Abstract Objective To analyse the risk factors for intracranial infection after neuroendoscopic transnasal pituitary adenoma resection (NTPAR) to provide a reference for the prevention and treatment of postoperative intracranial infection. Methods The clinical data of 387 patients who underwent NTPAR in the Department of Neurosurgery of the First People’s Hospital of Yichang from March 2013 to March 2021 were retrospectively analysed. The patients were divided into an infected group and a noninfected group according to the occurrence of intracranial infection. The detailed clinical data of the two groups were collected. Univariate and multivariate logistic regression was used to analyse the risk factors for intracranial infection after NTPAR. Results Among the 387 surgical patients, 32 patients (8.27%) were in the intracranially infected group and 355 patients (91.73%) were in the noninfected group. The results of the univariate analysis suggested that age > 45 years, tumour size > 1 cm, operation time > 240 min, blood loss > 400 ml, Kelly Grade of cerebrospinal fluid (CSF) leakage > Grade 2, postoperative CSF leakage, lumbar cistern drainage and blood transfusion were the influencing factors for postoperative intracranial infection, while the results of multivariate logistic regression analysis implied that intraoperative CSF leakage (Kelly Grade > 2) and postoperative CSF leakage were independent influencing factors for intracranial infection after NTPAR, and perioperative use of antibiotics was an independent protective factor for postoperative intracranial infection. Conclusions There are a variety of risk factors for intracranial infection after NTPAR, which indicates that it is necessary to develop different repair strategies for CSF leakage according to the Kelly Grade, timely treatment of postoperative CSF leakage and perioperative use of antibiotics. These measures have been shown to effectively reduce the probability of intracranial infection after NTPAR.
Glioma is the most common type of malignant intracranial tumor in adults and is associated with the highest mortality rate. Although surgery, radiotherapy, chemotherapy and other treatment methods have progressed, the median survival of patients with glioma is only 14‑15 months. Glioma cells are able to penetrate along blood vessels and invade into the surrounding normal brain tissue so that an overall resection of the tumor cannot be performed. In the process of metastasis, the resistance of cancer cells to anoikis has an important role. When tumor cells escape from their original environment, anoikis resistance aids their survival. In the present study, reverse transcription‑semi‑quantitative polymerase chain reaction (RT‑sqPCR), RT‑quantitative PCR and western blotting demonstrated that the transcription factor, motor neuron and pancreas homeobox 1 (MNX1), was ectopically expressed in glioma cells compared with normal HUVEC‑C human umbilical vein endothelial cells. Furthermore, its expression was higher in more malignant glioma cell lines (T98G and M059K) compared with the less malignant glioma cell line (U‑87 MG) and normal HUVEC‑C cells. An adhesion assay using fibronectin demonstrated that MNX1 and tyrosine kinase receptor B (TrkB) overexpression in HUVEC‑C and U‑87 MG cells reduced adhesion and forced them to suspend. Additionally, MNX1 and TrkB overexpression was demonstrated to increase the ability of cells to bypass anoikis. MNX1 and TrkB knockdown increased adhesion and promoted apoptosis after suspension. It was further demonstrated that MNX1 functioned as a transcription factor binding in the upstream regulatory region of TrkB to activate its expression. The results of the present study suggested that MNX1 may suppress the adhesion and apoptosis rates of tumor cells by activating TrkB. The results of the present study suggest that MNX1 may represent a novel therapeutic target for the treatment of gliomas.
