保留中央凹或标准内界膜剥除联合玻璃体切割术治疗近视牵引性黄斑病变的Meta分析

目的:评估玻璃体切割术中保留中央凹(FSIP)或标准内界膜剥除(CMIP)治疗近视牵引性黄斑病变(MTM)的疗效及安全性。方法:计算机检索中国知网、万方、维普、PubMed、Embase、Cochrane Library、Web of Science数据库,搜集2000-01-01/2022-07-01玻璃体切割术中FSIP或CMIP治疗MTM的对比研究。比较两组患者术后最佳矫正视力(BCVA)的变化值和改善率、术后全层黄斑裂孔(FTMH)发生率、视网膜中央凹厚度(CFT)变化值、术后中心凹完全解剖复位率。结果:共12篇文献484眼纳入研究,其中FSIP组203眼,CMIP组281眼。Meta分析结果显示:FSIP组患者术后BCVA的变化值(SMD=0.52,95%CI:0.20~0.85,P=0.002)、BCVA改善率(RR=1.50,95%CI:1.22~1.85,P=0.0002)及术后FTMH发生率(RR=0.23,95%CI:0.10~0.54,P=0.0008)优于CMIP组,两组患者CFT变化值(SMD=0.04,95%CI:-0.19~0.26,P=0.75)及术后中心凹完全解剖复位率(RR=1.12,95%CI:0.94~1.32,P=0.20)比较均无差异。结论:现有证据表明,两种术式解剖改善结果相似,但在改善视觉效果及降低术后全层黄斑裂孔发生率方面,FSIP明显优于CMIP。

Targeting long non-coding RNA MALAT1 alleviates retinal neurodegeneration in diabetic mice

●AIM:To observe the effect of inhibiting long non-coding RNA(lncRNA)metastasis-associated lung adenocarcinoma transcript 1(MALAT1)on diabetic neurodegeneration.●METHODS:Thirty-six 8-week-old C57 BL/6 mice were randomly divided into normal control,diabetic control,diabetic scrambled small interfering RNAs(siRNAs)and diabetic MALAT1-siRNA groups.After diabetic induction with streptozocin intraperitoneally-injection,the diabetic M A L AT 1-s i R N A g ro u p w a s i n t r av i t r e a l l y i n j e c te d with 1μL 20μmol/L MALAT1 siRNA,and the diabetic scrambled siRNA group was injected with the same amount of scrambled siRNA.Electroretinography was performed to examine photoreceptor functions 16 wk after diabetes induction.MALAT1 expression was detected via real time polymerase chain reaction.Cone morphological changes were examined using immunofluorescence.Rod morphological changes were examined by determining outer nuclear layer(ONL)thickness.●RESULTS:The upregulation of retinal MALAT1 expression was detected in the diabetic control mice,while MALAT1 expression in the diabetic MALAT1-siRNA mice was decreased by 91.48%compared to diabetic control mice.The diabetic MALAT1-siRNA and diabetic control mice showed lower a-wave and b-wave amplitudes than did the normal control mice in scotopic and photopic electroretinogram,while the diabetic MALAT1-siRNA mice showed higher amplitudes than diabetic control mice.Morphological examination revealed that ONL thickness in the diabetic MALAT1-siRNA and diabetic control mice was lower than normal control mice.However,ONL thickness was greater in the diabetic MALAT1-siRNA mice than diabetic control mice.Moreover,the diabetic control mice performed a sparser cone cell arrangement and shorter outer segment morphology than diabetic MALAT1-siRNA mice.●CONCLUSION:Inhibiting retinal MALAT1 results in mitigative effects on the retinal photoreceptors,thus alleviating diabetic neurodegeneration.

Sub-channel shared resource allocation for multi-user distributed MIMO-OFDM systems

Well-controlled resource allocation is crucial for promoting the performance of multiple input multiple output orthogonal frequency division multiplexing(MIMO-OFDM) systems. Recent studies have focused primarily on traditional centralized systems or distributed antenna systems(DASs), and usually assumed that one sub-carrier or sub-channel is exclusively occupied by one user. To promote system performance, we propose a sub-channel shared resource allocation algorithm for multiuser distributed MIMO-OFDM systems. Each sub-channel can be shared by multiple users in the algorithm, which is different from previous algorithms. The algorithm assumes that each user communicates with only two best ports in the system. On each sub-carrier, it allocates a sub-channel in descending order, which means one sub-channel that can minimize signal to leakage plus noise ratio(SLNR) loss is deleted until the number of remaining sub-channels is equal to that of receiving antennas. If there are still sub-channels after all users are processed, these sub-channels will be allocated to users who can maximize the SLNR gain. Simulations show that compared to other algorithms, our proposed algorithm has better capacity performance and enables the system to provide service to more users under the same capacity constraints.