Deficiency of platelet-derived growth factor receptor-α-positive cells in Hirschsprung's disease colon

AIM: To investigate whether the expression of platelet-derived growth factor receptor-α-positive (PDGFRα+)-cells is altered in Hirschsprung’s disease (HD).METHODS: HD tissue specimens (n = 10) were collected at the time of pull-through surgery, while colonic control samples were obtained at the time of colostomy closure in patients with imperforate anus (n = 10). Immunolabelling of PDGFRα+-cells was visualized using confocal microscopy to assess the distribution of these cells, while Western blot analysis was undertaken to quantify PDGFRα protein expression.RESULTS: Confocal microscopy revealed PDGFRα+-cells within the mucosa, myenteric plexus and smooth muscle in normal controls, with a marked reduction in PDGFRα+-cells in the HD specimens. Western blotting revealed high levels of PDGFRα protein expression in normal controls, while there was a striking decrease in PDGFRα protein expression in the HD colon.CONCLUSION: These findings suggest that the altered distribution of PDGFRα+-cells in both the aganglionic and ganglionic HD bowel may contribute to the motility dysfunction in HD.

Vascular endothelial growth factor/platelet-derived growth factor receptor pathway is involved in bone marrow mesenchymal stem cell differentiation and directional migration toward gliomas

BACKGROUND： Vascular endothelial growth factor （VEGF） induces bone marrow-derived mesenchymal stem cell （BMSC） differentiation into vascular endothelial-like cells and promotes BMSC migration toward gliomas. However, the molecular mechanisms by which VEGF induces BMSC differentiation and migration remain poorly understood. OBJECTIVE; To investigate the role of platelet-derived growth factor （PDGF） receptor （PDGFR） in BMSC differentiation and migration induced by VEGE DESIGN, TIME AND SETTING： A parallel, controlled, in vitro experiment was performed at the Molecular Neurobiology ＆ Neural Regeneration and Repairing Laboratory, Anhui Provincial Hospital of Anhui Medical University, China from June 2008 to March 2009. MATERIALS： U87 glioma cells were purchased from Shanghai Institutes for Biological Sciences; mouse anti-human PDGFR and VEGF receptor （VEGFR） monoclonal antibodies were purchased from Peprotech, USA. METHODS： Isolated BMSCs were precultured with neutralizing antibody for VEGFR-1, VEGFR-2, PDGFR-α, and PDGFR-β to block biological activity of related receptors, followed by induced differentiation with 50μg/L VEGF. BMSCs induced with 50μg/L VEGF alone served as the VEGF-induced group. The control group remained untreated. MAIN OUTCOME MEASURES： Cell surface markers were identified by flow cytometry; BMSC surface cytokine receptor expression was detected by reverse transcription-polymerase chain reaction; the Transwell model was used to observe cell migration. RESULTS： After blocking the PDGFR, VEGF did not induce BMSC cell surface marker CD-31 or von Willebrand factor （vWF） expression. However, inhibition with VEGF receptor blocking agents, VEGF induced BMSCs to express CD-31 and vWE Following inhibition of the PDGFR, the number of cells migrating through the polycarbonate membrane Transwell chamber was decreased, as well as the number of BMSCs migrating to glioma cells. However, through the use of VEGF receptor blocking agents, the number of migrating cells remained unchanged. VEGF preculture increased the number of BMSCs migrating to gliomas. CONCLUSION： VEGF interacts with PDGFRs on the BMSC surface to attract BMSC directional migration and induce BMSC differentiation. The VEGF/PDGFR pathway participates in BMSC directional migration to glioma. VEGF pretreatment increased efficiency of BMSC migration to glioma.

KIT and platelet-derived growth factor receptor α wild-type gastrointestinal stromal tumor associated with neurofibromatosis type 1: Two case reports

