Objective To explore the incidence and risk factors of perioperative ischemic stroke in non-cardiac and non-neurosurgical surgeries and its correlation with preoperative risk assessment of cerebrovascular events, so as to guide perioperative risk management. Methods A retrospective study was conducted on 40 patients aged ≥18 years who underwent non-cardiac and non-neurosurgical surgeries and experienced perioperative ischemic stroke in the First Affiliated Hospital of Henan University of Science and Technology from January 2015 to January 2022, forming the stroke group. A control group of 160 patients without perioperative ischemic stroke was selected in a 1:4 case-control ratio, matched for gender, age, date of operation, and the surgeon. Clinical data and preoperative risk assessment of cerebrovascular events (including the single or combined application of head CT/MRI, transcranial Doppler ultrasound, carotid ultrasound, and neurological consultation) of the two groups of patients were collected and statistically analyzed. Multiple logistic regression analysis was used to identify risk factors associated with perioperative ischemic stroke. Results The incidence of perioperative ischemic stroke was 0.042%. Multiple logistic analysis results showed that hypertension (OR=7.858, 95%CI 2.175-28.388, P=0.002), hyperlipidemia (OR=4.457, 95%CI 1.320-15.049, P=0.016), renal insufficiency (OR=8.277, 95%CI 1.480-46.282, P=0.016), and intraoperative hypotension (OR=3.862, 95%CI 1.211-12.317, P=0.022) were independent risk factors for perioperative ischemic stroke in non-cardiac and non-neurological surgeries; preoperative cerebrovascular risk assessment (OR=0.130, 95%CI 0.031-0.542, P=0.005) was a protective factor against it. Conclusions The incidence of perioperative ischemic stroke in non-cardiac and non-neurosurgical surgery is low but has a poor prognosis. Hypertension, hyperlipidemia, renal insufficiency, and postoperative hypotension are risk factors for perioperative ischemic stroke, while preoperative cerebrovascular event risk assessment is beneficial to reducing its incidence.

Objective To summarize the clinical characteristics of 2 cases of styloid-carotid syndrome(SCS) and review the literature to enhance understanding of the disease. Methods A retrospective analysis was conducted on the clinical manifestations, auxiliary examinations, and diagnosis and treatment of 2 patients with SCS admitted to the Neurology Department of Kaifeng Central Hospital. Additionally, relevant literature was searched through domestic and foreign databases such as PubMed, WOS, Embase, CNKI and VIP. The clinical characteristics of SCS were summarized based on the literature results. Results The 2 cases were diagnosed as transient cerebral ischemia (TIA) combined with SCS through head and neck CT angiography (CTA) and styloid process CT. Apart from the 2 cases treated in our hospital, a total of 11 cases of SCS have been reported in Chinese and English literature up to October 2023. Among the 13 cases, 11 cases (84.6%) started with episodic TIA symptoms, and 11 cases (84.6%) had obvious inducing factors related to specific head position changes. Common clinical manifestations included unilateral limb weakness with or without sensory disturbance (10 cases, 76.9%), slurred speech (7 cases, 53.8%), unilateral limb sensation disorder (4 cases, 30.7%), syncope (3 cases, 23.1%) and amaurosis (2 cases, 15.4%). All 13 cases underwent 64-row head and neck CTA examination, and 6 cases (46.2%) dynamically observed the changes in blood flow velocity through examinations such as transcranial Doppler ultrasound (TCD), cervical vascular ultrasound, and digital subtraction angiography (DSA). All patients were followed up for more than 3 months; and 10 cases (76.9%) achieved clinical cure after treatment, of which 8 cases underwent styloid process shortening surgery; 3 cases (23.1%) achieved clinical symptom improvement after treatment. Conclusions For patients with recurrent TIA and/or cerebral infarction, it is necessary to identify whether there are inducing factors related to specific body position changes. For patients highly suspected of SCS, routine examinations such as styloid process CT and 64-row head and neck CTA should be performed, and if necessary, whole brain DSA, dynamic TCD and/or carotid ultrasound should be conducted to guide the diagnosis and treatment. When non-surgical treatment is ineffective, radical styloid process truncation can be considered as a treatment option.

