神经病理性疼痛不同性质疼痛患者血清BDNF、TLR4表达水平差异及其诊断价值分析

摘要 目的：分析神经病理性疼痛（NP）不同性质疼痛患者血清脑源性神经生长因子（BDNF）、Toll受体4（TLR4）表达水平差异及其诊断价值。方法：选取2021年5月～2022年5月本院收治的80例NP患者和100例健康体检者作为研究对象,将NP患者其纳入NP组,将健康体检者纳入对照组,并参照神经病理性疼痛量表（NPS）区分NP组患者的疼痛性质（钝痛20例,不适感28例,深部痛17例,体表痛15例）,分别检测两组患者和NP组不同性质疼痛患者的血清BDNF、TLR4表达水平,采用双变量Spearman相关性检验血清BDNF、TLR4与NP不同性质疼痛的相关性,同时建立多因素Logistic模型,分析NP不同性质疼痛的影响因素,并比较其诊断效能。结果：与对照组比较,NP组血清BDNF表达水平较低,TLR4表达水平较高（P＜0.05）;NP钝痛、不适感、深部痛、体表痛的血清BDNF、TLR4表达水平比较（P＜0.05）;血清BDNF与NP钝痛、不适感、深部痛、体表痛呈负相关性,血清TLR4与NP钝痛、不适感、深部痛、体表痛呈正相关性（P＜0.05）;Logistic多因素分析结果显示,BDNF、TLR4均是NP钝痛、不适感、深部痛、体表痛的独立危险因素（P＜0.05）;血清BDNF、TLR4和BDNF+TLR4对NP钝痛、不适感、深部痛、体表痛的ACU均＞0.70。结论：血清BDNF、TLR4与钝痛、不适感、深部痛、体表痛等性质的NP均存在一定关联,在诊断不同NP性质方面具有较高的敏感性和特异性,有利于为临床治疗提供参考依据。     

腕踝针联合耳穴压豆治疗肝癌癌痛的疗效及对心理状态和血清疼痛介质的影响

摘要 目的：观察腕踝针联合耳穴压豆治疗原发性肝癌（PHC）癌痛的疗效及对心理状态和血清疼痛介质的影响。方法：选取湖南中医药大学第一附属医院2020年3月~2022年12月期间收治的PHC癌痛患者117例,按随机数字表法分为对照组和联合组,例数分别为58例和59例。两组患者均接受常规疼痛处理,对照组患者接受耳穴压豆治疗,联合组在对照组的基础上接受腕踝针治疗。对比两组疼痛缓解率、临床指标、心理状态和疼痛介质水平。结果：联合组的疼痛缓解率高于对照组（P<0.05）。联合组的数字疼痛法（NRS）评分低于对照组,止痛起效时间、每次疼痛持续时间短于对照组,爆发痛次少于对照组（P<0.05）。治疗后,两组焦虑自评量表（SAS）、抑郁自评量表（SDS）评分下降,且联合组低于对照组（P<0.05）。治疗后,两组5-羟色胺（5-HT）、P物质（SP）、前列腺素E₂（PGE₂）下降,且联合组低于对照组（P<0.05）。结论：腕踝针联合耳穴压豆治疗PHC癌痛,可有效减轻疼痛症状,降低血清疼痛介质水平,同时还可有效调节患者的心理状态,应用价值较好。     

经皮穴位电刺激联合常规镇痛对无痛人流术后宫缩痛镇痛效果及机制研究

摘要 目的：探讨经皮穴位电刺激联合常规镇痛对无痛人流术后宫缩痛镇痛效果及机制。方法：选择来我院行无痛人流患者100例。根据随机数字表法分为两组。对照组行术后常规镇痛治疗,同时在内关、合谷、三阴交最酸胀处黏贴电极但是不进行穴位刺激。观察组在术后常规镇痛基础上行经皮穴位电刺激治疗。对比不同时间点两组患者的机体一般情况、不同时间点两组患者的宫缩痛疼痛情况、T3时正性负性情绪量表评分、T3时血清P物质、前列腺素、5-羟色胺、β-内啡肽、强啡肽水平、T4点时的心理状态评分及满意度评分。结果：对照组T1、T2点时的BP、HR、RR、SpO₂明显较同组T0点低,对照组T3点与观察组T1、T2、T3点时BP、HR、RR、SpO₂与同组T0点对比无统计学意义（P>0.05）;对照组T1、T2点时的BP、HR、RR、SpO₂明显较观察组同时间点低（P<0.05）。T0点,两组VAS评分对比无统计学意义（P>0.05）;T1、T2、T3点时间,观察组的VAS评分明显较对照组低（P<0.05）;对照组T1、T2点的VAS评分明显较同组T0点高,观察组T1、T2、T3点的VAS评分明显较T0点低（P<0.05）。观察组的正性情绪明显较对照组高,负性情绪明显较对照组低（P<0.05）。观察组的血清P物质、前列腺素、5-羟色胺、β-内啡肽、强啡肽水平明显较对照组低（P<0.05）。观察组的心理状态评分明显较对照组低,满意度评分明显较对照组高（P<0.05）。结论：经皮穴位电刺激联合常规镇痛可明显改善无痛人流术后宫缩痛镇痛效果、患者心理状态及满意度,可能与其可降低血清P物质、前列腺素、5-羟色胺、β-内啡肽、强啡肽水平有关。     

