Cisternostomy is not beneficial to reduce the occurrence of post-traumatic hydrocephalus in Traumatic Brain Injury.

BACKGROUND: The Cisternostomy is a novel surgical concept in the treatment of Traumatic Brain Injury (TBI), which can effectively drain the bloody cerebrospinal fluid from the skull base cistern, reduce the intracranial pressure, and improve the return of bone flap, but its preventive role in post-traumatic hydrocephalus (PTH) is unknow. The purpose of this paper is to investigate whether Cisternostomy prevents the occurrence of PTH in patients with moderate and severe TBI. METHODS: A retrospective analysis of clinical data of 86 patients with moderate and severe TBI from May 2019 to October 2021 was carried out in the Brain Trauma Center of Tianjin Huanhu Hospital. Univariate analysis was performed to examine the gender, age, preoperative Glasgow Coma Scale (GCS) score, preoperative Rotterdam CT score, decompressive craniectomy rate, intracranial infection rate, the incidence of subdural fluid, and incidence of hydrocephalus in patients between the Cisternostomy group and the non-Cisternostomy surgery group. we also analyzed the clinical outcome indicators like GCS at discharge,6 month GOS-E and GOS-E ≥ 5 in two groups.Additionaly, the preoperative GCS score, decompressive craniectomy rate, age, and gender of patients with PTH and non hydrocephalus were compared. Further multifactorial logistic binary regression was performed to explore the risk factors for PTH. Finally, we conducted ROC curve analysis on the statistically significant results from the univariate regression analysis to predict the ability of each risk factor to cause PTH. RESULTS: The Cisternostomy group had a lower bone flap removal rate(48.39% and 72.73%, p = 0.024)., higer GCS at discharge(11.13 ± 2.42 and 8.93 ± 3.31,p = 0.000) and better 6 month GOS-E(4.55 ± 1.26 and 3.95 ± 1.18, p = 0.029)than the non-Cisternostomy group However, there was no statistical difference in the incidence of hydrocephalus between the two groups (25.81% and 30.91%, p = 0.617). Moreover, between the hydrocephalus group and no hydrocephalus group,there were no significant differences in the incidence of gender, age, intracranial infection, and subdural fluid. While there were statistical differences in peroperative GCS score, Rotterdam CT score, decompressive craniectomy rate, intracranial infection rate, and the incidence of subdural fluid in the two groups, there was no statistical difference in the percentage of cerebral cisterns open drainage between the hydrocephalus group and no hydrocephalus group (32.00% and 37.70%, p = 0.617). Multifactorial logistic binary regression analysis results revealed that the independent risk factors for PTH were intracranial infection (OR = 18.460, 95% CI: 1.864-182.847 p = 0.013) and subdural effusion (OR = 10.557, 95% CI: 2.425-35.275 p = 0.001). Further, The ROC curve analysis showed that peroperative GCS score, Rotterdam CT score and subdural effusion had good ACU(0.785,0.730,and 0.749), with high sensitivity and specificity to predict the occurrence of PTH. CONCLUSIONS: Cisternostomy may decrease morbidities associated with removal of the bone flap and improve the clinical outcome, despite it cannot reduce the disability rate in TBI patients.Intracranial infection and subdural fluid were found to be the independent risk factors for PTH in patients with TBI,and the peroperative GCS score, Rotterdam CT score and subdural effusion had higher sensitivity and specificity to predict the occurrence of PTH. And more importantly, no correlation was observed between open drainage of the cerebral cisterns and the occurrence of PTH, indicating that Cisternostomy may not be beneficial in preventing the occurrence of PTH in patients with moderate and severe TBI.

Related factors of delirium after transsphenoidal endoscopic pituitary adenoma resection-A matched retrospective cohort study.

