spontaneous repair leads to sustained impairment in voluntary control of movement below the injury. For decades, axonal regeneration and reconnection have been considered the opitome of spinal cord injury repair with the goal being the repair of the damaged long motor and sensory tracts in a complex process that involves:(1) resealing injured axons;(2) reconstructing the cytoskeletal structure inside axons;(3) re-establishing healthy growth cones;and(4) assembling axonal cargos. These biological processes require an efficient production of adenosine triphosphate, which is affected by mitochondrial dysfunction after spinal cord injury. From a pathological standpoint, during the secondary stage of spinal cord injury, mitochondrial homeostasis is disrupted, mainly in the distal segments of severed axons. This result in a reduction of adenosine triphosphate levels and subsequent inactivation of adenosine triphosphate-dependent ion pumps required for the regulation of ion concentrations and reuptake of neurotransmitters, such as glutamate. The consequences are calcium overload, reactive oxygen species formation, and excitotoxicity. These events are intimately related to the activation of necrotic and apoptotic cell death programs, and further exacerbate the secondary stage of the injury, being a hallmark of spinal cord injury. This is why restoring mitochondrial function during the early stage of secondary injury could represent a potentially effective therapeutic intervention to overcome the motor and sensory failure produced by spinal cord injury. This review discusses the most recent evidence linkin

关键词： adenosine triphosphate axonal regeneration creatine mitochondria dysfunction mitochondria spinal cord injury

Subclinical abnormal glucose tolerance is a predictor of death in liver cirrhosis

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World journal of Gastroenterology 2014年第22期20卷 7011-7018页

作者： Diego García-Compeán joel Omar jáquez-Quintana Fernando javier Lavalle-González josé Alberto González-González Linda Elsa Mu?oz-Espinosa jesús Zacarías Villarreal-PérezEndocrinology Service and Department of Internal Medicine University hospital "Dr. josé E. González" and Medical School Universidad Autónoma de Nuevo León Monterrey 64320 México héctor j maldonado-garza Gastroenterology Service and Department of Internal Medicine University Hospital "Dr. José E. Gonzalez" and Medical SchoolUniversidad Autónoma de Nuevo LeónMonterrey 64320México Endocrinology Service and Department of Internal Medicine University Hospital "Dr. José E. González" and Medical SchoolUniversidad Autónoma de Nuevo LeónMonterrey 64320México Liver Unit University Hospital "Dr. José E. González" and Medical SchoolUniversidad Autónoma de Nuevo LeónMonterrey 64320México

AIM:To determine if subclinical abnormal glucose tolerance(SAGT)has influence on survival of non-diabetic patients with liver cirrhosis.METhODS:In total,100 patients with compensatedliver cirrhosis and normal fasting plasma glucose were included.Fasting plasma insulin(FPI)levels were measured,and oral glucose tolerance test(OGTT)was performed.According to OGTT results two groups of patients were formed:those with normal glucose tolerance(NGT)and those with SAGT.Patients were followed every three months.The mean follow-up was932 d(range of 180-1925).Survival was analyzed by the Kaplan-Meyer method,and predictive factors of death were analyzed using the Cox proportional hazard regression model.RESULTS:Of the included patients,30 showed NGT and70 SAGT.Groups were significantly different only in age,INR,FPI and hOMA2-IR.Patients with SAGT showed lower 5-year cumulated survival than NGT patients(31.7%vs 71.6%,P=0.02).Differences in survival were significant only after 3 years of follow-up.SAGT,Child-Pugh B,and high Child-Pugh and Model for EndStage Liver Disease(MELD)scores were independent predictors of death.The causes of death in 90.3%of cases were due to complications related to liver disease.CONCLUSION:SAGT was associated with lower survival.SAGT,Child-Pugh B,and high Child-Pugh and MELD scores were independent negative predictors of survival.

