Traumatic brain injury (TBI) is a critical neurological condition, with neuronal damage being its fundamental pathological basis. However, molecular targets for the prevention and treatment of neuronal injury remain to be further explored. Parkin is an important molecule closely associated with neurodegenerative diseases, yet relatively few studies have investigated its relationship with TBI. In this study, we first established and validated both the controlled cortical impact (CCI) and traumatic neuronal injury (TNI) models. Using these models, we revealed that TBI led to the upregulation of Parkin expression, with a peak occurring 24 h post-injury. Furthermore, at the in vitro level, lentivirus-mediated modulation of Parkin expression revealed that Parkin overexpression alleviated TNI-induced neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction, whereas Parkin knockdown exacerbated neuronal damage. At the mechanistic level, the study demonstrated that Parkin promoted mitochondrial biogenesis and fission while inhibiting mitochondrial fusion and attenuated the impairment of mitophagy after TBI. In other words, Parkin exerts a neuroprotective role through regulating mitochondrial quality control. We further employed adeno-associated viruses and Parkin knockout mice to modulate Parkin expression in vivo. The results showed that Parkin attenuated CCI-induced brain damage, edema, and behavioral deficits, whereas Parkin knockout exacerbated brain injury and functional impairments. Finally, we designed and synthesized a recombinant Parkin protein and preliminarily validated its protective effects at the cellular level. In summary, this study provides new insights for the therapeutic targets against TBI.

This study aimed to evaluate the efficacy of a skull base reconstruction strategy for treating intraoperative high-flow cerebrospinal fluid (CSF) leaks during endoscopic endonasal approach (EEA) in the sellar region. This single-institution prospective study included patients who underwent EEA with multi-layer reconstruction between May 2023 and April 2025. Patients were divided into groups 1, 2, & 3, based on the quality of the pedicled nasoseptal flap (PNSF): high-quality, low-quality, and unavailable PNSF, respectively. We analyzed postoperative complications (failed skull base reconstruction and meningitis), time in bed, and length of hospital stay. Of 86 patients enrolled, we encountered three cases of failed skull base reconstruction (3.5%) and four cases of meningitis (4.7%), indicating a reduction in the postoperative complication rate. There were no significant differences in postoperative complications between the three groups (P > 0.05). There was no significant difference in lengths of hospital stay (10.82 ± 3.80 vs. 12.41 ± 2.26, P > 0.05) and time in bed (9.00 ± 4.06 vs. 10.00 ± 2.36, P > 0.05) between Groups 1 and 2, respectively. Group 3 had longer lengths of hospital stay and time in bed than the other groups (P < 0.001). The modified multi-layer skull base reconstruction based on the quality of PNSF is a reliable method for treating intraoperative high-flow CSF leak during EEA surgeries and was associated with low complications rates in this cohort.

Phosphoglycerate dehydrogenase (PHGDH) is a key molecule in the progression of Alzheimer's disease. Herein, we report that PHGDH exerts a significant influence on cerebral ischemia-reperfusion injury (CIRI). Ischemia-reperfusion injury is predominantly triggered by oxidative stress and inflammatory responses; however, the underlying molecular mechanisms remain incompletely understood. Our findings demonstrate that PHGDH displays predominant expression in brain astrocytes and undergoes time-dependent alterations in reactive astrocytes following cerebral ischemia-reperfusion. Specifically, targeted knockdown of PHGDH expression in astrocytes substantially exacerbates pathological damage and neurological deficits post cerebral ischemia-reperfusion. Subsequent mechanistic analyses unveiled that PHGDH knockdown predominantly facilitates astrocyte pyroptosis and neuroinflammation. Specifically, downregulation of PHGDH in astrocytes induces oxidative stress, augments ROS production, and diminishes antioxidant levels of GSH and NADPH. Moreover, PHGDH downregulation disrupts the mitochondrial respiratory chain, triggering mitochondrial damage and dsDNA release during ischemia-reperfusion, thereby exacerbating oxidative stress. Collectively, these mechanisms culminate in AIM2 inflammasome activation, as evidenced by substantial increases in AIM2, ASC, and Cleaved Caspase-1 expression. Notably, exogenous depletion of serine and glycine fails to fully explain the astrocyte pyroptosis triggered by PHGDH knockdown. In conclusion, downregulation of PHGDH in astrocytes post cerebral ischemia-reperfusion predominantly drives astrocyte pyroptosis via oxidative stress, resulting in the release of pro-inflammatory cytokines (e.g., IL-1β and IL-18) and subsequent exacerbation of ischemia-reperfusion injury. These novel insights into the role of PHGDH may inform the development of targeted therapeutic strategies for cerebral ischemia-reperfusion.

