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Research Progress on the Relationship between Coronary Artery Calcification and Chronic Renal Failure

Chinese Medical Journal 2018年第5期131卷 608-614页

作者： Jun Lai gael akindavyi Qiang Fu Zhi-Liang Li Hui-Min Wang Li-Hua Wen Department of Cardiology Zhujiang Hospital Southern Medical University Guangzhou Guangdong 510280 China

Objective： Coronary artery calcification （CAC） is thought to be a controlled metabolic process that is very similar to the formation of new bone. In patients with chronic renal failure （CRF）, CAC is very common, and CAC severity correlates with the deterioration of renal lilnction. We summarized the current understanding and emerging findings of the relationship between CAC and CRF. Data Sources： All studies were identified by systematically searching PubMed, Embase, and CNKI databases for the terms ＂coronary calcification＂, ＂＇chronic renal failure＂, ＇~vascular smooth muscle cell＂, and their synonyms until September 2017. Study Selection： We examined the titles and abstracts of all studies that met our search strategy thoroughly. The full text of relevant studies was evaluated. Reference lists of retrieved articles were also scrutinized for the additional relevant studies. Results： CRF can accelerate CAC progression. CRF increases the expression of pro-inflamrnatory factors, electrolyte imbalance （e.g., of calcium, phosphorus）, parathyroid hon^none, and uremic toxins and their ability to promote calcification. These factors, through the relevant signaling pathways, trigger vascular smooth muscle cells to transtbrm into osteoblast-like cells while inhibiting the reduction of vascular calcification factors, thus inducing further CAC. Conclusions： Coronary heart disease in patients with CRF is due to multiple factors. Understanding the mechanism of CAC can help interventionists to protect the myocardium and reduce the prevalence of coronary heart disease and mortality.

关键词： Chronic Renal Failure Coronary Calcification Vascular Smooth Muscle Cell

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真武汤可延缓尿毒症心肌病大鼠心室肥厚

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南方医科大学学报 2019年第1期39卷 113-119页

作者：赖俊吴英智杭丽玮 gael akindavyi 邓婷严全能傅强李志樑南方医科大学珠江医院心内科广东广州510280

目的探讨真武汤对尿毒症心肌病大鼠心室肥厚的作用及可能机制。方法(1)提取SD乳鼠心肌细胞,将其分为对照组及硫酸吲哚酚(indoxyl sulfate, IS)组(10μm刺激),通过[3H]亮氨酸掺入法、Western blot(WB)检测两组细胞蛋白表达情况;(2)将50... 详细信息

目的探讨真武汤对尿毒症心肌病大鼠心室肥厚的作用及可能机制。方法(1)提取SD乳鼠心肌细胞,将其分为对照组及硫酸吲哚酚(indoxyl sulfate, IS)组(10μm刺激),通过[3H]亮氨酸掺入法、Western blot(WB)检测两组细胞蛋白表达情况;(2)将50只SD大鼠随机分成假手术组、模型组、真武汤低(4.5 g/kg)、高剂量干预组(13.5 g/kg),除假手术组外,其他各组均予5/6肾切除术。术后4周,低剂量组及高剂量组分别每天给与真武汤灌胃,假手术组和模型组给予等量蒸馏水灌胃。给药4周后,检测各组大鼠血生化、血浆硫酸吲哚酚水平(IS),心脏及心室重量指数、心脏彩超、心肌组织BNP、p-ERK1/2、p-p38及p-JNK蛋白表达等情况。结果(1)细胞实验中,IS组心肌细胞蛋白质合成速率明显增加,而BNP、p-ERK1/2、p-p38表达均较对照组升高(均P<0.01),而P-JNK蛋白则与对照组相比未见明显差异;(2)与假手术组相比,模型组的血肌酐(SCr)、尿素氮(BUN)、24小时尿蛋白(24hUpro)、IS及左室质量指数(LVMI)、全心质量指数(HMI)均升高(P<0.01);左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)均有显著降低,左心室前壁收缩末期厚度(LVAWS)、左心室前壁舒张末期厚度(LVAWD)、左心室后壁收缩期厚度(LVPWS)、左心室后壁舒张期厚度(LVPWD)则明显增厚;HE染色示心肌细胞肥大。心肌组织蛋白BNP、p-ERK1/2、p-p38、p-jnk的表达均升高(P<0.01);(3)低剂量和高剂量组SCr、BUN、24 hUpro及IS较模型组降低(P<0.05),LVMI及HMI在低剂量、高剂量组中下降;LVESD、LVEDD、LVPWS、LVAWS、LVAWD等在高剂量组中改善较为显著,心肌组织蛋白BNP、p-ERK1/2、pp38及p-JNK的表达下调。结论真武汤可降低尿毒症心肌病大鼠血浆IS水平,进而延缓IS对心肌肥厚作用,延缓心室重构。