BACKGROUND Gastrointestinal stromal tumors(GISTs) associated with neurofibromatosis are uncommon compared to their gastrointestinal counterparts. Patients with neurofibromatosis type 1(NF-1) have an increased risk of developing gastrointestinal tumors, including rare types such as GIST.CASE SUMMARY A 60-year-old male Chinese patient was diagnosed with NF-1 10 years ago and presented with upper abdominal discomfort and black stools. Endoscopic ultrasonography and an enhanced abdominal computed tomography scan revealed a mass located 4 cm from the muscular layer of the descending duodenum. A 59-year-old Chinese woman who was diagnosed with NF-1 25 years ago presented with sudden unconsciousness and black stools. Multiple masses in the duodenum were noted by echogastroscopy and an enhanced abdominal computed tomography scan. Both patients presented with cutaneous neurofibromas. The histologic examination of tumors from both patients revealed spindle cells and low mitotic activity. Immunohistochemically, the tumor cells showed strong positivity for KIT(CD117), DOG-1, CD34, and Dehydrogenase Complex Subunit B, and negativity for SMA, desmin, S-100, and β-catenin. None of the six tumors from two patients had KIT exon 9, 11, 13, or 17 or platelet-derived growth factor receptor α exon 12 or 18 mutation, which is a typical finding for sporadic GISTs. None of the six tumors from the two patients had a BRAFV600 E mutation. The patients were alive and well during the follow-up period(range:0.6-5 yr).CONCLUSION There have been only a few previous reports of GISTs associated with NF-1.Although GISTs associated with NF-1 have morphologic and immunohistochemical similarities with GISTs, the pathogenesis, incidence,genetic background, and prognosis are not completely known. A medical history of NF-1 in a patient who has gastrointestinal bleeding or anemia and an intraabdominal mass with nonspecific computed tomography features may help in diagnosing GIST by virtue of the well-known association of these two entities.Molecular genetic studies of cases indicated that GISTs in NF-1 patients have a different pathogenesis than sporadic GISTs.

Expression of NG2 and platelet-derived growth factor receptor alpha in the developing neonatal rat brain

Platelet-derived growth factor receptor alpha （PDGFRct） is a marker of oligodendrocyte precursor cells in the central nervous system. NG2 is also considered a marker of oligodendrocyte precursor cells. However, whether there are differences in the distribution and morphol- ogy of oligodendrocyte precursor cells labeled by NG2 or PDGFRa in the developing neonatal rat brain remains unclear. In this study, by immunohistochemical staining, NG2 positive （NG2＋） cells were ubiquitous in the molecular layer, external pyramidal layer, internal pyramidal layer, and polymorphic layer of the cerebral cortex, and corpus callosum, external capsule, piriform cortex, and medial septal nucleus. NG2~ cells were stellate or fusiform in shape with long processes that were progressively decreased and shortened over the course of brain development. The distribution and morphology of PDGFRct positive （PDGFRa＋） cells were coincident with NG2＋ cells. The co- localization of NG2 and PDGFRu in the cell bodies and processes of some cells was confirmed by double immunofluorescence labeling. Moreover, cells double-labeled for NG2 and PDGFRa were predominantly in the early postnatal stage of development. The numbers of NG2＋/PDGFRa＋ cells and PDGFRa＋ cells decreased, but the number of NG2＋ cells increased from postnatal days 3 to 14 in the developing brain. In addition, amoeboid microglial cells of the corpus callosum, newborn brain macrophages in the normal developing brain, did not express NG2 or PDGFRu, but NG2 expression was detected in amoeboid microglia after hypoxia. The present results suggest that NG2 and PDGFRct are specific markers of oligodendrocyte precursor cells at different stages during early development. Additionally, the NG2 protein is involved in inflammatory and pathological processes of amoeboid microglial cells.

Three-dimensional-arterial spin labeling perfusion correlation with diabetes-associated cognitive dysfunction and vascular endothelial growth factor in type 2 diabetes mellitus rat

BACKGROUND Type 2 diabetes mellitus(T2DM) has been strongly associated with an increased risk of developing cognitive dysfunction and dementia.The mechanisms of diabetes-associated cognitive dysfunction(DACD) have not been fully elucidated to date.Some studies proved lower cerebral blood flow(CBF) in the hippocampus was associated with poor executive function and memory in T2DM.Increasing evidence showed that diabetes leads to abnormal vascular endothelial growth factor(VEGF) expression and CBF changes in humans and animal models.In this study,we hypothesized that DACD was correlated with CBF alteration as measured by three-dimensional(3D) arterial spin labeling(3D-ASL) and VEGF expression in the hippocampus.AIM To assess the correlation between CBF(measured by 3D-ASL and VEGF expression) and DACD in a rat model of T2DM.METHODS Forty Sprague-Dawley male rats were divided into control and T2DM groups.The T2DM group was established by feeding rats a high-fat diet and glucose to induce impaired glucose tolerance and then injecting them with streptozotocin to induce T2DM.Cognitive function was assessed using the Morris water maze experiment.The CBF changes were measured by 3D-ASL magnetic resonance imaging.VEGF expression was determined using immunofluorescence.RESULTS The escape latency time significantly reduced 15 wk after streptozotocin injection in the T2DM group.The total distance traveled was longer in the T2DM group;also,the platform was crossed fewer times.The percentage of distance in the target zone significantly decreased.CBF decreased in the bilateral hippocampus in the T2DM group.No difference was found between the right CBF value and the left CBF value in the T2DM group.The VEGF expression level in the hippocampus was lower in the T2DM group and correlated with the CBF value.The escape latency negatively correlated with the CBF value.The number of rats crossing the platform positively correlated with the CBF value.CONCLUSION Low CBF in the hippocampus and decreased VEGF expression might be crucial in DACD.CBF measured by 3D-ASL might serve as a noninvasive imaging biomarker for cognitive impairment associated with T2DM.