OBJECTIVES: The primary aim of this study is to explore the factors associated with delirium incidence in postoperative patients who have undergone endoscopic transsphenoidal approach surgery for pituitary adenoma. METHODS: The study population included patients admitted to Tianjin Huanhu Hospital's Skull Base Endoscopy Center from January to December 2022, selected through a retrospective cohort study design. The presence of perioperative delirium was evaluated using the 4 'A's Test (4AT) scale, and the final diagnosis of delirium was determined by clinicians. Statistical analysis included Propensity Score Matching (PSM), χ2 Test, and Binary Logistic Regression. RESULTS: A total of 213 patients were included in this study, and the incidence of delirium was found to be 29.58 % (63/213). Among them, 126 patients were selected using PSM (delirium:non-delirium = 1:1), ensuring age, gender, and pathology were matched. According to the results of univariate analysis conducted on multiple variables, The binary logistic regression indicated that a history of alcoholism (OR = 6.89, [1.60-29.68], P = 0.010), preoperative optic nerve compression symptoms (OR = 4.30, [1.46-12.65], P = 0.008), operation time ≥3 h (OR = 5.50, [2.01-15.06], P = 0.001), benzodiazepines for sedation (OR = 3.94, [1.40-11.13], P = 0.010), sleep disorder (OR = 3.86, [1.40-10.66], P = 0.009), and physical restraint (OR = 4.53, [1.64-12.53], P = 0.004) as independent risk factors for postoperative delirium following pituitary adenoma surgery. CONCLUSIONS: For pituitary adenoma patients with a history of alcoholism and presenting symptoms of optic nerve compression, as well as an operation time ≥3 h, enhancing communication between healthcare providers and patients, improving perioperative sleep quality, and reducing physical restraint may help decrease the incidence of postoperative delirium.

YY1: a key regulator inhibits gastric cancer ferroptosis and mediating apatinib-resistance.

OBJECTIVE: Gastric cancer (GC) stands as a prevalent and deadly global malignancy. Despite its role as a preoperative neoadjuvant therapy, Apatinib's effectiveness is curtailed among GC patients exhibiting elevated YY1 expression. YY1's connection to adverse prognosis, drug resistance, and GC metastasis is established, yet the precise underlying mechanisms remain elusive. This study aims to unravel potential pathogenic pathways attributed to YY1. DESIGN: Utilizing bioinformatics analysis, we conducted differentially expressed genes, functional annotation, and pathway enrichment analyses, and further validation through cellular and animal experiments. RESULTS: Higher YY1 expression correlated with diminished postoperative progression-free survival (PFS) and disease-specific survival (DSS) rates in TCGA analysis, identifying YY1 as an independent DSS indicator in gastric cancer (GC) patients. Notably, YY1 exhibited significantly elevated expression in tumor tissues compared to adjacent normal tissues. Bioinformatics analysis revealed noteworthy differentially expressed genes (DEGs), transcriptional targets, factors, and co-expressed genes associated with YY1. LASSO Cox analysis unveiled Transferrin as a prospective pivotal protein regulated by YY1, with heightened expression linked to adverse DSS and PFS outcomes. YY1's role in governing the p53 signaling pathway and ferroptosis in GC cells was further elucidated. Moreover, YY1 overexpression dampened immune cell infiltration within GC tumors. Additionally, YY1 overexpression hindered GC cell ferroptosis and mediated Apatinib resistance via the p53 pathway. Remarkably, IFN-a demonstrated efficacy in reversing Apatinib resistance and immune suppression in GC tissues. CONCLUSIONS: Our findings underscore the pivotal role of YY1 in driving GC progression and influencing prognosis, thus pinpointing it as a promising therapeutic target to enhance patient outcomes.

Is Pathologic Complete Response a Good Predictor for the Long-Term, Clinical Outcome in Patients with Gastric Cancer After Neoadjuvant Chemotherapy? A Retrospective, Multi-institution Study in China.

BACKGROUND: Many studies have used pathologic complete response (pCR) after neoadjuvant chemotherapy (NAC) as the primary endpoint for the short-term efficacy in gastric cancer, but whether it is a good indicator for overall survival is poorly understood. METHODS: This study reviewed a multi-institution database of patients who underwent radical gastrectomy and achieved pCR after NAC. Cox regression models were used to identify clinicopathologic predictors of overall survival (OS) and disease-free survival (DFS). Survival curves were calculated by using the Kaplan-Meier method and compared by means of the log-rank test. RESULTS: OS and DFS in patients with pCR were significantly higher than in those with non-pCR (both P < 0.001). Multivariable analysis confirmed pCR was an independent prognostic factor for OS and DFS (P = 0.009 and P = 0.002 for OS and DFS, respectively). However, the survival benefit for pCR was present only for ypN0 tumors (P = 0.004 and P = 0.001 for OS and DFS, respectively), and OS (P = 0.292) and DFS (P = 0.285) among patients with ypN+ gastric cancer could not be stratified by pCR. CONCLUSIONS: In our study, pCR is an independent prognostic factor for OS and DFS, but the survival benefit for pCR is present only for ypN0 tumors but not ypN+ tumors.

PLOD3 contributes to HER-2 therapy resistance in gastric cancer through FoxO3/Survivin pathway.