Selective neuron death or loss, which induced by specific pathogen- and damage-associated molecular patterns (PAMPs and DAMPs), was the main reason results in high morbidity, disability, and mortality of transient ischemic attack (TIA) in man and postmenopausal women. Shank3, a key postsynaptic density, is correlated with synaptic dysfunction, oxidative stress, inflammatory, apoptosis and poor outcomes in ischemic stroke, although its role in menopausal women TIA remains elusive. Here we discovered that Shank3 direct binds Gal-3, a positive regulator of aging and inflammation, then regulates innate immune sensors ZBP-1, to drive inflammatory signaling and inflammatory cell death, PANoptosis, during TIA. Base on the defeminization TIA models (a stable female mouse OVX + TIA model was first established as well as an in vitro cultured primary neuron desexualization + tOGD/R model), blockade of Shank3 amplify neuron PANoptosis, oxidative stress and inflammation, arouse persistent behavioral deficits and infarction formation, which does not appear in de-estrogen combination with TIA damage mice. We also observed that Shank3, Gal-3 and ZBP-1 were members of a large multi-protein complex along with Caspase 3, 7, 8, 9, 1, NLRP 3, GSDMD, GSDME, RIPK 1, RIPK 3 and MLKL that drove neuronal-special PANoptosis. In addition, administration of a natural inflammatory inhibitor, D-allose, used for food sweetener, produces anti-PANoptosis effects via activating Shank3 but inhibiting Gal-3 and ZBP-1. Collectively, our findings establish a previously unknown regulatory connection and molecular interaction among Shank3, Gal-3 and ZBP-1 as a driver of neuron-specific PANoptosis in postmenopausal female TIA, and reveal activate of Shank3, such as, D-allose, maybe a potential strategy to halt neuronal loss during TIA.

DNA damage binding protein 1 (DDB1), a substrate receptor of CUL4-DDB1 E3 ligase, is overexpressed in various cancers and acts as a tumor promoting factor. However, the role of DDB1 in the metabolism of pituitary adenoma (PA) remains unclear. Here, we found that DDB1 was upregulated in PA tissues, and silencing DDB1 significantly inhibited the proliferation, cell cycle, prolactin (PRL) secretion and aerobic glycolysis in PA cells, whereas DDB1 overexpression had the opposite effect. We also confirmed that the co-localization and interaction of DDB1 and PAK1 using Co-IP and dual immunofluorescence experiments. Further analysis of cell functions showed that PAK1 knockdown or 2DG treatment reversed the effect of DDB1 overexpression on proliferation, cell cycle, PRL secretion, aerobic glycolysis, and apoptosis in PA cell lines. Importantly, we observed that overexpression of DDB1 in vivo promoted tumor growth in xenograft mice, which could be reversed by knockout of PAK1. In short, DDB1 promotes PA tumor growth and PRL secretion by enhancing PAK1-mediated aerobic glycolysis. Our results reveal that targeting the DDB1/PAK1 axis may provide a potential therapeutic strategy for PA.

