Objective To investigate the association between the serum creatinine/cystatin C ratio (SCr/Cys C) as a Sarcopenia index (SI) and the incidence of in-hospital adverse events in patients with acute myocardial infarction (AMI) undergoing emergency percutaneous coronary intervention (PCI). Additionally, we evaluate the predictive efficacy of the SI in predicting major adverse cardiovascular events (MACEs) during hospitalization. Methods A total of 306 patients with AMI who underwent emergency PCI in the 904th Hospital of PLA Joint Logistics Support Force from January 2020 to March 2023 were consecutively included in this retrospective analysis. Patients were divided into two groups based on the occurrence of MACEs during hospitalization: MACEs group (n=43) and non-MACEs group (n=263). Clinical characteristics and pre-PCI laboratory test results were collected. Univariate and multivariate logistic regression analyses were performed to identify independent risk factors for MACEs. The predictive performance of SI was assessed using receiver operating characteristic (ROC) curve analysis. Results The incidence of in-hospital MACEs in AMI patients was 14.1%.The results of the independent samples t-test showed that the SI level in MACEs group was significantly lower than that in non-MACEs group, with a statistically significant difference (P<0.001). The results of the multivariate logistic regression analysis suggested that new-onset atrial fibrillation, Killip class 2-4, SI, and TG were independent risk factors for in-hospital adverse events after emergency PCI. The ROC curve results showed that the predictive value of SI (AUC=0.741, 95%CI 0.666-0.816) using the SCr/Cys C ratio was superior to that of single Cys C (AUC=0.658, 95%CI 0.570-0.746) for predicting post-PCI MACEs, with a statistically significant difference (P<0.05), and the optimal cutoff value for SI was 78.14. After stratifying SI based on the cutoff value, the results of the independent samples t-test showed that compared to the higher SI group, the lower SI group had a higher occurrence of specific adverse events such as heart failure (P<0.001), malignant arrhythmias (P=0.009), and strokes (P=0.003), with statistically significant differences. Conclusions The results highlight SI as an independent risk factor for MACEs during hospitalization after emergency PCI in AMI patients. Furthermore, SI has proven to be an effective prognostic index for patient outcomes.

Objective To investigate the independent risk factors of comprehensive complication index (CCI) ≥26.2 after radical resection of colon cancer, and use these factors to establish and verify a dynamic web-based nomogram model. Methods The clinical data of colon cancer patients who underwent radical resection in the Affiliated Hospital of Jiangnan University from November 2020 to April 2022 were retrospectively collected, and divided into main cohort (November 2020 to October 2021, n=438) and validation cohort (November 2021 to April 2022, n=196). CCI scores of all patients were obtained based on CCI calculator (http://www.assessurgery.com). Univariate and multivariate logistic regression analysis were performed to identify the risk factors for CCI ≥26.2, and a nomogram model was constructed. Receiver operator characteristic curve (ROC), C index and calibration curve were used to evaluate the differentiation and consistency of predictive nomogram model, and the decision curve analysis was conducted to assess the clinical benefits of the model. Internal validation of the model is performed in the validation cohort. Results A total of 438 patients were identified in present study, of which 63 cases (14.4%) had CCI ≥26.2. Multivariate logistic regression analysis revealed that age ≥60 years (OR=2.662, 95%CI 1.341-5.285, P=0.005), low third lumbar spine skeletal muscle mass index (L₃MI; OR=4.572, 95%CI 2.435-8.583, P<0.001), NRS2002 ≥3 (OR=4.281, 95%CI 2.304-7.952, P<0.001), and preoperative bowel obstruction (OR=3.785, 95%CI 1.971-7.268, P<0.001) were significant independent risk factors for postoperative CCI ≥26.2. Based on these results, a static and web-based dynamic nomogram was established (https://jndxfsyywcwksyf.shinyapps.io/DynNomCCI/). The C-index and area under the curve (AUC) of the nomogram were 0.742 and 0.787, respectively. The calibration curve indicated a good consistency between the predicted probability and the actual probability. In the validation cohort, the nomogram also presented good discrimination (C-index=0.722, AUC=0.795) and predictive consistency. The decision curve analysis indicated the clinical benefit and application value of the nomogram prediction model. Conclusion This easy-to-use dynamic nomogram based on 4 independent risk factors can conveniently and reliably predict the probability of CCI ≥26.2 after radical resection of colon cancer, which helps optimize the preoperative evaluation system, formulate precise individualized treatment strategies, and enhance recovery after surgery.