关键词：真武汤心肌肥厚心室重构尿毒症心肌病

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Gingerol improves cardiac function in rats with cardiorenal syndrome via inhibiting fibrosis

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South China Journal of Cardiology 2021年第2期22卷 135-144,F0003页

作者： DENG Ting WU Ying-zhi akindavyi gael LIU Yun-feng LI Zhi-liang FU Qiang DENG Xiao-fang Department of Cardiovascular Disease First Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou510006China Department of Cardiology Zhujiang HospitalSouthern Medical UniversityGuangzhou510280China Department of Cardiology South China hospital of Shenzhen UniversityShenzhen518110China Department of Cardiology Shenzhen HospitalSouthern Medical UniversityShenzhen518110China Department of neonatology Guangdong Provincial People's HospitalGuangzhou510080China

Background Cardiorenal syndrome(CRS)is a clinical syndrome with a complex mechanism,and there is currently no specific *** was confirmed to possess anti-inflammatory,antioxidant and cardiotonic properties as cardiovascular pharmacological ***,in vivo studies have yet to prove that it can improve cardiac function and inhibit fibrosis in rats with cardiorenal *** In this study,34 male Sprague-Dawley(SD)rats were randomly divided into control(n=9),model(n=12)and gingerol groups(n=13).The model and the gingerol groups underwent ligation of the left anterior descending coronary artery and 5/6 subtotal nephrectomy to construct a type 2 cardiorenal syndrome rat *** rats in gingerol group were injected intraperitoneally with 50 mg/kg *** same amount of saline was administered to both the control and the model *** 4 weeks of treatment,the rat cardiac function and myocardial fibrosis were evaluated by cardiac ultrasound and blood *** Biochemical results showed that the brain natriuretic peptide(BNP)levels of gingerol group decreased(P<0.05).Cardiac ultrasound revealed that gingerol improved cardiac systolic function and ventricular remodeling(P<0.05).The systolic function of the model group was significantly decreased compared with the control *** staining confirmed that the fibrosis area in the model group was significantly augmented than that in the control group,while the area of fibrosis in the gingerol group was diminished compared to the model group(P<0.01).Moreover,immunofluorescence showed that compared with the control group,the expression of collagen 1,TGF-β1 andα-SMA was significantly increased in the model group,and both collagen deposition and the expression of collagen I,TGF-β1 andα-SMA decreased in gingerol *** revealed that the expression of collagen 1 andα-SMA was significantly increased in the model group compared with the control group,while

关键词： gingerol cardiorenal syndrome fibrosis heart function

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炎症小体Nlrp3通路激活在尿毒症心肌病模型小鼠左心室重构的作用

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实用医学杂志 2020年第9期36卷 1172-1177页

作者：文俪桦傅强严全能李晚泉贺不凡 gael akindavyi 李志樑南方医科大学珠江医院心内科广州510280 南方医科大学深圳医院心内科广东深圳518101 佛山市三水区人民医院广东佛山528100

目的探讨Nlrp3炎症小体通路激活与尿毒症心肌病小鼠左心室重构的关系及可能机制。方法将20只小鼠随机分为假手术组和模型组。模型组予5/6肾脏切除术。两组小鼠术后第8周行心脏超声检查,检测血肌酐(Scr)、血尿素氮(BUN)、血浆硫酸吲哚酚(... 详细信息