Objective To explore the effects of circ_100284 in affecting the invasion of esophageal squamous cell carcinoma (ESCC) cells and their sensitivity to 5-fluorouracil (5-FU) chemotherapy via regulating miR-217/mitogen-activated protein kinase 1 (MAPK1) acting as a competing endogenous RNA (ceRNA). Methods The bioinformatics approach was used to analyze the differentially expressed circRNAs in ESCC. qRT-PCR was used to detect the expression of circ_100284 in ESCC tissues and cells. The 5-FU-resistant KYSE450 cell line (KYSE45-R) was established by increasing concentrations of 5-FU. The IC₅₀ of 5-FU in KYSE450 and KYSE450-R cells was determined through MTT assay. qRT-PCR was used to detect the expression of circ_100284, miR-217, and MAPK1 mRNA in KYSE450 and KYSE450-R cells, while Western blotting detecting the protein expression of MAPK1. In the experiments with KYSE450-R cells, we set up the following groups: (1) blank group (without treatment), si-NC group (transfected with si-NC), si-circ_100284 group (transfected with si-circ_100284), pc-Control group (transfected with pc-Control), pc-circ_100284 group (transfected with pc-circ_100284), pc-circ_100284+mimic NC group (transfected with pc-circ_100284 and mimic NC), and pc-circ_100284+miR-217 mimic group (transfected with pc-circ_100284 and miR-217 mimic). These groups were subjected to MTT assay to detect cell viability, Transwell assay to detect cell invasion, and flow cytometry to detect cell apoptosis. (2) Blank group (without treatment), si-NC group (transfected with si-MAPK1 negative control), si-MAPK1 group (transfected with si-MAPK1), si-MAPK1+inhibitor NC group (transfected with si-MAPK1 and inhibitor NC), and si-MAPK1+miR-217 inhibitor group (transfected with si-MAPK1 and miR-217 inhibitor). We detected the mRNA and protein expression of MAPK1 using qRT-PCR and Western blotting. We evaluated cell viability using MTT assay, invasion with Transwell assay, and apoptosis by flow cytometry. circ_100284-WT or circ_100284-MUT reporter plasmids, as well as MAPK1-WT or MAPK1-MUT reporter plasmids, were co-transfected with miR-NC or miR-217 mimic into KYSE450-R cells for 48 h, and dual luciferase reporter assay was used to measure luciferase activity. Results The bioinformatics analysis revealed significant upregulation of circ_100284 in ESCC. Compared with adjacent normal tissues, the expression of circ_100284 in ESCC tissues is enhanced (P<0.05); compared with the HECC cells, the TE-11, ECA109 and KYSE450 ESCC cell lines showed enhanced expression of circ_100284 (P<0.05). Compared with the KYSE450 cells, KYSE450-R cells demonstrated increased IC₅₀ with enhanced expression of circ_100284 and MAPK1 but suppressed expression of miR-217 (P<0.05). Compared with the si-NC group, the si-circ_100284 group demonstrated inhibited invasion and proliferation of cells with increased apoptosis (P<0.05). Compared with pc-Control group, the invasion and proliferation of cells in the pc-circ_100284 group are increased, and cell apoptosis is decreased (P<0.05). Over-expression of miR-217 reversed the malignant biological behavior of ESCC cells induced by pc-circ_100284 (P<0.05). Compared with si-NC group, in the si-MAPK1 group, we observed decreased cell invasion and proliferation, and increased apoptosis (P<0.05), but miR-217 inhibitor reversed the effect of si-MAPK1 on the biological behavior of ESCC cells (P<0.05). The targeting relationship of circ_100284 and miR-217, miR-217 and MAPK1 is confirmed. Conclusion circ_100284 promotes ESCC cell invasion by regulating miR-217/MAPK1, inhibits the chemosensitivity of ESCC cells to 5-FU, and acts as a tumor-promoting factor in ESCC.

Hemophilia, which includes different types such as hemophilia A and hemophilia B, is a hemorrhagic disorder with inherited blood clotting abnormalities. The main clinical manifestations are spontaneous bleeding of joints, muscles and deep tissues or repeated bleeding after trauma. It often starts at an early age and affects the whole life. The treatment of hemophilia patients is still dominated by alternative therapy, supplementing the corresponding clotting factors. In addition, non-factor drug therapy is adopted such as bispecific monoclonal antibodies and gene therapy. In recent years, the research on the pathogenesis of hemophilia A has made great progress, which is no longer limited to the mutation of the coding sequence of coagulation factor gene as the only cause of hemophilia. Many studies have found that abnormal expression of non-coding RNA (ncRNA) is involved in the regulation of coagulation factor Ⅷ (FⅧ) mRNA and protein, which not only explains why patients with normal FⅧ genotypes still present with hemophilia A, but also provides new directions for understanding the pathogenesis of other types of hemophilia. This paper reviews the research progress on the regulatory mechanism of ncRNA in hemophilia A.

