Activation of endogenous neurogenesis and angiogenesis by basic fibroblast growth factor-chitosan gel in an adult rat model of ischemic stroke

Attempts have been made to use cell transplantation and biomaterials to promote cell proliferation,differentiation,migration,and survival,as well as angiogenesis,in the context of brain injury.However,whether bioactive materials can repair the damage caused by ischemic stroke by activating endogenous neurogenesis and angiogenesis is still unknown.In this study,we applied chitosan gel loaded with basic fibroblast growth factor to the stroke cavity 7 days after ischemic stroke in rats.The gel slowly released basic fibroblast growth factor,which improved the local microenvironment,activated endogenous neural stem/progenitor cells,and recruited these cells to migrate toward the penumbra and stroke cavity and subsequently differentiate into neurons,while enhancing angiogenesis in the penumbra and stroke cavity and ultimately leading to partial functional recovery.This study revealed the mechanism by which bioactive materials repair ischemic strokes,thus providing a new strategy for the clinical application of bioactive materials in the treatment of ischemic stroke.

The Combined Effect of Lumenato and Ceramide in the Protection of Collagen Damage Induced by Neutrophils in Normal Human Dermal Fibroblasts

Introduction: Collagen is the primary structural protein fibroblasts produce in the skin’s extracellular matrix. Infiltration of neutrophils into the epidermis and dermis by exposure to UV causes collagen damage and contributes to photoaging. Methods: To study the combined effect of Lumenato and ceramide in preventing collagen-1 damage induced by phagocytes, we used co-cultures of normal human dermal fibroblasts (fibroblasts) and activated human neutrophils. The present study aimed to determine the protective effect of the combination of Lumenato and ceramide on fibroblast collagen-1 damage induced by neutrophils. Results: Lumenato (in the range of 6.5 - 208 μg/ml) or ceramide (in the range of 0.1 - 50 μM) inhibited the production of superoxides and MPO by TNFα-stimulated neutrophils, as well as the production of NO by LPS-stimulated macrophages in a dose-dependent manner. The combinations of Lumenato and ceramide, in low concentrations, caused synergistic prevention of fibroblasts’ collagen-1 damage induced by TNFα-activated neutrophils, detected by fluorescence immunostaining and WB analysis. MPO activity in the supernatants of the co-cultures was also synergistically inhibited. Adding Lumenato or ceramide singly or in combinations in these low concentrations to the fibroblast cultures did not affect the expression of collagen-1. The combinations of Lumenato or ceramide in these concentrations also caused a synergistic inhibition of NO production by activated macrophages. Conclusions: The results suggest that combining low concentrations of Lumenato and ceramide results in synergistic protection against fibroblasts’ collagen-1 damage induced by neutrophils, thus indicating their possible potential for enhanced skin health.

LYVE1+巨噬细胞在RA患者关节滑膜组织中表达变化及对RA-FLS细胞迁移、侵袭、FMT的抑制作用

目的观察淋巴管内皮受体-1(LYVE1)+巨噬细胞在类风湿性关节炎(RA)患者关节滑膜组织中的表达变化及对RA成纤维样滑膜细胞(RA-FLS)迁移、侵袭、向肌成纤维细胞转化(FMT)的抑制作用。方法采用免疫荧光染色法对45例RA患者及45例骨关节炎(OA)患者滑膜组织LYVE1、CD68进行定性、定量检测。取对数生长期人单核白血病细胞THP-1,在培养液中加入LYVE1过表达慢病毒,培养48 h获得表达LYVE1的THP-1细胞,在表达LYVE1的THP-1细胞中加入100 ng/mL的佛波酯(PMA)诱导培养48 h,获得LYVE1+巨噬细胞;另取部分THP-1细胞,仅加入100 ng/mL的PMA诱导培养48 h获得LYVE1-巨噬细胞。取对数生长期人类风湿性关节炎成纤维细胞MH7A分为LYVE1+巨噬细胞组、LYVE1-巨噬细胞组,分别加入LYVE1+巨噬细胞、LYVE1-巨噬细胞,另将仅含培养基的小室设为空白对照组,采用划痕实验观察各组细胞的迁移能力。取MH7A细胞分为A组、B组,分别加入LYVE1+巨噬细胞、LYVE1-巨噬细胞,将仅含培养基小室设为C组,采用Transwell侵袭实验观察各组细胞的侵袭能力。取MH7A细胞分为一组、二组,分别加入LYVE1+巨噬细胞、LYVE1-巨噬细胞,将仅含培养基小室设为空白组,培养48 h时采用实时定量PCR法检测各组MH7A细胞FMT相关基因(COL1A1、fibronectin、α-SMA)的mRNA。结果RA与OA患者滑膜组织中LYVE1、CD68表达位置基本重叠;RA与OA患者滑膜组织LYVE1相对表达量分别为0.319±0.033、1.000±0.159,二者比较,P<0.05。与LYVE1-巨噬细胞组、空白对照组比较,培养24、48 h时LYVE1+巨噬细胞组细胞划痕愈合比低(P均<0.05);与B组、C组比较,培养24 h时A组细胞穿膜细胞数少(P均<0.05);与二组、空白组比较,培养48 h时一组细胞COL1A1 mRNA、fibronectin mRNA、α-SMA mRNA相对表达量少(P均<0.05)。结论RA患者关节滑膜组织中LYVE1+巨噬细胞低表达。LYVE1+巨噬细胞可抑制RA-FLS的迁移、侵袭及FMT。