To evaluate the efficacy of neuronavigation-assisted stereotactic drilling drainage compared with that of craniotomy in the treatment of massive intracerebral haemorrhage (ICH) in elderly patients. This was a randomized, controlled, blind endpoint clinical study. Elderly patients with massive ICH treated at our neurosurgery department, without the formation of brain herniation preoperatively, all underwent neurosurgical intervention. Patients were randomly assigned to two groups: the minimally invasive surgery (MIS) group, which received neuronavigation-assisted stereotactic drilling drainage, and the craniotomy haematoma removal surgery (CHRS) group. Patient characteristics, surgical anaesthesia methods, surgery duration, intraoperative bleeding volume, duration of ICU stay duration of hospital stay, complications, and modified Rankin scale (mRS) scores at 90 days posttreatment were compared between the two groups. Statistical analysis was performed on the collected data. A total of 67 patients were randomly assigned, with 33 (49.25%) in the MIS group and 34 (50.75%) in the CHRS group. Compared with the CHRS group, the MIS group had advantages, including the use of local anaesthesia, shorter surgery duration, less intraoperative bleeding, shorter ICU stay, and fewer complications (P < 0.05). The MIS group had a significantly improved patient prognosis at 90 days (mRS 0–3). However, there were no significant differences in hospital stay or 90-day survival rate between the two groups (P > 0.05). For elderly patients with massive ICH without brain herniation, stereotactic drilling drainage is a simple surgical procedure that can be performed under local anaesthesia. Patients treated with this approach seem to have better outcomes than those treated with craniotomy. In clinical practice, neuronavigation-assisted stereotactic drilling drainage is recommended for surgical treatment in elderly patients with massive ICH without brain herniation. Clinical trial registration number: NCT04686877
Abstract Background: The protein expression of ERCC1 in DNA repair genes was related to resistance platinum and predicting treatment outcomes in various malignant carcinoma ,the level of plasma Epstein-Barr virus（EBV）DNA concentrations is positively correlated with clinical stages of nasopharyngeal carcinoma(NPC), but the predictive value of ERCC1 mRNA and EBV-DNA level for stratified treatment with stage II NPC is unclear precisely. This study aimed to assess the predictive value of combined EBV-DNA and ERCC1 in stage II NPC patients treated with intensity-modulated radiotherapy (IMRT) with concurrent cisplatin and provide guidance for future stratified treatment. Methods: A total 78 stage II NPC patients who received IMRT and concurrent cisplatin-based chemotherapy had measurements of ERCC1 mRNA and pre-treatment EBV DNA levels by real-time PCR (RT-PCR) analysis were analyzed. Associations of ERCC1 mRNA and pre-treatment EBV DNA levels with clinical characteristics and survivals were evaluated. Results: Cut-off value of ERCC1 mRNA obtained from ROC curve was used and there were significant differences in progression-free survival (PFS) and overall survival (OS) between high expression group as compared to low expression group ( P =0.021 and 0.030, respectively). Patients with pretreatment EBV-DNA<2000 copies/ml had significantly better PFS ( P = 0.024) than those with pretreatment EBV-DNA≥2000 copies/ml, but there was no significant difference in OS ( P = 0.062). Patients were divided into three groups by combination of ERCC1 mRNA and EBV-DNA level ERCC1 mRNA low expression/pre EBV-DNA<2000 copies/ml, ERCC1 mRNA low expression/pre EBV-DNA≥2000 copies/ml, ERCC1 mRNA high expression/pre EBV-DNA≥2000 copies/ml. In these groups, 1-year, 3-year, 5‐year OS were 100%, 100%, 100%; 100%, 94.1%, 90.9%; 100%, 85%, 72.9%, respectively ( P =0.038); 1-year, 3-year, 5‐year PFS were 100%, 100%, 100%; 97.1%, 91.2%, 84.8%; 95%, 85%, 71.4%, respectively ( P =0.028). Multivariate analysis showed combination of ERCC1 mRNA and EBV-DNA levels remained independent prognostic factor but not ERCC1 mRNA and EBV-DNA alone. Conclusion: Combined ERCC1 mRNA and pre EBV-DNA is a better prognostic factor in stage II NPC patients treated with concurrent chemoradiation. Patients with ERCC1 mRNA high expression/pre EBV-DNA≥2000 copies/ml should be treated with more aggressive regimen.
Abstract Renal cell carcinoma (RCC) is one of the most common urological cancers in adults. Forkhead box k1 (FOXK1) is a transcription factor involved in the progression of various malignant tumors. In this study, we aimed to investigate the expression and roles of FOXK1 in RCC development. Our findings revealed increased expression of FOXK1 in RCC tumor tissues and cell lines compared with normal controls. Functional assays demonstrated that knockdown of FOXK1 significantly inhibited proliferation, migration, invasion, and promoted apoptosis in RCC cells. Furthermore, FOXK1 knockdown suppressed epithelial‐mesenchymal transition and Wnt signaling in RCC cells. Additionally, we observed a correlation between FOXK1 upregulation and tumor associated macrophages infiltration in RCC. These results suggest that FOXK1 acts as an oncogene in RCC and may serve as a potential therapeutic target for RCC treatment.
Objective
To observe the incidence of hypothermia, acidosis and coagulopathy in the patients with multiple trauma and to explore the potential relationship among them.