Nerve growth factor in muscle afferent neurons of peripheral artery disease and autonomic function

In peripheral artery disease patients,the blood supply directed to the lower limbs is reduced.This results in severe limb ischemia and thereby enhances pain sensitivity in lower limbs.The painful perception is induced and exaggerate during walking,and is relieved by rest.This symptom is termed by intermittent claudication.The limb ischemia also amplifies autonomic responses during exercise.In the process of pain and autonomic responses originating exercising muscle,a number of receptors in afferent nerves sense ischemic changes and send signals to the central nervous system leading to autonomic responses.This review integrates recent study results in terms of perspectives including how nerve growth factor affects muscle sensory nerve receptors in peripheral artery disease and thereby alters responses of sympathetic nerve activity and blood pressure to active muscle.For the sensory nerve receptors,we emphasize the role played by transient receptor potential vanilloid type 1,purinergic P2X purinoceptor 3 and acid sensing ion channel subtype 3 in amplified sympathetic nerve activity responses in peripheral artery disease.

Impaired pericyte-Müller glia interaction via PDGFRβ suppression aggravates photoreceptor loss in a rodent model of light-induced retinal injury

AIM:To investigate the involvement of pericyte-Müller glia interaction in retinal damage repair and assess the influence of suppressing the platelet-derived growth factor receptorβ(PDGFRβ)signaling pathway in retinal pericytes on photoreceptor loss and Müller glial response.METHODS:Sprague-Dawley rats were exposed to intense light to induce retinal injury.Neutralizing antibody against PDGFRβwere deployed to block the signaling pathway in retinal pericytes through intravitreal injection.Retinal histology and Müller glial reaction were assessed following light injury.In vitro,normal and PDGFRβ-blocked retinal pericytes were cocultured with Müller cell line(rMC-1)to examine morphological and protein expression changes upon supplementation with light-injured supernatants of homogenized retinas(SHRs).RESULTS:PDGFRβblockage 24h prior to intense light exposure resulted in a significant exacerbation of photoreceptor loss.The upregulation of GFAP and p-STAT3,observed after intense light exposure,was significantly inhibited in the PDGFRβblockage group.Fur ther upregulation of cytokines monocyte chemoattractant protein 1(MCP-1)and interleukin-1β(IL-1β)was also observed following PDGFRβinhibition.In the in vitro coculture system,the addition of light-injured SHRs induced pericyte deformation and upregulation of proliferating cell nuclear antigen(PCNA)expression,while Müller cells exhibited neuron-like morphology and expressed Nestin.However,PDGFRβblockage in retinal pericytes abolished these cellular responses to light-induced damage,consistent with the in vivo PDGFRβblockage findings.CONCLUSION:Pericyte-Müller glia interaction plays a potential role in the endogenous repair process of retinal injury.Impairment of this interaction exacerbates photoreceptor degeneration in light-induced retinal injury.

Myeloid neoplasm with eosinophilia and rearrangement of plateletderived growth factor receptor beta gene in children: Two case reports

BACKGROUND Myeloid neoplasm(MN)with eosinophilia and rearrangement of platelet-derived growth factor receptor beta(PDGFRB)shows a good therapeutic response to imatinib in adults.MN is rarely found in children,and the efficacy of imatinib on pediatric patients remain unclear.CASE SUMMARY We report 2 pediatric cases diagnosed with MN with eosinophilia and PDGFRB rearrangement who were treated with imatinib.Case 1 was a 1-year-old girl admitted to the hospital because of“abdominal distension with hyperleukocytosis for 3 mo”.She had leukocytosis,anemia,and eosinophilia(the absolute eosinophil count(AEC)was 8960/μL),and her fluorescence in situ hybridization(FISH)test revealed that PDGFRB rearrangement was detected in 70%of 500 interphase cells.Case 2 was a 2-year-old girl admitted to the hospital because of“recurrent fever and rashes for 1 mo”.Her blood cell count showed an AEC of 3540/μL.The FISH test revealed that PDGFRB rearrangement was detected in 71%of 500 interphase cells.Both patients were diagnosed as MN with eosinophilia and PDGFRB rearrangement.Imatinib was added into their treatment regimen.As expected,complete hematologic remission was achieved after 1 mo of treatment,and symptoms disappeared.CONCLUSION Although MN with eosinophilia and PDGFRB rearrangement usually occurs in adults,it can be found in children.The therapeutic benefits of imatinib in these 2 pediatric patients were consistent with its reported effects in adult patients.