Lysine demethylase 5B transcriptionally regulates TREM1 in human cardiac fibroblasts

Background:A differential gene,triggering receptor expressed on myeloid cells 1(TREM1),was identified in blood sequencing datasets from myocardial infarction patients and healthy controls.Myocardialfibrosis following myocardial infarction significantly contributes to cardiac dysfunction.Objectives:This study aimed to unveil the intrinsic regulatory mechanism of TREM1 in myocardialfibrosis.Methods:Mimicking pathology by angiotensin II(Ang II)treatment of human cardiacfibroblasts(HCFs),the impacts of TREM1 knockdown on its proliferation,migration,and secretion of the pro-fibrotic matrix were identified.Using the Human Transcription Factor Database(HumanTFDB)website,lysine-specific demethylase 5B(KDM5B)was found to bind to the TREM1 promoter,which was further validated through luciferase reporter and chromatin immunoprecipitation(ChIP).By promoting KDM5B overexpression,its effect on the regulation of TREM1 was examined.Results:TREM1 knockdown suppressed the proliferation,migration,and secretion of the pro-fibrotic matrix in HCFs upon Ang II treatment.KDM5B bound to the TREM1 promoter and upregulated its transcriptional expression.Furthermore,KDM5B overexpression reversed the regulation of the above cellular phenotypes by TREM1 knockdown.Conclusion:This study sheds light on the positive regulation of TREM1 by KDM5B,demonstrating their role in promoting myocardialfibrosis.Thisfinding provides a theoretical foundation for understanding disease pathology and potentially advancing the development of new targeted therapies.

CRABP2 regulates infiltration of cancer-associated fibroblasts and immune response in melanoma

Finding biomarkers for immunotherapy is an urgent issue in cancer treatment.Cellular retinoic acid-binding protein 2(CRABP2)is a controversial factor in the occurrence and development of human tumors.However,there is limited research on the relationship between CRABP2 and immunotherapy response.This study found that negative correlations of CRABP2 and immune checkpoint markers(PD-1,PD-L1,and CTLA-4)were observed in breast invasive carcinoma(BRCA),skin cutaneous melanoma(SKCM),stomach adenocarcinoma(STAD)and testicular germ cell tumors(TGCT).In particular,in SKCM patients who were treated with PD-1 inhibitors,high levels of CRABP2 predicted poor prognosis.Additionally,CRABP2 expression was elevated in cancer-associated fibroblasts(CAFs)at the single-cell level.The expression of CRABP2 was positively correlated with markers of CAFs,such as MFAP5,PDPN,ITGA11,PDGFRα/βand THY1 in SKCM.To validate the tumor-promoting effect of CRABP2 in vivo,SKCM xenograft mice models with CRABP2 overexpression have been constructed.These models showed an increase in tumor weight and volume.Enrichment analysis indicated that CRABP2 may be involved in immunerelated pathways of SKCM,such as extracellular matrix(ECM)receptor interaction and epithelial-mesenchymal transition(EMT).The study suggests that CRABP2 may regulate immunotherapy in SKCM patients by influencing infiltration of CAFs.In conclusion,this study provides new insights into the role of CRABP2 in immunotherapy response.The findings suggest that CRABP2 may be a promising biomarker for PD-1 inhibitors in SKCM patients.Further research is needed to confirm these findings and to explore the clinical implications of CRABP2 in immunotherapy.