Objective To investigate the changes of serum neuroglobulin (NGB) levels in patients with aneurysmal subarachnoid hemorrhage (aSAH) and its clinical value in predicting of delayed cerebral ischemia (DCI). Methods A total of 217 patients with aSAH who were diagnosed and treated in the Department of Neurology of Wuwei People's Hospital from October 2019 to October 2022 were selected. They were divided into DCI group and non-DCI group according to the occurrence of DCI after aSAH. The clinical data, and serum NGB levels on day 1 and day 3 after admission were compared between the two groups, and the value of serum NGB in prediction of DCI was evaluated by ROC curve. Logistic regression was used to analyze the risk factors to DCI in aSAH patients. Results DCI occurred in 43 of 217 patients with aSAH (19.8%). Hunt-Hess grade and modified Fisher grade in DCI group were higher than those in non-DCI group (P<0.05). The level of serum NGB in DCI group was higher than that in non-DCI group on day 1 and day 3 after admission (P<0.05), and the levels of serum NGB on day 3 after admission were lower than that on day 1 in two groups (P<0.05). The decrease of serum NGB level in DCI group was lower than that in non-DCI group (P<0.05). ROC curves showed that serum NGB at 3 d after admission predicted a greater AUC for DCI (0.838) than serum NGB at 1 d after admission (0.706)(Z=2.139, P<0.05), with an optimal cutoff of 10.19 ng/ml of serum NGB, the sensitivity and specificity were 74.4% and 86.8% respectively. Logistic regression analysis showed that the risk factors of DCI in patients with aSAH were modified Fisher Grade Ⅲ-Ⅳ (OR=3.790, 95%CI 1.531-9.382), Hunt-Hess grade Ⅲ-Ⅴ(OR=2.448, 95%CI 1.023-5.858) and increased serum NGB at 3 d after admission (OR=1.835, 95%CI 1.496-2.251). Conclusions The serum NGB level is relatively high in patients with DCI after aSAH in the early stage. The serum NGB level, modified Fisher grade, and Hunt-Hess grade are related to the development of DCI after aSAH, and the serum NGB level on 3 d after admission has high predictive value.

Objective To investigate the genotypic and phenotypic characteristics of AB type GM2 gangliosidosis (GM2-GLS) with onset during childhood. Methods The report analyzed the clinical data and gene detection results of a 4-year-old child with AB type GM2-GLS diagnosed by Trio whole exome detection in March 2022 admitted to the Department of Pediatrics of Guangxi Zhuang Autonomous Region People's Hospital. The clinical data and genetic testing results are analyzed. A literature review was also conducted on relevant studies published between 1991 and 2022 in the PubMed database. Results The results of Trio whole exome sequencing and Sanger verification showed that the GM2A gene carried two compound heterozygous mutations: c.158_159delTG and c.496G>A, which caused p.L53Rfs*3 frameshift mutation and p.G166R missense mutation, respectively. A total of 20 cases were reported in 22 articles. A total of 11 mutation types of GM2A gene were included in the ClinVar Database. Conclusions AB type GM2-GLS is a rare autosomal recessive lysosomal storage disease, and its gene test is helpful for definite diagnosis.

Objective To investigate the protective effect of placental mesenchymal stem cells (P-MSCs) on pancreatic trauma (PT) in rats. Methods Sixty healthy adult male SD rats were randomly divided into control group, pancreatic trauma group (inject 1 ml of PBS solution locally in the pancreatic injury area and around the trauma area), and P-MSCs group [inject 1 ml of P-MSCs (1×10⁶/ml) locally in the pancreatic injury area and around the trauma area], with 20 rats in each group. The pancreatic trauma rat model was established using a traumatic pressure of 400 kPa. Five rats were sacrificed at 1, 3, 5, and 7 d after modeling in each group, and serum and pancreatic tissue were collected. HE staining was used to observe the pathological changes of pancreatic tissue and pathological scores were performed. The ELISA method was used to measure the concentrations of serum amylase (AMS), lipase (LPS), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10, and transforming growth factor-β₁ (TGF-β₁), as well as the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) in pancreatic tissue. The TUNEL method was used to observe the level of apoptosis in pancreatic tissue was observed by the TUNEL method. Results Compared with control group, pancreatic trauma group and P-MSCs group showed significant differences after pancreatic trauma, including the generation of peritoneal fluid increased (P<0.05), the ratio of pancreas to body weight and the total score of pancreatic tissue pathological damage increased (P<0.05), and serum levels of AMS, LPS, TNF-α, IL-6, and MPO activity increased early and showed a decreasing trend over time (P<0.05), while anti-inflammatory factors IL-10 and SOD activity showed an increasing trend over time (P<0.01), level of TGF-β₁ in the early decline showed an upward trend over time (P<0.01), and the apoptosis index (AI) significantly increased (P<0.001). Compared with pancreatic trauma group, P-MSCs group showed an improvement in the overall morphology of pancreatic tissue, the generation of peritoneal fluid decreased (P<0.001), the pancreas to body weight ratio and the total score of pancreatic tissue pathological damage decreased (P<0.05), and serum levels of AMS, LPS, IL-6, TNF-α and MPO activity returned to normal levels faster (P<0.05); and the rate of anti-inflammatory factors IL-10, TGF-β₁ and SOD activity elevation increased (P<0.05), the AI increased (P<0.001). Conclusion P-MSCs can achieve therapeutic effects on pancreatic trauma in rats by promoting pancreatic tissue repair, reducing local and systemic inflammation, improving tissue oxidative stress, and enhancing pancreatic acinar cell apoptosis.