目的探讨Nlrp3炎症小体通路激活与尿毒症心肌病小鼠左心室重构的关系及可能机制。方法将20只小鼠随机分为假手术组和模型组。模型组予5/6肾脏切除术。两组小鼠术后第8周行心脏超声检查,检测血肌酐(Scr)、血尿素氮(BUN)、血浆硫酸吲哚酚(indoxyl sulfate,IS)水平,心肌组织ANP、BNP、Nlrp3、Pro-caspase1、IL-1β和p-P65蛋白表达。培养小鼠巨噬细胞RAW264.7,分为对照组及IS组,检测两组细胞Nlrp3、Pro-caspase1和IL-1β蛋白表达。结果与假手术组相比,模型组小鼠Scr、BUN和IS水平均升高(P<0.05);左心室前壁舒张末期厚度(LVAWd)和左心室后壁舒张末期厚度(LVPWd)增厚,射血分数(EF)和短轴缩短率(FS)降低。更进一步,左心室等容舒张时间和E/A上升,LVFS/MPI下降。HE染色可见心肌细胞肥大。模型组心肌组织ANP、BNP、Nlrp3、Pro-caspase1、IL-1β和p-P65蛋白表达均上调。IS刺激小鼠巨噬细胞Nlrp3、Pro-caspase1和IL-1β蛋白表达均上调。以上结果均具有统计学意义。结论尿毒症心肌病小鼠左心室肥厚与血浆IS水平上调密切相关,可能与NF-κB信号通路激活炎症小体Nlrp3高度相关。

关键词： Nlrp3 炎症小体尿毒症心肌病左室重构

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高通量技术筛选主动脉夹层生物标志物的研究

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临床心血管病杂志 2021年第10期37卷 952-958页

作者：傅强邓小芳 akindavyi gael 刘云峰王慧敏邓钰莹李志樑邓婷南方医科大学深圳医院心内科广东深圳518110 南方医科大学珠江医院心内科广东省人民医院新生儿科深圳大学平湖医院心内科广州中医药大学第一附属医院心内科

目的:通过iTRAQ联合Label-free法筛选主动脉夹层潜在诊断标志物。方法:入选急性主动脉夹层及对照组(急性冠状动脉综合征)血清各50例。将两组患者中各15例血清标本用于iTRAQ及Label-free分析筛选表达差异蛋白。对所有收集血清进行差异蛋... 详细信息

目的:通过iTRAQ联合Label-free法筛选主动脉夹层潜在诊断标志物。方法:入选急性主动脉夹层及对照组(急性冠状动脉综合征)血清各50例。将两组患者中各15例血清标本用于iTRAQ及Label-free分析筛选表达差异蛋白。对所有收集血清进行差异蛋白的免疫吸附测定(ELISA)验证。结果:两组血清标本使用iTRAQ方法共鉴定出84种差异表达蛋白质,Label-free方法共鉴定有或无差异蛋白20种。通过Panther软件进行生信分析与主动脉夹层发病机制9种相关蛋白作为候选生物标志物。进行ELISA验证后得出2种差异蛋白Lumican、PI16有统计学差异,且特异性和敏感性较高。结论:蛋白Lumican、PI16可能成为主动脉夹层潜在的诊断标志物。

关键词：主动脉夹层蛋白质组学 iTRAQ Label-free Lumican PI16

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4例顽固性室性心动过速患者行ECMO+心外膜射频消融的术中护理

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护理学报 2020年第7期27卷 55-57页

作者：王玉珊陈健聪付晓华冷坷何维娟 akindavyi gael 南方医科大学珠江医院广东广州510282 暨南大学附属第一医院广东广州510630

目的总结4例顽固性室性心动过速患者在静脉-动脉体外肺膜氧合(VA-ECMO)辅助下行心包穿刺心外膜射频消融术的术中护理经验。方法4例患者在心血管内科、ICU、麻醉科、介入手术室、护理等多学科团队协作下,术前制定周密的手术方案、应急预... 详细信息

目的总结4例顽固性室性心动过速患者在静脉-动脉体外肺膜氧合(VA-ECMO)辅助下行心包穿刺心外膜射频消融术的术中护理经验。方法4例患者在心血管内科、ICU、麻醉科、介入手术室、护理等多学科团队协作下,术前制定周密的手术方案、应急预案和具体分工,由多学科团队联合提供手术全程监护,术中护理重点包括:注重术中的低体温、出血、溶血及灌注量变化、管道的管理、并发症的预防等问题,严密观察病情和配合手术,加强生命体征监测和出凝血监测,进行管道和穿刺口安全管理。结果4例患者手术成功,术中未发生严重并发症,住院时间为(12.50±2.06)d。1例在术后当天出现心源性休克,及时以CRRT配合治疗后好转出院。结论VA-ECMO能在术中提供血流动力学支持,提高手术成功率。术中护士与团队紧密配合,加强术中体温、出血/溶血、灌注量的监护,实施并发症的预见护理,可为手术提供安全保障。