Up and Down Expression of Androgen Receptor, Estrogen Receptor beta and Platelet Derived Growth Factor beta by Testosterone in Aortic Vascular Smooth Muscle Tissues

Objectives To investigate the effects of testosterone enanthate (TE) on serum lip- ids and lipoproteins metabolism and the expression of androgen receptor (AR) , estrogen receptor beta ( ER - β) and platelet derived growth factor beta ( PDGFR - β) in aortic vascular smooth muscle tissues (VSMTs). Methods Forty aged male rats were ran- domly divided into 4 groups, group A (placebo group) , group B (2. 5 mg/kg intramuscular injection of TE once a week ) , group C (5.0 mg/kg intramuscular injection of TE once a week ) , group D ( 10. 0 mg/kg intramus- cular injection of TE once a week). All animals were fed freely during 16 - week treatment periods. The ex- pression of AR ,ER - βand PDGFR - β were studied by Western bolt. Results Average serum LDL - C was lower in group D than that in group A ( p < 0. 01 ). Compared with the other groups, average serum TC was also lower in group D (p <0. 05). AR expression in aortic vascular smooth muscle tissues could be regulated by TE: 99.50 ±21.74, 125.38 ±28.68 and 101.98 ± 15.42 for TE concentrations at 2.5 mg/kg, 5.0 mg/kg and 10.0 mg/kg, respectively , the expression of ER - β could be regulated by TE: 92. 34 ± 18. 68, 47. 72 ± 18.12, 82.13 ±23.50, and the expression of PDGFR - β could be regulated as well by TE: 219.70 ±45. 59, 50.16 ±9. 72, 125.36 ±15. 74(Data for AR ,ER-β and PDGFR - β protein band intensity were expressed with x ± s, with control group taken as 100 ).Conclusions This study indicates that androgens have significant effects on serum lipids and lipoprotein metabolism. Testosterone enanthate at 5. 0 mg/kg can stimulate the expression of AR, but inhibite the expres- sion of PDGFR. Testosterone enanthate at the concen- trations of 5. 0 mg/kg and 10. 0 mg/kg can inhibite the expression of ER - β.

Effects of ribozyme targeting platelet-derived growth factor receptor β subunit gene on the proliferation and apoptosis of hepatic stellate cells in vitro

Background Activation and proliferation of hepatic stellate cells (HSC) is essentially involved in the development and progression of hepatic fibrosis. The most potent growth factor for HSC is platelet-derived growth factor receptor (PDGF) and PDGF receptor β subunit (PDGFR-β) is the predominant signal transduction pathyway of PDGF which is overexpressed in activated HSC. This study investigated the cleavage activity of hammerhead ribozyme targeting PDGFR-β mRNA in HSC and the effect on biological characteristics of HSC.Methods Expression vector of anti-PDGFR-β ribozyme was constructed and transfected into rat activated HSC with lipofectamin. The positive cell clones were gained by G418 selection. The expression of PDGFR-β, α-smooth muscle actin, and typeⅠand type Ⅲ collagen were detected by using Northern blot, Western blot and immunocytochemical staining, respectively. The cell proliferation was determined with MTT colorimetric assay. The cell apoptosis was analyzed by using flow cytometry, acridine orange fluorescence vital staining and transmission electron microscopy.Results The expression of PDGFR-β at mRNA and protein level was markedly reduced in ribozyme-transfected HSC by 49%-57% ( P <0.05-0.01). The proliferation and α-smooth muscle actin expression of ribozyme-transfected HSC were significantly decreased ( P <0.05-0.01), and the type Ⅰ and type Ⅲ collagen synthesis were also reduced ( P <0.01). In addition, the proliferative response of ribozyme-transfected HSC to PDGF BB was significantly inhibited. Otherwise, the apoptotic cells were significantly increased in ribozyme-transfected HSC ( P <0.01), and typical apoptotic cells could be found under transmission electron microscopy.Conclusions The anti-PDGFR-β ribozyme effectively cleaved the target RNA and significantly inhibited its expression, which blocked the signal transduction of PDGF at receptor level, inhibited HSC proliferation and collagen synthesis, and induced HSC apoptosis. These results suggest that inhibiting PDGFR-β expression of HSC may be a new target for the therapy of liver fibrogenesis, and ribozyme may be a useful tool for inhibiting PDGFR-β expression.