Effects of Serum Concentration, Synchronization Time and Confluence on the Cell-Cycle Synchronization Efficiency of Goat Fibroblasts

This study aims to evaluate the effect of serum concentration, synchronization time, and confluence degree on the synchronisation efficiency of goat fibroblast cycle. The results indicated that there was no difference in the percentage of nucleated fibroblasts in the G0/G1 stage between serum concentrations of 0.3% and 0.4% (83.89% and 82.69%, respectively, P > 0.05) as well as between serum concentrations of 0.2% and 0.5% (76.95% and 75.46%, respectively, P > 0.05). The percentage of nucleated fibroblasts in the G0/G1 stage was highest at the concentration of 0.3% and lowest in the control group (83.89% vs. 62.67%, P 0.05). The beneficial effect of high confluence was confirmed by the large percentage of nucleated fibroblasts at the G0/G1 stage. The 60% confluency was significantly lower than the 80% and 100% confluency (73.44%, 86.63%, and 87.17%, respectively, P < 0.05). The results indicate that the goat fibroblast cycle synchronization is the most effective at the serum concentration of 0.3%, 72 hours of synchronization and 100% confluency.

FLS模式康复护理对老年股骨粗隆间骨折切开复位内固定术后患者生活质量的影响分析

目的分析FLS模式康复护理在老年股骨粗隆间骨折切开复位内固定术后的应用效果。方法采用随机数字表法将2022年7月至2023年7月期间在我院接受老年股骨粗隆间骨折切开复位内固定术治疗的131例患者分为两组,对照组(65例)接受常规护理,观察组(66例)接受FLS模式康复护理,对比两组功能评定优良率、护理满意度和遵医行为、生活质量。结果观察组功能评定优良率高于对照组(P<0.05),遵医行为评分在用药、饮食、功能锻炼、并发症预防及遵医行为总分方面均高于对照组(P<0.05),生活质量评分在躯体功能、心理功能、物质生活及社会功能方面均高于对照组(P<0.05),护理满意度均高于对照组(P<0.05)。结论老年股骨粗隆间骨折切开复位内固定术后应用FLS模式康复护理,有助于提升患者遵医行为,可以促进患者肢体功能尽快恢复,改善患者生活质量,患者对护理也更加满意度。

Computed tomography-based radiomics predicts the fibroblastrelated gene EZH2 expression level and survival of hepatocellular carcinoma

BACKGROUND Hepatocellular carcinoma(HCC)is the most common subtype of liver cancer.The primary treatment strategies for HCC currently include liver transplantation and surgical resection.However,these methods often yield unsatisfactory outcomes,leading to a poor prognosis for many patients.This underscores the urgent need to identify and evaluate novel therapeutic targets that can improve the prognosis and survival rate of HCC patients.AIM To construct a radiomics model that can accurately predict the EZH2 expression in HCC.METHODS Gene expression,clinical parameters,HCC-related radiomics,and fibroblastrelated genes were acquired from public databases.A gene model was developed,and its clinical efficacy was assessed statistically.Drug sensitivity analysis was conducted with identified hub genes.Radiomics features were extracted and machine learning algorithms were employed to generate a radiomics model related to the hub genes.A nomogram was used to illustrate the prognostic significance of the computed Radscore and the hub genes in the context of HCC patient outcomes.RESULTS EZH2 and NRAS were independent predictors for prognosis of HCC and were utilized to construct a predictive gene model.This model demonstrated robust performance in diagnosing HCC and predicted an unfavorable prognosis.A negative correlation was observed between EZH2 expression and drug sensitivity.Elevated EZH2 expression was linked to poorer prognosis,and its diagnostic value in HCC surpassed that of the risk model.A radiomics model,developed using a logistic algorithm,also showed superior efficiency in predicting EZH2 expression.The Radscore was higher in the group with high EZH2 expression.A nomogram was constructed to visually demonstrate the significant roles of the radiomics model and EZH2 expression in predicting the overall survival of HCC patients.CONCLUSION EZH2 plays significant roles in diagnosing HCC and therapeutic efficacy.A radiomics model,developed using a logistic algorithm,efficiently predicted EZH2 expression and exhibited strong correlation with HCC prognosis.