D-allose, a rare sugar with anti-oxidant, anti-inflammatory, anti-cancer, immunosuppressing and other physiological functions, has become a research hotspot in recent years. This paper describes the physical and chemical properties, synthesis methods, metabolism, physiological functions, and applications of D-allose, aiming to promote the functional development of D-allose and facilitate the application of D-allose in the food field and clinical treatment.

Homer1a and A2 astrocytes are involved in the regulation of inflammation induced by intracerebral hemorrhage (ICH). However, there is no anticipated treatment strategy based on the anti-inflammatory effect of Homer1a and A2 astrocytes. Here, we successfully induced A2 astrocytes in vitro, and then we report an efficient method to prepare Homer1a+ EVs derived from A2 astrocytes which making it more stable, safe, and targetable to injured neurons. Homer1a+ EVs promotes the conversion of A1 to A2 astrocytes in ICH mice. Homer1a+ EVs inhibits activation and nuclear translocation of NF-κB, thereby regulating transcription of IL-17A in neurons. Homer1a+ EVs inhibits the RAGE/NF-κB/IL-17 signaling pathway and the binding ability of IL-17A: IL17-AR and RAGE: DIAPH1. In addition, Homer1a+ EVs ameliorates the pathology, behavior, and survival rate in GFAPCreHomer1fl/−Homer1a± and NestinCreRAGEfl/fl ICH mice. Our study provides a novel insight and potential for the clinical translation of Homer1a+ EVs in the treatment of ICH.

Objective: Cerebral ischemia-reperfusion injury (CIRI) is a particularly severe pathological condition that arises when blood is restored to an injured area after cerebral ischemia. Neuronal cell death stands out as the most severe detrimental outcome of CIRI. Therefore, it is critical to explore neuroprotective strategies following CIRI. This study aimed to assess the potential neuroprotective effects of D-allose in the context of CIRI by targeting the Gal-3/NLRP3 pathway and reducing neuronal cell death. Methods: In this study, we employed a middle cerebral artery occlusion (MCAO) model that included pretreatment with D-allose. Assessment of MCAO injury included behavioral analysis, neurological function scoring, and triphenyl tetrazolium chloride (TTC) staining. Apoptosis following CIRI and D-allose treatment was determined using TUNEL. Furthermore, we examined the expression of pyroptosis related molecules and Gal-3 using q-PCR, Western Blotting, and immunofluorescence staining. Results: Behavioral analysis, neurological function scoring and TTC staining, revealed that pretreatment with D-allose alleviated MCAO-induced brain injury. Additionally, D-allose treatment was associated with reduced expression of pyroptosis-related molecules and Gal-3 following CIRI. In the MCAO+AAV-shGal-3 group, wherein Gal-3 expression was down-regulated, the expression of pyroptosis-related molecules was lower compared to the MCAO+NC group. However, D-allose treatment did not further enhance this reduction. Conclusions: These findings strongly indicate that D-allose might play a neuroprotective role in CIRI by downregulating Gal-3 expression, thereby inhibiting activation of the pyroptosis pathway.

