基于TGF-β/smad信号通路探讨七方胃痛颗粒对人胃腺癌AGS细胞上皮间质转化过程的影响＊

目的 探究七方胃痛颗粒对转化生长因子-β1（TGF-β1）诱导人胃腺癌细胞AGS上皮间质转化（Epithelial-mesenchymal transition， EMT）过程的影响及其潜在分子机制。方法 为了探究七方胃痛颗粒对TGF-β1处理的AGS细胞增殖、迁移和侵袭的影响，实验分为四组：AGS细胞对照组，EMT空白模型组，中药血清组，TGF-β/smad通路抑制剂组，分别利用CCK8、细胞划痕实验和Transwell实验检测细胞增殖、迁移和侵袭能力。此外，通过免疫荧光检测EMT过程中相关蛋白（E-cadherin、N-cadherin、14-3-3ζ、Smad2和p-Smad2/3）的表达水平。结果 与AGS细胞对照组相比，TGF-β1诱导EMT过程，显著促进AGS细胞增殖、迁移和侵袭，下调了E-cadherin的表达，上调了N-cadherin、14-3-3ζ、Smad2和p-Smad2/3的表达；与EMT空白模型组相比，中药血清组、TGF-β/smad通路抑制剂组显著抑制了细胞增殖、迁移和侵袭，上调了E-cadherin的表达，降低了N-cadherin、14-3-3ζ、Smad2和p-Smad2/3的表达。结论 七方胃痛颗粒通过调控TGF-β/smad信号通路从而抑制人胃腺癌AGS细胞的EMT过程。     

Physiological determinants of residual cerebral arterial pulsatility on best medical treatment after TIA or minor stroke

Cerebral arterial pulsatility is strongly associated with cerebral small vessel disease and lacunar stroke yet its dependence on central versus local haemodynamic processes is unclear. In a population-based study of patients on best medical managment, 4–6 weeks after a TIA or non-disabling stroke, arterial stiffness and aortic systolic, diastolic and pulse pressures were measured (Sphygmocor). Middle cerebral artery peak and trough flow velocities and Gosling’s pulsatility index were measured by transcranial ultrasound. In 981 participants, aortic and cerebral pulsatility rose strongly with age in both sexes, but aortic diastolic pressure fell more with age in men whilst cerebral trough velocity fell more in women. There was no significant association between aortic systolic or diastolic blood pressure with cerebral peak or trough flow velocity but aortic pulse pressure explained 37% of the variance in cerebral arterial pulsatility, before adjustment, whilst 49% of the variance was explained by aortic pulse pressure, arterial stiffness, age, gender and cardiovascular risk factors. Furthermore, arterial stiffness partially mediated the relationship between aortic and cerebral pulsatility. Overall, absolute aortic pressures and cerebral blood flow velocity were poorly correlated but aortic and cerebral pulsatility were strongly related, suggesting a key role for transmission of aortic pulsatility to the brain.     

香萱益神方对血管性痴呆模型大鼠神经元凋亡机制研究

目的:探讨香萱益神方治疗血管性痴呆(VD)模型大鼠认知功能作用及其对神经元凋亡机制的研究。方法:两血管阻断法建立VD大鼠模型,给予中药方香萱益神方灌胃治疗6周,分别于造模后、中药喂养6周后进行Morris水迷宫行为学检测,测试大鼠认知行为能力改变,行为学测试结束后,检测VD模型大鼠海马中海马组织脑源性神经营养因子(BDNF)表达水平的变化。结果:香萱益神方治疗6周后,血管性痴呆大鼠模型学习记忆能力得到改善,上调脑内海马组织神经营养因子水平,海马神经元凋亡率下降。结论:香萱益神方是治疗血管性痴呆的有效方剂,可以有效改善VD大鼠模型认知行为功能的障碍情况,起到减少海马神经元细胞凋亡,诱导海马神经元细胞修复的作用。香萱益神方可能是通过激活BDNF相关通路,起到保护海马神经元的作用。     

ERCC1在结直肠癌组织中的表达及预后价值

目的:探究核苷酸切除修复交叉互补基因1（excision repair cross-complementation gene 1，ERCC1）表达对结直肠癌（colorectal cancer，CRC）患者铂类辅助化疗的预后价值。方法:选取2011年01月至2013年01月安徽医科大学附属六安医院行CRC根治术后接受mFOLFOX6方案化疗的患者共84例，通过免疫组化方法评估ERCC1在CRC组织中表达情况，分析ERCC1表达与预后的关联。结果:ERCC1高表达30例（35.7%）。Kaplan-Meier曲线显示ERCC1高表达的CRC患者无病生存期（DFS）和总生存期（OS）均缩短（P均<0.001）。多因素COX分析显示ERCC1高表达（DFS HR=4.645，95%CI:2.045~10.548，P<0.001；OS HR=4.898，95%CI:1.971~12.170，P<0.001）是CRC患者预后的不良因素，分析各亚组患者中ERCC1表达与生存相关性得到相似的结果。复发患者中ERCC1高表达的肝肺转移占68.8%（11/16），低表达的腹腔转移为70.0%（7/10），ERCC1表达与首次复发模式显著相关（P=0.006）。结论:ERCC1表达可作为评价CRC患者预后的重要指标。ERCC1表达可能有助于预测CRC患者辅助化疗后首次复发模式。ERCC1表达的预后价值需进一步研究。     

COVID-19, chronic inflammatory rheumatic disease and anti-rheumatic treatments

Clinical Rheumatology - Since December 2019, the pandemic caused by coronavirus disease 2019 (COVID-19) raises a real public health problem. COVID-19 appeared in Wuhan (Hubei province) in China....     

Putative protective neural mechanisms in prereaders with a family history of dyslexia who subsequently develop typical reading skills

Developmental dyslexia affects 40–60% of children with a familial risk (FHD+) compared to a general prevalence of 5–10%. Despite the increased risk, about half of FHD+ children develop typical reading abilities (FHD+Typical). Yet the underlying neural characteristics of favorable reading outcomes in at‐risk children remain unknown. Utilizing a retrospective, longitudinal approach, this study examined whether putative protective neural mechanisms can be observed in FHD+Typical at the prereading stage. Functional and structural brain characteristics were examined in 47 FHD+ prereaders who subsequently developed typical (n = 35) or impaired (n = 12) reading abilities and 34 controls (FHD?Typical). Searchlight‐based multivariate pattern analyses identified distinct activation patterns during phonological processing between FHD+Typical and FHD?Typical in right inferior frontal gyrus (RIFG) and left temporo‐parietal cortex (LTPC) regions. Follow‐up analyses on group‐specific classification patterns demonstrated LTPC hypoactivation in FHD+Typical compared to FHD?Typical, suggesting this neural characteristic as an FHD+ phenotype. In contrast, RIFG showed hyperactivation in FHD+Typical than FHD?Typical, and its activation pattern was positively correlated with subsequent reading abilities in FHD+ but not controls (FHD?Typical). RIFG hyperactivation in FHD+Typical was further associated with increased interhemispheric functional and structural connectivity. These results suggest that some protective neural mechanisms are already established in FHD+Typical prereaders supporting their typical reading development.