Uniportal video-assisted thoracoscopic fissureless right upper lobe anterior segmentectomy for inflammatory myofibroblastic tumor:A case report

BACKGROUND Inflammatory myofibroblastic tumors(IMTs)are exceptionally rare neoplasms with intermediate malignant potential.Surgery is the accepted treatment option,aiming for complete resection with clear margins.CASE SUMMARY A 39-year-old woman presented with a growing solitary pulmonary nodule measuring 2.0 cm in the right upper lobe(RUL)of the lung.The patient underwent a RUL anterior segmentectomy using uniportal video-assisted thoracoscopy.A preliminary tissue diagnosis indicated malignancy;however,it was later revised to an IMTs.Due to the absence of a minor fissure between the right upper and middle lobes,an alternative resection approach was necessary.Therefore,we utilized indocyanine green injection to aid in delineating the intersegmental plane.Following an uneventful recovery,the patient was discharged on the third postoperative day.Thereafter,annual chest tomography scans were scheduled to monitor for potential local recurrence.CONCLUSION This case underscores the challenges in diagnosing and managing IMTs,showing the importance of accurate pathologic assessments and tailored surgical strategies.

Impact of STAT-signaling pathway on cancer-associated fibroblasts in colorectal cancer and its role in immunosuppression

Colorectal cancer(CRC)remains one of the most commonly diagnosed and deadliest types of cancer worldwide.CRC displays a desmoplastic reaction(DR)that has been inversely associated with poor prognosis;less DR is associated with a better prognosis.This reaction generates excessive connective tissue,in which cancer-associated fibroblasts(CAFs)are critical cells that form a part of the tumor microenvironment.CAFs are directly involved in tumorigenesis through different mechanisms.However,their role in immunosuppression in CRC is not well understood,and the precise role of signal transducers and activators of transcription(STATs)in mediating CAF activity in CRC remains unclear.Among the myriad chemical and biological factors that affect CAFs,different cytokines mediate their function by activating STAT signaling pathways.Thus,the harmful effects of CAFs in favoring tumor growth and invasion may be modulated using STAT inhibitors.Here,we analyze the impact of different STATs on CAF activity and their immunoregulatory role.

Fibroblast growth factor 21 inhibits ferroptosis following spinal cord injury by regulating heme oxygenase-1

Interfering with the ferroptosis pathway is a new strategy for the treatment of spinal cord injury.Fibroblast growth factor 21 can inhibit ferro ptosis and promote neurofunctional recovery,while heme oxygenase-1 is a regulator of iron and reactive oxygen species homeostasis.The relationship between heme oxygenase-1and ferroptosis remains controve rsial.In this study,we used a spinal co rd injury rat model to show that the levels of fibroblast growth factor 21 in spinal co rd tissue decreased after spinal cord injury.In addition,there was a significant aggravation of ferroptosis and a rapid increase in heme oxygenase-1 expression after spinal cord injury.Furthe r,heme oxygenase-1 aggravated fe rroptosis after spinal cord injury,while fibroblast growth factor 21 inhibited fe rroptosis by downregulating heme oxygenase-1.Thus,the activation of fibroblast growth factor 21 may provide a potential treatment for spinal co rd injury.These findings could provide a new potential mechanistic explanation for fibroblast growth factor 21 in the treatment of spinal cord injury.

Roles of fibroblast growth factors in the treatment of diabetes

Diabetes affects about 422 million people worldwide,causing 1.5 million deaths each year.However,the incidence of diabetes is increasing,including several types of diabetes.Type 1 diabetes(5%-10%of diabetic cases)and type 2 diabetes(90%-95%of diabetic cases)are the main types of diabetes in the clinic.Accumulating evidence shows that the fibroblast growth factor(FGF)family plays important roles in many metabolic disorders,including type 1 and type 2 diabetes.FGF consists of 23 family members(FGF-1-23)in humans.Here,we review current findings of FGFs in the treatment of diabetes and management of diabetic complications.Some FGFs(e.g.,FGF-15,FGF-19,and FGF-21)have been broadly investigated in preclinical studies for the diagnosis and treatment of diabetes,and their therapeutic roles in diabetes are currently under investigation in clinical trials.Overall,the roles of FGFs in diabetes and diabetic complications are involved in numerous processes.First,FGF intervention can prevent high-fat diet-induced obesity and insulin resistance and reduce the levels of fasting blood glucose and triglycerides by regulating lipolysis in adipose tissues and hepatic glucose production.Second,modulation of FGF expression can inhibit renal and cardiac fibrosis by regulating the expression of extracellular matrix components,promote diabetic wound healing process and bone repair,and inhibit cancer cell proliferation and migration.Finally,FGFs can regulate the activation of glucoseexcited neurons and the expression of thermogenic genes.

