两例 SMILE 术中特殊情况更改 SBK 手术的疗效观察

目的：通过对同一患者双眼不同手术方式的自身对比，了解飞秒扫描后改SBK手术的疗效差异，为不同患者屈光手术方式的选择提供临床指导依据。方法回顾分析2例右眼行飞秒激光小切口透镜取出术（ SMILE），左眼SMILE术中负压环脱失和激光扫描不良透镜分离困难而改行机械刀制瓣准分子激光手术（ SBK）的患者，比较术后视力、等效球镜（ SE）、对比敏感度（ CSF）、波前像差（ HAOS）以及泪膜破裂时间（ BUT）、泪液分泌功能试验（ Schimer I）和SPEED、OSDI干眼症状问卷调查分析差异。结果（1）术后个月，均能达到最佳矫正视力（BSCVA），等效球镜均在±0．75 D以内，双眼比较无显著性差异。（2）CSF的比较，左右眼无显著性差异，略低于正常水平。（3）术后3个月，BUT和Schimer检查中，双眼无显著性差异。（4）HAOS比较中，总像差RMS和高阶像差这两项， SMILE眼低于SBK眼；球差（S）的比较，SMILE眼高于SBK眼。（5）SPEED和OSDI问卷评分双眼无显著差异。结论 SMILE失败眼改SBK后视觉质量与SMILE眼无显著差异，其视觉质量、疗效不受影响。     

Adolescent neighborhood quality predicts adult dACC response to social exclusion

Neuroimaging studies using the social-exclusion paradigm Cyberball indicate increased dorsal anterior cingulate cortex (dACC) and right insula activity as a function of exclusion. However, comparatively less work has been done on how social status factors may moderate this finding. This study used the Cyberball paradigm with 85 (45 females) socio-economically diverse participants from a larger longitudinal sample. We tested whether neighborhood quality during adolescence would predict subsequent neural responding to social exclusion in young adulthood. Given previous behavioral studies indicating greater social vigilance and negative evaluation as a function of lower status, we expected that lower adolescent neighborhood quality would predict greater dACC activity during exclusion at young adulthood. Our findings indicate that young adults who lived in low-quality neighborhoods in adolescence showed greater dACC activity to social exclusion than those who lived in higher quality neighborhoods. Lower neighborhood quality also predicted greater prefrontal activation in the superior frontal gyrus, dorsal medial prefrontal cortex and the middle frontal gyrus, possibly indicating greater regulatory effort. Finally, this effect was not driven by subsequent ratings of distress during exclusion. In sum, adolescent neighborhood quality appears to potentiate neural responses to social exclusion in young adulthood, effects that are independent of felt distress.     

Melatonin induces apoptosis of colorectal cancer cells through HDAC4 nuclear import mediated by CaMKII inactivation

Melatonin induces apoptosis in many different cancer cell lines, including colorectal cancer. However, the precise mechanisms involved remain largely unresolved. In this study, we provide evidence to reveal a new mechanism by which melatonin induces apoptosis of colorectal cancer LoVo cells. Melatonin at pharmacological concentrations significantly suppressed cell proliferation and induced apoptosis in a dose‐dependent manner. The observed apoptosis was accompanied by the melatonin‐induced dephosphorylation and nuclear import of histone deacetylase 4 (HDAC4). Pretreatment with a HDAC4‐specific siRNA effectively attenuated the melatonin‐induced apoptosis, indicating that nuclear localization of HDAC4 is required for melatonin‐induced apoptosis. Moreover, constitutively active Ca²⁺/calmodulin‐dependent protein kinase II alpha (CaMKIIα) abrogated the melatonin‐induced HDAC4 nuclear import and apoptosis of LoVo cells. Furthermore, melatonin decreased H3 acetylation on bcl‐2 promoter, leading to a reduction of bcl‐2 expression, whereas constitutively active CaMKIIα(T286D) or HDAC4‐specific siRNA abrogated the effect of melatonin. In conclusion, the present study provides evidence that melatonin‐induced apoptosis in colorectal cancer LoVo cells largely depends on the nuclear import of HDAC4 and subsequent H3 deacetylation via the inactivation of CaMKIIα.