角膜生物力学分析仪评估SMILE与FS-LASIK术后角膜生物力学的变化

目的：利用角膜生物力学分析仪(Corvis ST)评估行飞秒激光小切口角膜基质透镜取出术(SMILE)和飞秒激光辅助的准分子激光原位角膜磨镶术(FS-LASIK)治疗的中度屈光不正患者术后角膜生物力学的变化特征。方法：前瞻性队列研究。选取2020-11/2021-11在宁夏眼科医院视光中心拟行角膜屈光手术的中度近视患者65例130眼，考虑双眼存在关联，双眼同时满足条件选右眼进行研究，其中SMILE组30眼，FS-LASIK组35眼。应用Corvis ST观察两组患者术前、术后1、3mo角膜生物力学参数综合半径(IR)、反向凹面半径(ICR)、形变幅度比值(DAR2)、硬度指数(SP-A1)、相关厚度-水平方向(ARTh)和最大压陷曲率半径(HC-Radius)的变化。结果：两组间患者术前，术后1、3mo生物力学参数比较均无差异(P>0.05)。各组患者术后1、3mo IR、ICR、DAR2均较术前明显增加，SP-A1、ARTh、HC-Radius均较术前明显降低(均P<0.05)，术后1mo与术后3mo生物力学参数比较无差异(P>0.05)。两组患者术后3mo中央角膜厚度(CCT)与ARTh和SP-A1呈正相关(FS-LASIK组： r=0.727、0.819，SMLIE组： r=0.683、0.434，均P<0.05)，与IR和ICR呈负相关(FS-LASIK组： r=-0.697、-0.622，SMLIE组： r=-0.447、-0.491，均P<0.05)。结论：对于中度近视患者，SMILE和FS-LASIK术后均可导致角膜生物力学稳定性降低，两种手术方式对生物力学的影响无明显差异，且在术后1mo时生物力学趋于稳定，术后CCT与生物力学参数ARTh、SP-A1、IR和ICR存在相关性。     

康柏西普两种给药方案治疗息肉样脉络膜血管病变的疗效比较

目的:观察康柏西普不同给药方案治疗息肉样脉络膜血管病变(PCV)的效果。方法:将21例符合入组条件的,就诊于我院的PCV患者随机分为两组,A组:3+Q12W方案(固定给药组),9例9眼,连续3次每4wk玻璃体腔注射0.5mg康柏西普眼用注射液,之后每12wk给药1次;B组:3+TAE方案(延长给药组),12例12眼,连续3次每4wk玻璃体腔注射0.5mg康柏西普眼用注射液,之后根据每次访视评估结果确定下次给药的时间,至下一次访视/治疗间隔最短4wk,最长不超过12wk。分别于治疗12、48wk时比较两组最佳矫正视力(BCVA)及中心视网膜厚度(CRT)及给药的次数。结果:治疗12、48wk时固定给药组的BCVA分别为74.78±11.23、74.67±13.94个字母,分别比治疗前提高了7.00±4.21、6.89±4.48个字母;在治疗12、48wk时延长给药组BCVA分别为77.83±5.46、77.58±8.59个字母,分别比治疗前提高了8.75±7.54、8.50±5.60个字母。注射后12、48wk固定给药组黄斑CRT分别为276.33±44.34、240.56±40.11μm,分别比治疗前下降了43.22±42.21、79.00±53.64μm;注射后第12、48wk延长给药组黄斑CRT分别为271.58±63.08、241.00±43.91μm,分别比治疗前下降了57.42±45.33、88.00±61.16μm。固定给药组和延长给药组球内注射康柏西普次数分别为6.00±0.00、7.75±1.14次。结论:两种康柏西普给药方案均可以减轻PCV患者CRT,提高视力,固定给药组球内注射的次数少于延长给药组。     

Role of gut microbiota in the pathogenesis and therapeutics of minimal hepatic encephalopathy via the gut-liver-brain axis

Minimal hepatic encephalopathy (MHE) is a frequent neurological and psychiatric complication of liver cirrhosis. The precise pathogenesis of MHE is complicated and has yet to be fully elucidated. Studies in cirrhotic patients and experimental animals with MHE have indicated that gut microbiota dysbiosis induces systemic inflammation, hyperammonemia, and endotoxemia, subsequently leading to neuroinflammation in the brain via the gut-liver-brain axis. Related mechanisms initiated by gut microbiota dysbiosis have significant roles in MHE pathogenesis. The currently available therapeutic strategies for MHE in clinical practice, including lactulose, rifaximin, probiotics, synbiotics, and fecal microbiota transplantation, exert their effects mainly by modulating gut microbiota dysbiosis. Microbiome therapies for MHE have shown promised efficacy and safety; however, several controversies and challenges regarding their clinical use deserve to be intensively discussed. We have summarized the latest research findings concerning the roles of gut microbiota dysbiosis in the pathogenesis of MHE via the gut-liver-brain axis as well as the potential mechanisms by which microbiome therapies regulate gut microbiota dysbiosis in MHE patients.     