关键词： Diabetes mellitus Liver cirrhosis Oral glu-cose to

Loss of tau expression attenuates neurodegeneration associated with α-synucleinopathy

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Translational Neurodegeneration 2022年第1期11卷 426-442页

作者： Scott C.Vermilyea Anne Christensen joyce Meints Balvindar Singh héctor Martell-Martínez MdRazaul Karim Michael K.Lee Department of Neuroscience University of Minnesota-Twin Cities321 Church Street S.E.MinneapolisMNUSA6-145 Jackson Hall Institute for Translational Neuroscience University of Minnesota-Twin CitiesMin-neapolisMNUSA Aligning Science Across Parkinson’s(ASAP)Collaborative Research Network Chevy ChaseMDUSA University of Minnesota Medical School 420 Delaware Street SEMinneapolisMN 55455USA.

Background: Neuronal dysfunction and degeneration linked to α-synuclein (αS) pathology is thought to be responsible for the progressive nature of Parkinson’s disease and related dementia with Lewy bodies. Studies have indicated bidirectional pathological relationships between αS pathology and tau abnormalities. We recently showed that A53T mutant human αS (huαS) can cause post-synaptic and cognitive deficits that require microtubule-associated protein tau expression. however, the role of tau in the development of αS pathology and subsequent neuronal dysfunction has been controversial. herein, we set out to determine the role of tau in the onset and progression of αS pathology (α-synucleinopathy) using a transgenic mouse model of α-synucleinopathy lacking mouse tau expression. Methods: Transgenic mice expressing A53T mutant huαS (TgA53T) were crossed with mTau−/− mice to generate TgA53T/mTau−/−. To achieve more uniform induction of α-synucleinopathy in mice, we used intramuscular injections of αS preformed fibrils (PFF) in non-transgenic (nTg), TgA53T, TgA53T/mTau−/−, and mTau−/− mice. Motor behavior was analyzed at 70 days post inoculation (dpi) of PFF and tissues for biochemical and neuropathological analysis were collected at 40 dpi, 70 dpi, and end stage. Results: Loss of tau expression significantly delayed the onset of motor deficits in the TgA53T model and the progression of α-synucleinopathy disease, as evidenced by a significant reduction in histopathological and behavioral markers of neurodegeneration and disease, and a significant improvement in survival. In vitro application of PFF to primary mouse hippocampal neurons demonstrated no changes in PFF uptake and processing or pS129 αS aggregation as a function of tau expression. however, PFF-induced neurotoxicity, including morphological deficits in nTg neurons, was prevented with tau removal. Conclusions: Collectively, our data suggest that tau is likely acting downstream of αS pathology to affect neuronal homeostasis and survival. This work further supp

关键词： α-Synuclein Tau Parkinson’s disease Lewy body disease Neurodegeneration

碱性介质中界面电场对铁原子吸附修饰Pt(111)表面hER性能的影响

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Chinese journal of Catalysis 2022年第11期43卷 2826-2836页

作者： Francisco j.Sarabia Víctor Climent juan M.Feliu 阿利坎特大学电化学研究所西班牙阿利坎特

鉴于析氢反应(hER)与制氢技术直接相关,而氢气是氢经济中的能量载体,因此,深入理解析氢反应(hER)速率的控制参数非常重要.前期关于碱性介质中Ni(Oh)_(2)修饰的Pt(111)上激光诱导温度跃迁(LITj)实验结果已经揭示了界面电场对hER速率有较... 详细信息