目的 探讨D-阿洛糖(D-allose)对小鼠脑缺血再灌注损伤(CIRI)的神经功能恢复、半乳糖凝集素-3(Gal-3)、腺苷一磷酸活化蛋白激酶/哺乳动物雷帕霉素靶蛋白(AMPK/mTOR)及部分炎症因子表达的影响.方法 C57BL/6雄性小鼠50只,随机分为对照组(Con组)、假手术组(Sham组)、脑缺血再灌注损伤组(MCAO组)、脑缺血再灌注损伤+D-阿洛糖组(MCAO+D-allose组)及脑缺血再灌注损伤+改良柑橘果胶组(MCAO+MCP组).采用线栓法建立大脑中动脉闭塞/再灌注(MCAO/R)模型.造模成功后对小鼠进行Longa神经功能评分及转棒行走评分;采用TTC染色法观察脑梗死灶体积;通过Western blot及RT-PCR技术检测Gal-3、自噬相关分子的表达水平;免疫荧光技术检测脑组织中Gal-3的分布情况;试剂盒检测TNF-α,IL-8分泌.结果 相较于Con组和Sham组,MCAO模型可增加小鼠神经功能评分(P＜0.01)、增加脑梗死体积(P＜0.01)、上调Gal-3的表达并增强自噬(P＜0.01).给予D-阿洛糖及Gal-3抑制剂MCP治疗后可改善神经功能障碍、减小脑梗死体积(P＜0.01),并降低Gal-3的表达(P＜0.01),抑制AMPK磷酸化,促进mTOR磷酸化,抑制自噬(P＜0.01).结论 D-阿洛糖可有效促进CIRI小鼠神经功能恢复和减小梗死灶体积,其机制可能是通过下调Gal-3的表达进而抑制组织损伤后细胞过度自噬,并减少TNF-α,IL-8等炎性因子释放,从而发挥神经保护作用.

Ischemic stroke is an acute brain disease with a high mortality rate. Currently, the only effective method is to restore the blood supply. But the inflammation and oxidative stress induced by this approach can damage the integrity of the endothelial system, which hampers the patient's outcome. D-allose has the biological activity to protect against ischemia-reperfusion injury, however, the underlying mechanism remains unclear. Here, brain microvascular endothelial cells (RBMECs) were used as the study material to establish an IR-injury model. Cell viability of RBMECs was suppressed after hypoxia/reoxygenation (H/R) treatment and significantly increased after D-allose supplementation. RNAseq results showed 180 differentially expressed genes (DEGs) between the therapy group (H/R + Dal) and the model group (H/R), of which 151 DEGs were restored to control levels by Dallose. Enrichment analysis revealed that DEGs were mainly involved in protein processing in endoplasmic reticulum. 6 DEGs in the unfolded protein response (UPR) pathway were verified by qRT-PCR. All of them were significantly down-regulated by D-allose, indicating that endoplasmic reticulum stress (ERS) was relieved. In addition, D-allose significantly inhibited the phosphorylation level of eIF2 alpha, a marker of ERS. The downstream molecules of Phosphorylation of eIF2 alpha, Gadd45a and Chac1, which trigger cycle arrest and apoptosis, respectively, were also significantly inhibited by D-allose. Thus, we conclude that D-allose inhibits the UPR pathway, attenuates eIF2 alpha phosphorylation and ERS, restores the cell cycle, inhibits apoptosis, and thus enhances endothelial cell tolerance to H/R injury.

Background Ischemic stroke (IS) occurs when a blood vessel supplying the brain becomes obstructed, resulting in cerebral ischemia. This type of stroke accounts for approximately 87% of all strokes. Globally, IS leads to high mortality and poor prognosis and is associated with neuroinflammation and neuronal apoptosis. D-allose is a bio-substrate of glucose that is widely expressed in many plants. Our previous study showed that D-allose exerted neuroprotective effects against acute cerebral ischemic/reperfusion (I/R) injury by reducing neuroinflammation. Here, we aimed to clarify the beneficial effects D-allose in suppressing IS-induced neuroinflammation damage, cytotoxicity, neuronal apoptosis and neurological deficits and the underlying mechanism in vitro and in vivo. Methods In vivo, an I/R model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R) in C57BL/6 N mice, and D-allose was given by intraperitoneal injection within 5 min after reperfusion. In vitro, mouse hippocampal neuronal cells (HT-22) with oxygen–glucose deprivation and reperfusion (OGD/R) were established as a cell model of IS. Neurological scores, some cytokines, cytotoxicity and apoptosis in the brain and cell lines were measured. Moreover, Gal-3 short hairpin RNAs, lentiviruses and adeno-associated viruses were used to modulate Gal-3 expression in neurons in vitro and in vivo to reveal the molecular mechanism. Results D-allose alleviated cytotoxicity, including cell viability, LDH release and apoptosis, in HT-22 cells after OGD/R, which also alleviated brain injury, as indicated by lesion volume, brain edema, neuronal apoptosis, and neurological functional deficits, in a mouse model of I/R. Moreover, D-allose decreased the release of inflammatory factors, such as IL-1β, IL-6 and TNF-α. Furthermore, the expression of Gal-3 was increased by I/R in wild-type mice and HT-22 cells, and this factor further bound to TLR4, as confirmed by three-dimensional structure prediction and Co-IP. Silencing the Gal-3 gene with shRNAs decreased the activation of TLR4 signaling and alleviated IS-induced neuroinflammation, apoptosis and brain injury. Importantly, the loss of Gal-3 enhanced the D-allose-mediated protection against I/R-induced HT-22 cell injury, inflammatory insults and apoptosis, whereas activation of TLR4 by the selective agonist LPS increased the degree of neuronal injury and abolished the protective effects of D-allose. Conclusions In summary, D-allose plays a crucial role in inhibiting inflammation after IS by suppressing Gal-3/TLR4/PI3K/AKT signaling pathway in vitro and in vivo.

