Neck and mediastinal hematoma caused by a foreign body in the esophagus with diagnostic difficulties: A case report.

BACKGROUND: Esophageal foreign body (FB) is a common clinical emergency. Clinically, computed tomography (CT) scans are important in the diagnosis of FBs in the esophagus. Here, we report a case of esophageal perforation and cervical hematoma, caused by a FB, whose uniqueness made rapid diagnosis difficult. CASE SUMMARY: A 42-year-old man was transferred to our hospital with esophageal perforation, which was accompanied by cervical and mediastinal hematoma. CT scans only revealed a black shadow, approximately 2.5 cm in diameter, in the upper esophagus. After multidisciplinary discussion, he was quickly subjected to mediastinal hematoma resection, peripheral nerve compression release, esophageal FB removal and esophagectomy. Eventually, we removed a small crab with a pointed tip from his esophagus. CONCLUSION: This was an unusual case of occurrence of sharp polygonal esophageal FBs caused by a small crab. Rapid diagnosis of this FB was difficult, mainly due to its translucent nature. Occurrence of sharp FBs, with cavities that sometimes only appear as black shadows on CT scans, can easily be mistaken for esophageal lumens. More attention should be paid to such sharp polygonal FBs.

Evaluation of a tumor electric field treatment system in a rat model of glioma.

OBJECTIVE: Glioma is a devastating disease lacking effective treatment. Tumor electric field therapy is emerging as a novel non-invasive therapy. The current study evaluates the efficacy and safety of a self-designed tumor electric field therapy system (TEFTS ASCLU-300) in a rat orthotopic transplantation model of glioma. METHODS: A model of intracranial orthotopic transplantation was established in rats using glioma C6 cells. For electric field therapy, glioma-bearing rats were exposed to alternating electric fields generated by a self-developed TEFTS starting on either 1st (Group 2) or 3rd (Group 3) day after transplantation, while other conditions were maintained the same as non-treated rats (Group 1). Glioma size, body weight, and overall survival (OS) were compared between groups. Immunohistochemical staining was applied to access tumor cell death and microvessel density within the tumor. In addition, the systemic effects of TEFTS on blood cells, vital organs, and hepatorenal functions were evaluated. RESULTS: TEFTS treatment significantly elongated the OS of tumor-bearing rats compared with non-treated rats (non-treated vs treated: 24.77 ± 7.08 days vs 40.31 ± 19.11 days, P = .0031). Continuous TEFTS treatment starting on 1st or 3rd day significantly reduced glioma size at 2 and 3 weeks after tumor cell inoculation (Week 2: Group 1:289.95 ± 101.69 mm3 ; Group 2:70.45 ± 17.79 mm3 ; Group 3:73.88 ± 33.21 mm3 , P < .0001. Week 3: Group 1:544.096 ± 78.53 mm3 ; Group 2:187.58 ± 78.44 mm3 ; Group 3:167.14 ± 109.96 mm3 , P = .0005). Continuous treatment for more than 4 weeks inhibited tumor growth. The TEFTS treatment promoted tumor cell death, as demonstrated by increased number of Caspase 3+ cells within the tumor (non-treated vs treated: 38.06 ± 10.04 vs 68.57 ± 8.09 cells/field, P = .0007), but had minimal effect on microvessel density, as shown by CD31 expression (non-treated vs treated: 1.63 ± 0.09 vs 1.57 ± 0.13% of positively stained areas, P > .05). No remarkable differences were observed in hepatorenal function, blood cell counts, or other vital organs between non-treated and treated groups. CONCLUSION: The TEFTS developed by our research team was proved to be effective and safe to inhibit tumor growth and improve general outcomes in a rat model of brain glioma.

Correlation of preoperative seizures with a wide range of tumor molecular markers in gliomas: An analysis of 442 glioma patients from China.

