Objective: To explore the early diagnosis and treatment plan of intracranial infection with Acinetobacter baumannii. Methods: The clinical data of a patient with intracranial infection caused by Acinetobacter baumannii after intracranial hemorrhage surgery were analyzed. Combined with literature review, analyze the treatment plan for intracranial infection of Acinetobacter baumannii. Results: During the hospitalization of this patient, cerebrospinal fluid culture and routine biochemical monitoring were combined with procalcitonin and C-reactive protein for auxiliary diagnosis. The antibiotic treatment regimen was intravenous injection of meropenem and vancomycin, combined with artificial cerebrospinal fluid replacement and lumbar cisterior drainage. After one week of treatment, the patient's condition improved and the bacterial culture of cerebrospinal fluid was negative. Conclusion: For intracranial infection caused by Acinetobacter baumannii, in this case, the patient was treated with meropenem + vancomycin via intravenous administration, combined with artificial cerebrospinal fluid replacement surgery + lumbar cistern drainage surgery. Although this treatment approach achieved relatively satisfactory therapeutic results, it is still a single-case empirical treatment. Due to the high rate of drug resistance and poor prognosis of intracranial Acinetobacter baumannii infection, there is currently no standardized unified treatment plan. More clinical studies are needed to accumulate data and further explore effective and with fewer adverse reactions treatment strategies to improve the clinical prognosis of such patients.

Glioblastoma (GBM) is the most common and lethal primary intracranial tumor, and glycolysis has been reported to play a critical role in its progression. Formin-binding protein 1 (FNBP1) has been implicated in GBM progression; however, the precise molecular mechanisms remain unclear. In this study, we demonstrated that FNBP1 expression was significantly higher in GBM tissues compared with adjacent tissues. Elevated FNBP1 expression was correlated with higher tumor grade and reduced 5-year survival in GBM patients. In vitro, knockdown of FNBP1 inhibited proliferation, invasion, and glycolysis, while promoting apoptosis in GBM cells. Mechanistically, RNA-binding motif protein 15B (RBM15B) increased the m6A modification level of FNBP1 mRNA, and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) recognized this m6A mark and enhanced the stability of FNBP1 mRNA. Furthermore, FNBP1 interacted with LIM and SH3 Domain Protein 1 (LASP1), upregulating LASP1 protein expression and subsequently activating the Smad3 signaling pathway to promote glycolysis. In vivo, subcutaneous xenograft models were established using U251/U87 cells, and a lung metastasis model was generated via tail vein injection of U87 cells. FNBP1 knockdown significantly suppressed tumor growth in the subcutaneous model and reduced the number of lung nodules in the metastasis model. In conclusion, FNBP1, regulated by the RBM15B-m6A-IGF2BP2 axis, promotes GBM progression by interacting with LASP1 to activate Smad3-mediated glycolysis.

NK cells are a type of antitumor immune cell with promising clinical application, following T cells. The activity of NK cells is primarily regulated by their surface receptors and immune microenvironment. In gliomas, the tumor microenvironment exerts a strong immunosuppressive effect, which significantly reduces the clinical efficacy of NK cell immunotherapy. Therefore, this review aims to discuss the latest research on the role of NK cells in glioma immunotherapy, focusing on aspects such as NK cell development, function, and localization. It summarizes information on the compounds, monoclonal antibodies, and cytokine therapies targeting NK cells while emphasizing the current status and trends of gene-modified NK cells in glioma treatment. Additionally, it explores the molecular mechanisms underlying immune escape in glioma cells, providing a theoretical foundation and new perspectives for NK cell-based immunotherapy in gliomas.

