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Feasibility of Scanopelvimetry in the medical Imaging department of the university hospital of Point “G”.

Open Journal of medical Imaging 2022年第3期12卷 157-164页

作者： Abdoulaye Koné Moussa Konaté Youssouf Koné Moussa Traore Youssouf Diawara Ibrahima Coulibaly Ouncoumba Diarra Fatoumata Kalapo Amadou Doumbia Kassim Sidibe Cheick Oumar Touré Oumar Aba Ata Mody A. Camara Mamadou Sima Coulibaly Salia Mahamadou Diallo Adama Diaman Keita Siaka Sidibé Faculty of Medicine and Odontostomatology Bamako Mali medical Imaging department of the university hospital of Point G Bamako Mali Radiology department of the Jacques Boutard hospital Saint-Yrieix-la-Perche France medical Imaging department of GABRIEL TOURE hospital Bamako Mali Radiology department of CSREF Commune III Bamako Mali medical Imaging Service Health Center of Ref Commune VI Bamako Mali DCSSA Kati Mali medical Imaging Service Health Center of Ref Commune IV Bamako Mali medical Imaging Service of the Mali hospital Bamako Mali. Surgery of Gynecology-Obstetrics CHU Point G Bamako Mali medical Imaging department CHU BSS Kati Mali

Purpose: The purpose of our study was to describe the technique of scanopelvimetry used in the radiology department of the Point G university hospital, to specify the indications of scanopelvimetry in the department and to evaluate the cost of radiopelvimetry. Patients and Method: This was a prospective, cross-sectional study that took place over a 12-month period from January 1 to December 31, 2018. It focused on pregnant women in whom scanopelvimetry was performed in the medical imaging department of Point G university hospital during the study period. Results: Out of 8615 CT examinations performed in the radiology department, we collected 65 cases of scanopelvimetry, i.e., 0.7% of the CT examinations. Primigravida and paucigravida dominated the study (40% each). In 60% of the pregnant women the height was less than 150 cm. The most frequent indication for CT scanning was clinical pelvic narrowing (50%). In 80% of the cases, the scanopelvimetry was performed after 37 weeks of amenorrhea. A predominance of narrowing of the superior strait was noted (40%). 4.6% of the pregnant women had a Magnin index of less than 20. CT scanopelvimetry is a feasible examination in our context but the level of demand is low because of the high cost of the examination (49500 fca). Conclusion: In light of the results obtained, we can say that CT pelvimetry allows us to predict the probable route of delivery and thus we can reduce the risk of fetomaternal morbidity and mortality to improve maternal and child health.

关键词： Scanopelvimetry Prognosis Magnin Index Delivery

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Effect of cytochrome P4502C19(CYP2C19)gene polymorphism and clopidogrel reactivity on long term prognosis of patients with coronary heart disease after PCI

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Journal of Geriatric Cardiology 2024年第1期21卷 90-103页

作者： Cheng-Yan HU Yan-Ling WANG Zhen-Xing FAN Xi-Peng SUN Shuai WANG Zhi LIU department of Geriatrics Fu Xing HospitalCapital Medical UniversityBeijingChina department of Cardiology Xuanwu Hospital Capital Medical UniversityBeijingChina Emergency department of Xuanwu hospital Capital Medical UniversityBeijingChina

Objective To investigate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity and its association with longterm clinical outcome in patients with coronary heart disease(CHD)undergoing percutaneous coronary intervention(PCI).Methods In total,675 patients were enrolled.Based on the platelet inhibition rate,patients were categorized into two groups:clopidogrel low responsiveness(CLR)and normal clopidogrel responsiveness(NCR).The CLR group was divided into ticagrelor and clopidogrel group based on the antiplatelet drugs used in the follow-up treatment.Patients were classified into three groups(normal metabolizer,intermediate metabolizer,and poor metabolizer)based on the CYP2C19 genotype.We aimed to evaluate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity.The cumulative rates of 12-month all-cause deaths,major adverse cardiovascular events(MACCEs),and bleeding events were calculated.Results CLR was observed in 44.4%of the overall population.Significant differences were observed in the platelet inhibition rate of clopidogrel among the three metabolic genotypes(P0.05).Conclusions Low response to clopidogrel in CHD patients is correlated with CYP2C19 gene polymorphism.CYP2C19 genotyping combined with platelet reactivity is an independent predictor of 12-months MACCEs in patients with clopidogrel treatment after PCI,which is better than either test alone.