Human epidermal growth factor receptor 2 (HER-2), a famous therapeutic target for breast cancer, is also associated with an increased risk of recurrence and poor outcomes of other malignancies, including gastric cancer. Yet the mechanism of HER-2 therapy resistance remains controversial due to the heterogeneity of gastric adenocarcinoma. We know, Procollagen-Lysine,2-Oxoglutarate 5-Dioxygenase 3 (PLOD3), a key gene coding enzymes that catalyze the lysyl hydroxylation of extracellular matrix collagen, plays an important contributor to HER-2 targeting agent Trastuzumab resistance in gastric cancer. Herein, we analyzed clinical samples of gastric cancer patients and gastric cancer cell lines and identified PLOD3, unveiled that depletion of PLOD3 leads to decreased cell proliferation, tumor growth and Trastuzumab sensitivity in these Trastuzumab resistant GC cell lines. Clinically, increased PLOD3 expression correlates with decreased Trastuzumab therapy responsiveness in GC patients. Mechanistically, we show that PLOD3 represses tumor suppressor FoxO3 expression, therefore upregulating Survivin protein expression that contributes to Trastuzumab resistance in GC. Therefore, our study identifies a new signaling axis PLOD3-FoxO3- Survivin pathway that may be therapeutically targeted in HER-2 positive gastric cancer.

Identification of a novel Calpain-2-SRC feed-back loop as necessity for ß-Catenin accumulation and signaling activation in hepatocellular carcinoma.

Rapid progression is the major cause of the poor prognosis of hepatocellular carcinoma (HCC); however, the underlying mechanism remained unclear. Here, we found Calpain-2 (CAPN2), a well-established protease that accelerates tumor progression in several malignancies, is overexpressed in HCC and acts as an independent predictor for poor outcomes. Furthermore, CAPN2 promoted the proliferation and invasion of HCC, and showed a positive correlation with the levels of invasion-related markers. Mechanistically, a novel CAPN2-SRC positive regulatory loop was identified upstream of ß-catenin to prevent its ubiquitination and degradation, and subsequently promoted HCC progression: CAPN2 could proteolyze PTP1B to form a truncation of approximately 42 kDa with increased phosphatase activity, resulting in reduced SRC Y530 phosphorylation and increased SRC kinase activity; meanwhile, CAPN2 itself was a bone fide substrate of SRC that was primarily phosphorylated at Y625 by SRC and exhibited increased proteolysis activity upon phosphorylation. Interestingly, the CAPN2-SRC loop could not only restrain most of cytoplasmic ß-catenin degradation by inhibiting GSK3ß pathway, but also prevented TRIM33-induced nuclear ß-catenin degradation even in ß-catenin-mutant cells. Present study identified a CAPN2-SRC positive loop responsible for intracellular ß-catenin accumulation and signaling activation, and targeting CAPN2 protease activity might be a promising approach for preventing HCC progression.

CircRNA UBAP2 serves as a sponge of miR-1294 to increase tumorigenesis in hepatocellular carcinoma through regulating c-Myc expression.

Circular RNAs (circRNAs) are a class of regulatory RNAs with complex roles in healthy and diseased tissues. However, the oncogenic role of circRNAs in hepatocellular carcinoma (HCC) remains poorly understood, including the mechanisms by which the circular ubiquitin-binding associated protein 2 (circUBAP2) contributes to tumorigenesis. We analyzed the expression of circUBAP2 in 20 paired samples of HCC and healthy tissue as well as in seven HCC cell lines via quantitative real-time polymerase chain reaction. Functional experiments, such as CCK8 viability assays, colony formation assays, wound healing, transwell assays and flow cytometry, were conducted to assess the effects of circUBAP2 in vitro. To further elucidate the mechanisms by which circUBAP2 acts, we conducted dual-luciferase assays, western blots, RNA pull-down assays and rescue experiments. CircUBAP2 was highly upregulated in most HCC tissues and was associated with poor prognosis. HCC patients with high circUBAP2 expression had greater vascular invasion and worse differentiation. Functionally, circUBAP2 overexpression enhanced HCC cell proliferation, migration and invasion and inhibited apoptosis. Furthermore, we found that circUBAP2 upregulated c-Myc expression by sponging miR-1294, thus contributing to hepatocarcinogenesis. Inhibiting circUBAP2 expression in HCC attenuated the oncogenic effects of c-Myc. These findings suggest that circUBAP2 promotes HCC growth and metastasis. CircUBAP2 may have value as an independent prognostic biomarker or as a new target for the treatment of HCC.

A multi-label classification model for full slice brain computerised tomography image.