鉴于析氢反应(hER)与制氢技术直接相关,而氢气是氢经济中的能量载体,因此,深入理解析氢反应(hER)速率的控制参数非常重要.前期关于碱性介质中Ni(Oh)_(2)修饰的Pt(111)上激光诱导温度跃迁(LITj)实验结果已经揭示了界面电场对hER速率有较大影响.推测认为,少量的Ni(Oh)_(2)会使电极的零自由电荷电势向析氢开始的方向负移,从而导致电场减弱.为进一步验证这一推测,本文将研究对象扩展到Fe(Oh)_(2)修饰的Pt(111)表面,对其伏安特性进行分析.伏安图在析氢区域显示出一个峰,表明修饰层发生Fe(Ⅱ)到Fe(0)的转变.与库仑分析结果一致,Oh吸附区的伏安特征与Fe物种被氧化至+3价有关.LITj结果显示,亲氧的Fe物质与水分子之间存在强烈的相互作用,其使熵最大处的电势远离hER的开始电势.因此,最具催化性的表面应该是Fe覆盖度最低的表面.

关键词：析氢反应铁吸附原子铂单晶 Pt(111) 激光诱导温度跃变方法界面电场零电荷电势

Arrhythmogenic mechanisms in ryanodine receptor channelopathies

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Science China(Life Sciences) 2015年第1期58卷 54-58页

作者： ZhAO Yan-Ting VALDIVIA Carmen R. GURROLA Georgina B. hERNNDEZ jonathan j. VALDIVIA héctor h. Center for Arrhythmia Research Department of Internal MedicineCardiovascular DivisionUniversity of Michigan

Ryanodine receptors(Ry Rs) are the calcium release channels of sarcoplasmic reticulum(SR) that provide the majority of calcium ions(Ca2+) necessary to induce contraction of cardiac and skeletal muscle cells.In their intracellular environment,Ry R channels are regulated by a variety of cytosolic and luminal factors so that their output signal(Ca2+) induces finely-graded cell contraction without igniting cellular processes that may lead to aberrant electrical activity(ventricular arrhythmias) or cellular remodeling.The importance of Ry R dysfunction has been recently highlighted with the demonstration that point mutations in RYR2,the gene encoding for the cardiac isoform of the Ry R(Ry R2),are associated with catecholaminergic polymorphic ventricular tachycardia(CPVT),an arrhythmogenic syndrome characterized by the development of adrenergically-mediated ventricular tachycardia in individuals with an apparently normal heart.here we summarize the state of the field in regards to the main arrhythmogenic mechanisms triggered by Ry R2 channels harboring mutations linked to CPVT.Most CPVT mutations characterized to date endow Ry R2 channels with a gain of function,resulting in hyperactive channels that release Ca2+ spontaneously,especially during diastole.The spontaneous Ca2+ release is extruded by the electrogenic Na+/Ca2+ exchanger,which depolarizes the external membrane(delayed afterdepolarization or DAD) and may trigger untimely action potentials.however,a rare set of CPVT mutations yield Ry R2 channels that are intrinsically hypo-active and hypo-responsive to stimuli,and it is unclear whether these channels release Ca2+ spontaneously during diastole.We discuss novel cellular mechanisms that appear more suitable to explain ventricular arrhythmias due to Ry R2 loss-of-function mutations.

关键词：心律失常细胞机制离子通道受体骨骼肌细胞碱细胞收缩钙释放通道

The spectrum of building block conformers sustains the biophysical properties of clinically-oriented self-assembling protein nanoparticles

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Science China Materials 2022年第6期65卷 1662-1670页

作者： Eric Voltà-Durán julieta M Sánchez hèctor-López-Laguna Eloi Parladé Laura Sánchez-García Alejandro Sánchez-Chardi Ario de Marco Ugutz Unzueta Esther Vázquez Antonio Villaverde Institut de Biotecnologia i de Biomedicina Universitat Autònoma de BarcelonaBellaterra 08193BarcelonaSpain Departament de Genètica i de Microbiologia Universitat Autònoma de BarcelonaBellaterra 08193BarcelonaSpain CIBER de Bioingeniería Biomateriales y Nanomedicina(CIBER-BBN) Bellaterra 08193BarcelonaSpain Instituto de Investigaciones Biológicas y Tecnológicas(IIBYT)(CONICET-Universidad Nacional de Córdoba) ICTA&Cátedra de Química BiológicaDepartamento de QuímicaFCEFyNUNC.Av.Velez Sarsfield 1611X 5016GCA CórdobaArgentina Servei de Microscòpia Universitat Autònoma de BarcelonaBellaterra 08193BarcelonaSpain Departament de Biologia Evolutiva Ecologia i Ciències AmbientalsFacultat de BiologiaUniversitat de Barcelona08028 BarcelonaSpain Laboratory for Environmental and Life Sciences University of Nova GoricaNova Gorica 5000Slovenia Biomedical Research Institute Sant Pau(IIB Sant Pau) Sant Antoni Ma Claret 16708025 BarcelonaSpain