关键词： CYP2C19 drugs PCI

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Clinical features, treatment strategies and outcomes of craniocervical junction arteriovenous fistulas: a cohort study of 193 patients

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Stroke & Vascular Neurology 2024年第1期9卷 18-29页

作者： Yongjie Ma Zihao Song Yinqing Wang Jiachen Wang Chuan He Guilin Li Peng Zhang Tao Hong Liyong Sun Peng Hu Ming Ye Hongqi Zhang department of Neurosurgery Xuanwu hospital Capital medical university

Background Craniocervical junction(CCJ)arteriovenous fistulas(AVFs)are rare.The current treatment strategies for AVFs with different angioarchitecture need to be clarified.The present study aimed to analyse the correlation between angioarchitecture and clinical characteristics,share our experience in treating this disease and identify risk factors associated with subarachnoid haemorrhage(SAH)and poor outcomes.Methods A total of 198 consecutive patients with CCJ AVFs from our neurosurgical centre were retrospectively reviewed.The patients were grouped according to their clinical manifestations,and their baseline clinical characteristics,angioarchitecture,treatment strategies and outcomes were summarised.Results The patients’median age was 56 years(IQR 47–62 years).The majority of patients were men with 166(83.8%)patients.The most common clinical manifestation was SAH(52.0%),followed by venous hypertensive myelopathy(VHM)(45.5%).The most common CCJ AVFs type was dural AVF,with 132(63.5%)fistulas.The most frequent fistula location was C-1(68.7%)and dural branch of vertebral artery(70.2%)was the most involved arterial feeders for fistulas.The most common direction of venous drainage was descending intradural drainage(40.9%),followed by ascending intradural drainage(36.5%).Microsurgery was the most common treatment strategy applied for 151(76.3%)patients,15(7.6%)patients were treated with interventional embolisation only,and 27(13.6%)received both interventional embolisation and microsurgical treatment.The learning curve for microsurgery only was analysed by cumulative summation method,and the turning point was the 70th case,and blood loss in post-group was lower than that in pre-group(p=0.034).At the last follow-up,there were 155(78.3%)patients with favourable outcomes(modified Rankin Scale(mRS)<3).Age≥56(OR 2.038,95%CI 1.039 to 3.998,p=0.038),VHM as the clinical manifestation(OR 4.102,95%CI 2.108 to 7.982,p<0.001)and pretreatment mRS≥3(OR 3.127,95%CI 1.617 to 6.047,p<0.001)were significantly associated with poor out

关键词： patients treatment hypertensive

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Mitochondrial transplantation confers protection against the effects of ischemic stroke by repressing microglial pyroptosis and promoting neurogenesis

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Neural Regeneration Research 2024年第6期19卷 1325-1335页

作者： Li Sun Zhaoyan Zhao Jing Guo Yuan Qin Qian Yu Xiaolong Shi Fei Guo Haiqin Zhang Xude Sun Changjun Gao Qian Yang department of Experimental Surgery The Second Affiliated Hospital of Air Force Medical University department of Anesthesiology The Second Affiliated Hospital of Air Force Medical University