关键词：顽固性室性心动过速体外肺膜氧合心包穿刺心外膜射频消融术术中护理

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Should we perform decompressive laparotomy during severe acute pancreatitis with intra-abdominal hypertension below 25 mmHg:Only the gut knows

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World Journal of Gastrointestinal Surgery 2024年第5期16卷 1470-1473页

作者： Thibault Vieille Melissa Crotet Celia Turco Paul Monasterolo Hadrien Winiszewski gael Piton Medical Intensive Care Unit Besancon University HospitalBesancon 25000France Intensive Care Unit Vesoul HospitalVesoul 70000France Department of Digestive Surgical Oncology-Liver Transplantation Unit Besancon University HospitalBesancon 25000France Inserm UMRS-938 Centre de Recherche Saint-Antoine(CRSA)Sorbonne UniversitéParis 10041NY212France Intensive Care Unit Nord Franche Comte HospitalTrevenans 90400France

We suggest that during severe acute pancreatitis(SAP)with intra-abdominal hypertension,practitioners should consider decompressive laparotomy,even with intra-abdominal pressure(IAP)below 25 ***,in this setting,non-occlusive mesenteric ischemia(NOMI)may occur even with IAP below this cutoff and lead to transmural necrosis if abdominal perfusion pressure is not promptly *** report our experience of 18 critically ill patients with SAP having undergone decompressive laparotomy of which one third had NOMI while IAP was mostly below 25 mmHg.

关键词： Acute pancreatitis Abdominal compartment syndrome Decompressive laparotomy Mesenteric ischemia Intra-abdominal pressure Abdominal perfusion pressure

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细胞质核苷酸结合寡聚化域样受体蛋白3炎症小体通路激活对硫酸吲哚酚诱导的心肌细胞肥大蛋白表达的影响

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中华高血压杂志 2020年第12期28卷 1134-1141页

作者：傅强刘家超杨镒宇李志樑 gaelakindavyi 刘云峰梁建光文俪桦李晚泉南方医科大学深圳医院心内科广东深圳518101 佛山市三水区人民医院心内科广州市妇女儿童医疗中心PICU 南方医科大学珠江医院心内科

目的探讨硫酸吲哚酚(IS)诱导细胞质核苷酸结合寡聚化域样受体蛋白3(NLRP3)炎症小体通路激活与心肌细胞肥大蛋白表达的关系及可能机制。方法提取原代心肌细胞,分为对照组和IS(10 mmol/L)组,IS干预后检测两组脑钠肽蛋白表达情况。细胞计... 详细信息

目的探讨硫酸吲哚酚(IS)诱导细胞质核苷酸结合寡聚化域样受体蛋白3(NLRP3)炎症小体通路激活与心肌细胞肥大蛋白表达的关系及可能机制。方法提取原代心肌细胞,分为对照组和IS(10 mmol/L)组,IS干预后检测两组脑钠肽蛋白表达情况。细胞计数套盒8(CCK8)法检测IS刺激小鼠单核巨噬细胞白血病细胞(RAW264.7)的最佳刺激浓度和时间。将RAW264.7分为对照组和IS组,Western blot检测NLRP3、含半胱氨酸的天冬氨酸蛋白水解酶-1前体(Pro-caspase 1)、白细胞介素-1β(IL-1β)、IL-18蛋白表达情况。酶联免疫吸附试验(ELISA)法检测对照组和IS组细胞上清液中炎症因子IL-18和IL-1β水平。将巨噬细胞培养基上清液与心肌细胞直接共培养,分为空白对照组、巨噬细胞培养基组、巨噬细胞培养基+IS组,检测各组NLRP3、Pro-caspase 1、IL-1β、IL-18、脑钠肽蛋白表达情况。结果IS刺激原代心肌细胞后,心房钠尿肽(ANP)和脑钠肽蛋白表达显著上调。由CCK8法检测发现IS刺激RAW264.7的最佳浓度是15 mmol/L,最佳干预时间为3 h。IS刺激RAW264.7后,与对照组相比炎症相关蛋白NLRP3、Pro-caspase 1、IL-1β、IL-18表达明显增加(均P<0.05)。通过ELISA法检测发现IS组巨噬细胞培养基上清液中炎症因子IL-1β和IL-18水平较对照组显著增加。在直接共培养实验中发现IS+巨噬细胞培养基组与空白对照组和巨噬细胞培养基组相比,NLRP3、Pro-caspase 1、IL-1β、IL-18、ANP和脑钠肽蛋白表达显著上调(均P<0.05)。结论IS可诱导NLRP3炎症小体活化,促进心肌细胞肥大蛋白表达。

