Transcatheter aortic valve replacement(TAVR)has become an important therapeutic approach for severe aortic stenosis.However,complications associated with TAVR cannot be overlooked,among which contrast agents induced acute kidney injury(AKI)is a common complication.To explore methods to reduce the occurrence of AKI,this article reports two cases of successful treatment of severe aortic stenosis by TAVR under pure echocardiographic guidance,both of whom were elderly women aged 75 and 69,respectively,and both were implanted with a Evolute Pro 26 mm valve.Postoperative echocardiography showed good valve positioning and function.

Objective:To investigate the effects of glimepiride on cerebral edema and apoptosis in a rat model of sub-arachnoid hemorrhage(SAH).Methods:An SAH model was established in rats using the internal carotid artery punc-ture method.Low-dose glimepiride was administered via intraperitoneal injection.Neurological deficits were assessed u-sing the modified Neurological Severity Score(mNSS),and brain water content was evaluated by measuring the wet-dry weight ratio of brain tissue.Cortical tissue from the surgical side was collected to measure the mRNA expression of sul-fonylurea receptor 1(SUR1)and transient receptor potential melastatin 4(TRPM4)using RT-qPCR,while the protein expression of Bcl-2 and Bax was detected by Western blot.Results:SAH rats exhibited impaired neurological function,increased brain water content,upregulation of SUR1 and TRPM4 mRNA expression,and a decreased Bcl-2/Bax ratio.Low-dose glimepiride did not affect blood glucose levels but significantly improved neurological function and reduced cerebral edema in SAH rats.Although glimepiride had no significant effect on SUR1 and TRPM4 mRNA expression,it increased the Bcl-2/Bax ratio.Conclusion:Glimepiride alleviates cerebral edema and inhibits apoptosis in SAH model rats by suppressing the SUR1-TRPM4 channel.

Objective:To explore the effect of melatonin on mitophagy in the brain tissue of rats with early subarach-noid hemorrhage(SAH).Methods:The rat model of SAH was established by internal carotid artery puncture and trea-ted with melatonin by intraperitoneal injection.At 24 hours after the operation,the neurological function of rats was de-tected by mNSS score and balance beam test.The contents of reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)and in brain tissue were detected by commercial reagent kits.The expression changes of PINK1/Parkin,microtubule-associated protein1A/1B-light chain3(LC3)and p62 in brain tissue were detected by Western blot.Results:Melatonin can significantly improve the neurological function of SAH rats,reduce the con-tents of MDA(P<0.05)and ROS(P<0.05),and increase the content of GSH(P<0.05).Meanwhile,Western blot detection indicated that melatonin could increase the expression of PINK1 and Parkin(P<0.05),increase the ratio of LC3-II/LC3-I(P<0.05),and reduce the expression of p62(P<0.05).Conclusion:Melatonin alleviates early brain injury in rats with subarachnoid hemorrhage through PINK1/Parkin-mediated mitophagy.

Objective:To evaluate the effect of deep brain stimulation(DBS)of the lateral cerebellar nucleus(LCN)on synaptic plasticity in a traumatic brain injury(TBI)rat model of the medial prefrontal cortex(mPFC).Methods:A controllable mPFC injury rat model was prepared using a hydraulic impact method.Two weeks after inju-ry,stimulation electrodes were implanted into the left LCN.Electrical stimulation was initiated at the 4th week after injury and continued for 30 days.The learning and memory function of the rats was evaluated using the Morris water maze.RT-qPCR and Western blot were used to detect the mRNA and protein expressions of brain-derived neurotrophic factor(BDNF),postsynaptic density protein 95(PSD95),and growth-associated protein 43(GAP43)in the mPFC region.Results:The learning and memory function of the mPFC-injured rats significantly decreased.The expressions of BDNF,PSD95,and GAP43 in mPFC decreased.DBS treatment significantly enhanced the learning and memory ability of mPFC-injured rats,and simultaneously upregulated the expressions of BDNF,PSD95,and GAP43 in mPFC.Conclusion:LCN DBS is an effective method for treating cognitive impairment caused by TBI,and it may achieve this through activating the neural plasticity mechanism of the mPFC.

Objective:To evaluate the effect of deep brain stimulation(DBS)of the lateral cerebellar nucleus(LCN)on synaptic plasticity in a traumatic brain injury(TBI)rat model of the medial prefrontal cortex(mPFC).Methods:A controllable mPFC injury rat model was prepared using a hydraulic impact method.Two weeks after inju-ry,stimulation electrodes were implanted into the left LCN.Electrical stimulation was initiated at the 4th week after injury and continued for 30 days.The learning and memory function of the rats was evaluated using the Morris water maze.RT-qPCR and Western blot were used to detect the mRNA and protein expressions of brain-derived neurotrophic factor(BDNF),postsynaptic density protein 95(PSD95),and growth-associated protein 43(GAP43)in the mPFC region.Results:The learning and memory function of the mPFC-injured rats significantly decreased.The expressions of BDNF,PSD95,and GAP43 in mPFC decreased.DBS treatment significantly enhanced the learning and memory ability of mPFC-injured rats,and simultaneously upregulated the expressions of BDNF,PSD95,and GAP43 in mPFC.Conclusion:LCN DBS is an effective method for treating cognitive impairment caused by TBI,and it may achieve this through activating the neural plasticity mechanism of the mPFC.