Objective To explore the clinical characteristics of pediatric patients with cerebral palsy (CP) who also have comorbid epilepsy. Methods A retrospective analysis was conducted on the clinical data of 155 pediatric patients with CP and comorbid epilepsy admitted to the Third Affiliated Hospital of Zhengzhou University from January 2019 to December 2022. Patients were divided into 4 groups based on CP subtype: spastic diplegia group (n=29), spastic hemiplegia group (n=33), spastic quadriplegia group (n=73), and non-spastic group (n=20). Differences in sex, season of birth, birth weight, gestational age, and the relationship between gestational age and weight were compared among the groups. Additionally, the relationships between perinatal risk factors, MRI classification system (MRICS), gross motor function classification system (GMFCS), and the age of the first onset of epilepsy with respect to CP subtype were analyzed. Results Among the 155 patients, 101 were male and 54 were female. A lower proportion of patients with spastic hemiplegia was observed with a gestational age of 28-31⁺⁶ weeks compared with those with spastic diplegia and spastic quadriplegia (P=0.009). The proportion of patients with a history of asphyxia in spastic hemiplegia group was significantly lower than that in the other 3 groups, and the proportion of patients with hypoxic-ischemic encephalopathy (HIE) in spastic hemiplegia group was significantly lower than in that both spastic quadriplegia group and non-spastic group (P<0.05). The proportion of patients in spastic quadriplegia group who had their first seizure at an age of <1 year was significantly higher than that in spastic diplegic group (P=0.041). The spastic diplegia group exhibited a higher percentage of white matter damage compared with the other 3 groups, and had a lower percentage of gray matter damage compared with both spastic hemiplegic group and non-spastic group (P=0.001). The proportion of patients with GMFCS levels Ⅳ－Ⅴ in spastic quadriplegia group was higher than those in the other 3 groups (P<0.001), and the proportion of patients with levels Ⅰ－Ⅲ in spastic hemiplegia group was significantly higher than those in spastic quadriplegia group and non-spastic group (P<0.001). Conclusion Significant differences were observed among pediatric patients with different subtypes of CP and comorbid epilepsy in factors such as gestational age, history of asphyxia, HIE history, age of first seizure, MRICS classification and GMFCS levels.

Objective To investigate the effect and mechanism of leucine zipper/EF-hand-containing transmembrane protein 1 (LETM1) on proliferation, migration, apoptosis, osteogenic differentiation, and tumorigenesis in vivo of human osteosarcoma MG63 and 143B cells. Methods The osteosarcoma MG63 and 143B cells were divided into blank control group (without adenovirus infection), negative control group (sh-NC group, infected with RNAi negative control virus), and LETM1 knockdown group (sh-LETM1 group, infected with sh-LETM1 adenovirus). Western blotting was performed to detect LETM1 expression in normal human osteoblasts hFOB1.19 and osteosarcoma cells, and to verify the knockdown effect of adenovirus; cell clone formation assays and CCK-8 method were used to detect the proliferation of MG63 and 143B cells; wound-healing assay and Transwell assay were used to test cell migration; DAPI staining and Annexin V-APC/7-AAD flow cytometry double staining were used to detect the apoptosis of MG63 and 143B cells; alkaline phosphatase (ALP) staining and Alizarin Red S staining were used to evaluate early and late osteogenic differentiation of MG63 and 143B cells. Ten nude mice were divided into sh-NC group (n=5, injected subcutaneously into nude mice with 143B cells infected with RNAi negative control virus) and sh-LETM1 group (n=5, injected subcutaneously into nude mice with 143B cells infected with sh-LETM1 adenovirus), and nude mice subcutaneous tumor formation assay was used to examine the in vivo tumor-forming ability of 143B cells in each group. Results Western blotting showed that the expression of LETM1 protein in osteosarcoma MG63 and 143B cells was significantly higher than that in human normal osteoblasts hFOB1.19 (P<0.05), and that the expression of LETM1 protein was markedly reduced after injection with sh-LETM1 adenovirus in MG63 and 143B cells. The results of cell clone formation assay and CCK-8 assay indicated that in MG63 and 143B osteosarcoma cells, the clone formation ability and proliferation ability were significantly reduced in sh-LETM1 group compared with sh-NC group and blank control group (P<0.01). The results of wound-healing assay and Transwell assay demonstrated that in MG63 and 143B osteosarcoma cells, the cell migration rate in sh-LETM1 group was significantly lower than that in sh-NC group and blank control group (P<0.01). DAPI staining and flow cytometry results revealed that the apoptosis rate in sh-LETM1 group was significantly higher than those in MG63 and 143B osteosarcoma cells in sh-NC group (P<0.01). Alkaline phosphatase staining and Alizarin red S staining experiments showed more stained areas and calcium salt nodules in MG63 and 143B osteosarcoma cells in sh-LETM1 group than those in sh-NC group and blank control group. The results of the subcutaneous tumor formation assay in nude mice indicated that subcutaneous tumor formation ability was reduced in 143B sh-LETM1 group compared with 143B sh-NC group. Conclusion LETM1 promotes the proliferation, migration and in vivo tumor formation of MG63 and 143B osteosarcoma cells and the mechanism may be related to the inhibition of apoptosis and osteogenic differentiation.

Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease characterized by excess fat accumulation within liver cells. The main causes include obesity, diabetes, and hyperlipidemia. In recent years, NAFLD and other metabolic diseases have become global public health issues. Although some progress has been made in the drug treatment of NAFLD, the efficacy is limited and there are many adverse effects. As a treatment method with high safety and few adverse effects, exercise therapy has good application prospects in the treatment of NAFLD and other metabolic diseases. However, challenges remain in overcoming patients' low exercise compliance and in finding safe and effective exercise therapy drug targets. This article explores the mechanisms and application prospects of exercise therapy in the treatment of NAFLD and other metabolic diseases, summarizes the energy consumption, metabolic pathways, and inter-organ communication induced by exercise, aiming to provide useful references for clinical practitioners.

Perioperative neurocognitive disorder (PND) significantly threatens brain health, leading to prolonged hospitalization, increased patient mortality risk, and poor long-term prognosis. Sleep disorder may substantially elevate the risk of neurocognitive dysfunction. However, the specific role of sleep in PND development remains to be elucidated. In addition, controversy exists over whether interventions for perioperative sleep disorder can effectively prevent PND. Therefore, this review aims to explore the basic function and regulatory principles of sleep, the clinical characteristics of perioperative sleep disorder, its role and potential mechanisms in PND development. Furthermore, we also provide new evidence on the potential therapeutic strategies to modulate sleep disorder for PND management, to improve patient's neurocognitive prognosis and long-term outcomes.

Remazolam is a γ-aminobutyric acid (GABA) receptor agonist. It is a short-acting benzodiazepine drug that has just been launched in China in recent years. Its mechanism of action is to enhance inhibitory neurotransmitters of GABA in the central nervous system. It has been widely used in clinical practice for sedation, hypnosis, anti anxiety, and the treatment of insomnia. Meanwhile, remazolam is mainly used for induction and maintenance of general anesthesia during the perioperative period, with a fast onset time and a brief duration of action. Recent studies have shown that remazolam can protect important organs and alleviate organ damage by reducing inflammatory responses and oxidative stress, regulating cell apoptosis, and other pathways. This article summarizes the protective effects and mechanisms of remazolam on the brain, heart, liver, and lung, providing a theoretical basis for the clinical application of remazolam.

Autophagy is an essential cellular metabolic process that involves clearance of damaged organelles and protein aggregates in cells through lysosomes, providing energy for cells, and maintaining cellular tissue homeostasis. Impaired autophagy is closely related to the pathophysiology of a variety of diseases. In the pathogenesis of atherosclerosis (AS), the dysfunction of autophagy of vascular cells plays a crucial role in the formation and progression of AS. The functional status, survival or death of vascular cells, including endothelial cells, vascular smooth muscle cells and macrophages, can influence the formation and stability of plaques, thereby affecting the progression of AS. This review summarizes the relationship between autophagy and AS, and details the impact of autophagy dysfunction on vascular cell function in the process of AS, as well as the role of mitophagy and inflammasome in the development of AS, aiming to provide novel insights for the prevention and treatment of AS.