目的:总结鞍区Rathke囊肿的临床特点和经鼻内镜手术治疗的临床技巧和疗效.方法:回顾性分析经鼻内镜手术治疗的46例鞍区症状性Rathke囊肿患者的临床资料,总结分析其疗效、并发症和手术优越性.其中38例行单鼻孔入路,8例行双鼻孔入路,观察组采用囊肿引流29例,采用囊液引流后囊壁部分切除17例作为对照组,依据不同手术进行颅底多层重建.结果:所有病例随访1～7年,对不同手术方式组临床资料进行比较.所有病例头痛症状缓解24(96.2％)例,视力改善12(92.3％)例,内分泌症状缓解26(92.9％)例;两组间比较无统计学差异(均P>0.05),术中出现4例(8.7％)脑脊液漏,不同入路组间比较有统计学差异(P<0.05);3例出现嗅觉减退,1例出现垂体功能低下,1例在术后3年复发,给予临床观察,随访无变化,组间比较无统计学差异(均P>0.05);所有病例术后未见脑脊液漏的发生.结论:经鼻内镜治疗鞍区症状性Rathke囊肿,能够有效缓解症状,疗效确切,临床应用前景较好.

Purpose: Stroke is a multifactorial and complex disease caused by the obstruction or rupture of cerebrovascular. To explore the influence of genetic factors on stroke susceptibility, we investigated the association between four single nucleotide polymorphisms (SNPs) in the paired-like homeodomain transcription factor 2 (PITX2) gene and stroke risk. Methods: A total of 977 volunteers including 476 stroke patients and 501 control individuals were recruited. The association between PITX2 polymorphisms and stroke risk was evaluated using genetic models and haplotype analyses. The strength of the association between each studied polymorphisms and stroke risk was evaluated by calculating odds ratios (ORs) and 95% confidence intervals (CIs). What's more, multifactor dimensionality reduction (MDR) was used to predict the interaction between SNPs. Results: Our study showed that rs6817105 in PITX2 was related to a significant increase in stroke susceptibility (OR = 1.42, 95% CI = 1.04-1.94, p = 0.028). Stratified analyses based on gender indicated that rs6817105, rs13143308, and rs6843082 polymorphisms were significantly associated with an increased risk of stroke in male (OR = 0.68, 95% CI = 0.47-0.99, p = 0.042; OR = 0.53, 95% CI = 0.30-0.96, p = 0.035; and OR = 0.55, 95% CI = 0.30-0.99, p = 0.047). Besides, SNP rs6817105 was significantly increased the risk of stroke in people at age over 65 years (OR = 1.87, 95% CI =1.12-3.11, p = 0.016). MDR showed that the interaction model of rs6817105 and rs3853445 emerged as the best predictor between the PITX2 gene and stroke susceptibility. Conclusions: This study indicated that there was a significant association between the PITX2 gene and stroke risk, and provided some data as far as possible to support the prevention of stroke.