关键词：细胞质核苷酸结合寡聚化域样受体蛋白3 炎症小体硫酸吲哚酚心肌肥大尿毒症心肌病

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Acute Kidney Injury in the Nephrology Department of the Brazzaville University Hospital: Epidemiological, Clinical and Evolutionary Aspects

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Open Journal of Nephrology 2024年第2期14卷 196-215页

作者： Daniel Tony Eyeni Sinomono gael Honal Mahoungou Eric Gabdzali Ngabé Audrey Missamou Mavi Bouloupy Richard Loumingou Department of Nephrology Brazzaville University Hospital Brazzaville Congo Department of Nephrology Adolphe Ciss General Hospital Pointe Noire Congo

Introduction: Acute kidney injury (AKI) is defined as a sudden and reversible deterioration in renal function. It is a life-threatening condition in hospitalized patients. Our objectives were to determine the prevalence of AKI in a nephrology department, list the causes, describe the evolutionary profile and identify the factors associated with death. Patients and Methods: We reviewed the records of patients hospitalised between 1 January 2016 and 31 October 2020 in the nephrology department of Brazzaville University Hospital. We included patients aged at least 18 years whose discharge diagnosis included the item AKI. Study variables were socio-demographic data, clinical and paraclinical signs, stage and type of AKI, etiology and evolutionary profile. Results: Of the 1823 patients hospitalised, 244 (13.38%) were hospitalised for AKI. Of these, 60.2% were boys and 39.8% girls, with an average age of 47 19 years. The average consultation time was 10 6.5 days. AKI was stage 3 in 69.57% of cases. It was functional, organic and obstructive in the order of 55.28%, 36.02% and 8.69%. Dialysis was indicated in 62 patients (38.51%) and performed in 24 patients (14.9%). In-hospital mortality was 27.95%, with an average hospital stay of 9.6 5.8 days. Metabolic acidosis and anemia were the main causes of death in 14.28% and 4.35% of patients respectively. Factors associated with death were male sex, socioeconomic level, coma, indication for dialysis and absence of dialysis, with a p Conclusion: AKI is more common in young adult males. Mortality is relatively low. Improving prognosis requires early management and access to dialysis.

关键词： AKI Epidemiology Diagnosis Evolution Brazzaville

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A Budd-Chiari Syndrome Due to C Protein Deficiency: A Case Report at YaoundéGeneral Hospital (Cameroon)

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Open Journal of Gastroenterology 2024年第4期14卷 117-124页

作者： Antonin Wilson Ndjitoyap Ndam Gilles gael Aghoagni Gouajio Armel Awana Tenone Danah Larry Tangie Ngek Mathurin Kowo Firmin Andoulo Ankouane Elie Claude Ndjitoyap Ndam Department of Internal Medicine Faculty of Medicine and Biomedical Sciences University of Yaoundé 1 Yaoundé Came-roon Department of Internal Medicine and Peadiatrics Faculty of Health Sciences University of Buéa Buéa Cameroon Department of Biomedical Sciences Faculty of Sciences University of Ngaoundéré Ngaoundéré Cameroon

Primary Budd-Chiari syndrome (BCS) is a spontaneously fatal disease characterized by an obstruction of the hepatic venous outflow tract due to thrombosis or a primary disease of the venous wall. The primary form of BCS is extremely rare. This is a disease mainly affecting young adults of both sexes. Clinical manifestations are variable;they can be asymptomatic, acute, or subacute but mostly chronic. Several causes have been identified, such as myeloproliferative syndrome, antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria, and inherited thrombotic disorders. Data on primary BCS in Sub-Saharan Africa is rare as most publications available are case reports. In these reports, the causes are unknown with poor prognosis in most cases often leading to patient death. We herein present a case report of a male patient diagnosed with a primary BCS at Yaoundé General Hospital (Cameroon) caused by a Protein C deficiency who presented with ascites decompensating liver cirrhosis. Treatment was based on anticoagulants, diuretics and laxatives administration. Two years after the diagnosis, the patient is alive with clinical and paraclinical improvement.

关键词： Budd-Chiari Syndrome Hepatic Veins Liver Cirrhosis Protein C Deficiency Cameroon

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