BACKGROUND At present, the conventional methods for diagnosing cerebral edema in clinical practice are computed tomography (CT) and magnetic resonance imaging (MRI), which can evaluate the location and degree of peripheral cerebral edema, but cannot realize quantification. When patients have symptoms of diffuse cerebral edema or high cranial pressure, CT or MRI often suggests that cerebral edema is lagging and cannot be dynamically monitored in real time. Intracranial pressure monitoring is the gold standard, but it is an invasive operation with high cost and complications. For clinical purposes, the ideal cerebral edema monitoring should be non-invasive, real-time, bedside, and continuous dynamic monitoring. The disturbance coefficient (DC) was used in this study to dynamically monitor the occurrence, development, and evolution of cerebral edema in patients with cerebral hemorrhage in real time, and review head CT or MRI to evaluate the development of the disease and guide further treatment, so as to improve the prognosis of patients with cerebral hemorrhage. AIM To offer a promising new approach for non-invasive adjuvant therapy in cerebral edema treatment. METHODS A total of 160 patients with hypertensive cerebral hemorrhage admitted to the Department of Neurosurgery, Second Affiliated Hospital of Xi’an Medical University from September 2018 to September 2019 were recruited. The patients were randomly divided into a control group (n = 80) and an experimental group (n = 80). Patients in the control group received conventional empirical treatment, while those in the experimental group were treated with mannitol dehydration under the guidance of DC. Subsequently, we compared the two groups with regards to the total dosage of mannitol, the total course of treatment, the incidence of complications, and prognosis. RESULTS The mean daily consumption of mannitol, the total course of treatment, and the mean hospitalization days were 362.7 ± 117.7 mL, 14.8 ± 5.2 days, and 29.4 ± 7.9 in the control group and 283.1 ± 93.6 mL, 11.8 ± 4.2 days, and 23.9 ± 8.3 in the experimental group (P < 0.05). In the control group, there were 20 patients with pulmonary infection (25%), 30 with electrolyte disturbance (37.5%), 20 with renal impairment (25%), and 16 with stress ulcer (20%). In the experimental group, pulmonary infection occurred in 18 patients (22.5%), electrolyte disturbance in 6 (7.5%), renal impairment in 2 (2.5%), and stress ulcers in 15 (18.8%) (P < 0.05). According to the Glasgow coma scale score 6 months after discharge, the prognosis of the control group was good in 20 patients (25%), fair in 26 (32.5%), and poor in 34 (42.5%); the prognosis of the experimental group was good in 32 (40%), fair in 36 (45%), and poor in 12 (15%) (P < 0.05). CONCLUSION Using DC for non-invasive dynamic monitoring of cerebral edema demonstrates considerable clinical potential. It reduces mannitol dosage, treatment duration, complication rates, and hospital stays, ultimately lowering hospitalization costs. Additionally, it improves overall patient prognosis, offering a promising new approach for non-invasive adjuvant therapy in cerebral edema treatment.

Glioblastoma, the most malignant primary brain tumor among gliomas, is characterized by a low cure rate, high recurrence rate, and invasive growth. Without chemotherapy, the median survival of patients is only 12.1 months. The standard treatment for glioblastoma primarily involves surgical resection, complemented by radiotherapy. Temozolomide (TMZ), a new oral alkylating agent, is currently used as the first-line chemotherapy drug for glioma. However, TMZ treatment only improves median survival by 2 months, largely because of the tumor's ability to develop resistance to the drug. The main mechanism underlying this resistance involves DNA repair processes, such as the action of O6⁃methylguanine DNA methyltransferase (MGMT), which repairs the DNA damage caused by TMZ, and other DNA repair mechanisms including mismatch repair and base excision repair. These mechanisms can effectively repair the DNA damage caused by TMZ, thereby reducing the sensitivity of tumor cells to the drug. This study summarized the recent research progress of TMZ resistance mechanism in glioblastoma, aiming to provide a theoretical basis for the development of new therapies. The mechanisms of glioma resistance to TMZ mainly involves DNA damage repair (as mentioned above), abnormal cell signaling pathways (p53-mediated signaling, reactive oxygen species-mediated signaling, endoplasmic reticulum stress and autophagy-related signaling, receptor tyrosine kinase-related signaling, transforming growth factors, β-mediated signaling pathway, Wnt/β-Catenin signaling pathway), glioma stem cells, tumor microenvironment (hypoxic microenvironment, nano-drug delivery system), epidermal growth factor receptor, and microRNAs.

Cysteine and glycine-rich protein 2 (CSRP2) is expressed differently in numerous cancers and plays a key role in carcinogenesis. However, the role of CSRP2 in glioma is unknown. This study sought to determine the expression profile and clinical significance of CSRP2 in glioma and explore its biological functions and mechanisms via lentivirus-mediated CSRP2 silencing experiments. Increased CSRP2 was frequently observed in gliomas, which was associated with clinicopathological characteristics and an unfavourable prognosis. Decreasing CSRP2 led to the suppression of malignant proliferation, metastasis and stemness in glioma cells while causing hypersensitivity to chemotherapeutic drugs. Mechanistic investigations revealed that CSRP2 plays a role in mediating the Notch signalling cascade. Silencing CSRP2 decreased the levels of Notch1, cleaved Notch1, HES1 and HEY1, suppressing the Notch signalling cascade. Reactivation of Notch markedly diminished the tumour-inhibiting effects of CSRP2 silencing on the malignant phenotypes of glioma cells. Notably, CSRP2-silencing glioma cells exhibited reduced potential in the formation of xenografts in nude mice in vivo, which was associated with an impaired Notch signalling cascade. These results showed that CSRP2 is overexpressed in glioma and has a crucial role in sustaining the malignant phenotypes of glioma, suggesting that targeting CSRP2 could be a promising strategy for glioma treatment.