BackgroundThe surgical treatment of the extended endoscopic endonasal approach (EEEA) is a safe and effective treatment for suprasellar craniopharyngiomas. However, due to damage to the hypothalamus and third ventricle floor (TVF), EEEA is generally regarded as unsuitable in treating intrinsic third ventricle craniopharyngioma (ITVC) that is entirely within the third ventricle. Until now, there have been only a small number of reports using EEEA to treat TVC via a supra-infrachiasmatic approach. Given that the translamina terminalis (TLT) corridor was used in the transcranial subfrontal approach, EEEA via a suprachiasmatic approach may be feasible and practical to treat ITVC. In the current study, we accumulated experience applying the suprachiasmatic translamina terminalis (STLT) corridor for anterior treatment of ITVC.MethodsFrom March 2016 to December 2020, 14 patients with ITVC in our center were analyzed retrospectively. All patients underwent surgery by EEEA via an STLT corridor. The multilayer reconstruction technique was adopted to achieve skull base reconstruction. Data concerning the patient’s tumor resection, vision, hypophyseal hormone, and complications were collected.ResultsGross-total resection was achieved in 13 (92.8%) of14 patients, with achievement of near-total (90%) resection in the remaining 1 patient. Nine cases (64.3%) were papillary craniopharyngiomas, and the other 5 cases were adamantinomatous subtypes. Postoperatively, 3 patients with pituitary insufficiency received hormone replacement therapy. No permanent diabetes insipidus or hypothalamic obesity was found. All pairs showed significant improvement or stability in vision except 1 patient who encountered visual deterioration. No other neurological deficit occurred postoperatively. Observation results for the exudation of nasal tissue and the length of hospitalization were satisfactory. After a mean follow-up period of 26.2 months, tumor recurrence was not observed.ConclusionTLT is a minimally invasive corridor used in EEEA for treating anterior ITVC without increasing risks of visual and hormonal deficits. The multilayered reconstruction technique we used is a safe and effective method for achieving watertight closure and avoiding cerebrospinal fluid leaks and infection. The endonasal approach via STLT provides a new, safe and efficacious operative strategy that should be considered a surgical alternative in treating ITVC.

缺血再灌注损伤是以器官供血受限,随后血流和供氧恢复,出现明显的结构、功能变化为特征的一种病理过程[1].血流恢复后可能导致潜在的有害影响,如细胞坏死、细胞肿胀以及组织各部分血流不均匀恢复等.再灌注阶段,血流的恢复导致破坏性炎症反应,产生大量活性氧,细胞内钙离子堆积,引起细胞凋亡蛋白释放,导致大量细胞凋亡[2].针对缺血再灌注的损伤机制,有研究[3-5]提出,可以使用如缺血预处理、爱帕琳肽、褪黑素等治疗方法或治疗药物减轻缺血再灌注损伤.近年来,D-阿洛糖被发现具有对抗缺血再灌注损伤的作用.最近的研究[6]发现,D-阿洛糖对抗缺血再灌注损伤时,主要在抑制中性粒细胞的激活、减少细胞因子与趋化因子的释放等方面发挥重要作用.因此,D-阿洛糖近年来已成为抗缺血再灌注损伤研究的热点靶向药物,相关基础分子机制研究为临床治疗提供了新思路和实验基础.