BACKGROUND: Screening of the brain computerised tomography (CT) images is a primary method currently used for initial detection of patients with brain trauma or other conditions. In recent years, deep learning technique has shown remarkable advantages in the clinical practice. Researchers have attempted to use deep learning methods to detect brain diseases from CT images. Methods often used to detect diseases choose images with visible lesions from full-slice brain CT scans, which need to be labelled by doctors. This is an inaccurate method because doctors detect brain disease from a full sequence scan of CT images and one patient may have multiple concurrent conditions in practice. The method cannot take into account the dependencies between the slices and the causal relationships among various brain diseases. Moreover, labelling images slice by slice spends much time and expense. Detecting multiple diseases from full slice brain CT images is, therefore, an important research subject with practical implications. RESULTS: In this paper, we propose a model called the slice dependencies learning model (SDLM). It learns image features from a series of variable length brain CT images and slice dependencies between different slices in a set of images to predict abnormalities. The model is necessary to only label the disease reflected in the full-slice brain scan. We use the CQ500 dataset to evaluate our proposed model, which contains 1194 full sets of CT scans from a total of 491 subjects. Each set of data from one subject contains scans with one to eight different slice thicknesses and various diseases that are captured in a range of 30 to 396 slices in a set. The evaluation results present that the precision is 67.57%, the recall is 61.04%, the F1 score is 0.6412, and the areas under the receiver operating characteristic curves (AUCs) is 0.8934. CONCLUSION: The proposed model is a new architecture that uses a full-slice brain CT scan for multi-label classification, unlike the traditional methods which only classify the brain images at the slice level. It has great potential for application to multi-label detection problems, especially with regard to the brain CT images.

[Clinical significance of ropivacaine local infiltration for postoperative analgesia after total laparoscopic radical gastrectomy in elderly patients].

OBJECTIVE: To explore the analgesic effects and postoperative recovery of ropivacaine incision infiltration in elderly patients after total laparoscopic radical gastrectomy. METHODS: The clinical data were obtained prospectively from 61 elderly patients ( ≥ 65y) undergoing traditional total laparoscopic radical gastrectomy under standard general anesthesia at our department during January 2012 and September 2013. After surgery, they were randomly double-blindly divided into 3 groups: local infiltration of ropivacaine group (0.5% ropivacaine incision infiltration, 40 ml, n = 22), local infiltration of sodium chloride group (0.9% sodium chloride injection incision infiltration, 40 ml, n = 20) and control group (no analgesic, n = 19). The intensity of postoperative pain was evaluated by numeric rating scale (NRS). And 10 mg of morphine was administered intramuscularly as rescue medication when NRS exceeded 4.NRS, cases on remedy analgesia and associated side effects were observed and recorded after 6 h postoperatively. A comparative study was made for postoperative first ambulation time, intestinal function recovery time, complication incidence, postoperative hospital stay and medical expenses among three groups. RESULTS: Significant postoperative difference existed in NRS at 6, 12, 24, 48 h among ropivacaine, sodium and control groups respectively (6 h: 2.65 ± 0.25 vs 5.47 ± 0.12 vs 5.63 ± 0.27, 12 h: 2.42 ± 0.34 vs 5.82 ± 0.63 vs 5.67 ± 0.49, 24 h: 2.27 ± 0.83 vs 3.95 ± 0.51 vs 3.84 ± 0.60, 48 h: 2.05 ± 0.90 vs 3.75 ± 0.72 vs 3.74 ± 0.56, P < 0.05) . The patients with ropivacaine local infiltration had a lower rate of remedy analgesia than those with sodium chloride injection incision infiltration or without analgesic (both P < 0.05). There was no obvious adverse effect of ropivacaine infiltration at 48 h postoperatively. Both postoperative first ambulation and peristalsis recovery time were shorter (P < 0.05) in ropivacaine group ((53 ± 9) and (80 ± 6) h) than sodium group ((91 ± 11) and (105 ± 9) h) and control group ((93 ± 11) and (109 ± 10) h) . Meanwhile, ropivacaine group had significance decreased postoperative hospital stay and medical expenses than that in local infiltration of sodium group and control group ((10.2 ± 1.3) vs (12.6 ± 1.3), (12.9 ± 1.6) days, (57 000 ± 5 000) vs (63 000 ± 6 000), (65 000 ± 6 000) yuan) (all P < 0.05). Occurrence of complications significantly differed among three groups (local infiltration of ropivacaine group 9.10% (2/22), local infiltration of sodium chloride group 25.00% (5/20) and control group 21.05% (4/19), P < 0.05). CONCLUSION: Ropivacaine infiltration may reduce postoperative pain after total laparoscopic radical gastrectomy, enable faster recovery and provide an alternative analgesia in elderly patients.