Transferring healthy and functional mitochondria to the lateral ventricles confers neuroprotection in a rat model of ischemia-reperfusion injury. Autologous mitochondrial transplantation is also beneficial in pediatric patients with cardiac ischemia-reperfusion injury. Thus, transplantation of functional exogenous mitochondria may be a promising therapeutic approach for ischemic disease. To explore the neuroprotective effect of mitochondria transplantation and determine the underlying mechanism in ischemic stroke, in this study we established a photo-thrombosis-induced mouse model of focal ischemia and administered freshly isolated mitochondria via the tail vein or to the injury site(in situ). Animal behavior tests, immunofluorescence staining, 2,3,5-triphenyltetrazolium chloride(TTC) staining, mRNA-seq, and western blotting were used to assess mouse anxiety and memory, cortical infarct area, pyroptosis, and neurogenesis, respectively. Using bioinformatics analysis, western blotting, co-immunoprecipitation, and mass spectroscopy, we identified S100 calcium binding protein A9(S100A9) as a potential regulator of mitochondrial function and determined its possible interacting proteins. Interactions between exogenous and endogenous mitochondria, as well as the effect of exogenous mitochondria on recipient microglia, were assessed in vitro. Our data showed that:(1) mitochondrial transplantation markedly reduced mortality and improved emotional and cognitive function, as well as reducing infarct area, inhibiting pyroptosis, and promoting cortical neurogenesis;(2) microglial expression of S100A9 was markedly increased by ischemic injury and regulated mitochondrial function;(3) in vitro, exogenous mitochondria enhanced mitochondrial function, reduced redox stress, and regulated microglial polarization and pyroptosis by fusing with endogenous mitochondria; and(4) S100A9 promoted internalization of exogenous mitochondria by the microglia, thereby amplifying their pro-proliferation and anti-inflammatory effects. Taken togeth

关键词： ischemic stroke microglia mitochondria transplantation neurogenesis pyroptosis

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New clinical trial design in precision medicine:discovery,development and direction

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Signal Transduction and Targeted Therapy 2024年第4期9卷 1293-1321页

作者： Xiao-Peng Duan Bao-Dong Qin Xiao-Dong Jiao Ke Liu Zhan Wang Yuan-Sheng Zang department of medical Oncology Changzheng HospitalNaval Medical UniversityShanghaiChina

In the era of precision medicine,it has been increasingly recognized that individuals with a certain disease are complex and different from each other.Due to the underestimation of the significant heterogeneity across participants in traditional"one-sizefits-all"trials,patient-centered trials that could provide optimal therapy customization to individuals with specific biomarkers were developed including the basket,umbrella,and platform trial designs under the master protocol framework.In recent years,the successive FDA approval of indications based on biomarker-guided master protocol designs has demonstrated that these new clinical trials are ushering in tremendous opportunities.Despite the rapid increase in the number of basket,umbrella,and platform trials,the current clinical and research understanding of these new trial designs,as compared with traditional trial designs,remains limited.The majority of the research focuses on methodologies,and there is a lack of in-depth insight concerning the underlying biological logic of these new clinical trial designs.Therefore,we provide this comprehensive review of the discovery and development of basket,umbrella,and platform trials and their underlying logic from the perspective of precision medicine.Meanwhile,we discuss future directions on the potential development of these new clinical design in view of the"Precision Pro","Dynamic Precision",and"Intelligent Precision".This review would assist trial-related researchers to enhance the innovation and feasibility of clinical trial designs by expounding the underlying logic,which be essential to accelerate the progression of precision medicine.

关键词： clinical approval successive

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Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage

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Neural Regeneration Research 2024年第4期19卷 825-832页

作者： Jiatong Zhang Qi Zhu Jie Wang Zheng Peng Zong Zhuang Chunhua Hang Wei Li department of Neurosurgery Nanjing Drum Tower HospitalAffiliated Hospital of Medical SchoolNanjing University department of Neurosurgery Nanjing Drum Tower HospitalClinical College of Nanjing Medical University

The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial dysfunction.Dysfunctional mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging cells.In response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological conditions.Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage.This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control mechanisms.It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.