Down-regulation of miR-17 family expression in response to retinoic acid induced neuronal differentiation

Whole-genome microRNA and gene expression analyses were used to monitor changes during retinoic acid induced differentiation of neuroblasts in vitro. Interestingly, the entire miR-17 family was over-represented among the down-regulated miRNA. The implications of these changes are considerable, as target gene prediction suggests that the miR-17 family is involved in the regulation of the mitogen-activated protein kinase (MAPK) signaling pathway, synaptic plasticity and other markers of neuronal differentiation. Significantly, many of the target responses predicted by changes in miRNA expression were supported by the observed changes in gene expression. As expected, markers of neuronal differentiation such as anti-apoptotic protein B-cell lymphoma 2 (BCL2), myocyte enhancer factor-2D (MEF2D) and zipper protein kinase (MAP3K12; aka ZPK/MUK/DLK) were each up-regulated in response to differentiation. The expression of these genes was also reduced in response to miR-17 and miR-20a transfection, and more specifically they were also shown to contain functional miRNA recognition elements for members of the miR-17 family by reporter gene assay. This suggests that the miR-17 family have an integral role in fine-tuning the pathways involved in the regulation of neuronal differentiation.     

miRNA参与肿瘤基因表达调控研究进展

调查表明,我国城乡居民恶性肿瘤死亡率属于世界较高水平,而且呈持续的增长趋势。近年来的研究发现在肿瘤的发生与发展过程中涉及到多种因素,其中mi RNA可能扮演了重要的作用。mi RNA是一种长度约为22 nt的非编码短序列RNA,通过介导特异性的基因沉默导致靶m RNA降解,促使相应蛋白质的转译受阻而失去原有编码蛋白质的功能。mi RNA在细胞分裂周期中影响着基因的表达调控,在此过程中基因表达的失控就可能导致疾病的发生。而肿瘤的发生是以细胞恶变为基础,细胞恶变则是与细胞周期调控因素失衡相关,由此提示了一些mi RNA可能参与了肿瘤的发生、发展过程并在其中发挥了重要作用。随着研究的深入,mi RNA逐渐成为肿瘤诊治的新研究方向。本文主要讨论mi RNA在肿瘤基因表达调控方面的研究进展。     

Calcium signaling and cellular senescence

Cellular senescence is a stable cell proliferation arrest induced by a variety of stresses including telomere shortening, oncogene activation and oxidative stress. This process plays a crucial role in many physiopathological contexts, especially during aging when cellular senescence favors development of age-related diseases, shortening lifespan. However, the molecular and cellular mechanisms controlling senescence are still a matter of active research. In the last decade, there has been emerging literature indicating a key involvement of calcium signaling in cellular senescence. In this review we will initially give an account of the direct evidence linking calcium and the regulation of senescence. We will then review our current knowledge on the role of calcium in some senescence-associated features and physiopathological conditions, which will shed light on additional ways in which calcium signaling is implicated in cellular senescence.     

Influence of surface anesthesia on the pressure pain threshold measured with different-sized probes

Transcutaneous pressure with pressure probes of arbitrary diameters have been commonly used for measuring the threshold and magnitude of muscle pain, yet this procedure lacks scientific validation. To examine the valid probe dimensions, we conducted physiological experiments using 34 human subjects. Pin-prick pain, pressure pain threshold (PPT) to pressure probes of various diameters, heat pain threshold, and electrical pain threshold of deep tissues were measured before and after application of surface lidocaine anesthesia to the skin surface over the brachioradial muscle in a double-blinded manner. The anesthesia neither affected PPT with larger probes (diameters: 1.6 and 15?mm) nor increased electric pain threshold of deep structures, whereas it diminished pain count in pin-prick test and PPT with a 1.0?mm diameter probe, suggesting that mechanical pain thresholds measured with 1.6 and 15?mm probes reflect the pain threshold of deep tissues, possibly muscle. Pain thresholds to heat did not change after application of the anesthesia. These results suggest that larger pressure probes can give a better estimation of muscular pain threshold.     

7,9-Diaryl-1,6,8-trioxaspiro[4.5]dec-3-en-2-ones: Readily accessible and highly potent anticancer compounds

7,9-Diaryl-1,6,8-trioxaspiro[4.5]dec-3-en-2-ones are a recently described group of spirocyclic butenolides that can be generated rapidly and as a single diastereomer through a cascade process between γ-hydroxybutenolides and aromatic aldehydes. The following outlines our findings that these spirocycles are potently cytotoxic and have a dramatic structure–function profile that provides excellent insight into the structural features required for this potency.