PURPOSE: Epileptic seizures often develop in 40-70 % of glioma patients and have a significant impact on patients' quality of life. Many biomarkers have been suggested to be associated with glioma-related preoperative seizures (GPS). The purpose of the present study was to investigate the possible correlation between GPS and clinicopathological factors and a wide range of glioma-associated molecular markers (GMMs). METHODS: First, a retrospective cohort study of 442 patients with glioma was evaluated at the PLA General Hospital. Univariate and multivariate logistic analyses were used to identify basic factors associated with GPS. Second, 40 pairs of cases who underwent deep sequencing of 68 GMMs were selected from both groups for in-depth analysis. RESULTS: Of the 442 patients examined in this study, 137 (31 %) had GPS. By analyzing the characteristics of these patients, the results showed that patient age (OR: 0.981, p = 0.037, 95 % CI: 0.964-0.999), WHO grade (OR: 0.678, p = 0.008, 95 % CI: 0.509-0.903) and IDH mutations (OR: 1.886, p = 0.013, 95 % CI: 1.143-3.11) in patients were associated with the occurrence of GPS. In our cohort, GPS did not differ by sex, tumor location, histopathological subtype, p53 expression, ARTX loss, MGMT gene promotor methylation, TERT promoter mutation, or 1p/19q co-deletion status. The results of the matching study showed that the paired groups had similar genetic expression profiles, and the mutation of these 68 GMMs was not correlated with the occurrence of GPS. CONCLUSION: The current study updates existing information on GPS and genetic markers in gliomas and explores the correlation of a wide range of GMMs and GPS. These factors may provide insights for developing effective treatment strategies aimed at seizure control.

Practice and reflection on the management mode of pain quality control in emergency pre-check and triage.

BACKGROUND: Triage decision making is crucial for patients arrived at emergency room as it influences the clinical outcome. Appropriate standard to discriminate patients into different category is challenging. We introduced a suitable emergency preview triage pain model for quality management methods through the pain assessment module. METHODS: The pain quality control and management of emergency pre-examination triage were realized by designing the pain assessment module of the intelligent triage system. Clinical nurses completed the assessment of pain score and PQRST pain content through the pain tool in the pain assessment module of the intelligent triage system. The computer system would automatically assess the triage category according to the pain score. Triage nurses determined the priority of emergency care based on the type of care. RESULTS: The pain quality control target monitoring reached 95% of the target management value in ten months. There were two months when the target management value was not reached 95%, June 2019 (94.28%), and December 2019 (94.28%), respectively, slightly lower than the target management value (95%). CONCLUSIONS: The application of the pain quality control management mode of emergency preexamination triage unifies the standards of emergency pre-examination triage pain, standardizes the pain assessment and improves the level of emergency pre-examination triage pain management.

Trichostatin A activates FOXO1 and induces autophagy in osteosarcoma.

INTRODUCTION: Histone deacetylase inhibitors (HDACIs) inhibit human osteosarcoma growth and cause apoptosis. Previously, we reported that HDACIs induce autophagy via the FOXO1 pathway. Whether there is involvement of autophagy in anti-osteosarcoma activity of HDACIs is still unknown. MATERIAL AND METHODS: Confocal microscopy was performed to determine the formation of GFP-LC3 puncta. Western blotting was conducted to measure FOXO1, and autophagy-related protein levels. Small interference RNA (siRNA) specific for FOXO1 was transfected into U2OS cells to knock down FOXO1 expression level. Flow cytometry was performed to quantify cell death. RESULTS: In this study, we first observed that trichostatin A (TSA) induces autophagy in human osteosarcoma cells. Moreover, we found that TSA treatment inhibits the mammalian target of rapamycin (mTOR) signaling pathway and enhances forkhead box O1 (FOXO1) transcriptional activity, which is responsible for the increased autophagy level, while suppression of FOXO1 function by siRNA knockdown markedly decreases TSA-induced autophagy. CONCLUSIONS: We found that inhibition of autophagy, either by autophagy inhibitors or ATG gene knockdown, markedly enhances TSA-caused cell death. Taken together, our studies reveal the function of autophagy in HDACI-caused osteosarcoma cell death and thus support the development of a novel therapeutic strategy by combining HDACIs and autophagy inhibitors in osteosarcoma treatment.

The significance of serum uric acid level in humans with acute paraquat poisoning.

Hyperuricemia is a strong and independent predictor of all-cause mortality in cardiovascular disease and has been found to play a role in diseases exacerbated by oxidative stress and inflammation. This study aimed to evaluate whether serum uric acid (UA) level is an indicator of outcome in patients with acute paraquat poisoning. A total of 205 subjects who had attempted suicide by oral ingestion of paraquat were admitted to the emergency room between January 2009 and June 2014. Initial serum UA level and other laboratory parameters were measured. A total of 66 patients died during the 30 days after admission, corresponding to a 32.2% cumulative incidence of mortality. UA levels were higher in non-survivors than survivors (P < 0.001) and 30-day mortality increased with increasing baseline serum UA level (P < 0.001). In a prediction analysis for 30-day mortality, the serum UA level had a cut-off concentration of 284 µmol/L in female patients and 352 µmol/L in male patients. Multivariate Cox proportional hazards regression analyses showed that white blood cell counts and UA were independent prognostic factors. In conclusion, we showed that serum UA may be an independent predictor of 30-day mortality in patients with paraquat poisoning.