Objective To investigate the effect and mechanism of proteasome inhibitor MG132 on memory impairment induced by chronic hypoxia in mice. Methods (1) A hypoxic model of the mouse midbrain dopaminergic neuron cell line MN9D was established using a hypoxia workstation. To observe the effects of hypoxia on the expression of TH, Ub-K48 and Ub-K63, MN9D cells were divided into normoxia group and hypoxia (12 h, 24 h and 48 h) groups. To observe the effects of MG132 on the expression of the above-mentioned proteins, MN9D cells were divided into normoxia group, hypoxia group and hypoxia + MG132 (25, 50, 100, 200 μmol/L) group. (2) A mouse model of memory impairment was established using a hypobaric chamber. To observe the effects of hypobaric hypoxia on the expression of TH, Ub-K48 and Ub-K63 in the substantia nigra compacta (SNc) of mice, thirty C57BL/6 mice were randomly and equally divided into normoxia group and hypobaric hypoxia (3 d and 21 d) groups, 10 in each group. To observe the effects of MG132 on spatial memory impairment induced by hypobaric hypoxia, twenty-four C57BL/6 mice were randomly and equally divided into normoxia group, hypobaric hypoxia 21 d group and hypobaric hypoxia 21 d+MG132 group, 8 in each group. (3) The protein expression levels of TH, Ub-K48, and Ub-K63 in MN9D cells which were either subjected to different durations of hypoxia treatment or pre-treated with MG132 prior to hypoxia treatment were detected using Western blotting (WB). The novel object recognition test was used to detect the memory function of mice. Immunofluorescence was used to detect the proportion of positive immunoreactive area of TH response in the SNc region. The expression levels of TH, Ub-K48, and Ub-K63 in the SNc region were detected by WB. Results (1) Compared with normoxia group, MN9D cells in hypoxia 24 h group showed increasing expression of Ub-K48 and Ub-K63 (P<0.05), and decreasing expression of TH (P<0.05), and MN9D cells in all hypoxia groups showed increasing expression of Ub-K48/TH and Ub-K63/TH (P<0.05). Compared with hypoxia group, MN9D cells showed decreasing expression of Ub-K48/TH and Ub-K63/TH in hypoxia + MG132 100 umol/L group and hypoxia + MG132 200 umol/L group (P<0.05). (2) Compared with the mice in normoxia group, mice in 3 d and 21 d hypobaric hypoxia groups showed decreasing expression of TH (P<0.001), and increasing expression of Ub-K48/TH and Ub-K63/TH (P<0.05) in the SNc region. Compared with normoxia group, the mice in 21 d hypobaric hypoxia group showed a lower new object recognition index (P<0.01), and the proportion of positive immunoreactive area of TH response in the SNc region (P<0.05). Compared with 21 d hypobaric hypoxia group, the mice in hypobaric hypoxia 21 d+MG132 group showed a higher new object recognition index (P<0.01). Conclusion The proteasome inhibitor MG132 could alleviate the memory impairment induced by chronic hypoxia in mice, and its mechanism may be related to the inhibition of Ub-K63 and Ub-K48, which in turn upregulates expression of TH in dopaminergic neurons.