关键词： mitochondrial biogenesis mitochondrial dynamics mitochondrial dysfunction mitochondrial fission and fusion mitochondrial quality control mitophagy subarachnoid hemorrhage

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Leveraging diverse cell-death patterns to predict the clinical outcome of immune checkpoint therapy in lung adenocarcinoma:Based on muti-omics analysis and vitro assay

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Oncology Research 2024年第2期32卷 393-407页

作者： HONGYUAN LIANG YANQIU LI YONGGANG QU LINGYUN ZHANG department of Radiology Shengjing Hospital of China Medical UniversityShenyangChina department of Nephrology The First Affiliated Hospital of China Medical UniversityShenyangChina department of Clinical Medicine China Medical UniversityShenyangChina department of medical Oncology The First Hospital of China Medical UniversityShenyangChina

Advanced LUAD shows limited response to treatment including immune therapy.With the development of sequencing omics,it is urgent to combine high-throughput multi-omics data to identify new immune checkpoint therapeutic response markers.Using GSE72094(n=386)and GSE31210(n=226)gene expression profile data in the GEO database,we identified genes associated with lung adenocarcinoma(LUAD)death using tools such as“edgeR”and“maftools”and visualized the characteristics of these genes using the“circlize”R package.We constructed a prognostic model based on death-related genes and optimized the model using LASSO-Cox regression methods.By calculating the cell death index(CDI)of each individual,we divided LUAD patients into high and low CDI groups and examined the relationship between CDI and overall survival time by principal component analysis(PCA)and Kaplan-Meier analysis.We also used the“ConsensusClusterPlus”tool for unsupervised clustering of LUAD subtypes based on model genes.In addition,we collected data on the expression of immunomodulatory genes and model genes for each cohort and performed tumor microenvironment analyses.We also used the TIDE algorithm to predict immunotherapy responses in the CDI cohort.Finally,we studied the effect of PRKCD on the proliferation and migration of LUAD cells through cell culture experiments.The study utilized the TCGA-LUAD cohort(n=493)and identified 2,901 genes that are differentially expressed in patients with LUAD.Through KEGG and GO enrichment analysis,these genes were found to be involved in a wide range of biological pathways.The study also used univariate Cox regression models and LASSO regression analyses to identify 17 candidate genes that were best associated with mortality prognostic risk scores.By comparing the overall survival(OS)outcomes of patients with different CDI values,it was found that increased CDI levels were significantly associated with lower OS rates.In addition,the study used unsupervised cluster analysis to divide 115 LUAD patients into two distinct cluste

关键词： Lung adenocarcinoma Programmed cell death Iron-death Drug sensitivity Cancer therapy

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Arginine methylation of ALKBH5 by PRMT6 promotes breast tumorigenesis via LDHA-mediated glycolysis

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Frontiers of Medicine 2024年第2期18卷 344-356页

作者： Xue Han Chune Ren Aifang Jiang Yonghong Sun Jiayi Lu Xi Ling Chao Lu Zhenhai Yu department of Reproductive Medicine Affiliated Hospital of Weifang Medical UniversityWeifang261053China department of Pathology Affiliated Hospital of Weifang Medical UniversityWeifang261053China

ALKBH5 is a master regulator of N6-methyladenosine(m6A)modification,which plays a crucial role in many biological processes.Here,we show that ALKBH5 is required for breast tumor growth.Interestingly,PRMT6 directly methylates ALKBH5 at R283,which subsequently promotes breast tumor growth.Furthermore,arginine methylation of ALKBH5 by PRMT6 increases LDHA RNA stability via m6A demethylation,leading to increased aerobic glycolysis.Moreover,PRMT6-mediated ALKBH5 arginine methylation is confirmed in PRMT6-knockout mice.Collectively,these findings identify a PRMT6-ALKBH5-LDHA signaling axis as a novel target for the treatment of breast cancer.