目的 分析颅脑损伤患者合并眼部损伤的临床特征.方法 回顾性分析2011年2月—2019年9月空军军医大学第一附属医院神经外科收治的中、重型颅脑损伤患者704例,其中合并眼部损伤121例(眼部损伤组),无眼部损伤583例(无眼部损伤组).回顾两组患者的临床和影像学资料,临床资料包括患者的年龄、性别、病史、视力、临床表现、实验室检查、手术记录及病情转归;影像学资料主要包括眼眶及头颅CT、MRI表现.比较两组患者伤因、伤型、临床病理、视觉功能及预后等方面差异.结果 颅脑损伤患者以中年男性为主,道路交通伤为首要致伤原因,眼部损伤以单眼伤较多(80.2％).与无眼部损伤组比较,眼部损伤组患者爆炸伤(3例)和锐器伤(4例)较多(P<0.001),均与眼部损伤直接相关,开放性颅脑损伤(58例)比例较高(P<0.001),前颅底硬脑膜破裂(57例,47.1％)和眶骨骨折(112例,92.6％)发生率更高(P<0.001),并出现多种眼部软组织和视神经损伤,但经治疗,视力恢复效果不容乐观.眼部损伤组总体预后(GOS评分)优于无眼部损伤组,院内病死率更低(P<0.001),虽也更影响伤者的生活质量.结论 爆炸伤和锐器伤所致的颅脑损伤患者更易合并眼部损伤;颅脑损伤合并眼部损伤的患者更易出现前颅底硬脑膜破裂和眶骨骨折,影响视觉功能.因此,神经外科与眼科医师需采取多学科诊疗方式,早期介入,加强协作,努力提高救治水平.

IntroductionThe endoscopic endonasal approach (EEA) is a safe and effective treatment for pituitary adenomas (PAs). Since extracapsular resection (ER) of PAs improves tumor resection and endocrine remission rates, the interface between the pseudocapsule and gland draws increasing attention. However, it is difficult to precisely dissect the tumor along the exact boundary, and complete removal of the tumor increases the risks of normal tissue damage and cerebrospinal fluid (CSF) leakage. In this study, we investigated the extracapsular resection as well as the pseudocapsule histology to evaluate the effectiveness and safety of pseudocapsule-related surgical interventions.MethodsFrom December 2017 to December 2019, 189 patients of PAs via EEA in our single center were analyzed retrospectively. The images, operative details, and clinical follow-up of patients were collected. Sixty-four patients underwent pseudocapsule-based ER, and 125 patients also underwent traditional intracapsular resection (IR) with or without intensive excision for FPAs. The clinical characteristics, tumor resection, endocrinological outcomes, and postoperative morbidities of the two groups were compared. Informed consent for publication of our article was obtained from each patient. Histological examination of pseudocapsule was performed using hematoxylin and eosin and reticulin staining.ResultsThe gross total recession was 62 (96.9%) in the ER group and 107 (85.6%) cases in the IR group, whereas the endocrine remission rate was 29/31 (93.5%) and 40/53 (75.5%) cases, respectively. Anterior pituitary functions were not aggravated postoperatively in any patient, but transient diabetes insipidus (DI) occurred more in the IR group (64.0%) than in ER (48.4%). Pseudocapsule specimens were obtained in 93 patients, and clusters of small cell aggregation were detected in 11 pseudocapsule specimens (11.8%) whereas other patients showed no remarkable developed pseudocapsule. Intraoperative CSF leak occurred more in the ER group (28.1%) than in the IR group (13.6%), but no difference was seen between two groups postoperatively. No case of intracranial hematoma or pituitary crisis occurred in both groups. After a mean follow-up of 22.8 months, tumor recurrence was observed in 4 (2.1%) cases.ConclusionPseudocapsule-based extracapsular resection of PAs via EEA is an effective and safe procedure to achieve complete resection with high and sustained endocrine remission and without deteriorating pituitary function.