Transcatheter aortic valve replacement(TAVR)has become an important therapeutic approach for severe aortic stenosis.However,complications associated with TAVR cannot be overlooked,among which contrast agents induced acute kidney injury(AKI)is a common complication.To explore methods to reduce the occurrence of AKI,this article reports two cases of successful treatment of severe aortic stenosis by TAVR under pure echocardiographic guidance,both of whom were elderly women aged 75 and 69,respectively,and both were implanted with a Evolute Pro 26 mm valve.Postoperative echocardiography showed good valve positioning and function.

Objective:To investigate the effects of glimepiride on cerebral edema and apoptosis in a rat model of sub-arachnoid hemorrhage(SAH).Methods:An SAH model was established in rats using the internal carotid artery punc-ture method.Low-dose glimepiride was administered via intraperitoneal injection.Neurological deficits were assessed u-sing the modified Neurological Severity Score(mNSS),and brain water content was evaluated by measuring the wet-dry weight ratio of brain tissue.Cortical tissue from the surgical side was collected to measure the mRNA expression of sul-fonylurea receptor 1(SUR1)and transient receptor potential melastatin 4(TRPM4)using RT-qPCR,while the protein expression of Bcl-2 and Bax was detected by Western blot.Results:SAH rats exhibited impaired neurological function,increased brain water content,upregulation of SUR1 and TRPM4 mRNA expression,and a decreased Bcl-2/Bax ratio.Low-dose glimepiride did not affect blood glucose levels but significantly improved neurological function and reduced cerebral edema in SAH rats.Although glimepiride had no significant effect on SUR1 and TRPM4 mRNA expression,it increased the Bcl-2/Bax ratio.Conclusion:Glimepiride alleviates cerebral edema and inhibits apoptosis in SAH model rats by suppressing the SUR1-TRPM4 channel.

Objective:To explore the effect of melatonin on mitophagy in the brain tissue of rats with early subarach-noid hemorrhage(SAH).Methods:The rat model of SAH was established by internal carotid artery puncture and trea-ted with melatonin by intraperitoneal injection.At 24 hours after the operation,the neurological function of rats was de-tected by mNSS score and balance beam test.The contents of reactive oxygen species(ROS),malondialdehyde(MDA),and glutathione(GSH)and in brain tissue were detected by commercial reagent kits.The expression changes of PINK1/Parkin,microtubule-associated protein1A/1B-light chain3(LC3)and p62 in brain tissue were detected by Western blot.Results:Melatonin can significantly improve the neurological function of SAH rats,reduce the con-tents of MDA(P<0.05)and ROS(P<0.05),and increase the content of GSH(P<0.05).Meanwhile,Western blot detection indicated that melatonin could increase the expression of PINK1 and Parkin(P<0.05),increase the ratio of LC3-II/LC3-I(P<0.05),and reduce the expression of p62(P<0.05).Conclusion:Melatonin alleviates early brain injury in rats with subarachnoid hemorrhage through PINK1/Parkin-mediated mitophagy.

Objective:Cerebral hemorrhage can lead to neuronal cell death,nervous system disorder and permanent disability.Chlorogenic acid(CGA)has antioxidant,anti-inflammatory and anti-apoptotic properties.This study was to investigate the neuroprotective effect of CGA on subarachnoid hemorrhage(SAH)in rats.Methods:SAH was induced by carotid artery puncture in male adult rats.CGA(30 mg/kg)was injected intraperitoneally 2 h after SAH.Neurologi-cal outcomes were assessed 24 h after SAH by modified Garcia scores and the beam balance test.The brain edema was evaluated by dry-wet ratio method.Oxidative stress was assessed by measuring reactive oxygen species(ROS)and su-peroxide dismutase(SOD)activity in rat cortex using commercial kits.Results:SAH caused severe neurobehavioral defects and cerebral edema in rats.The level of ROS in cerebral cortex increased,while the activity of SOD decreased.However,CGA treatment improved the neurobehavioral deficits induced by SAH,while reducing ROS levels and enhan-cing SOD activity.Conclusion:CGA plays a neuroprotective role through anti-oxidative stress.

Objective:To analyze the key differentially expressed genes and related pathways in patients with de-layed cerebral ischemia(DCI)occurring after aneurysmal subarachnoid hemorrhage(aSAH)based on gene expression database(GEO)datasets.Methods:Gene datasets meeting the study requirements were screened from the GEO data-base and divided into a patient group with DCI after aSAH and a control group without DCI,and differentially expressed genes(DEGs)analysis,gene ontology(GO)enrichment analysis,Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis,and gene set enrichment analysis(GSEA)were performed by using R software to find rele-vant genes and pathways.Results:A total 140 differentially expressed genes were identified.KEGG analysis showed that there were 10 significantly enriched signaling pathways(P＜0.05),mainly related to hypoxia-inducible factor-1(HIF-1)signaling pathway,glutamatergic synapses,cell adhesion molecules,and chemokine signaling pathways,etc.Twenty-six significantly enriched entries were obtained according to the functional analysis of GO,which involved entries in three categories,namely,biological processes,cellular components,and molecular functions.GSEA analysis showed that two pathways,extracellular matrix receptor interactions as well as peroxisomes,had significant enrichment differ-ences between the patient group and the control group.Conclusion:The development of DCI after aSAH involves sever-al genes such as COL17A1,RPL11,FCAMR,GNB2L1,HIF1A,and can affect the development of DCI through various pathways such as vascular dysfunction,inflammatory response,neurological injury,and oxidative stress.