天香百合、药百合黄酮醇合成酶FLS基因克隆和表达分析

以天香百合(Lilium auratum)和药百合(L.speciosum var.gloriosoides)为研究材料,分别克隆获得黄酮醇合成酶(flavonol synthase, FLS)基因,命名为LaFLS和LsFLS。实验结果表明,LaFLS和LsFLS基因均含完整的开放阅读框1 035 bp,均编码344个氨基酸,氨基酸序列高度保守,均具有DIOX-N结构域和2-酮戊二酸和铁(Ⅱ)依赖性双加氧酶结构域,属于2-酮戊二酸和铁(Ⅱ)依赖性双加氧酶超家族;系统进化分析表明,LaFLS和LsFLS除与东方系百合西伯利亚和索邦的FLS亲缘关系最近外,与百合科郁金香(Tulipa fosteriana)等亲缘关系较近;生物信息学分析显示,LaFLS和LsFLS蛋白无信号肽序列和跨膜结构域,均为亲水性蛋白,亚细胞定位结果显示二者主要定位在细胞质中。基因表达分析结果表明,在花蕾发育过程中,LaFLS和LsFLS随花蕾发育出现先上升后下降再上升的趋势,而且在花被片无色区的表达量显著高于有色区域。

Attenuation of the Activation of NLRP3 Inflammasome in Fibroblast Like Synoviocytes of Rheumatoid Arthritis by Baicalin through Regulating the Let-7i-3p/PI3K/Akt/NF-κB Signaling Axis

[Objectives]To study the effect and mechanism of baicalin on the activation of NLRP3 inflammasome in human fibroblast like synoviocytes of rheumatoid arthritis(HFLS-RA).[Methods]To confirm that baicalin alleviated the activation of NLRP3 inflammasome in HFLS-RA,the expression of NLRP3 before and after baicalin treatment was observed by immunofluorescence.Western blot was used to detect the protein expression of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1 after baicalin treatment for 48 h,and the contents of IL-1 and IL-18 in the supernatents were detected by ELISA.In order to explore the mechanism of baicalin alleviating the activation of NLRP3 inflammasome,the corresponding relationship between let-7i-3p and PIK3CA was verified by double luciferin and Westen blot analysis.The expression of let-7i-3p and PI3K before and after baicalin intervention was detected by RT-qPCR.let-7i-3p interference was used to verify whether baicalin mitigated the activation of enhanced NLRP3 inflammasome.[Results]Baicalin(50 and 100 mg/L)significantly reduced the activation of NLRP3 inflammasome,inhibited the protein expressions of p-PI3K,p-Akt,NF-κB p65,NLRP3,ASC and caspase-1,and the secretion of IL-1 and IL-18.let-7i-3p and PIK3CA had a targeted correspondence,and baicalin up-regulated the expression of let-7i-3p and down-regulated the expression of PIK3CA.Baicalin attenuated the activation of NLRP3 inflammasome enhanced by let-7i-3p interference.[Conclusions]Baicalin can up-regulate let-7i-3p expression,inhibit PI3K/Akt/NF-κB signal transduction,and thus reduce the activation of NLRP3 inflammasome in HFLS-RA.

RNA sequencing of exosomes secreted by fibroblast and Schwann cells elucidates mechanisms underlying peripheral nerve regeneration