Methods
A retrospective study was carried out to observe the incidences of hypothermia, acidosis, coagulopathy and shock from a database of 713 trauma patients consisting of 184 simple trauma patients and 529 multiple trauma patients. Moreover, the multiple trauma patients were classified into critical multiple trauma subgroup (CMT) , severe multiple trauma subgroup (SMT) and mild multiple trauma subgroup (MMT) by using injury severity score. The potential relationships among shock and hypothermia, acidosis, coagulopathy were analyzed.
Results
Analysis of data from the database indicated that the incidences of hypothermia, acidosis, coagulopathy and lethal triad in multiple trauma patients were 8.1%, 18.9%, 27.6% and 7.8%, respectively, which were significantly higher compared with simple trauma patients (P <0.05, P < 0.01) . As increase in disease severity, the incidence of lethal triad was significantly higher in CMT subgroup (11.1%) compared with SMT subgroup (7.1%) and MMT subgroup (2.0%) (P <0.05) . Multiple trauma patients, particularly with hypovolaemic shock, tended to have higher incidence of hypothermia, acidosis and coagulopathy (P <0.01) .
Conclusion
Our study demonstrates the high incidences of hypothermia, acidosis and coagulopathy are prominent in the patients with multiple trauma. Moreover, post-traumatic shock is the major factor to induce the occurrence of hypothermia, acidosis, coagulopathy and triad of death in the patients with multiple trauma.
Key words:
Multiple trauma; Hypothermia; Acidosis; Coagulopathy
Lactobacillus casei (L. casei) has four possible mechanisms: antimicrobial antagonism, competitional adhesion, immunoregulation, and the inhibition of bacterial toxins. To delineate the metabolic reactions of nucleotides from L. casei that are associated with mechanisms of inhibiting pathogens and immunoregulation, we report that a PyrR-deficient L. casei strain was constructed using the CRISPR-Cas9D10A tool. Furthermore, there were some changes in its basic biological characterization, such as its growth curve, auxotroph, and morphological damage. The metabolic profiles of the supernatant between the PyrR-deficient and wild strains revealed the regulation of the synthesis of genetic material and of certain targeting pathways and metabolites. In addition, the characteristics of the PyrR-deficient strain were significantly altered as it lost the ability to inhibit the growth of pathogens. Moreover, we identified PyrR-regulating pyrimidine biosynthesis, which further improved its internalization and colocalization with macrophages. Evidence shows that the PyrR gene is a key active component in L. casei supernatants for the regulation of pyrimidine biosynthesis against a wide range of pathogens.
Diabetes mellitus (DM) is a complex metabolic disease with significant neurological complications and is reported to be closely related to the blood-brain barrier (BBB) disruption. Azilsartan is an antagonist of the Angiotensin II receptor developed for the treatment of hypertension, and it has been recently reported to have neuroprotective effects. The present study aims to investigate the protective effect of Azilsartan against hyperglycemia-induced BBB disruption and its underlying mechanism. Male db/db mice were treated with Azilsartan (20 μg/day) for 10 consecutive days. Compared to the control group, increased BBB permeability, suppressed occludin expression, excessive release of inflammatory factors, and downregulation of krüppel-like factor 2 (KLF2) were observed in diabetic mice, all of which were dramatically reversed by Azilsartan treatment. In the in vitro experiments, elevated endothelial permeability and decreased expression of occludin and KLF2 were observed in high glucose-challenged endothelial cells, which were significantly alleviated by Azilsartan. Lastly, the silencing of KLF2 abolished the protective effects of Azilsartan against the high glucose-induced expression of occludin and endothelial monolayer permeability in bEnd.3 brain endothelial cells. Based on these observations, we concluded that Azilsartan protected against hyperglycemia-induced hyperpermeability of BBB via the KLF2/occludin axis.
To demonstrate the relationship between of sphingosine-1-phosphate (S1P) expression and subarachnoid hemorrhage (SAH).The basilar arteries from a "double-hemorrhage" rabbit model of SAH were used to investigate the relation between S1P expression and SAH. Various symptoms, including blood clots, basilar artery cross-sectional area, and S1P phosphatase expression were measured at day 3, 5, 7, 9.The expression of S1P was enhanced in the cerebral vasospasm after subarachnoid hemorrhage in the rabbits. And S1P expression was consistent with the basilar artery cross-sectional area changes at day 3, 5, 7, 9.Sphingosine-1-phosphate expression in the cerebral arterial may be a new indicator in the development of cerebral vasospasm after subarachnoid hemorrhage and provide a new therapeutic method for SAH.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)