Neuropharmacological insight into preventive intervention in posttraumatic epilepsy based on regulating glutamate homeostasis

Background

Posttraumatic epilepsy (PTE) is one of the most critical complications of traumatic brain injury (TBI), significantly increasing TBI patients' neuropsychiatric symptoms and mortality. The abnormal accumulation of glutamate caused by TBI and its secondary excitotoxicity are essential reasons for neural network reorganization and functional neural plasticity changes, contributing to the occurrence and development of PTE. Restoring glutamate balance in the early stage of TBI is expected to play a neuroprotective role and reduce the risk of PTE.

Aims

To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis.

Methods

We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance.

Results

TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective.

Discussion

Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson's disease, depression, and cognitive impairment.

Conclusion

It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.     

幽门螺杆菌抗生素耐药影响因素的研究进展

幽门螺杆菌是一种全球流行率较高的人类病原体，与胃肠道内外多种疾病有关，根除幽门螺杆菌对防治这些疾病至关重要。抗生素治疗仍然是目前根除幽门螺杆菌的主要手段，然而，幽门螺杆菌抗生素耐药性的出现使其根除成功率明显下降。除了用药敏试验和耐药基因的检测指导抗生素的有效使用，分析与抗生素耐药发病率增加相关的临床影响因素对临床医生经验性为患者选择合适的抗生素治疗同样意义重大。该文就与幽门螺杆菌抗生素耐药相关临床影响因素的研究现状和进展作一综述。     

酪酸梭菌联合四联疗法治疗幽门螺杆菌阳性胃溃疡的作用机制研究

摘要：目的  观察酪酸梭菌（Cb）联合四联疗法治疗幽门螺杆菌（Hp）阳性胃溃疡的作用。方法  选取Hp阳性胃溃疡102例，采取随机双盲方法，将其分为观察组和对照组。前2周，观察组口服埃索美拉唑镁肠溶片+枸橼酸铋剂钾片+阿莫西林胶囊+左氧氟沙星片+酪酸梭菌活菌胶囊，对照组在上述四联疗法基础上加空白胶囊；后2周，停用抗生素和枸橼酸铋剂钾片。疗程结束后1个月，比较两组治疗有效率、Hp根除率、不良反应发生率。结果  观察组有效率为89.46%，对照组为76.00%，经χ2检验，差异无统计学意义（P >0.05）。观察组HP根除率为82.69%，对照组HP为64.00%，经χ2检验，差异有统计学意义（P <0.05）。观察组不良反应发生率为11.54%，对照组为18.00%，经χ2检验，差异无统计学意义（P >0.05）。结论  Cb联合四联疗法能够提高胃溃疡Hp根除率。

     

Backscatter tensor imaging and 3D speckle tracking for simultaneous ex vivo structure and deformation measurement of myocardium

Objective: Biaxial mechanical testing is a common method for elucidation of mechanical properties of excised ventricular myocardium, especially in the context of structural remodeling that accompanies heart disease. Current imaging strategies in biaxial testing are based on optical camera imaging of the tissue surface, thus providing no information about the tissue microstructure and limiting strain measurements to two dimensions. Here, these limitations are overcome by replacing the camera with ultrasound imaging in order to measure both transmural fiber orientation and 3D tissue deformation during biaxial testing. Methods: Quasi-static biaxial mechanical testing is applied to four samples of excised porcine ventricular myocardium (two left- and two right-ventricular tissues). During testing, a rotational scan of an ultrasound linear array provides data for both backscatter tensor imaging and 3D speckle tracking, from which transmural fiber orientation and tissue deformation are computed, respectively. Ultrasound-derived fiber orientation and tissue strain are validated against histology and camera surface imaging, respectively. Discussion: Ultrasound-derived fiber angle and tissue strain exhibit good accuracy, with root-mean-square errors of 9.9° and 1.2% strain, respectively. Further investigation into the optimization of backscatter tensor imaging is warranted. Replacing the rotational scan of a linear array with volume imaging with a matrix array will improve the technique. Conclusion: Ultrasound imaging can replace the optical camera measurement during biaxial mechanical testing of ventricular myocardium in order to accurately provide measurements of transmural fiber orientation and tissue strain. In situ knowledge of transmural fiber structure and tissue deformation can enhance the inverse problem used to determine tissue mechanical properties from biaxial testing.