Exosomes exhibit complex biological functions and mediate a variety of biological processes,such as promoting axonal regeneration and functional recove ry after injury.Long non-coding RNAs(IncRNAs)have been reported to play a crucial role in axonal regeneration.Howeve r,the role of the IncRNA-microRNAmessenger RNA(mRNA)-competitive endogenous RNA(ceRNA)network in exosome-mediated axonal regeneration remains unclear.In this study,we performed RNA transcriptome sequencing analysis to assess mRNA expression patterns in exosomes produced by cultured fibroblasts(FC-EXOs)and Schwann cells(SCEXOs).Diffe rential gene expression analysis,Gene Ontology analysis,Kyoto Encyclopedia of Genes and Genomes analysis,and protein-protein intera ction network analysis were used to explo re the functions and related pathways of RNAs isolated from FC-EXOs and SC-EXOs.We found that the ribosome-related central gene Rps5 was enriched in FC-EXOs and SC-EXOs,which suggests that it may promote axonal regeneration.In addition,using the miRWalk and Starbase prediction databases,we constructed a regulatory network of ceRNAs targeting Rps5,including 27 microRNAs and five IncRNAs.The ceRNA regulatory network,which included Ftx and Miat,revealed that exsosome-derived Rps5 inhibits scar formation and promotes axonal regeneration and functional recovery after nerve injury.Our findings suggest that exosomes derived from fibro blast and Schwann cells could be used to treat injuries of peripheral nervous system.

金铁锁三萜类成分对衣霉素诱导RA-FLS细胞内质网应激的影响

目的基于内质网通路探索金铁锁三萜类成分皂皮酸、丝石竹皂苷元对衣霉素诱导类风湿性关节炎成纤维细胞(RA-FLS)的作用机制。方法以衣霉素诱导RA-FLS细胞为研究对象,给予皂皮酸、丝石竹皂苷元进行干预,检测细胞增殖活性,ELISA法检测肿瘤坏死因子-α(TNF-α)水平,流式细胞术检测细胞凋亡,Transwell实验检测细胞迁移能力,Western blot法检测细胞中转录激活因子6(ATF-6)、葡萄糖调节蛋白78(GRP78)、C/EBP同源蛋白(CHOP)、半胱氨酸蛋白酶蛋白-12(caspase-12)、抗凋亡Bcl-2蛋白表达,RT-qPCR法检测细胞中ATF-6、GRP78、CHOP mRNA表达。结果与模型组比较,皂皮酸、丝石竹皂苷元各剂量组RA-FLS细胞TNF-α水平均降低(P<0.01),细胞增殖、迁移能力均减弱(P<0.01),凋亡率均升高(P<0.01),细胞ATF-6、Bcl-2蛋白表达降低(P<0.05,P<0.01),CHOP、caspase-12蛋白表达升高(P<0.05,P<0.01);皂皮酸、丝石竹皂苷元低、中剂量组GRP78蛋白表达降低(P<0.05,P<0.01);皂皮酸、丝石竹皂苷元中剂量组ATF-6、GRP 78 mRNA表达降低(P<0.01),CHOP mRNA表达升高(P<0.01)。结论皂皮酸、丝石竹皂苷元可能通过调节内质网信号通路,降低相关炎症因子分泌,抑制RA-FLS细胞增殖及迁移,诱导细胞凋亡,起到对类风湿性关节炎的保护作用。

FLS模式护理对老年股骨颈骨折手术患者肢体功能康复的影响

目的探讨在老年股骨颈骨折手术患者中开展骨折联络服务(FLS)模式护理的临床效果。方法选择2021年1月—2022年5月医院收治的95例老年股骨颈骨折手术患者,按照组间基线资料可比的原则分为对照组47例和观察组48例,对照组给予常规护理,观察组在对照组基础上给予FLS模式护理干预,对比两组临床效果。结果与干预前相比,干预后两组髋关节功能评分表(Harris)各项评分、一般自我效能感量表(GSES)评分均升高,且观察组评分较对照组高,差异有统计学意义(P<0.05);干预后两组自我感受负担量表(SPB)评分较干预前均下降,且观察组分值较对照组低,差异有统计学意义(P<0.05);较之对照组,观察组首次下床时间及住院时间更短,差异有统计学意义(P<0.05)。术后随访1年,观察组骨折再发率为2.08%,低于对照组的14.89%,但组间差异无统计学意义(P<0.05)。结论FLS模式护理干预可促进老年股骨颈骨折手术患者自我效能感及肢体功能改善,有助于缓解患者自我感受负担,能够缩短患者康复进程。