Glioma has a high malignant degree and poor prognosis, which seriously affects the prognosis of patients. Traditional treatment methods mainly include craniotomy tumor resection, postoperative radiotherapy and chemotherapy. Although above methods have achieved remarkable curative effect, they still have certain limitations and adverse reactions. With the introduction of the concept of minimally invasive surgery and its clinical application as well as the development and progress of imaging technology, minimally invasive treatment of glioma has become a research hotspot in the field of neuromedicine, including photothermal treatment, photodynamic therapy, laser-induced thermal theraphy and TT-Fields of tumor. These therapeutic methods possess the advantages of precision, minimally invasive, quick recovery and significant curative effect, and have been widely used in clinical practice. The purpose of this review is to introduce the progress of minimally invasive treatment of glioma in recent years and the achievements and prospects for the future.

Brain glioma, which is highly invasive and has a poor prognosis, is the most common primary intracranial tumor. Several studies have verified that the extent of resection is a considerable prognostic factor for achieving the best results in neurosurgical oncology. To obtain gross total resection (GTR), neurosurgery relies heavily on generating continuous, real-time, intraoperative glioma descriptions based on image guidance. Given the limitations of existing devices, it is imperative to develop a real-time image-guided resection technique to offer reliable functional and anatomical information during surgery. At present, the application of intraoperative ultrasound (IOUS) has been indicated to enhance resection rates and maximize brain function preservation. IOUS, which is promising due to its lower cost, minimal operational flow interruptions, and lack of radiation exposure, can enable real-time localization and precise tumor size and form descriptions while assisting in discriminating residual tumors and solving brain tissue shifts. Moreover, the application of new advancements in ultrasound technology, such as contrast-enhanced ultrasound (CEUS), three-dimensional ultrasound (3DUS), noninvasive ultrasound (NUS), and ultrasound elastography (UE), could assist in achieving GTR in glioma surgery. This article reviews the advantages and disadvantages of IOUS in glioma surgery.

目的:探讨烟酰胺经调控p38MAPK信号通路对高血压脑出血大鼠的脑保护作用机制.方法:选择48只SD大鼠,随机选择12只作为假手术组,其余36只进行高血压脑出血造模,对比4组大鼠的血肿体积、左扭转比率、神经功能变化、出血脑组织p-p38MAPK、p38MAPK蛋白表达、烟酰胺腺嘌吟二核苷酸、凋亡诱导因子含量及脑组织含水量.结果:与模型组相比,尼莫地平组、烟酰胺组的血肿体积明显缩小;与烟酰胺组相比,尼莫地平组的血肿体积明显缩小(P＜0.05);与干预前相比,干预后烟酰胺组、尼莫地平组的血肿体积明显缩小,模型组的血肿体积明显增多(P＜0.05).与模型组相比,假手术组、尼莫地平组、烟酰胺组的向左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌吟二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低;与烟酰胺组相比,尼莫地平组、假手术组的左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌呤二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低;与尼莫地平组相比,假手术组的左扭转比率、p-p38MAPK/p38MAPK、烟酰胺腺嘌呤二核苷酸明显较高,脑组织含水量、凋亡诱导因子含量明显较低(P＜0.05).结论:在高血压脑出血大鼠中,p38MAPK介导的细胞凋亡途径会加剧高血压脑出血的脑损伤,烟酰胺会经过抑制p38MAPK信号通路减轻高血压脑出血后的脑损伤.

The diagnosis of cerebral edema mainly relies on traditional monitoring techniques such as CT and MRI, but traditional techniques often do not have the ideal monitoring method of economy, real-time dynamic, and bedside monitoring. At present, there are an increasing number of new Brain edema monitoring devices that are popular at home and abroad. These new non-invasive monitoring technologies are used to monitor the situation of brain edema in patients with craniocerebral injury and the profile of intracranial pressure in high-risk populations with craniocerebral diseases. It may play a key role in assisting and guiding the decision-making of specialized medical behavior. Therefore, a reliable, inexpensive and widely applicable brain edema monitoring technology has become an urgent need for scientific researchers, clinical staff and patients. This article reviews the research status and prospect of noninvasive brain edema monitoring techniques.