血清PDGF联合BNP预测非体外循环冠状动脉搭桥术患者术后新发心房颤动的临床价值

目的探讨血小板源性生长因子(PDGF)联合血清脑钠肽(BNP)预测非体外循环冠状动脉搭桥术(OPCABG)患者术后新发心房颤动(房颤)的临床价值。方法选取2021年1月至2023年1月于邯郸市中心医院心血管外科收治的197例择期行OPCABG术的患者作为研究对象。所有患者于术前检测血清PDGF水平(酶联免疫吸附法)和血清BNP水平(放射免疫法)。根据患者术后住院期间是否发生房颤分为新发房颤组(n=37)和非新发房颤组(n=160)。采用受试者工作特性(ROC)曲线评估血清PDGF、BNP对OPCABG患者术后是否新发房颤的预测价值;采用多因素Logistic回归分析探讨OPCABG患者术后新发房颤的影响因素。结果新发房颤组血清BNP、PDGF水平高于非新发房颤组(P<0.05)。新发房颤组患者年龄、右冠状动脉狭窄率、术后主动脉内球囊反搏(IABP)辅助比例、机械通气时间、空腹血糖(FPG)、左心房容积指数(LAVI)均高于非新发房颤组,左室射血分数(LVEF)低于非新发房颤组(P<0.05)。多因素Logistic回归分析显示,右冠状动脉近段狭窄≥75%(OR=2.090,95%CI:1.495~2.922)、BNP≥287.64 pg/ml(OR=2.746,95%CI:1.798~4.193)、PDGF≥398.57μg/L(OR=2.601,95%CI:1.765~3.835)是OPCABG患者术后发生房颤的影响因素(P<0.05)。血清BNP、PDGF预测OPCABG患者术后新发房颤的AUC(95%CI)分别为0.781(0.756~0.818)、0.825(0.797~0.861),两者联合预测的AUC(95%CI)为0.901(0.874~0.935)。结论OPCABG术后新发房颤患者血清PDGF、BNP水平均升高,二者可作为OPCABG患者术后新发房颤的预测指标,且联合检测预测效能更高,可为临床早期治疗提供依据。

冠状动脉旁路移植患者术后疲劳发展轨迹及影响因素研究

目的探讨冠状动脉旁路移植术(coronary artery bypass grafting,CABG)患者术后疲劳发展轨迹及其影响因素。方法采用便利抽样法,选取2022年10月-2023年8月在我院心脏外科行CABG的145例患者为研究,随访过程中剔除18例,最终共纳入124例患者。分别在出院前1 d及出院后1、2、4个月采用一般资料调查表、中文版多维疲劳量表(multidimensional fatigue inventory-20,MFI-20)及Barthel指数评定量表对患者术后疲劳水平进行追踪调查,利用潜类别增长模型(latent class growth model,LCGM)识别潜在的术后疲劳轨迹类别,采用多分类logistic回归分析患者术后疲劳轨迹类别的影响因素。结果患者术后MFI-20得分随时间呈下降趋势(F=310.039,P<0.001),得分从出院前1 d(58.44±8.65)分降至出院后4个月(36.92±9.89)分;最终识别出3种术后疲劳轨迹类别,根据其特征分别命名为中至轻度明显下降组、中度缓慢下降组、重至中度缓慢下降组,分别占比53.2%、32.3%、14.5%。单因素分析显示:有无心肌梗死病史、有无脑卒中病史、NYHA心功能分级、术后ICU停留天数、术后左室射血分数(LVEF)、红细胞计数、血红蛋白、总胆固醇、低密度脂蛋白、日常生活活动能力与术后疲劳轨迹类别有关(均P<0.05);多因素logistic回归分析显示:术后ICU停留天数、有无心肌梗死病史、NYHA心功能分级、有无脑卒中病史、日常生活活动能力是CABG患者术后疲劳轨迹类别的主要影响因素(均P<0.05)。结论CABG患者术后疲劳发展轨迹存在异质性,医护人员应根据不同变化轨迹制定针对性护理措施,积极改善可控因素,缓解患者术后疲劳程度。