基于FLS模式护理干预脊柱骨折合并脊髓损伤患者术后疗效观察

目的:基于骨折联络服务(FLS)模式观察护理干预对脊柱骨折合并脊髓损伤患者术后的临床疗效。方法:选取甘肃省中医院脊柱骨三科2021年6月—2022年9月收治的60例骨科术后的患者,采用随机数字表法将患者分为实验组(30例)和对照组(30例),对照组采用常规骨科护理;实验组在骨科常规护理基础上进行FLS模式护理;比较2组患者护理干预前后临床疗效及生活质量差异变化。结果:2组患者在干预前、后腰痛视觉模拟评分(VAS)、Oswestry功能障碍指数(ODI)、Barthel指数(BMI)及脊髓损伤水平(ASIA)评分进行对比观察,实验组各项评分均低于对照组;干预前后功能锻炼知识评分、依从性评分及生活质量评分比较实验组的分均优于对照组,差异均有统计学意义。结论:基于骨折联络服务(FLS)模式护理干预对脊柱骨折合并脊髓损伤患者可有效提高患者的依从性,提高患者术后生活质量及住院期间患者对护理工作的满意度。

斑地锦黄酮醇合成酶基因(EmFLS)及其启动子克隆及表达分析

【目的】克隆斑地锦黄酮醇合成酶基因(EmFLS)及其启动子序列,并检测EmFLS基因在斑地锦不同生长期不同组织中的表达模式,为后续研究该基因对黄酮醇化合物生物合成的调控机制提供理论参考。【方法】以斑地锦为材料,采用cDNA末端快速扩增(RACE)技术和热不对称交互式PCR(Tail-PCR)技术克隆EmFLS基因及启动子序列,对其进行生物信息学分析,并通过实时荧光定量PCR检测其在不同生长期不同组织中的表达模式。【结果】扩增获得EmFLS基因开放阅读框(ORF)(GenBank登录号ON821211.1),长度为1002 bp,编码333个氨基酸残基,蛋白相对分子质量为37.62 kD,定位于细胞质,为不稳定的亲水性蛋白,属于2OG-Fe(II)加氧酶超家族。EmFLS蛋白与其他13种植物FLS蛋白的氨基酸序列相似性为63.55%~70.51%,其中与木薯FLS蛋白的氨基酸序列相似性最高,且在系统发育进化树上处于一个独立的分支。EmFLS基因启动子约1800 bp,除含有真核生物启动子核心元件TATA-box和CAAT-box外,还含激素响应、胁迫响应和光响应等顺式作用元件。EmFLS基因在营养生长期和生殖生长期的根、茎、叶和果中均有表达,但在根和茎中的相对表达量显著高于叶和果(P<0.05,下同),斑地锦从营养生长期到生殖生长期EmFLS基因在根和茎中的相对表达量显著下降,而在叶中无显著变化(P>0.05)。【结论】EmFLS基因表达具有组织特异性,且在根和茎中具有发育阶段特异性,推测EmFLS基因主要参与调控斑地锦根和茎中黄酮醇化合物的生物合成。

Calcitriol Suppressed Isoproterenol-induced Proliferation of Cardiac Fibroblasts via Integrinβ3/FAK/Akt Pathway

Objective Cardiac fibroblasts(CFs)proliferation and extracellular matrix deposition are important features of cardiac fibrosis.Various studies have indicated that vitamin D displays an anti-fibrotic property in chronic heart diseases.This study explored the role of vitamin D in the growth of CFs via an integrin signaling pathway.Methods MTT and 5-ethynyl-2′-deoxyuridine assays were performed to determine cell viability.Western blotting was performed to detect the expression of proliferating cell nuclear antigen(PCNA)and integrin signaling pathway.The fibronectin was observed by ELISA.Immunohistochemical staining was employed to evaluate the expression of integrinβ3.Results The PCNA expression in the CFs was enhanced after isoproterenol(ISO)stimulation accompanied by an elevated expression of integrin beta-3(β3).The blockade of the integrinβ3 with a specific integrinβ3 antibody reduced the PCNA expression induced by the ISO.Decreasing the integrinβ3 by siRNA reduced the ISO-triggered phosphorylation of FAK and Akt.Both the FAK inhibitor and Akt inhibitor suppressed the PCNA expression induced by the ISO in the CFs.Calcitriol(CAL),an active form of vitamin D,attenuated the ISO-induced CFs proliferation by downregulating the integrinβ3 expression,and phosphorylation of FAK and Akt.Moreover,CAL reduced the increased levels of fibronectin and hydroxyproline in the CFs culture medium triggered by the ISO.The administration of calcitriol decreased the integrinβ3 expression in the ISO-induced myocardial injury model.Conclusion These findings revealed a novel role for CAL in suppressing the CFs growth by the downregulation of the integrinβ3/FAK/Akt pathway.