histidine-rich peptides confer self-assembling properties to recombinant proteins through the supramolecular coordination with divalent cations.This fact allows the cost-effective,large-scale generation of microscopic and macroscopic protein materials with intriguing biomedical properties.Among such materials,resulting from the simple bioproduction of protein building blocks,homomeric nanoparticles are of special value as multivalent interactors and drug carriers.Interestingly,we have here identified that the assembly of a given his-tagged protein might render distinguishable categories of self-assembling protein nanoparticles.This fact has been scrutinized through the nanobody-containing fusion proteins EM1-GFP-h6 and A3C8-GFP-h6,whose biosynthesis results in two distinguishable populations of building blocks.In one of them,the assembling and disassembling is controllable by cations.however,a second population immediately self-assembles upon purification through a non-regulatable pathway,rendering larger nanoparticles with specific biological properties.The structural analyses of both model proteins and nanoparticles revealed important conformational variability in the building blocks.This fact renders different structural and functional categories of the final soft materials resulting from the participation of energetically unstable intermediates in the oligomerization process.These data illustrate the complexity of the hismediated protein assembling in recombinant proteins but they also offer clues for a better design and refinement of protein-based nanomedicines,which,resulting from biological fabrication,show an architectonic flexibility unusual among biomaterials.

关键词： recombinant proteins self-assembling protein materials nanoparticles biomaterials

Population dynamics of three lizard species from the genus Sceloporus:short-term changes in demographic parameters

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Integrative Zoology 2019年第6期14卷 542-560页

作者： Selene VARGAS-GARCÍA Víctor ARGAEZ Israel SOLANO-ZAVALETA j.jaime ZÚÑIGA-VEGA Graduate Program in Biological Sciences National Autonomous University of MexicoUniversity CityMexico CityMéxico Department of Ecology and Natural Resources Faculty of SciencesNational Autonomous University of MexicoUniversity CityMexico CityMéxico.

Most demographic studies focus on numerical changes that occur within populations across years.however,typically studies at an interannual scale do not provide information on the particular times of the year(particular months or seasons)when rates of survival,recruitment,or migration increase or decrease due to physiological,behavioral or ecological processes.These monthly or seasonal changes in demographic parameters may lead to substantial variations in population abundance.In this study,we collected capture-mark-recapture data on 3 species of lizards of the genus Sceloporus(Sceloporus torquatus,Sceloporus grammicus and Sceloporus megalepidurus)found in ecologically similar habitats to examine potential changes in demographic rates among 3 different climatic seasons:rainy,cold-dry and warm-dry seasons.We tested different hypotheses about the effect of these seasons on survival,recruitment of new adults,and temporary emigration.We found that during the season with severe thermal constraints,the cold-dry season,survival of S.torquatus decreased markedly.We also detected a considerable increase in the recruitment rate of S.grammicus during the rainy season,when these lizards are establishing territories and finding mates.In contrast,we found no evidence of intra-annual changes in the rate of temporary emigration.In addition,we calculated abundance and population growth rates for each species and for each season.Our study represents a significant contribution to the understanding of intra-annual demographic variation in lizards.

关键词： abundance recruitment Sceloporus lizards survival temporary emigration