生长分化因子15和碱性磷酸酶水平对冠心病患者冠状动脉病变程度的预测价值

目的探讨生长分化因子15(GDF-15)和碱性磷酸酶(ALP)对冠心病(冠状动脉粥样硬化性心脏病)患者冠状动脉病变程度的预测价值。方法选取2021年1月至2023年12月在内蒙古自治区人民医院心血管内科住院的患者140例。根据最终诊断分为冠心病合并糖尿病组(46例)、冠心病组(51例)和对照组(冠状动脉造影检查未见明显狭窄病变的非冠心病患者,43例)。比较3组GDF-15、ALP水平及Gensini评分,3组不同民族构成比和不同民族患者间以上指标的差异。分析GDF-15、ALP水平与冠心病发生风险的关系及二者对冠状动脉病变程度的预测价值。结果冠心病组、冠心病合并糖尿病组GDF-15、ALP水平及Gensini评分均高于对照组,冠心病合并糖尿病组高于冠心病组(均P<0.05)。3组患者不同民族构成比差异无统计学意义(P>0.05)。汉族与蒙古族患者GDF-15、ALP水平和Gensini评分差异均无统计学意义(均P>0.05)。Logistic回归分析结果显示,冠心病发生风险随GDF-15(比值比=2.356,95%置信区间:1.608~3.451,P<0.001)和ALP(比值比=1.117,95%置信区间:1.019~1.225,P=0.019)水平的升高而增加。受试者工作特征曲线分析结果显示,GDF-15、ALP及二者联合预测冠状动脉病变程度的曲线下面积(AUC)分别为0.929、0.796和0.939,二者联合预测的AUC大于单个指标(均P<0.05)。结论冠心病患者GDF-15、ALP表达水平升高,且与糖尿病、冠状动脉病变程度相关,二者联合检测对冠状动脉病变严重程度具有良好预测价值。

微RNA-296、血管内皮生长因子-B的表达与冠心病患者冠脉病变程度的关系

目的 探讨微RNA-296(mi R-296)、血管内皮生长因子-B(VEGF-B)的表达与冠心病(CHD)患者冠脉病变程度的关系。方法 选取2019年1月至2022年11月山东省聊城市第二人民医院收治的93例CHD患者,根据冠状动脉病变支数分为单支病变组38例、双支病变组33例、多支病变组22例,再根据Gensini积分将其分为冠状动脉狭窄(CAS)轻度组30例、中度组34例、重度组29例。采用实时荧光定量聚合酶链式反应检测mi R-296,酶联免疫吸附试验检测血清VEGF-B。通过双萤光素酶报告基因验证mi R-296与VEGF-B的关系。采用Pearson相关性分析CHD患者mi R-296、VEGF-B表达的相关性,采用Spearman相关性分析CHD患者mi R-296、VEGF-B表达与Gensini积分及冠脉病变支数的相关性。结果 多支病变组mi R-296表达低于单支病变组和双支病变组,VEGF-B水平高于单支病变组和双支病变组,且双支病变组mi R-296表达低于单支病变组,VEGF-B高于单支病变组,差异有统计学意义(P<0.05)。重度组mi R-296表达低于轻度组和中度组,VEGF-B水平高于轻度组和中度组,且中度组mi R-296表达低于轻度组,VEGF-B水平高于轻度组,差异有统计学意义(P<0.05)。双萤光素酶报告基因显示,VEGF-B是mi R-296的靶点。Pearson相关性分析显示,CHD患者mi R-296与VEGF-B表达呈负相关(r=-0.731,P<0.05)。Spearman相关性分析显示,CHD患者mi R-296表达与Gensini积分及病变支数呈负相关(rs=-0.719、0.638,P<0.05),VEGF-B表达与Gensini积分及病变支数呈正相关(rs=0.727、0.698,P<0.05)。结论CHD患者mi R-296低表达,VEGF-B高表达,两者与CAS病变程度密切相关。

