Scarf联合Akin截骨术治疗中、重度踇外翻的临床疗效

目的评价Scarf联合Akin截骨术治疗中、重度踇外翻畸形的临床疗效。方法选取2012年4月-2016年4月郑州大学附属郑州市中心医院采用Scarf联合Akin截骨术治疗中、重度踇外翻畸形患者60例(98足)。术前术后均行患足X射线检查,观察疗效及影像学改变,同时采用美国足踝外科学会足功能评分系统(AOFAS)评价治疗效果。结果60例患者均获得随访,随访时间6~20个月,术后2例(2足)患者出现趾背内侧皮肤麻木,考虑为神经损伤,2~4个月后好转,手术切口均一期愈合,截骨处无延迟愈合或不愈合,愈合时间14周。术后踇外翻角度(11.1±3.2)°、第1、2跖骨间角(7.1±2.6)°和胫侧籽骨位置(2.13±0.50)级均低于术前[(39.8±6.2)°、(18.2±4.6)°和(4.79±0.53)级],AOFAS评分[(86.2±8.2)分]高于术前[(36.8±9.2)分](P<0.05)。结论Scarf联合Akin截骨术治疗中重度踇外翻畸形临床疗效良好,并发症少,复发率低。

Microglia in neurodegenerative diseases

A major feature of neurodegeneration is disruption of central nervous system homeostasis,during which microglia play diverse roles.In the central nervous system,microglia serve as the first line of immune defense and function in synapse pruning,injury repair,homeostasis maintenance,and regulation of brain development through scavenging and phagocytosis.Under pathological conditions or various stimulations,microglia proliferate,aggregate,and undergo a variety of changes in cell morphology,immunophenotype,and function.This review presents the features of microglia,especially their diversity and ability to change dynamically,and reinterprets their role as sensors for multiple stimulations and as effectors for brain aging and neurodegeneration.This review also summarizes some therapeutic approaches for neurodegenerative diseases that target microglia.

Human induced pluripotent stem cells labeled with fluorescent magnetic nanoparticles for targeted imaging and hyperthermia therapy for gastric cancer

Objective: Human induced pluripotent stem(i PS) cells exhibit great potential for generating functional human cells for medical therapies. In this paper, we report for use of human i PS cells labeled with fluorescent magnetic nanoparticles(FMNPs) for targeted imaging and synergistic therapy of gastric cancer cells in vivo. Methods: Human i PS cells were prepared and cultured for 72 h. The culture medium was collected, and then was coincubated with MGC803 cells. Cell viability was analyzed by the MTT method. FMNP-labeled human i PS cells were prepared and injected into gastric cancer-bearing nude mice. The mouse model was observed using a small-animal imaging system. The nude mice were irradiated under an external alternating magnetic field and evaluated using an infrared thermal mapping instrument. Tumor sizes were measured weekly. Results: iP S cells and the collected culture medium inhibited the growth of MGC803 cells. FMNP-labeled human iP S cells targeted and imaged gastric cancer cells in vivo, as well as inhibited cancer growth in vivo through the external magnetic field. Conclusion: FMNP-labeled human i PS cells exhibit considerable potential in applications such as targeted dual-mode imaging and synergistic therapy for early gastric cancer.

The updated landscape of tumor microenvironment and drug repurposing

Accumulating evidence shows that cellular and acellular components in tumor microenvironment(TME)can reprogram tumor initiation,growth,invasion,metastasis,and response to therapies.Cancer research and treatment have switched from a cancercentric model to a TME-centric one,considering the increasing significance of TME in cancer biology.Nonetheless,the clinical efficacy of therapeutic strategies targeting TME,especially the specific cells or pathways of TME,remains unsatisfactory.Classifying the chemopathological characteristics of TME and crosstalk among one another can greatly benefit further studies exploring effective treating methods.Herein,we present an updated image of TME with emphasis on hypoxic niche,immune microenvironment,metabolism microenvironment,acidic niche,innervated niche,and mechanical microenvironment.We then summarize conventional drugs including aspirin,celecoxib,β-adrenergic antagonist,metformin,and statin in new antitumor application.These drugs are considered as viable candidates for combination therapy due to their antitumor activity and extensive use in clinical practice.We also provide our outlook on directions and potential applications of TME theory.This review depicts a comprehensive and vivid landscape of TME from biology to treatment.

NAT 10 promotes gastric cancer metastasis via N4-acetylated COL5A1

Dear Editor,Gastric cancer(GC)is among the most prevalent gastrointestinal malignancies.The occurrence of local deep infiltration or distant metastasis in GC is commonly associated with weak treatment and poor prognosis.1 Although,N4-Acetylcytidine(ac4C)represents one of the extensive chemical modifications in mRNAs that plays a pivotal role in modulating mRNA stability and the mRNA translation process(Fig.1b).

Non-catalytic roles for TET1 protein negatively regulating neuronal differentiation through srGAP3 in neuroblastoma cells

The methylcytosine dioxygenases TET proteins （TET1, TET2, and TET3） play important regulatory roles in neural function. In this study, we investigated the role of TET proteins in neuronal differentiation using Neuro2a cells as a model. We observed that knockdown of TET1, TET2 or TET3 promoted neuronal differentiation of Neuro2a cells, and their overexpression inhibited VPA （valproic acid）-induced neuronal differentiation, suggesting all three TET proteins negatively regulate neu- ronal differentiation of Neuro2a cells. Interestingly, the inducing activity of TET protein is independent of its enzymatic activity. Our previous studies have demon- strated that srGAP3 can negatively regulate neuronal differentiation of Neuro2a cells. Furthermore, we revealed that TET1 could positively regulate srGAP3 expression independent of its catalytic activity, and srGAP3 is required for TET-mediated neuronal differentiation of Neuro2a cells. The results presented here may facilitate better understanding of the role of TET proteins in neuronal differentiation, and provide a possible therapy target for neuroblastoma.

The arsenal of TP53 mutants therapies:neoantigens and bispecific antibodies

A recent research published in Science by Hsiue et al.1 introduced a CD3-targeting bispecific antibody that can bind to tumor cells by recognizing mutation-associated neoantigens and activate T cell-mediated tumor killing by binding to CD3.The tumor suppressor gene TP53 is the most commonly mutated gene in various cancers.

Drug repurposing for cancer therapy

Cancer,a complex and multifactorial disease,presents a significant challenge to global health.Despite significant advances in surgical,radiotherapeutic and immunological approaches,which have improved cancer treatment outcomes,drug therapy continues to serve as a key therapeutic strategy.However,the clinical efficacy of drug therapy is often constrained by drug resistance and severe toxic side effects,and thus there remains a critical need to develop novel cancer therapeutics.One promising strategy that has received widespread attention in recent years is drug repurposing:the identification of new applications for existing,clinically approved drugs.Drug repurposing possesses several inherent advantages in the context of cancer treatment since repurposed drugs are typically cost-effective,proven to be safe,and can significantly expedite the drug development process due to their already established safety profiles.In light of this,the present review offers a comprehensive overview of the various methods employed in drug repurposing,specifically focusing on the repurposing of drugs to treat cancer.We describe the antitumor properties of candidate drugs,and discuss in detail how they target both the hallmarks of cancer in tumor cells and the surrounding tumor microenvironment.In addition,we examine the innovative strategy of integrating drug repurposing with nanotechnology to enhance topical drug delivery.We also emphasize the critical role that repurposed drugs can play when used as part of a combination therapy regimen.To conclude,we outline the challenges associated with repurposing drugs and consider the future prospects of these repurposed drugs transitioning into clinical application.