目的 探讨优质护理对脑膜瘤切除术后并发症的预防效果.方法 选取2019年12月至2021年12月间西安医学院第二附属医院收治的90例脑膜瘤切除术患者,根据随机数字表法分为观察组和对照组,每组45例.对照组患者采用常规护理,观察组患者采用优质护理,比较两组患者的负性情绪、术后恢复指标、并发症总发生率和满意度.结果 护理后,观察组患者焦虑和抑郁评分均降低,且观察组低于对照组,差异均有统计学意义(均P<0.05).观察组患者肛门首次排气、首次下床时间和住院时间均短于对照组,差异均有统计学意义(均P<0.05).观察组患者并发症总发生率为2.2％,低于对照组的17.8％,差异有统计学意义(P<0.05).观察组患者护理满意度为95.6％,高于对照组的75.6％,差异有统计学意义(P<0.05).结论 优质护理可有效减轻脑膜瘤切除术患者的焦虑、抑郁等不良情绪,缩短术后机体恢复时间,降低并发症发生率,提高护理满意度.

Protein tyrosine phosphatase non-receptor type 21 (PTPN21) has been recognised as a new tumour-associated protein that is implicated in diverse tumours. However, the correlation between PTPN21 and glioma remains unaddressed. This investigation focused on the relevance of PTPN21 in glioma. The Cancer Genome Atlas (TCGA) analysis identified PTPN21 as being up-regulated in glioma tissue. The elevation of PTP21 in glioma was validated by evaluating clinical specimen. Kaplan-Meier plot analysis revealed that a high PTPN21 level predicted poor survival rate in glioma patient. Silencing of PTPN21 produced remarkable anticancer effects in glioma cells including proliferation inhibition, cell cycle arrest, metastasis suppression and enhanced chemosensitivity. Mechanistic studies uncovered that PTPN21 contributes to mediation of the phosphatidyl-inositole-3 kinase (PI3K)/AKT pathway via the regulation of epidermal growth factor receptor (EGFR). Restraint of EGFR diminished PTPN21 overexpression-induced promoting effect on PI3K/AKT pathway. Reactivation of AKT reversed PTPN21 silencing-evoked antitumor effect. The tumorigenic potential of PTPN21-silenced glioma cells in vivo was markedly compromised. In summary, this study demonstrates that silencing of PTPN21 produces remarkable anticancer effects in glioma by restraining the EGFR/PI3K/AKT pathway.

目的 探讨对重症脑出血患者实施早期肠内营养(EEN)支持的临床效果.方法 选取2020年9月至2021年10月本院收治的300例重症脑出血患者为研究对象,采用随机排列法分为对照组和实验组,各150例.两组患者在入院12～48 h内均给予营养支持,其中对照组采用常规鼻饲饮食,实验组给予EEN干预.分别于入院第1 d和入院2周后比较患者营养状况和免疫功能的差异,观察患者预后情况.结果 两组干预前血清白蛋白(ALB)、前清蛋白(PA)、血清总蛋白(TP)三项营养状况指标水平和免疫球蛋白G(IgG)、免疫球蛋白A(IgA)和免疫球蛋白M(IgM)三项免疫功能指标水平比较差异无统计学意义(P＞0.05);干预后,对照组营养状况指标和免疫功能指标水平均低于本组干预前,差异有统计学意义(P＜0.05),而实验组营养状况指标和免疫功能指标水平均高于本组干预前,差异有统计学意义(P＜0.05);且实验组干预后ALB、PA、TP、IgG、IgA和IgM水平高于对照组,差异有统计学意义(P＜0.05).实验组并发症总发生率6％低于对照组25.33％,差异有统计学意义(P＜0.05).结论 EEN支持可以有效改善重症脑出血患者营养状况,提高患者的免疫功能,减少并发症的发生,为患者预后转归创造良好条件.