血清HIF-1α、LP(a)、VEGF、LP-PLA2水平与冠心病病情的相关性研究

目的分析血清低氧诱导因子-1α(HIF-1α)、脂蛋白a[LP(a)]、血管内皮生长因子(VEGF)、脂蛋白相关磷脂酶A2(LP-PLA2)在监测冠心病病情方面的临床意义。方法回顾性分析我院收治的冠心病患者192例,依据冠脉造影检查结果对其进行分组,分为单支、双支、多支冠脉病变组以及轻度、中度以及重度狭窄组;另选健康体检者为对照组;对比不同检查结果下冠心病患者、对照组之间的血清HIF-1α、LP(a)、VEGF、LP-PLA2水平,分析各指标间的差异以及对病情程度的监测意义。结果比较不同冠脉分支组的血清HIF-1α、LP(a)、VEGF、LP-PLA2水平,病变组均高于对对照组,其中多支病变组水平最高,单支病变组最低;不同病情程度的指标水平对比,病变组高于对照组,重度组水平高于中度组,中度组高于轻度组,差异具有统计学意义(P<0.05);ROC曲线分析,血清HIF-1α、LP(a)、VEGF、LP-PLA2评估中重度冠心病的AUC分别为0.865、0.751、0.799、0.782,联合评估AUC为0.887。结论血清HIF-1α、LP(a)、VEGF、LP-PLA2水平变化与冠心病患者病情变化相关,临床可通过检测这4项指标变化评估冠心病患者具体病情。

血清PTX3、GDF-15、IL-17在川崎病患儿中的表达及与冠脉损伤的关系

目的 探讨血清生长分化因子-15(GDF-15)、正五聚蛋白3(PTX3)、白细胞介素-17(IL-17)在川崎病(KD)患儿中的表达及与冠脉损伤的关系。方法 回顾性分析2020年5月至2023年5月郑州大学附属郑州中心医院收治的114例KD患儿为研究对象,根据冠脉损伤情况分为损伤组(48例)和无损伤组(66例),另选取同时期114例健康体检儿童为对照组;根据冠状动脉内径将冠脉损伤患儿分为轻度扩张(21例)、中度扩张(18例)、冠状动脉瘤(9例)3个亚组。比较3组不同冠状动脉扩张程度患儿入院时血清GDF-15、PTX3、IL-17水平,分析入院时血清GDF-15、PTX3、IL-17水平与冠脉损伤及冠状动脉内径的相关性,偏回归分析KD患儿发生冠脉损伤的危险因素,受试者工作特征曲线(ROC)分析入院时血清IL-17、PTX3、GDF-15水平联合诊断KD患儿发生冠脉损伤的价值。结果 损伤组入院时血清GDF-15、PTX3、IL-17水平>无损伤组>对照组(P<0.05)。不同冠状动脉扩张程度患儿入院时血清IL-17、PTX3、GDF-15水平比较:冠状动脉瘤>中度扩张>轻度扩张(P<0.05)。相关性分析显示,入院时血清GDF-15、PTX3、IL-17水平与冠脉损伤、冠状动脉内径呈正相关(P<0.05)。logistic回归分析显示,入院时血清IL-17、PTX3、GDF-15水平为KD患儿发生冠脉损伤的危险因素(P<0.05)。ROC曲线分析显示,入院时血清GDF-15、PTX3、IL-17水平联合诊断KD患儿发生冠脉损伤的曲线下面积(AUC)为0.818,最佳诊断敏感度为93.75%,特异度为69.70%,高于各指标单独诊断(P<0.05)。结论 GDF-15、PTX3、IL-17参与KD患儿发生冠脉损伤过程,且在辅助临床早期诊断KD患儿发生冠脉损伤方面具有较高效能。

血清FGF23对2型糖尿病患者冠状动脉钙化的预测价值

目的评估血清全段成纤维细胞生长因子(FGF23)对2型糖尿病患者冠状动脉钙化的预测价值。方法选择2022年1月至2023年1月门诊及住院的2型糖尿病患者共86例为2型糖尿病患者组,选择年龄、性别匹配的80例健康体检者为对照组。比较两组患者的临床资料,血压、血脂、肾功能、钙磷代谢指标,血清FGF23及冠状动脉钙化发生率等。分析血清FGF23及碱性磷酸酶(AKP)对2型糖尿病患者冠状动脉钙化的预测价值。结果2型糖尿病患者组的糖化血红蛋白(HbA1c)、血清FGF23、收缩压(SBP)、舒张压(DBP)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三脂(TG)、尿蛋白肌酐比值(UACR)、血磷、钙磷乘积、AKP以及冠状动脉钙化发生率均明显高于对照组,高密度脂蛋白胆固醇(HDL-C)低于对照组,差异均有统计学意义(t分别=6.32、5.12、3.65、4.25、5.78、2.47、3.45、5.12、2.45、2.47、3.89,χ^(2)=3.46,t=-2.46,P均<0.05)。多元线性回归分析,logFGF23与吸烟、血磷、AKP、UACR、冠状动脉钙化有相关性(t分别=9.02、5.69、6.35、7.65、12.89,P均<0.05)。受试者工作特征曲线(ROC)结果显示,血清FGF23预测2型糖尿病患者合并冠状动脉钙化的曲线下面积为0.70(95%CI 0.62~0.78),当检测的截点为305.52 pg/mL时,其灵敏度及特异度分别为76.73%及68.12%。血清AKP预测2型糖尿病患者合并冠状动脉钙化的曲线下面积为0.62(95%CI 0.55~0.70),当检测的截点为67.15 mmol/L,其灵敏度及特异度分别为66.52%及58.26%。结论2型糖尿病患者有更高的血清FGF23水平,血清FGF23对2型糖尿病患者合并冠状动脉钙化具有较好的预测价值。