Objective To investigate the expression of prolyl 4-hydroxylase β‑polypeptide (P4HB) in glioblastoma multiforme (GBM) and its impact on clinical prognosis, as well as on the proliferation and migration of U87 cells. Methods (1) According to the Cancer Genome Atlas (TCGA) database, GTEx database and GEPIA2 database, the difference expression of P4HB in GBM and normal brain tissues were analyzed by R software. (2) A total of 52 patients with GBM who underwent surgical treatment from February 2017 to December 2019 were collected from Department of Neurosurgery, the Second People's Hospital of Guiyang. The normal brain tissues of 10 patients were selected as controls. Immunohistochemical method was used to detect the expression level of P4HB in tumor tissues and normal tissues. The Kaplan-Meier method with the log-rank test was employed for survival analysis. Receiver operating characteristic (ROC) curve was used to analyze the predictive valuable of P4HB expression in survival rate of GBM. Univariate and multivariate Cox regression analysis were used to identify the expression of P4HB and related clinicopathological factors affecting the survival and prognosis of the patients. (3) Human GBM U87 cells were randomly assigned into three groups: control group, NC-siRNA group and P4HB-siRNA group. P4HB expression was interfered with by the transfection of siRNA in P4HB-siRNA group. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the content of P4HB mRNA in U87 cells. Cell counting kit-8 (CCK-8) and immunofluorescence assay were used to analyze the effects of P4HB on the proliferation of U87 cells. Scratch test was used to analyze the effects of P4HB on cell migration. Results The expression of P4HB was significantly upregulated in GBM tissues compared with normal brain tissues (P<0.05). The γδ T cells (r=-0.227) and follicular helper T cells (r=-0.226) were negatively correlated with the expression of P4HB, while natural killer cell (r=0.417), macrophages (r=0.374), neutrophils (r=0.344), and immature dendritic cells (r=0.263) were positively correlated with the expression of P4HB. Kaplan-Meier survival analysis showed that the progression-free survival and disease-specific survival of GBM patients with high P4HB expression were significantly lower than those with low expression (P<0.05). ROC curve showed that the area under the curve (AUC) of P4HB in predicting overall survival rate of GBM patients was 0.982, and 1-year, 3-year, and 5-year survival was 0.655, 0.724, 0.861, respectively. The immunohistochemistry results suggested that P4HB protein was significantly highly expressed in GBM tumors. Survival analysis indicated that high expression of P4HB was associated with bad prognosis in GBM patients (P<0.05). Multivariate Cox regression analysis indicated that high expression of P4HB and TERT promoter mutations were the independent prognostic risk factors for GBM (P<0.05). Compared with control group and NC-siRNA group, the expression levels of P4HB were decreased significantly after transfected with siRNA in U87 cells of P4HB-siRNA group (P<0.01), and the proliferation ability and the wound healing rate were decreased significantly in P4HB-siRNA group (P<0.001). Conclusions P4HB is significantly highly expressed in GBM, which indicates that the prognosis of patients is poor. Knockout of P4HB could inhibit cellular proliferation and migration of GBM U87 cells. P4HB may be used as the relevant predictive marker and potential therapeutic target in GBM.

Histone deacetylases (HDACs) can deacetylate histones, leading to tighter DNA binding, and thereby playing a role in inhibiting gene transcription. On the contrary, histone deacetylase inhibitors (HDACis) can promote chromatin relaxation, enabling various transcription factors to bind specifically to DNA and activate transcription genes. Dental stem cells (DSCs) are human adult stem cells. These cells have the characteristics of less damage and low immune rejection during sampling, and are especially important seed cells in the process of osteogenesis, odontogenesis and other differentiation. A large number of experimental studies have shown that HDACs and HDACis together play important roles in cell division and differentiation, signal transduction, regulation of cellular inflammation and other life processes. This review summarizes the research progress of HDACs and HDACis in regulating osteogenic and odontogenic differentiation of DSCs, aiming to provide insights into the study of the interaction between HDACs and HDACis, and potentially guide clinical application of DSCs in the treatment of tooth and bone injury.

Epilepsy is a chronic disease characterized by recurrent, sudden, and excessive synchronous discharge of neurons in the brain, leading to transient brain dysfunction, and inflammatory responses in specific regions within the central nervous system are common features of epilepsy. In recent years, there has been increasing evidence that endoplasmic reticulum stress is involved in the pathology of epilepsy, which activates the unfolded protein response, then regulate and control nuclear factor kappa-B (NF-κB), efficiently induces glial cell activation through the release of pro-inflammatory signals, in turn affects epileptogenesis and seizures by triggering neuroinflammation. This review focuses on the close link between endoplasmic reticulum stress and glial cell activation-mediated neuroinflammation in epilepsy pathology, aiming to provide insights for a deeper understanding of epilepsy.

Breast cancer is one of the most prevalent malignancies in the world, and many advances have been made in various types of tumor research in recent years. With the deepening understanding of tumors, the microenvironment for tumor cell growth has attracted more and more attention for its impact on the development and progression of cancer. Cancer-associated fibroblasts (CAFs) as the most important components of the tumor microenvironment, can release cytokines, exosomes, and so forth in many ways to regulate immune microenvironment, remodel extracellular matrix and promote formation, migration, invasion, and resistance of tumors, while at the same time CAFs can be regulated by tumor cells. This paper attempts to explain the interaction mode between CAFs and tumors in the immune microenvironment and various ways in which CAFs can promote tumor proliferation, growth, invasion, metastasis, drug resistance and other malignant biological behaviors. Finally, the possibility of using CAFs as an early screening technique and new treatment method for breast tumors is discussed.