Isorhynchophylline (IRN), a component of traditional Chinese herb Uncaria rhynchophylla, possesses strong antioxidant activity. Ferroptosis induced by iron overload causes cell oxidative stress after intracerebral hemorrhage (ICH). Therefore, this study aims to explore the effects of IRN on the ferroptosis following ICH. In this study, mouse hippocampal HT-22 cells were treated with ferric ammonium citrate (FAC) alone or together with IRN, and we found IRN reduced the FAC-induced cell damage. Then, cells were treated with IRN following treatment with FAC after transfection with miR-122-5p inhibitor, and the results showed IRN reduced the FAC-induced decrease of miR-122-5p levels and relieved the ferroptosis by detecting ferroptotic marker proteins, iron ion concentration and oxidative stress level; after transfection with miR-122-5p inhibitor, the protective effects of IRN against FAC-induced ferroptosis in these cells were weakened. TP53 (also known as p53) was verified as a target of miR-122-5p by using dual luciferase reporter assay, and restoration of TP53 attenuated the effects of miR-122-5p on ferroptotic marker proteins expression, iron ion concentration and lipid ROS levels, as well as solute carrier family seven member 11 (SLC7A11) mRNA expression. SLC7A11 siRNA reversed the inhibitory effects of IRN on FAC-induced ferroptosis and oxidative stress levels. Subsequently, IRN increased the mNSS score, and decreased brain water content and EB content in ICH model. Moreover, IRN decreased ferroptosis and lipid ROS level, upregulated the expression of miR-122-5p and SLC7A11 mRNA, and inhibited TP53 expression. Our findings reveal that IRN protects neurocyte from ICH-induced ferroptosis via miR-122-5p/TP53/SLC7A11 pathway, which may provide a potential therapeutic mechanism for ICH.

目的 探讨盐酸氨溴索联合头孢哌酮舒巴坦治疗脑出血术后肺部感染的临床疗效及其对氧合指数的影响.方法 选取西安医学院第二附属医院2018年9月—2020年9月收治的脑出血术后肺部感染患者82例,按照随机数字表法分为对照组与观察组,各41例.对照组予以注射用头孢哌酮舒巴坦治疗,观察组予以盐酸氨溴索治疗.比较2组临床疗效,治疗前后临床症状及体征评分、后氧合指数、炎性细胞因子[C反应蛋白(CRP)、白介素6(IL-6)和肿瘤坏死因子α(TNF-α)],并观察2组不良反应发生情况.结果 观察组治疗总有效率高于对照组(P＜0.05).治疗前2组症状评分、体征评分、X线评分比较,差异无统计学意义(P＞0.05);治疗后观察组症状评分、体征评分、X线评分低于对照组(P＜0.05).治疗前2组氧合指数比较,差异无统计学意义(P＞0.05);治疗后观察组氧合指数高于对照组(P＜0.05).治疗前2组CRP、IL-6、TNF-α水平比较,差异无统计学意义(P＞0.05);治疗后观察组CRP、IL-6、TNF-α水平低于对照组(P＜0.05).2组不良反应发生率比较,差异无统计学意义(P＞0.05).结论 盐酸氨溴索联合头孢哌酮舒巴坦治疗脑出血术后肺部感染的临床疗效确切,可减轻肺部炎症损伤,促进临床症状及体征消失,增强肺氧合功能,且安全性较高.

目的 通过Meta分析探讨高血压脑出血(HICH)术后再出血的相关危险因素,为防止发生术后再出血提供循证医学依据.方法 通过检索中国知网(CNKI)、万方数据库、维普数据库(VIP)、中国生物医学数据库(CBM)及PubMed、Embase、Web of Science、Cochrane Library数据库,查找2015年1月1日-2020年1月31日发表的,关于高血压脑出血术后再出血危险因素研究的相关文献;同时追溯纳入文献的参考文献,以尽可能查全文献.采用Stata15.1、RevMan5.3软件对纳入文献的研究结果进行Meta分析.结果 最终纳入17篇文献,总样本例数为3 544例.Meta分析结果显示,高血压脑出血术后再出血的危险因素为发病至手术时间≤6 h(OR =3.98,95％ CI:2.98～5.33)、凝血功能异常(OR =3.13,95％ CI:2.28 ～4.30)、术前收缩压≥200 mmHg(OR =2.91,95％ CI: 1.94～4.36)、术前舒张压≥120 mmHg(OR=6.28,95％ CI:3.58～10.99)、术后收缩压≥200 mmHg(OR=6.48,95％ CI:3.60 ～ 11.65)、术前血肿量≥60 mL(OR=2.23,95％CI:1.72 ～2.88)、术中止血困难(OR =4.14,95％ CI:2.47 ～ 6.92)及合并糖尿病(OR=1.84,95％ CI: 1.27～2.65).结论 发病至手术时间≤6 h、凝血功能异常、术前收缩压≥200 mmHg、术前舒张压≥120 mmHg、术后收缩压≥200 mmHg、术前血肿量≥60 mL、术中止血困难、合并糖尿病是高血压脑出血术后再出血的危险因素;了解及预防、处理这些危险因素可降低高血压脑出血术后再出血的发生率.