Objective The aim of the study is to summarize and analyze the efficacy of the multilayered skull base reconstruction using in situ bone flap in endoscopic endonasal approach (EEA) for craniopharyngiomas. Methods A retrospective review of 65 patients who underwent resection of their histopathology confirmed craniopharyngiomas performed at a single institution. Based on the team's understanding and mastery of skull base reconstruction techniques, patients were divided into two groups according to the methods of reconstruction in two periods. First (March 2015 through August 2016), osseous reconstruction was not adopted and served as the control group (34 cases). Second (September 2016 through July 2019), in situ bone flap repair of the skull base (complete osseous reconstruction) served as observation group (31 cases). The length of hospitalization and nasal exudation, bed rest time of hospital discharge, the incidence of cerebrospinal fluid leaks, lumbar drainage, and intracranial/pulmonary infections were collected and compared. Results Compared with the control group, patients in the observation group had obviously less lumbar drainage and CSF leakage ( p <0.05), but had no significant difference in cases of re-operation, meningitis, and pulmonary infection. At the meantime, cases of nasal exudation, bed rest, and hospitalization of the observation group were significantly reduced ( p <0.05) in the observation group. Conclusion The multilayered reconstruction technique (especially using in situ bone flap, combined with vascularized pedicled nasoseptal flap) is a safe and effective method in achieving watertight closure after EEEA, and can significantly reduce the incidence of cerebrospinal fluid leaks, and facilitate rehabilitation in skull base reconstruction of craniopharyngiomas.

Objective:To explore the method of identifying the boundary of the normal pituitary gland during neuroendoscopic transnasal pituitary adenoma resection and its clinical significance.Methods:A retrospective analysis was conducted on the clinical data of 502 patients with pathologically confirmed pituitary adenomas who were admitted to the Department of Neurosurgery, Xijing Hospital, Air Force Medical University from January 2010 to December 2013. We analyzed the patients′ preoperative imaging and surgical video data, and summarized the methods for determining the pituitary border and pituitary protection. According to the preoperative and postoperative MRI images, the degree of tumor resection was evaluated. The occurrence of postoperative complications was confirmed.Results:Among 502 patients, total resection was achieved in 463 (92.2%). Through preoperative imaging and direct observation under neuroendoscope or through intraoperative diving technique, we were able to recognize the normal pituitary gland and the boundary between the pituitary gland and the tumor tissue in 483 cases (96.2%) during the operation, and the pituitary gland tissue was well preserved; we were unable to identify the pituitary tissue in 19 cases (3.8 %), and frozen section was made from the possible pituitary border tissue during the operation for pathological examination. The results showed that there were 12 cases of pure pituitary tissue, 3 cases of pituitary tissue invaded by tumor, and 4 cases of merely tumor tissue. Postoperative complications included loss of smell (1.6%, 8/502), diabetes insipidus (1.4%, 7/502), electrolyte disturbance (1.0%, 5/502), cerebrospinal fluid rhinorrhea (1.0%, 5/502), meningitis (0.4%, 2/502) and hypopituitarism (0.4%, 2/502). There were no deaths in this series.Conclusions:For most patients with pituitary adenomas, the boundary between the pituitary tissue and the tumor could be identified through preoperative imaging combined with intraoperative endoscopic direct vision or intraoperative diving techniques. For patients whose pituitary boundaries are difficult to identify, frozen section for rapid pathological examinations can be applied to confirm the boundaries during the operation. This method can be used to improve the recognition rate of pituitary tissue, which facilitates the protection of the pituitary, thereby reducing postoperative complications.

针对神经外科学教学中存在的问题,为提高教学质量,对临床教学进行整合改革.运用整合医学(HIM)理念,调整教学计划,建立有利于临床诊疗思维能力、创新精神培养和综合素质提高的HIM教学体系.运用整合教学方式后,有效地提高了神经外科的临床教学质量,学生不仅具备了一定的专业知识和较强的临床能力,而且学习兴趣明显增强.因此,将HIM理念贯穿于神经外科临床教学,对医学生临床思维的培养和手术技巧进步具有重要意义,特别是能够加快年轻医生的成长,对于专培医生效果更加显著.