PI、RI 指数结合血清sFlt-1 在子宫肌瘤患者中的诊断作用

目的:探讨超声评价PI和RI结合sFlt-1诊断子宫肌瘤的临床价值。方法:选取2020年1月~2022年8月收治的150例,怀疑患有子宫腺肌病或子宫肌瘤患者作为研究对象,计算PI和RI指数,检测患者血清sFlt-1水平。Logistic回归模型结合ROC曲线评价各指标单独及联合检测对子宫肌瘤诊断的临床价值。结果:子宫肌瘤患者RI及PI参数值均显著低于子宫腺肌病患者,而血清sFlt-1表达水平升高(P<0.001)。子宫动脉超声、血清sFlt-1水平联合检测诊断效能高于单项检测(P<0.05)。结论:子宫动脉超声联合血清sFlt-1检查可提高子宫肌瘤患者诊断的灵敏度和特异性,对于子宫肌瘤患者诊断具有潜在应用价值。

阿托伐他汀对缺血伴非阻塞性冠状动脉粥样硬化性心脏病患者相关细胞因子的影响

目的他汀类药物已被推荐用于缺血伴非阻塞性冠状动脉粥样硬化性心脏病(ischemia and non-obstructive coronary artery disease,INOCA)患者二级预防,本文研究阿托伐他汀治疗对INOCA患者外周血基质细胞衍生因子-1(stromal cell derived factor-1,SDF-1)和血管内皮生长因子(vascular endothelial growth factor,VEGF)短期内的影响。方法选择2020年1月至2020年12月上海市杨浦区市东医院冠状动脉计算机断层扫描血管造影(computed tomography angiography,CTA)或冠状动脉造影提示冠状动脉血管正常或冠状动脉血管狭窄小于50%的100例患者,分成危险因素控制组(Risk组)(50例)和INOCA组(50例),检测阿托伐他汀治疗前后SDF-1和VEGF浓度的变化。结果与危险因素控制组患者相比,INOCA组患者的VEGF浓度差异无统计学意义(t=-0.252,P=0.801);SDF-1浓度较低,差异有统计学意义(t=2.103,P=0.039)。阿托伐他汀治疗后,INOCA组患者的VEGF和SDF-1浓度显著升高,差异有统计学意义(t=-3.850,P=0.000;t=-2.313,P=0.025),且治疗后两者表达呈正相关(r=0.415,P=0.003)。结论阿托伐他汀治疗INOCA患者可使VEGF与SDF-1浓度短期内升高,进而协同促进血管增生,改善INOCA患者预后。

The correlation of serum PDGF and Ang-2 contents with atherosclerotic plaque features in patients with coronary heart disease

Objective:To study the correlation of serum PDGF and Ang-2 contents with atherosclerotic plaque features in patients with coronary heart disease.Methods: A total of 80 patients with coronary heart disease who were treated in our hospital between January 2013 and April 2016 were collected as the observation group, and 50 healthy subjects who received medical examination in our hospital during the same period were selected as the normal control group. Serum PDGF and Ang-2 contents of two groups of patients were detected, and the observation group were further divided into the high PDGF group and low PDGF group (n = 40) as well as the high Ang-2 group and low Ang-2 group (n = 40) according to the median of PDGF and Ang-2 contents. Ultrasonic contrast technology was used to assess the atherosclerotic plaque characteristics in patients with coronary heart disease.Results: Serum PDGF and Ang-2 contents of observation group were significantly higher than those of control group;ultrasound parameters P and AUC levels of high PDGF group were higher than those of low PDGF group while Tp and MTT levels were lower than those of low PDGF group;ultrasound parameters P and AUC levels of high Ang-2 group were higher than those of low Ang-2 group while Tp and MTT levels were lower than those of low Ang-2 group.Conclusion:Serum PDGF and Ang-2 contents increase in patients with coronary heart disease and are negatively correlated with the atherosclerotic plaque stability.