脑水肿是由多种原因引起的脑组织继发性病理改变,主要表现是含水量和脑容量增加,可导致颅内压升高、脑中线结构位移等,甚至导致脑疝[1].脑水肿的发生和发展直接关系到脑功能损害的程度,与病人的预后密切相关[2].因此,及时发现脑水肿、准确监测脑水肿、准确掌握颅内压的变化,并采用药物、手术等方法缓解脑水肿,降低颅内压,是抢救成败、改善病情发展及转归的关键[3].

目的 探讨转铁蛋白受体(TFRC)在替莫唑胺抑制U87胶质瘤细胞增殖和侵袭中的作用.方法 体外培养U87胶质瘤细胞,加入50 μmol/L、100 μmol/L和200 μmol/L替莫唑胺作用;构建control siRNA、siTFRC转染U87细胞沉默TFRC表达,构建pcDNA3.1空载体、pcDNA3.1/TFRC转染U87细胞过表达TFRC;利用CCK-8方法检测U87细胞增殖;利用Transwell小室实验检测U87细胞侵袭能力;实时荧光定量PCR和免疫印迹法检查U87细胞TFRC mRNA和蛋白表达.结果 与空白组相比,替莫唑胺处理后,U87细胞的增殖和侵袭能力显著下降(P＜0.05),TFRC mRNA和蛋白表达水平显著降低(P＜0.05),当替莫唑胺浓度为200 μmol/L时,对U87细胞的抑制能力最强(P＜0.05).当利用pcDNA3.1/TFRC过表达U87细胞TFRC处理后,替莫唑胺对U87细胞增殖和侵袭的抑制能力显著下降(P＜0.05);而当利用siTFRC沉默U87细胞TFRC表达后,替莫唑胺对U87细胞增殖和侵袭的抑制能力显著增强(P＜0.05).结论 替莫唑胺可能通过抑制TFRC的表达而抑制U87胶质瘤细胞的增殖和侵袭.

目的:探讨阿托伐他汀对2型糖尿病心肌病心功能、脑钠肽(BNP)及超敏C反应蛋白(hs-CRP)的影响.方法:将59例2型糖尿病心肌病患者随机分为一般治疗组(n=29例)和阿伐他汀治疗组(n=30例),一般治疗组和阿伐他汀治疗组在治疗中严格控制血糖及给予抗心衰规范化治疗,阿伐他汀治疗组在此治疗基础上,加用阿伐他汀(20 mg/d)治疗.所有患者在治疗前和治疗8周后,左室射血分数(LVEF)、检测左室舒张末期内径(LVDd)、血浆脑钠肽前体检氨基端片段(BNP)和血清超敏C反应蛋白(hs-CRP).结果:两组患者在治疗前LVEF、LVDd、BNP及hs-CRP差异均无统计学意义(P>0.05),经8周治疗后,一般治疗组和阿托伐他汀治疗组,LVEF较治疗前明显改善(P<0.05),BNP及HS-CRP水平较治疗前明显降低(P<0.05),但LVDd未见明显改善(P>0.05),两组患者在治疗后,阿托伐他汀治疗组较一般治疗组BNP及hs-CRP明显降低(P<0.05),但LVEF和LVDd没有显著变化(P>0.05).结论:阿托伐他汀改善糖尿病心肌病心功能,可能与降低血浆中脑钠肽水平及炎症因子相关.

目的 探讨慢性硬膜下血肿(CSDH)钻孔引流术后脑膨胀不良的原因及治疗体会.方法 选择2015年1月至2018年5月于我院进行CSDH钻孔引流治疗后出现术后脑膨胀不良的34例患者为研究对象,出院后给予其阿托伐他汀治疗.结果 34例患者经不同疗程阿托伐他汀治疗后脑膨胀良好,硬膜下积液消失.结论 不同疗程的阿托伐他汀(20 mg/次,1次/d)辅助治疗CSDH钻孔引流术后脑膨胀不良效果显著,值得推广.