关键词： PRMT6 ALKBH5 N6-methyladenosine glycolysis tumor growth

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SENP3 Promotes Mantle Cell Lymphoma Development through Regulating Wnt10a Expression

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Current medical Science 2024年第1期44卷 134-143页

作者： Yan-ni MA Yun-ding ZOU Zhi-long LIU Gui-xian WU Yuan-ze ZHOU Cheng-xin LUO Xiang-tao HUANG Ming-ling XIE Shuang-nian XU Xi LI department of Hematology Southwest HospitalThird Military Medical University(Army Medical University)Chongqing 400038China department of Hematology the Third Affiliated Hospital(Daping Hospital)Third Military Medical University(Army Medical University)Chongqing 400042China

Objective SUMO-specific protease 3(SENP3),a member of the SUMO-specific protease family,reverses the SUMOylation of SUMO-2/3 conjugates.Dysregulation of SENP3 has been proven to be involved in the development of various tumors.However,its role in mantle cell lymphoma(MCL),a highly aggressive lymphoma,remains unclear.This study was aimed to elucidate the effect of SENP3 in MCL.Methods The expression of SENP3 in MCL cells and tissue samples was detected by RT-qPCR,Western blotting or immunohistochemistry.MCL cells with stable SENP3 knockdown were constructed using short hairpin RNAs.Cell proliferation was assessed by CCK-8 assay,and cell apoptosis was determined by flow cytometry.mRNA sequencing(mRNA-seq)was used to investigate the underlying mechanism of SENP3 knockdown on MCL development.A xenograft nude mouse model was established to evaluate the effect of SENP3 on MCL growth in vivo.Results SENP3 was upregulated in MCL patient samples and cells.Knockdown of SENP3 in MCL cells inhibited cell proliferation and promoted cell apoptosis.Meanwhile,the canonical Wnt signaling pathway and the expression of Wnt10a were suppressed after SENP3 knockdown.Furthermore,the growth of MCL cells in vivo was significantly inhibited after SENP3 knockdown in a xenograft nude mouse model.Conclusion SENP3 participants in the development of MCL and may serve as a therapeutic target for MCL.

关键词： mantle cell lymphoma SENP3 cell proliferation apoptosis

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HSP110 aggravates ischemia-reperfusion injury after liver transplantation by promoting NF-κB pathway

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Hepatobiliary & Pancreatic Diseases International 2024年第4期23卷 344-352页

作者： Qing-Zhi Hu Zhen-Rui Cao Wei-Xiong Zheng Min-Jie Zhao Jun-Hua Gong Cong Chen Zhong-Jun Wu Rui Tao department of Hepatobiliary Surgery Bishan Hospital of Chongqing Medical UniversityChongqing 402760China department of Cardiothoracic Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China c department of Hepatobiliary Surgery the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016China department of Hepatobiliary Surgery the Second Affiliated Hospital of Chongqing Medical UniversityChongqing 400010China

Background:Ischemia-reperfusion injury(IRI)poses a significant challenge to liver transplantation(LT).The underlying mechanism primarily involves overactivation of the immune system.Heat shock protein 110(HSP110)functions as a molecular chaperone that helps stabilize protein structures.Methods:An IRI model was established by performing LT on Sprague-Dawley rats,and HSP110 was silenced using siRNA.Hematoxylin-eosin staining,TUNEL,immunohistochemistry,ELISA and liver enzyme analysis were performed to assess IRI following LT.Western blotting and quantitative reverse transcription-polymerase chain reaction were conducted to investigate the pertinent molecular changes.Results:Our findings revealed a significant increase in the expression of HSP110 at both the mRNA and protein levels in the rat liver following LT(P<0.05).However,when rats were injected with siRNAHSP110,IRI subsequent to LT was notably reduced(P<0.05).Additionally,the levels of liver enzymes and inflammatory chemokines in rat serum were significantly reduced(P<0.05).Silencing HSP110 with siRNA resulted in a marked decrease in M1-type polarization of Kupffer cells in the liver and downregulated the NF-κB pathway in the liver(P<0.05).Conclusions:HSP110 in the liver promotes IRI after LT in rats by activating the NF-κB pathway and inducing M1-type polarization of Kupffer cells.Targeting HSP110 to prevent IRI after LT may represent a promising new approach for the treatment of LT-associated IRI.

关键词： Ischemia-reperfusion injury Liver transplantation Inflammation HSP110 Heat shock proteins NF-κB

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